Part 1 -

Fundamentals
of
ECG recording,
reporting and
interpretation
Dr Naila BUMS MD BAMS(Intg)
Chief Medical Officer
GUMCH
Bangalore
Presentation
• Part -1
 Introduction
 Leads
 steps of recording ECG
 ECG paper
 Wave forms

• Part -2
 Steps of ECG interpretation – Rule of fours
• Part – 3
 Abnormal ECG
ECG
Part -1
 • ‘ECG’ stands for electrocardiogram, or
electrocardiograph

• The device used to obtain and display

the conventional (12-lead) ECG is called
the electrocardiograph, or more
informally, the ECG machine.

• The electrocardiogram (ECG or EKG) is a

special type of graph that represents
cardiac electrical activity

• Graphical recording as the

electrocardiogram and the recording
device as the electrocardiograph

• ECG provides a time-voltage chart of the

Introduction heartbeat.
Electrical activity of heart
The term electrical activation (stimulation) was applied to the
spread of electrical signals through the atria and ventricles.

The more technical term for the cardiac activation process is

depolarization.

The return of heart muscle cells to their resting state following

depolarization is called repolarization.
 • SA node cells:
• Atrial cells: 55- • AV node: 45-50
60-100 BPM
60 BPM BPM
(beats per minute)

• Bundle of His • Bundle branch • Purkinje cells:

cells: 40-45 BPM cells: 40-45 BPM 20-40 BPM
 ECG Leads
• LIMB (EXTREMITY) LEADS

Standard Limb Leads: I, II, and III

Augmented Limb Leads: aVR, aVL, and Avf

• CHEST (PRECORDIAL) LEADS

 Electrodes are One electrode is provide six ‘limb
different views of
placed on the chest attached to each leads’ or six different
the heart's electrical
and limbs of the limb. These four views of the heart in
activity.
patient to record electrodes a vertical Plane

Six electrodes are Accurate placement

These are called
attached to the of these electrodes
leads I, II, III, VL, VF ECGs.
chest, recording is essential for
and VR.
leads V1 to V6. comparing later

These leads ‘look at’

the heart from the
front in a horizontal
plane
Localising pathology on the ECG
Before Electrodes should be selected for maximum

recording adhesiveness and minimum discomfort,

electrical noise

ECG Effective contact between electrode and skin

is essential. Sites with skin irritation or
skeletal abnormalities should be avoided

Calibration of the ECG signal is typically 1 mV

= 10 mm.

ECG paper speed is typically 25 mm per

second

It is important that the patient remain supine

during recording of the ECG
STANDARDIZATION (CALIBRATION)
MARK

The electrocardiograph Paper speed and

is generally calibrated standardization at the
such that a 1-mV signal bottom of the ECG paper
produces a 10-mm (“25 mm/sec, 10
deflection. mm/mV”).
 Paper output speed is the rate at which
the ECG machine produces a trace

The standard paper speed is

Understand 25mm/sec:
ing ECG
paper 1mm (small square) = 0.04 sec (40ms)

5mm (large square) = 0.2 sec (200ms)

The ECG
Complex
 ECG Wave forms

• The P wave represents atrial

depolarization.
• The PR interval is the time from initial
stimulation of the atria to initial
stimulation of the ventricles.
• The QRS complex represents ventricular
depolarization.
• The ST segment, T wave, and U wave
are produced by ventricular repolarization
WHY IS ECG SO USEFUL?

1 2
Diagnosing dangerous cardiac Providing immediate information
electrical disturbances causing about clinically important
brady- and tachyarrhythmias. problems, including myocardial
ischemia/infarction, electrolyte
disorders, and drug toxicity, as
well as hypertrophy and other
types of chamber overload.
ECG Part -2
 Method 1
seven step approach
to ECG rhythm analysis
 Tachycardia or
bradycardia?
1. Rate
Normal rate is
60-100/min.
2. Pattern of QRS complexes

If irregular, is it
Regular or regularly irregular
irregular? or irregularly
irregular?
3. QRS Narrow complex: sinus, atrial
or junctional origin.
morpholo
gy
Wide complex: ventricular
origin, or supraventricular
 Absent: sinus arrest, atrial
fibrillation
4. P
waves
Present: morphology and PR
interval may suggest sinus,
atrial, junctional or even
retrograde from the ventricles.
5. AV association (may be difficult to
distinguish from isorhythmic dissociation)
Relationsh
ip AV dissociation
between P
waves and complete: atrial and ventricular activity is
QRS always independent.

complexes
incomplete: intermittent capture
6. Onset and termination

Abrupt: suggests Gradual: suggests

re-entrant increased
process. automaticity.
 Sinus tachycardia, ectopic atrial
tachydysrhythmia
7. Response
to vagal Atrial fibrillation and atrial flutter:
gradual slowing during the
manoeuvres manoeuvres.

VT: no response.
 Method 2

12 parameters
Method 2

Cardiac The cardiac

The heart rate The P wave
rhythm axis

The size of R The width of

The PR The QRS
and S waves in the QRS
interval complex
the chest leads complex

The ST The QT
Q waves The T wave
segment interval
The ECG ‘Rule of Fours’

Four Initial Four

Features Waves

Four
Intervals
1. The FOUR INITIAL FEATURES

History and clinical picture

Rate

Rhythm

Axis
 (1) P wave

2. Four
The waves
F22OUR
W4AVES (or (2) QRS complexes (or QRS “waves”)
complexes) on
an ECG
(3) T waves

(4) U waves
 3. The FOUR INTERVALS (or
segments)
PR interval

QRS width / interval

ST segment

QT interval
1. The FOUR INITIAL
FEATURES
1. The FOUR INITIAL FEATURES

History and clinical picture

Rate

Rhythm

Axis
 The FOUR INITIAL FEATURES
(1) History/ Clinical Picture
• This is THE MOST IMPORTANT thing to look at on ANY ECG.
• Simple things need to be recorded, like the name, age,
time, patient symptoms (e.g. chest pain) and other clinical
features.
Also do a quick check for lead placement errors :
• Limb leads: (a) check aVR for upside down P, QRS and T
waves, (b) aVL and aVR should generally be mirror images.
• Chest leads: look for RS pattern in V1 – changing
progressively to QR pattern in V6.
(2) Rate

The normal value is between 60-100/min. Lower

than this is bradycardia, higher is tachycardia.

(3) Rhythm

Is the rhythm sinus or is it another rhythm? If so,

what?

(4) Axis
 • The rhythm is best analyzed by
looking at a rhythm strip.
2. ECG
Rhythm • On a 12 lead ECG this is
usually a 10 second recording
Evaluation from Lead II.
 Normal sinus rhythm (NSR) is an impulse that originates in the sinus
node.

It is recognized by the P wave morphology that is:

Normal Heart rate 60-100 BPM

Sinus Regular rhythm

rhythm Normal PR Interval and QT interval

Every P wave is followed by QRS complex

• upright P in leads I, II and aVF
• inverted in aVR
• upright in leads V4-V6 (in 12-lead ECG)
• most often biphasic (positive-negative) in leads V1 and V2
 A. Large square method
• 300 large squares is equal to 1 minute
at a paper speed of 25mm/sec
3. • We can thus calculate bpm by dividing
300 by the number of LARGE squares
HEART between each R-R interval (space
between two consecutive R waves =
RATE 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
 1500 is divided by the
B. Small number of SMALL squares
between consecutive R waves
square
method For example, 10 small squares
between R-R interval implies
a rate of 150 bpm, 15 implies
a rate of 100 bpm,
 Rate = Number of R waves (rhythm strip) X 6

C. R The number of complexes (count R waves) on the

wave 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)

method
Useful for slow and/or irregular rhythms
Count r waves in
6 seconds
multiply by 10
Many electrocardiographic recordings conveniently provide markers at 3-
second intervals
Count the number of cardiac cycles in 6 seconds and to multiply by 10.
4. AXIS
 Mean axis of the QRS projected on the frontal
plane
4. ECG Axis
Interpretat Since the left ventricle makes up most of the
ion 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”).
A. The Quadrant
• The most efficient way
Method – (Lead I and to estimate axis is to
aVF) look at LEAD I and LEAD
aVF.

• Examine the QRS

complex in each lead
and determine if it is
Positive, Isoelectric
(Equiphasic) or
Negative:
 • The combined evaluation of
Lead I, Lead II and aVF –
Method 2: allows rapid and accurate
Three Lead QRS assessment.
analysis –
(Lead I, Lead • The addition of Lead II can
help determine pathological
II and aVF) LAD from normal
axis/physiological LAD
Method 3 –
The
Isoelectric
Lead
• This method
allows a more
precise
estimation of
QRS axis, using
the axis diagram
Identify the transitional lead by locating the lead in which the QRS
complex has the most nearly equal positive and negative
components.

2. Identify the lead that is oriented perpendicular to the transitional

lead by using the hexaxial reference system.

3. Consider the predominant direction of the QRS complex in the

lead identified in step 2.

If the direction is positive, the axis is the same as the positive pole
of that lead. If the direction is negative, the axis is the same as the
negative pole of the lead.
-30
60
-90
-60
-30
2. The FOUR WAVES (or
complexes) on an ECG
 (1) P wave
• Lead II is usually the best lead place to look at the P wave
morphology.
The FOUR • Observe the P-wave morphology e.g. in particular P pulmonale
or P mitrale.

WAVES (or (2) QRS complexes (or QRS “waves”)

complexes) on • Look in ALL leads for the presence of Q waves.
• Observe the QRS amplitude and look for QRS progression
an ECG through the chest leads.

(3) T waves
• Look in ALL leads for T waves.
• Look for T wave inversion, T wave concordance or discordance
with QRS and the presence of T wave flattening.

(4) U waves
• Are U waves present or not?
 The P wave is the first positive deflection on the ECG

It represents atrial depolarization

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

Atrial abnormalities are most easily seen in the inferior

leads (II, III and aVF) and lead V1, as the P waves are most
prominent in these leads.

Normal duration: < 0.12 s (< 120ms or 3 small squares)

 Morphology
Smooth contour

Characteris Monophasic in lead II

tics of the Biphasic in V1

Normal Duration
Sinus P < 0.12 s (<120ms or 3 small squares)
Wave Amplitude
< 2.5 mm (0.25mV) in the limb leads
< 1.5 mm (0.15mV) in the precordial leads
 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
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)
 • Right atrial enlargement
Right Atrial causes increased height
Enlargement – (> 1.5mm) in V1 of the
initial positive deflection
Lead V1 of the P wave.
 In left atrial enlargement, left atrial
depolarisation lasts longer than normal
Left but its amplitude remains unchanged
Atrial Therefore, the height of the resultant P
Enlargem wave remains within normal limits but
its duration is longer than 120 ms
ent –
Lead II A notch (broken line) near its peak may
or may not be present (“P mitrale”)
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.
 The presence of
broad, notched (bifid)
P waves in lead II is a
sign of left atrial
enlargement,
classically due to
mitral stenosis.
 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).
QRS
complex
QRS
QRS complex

Width Height Morphology

 QRS The QRS interval represents
Interval the time required for a
(Width or stimulus to spread through
Duration) the ventricles (ventricular
depolarization) and is
normally about ≤0.12 sec
Width can
NARROW BROAD (>
be
(< 0.12 0.12
described
seconds) seconds):
as
 when the impulse is conducted
down the bundle of His and the
Purkinje fibre to the ventricles.

Narrow This results in well organised

QRS synchronised ventricular
depolarisation.

complex
< 0.12 seconds
 A broad QRS complex occurs if there is an abnormal
depolarisation sequence

Broad > 0.12 seconds

QRS
complex
a ventricular ectopic where the impulse spreads slowly
across the myocardium from the focus in the ventricle.

a bundle branch block results in a broad QRS complex

because the impulse gets to one ventricle rapidly down
the intrinsic conduction system then has to spread
slowly across the myocardium to the other ventricle.
Height of QRS • Small complexes are defined as < 5mm in
the limb leads or < 10 mm in the chest
leads.
• Tall complexes imply ventricular
hypertrophy
Morphology
 • 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
The Q left-sided leads (I, aVL, V5 and V6)
Wave
 Small Q waves are normal in
Q waves most leads

in
Deeper Q waves (>2 mm) may
different be seen in leads III and aVR as a
normal variant
leads
Under normal circumstances, Q
waves are not seen in the right-
sided leads (V1-3)
 leads (V1, V2, and V3), the presence of any Q wave should be
considered abnormal, whereas in all other leads (except rightward-
oriented leads III and aVR), a “normal” Q wave is very small
Pathologic Q waves are
considered > 40 ms (1 mm) wide
al Q Waves pathological if:

> 25% of depth of

> 2 mm deep
QRS complex

Pathological Q waves
usually indicate
Seen in leads V1-3
current or prior
myocardial infarction.
Differenti Myocardial infarction

al Cardiomyopathies — Hypertrophic
Diagnosi (HCM), infiltrative myocardial
disease
s
Lead placement errors — e.g. upper
limb leads placed on lower limbs
 • Inferior infarction: Q waves affecting
Once Q waves leads II, III, aVF
• Anterior infarction: Q waves affecting
have developed leads V2-V5
• Lateral infarction: Q waves affecting
it is permanent. leads V5-V6, I, aVL
• NOTE: a posterior infarction is not
associated with Q waves on a normal
12-lead ECG.
• In this type of myocardial infarction
there is a dominant R wave in V1
similar to the findings in right
ventricular hypertrophy.
 The absence of small septal
Loss of Q waves in leads V5-6 should
normal Q be considered abnormal.

waves
Absent Q waves in V5-6 is
most commonly due to LBBB.
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
Lateral Q waves (I, aVL) with
ST elevation due to acute MI
Anterior Q waves
(V1-4) with ST
elevation due to
acute MI
Anterior Q waves (V1-4)
with T-wave inversion
due to recent MI
 R wave

The R wave is the first upward deflection after the P or Q wave.

The R wave represents early ventricular depolarization

The cardiac electrical activity progressing from the thinner right ventricle
across the thicker left ventricle, the positive R wave normally increases in
amplitude and duration from lead V1 to lead V4 or V5
 There are three key R wave abnormalities:

Dominant R wave in V1.

Abnormal
ities of larger R waves in leads V1 and V2, can be produced
by right-ventricular hypertrophy
the R Larger R waves in leads V5 and V6, can be produced
wave by left-ventricular hypertrophy.
Dominant R wave in aVR

Poor R wave progression

 Causes of Dominant R wave in V1
• Normal in children and young adults
• Right Ventricular Hypertrophy (RVH)
• Right Bundle Branch Block (RBBB)
Dominan • Posterior Myocardial Infarction (ST elevation
t R wave in Leads V7, V8, V9)
in V1 • Incorrect lead placement (e.g. V1 and V3
reversed)
• Dextrocardia
• Hypertrophic cardiomyopathy
 Poisoning with
sodium-channel
2.Domina Dextrocardia
blocking drugs
nt R wave (e.g. TCAs)
in aVR
Incorrect lead Commonly
placement elevated in
(left/right arm ventricular
leads reversed) tachycardia (VT)
3. Poor R wave progression

Loss of normal R-wave progression from lead V1 to lead V4 may indicate loss of
left-ventricular myocardium, as occurs with myocardial infarction
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
 • The S wave also has a normal sequence of
progression in the precordial leads.
• It should be large in V1, larger in V2, and
then progressively smaller from V3 through
V6

S Waves
 The T wave is the positive deflection after each
QRS complex.

It represents ventricular repolarisation.

T wave Upright in all leads except aVR and V1

Amplitude < 5mm in limb leads, < 10mm in

precordial leads (10mm males, 8mm females)
 Peaked T waves

Hyperacute T waves

T wave Inverted T waves

abnormalities Biphasic T waves

‘Camel Hump’ T waves

Flattened T waves
 T waves are considered tall if they are:

> 5mm in the limb leads AND

> 10mm in the chest leads (the same criteria as ‘small’ QRS
Tall T complexes)

waves Tall T waves can be associated with:

Hyperkalaemia (“tall tented T waves”)

Hyperacute STEMI
Peaked T
waves
Hyperacute T waves (HATW)

Broad, asymmetrically peaked Particular attention should be

or ‘hyperacute’ T-waves paid to their size in relation to
(HATW) are seen in the early the preceding QRS complex, as
stages of ST-elevation MI HATW may appear ‘normal’ in
(STEMI), and often precede the size if the preceding QRS
appearance of ST elevation and complex is of a small
Q waves. amplitude.
Loss of precordial T-wave
balance

The normal T
Loss of precordial
wave in V1 is This finding
T-wave balance
inverted. An indicates a high
occurs when the
upright T wave in likelihood of
upright T wave is
V1 is considered coronary artery
larger than that
abnormal — disease, and
in V6. This is a
especially if it is when new
type of
tall (TTV1), and implies acute
hyperacute T
especially if it is ischemia
wave.
new (NTTV1).
 T wave inversion in lead III is a
normal variant.

T wave New T-wave inversion (compared

inversio with prior ECGs) is always
abnormal.
n
Pathological T wave inversion is
usually symmetrical and deep
(>3mm).
Inverted T waves

• T waves are normally inverted in V1 and

inversion in lead III is a normal variant.
• Ischaemia
• Bundle branch blocks (V4-6 in LBBB and
V1-V3 in RBBB)
• Pulmonary embolism
• Left ventricular hypertrophy (in the
lateral leads)
• Hypertrophic cardiomyopathy
(widespread)
• General illness
 The U wave is a small (0.5 mm)
deflection immediately following
the T wave

U wave is usually in the same

U Wave direction as the T wave.

U wave is best seen in leads V2

and V3.
 The source of the U wave is unknown.
Three common theories regarding its
origin are:

Source
of the U
Delayed repolarisation of Purkinje fibres

wave Prolonged repolarisation of mid-

myocardial “M-cells”

After-potentials resulting from mechanical

forces in the ventricular wall
 • The U wave normally goes in the same
direction as the T wave
• U -wave size is inversely proportional to heart
Features rate: the U wave grows bigger as the heart rate
of slows down
• U waves generally become visible when the
Normal U heart rate falls below 65 bpm
waves • 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
Abnormal
Prominent U
ities of waves
the U
wave
Inverted U
waves
 Prominent U waves

Prominent U
most commonly Bradycardia
found with:

waves Severe
Hypocalcaemia

>1-2mm or
hypokalaemia.

25% of the Hypomagnesaemia Hypothermia

height of the
T wave. Raised intracranial
pressure
Left ventricular
hypertrophy

Hypertrophic
cardiomyopathy
 Inverted U waves
A negative U wave is highly specific for the presence of heart
disease

Common causes
Coronary artery Valvular heart
of inverted U Hypertension
disease disease
waves

Congenital heart
Cardiomyopathy Hyperthyroidism
disease
U waves are not a common finding.

The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.

These become larger the slower the bradycardia – classically U waves are seen
in various electrolyte imbalances, hypothermia and secondary to
antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).
 3. The FOUR
INTERVALS (or
segments)
 3. The FOUR INTERVALS (or
segments)
PR interval

QRS width / interval

ST segment

QT interval
1. PR INTERVAL

It is the time required for an electrical impulse to travel from the atrial
myocardium adjacent to the sinoatrial (SA) node to the ventricular
myocardium adjacent to the fibers of the Purkinje network

Normally from 0.10 to 0.21 second

PR interval varies with the heart rate, being shorter at faster rates
when the sympathetic component predominates, and vice versa
In adults the normal PR interval is between 0.12 and 0.2 sec (three to five small box sides)
prolongation of the PR interval above 0.2 sec is called first-degree heart block
sinus tachycardia, AV conduction may be facilitated by increased sympathetic and decreased vagal tone modulation.
Accordingly, the PR may be relatively short, e.g., about 0.10–0.12 sec,
1. PR interval

The PR interval is normally

between 0.12-0.20 seconds
(3-5 small squares).

A prolonged or changing (esp

lengthening) PR interval
indicates heart block.

Shortened PR intervals can be

because of WPW or a
junctional rhythm
Prolonge
d PR
interval
Shortened PR interval
2. QRS width /
A widened
The QRS- QRS width
interval is indicates
normally less some sort of
than 0.12 conduction
seconds (3 defect with
interval

small the left or

squares). right bundle
branches.
 Main features to consider:

Width of the complexes: Narrow versus

QRS broad.

Interval Voltage (height) of the complexes.

Spot diagnoses: Specific morphology

patterns that are important to recognize.
QRS Width

• Normally ranges from 0.07 to 0.11 second {2 / 2 ½ small

squre}
• 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).
3. ST segment (“ST-interval”)

This is probably the most

important thing to look at.

…then look at it a 2nd and

3rd time.

Look for sloping (especially

downsloping) or flattening
of the ST segments.
 J point
• The very beginning of
the ST segment
(actually the junction
between the end of the
QRS complex and the
beginning of the ST
segment) is called the J
point
Isolated J point elevation may occur as a normal variant with the early repolarization pattern

As a marker of systemic hypothermia

J point elevation may also be part of ST elevations with acute pericarditis, acute myocardial
ischemia, left bundle branch block or left ventricular hypertrophy (leads V1 to V3 usually)

J point depression may occur in a variety of contexts, both physiologic and pathologic
 The QT interval is the time from the start of
the Q wave to the end of the T wave.

4. QT interval
If the QT interval The normal QTc is
different for Men and
is prolonged there Women:
is an increased
risk of developing
polymorphic VT Men: 350 - 440 ms
(Torsades de
pointes) and
sudden death.
Women: 350 - 460 ms
• A long QT interval (known as “long QT”) is especially important to
identify in patients with a history of collapse or transient loss of
consciousness.
ECG Part -3
Abnormal Wave
Morphology
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
Chamber Enlargement
ATRIAL ENLARGEMENT
VENTRICULAR ENLARGEMENT
ECG SEGMENTS VS. ECG INTERVALS
There are three basic segments:
1. PR segment: end of the P wave to beginning of the QRS complex
2. ST segment: end of the QRS complex to beginning of the following T wave.
3. TP segment: end of the T wave to beginning of
the P wave.
four sets of intervals
2. The PR interval is measured from the beginning of the P wave to the beginning of the QRS
complex.
3. The QRS interval (duration) is measured from the beginning to the end of the same QRS.
4. The QT interval is measured from the beginning of the QRS to the end of the T wave. When
this interval is corrected (adjusted for the heart rate), the designation QTc is used,
5. The RR (QRS–QRS) interval is measured from one point (sometimes called the R-point) on a
given QRS complex to the corresponding point on the next.