Ecg interpretation

Yemen – Sana’a Governorate .
2021

Copyright © 2021, 2022 by Dr. Eba’a Gamil .
This eBook also can be obtained by sending request to
Dr.eba’a’s official email at rudus.azeer@yahoo.com

ECG interpretation is a vital skill for all medical students and doctors as ECGs are
the most commonly used and widely available investigation used to diagnose
heart disease.
 The ability to interpret ECGs correctly means that the correct management can
be chosen for the patient and avoids otherwise preventable adverse events.
 Training in ECG interpretation often varies a lot between medical students so I
felt that it, for these reasons, was important to produce a guide.
 To produce a short guide to the interpretation of ECGs (electrocardiograms)
aimed at medical students enabling them to:
A. determine features of a normal ECG
B. assess rate and rhythm
C. Identify a clear myocardial infarction
 To reflect upon what I have learnt from producing this educational material.
Both when interpreting ECGs and presenting your findings, it is important to do so
in logical and structured manner to avoid misinterpretation. When presenting an
ECG, one should first say the patients name, age and the date the recording was
done.

This book contents mainly aimed to out reached the ultimate
educational propose and improves the ECG interpolation skills along
with avoiding some common misperceptions and mistakes during
interacting with ECG reports .
I intended to write this book in manner that all health care providers
will be able to interact and understand the general concept of this
book , The introductory chapters are of mandatory propose to
understand the further more details of each chapter , the headlines
are intended to be printed on each page along with the sub-headline
to simplified the coordination sequence of the topics .

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A hollow muscular organ, pyramidal in shape , somewhat larger than a
closed fist , consists of four chambers (right and left atria, right and left
ventricles)
Structure of the Heart
The heart is enclosed in a pericardial sac that is lined with the parietal
layers of a serous membrane. The visceral layer of the serous membrane
forms the pericardium.
Layers of the Heart Wall
Three layers of tissue form the heart wall:
 The outer layer of the heart wall is the epicardium .
 the middle layer is the myocardium .
 the inner layer is the endocardium .
Principles
Of Cardiac Anatomy .
Figure No ( 1 )

Chambers of the Heart The internal cavity of the
heart is divided into four chambers:
 The Two Atria:
are thin-walled chambers that receive blood from the veins.
 The Two Ventricles :
are thick-walled chambers that forcefully pump blood out of the heart.
• Differences in thickness of the heart chamber walls are due to variations in
the amount of myocardium present, which reflects the amount of force each
chamber is required to generate.
 The Right Atrium :
receives deoxygenated blood from systemic veins .
 The Left Atrium:
receives oxygenated blood from the pulmonary veins.
The Heart
Principles
Structure of the Heart .
Figure No ( 2 )

 Valves Of The Heart :
Aortic valve.
The aortic valve is located between the
left ventricle and the aorta.
Mitral valve.
This valve is located between the left
atrium and the left ventricle. It has only 2
leaflets.
Pulmonary valve.
The pulmonary valve is located between
the right ventricle and the pulmonary
artery.
Tricuspid valve.
This valve is located between the right
atrium and the right ventricle.
Principles
Figure No ( 3 ) Figure No ( 4 )
Figure No ( 5 )

Principles
Circulation of blood through the heart .
Figure No ( 6 )

PATHWAY OF BLOOD THROUGH THE HEART
Principles
Figure No ( 7 )

 Blood Supply To The Myocardium :
The major vessels of the coronary circulation are the
 Left Main Coronary : that divides into
 left anterior descending .
 circumflex branches .
 Right Main Coronary Artery :
The left and right coronary arteries originate at the base of the
aorta from openings called the coronary ostia located behind the
aortic valve leaflets
Principles

Nerves To The Heart Include:
Vagus nerve
Function: reducing the heart rate,
reducing the force of contraction of
the heart, vasoconstriction of the
coronary arteries
Parasympathetic Efferent
Fibers
Cardiac nerves from the lower
cervical and upper thoracic ganglia
Function: increasing heart rate,
increasing the force of contraction of
the myocardium
Sympathetic Efferent Fibers
Vagal cardiac nerves
Function: feedback on blood
pressure
Afferent Parasympathetic
Fibers
Afferents to upper thoracic and
lower cervical ganglia
Function: feedback on blood
pressure, pain sensation
Afferent Sympathetic Fibers
Cardiac plexus injury, referred pain
Clinical Relations
Principles
Innervation Of The Heart :
Table No. ( 1 )

Principles
Innervation Of The Heart :
Figure No ( 10 )

Principles
Figure No ( 11 )

Conducting System of the Heart :
The Cardiac Conduction System Is A Group Of Specialized Cardiac Muscle
Cells In The Walls Of The Heart That Send Signals To The Heart Muscle
Causing It To Contract
 Cardiac Muscle Tissue Has Intrinsic Ability To:
• Generate and conduct impulses
• Signal these cells to contract rhythmically
 Conducting system :
• A series of specialized cardiac muscle cells .
• Sino-atrial (SA) node sets the inherent rate of contraction .
Conduction System: [ SA AV Bundle Branch / Purkinje fibers.]
Anatomy
Of Conducting System .
Figure No ( 12 )

Anatomy
Conducting System of the Heart.
Figure No ( 13 )


 Called the pacemaker cell (P cell)
 Located at the junction of right atrium and superior vena cava,
upper part of the sulcus terminalis, under the epicardium .

 Located in the lower part of inter-atrial septum just above the
orifice of coronary sinus, under the endocardium
 Lower part related to membranous part of inter-ventricular septum

 Passes forward through right fibrous trigon to reach inferior border
of membranous part .
 Divides into right and left branches at upper border of muscular
part of inter-ventricular septum

 are located in the inner ventricular walls of the heart, just beneath
the endocardium in a space called the subendocardium.
Anatomy

Anatomy
Figure No ( 14 )

Electrocardiography.
 Introduction to ECG :
An electrocardiogram also termed an ECG or EKG (K means kardia for heart in
Greek) or a 12 lead ECG. is a simple non-invasive test that records the heart's
electrical activity and the electrical signals that control heart rhythm. The test
measures how electrical impulses move through the heart muscle as it contracts and
relaxes.
 Electrocardiogram translates the heart's electrical activity into line tracings on
paper. The spikes and dips in the line tracings are called waves.
 It provides information about the function of the intra-cardiac conducting tissue
of the heart and reflects the presence of cardiac disease through its electrical
properties.
 Understanding ECG helps to understand how the heart works.
 With each heartbeat, an electrical impulse starts from the superior part of the
heart to the bottom. The impulse prompts the heart to contract and pumps blood.
 It was invented by a Dutch physician, William Einthoven in 1902.
Figure No ( 15 )

Parts of an ECG
 Electrodes and Leads
 ECG Paper
 Electrodes and Leads :
To measure the heart's electrical activity accurately, proper electrode
placement is crucial.in a 12-lead ECG, there are 12 leads calculated
using 10 electrodes :
 Six of the leads are considered ―limb leads‖ because they are placed on the
arms and/or legs of the individual.
 The other six leads are considered ―precordial leads‖ because they are
placed on the torso (precordium) .
ECG Electrode Color Coding :
1. International Electro-technical Commission (IEC) Electrode
Color Coding :
A. Limb Electrodes :
 Right arm: red, marked with the letter R.
 Left arm: yellow, marked with the letter L.
 Left leg: green, marked with the letter F.
 Right leg: black, marked with the letter N for neutral.
B. Precordial Electrodes :
 V1: red, marked with letters C1.
 V2: yellow (C2).
 V3: green (C3).
 V4: brown (C4).
 V5: black (C5).
 V6: violet (C6).

Parts of an ECG .
2. American Heart Association (AHA) Electrode Color Coding :
A. Limb Electrodes:
 Right arm: white, marked with letters RA.
 Left arm: black, marked with letters LA.
 Left leg: red, marked with the letter LL.
 Right leg: green, marked with the letter RL
B. Precordial Electrodes :
 V1: red, marked with letters V1.
 V2: yellow (V2).
 V3: green (V3).
 V4: blue (V4).
 V5: orang (V5).
 V6: purple (V6).
Figure No ( 16 )

 Chest (Precordial) Electrodes And Placement :
» V1 - Fourth intercostal space on the right sternum .
» V2 - Fourth intercostal space at the left sternum .
» V3 - Midway between placement of V2 and V4 .
» V4 - Fifth intercostal space at the mid-clavicular line .
» V5 - Anterior axillary line on the same horizontal level as V4 .
» V6 - Mid-axillary line on the same horizontal level as V4 and V5 .
Mid-clavicular line
Anterior axillary line
Mid-axillary line
Sternum
Manubrium
Sternal angel
Costal cartilage
Costal margin
Parts of an ECG .
Figure No ( 17 )

 Limb (Extremity) Electrodes and Placement :
» RA (Right Arm) - Anywhere between the right shoulder and right elbow
» RL (Right Leg) - Anywhere below the right torso and above the right ankle
» LA(Left Arm) - Anywhere between the left shoulder and the left elbow
» LL (Left Leg) - Anywhere below the left torso and above the left ankle
Parts of an ECG .
Figure No ( 18 )

Figure No ( 19 )
Parts of an ECG .
 The areas of Electrodes represented on the ECG are summarized
below :
 V1, V2 = RV
 V3, V4 = septum
 V5, V6 = L side of the heart
 Lead I = L side of the heart
 Lead II = inferior territory
 Lead III = inferior territory
 aVF = inferior territory (remember ‘F’ for ‘feet’)
 aVL = L side of the heart
 aVR = R side of the heart
Figure No ( 20 )

 Additional notes on 12-lead ECG Placement:
o The limb leads can also be placed on the upper arms and thighs.
However, there should be uniformity in your placement. For instance, do
not attach an electrode on the right wrist and one on the left upper arm.
o For female patients, place leads V3-V6 under the left breast.
o Do not use nipples as reference points in placing electrodes for both men
and women as nipple locations vary from one person to another.
o Always protect the patient‘s privacy and dignity by draping with a sheet
to minimize exposure.
o Lead placement and patient positioning should be the same for
subsequent ECGs on any individual patient.
o During the procedure, record any clinical signs (e.g. chest pain) in the
notes or on the ECG tracing itself.
Parts of an ECG .

 ECG Paper :
The ECG paper is a strip of graph paper with large and small grids with
horizontal axis (Time in seconds) and vertical axis(amplitude in volts).
 Each 1 mm square (the smallest square) represents 0.04 second and each
large square (5 mm) represents 0.20 seconds.
 On the vertical axis, each large square represents 0.5mV and each small
block equals 0.1mV.
Parts of an ECG .
Figure No ( 21 )

 Medical Uses :
The overall goal of performing an ECG is to obtain information about the
electrical function of the heart.

Medical uses .

Normal
Components of the ECG .
 P wave
 QRS complex
 T wave
 ST segment
 PR interval
 QT interval
 U wave
Normal Components of the ECG Waveform :
Figure No ( 22 )

 The first wave P wave :
represents atrial depolarization (ventricular filling)
 Q wave :
representing septal depolarization
 R wave:
representing ventricular depolarization
 S wave:
representing depolarization of the Purkinje fibers
 QRS complex :
is ventricular depolarization
 T wave :
is ventricular repolarization
 ST segment :
is a flat line any change shows myocardial infarction
 P wave, QRS complex, and T wave show the 3 phase of cardiac cycle in
one heart beat.
 after the PQRST complex a U wave, seen in electrolyte
imbalance(potassium)
Normal Components of the ECG Waveform .
Normal Components of the ECG .

 P wave :
• Indicates atrial depolarization, or contraction of the atrium.
• Normal duration is not longer than 0.11 seconds (less than 3 small
squares)
• Amplitude (height) is no more than 3 mm
• No notching or peaking
 QRS complex
• Indicates ventricular depolarization, or contraction of the ventricles.
• Normally not longer than .10 seconds in duration
• Amplitude is not less than 5 mm in lead II or 9 mm in V3 and V4
• R waves are deflected positively and the Q and S waves are
negative
 T wave
• Indicates ventricular repolarization
• Not more that 5 mm in amplitude in standard leads and 10 mm in
precordial leads
• Rounded and asymmetrical

 ST segment
• Indicates early ventricular repolarization
• Normally not depressed more than 0.5 mm
• May be elevated slightly in some leads (no more than 1 mm)
 PR interval P wave + PR Segment.
• Indicates AV conduction time
• Duration time is 0.12 to 0.20 seconds
• Duration: 3-5 small squares/120-220 ms
Figure No ( 23 )

 QT interval
• Measured from the Q wave to the end of the T wave .
• Represents ventricular depolarization and repolarization (sodium influx
and potassium efflux)
• V3, V4 or lead II optimize the T-wave.
• QT usually less than half the R-R interval
• (0.32-0.40 seconds when rate is 65-90/minute)
• QT varies with rate. Correct for rate by dividing QT by the square root
of the RR interval.
o Normal corrected is < 0.46 for women and < 0.45 for men.
• Prolonged QT may be inherited or acquired (predisposes to long QT
syndrome and torsades de pointe)
• Inherited - defective sodium or potassium channels
• Acquired - drugs, electrolyte imbalance or MI
o Atleast, 50 drugs known to affect QT (including: quinidine,
amiodarone and dofetilide)
Figure No ( 24 )

Figure No ( 25 )

 U wave :
• The U wave is a small (0.5 mm) deflection immediately following
the T wave
• U wave is usually in the same direction as the T wave.
• U wave is best seen in leads V2 and V3.
Figure No ( 26 )

ST Segment
QRS
Complex
PR Interval
P Wave
Interval between
ventricular
depolarization
and
repolarization
Ventricular
depolarizatio
n
atrial
depolarization
and
delay at the AV
Node
(AV conduction
time)
Atrial
depolarization
Represents
Measure from
end of
QRS (J-point) to
beginning of T
wave
0.06 - 0.11
seconds
0.11 - 0.20
seconds
< 0.12
seconds
Duration
Q- First
negative
deflection
R- First
positive
deflection
S- Negative
deflection
after R wave
Measure start
of P wave
to start of QRS
< 2.5 mm
Height
In relation to
isoelectric line:
Depression/Neg
ative
indicates
ischemia
Elevation/Positiv
e
indicates injury
Prolonged
indicates a
conduction block
Shortened
indicates
accelerated
conduction or
junctional in
origin
Smooth
Shape
Positive in
Leads
I, II, aVF, V4
Negative in
aVR
Orientation
SUMMARY
Table No. ( 2 )

1. Patient Data ID :
A. Name
B. Age
C. Gender
D. Date
E. Time
F. Machine Diagnosis ( not all modalities )
2. Blood Pressure ( not all modalities )
3. Parameters Values :
A. Standard Calibration And Speed Of Paper
B. Heart Rate
C. Heart Rhythm
D. Electrical Heart Axis
4. 12 lead Waveform Data :
• I . II. III
• aVR, aVL, and aVF
• V1. V2 . V3 . V4 . V5 . V6
Interpretation Of
ECG .
ECG Paper Data Content

Patient Data ID :
• Patient‘s name, date of birth and hospital number .
• Location .
• This becomes important as in the ED or acute medical setting doctors are often
shown multiple ECGs. You need to know where your patient is in order to
ensure that they can be moved to a higher dependency area if appropriate.
• When was the ECG done?
• The time
• The number of the ECG if it is one of a series
• If you are concerned that there are dynamic changes in an ECG it is helpful to
ask for serial ECGs (usually three ECGs recorded 10 minutes apart) so they
can be compared. These should always be labelled 1, 2 and 3.
• Did the patient have chest pain at the time?
• Or other relevant clinical details. For example, if you are wanted an ECG to
look for changes of hyperkalemia, note the patient‘s potassium level on the
ECG.
ECG paper contents - Patient Data ID .
Interpretation Of ECG .

Figure No ( 27 )

Figure No ( 28)

A. Standard Calibration And Speed Of Paper
 Standardization: full standard is two large squares (1 mV, 10 mm)
and half standard is one large square (0.5mV, 5 mm)
 Paper speed: The standard paper speed is 25 mm (5 large
squares)/sec. This means that if the interval between two beats (R-R)
is 5 large squares, the HR is 60 beat/min.
Parameters Values :
ECG paper contents - Parameters Values - Standard
Calibration And Speed Of Paper .

A. The standard paper speed is 25mm/sec:
 1mm (small square) = 0.04 sec (40ms)
 5mm (large square) = 0.2 sec (200ms)
B. Heart Rate
Figure No ( 31 )
ECG paper contents - Parameters Values - Heart Rate .

B. Paper speed: 50mm/sec :
 1mm (small square) = 0.02 sec (20ms)
 5mm (large square) = 0.1 sec (100ms)
Figure No ( 32 )

 HR ( Heart Rate )
• Number of P‘s (atrial) R‘s (ventricular) per minute (6 second [30
squares] X 10 = minute rate).
• 1500/No of small squares (or)
• 300/No of large squares:
 The HR may be counted by simply dividing 300 by the number of
the large squares between two heart beats (R-R).
 If the interval between two beats is one large square, the HR is 300
beat/min, 2 squares →150, 3 squares →100, 4 squares → 75, 5
squares → 60, 6 squares → 50 beat/min.
Figure No ( 33 )

Estimate the rate :
 REGULAR rhythms :
 Rate = 300 / number of LARGE squares between consecutive R waves.
 Very FAST rhythms:
 Rate = 1500 / number of SMALL squares between consecutive R waves.
 SLOW or IRREGULAR rhythms:
 Rate = Number of R waves 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)

Estimate the rate :
 Example of 1500 (small squares) versus 300 (large square) method
Figure No ( 34 )

Estimate the rate :
 Now adding the R wave (10 second rhythm strip)
Note:
Calculate atrial and ventricular rates separately if they are different (e.g. complete
heart block) .
Atrial Rate By ( P ) Wave Ventricular Rate By ( R ) Wave
Figure No ( 35 )

 Interpretation (adults) :
 Normal: 60–100 beats/min
 Tachycardia: >100 beats/min
 Bradycardia: <60 beats/min
 Interpretation ( Children ) :
 Newborn: 110 – 150 bpm
 2 years: 85 – 125 bpm
 4 years: 75 – 115 bpm
 6 years+: 60 – 100 bpm

 Between R-R ( Must Compare Between 3-4 Cycles) (Big Square)
 Rhythm = Regular Or Irregular. Map P-P And R-R Intervals.
C. Heart Rhythm
Rhythm:
 The cardiac myocytes have an inherent automaticity and can generate
an electric impulse.
 The SA nodal cells have the fastest automaticity (pacemaker) and
hence control the heart rate and rhythm.
 There are 4 levels of conductions and potential pacemakers in the
heart from fastest to slowest: SA node → atria → AV node →
ventricles.
 If the rhythm is not sinus, we have to determine the origin of the
pacemaker and where the impulse is initiated.
ECG paper contents - Parameters Values - Heart Rhythm .
Figure No ( 36 )

A. SA nodal rhythm (normal sinus rhythm) :
 The sinus node is located at the SVC/right atrial junction. Sinus rhythm
requires ALL of the following 3 criteria:
1. One P wave preceding each QRS complex
2. All P waves should be uniform in shape
3. Normal P wave axis is in the left lower quadrant (0-90 degrees),
i.e. upright in both lead I and aVF (unless there is dextrocardia)
 The R-R interval in NSR does not have to be identical as it may change
with breathing (sinus arrhythmia)
 The sinus arrhythmia is easier to appreciate with slower heart rates.
 HR increases during inspiration due to:
• Increased venous return
• Increased sympathetic tone
 HR decreases during expiration due to:
• Decreased venous return
• Increased parasympathetic tone

B. Atrial Rhythm :
 Characterized by narrow QRS complexes preceded by P waves that do
not fulfill one or more of the normal sinus rhythm (NSR) criteria mentioned
earlier.
 If the P wave morphology changes, this may indicate a multifocal origin
which is called "wandering pacemaker―
C. AV Nodal Or Junctional Rhythm :
 Characterized by narrow QRS complexes that are not preceded by P
waves.
 An inverted P wave may be seen following the QRS due to retrograde
conduction
D. Ventricular rhythm :
 Characterized by wide QRS complexes that are not preceded by P
waves.
If the sinus node fails to initiate the impulse, an atrial focus will take over as
the pacemaker, which is usually slower than the NSR. When the atrial focus
fails, the AV node will take over. Subsequently, if the AV node fails, the
ventricular focus, which is the slowest, will take over as a pacemaker. Each
time the focus is downgraded, the heart rate becomes slower based on the
inherent automaticity of the pacemaker.

Figure No ( 37 )
Figure No ( 38 )
Figure No ( 39 )

Figure No ( 40 )
Figure No ( 41 )

ECG Rhythm Evaluation
The rhythm is best analyzed by looking at a rhythm strip. On a 12 lead ECG this is
usually a 10 second recording from Lead II.
 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)
• complete: atrial and ventricular activity is always independent.
• incomplete: intermittent capture.
6. Onset and termination
• Abrupt: suggests re-entrant process.
• Gradual: suggests increased automaticity.
7. Response to vagal 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.

Differential Diagnosis:
Narrow Complex (Supraventricular) Tachycardia .
1. ATRIAL – REGULAR
• Sinus tachycardia
• Atrial tachycardia
• Atrial flutter
• Inappropriate sinus tachycardia
• Sinus node re-entrant tachycardia
2. ATRIAL – IRREGULAR
• Atrial fibrillation
• Atrial flutter with variable block
• Multifocal atrial tachycardia
3. ATRIOVENTRICULAR
• Atrioventricular re-entry tachycardia (AVRT)
• AV nodal re-entry tachycardia (AVNRT)
• Automatic junctional tachycardia

Broad Complex Tachycardia (BCT)
1. REGULAR BCT
• Ventricular tachycardia
• Antidromic atrioventricular re-entry tachycardia (AVRT).
• Any regular supraventricular tachycardia with aberrant conduction
— e.g. due to bundle branch block, rate-related aberrancy.
2. IRREGULAR
• Ventricular fibrillation
• Polymorphic VT
• Torsades de Pointes
• AF with Wolff-Parkinson-White syndrome
• Any irregular supraventricular tachycardia with aberrant conduction
— e.g. due to bundle branch block, rate-related aberrancy.

2. IRREGULAR :
• Bradycardia
 P Waves Present :
I. Every P wave is followed by a QRS complex (= sinus node
dysfunction)
 Sinus bradycardia
 Sinus node exit block
 Sinus pause / arrest
II. Not every P wave is followed by a QRS complex (= AV node
dysfunction)
 AV block: 2nd degree, Mobitz I (Wenckebach)
 AV block: 2nd degree, Mobitz II (Hay)
 AV block: 2nd degree, ―fixed ratio blocks‖ (2:1, 3:1)
 AV block: 2nd degree, ―high grade AV block‖
 AV block: 3rd degree (complete heart block)
 P Waves Absent :
 Narrow complex: Junctional escape rhythm
 Broad complex: Ventricular escape rhythm
For escape rhythms to occur there must be a failure of sinus node impulse
generation or transmission by the AV node.

Axis Of ECG
• Determine both P wave and QRS axes. The net summation of
positive and negative deflection is used to determine the axis. Look
for two perpendicular leads (usually lead I and aVF) to determine in
which quadrant the axis is located.
• The axis of the ECG is the major direction of the overall electrical
activity of the heart.
 It can be :
 Normal (normal axis deviation)
 leftward (left axis deviation, or LAD)
 rightward (right axis deviation, or RAD)
 indeterminate (northwest axis).
D. Electrical Heart Axis
ECG paper contents - Parameters Values - Heart Axis .
Figure No ( 42 )

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)
 Negative:
As Explained In The Figure
Figure No ( 43 )
Figure No ( 45 )

 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).
Figure No ( 46 )

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).
Figure No ( 47 )

• 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
Figure No ( 48 )

Method 3 – The Isoelectric Lead
This method allows a more precise estimation of QRS axis, using the
axis diagram below.
 Key Principles :
 If the QRS is POSITIVE in any given lead, the axis points in roughly the
same direction as this lead.
 If the QRS is NEGATIVE in any given lead, the axis points in roughly the
opposite direction to this lead.
 If the QRS is ISOELECTRIC (equiphasic) in
any given lead (positive deflection = negative
deflection), the axis is at 90° to this lead
Figure No ( 49 )

Example 1
Answer – Lead I, II, aVF (Three Lead method )
• Lead I = POSITIVE
• Lead II = POSITIVE
• aVF = POSITIVE
• This puts the axis in the quadrant between 0° and +90° – i.e. normal
axis
Answer – Isoelectric Lead Method
• From the diagram above, we can see that aVL is located at -30°.
• The QRS axis must be ± 90° from lead aVL, either at +60° or -120°
• With leads I (0), II (+60) and aVF (+90) all being positive, we know that
the axis must lie somewhere between 0 and +90°.
• This puts the QRS axis at +60° – i.e. normal axis
Figure No ( 50 )

Answer – Quadrant Method
 Lead I = NEGATIVE
 Lead II = Equiphasic
 Lead aVF = POSITIVE
 This puts the axis in the quadrant, between +90° and +180°, i.e. RAD.
 Lead II (+60°) is the isoelectric lead.
 The QRS axis must be ± 90° from lead II, at either +150° or -30°.
 The more rightward-facing leads III (+120°) and aVF (+90°) are positive,
while aVL (-30°) is negative.
 This puts the QRS axis at +150°
Example 2
Figure No ( 51 )

• Lead I = POSITIVE
• Lead II = Equiphasic
• Lead aVF = NEGATIVE
• This puts the axis in the quadrant between 0° and -90°, i.e. normal or LAD.
• Lead II is neither positive nor negative (isoelectric), indicating physiological
LAD
• Lead II (+60°) is isoelectric.
• The QRS axis must be ± 90° from lead II, at either +150° or -30°.
• The more leftward-facing leads I (0°) and aVL (-30°) are positive, while
lead III (+120°) is negative.
• This confirms that the axis is at -30°.
Example 3
Figure No ( 52 )

• Lead I = NEGATIVE
• Lead II = NEGATIVE
• Lead aVF = NEGATIVE
• This puts the axis in the upper right quadrant, between -90° and 180°,
i.e. extreme axis deviation.
• The most isoelectric lead is aVL (-30°).
• The QRS axis must be at ± 90° from aVL at either +60° or -120°.
• Lead aVR (-150°) is positive, with lead II (+60°) negative.
• This puts the axis at -120°.
Example 4
Figure No ( 53 )

Causes Of Axis Deviation
A. 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

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

The ECG is one of the most useful investigations in medicine. Electrodes
attached to the chest and/or limbs record small voltage changes as
potential difference, which is transposed into a visual tracing
 Basic landmarks
ECG Lead Positioning
ECG Lead Positioning.
Figure No ( 54 )

A. 3- Electrode System :
 Uses 3 electrodes (RA, LA and LL)
 Monitor displays the bipolar leads (I, II and III)
 To get best results – Place electrodes on the chest wall equidistant from
the heart (rather than the specific limbs)
Electrode Systems.
Figure No ( 55 )

B. 5- Electrode System :
 Uses 5 electrodes (RA, RL, LA, LL and Chest)
 Monitor displays the bipolar leads (I, II and III)
 AND a single unipolar lead (depending on position of the brown chest
lead (positions V1–6))
Electrode Systems.
Figure No ( 56 )

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

12-lead Precordial lead placement : as mentioned previously
 V1: 4th intercostal space (ICS), RIGHT margin of the sternum
 V2: 4th ICS along the LEFT margin of the sternum
 V4: 5th ICS, mid-clavicular line
 V3: midway between V2 and V4
 V5: 5th ICS, anterior axillary line (same level as V4)
 V6: 5th ICS, mid-axillary line (same level as V4)
Electrode Systems.
Figure No ( 59 )

E. Additional Lead placements
1. Right sided ECG electrode placement ( Dextrocardia ) :
There are several approaches to recording a right-sided ECG:
 A complete set of right-sided leads is obtained by placing leads V1-6 in
a mirror-image position on the right side of the chest
 It can be simpler to leave V1 and V2 in their usual positions and just
transfer leads V3-6 to the right side of the chest (i.e. V3R to V6R)
 The most useful lead is V4R, which is obtained by placing the V4
electrode in the 5th right intercostal space in the mid-clavicular line.
 ST elevation in V4R has a sensitivity of 88%, specificity of 78% and
diagnostic accuracy of 83% in the diagnosis of RV MI.
Electrode Systems.

Electrode Systems.
Figure No ( 60 )

2. Posterior leads :
Leads V7-9 are placed on the posterior chest wall in the following
positions:
 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.
Electrode Systems.
Figure No ( 61 )

ECG Artifact:
Electrocardiograph (ECG) artifacts are defined as ECG abnormalities, which are a
measurement of cardiac potentials on the body surface and are not related to
electrical activity of the heart.
 As a result of artifacts, normal components of the ECG can be distorted.
 It is very important to recognize these artifacts, otherwise they can lead to
unnecessary testing and therapeutic interventions. In this chapter, we will present
the common causes and ways to characterize ECG artifacts.
Causes of ECG artifact :
ECG artifacts can be generated by internal and external causes
A. Internal
These are physiological causes that could be due to:
 Patient's motion: Does not allow electronic filtration (large swings, usually by
epidermal stretching).
• Tremors and shivering cause motion artifacts.
• Simple movements such as brushing and combing the hair can produce ECG
disturbances during ambulatory ECG monitoring.
 Muscular activity: Allows electronic filtration (small spikes)
ECG Artifact .

B. External
These are non-physiological causes associated with other electrical devices
attached to or implanted (e.g. deep brain stimulator) in the body and includes the
following :
 Electromagnetic interference:
• Power line electrical disturbances/ Light fixtures
• Electro-cautery
• Electrical devices in the room
• Radiofrequency based commercial (e.g. mobile phones) products
 Cable and electrode malfunction:
• Insufficient electrode gel
• Misplaced leads
• Inappropriate filter settings
• Broken wires
• Loose connections
• Accumulation of static energy
 Medical equipment's:
In operation theatres and intensive care unit various equipment's can affect ECG
monitoring system (e.g. electrodes, leads, amplifier, filters)
ECG Artifact .

Type of equipment Artifact
IVAC intravenous infusion controller
Atrial or ventricular extrasystoles,
pseudowaves (QRS)
Cardiopulmonary bypass pump Uninterpretable tracing, non-specific
Pressure-controlled irrigation pump Atrial flutter
COBE Prisma System for continuous
venovenous hemofiltration
Atrial flutter
Flexible bronchoscope Atrial fibrillation
Deep brain stimulator Uninterpretable tracing
Straight shot microdebrider (nasal
endoscopy)
Ventricular tachycardia
Intra-aortic balloon pump
Pseudowaves (P), premature atrial
contraction
Somatosensory evoked potential
monitoring units
Supraventricular tachycardia
High-frequency oscillatory ventilation
Atrial flutter, atrial fibrillation, ventricular
tachycardia
Intraoperative high-field MRI
Ventricular tachycardia, ventricular
fibrillation, non-specific
Transcutaneous electrical nerve stimulator
Spikes, runaway pacemaker, ventricular
Peripheral nerve stimulator Spikes, loss of pacemaker spikes
Medical equipment related EKG artifacts
ECG Artifact .
Table No. ( 3 - 1)

Cardiopulmonary bypass pump Uninterpretable tracing, non-specific
COBE Prisma System for continuous
venovenous hemofiltration
Atrial flutter
tachycardia
contraction
pseudowaves (QRS)
monitoring units
Straight shot microdebrider (nasal
endoscopy)
Transcutaneous electrical nerve stimulator
Spikes, runaway pacemaker, ventricular
ECG Artifact .
Table No. ( 3 – 2 )

Straight shot micro-debrider (nasal
endoscopy)
monitoring units
pseudowaves (QRS)
contraction
tachycardia
ECG Artifact .
Table No. ( 3 – 3 )

Differentiating an Artifact from Ventricular tachycardia :
Sometimes, ECG changes may mimic specific arrhythmias like ventricular
tachycardia and atrial flutter or fibrillation. It is important to differentiate these, as
misdiagnosis can lead to inadvertent use of medications and procedures in such a
patient .
Characteristics that can help in differentiate an artifact from ventricular
tachycardia include :
 Absence of hemodynamic deterioration during the event.
 Normal QRS complexes within the artifact.
 An unstable baseline on the ECG before the event, after the event, or both.
 Association with bodily movement.
Presence of any of these signs is suggestive of pseudo-ventricular tachycardia:
o "Sinus" sign: One of the frontal leads (I, II and III) may present with sinus
rhythm showing normal P, QRS, and T waves. The reason is that one of the
upper limbs may be free off tremor.
o "Spike" sign: Presence of regular or irregular tiny spikes among wide-QRS
complexes.
o "Notch" sign: Notches superimposed in the wide-QRS-like complex
artifact, coinciding with the cycle length when sinus rhythm was recorded.
ECG Artifact .

Electrode misplacement :
Electrode misplacements are a common artifact that can mimic life-threatening
arrhythmias. Early identification and replacement of electrodes can help in
avoiding unnecessary therapies. An algorithm has been described previously ,
which may help in recognizing these artifacts .
ECG findings Explanation
R
R wave is positive in lead aVR
(P wave also positive)
Reversal of left arm and right
arm electrodes
E
Extreme axis deviation : QRS
axis between -90 and +180
arm electrodes
V
Very low (<0.1 mV) voltage in
an isolated limb lead
Reversal of right leg and left
arm or right arm electrodes
E
Exchanged amplitude of P
waves (P wave in lead I >
lead II)
Reversal of left arm and left
leg electrodes
R
R wave abnormal progression
in precordial lead (pre-
dominal R in V1 and S in V6)
Reversal of precordial
electrodes (V1 through V6)
S
Suspect dextrocardia
(negative P waves in lead I)
arm electrodes
E
Eliminate noise and
interference (artifact
mimicking tachycardias or ST-
T changes
ECG Artifact .
Table No. ( 4 )

Other Common Artifacts :
 Electrodes on the torso: Placement of the electrodes on torso may lead to a
change in vectors and produce pseudo-Q waves and pseudo-ST segment
elevation, mimicking myocardial infarction.
 Telemetry interference: Superimposition of telemetry electrodes over the ECG
electrodes or vice versa may cause ST segment deviation due to
electromagnetic interference.
 Loose wire: Straight line may resemble systole and a wavy line may resemble
fibrillation. However, it will be limited to one or two leads only.
 Tall T wave: A tall T wave may be mistaken for an R wave and the digital
heart rate would be higher than the actual pulse rate.
 Lead placement: Obscuring of P waves may resemble a heart block.
 Motion artifact: Chest percussions or physiotherapy may mimic ventricular
fibrillation.
ECG Artifact .

Correction OF ECG Artifact :
• Attention to basic principles such as proper electrodes placement and lead
connections (as mentioned above) is required during ECG monitoring.
• Well designed and maintained ECG measurement devices can withstand routine
internal or external electrical and motion-related disturbances. However, it is not
always possible to eliminate artifacts completely.
• It is essential that physicians keep high vigilance and interpret EKG keeping
artifacts in their differential diagnosis list.
A slight ECG artifact is not uncommon. However, you can reduce further
interference through the following steps:
 Switch off non-essential electrical devices and equipment within the vicinity if
possible.
 Check for cable loops and avoid running cables adjacent to metallic objects as
they can affect the signal.
 Inspect wires and cables for cracks or breaks. Replace as needed.
 If possible, use surge suppressors with the power supply.
 Ensure that filters and preamplifiers are appropriately adjusted.
 Ensure securely connection between patient cable and the ECG device. Double
check for gaps between connectors
ECG Artifact .

Examples of Artifacts :
Movement artifacts
Increasing movement artifacts in a Parkinson patient.
ECG Artifact .
Figure No ( 62 )
Figure No ( 63 )

Cardio-version from atrial fibrillation to sinus rhythm, with clear baseline drift.
Baseline drift. The amplifier in the ECG machine has to re-find the 'mean'.
This often occurs right after lead connection and after electric cardio-version.
ECG Artifact .
Figure No ( 64 )
Figure No ( 65 )

Another example of an artifact caused by an electrical appliance. The
patients rhythm is regular. This strip shows 10 QRS complexes.
Electrical interference from a nearby electrical appliance. A typical example
is a 100 Hz background distortion from fluorescent lights. Not to be confused
with atrial fibrillation.
ECG Artifact .
Figure No ( 66 )
Figure No ( 67 )

A. Waves:
1. P Wave
• 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-Atrium Depolarization
Duration: < 0.12 s (<120ms or 3 small squares) less than 2.5 mm high
Normal Vs Abnormal
ECG Components .
Normal Vs Abnormal ECG
Components .
Figure No ( 68 )

 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
Waves : P
Normal Vs Abnormal ECG Components . Normal
Figure No ( 69 )

 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
 Normal P-wave Morphology – Lead V1
The P wave is typically biphasic in V1, with similar sizes of the positive
and negative deflections
Waves : P
Figure No ( 70 )

 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 – Lead V1
Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm
deep) in V1 of the terminal negative portion of the P wave.
Waves : P - Abnormalities of the P wave .
Normal Vs Abnormal ECG Components . Abnormal
Figure No ( 71 )

 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).
Lead II Lead V1
Figure No ( 74 )

 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‘)
Lead II Lead V1
Figure No ( 75 )
Figure No ( 76 )

 Biatrial Enlargement
Biatrial enlargement is diagnosed when criteria for both right and left atrial
enlargement are present on the same ECG. The spectrum of P-wave
changes in leads II and V1 with right, left and bi-atrial enlargement is
summarised in the following diagram:
Figure No ( 77 )

 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.
1. 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.
2. 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).
Figure No ( 78 )
Figure No ( 79 )

3. 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):
4. 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:
Figure No ( 80 )
Figure No ( 81 )
Figure No ( 82 )

A Q wave is any negative deflection that precedes an R wave
 The Q wave represents the normal left-to-right depolarisation of the inter-
ventricular 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)
A. Waves:
2. Q Wave
Waves : Q
Figure No ( 83 )

Pathological Q Waves :
Q waves are considered pathological if:
 > 40 ms (1 mm) wide
 > 2 mm deep
 > 25% of depth of QRS complex
 Seen in leads V1-3
 Pathological Q waves usually indicate current or prior myocardial
infarction.
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.
 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
Waves : Q - Abnormalities of the Q wave .

Inferior Q waves (II, III, aVF) with ST elevation due to acute MI
Inferior Q waves (II, III, aVF) with T-wave inversion due to previous MI
Example 1
Example 2
Figure No ( 84 )
Figure No ( 85 )

Lateral Q waves (I, aVL) with ST elevation due to acute MI
Anterior Q waves (V1-4) with ST elevation due to acute MI
Example 3
Example 4
Figure No ( 87 )
Figure No ( 86 )

Anterior Q waves (V1-4) with T-wave inversion due to recent MI
Example 5
Figure No ( 88 )

 The U wave is a small (0.5 mm) deflection immediately following the T
wave .
 It comes after the T wave of ventricular repolarization and may not always
be observed as a result of its small size.
 U wave is usually in the same direction as the T wave.
 U wave is best seen in leads V2 and V3 .
 The normal U wave is best seen at rest in the precordial leads and is more
commonly seen during sinus bradycardia.
A. Waves:
3. U Wave
Waves : U
Figure No ( 89 )
Figure No ( 90 )

 Source of the U wave :
The source of the U wave is unknown. Three common theories regarding its
origin are:
1. Delayed repolarisation of Purkinje fibres
2. Prolonged repolarisation of mid-myocardial ‗M-cells‘
3. After-potentials resulting from mechanical forces in the ventricular wall
 Features of Normal U waves :
 The U wave normally goes in the same direction as the T wave
 U -wave size is inversely proportional to heart rate: the U wave grows
bigger as the heart rate slows down
 U waves generally become visible when the heart rate falls below 65
bpm
 The voltage of the U wave is normally < 25% of the T-wave voltage:
disproportionally large U waves are abnormal
 Maximum normal amplitude of the U wave is 1-2 mm
Waves : U
Figure No ( 91 )

 Abnormalities of the U wave :
A. Prominent U waves
B. Inverted U waves
Prominent U waves Inverted U waves
Normal physiological U waves
Waves : U - Abnormalities of the U wave .
Figure No ( 92 )

A. Prominent U waves
U waves are described as prominent if they are >1-2mm or 25% of the
height of the T wave.
 Prominent U waves may be present with:
 Hypocalcaemia
 Hypomagnesaemia
 Hypothermia
 Raised intracranial pressure
 Left ventricular hypertrophy
 Hypertrophic cardiomyopathy
 Drugs associated with prominent U waves:
• Digoxin
• Phenothiazines (thioridazine)
• Class Ia antiarrhythmics (quinidine, procainamide)
• Class III antiarrhythmics (sotalol, amiodarone)
**Note :
many of the conditions causing prominent U waves will also cause a long
QT.
Figure No ( 95 )

Prominent U waves due to sinus bradycardia
U waves associated with hypokalemia
A. Prominent U waves ( Examples )
Example 1
Example 2
Figure No ( 96 )
Figure No ( 97 )

U waves associated with left ventricular hypertrophy
U waves associated with digoxin use
Example 3
Example 4
Figure No ( 98 )
Figure No ( 99 )

U waves associated with quinidine use
Example 5
Figure No ( 100 )

B. 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
 Common causes of inverted U waves :
 Coronary artery disease
 Hypertension
 Valvular heart disease
 Congenital heart disease
 Cardiomyopathy
 Hyperthyroidism

Unstable Angina
Inverted U Waves In Prinzmetal Angina
B. Inverted U waves ( Examples )
Example 1
Example 2
Figure No ( 101 )
Figure No ( 102 )

A. Waves:
4. R Wave
 The R wave is the first upward deflection after the P wave.
 The R wave represents early ventricular depolarisation .
 R-wave amplitude in V6 + S-wave amplitude in V1 should be <35 mm.
 R-wave amplitude in aVL should be ≤ 12 mm. R-wave amplitude in
leads I, II and III should all be ≤ 20 mm.
 If R-wave in V1 is larger than S-wave in V1, the R-wave should be <5
mm
Waves : R
Figure No ( 103 )

 Abnormalities of the R wave
There are three key R wave abnormalities:
A. Dominant R wave in V1
B. Dominant R wave in aVR
C. Poor R wave progression
Waves : R - Abnormalities of the R wave .

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

Dominant R wave in V1 : ( Examples )
 Normal paediatric ECG (2 yr old)
 Right Bundle Branch Block
 Right Ventricular Hypertrophy (RVH)
Figure No ( 104 )
Figure No ( 105 )
Figure No ( 106 )

 Right Bundle Branch Block MoRRoW
 Posterior MI
 Wolff-Parkinson-White (WPW) Type A
Figure No ( 107 )
Figure No ( 108 )
Figure No ( 109 )

 Leads V1 and V3 reversed
**Note :
biphasic P wave (typically seen in only in V1) in lead ―V3‖
 Muscular dystrophy
Figure No ( 110 )
Figure No ( 111 )

B. 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)
 Dominant R wave in aVR : ( Examples )
 Poisoning With Sodium-channel Blocking Drugs :
• Causes a characteristic dominant terminal R wave in aVR
• Poisoning with sodium-channel blocking agents is suggested if:
 R wave height > 3mm
 R/S ratio > 0.7
Figure No ( 112 )

 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)
Figure No ( 113 )

 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
Figure No ( 114 )

 Ventricular Tachycardia
Figure No ( 115 )

C. 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
***Note
that absent R wave progression is characteristically seen in dextrocardia (see
previous ECGs).
Figure No ( 116 )

 J Point In :
a normal .
b – c J point elevation.
d J point depression.
e with J wave (Osborn wave)
A. Waves:
5. Osborn (J Wave ) :
The Osborn wave (J wave) is a positive deflection at the J point (negative in
aVR and V1). It is usually most prominent in the precordial leads.
Waves : Osborn (J Wave ) .
Figure No ( 117 )

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

Osborn Wave ECG : ( examples )
Example 1
 Subtle J waves in mild hypothermia [Temp: 32.5°C (90.5°F)]
 The height of the J wave is roughly proportional to the degree of
hypothermia
Example 2
 J waves in moderate hypothermia. [Temp: 30°C (86°F)
Osborn (J) Wave .
Figure No ( 118 )
Figure No ( 119 )

Example 3
 J waves in moderate hypothermia. [Temp: 28°C (82.4°F)]
Example 4
 Marked J waves in severe hypothermia [Temp: 26°C (78.8°F)]
Osborn (J) Wave .
Figure No ( 120 )
Figure No ( 121 )

A. Waves:
6. T Wave
The T wave is the positive deflection after each QRS complex.It represents
ventricular repolarisation.
 Characteristics of the normal T wave :
Upright in all leads except aVR and V1
Amplitude < 5mm in limb leads, < 10mm in precordial leads (10mm in
men, 8mm in women)
Duration 0.10 to 0.25 seconds
 T wave abnormalities :
1. Peaked T waves
2. Hyperacute T waves
3. Inverted T waves
4. Biphasic T waves
5. ―Camel Hump‖ T waves
6. Flattened T waves
Waves : T .
Figure No ( 122 )

1. Peaked T waves
Tall, narrow, symmetrically peaked T-waves are characteristically seen
in hyperkalemia.
2. Hyper-acute T waves
Broad, asymmetrically peaked or ―hyper-acute‖ T-waves are seen in the
early stages of ST-elevation MI (STEMI) and often precede the
appearance of ST elevation and Q waves.
They are also seen with Prinzmetal angina.
T Wave Abnormalities :
Waves : T - Abnormalities of the T Wave .
Figure No ( 123 )
Figure No ( 124 )

3. Inverted T 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).
Inverted T waves are seen in the following conditions:
 Normal finding in children
 Persistent juvenile T wave pattern
 Myocardial ischaemia and infarction
 Bundle branch block
 Ventricular hypertrophy (―strain‖ patterns)
 Pulmonary embolism
 Hypertrophic cardiomyopathy
 Raised intracranial pressure
**Note :
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).
Figure No ( 125 )

 Pediatric T Waves :
Inverted T-waves in the right precordial leads (V1-3) are a normal finding
in children, representing the dominance of right ventricular forces.
Pediatric T Waves Normal T Waves 2 Year Old Boy
 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.
Inverted T Waves Conditions :
Figure No ( 126 )
Figure No ( 127 )

 Myocardial Ischemia and Infarction :
T-wave inversions due to myocardial ischemia or infarction occur in
contiguous leads based on the anatomical location of the area of ischemia
/infarction:
 Inferior = II, III, aVF
 Lateral = I, aVL, V5-6
 Anterior = V2-6
Inferior T Wave Inversion Due To Acute Ischaemia
**NOTE :
• Dynamic T-wave inversions are seen with acute myocardial ischemia.
• Fixed T-wave inversions are seen following infarction, usually in
association with pathological Q waves.
Figure No ( 128 )

Inferior T Wave Inversion With Q Waves – Prior Myocardial Infarction
T Wave Inversion In The Lateral Leads Due To Acute Ischemia
Anterior T Wave Inversion With Q Waves Due To Recent MI
Figure No ( 129 )
Figure No ( 130 )
Figure No ( 131 )

 Bundle Branch Block :
A. Left Bundle Branch Block (with T-wave inversion )
Left bundle branch block produces T-wave inversion in the lateral leads I,
aVL and V5-6.
B. Right Bundle Branch Block (with T-wave inversion )
Right bundle branch block produces T-wave inversion in the right precordial
leads V1-3.
Figure No ( 132 )
Figure No ( 133 )

 Ventricular Hypertrophy :
A. Left Ventricular Hypertrophy (With T-wave Inversion )
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.
B. Right Ventricular Hypertrophy (With T-wave Inversion )
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).
Figure No ( 134 )
Figure No ( 135 )

 Pulmonary Embolism :
T-wave inversions in the right precordial (V1-3) and inferior (II, III, aVF)
leads.
 Hypertrophic Cardiomyopathy (HCM) :
Hypertrophic Cardiomyopathy is associated with deep T wave inversions in
all the precordial leads.
Figure No ( 136 )
Figure No ( 137 )

 Raised intracranial pressure (ICP) :
Events causing a sudden rise in intracranial pressure (e.g. subarachnoid
hemorrhage) produce widespread deep T-wave inversions with a bizarre
morphology.
Figure No ( 138 )

4. Biphasic T waves
There are two main causes of biphasic T waves:
 Myocardial ischemia
T waves go UP then DOWN
 Hypokalemia
The two waves go in opposite directions:
T waves go DOWN then UP
Figure No ( 139 )
Figure No ( 140 )
Figure No ( 141 )

5. ‘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 Hypokalemia .
 Hidden P waves :
Embedded In The T Wave, As Seen In Sinus Tachycardia And Various
Types Of Heart Block .
Figure No ( 142 )
Figure No ( 143 )

6. Flattened T waves
Flattened T waves are a non-specific finding, but may represent :
 Ischemia (If Dynamic Or In Contiguous Leads) Or
 Electrolyte Abnormality, E.G. Hypokalemia (If Generalized).
 Ischemia :
Dynamic T-wave flattening due to anterior ischemia .
T waves return to normal once the ischemia resolves .
Dynamic T wave flattening due to
anterior ischemia
T waves return to normal as
ischemia resolves

 Hypokalemia :
Note generalized T-wave flattening in hypokalemia associated with
prominent U waves in the anterior leads (V2 and V3).
Figure No ( 146 )

A. Waves:
7. Epsilon Wave
• The epsilon wave is a small positive deflection (―blip‖ or ―wiggle‖) buried
in the end of the QRS complex. Epsilon waves are caused by
postexcitation of the myocytes in the right ventricle.
Waves : Epsilon Wave - Abnormalities of the Epsilon
Wave .

Epsilon waves are the most characteristic finding in :
 Arrhythmo-genic Right Ventricular Dysplasia (ARVD/C).
Here myocytes are replaced with 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 and causes the little wiggles seen during the ST segment
of the ECG.
The ECG changes in Arrhythmo-genic Right Ventricular Dysplasia include:
• Epsilon wave (most specific finding, seen in 30% of patients)
• T wave inversions in V1-3 (85% of patients)
• Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)
• Localized QRS widening of 110ms in V1-3
• Paroxysmal episodes of ventricular tachycardia with a LBBB
morphology.
Wave .
Figure No ( 149 )

Example 1 12-lead ECG is a typical example of ARVD.
Arrhythmo-genic Right Ventricular Dysplasia (ARVD) : Examples
Example 2 VT with LBBB morphology due to ARVD
Wave .
Figure No ( 150 )
Figure No ( 151 )

A. Waves:
8. Delta Wave
The Delta wave is a slurred upstroke in the QRS complex often associated
with a short PR interval. It is most commonly associated with pre-excitation
syndrome such as Wolff-Parkinson-White syndrome ( WPW ) .
The characteristic ECG findings in the Wolff-Parkinson-White
syndrome are:
 Short PR interval (< 120ms)
 Broad QRS (> 100ms)
 A slurred upstroke to the QRS complex (the delta wave)
Waves : Delta Wave - Abnormalities of the Delta
Wave .
Figure No ( 152 )

B. Segments :
1. ST Segment
 The ST segment is the flat, isoelectric section of the ECG between
the end of the S wave (the J point) and the beginning of the T wave.
 The ST Segment represents the interval between ventricular
depolarization and repolarization.
 The most important cause of ST segment abnormality (elevation or
depression) is myocardial ischemia or infarction.
S e gmen ts : ST Segment .
Figure No ( 153 )

 Causes of ST Segment Elevation :
 Acute myocardial infarction
 Coronary vasospasm (Printzmetal‖s angina)
 Pericarditis
 Benign early repolarization
 Left bundle branch block
 Left ventricular hypertrophy
 Ventricular aneurysm
 Brugada syndrome
 Ventricular paced rhythm
 Raised intracranial pressure
 Takotsubo Cardiomyopathy
S e gmen ts : ST Segment - Abnormalities of the ST
Segment - ST Elevation .

 Acute ST Elevation Myocardial Infarction (STEMI) :
ST segment elevation and Q-wave formation in contiguous leads
• Septal (V1-2)
• Anterior (V3-4)
• Lateral (I + aVL, V5-6)
• Inferior (II, III, aVF)
• Right ventricular (V1, V4R)
• Posterior (V7-9)
Figure No ( 154 )

 Pericarditis :
Acute Pericarditis causes widespread concave (‗saddleback‘) ST segment
elevation with PR segment depression in multiple leads, typically
involving I, II, III, aVF, aVL, and V2-6.
 Concave ‗saddleback‘ ST elevation in leads I, II, III, aVF, V5-6 with
depressed PR segments.
 There is reciprocal ST depression and PR elevation in leads aVR and
V1.
 Spodick‖s sign was first described by David H. Spodick in 1974 as a
downward sloping TP segment with specificity for acute pericarditis
Figure No ( 155 )

 Benign Early Repolarization :
Benign Early Repolarization (BER) causes mild ST elevation with tall T-
waves mainly in the precordial leads. BER is a normal variant commonly seen
in young, healthy patients. There is often notching of the J-point — the ‗fish-
hook‘ pattern.
The ST changes may be more prominent at slower heart rates and disappear in
the presence of tachycardia.
There is slight concave ST elevation in the precordial and inferior
leads with notching of the J-point (the ―fish-hook‖ pattern)
Figure No ( 156 )

 Left Bundle Branch Block (LBBB) :
In Left bundle branch block (LBBB), the ST segments and T waves show
‗appropriate discordance‘ — i.e. they are directed opposite to the main
vector of the QRS complex.
This produces ST elevation and upright T waves in leads with a negative
QRS complex (dominant S wave), while producing ST depression and T
wave inversion in leads with a positive QRS complex (dominant R wave).
Note :
 the ST elevation in leads with deep S waves — most apparent in V1-3.
 Also note the ST depression in leads with tall R waves — most apparent
in I and aVL
Figure No ( 157 )

 Left Ventricular Hypertrophy (LVH) :
Left Ventricular Hypertrophy (LVH) causes a similar pattern of repolarization
abnormalities as LBBB, with ST elevation in the leads with deep S-waves
(usually V1-3) and ST depression/T-wave inversion in the leads with tall R
waves (I, aVL, V5-6).
• Deep S waves with ST elevation in V1-3
• ST depression and T-wave inversion in the lateral leads V5-6
• Note in this this case there is also right axis deviation, which is
unusual for LVH and may be due to associated left posterior fascicular
block.
Figure No ( 158 )

 Ventricular Aneurysm :
This is an ECG pattern of Ventricular Aneurysm – residual ST elevation and
deep Q waves seen in patients with previous myocardial infarction. It is
associated with extensive myocardial damage and paradoxical movement of
the left ventricular wall during systole.
• There is ST elevation with deep Q waves and inverted T waves in V1-3.
• This pattern suggests the presence of a left ventricular aneurysm due to a
prior anteroseptal MI.
Figure No ( 159 )

 Brugada Syndrome :
Brugada Syndrome is an inherited channelo-pathy (a disease of myocardial
sodium channels) that leads to paroxysmal ventricular arrhythmias and
sudden cardiac death in young patients.
The tell-tale sign on the resting ECG is the ‗Brugada sign‘ — ST elevation
and partial RBBB in V1-2 with a ‗coved‘ morphology.

There is ST elevation and partial RBBB in V1-2 with a coved morphology - the
‚Brugada sign‛.
Figure No ( 162 )

 Brugada Syndrome :
 Type 1 :
• Coved ST segment elevation >2mm in >1 of V1-V3 followed by a
negative T wave.
• This is the only ECG abnormality that is potentially diagnostic.
• It is often referred to as Brugada sign.
This ECG abnormality must be associated with one of the following clinical criteria
to make the diagnosis:
o Documented ventricular fibrillation (VF) or polymorphic ventricular
tachycardia (VT).
o Family history of sudden cardiac death at <45 years old .
o Coved-type ECGs in family members.
o Inducibility of VT with programmed electrical stimulation .
o Syncope.
o Nocturnal agonal respiration
Figure No ( 163 )

 Type2:
• Brugada Type 2 has >2mm of saddleback shaped ST elevation.
Figure No ( 164 )

 Type3:
• Brugada type 3: can be the morphology of either type 1 or type
2, but with <2mm of ST segment elevation.
Figure No ( 165 )

 Ventricular Paced Rhythm :
Ventricular pacing (with a pacing wire in the right ventricle) causes ST
segment abnormalities identical to that seen in LBBB. There is appropriate
discordance, with the ST segment and T wave directed opposite to the main
vector of the QRS complex.
Figure No ( 166 )

 Raised Intracranial Pressure :
Raised Intracranial Pressure (ICP) (e.g. due to intracranial haemorrhage,
traumatic brain injury) may cause ST elevation or depression that simulates
myocardial ischaemia or pericarditis.
More commonly, raised ICP is associated with widespread, deep T-wave
inversions (‗cerebral T waves‗).
Widespread ST elevation with concave (pericarditis-like) morphology in a patient with
severe traumatic brain injury.
Figure No ( 167 )

 Takotsubo Cardiomyopathy :
Takotsubo Cardiomyopathy: A STEMI mimic producing ischaemic chest
pain, ECG changes +/- elevated cardiac enzymes with characteristic regional
wall motion abnormalities on echocardiography.
• Typically occurs in the context of severe emotional distress (‗broken
heart syndrome‗).
• Commonly associated with new ECG changes (ST elevation or T
wave inversion) or moderate troponin rise.
Figure No ( 168 )

 Less Common Causes of ST segment Elevation :
o Pulmonary embolism and acute cor pulmonale (usually in lead III)
o Acute aortic dissection (classically causes inferior STEMI due to
RCA dissection)
o Hyperkalaemia
o Sodium-channel blocking drugs (secondary to QRS widening)
o J-waves (hypothermia, hypercalcaemia)
o Following electrical cardioversion
o Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease
Transient ST elevation after DC cardioversion from VF .
J waves in hypothermia simulating ST elevation
Figure No ( 169 )
Figure No ( 170 )

 Causes of ST Depression :
 Myocardial ischemia / NSTEMI
 Reciprocal change in STEMI Posterior MI
 Digoxin effect
 Hypokalemia
 Supraventricular tachycardia
 Right bundle branch block
 Right ventricular hypertrophy
 Left bundle branch block
 Left ventricular hypertrophy
 Ventricular paced rhythm
Segment - ST Depression .

Morphology of ST Depression
• ST depression can be either up-sloping, down-sloping, or horizontal.
• Horizontal or down-sloping ST depression ≥ 0.5 mm at the J-point in ≥
2 contiguous leads indicates myocardial ischemia (according to the
2007 Task Force Criteria).
• Up-sloping ST depression in the precordial leads with prominent De
Winter T waves is highly specific for occlusion of the LAD.
• Reciprocal change has a morphology that resembles ‗upside down‘ ST
elevation and is seen in leads electrically opposite to the site of
infarction.
• Posterior MI manifests as horizontal ST depression in V1-3 and is
associated with upright T waves and tall R waves.

ST segment morphology in myocardial ischemia
Figure No ( 171)
Figure No ( 172 )

Reciprocal change
ST segment morphology in posterior MI
Figure No ( 173 )
Figure No ( 174 )

 Myocardial Ischemia :
ST depression due to sub-endocardial ischemia may be present in a variable
number of leads and with variable morphology. It is often most prominent
in the left precordial leads V4-6 plus leads I, II and aVL.
Widespread ST depression with ST elevation in aVR is seen in left main
coronary artery occlusion and severe triple vessel disease.
**NOTE :
ST depression localized to the inferior or high lateral leads is more likely to
represent reciprocal change than sub-endocardial ischemia. The corresponding
ST elevation may be subtle and difficult to see, but should be sought.
Figure No ( 175 )

 Reciprocal Change :
ST elevation during acute STEMI is associated with simultaneous ST
depression in the electrically opposite leads:
• Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
• Lateral or anterolateral STEMI produces reciprocal ST depression in III
and aVF (± lead II).
• Reciprocal ST depression in V1-3 occurs with posterior infarction (see
below).
Reciprocal ST depression in aVL with inferior STEMI
Figure No ( 176 )

Reciprocal ST depression in III and aVF with high lateral STEMI
Figure No ( 177 )

 Posterior Myocardial Infarction :
 Acute posterior STEMI causes ST depression in the anterior leads V1-3,
 along with dominant R waves (‗Q-wave equivalent‘) and upright T
waves.
 There is ST elevation in the posterior leads V7-9.
Figure No ( 178 )

 De Winter T Waves :
De Winter T waves: a pattern of up-sloping ST depression with
symmetrically peaked T waves in the precordial leads is considered to be a
STEMI equivalent, and is highly specific for an acute occlusion of the
LAD.
Figure No ( 179 )

 Digoxin Effect :
Digoxin Effect: Treatment with digoxin causes downsloping ST depression
with a ‗sagging‘ morphology, reminiscent of Salvador Dali‖s moustache.
Figure No ( 180 )

 Hypokalemia :
Hypokalemia causes widespread down-sloping ST depression with T-wave
flattening/inversion, prominent U waves and a prolonged QU interval.
Figure No ( 181 )

 Right ventricular hypertrophy (RVH) :
Right ventricular hypertrophy (RVH) causes ST depression and T-wave
inversion in the right precordial leads V1-3.
Figure No ( 182 )

 Right Bundle Branch Block (RBBB) :
Right Bundle Branch Block (RBBB) may produce a similar pattern of
repolarization abnormalities to RVH, with ST depression and T wave
inversion in V1-3.
Figure No ( 183 )

 Supraventricular Tachycardia (SVT) :
Supraventricular tachycardia (e.g. AVNRT) typically causes widespread
horizontal ST depression, most prominent in the left precordial leads (V4-6).
This rate-related ST depression does not necessarily indicate the presence of
myocardial ischemia, provided that it resolves with treatment.
Figure No ( 184 )
Figure No ( 185 )

B. Segments :
2. PR segment
The PR segment is the flat, usually isoelectric segment between the end of
the P wave and the start of the QRS complex.
 PR segment abnormalities :
These occur in two main conditions:
 Pericarditis
 Atrial Ischemia
S e gmen ts : PR Segment .
Figure No ( 186 )

 Pericarditis :
The characteristic changes of acute pericarditis are:
 PR segment depression.
 Widespread concave (―saddle-shaped‖) ST elevation.
 Reciprocal ST depression and PR elevation in aVR and V1
 Absence of reciprocal ST depression elsewhere.
.
**Note :
PR segment changes are relative to the baseline formed by the T-P segment
S e gmen ts : PR Segment - Abnormalities of the PR
Segment .
Figure No ( 187 )

PR elevation in aVR due to
acute pericarditis (note the
reciprocal ST depression)
PR segment depression in V5 due
to acute pericarditis (note also
some concave ST elevation)
Typical ECG of acute pericarditis.
Segment .
Figure No ( 188 )

 Atrial ischemia :
 PR segment elevation or depression in patients with myocardial
infarction indicates concomitant atrial ischemia or infarction.
 This finding has been associated with poor outcomes following MI,
increased risk for the development of atrio-ventricular block,
supraventricular arrhythmias and cardiac free-wall rupture.
Liu‖s criteria for diagnosing atrial ischemia / infarction include:
 PR elevation >0.5 mm in V5 & V6 with reciprocal PR depression in V1 & V2
 PR elevation >0.5 mm in lead I with reciprocal PR depression in leads II & III
 PR depression >1.5 mm in the precordial leads
 PR depression >1.2 mm in leads I, II, & III
 Abnormal P wave morphology: M- shaped, W-shaped ,irregular ,or notched
(minor criteria)
Segment .

PR depression in inferior STEMI indicating concomitant atrial infarction
 Profound PR-segment depression in inferior leads:
(A) with clear-cut TP segment;
(B) without clear-cut TP segment; in acute inferior myocardial infarction.
(A) (B)
**Note :
Also St-segment Elevation In Inferior Leads. (Reproduced From Jim Et Al.)
Segment .
Figure No ( 191 )

Measurement of PR-segment depression:
(A) with clear-cut TP segment;
(B) without clear-cut TP segment. (Reproduced from Jim et al.)
Segment .
Figure No ( 192 )

C. Intervals :
1. PR Interval
The PR interval is the time from the onset of the P wave to the start of the
QRS complex. It reflects conduction through the AV node.
• The normal PR interval is between 120 – 200 ms (0.12-0.20s) in
duration (three to five small squares).
• If the PR interval is > 200 ms, first degree heart block is said to be
present.
• PR interval < 120 ms suggests pre-excitation (the presence of an
accessory pathway between the atria and ventricles) or AV nodal
(junctional) rhythm.
In ter vals : PR Interval .
Figure No ( 193 )

A. Prolonged PR Interval – AV block (PR >200ms) :
Delayed conduction through the AV node
May occur in isolation or co-exist with other blocks (e.g., second-degree AV block,
trifascicular block)
 First degree AV block :
Sinus rhythm with marked 1st degree heart block (PR interval 340ms)
 Second degree AV block (Mobitz I) with prolonged PR interval :
• Second degree heart block, Mobitz type I (Wenckebach
phenomenon).
• Note how the baseline PR interval is prolonged, and then further
prolongs with each successive beat, until a QRS complex is dropped.
• The PR interval before the dropped beat is the longest (340ms),
while the PR interval after the dropped beat is the shortest (280ms).
In ter vals : PR Interval -Abnormalities of the PR
Interval .
Figure No ( 194 )
Figure No ( 195 )

A. Short PR interval (<120ms) :
A short PR interval is seen with:
1. Pre-excitation syndromes .
2. AV nodal (junctional) rhythm .
.
1. Pre-excitation syndromes :
• Wolff-Parkinson-White (WPW)
• Lown-Ganong-Levine (LGL) syndromes.
 These involve the presence of an accessory pathway connecting the atria and
ventricles.
 The accessory pathway conducts impulses faster than normal, producing a short
PR interval.
 The accessory pathway also acts as an anatomical re-entry circuit, making
patients susceptible to re-entry tachyarrhythmias.
 Patients present with episodes of paroxsymal supraventricular tachycardia
(SVT), specifically atrioventricular re-entry tachycardia (AVRT), and
characteristic features on the resting 12-lead ECG
Interval .

• Wolff-Parkinson-White syndrome :
The characteristic features of Wolff-Parkinson-White syndrome are a short PR
interval (<120ms), broad QRS and a slurred upstroke to the QRS complex, the
delta wave.
• Lown-Ganong-Levine syndrome :
The features of Lown-Ganong-Levine syndrome LGL syndrome are a very short
PR interval with normal P waves and QRS complexes and absent delta waves.
Interval .
Figure No ( 196 )
Figure No ( 197 )

2. AV nodal (junctional) rhythm :
 Junctional rhythms are narrow complex, regular rhythms arising from
the AV node.
 P waves are either absent or abnormal (e.g. inverted) with a short PR
interval (=retrograde P waves).
 ECG: Accelerated junctional rhythm demonstrating inverted P waves
with a short PR interval (retrograde P waves)
Interval .
Figure No ( 198 )

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