Electrocardiogram:

Indications,
Utilization, &
Clinical
Correlation
Michael Anthony C. Estur, MD, FPCP, FPCC
objectives
At the end of the session, the students should be able to:
1. Define electrocardiography
2. Discuss indications and utilization of ECG
3. Identify normal ECG tracings
4. Correlate abnormal ECG findings with clinical
conditions
ELECTROCARDIOGRAM (ECG or EKG)
 It is a graphic recording of electric potentials generated by the heart.

 The signals are detected by means of metal electrodes attached to the

extremities and chest wall and then are amplified and recorded by the
electrocardiograph.

 ECG leads actually display the instantaneous differences in potential between

the electrodes.

*Harrison’s Principles of Internal Medicine, 18 th edition.

THE CARDIAC CONDUCTION SYSTEM
Pacemakers of the heart
ECG WAVEFORMS
 avR avL
ECG ELECTRODES &
LEADS I

 3 Bipolar Limb II III

Leads

 3 Augmented
Limb Leads

avF
 aVR aVL

III II
aVF

Standard Locations of Limb Leads

Lead placement
CHEST LEADS LIMB LEADS
12-lead ecg

SEPTAL WALL ANTERIOR WALL LATERAL WALL

WHAT IS A NORMAL ECG
Normal ecg waveform
Waves:
Atrial depolarization
P

Q Ventricular
depolarization
R

S Ventricular
repolarization
T
Normal ecg waveform
Segments:
 end of the P to the onset
 PR of QRS
 duration of conduction
from AVN to the His
bundle
 Normally ISOELECTRIC

 end of S to the onset of T

wave
 ST  duration between
ventricular depolarization
and repolarization
 Normally ISOELECTRIC
Normal ecg waveform
Intervals:
• Time between atrial
 PR and ventricular
depolarization
• onset of P to the
onset of QRS
• 0.12 to 0.20 seconds
 QRS • physiologic delay
imposed by
stimulation of cells in
the AV junction area

 QT
Normal ecg waveform
Intervals:
• onset of Q to
 PR the end of the S
wave
• measure of the
duration of
 QRS ventricular
depolarization
• normally ≤0.10
sec
 QT
Normal ecg waveform
Intervals:
 PR
• Onset of the QRS
complex and ends at
the end of the T-wave
• ventricular
 QRS
depolarization and
repolarization times
• varies inversely with
heart rate
 QT • Normal: 0.39 sec to
0.45sec in Males /
0.46 sec in Females
 The ecg paper

1 small box = 0.04 sec

 The ecg paper

1 big box = 0.2 sec

 THE ECG PAPER

• Horizontally
• One small box - 0.04 s
• One large box - 0.20 s
• Vertically
• One large box – 5mm
or 0.5 mV
 THE ECG PAPER
3 sec 3 sec

• Every 3 seconds (15 large boxes) is marked

by a vertical line.
• This helps when calculating the heart rate.
 R

PR ST
segment
segment
T
P

S
 Reading 12-Lead ECGs

• Calculate RATE
• Determine RHYTHM
• Determine AXIS
• Assess for HYPERTROPHY
• Look for evidence of INFARCTION
• Check for MISCELLANEOUS FINDINGS
 Rhythm Analysis

• Step 1: Calculate rate.

• Step 2: Determine regularity.
• Step 3: Assess the P waves.
• Step 4: Determine PR interval.
• Step 5: Determine QRS duration.
 Normal values
• Heart rate - 60-100
• PR interval - 0.12-0.20 secs
• QRS duration - <0.12 secs
• QT interval - 0.30-0.44 (0.45 for women)
second
• A rate-related ("corrected") QT interval, QTc,
can be calculated as QT/√R-R and normally is
0.44 s. (Some references give QTc upper normal limits
as 0.43 s in men and 0.45 s in women.)
Step 1: Calculate Rate

• Formula 1
300
# of big squares between R-R

• Formula 2
1500
# of small squares between R-R
Step 1: Calculate Rate

R
wave
• Option 2
• Find a R wave that lands on a bold line.
• Count the # of large boxes to the next R wave.
If the second R wave is 1 large box away the
rate is 300, 2 boxes - 150, 3 boxes - 100, 4
boxes - 75, etc. (cont)
Step 1: Calculate Rate
3 1 1
0 5 0 7 6 5
0 0 0 5 0 0

• Option 2 (cont)
• Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50

Interpretation? Approx. 1 box less than 100

= 95 bpm
Step 1: Calculate Rate
3 sec 3 sec

• Option 3 (For irregular rhythm)

• Count the # of R waves in a 6 second rhythm
strip, then multiply by 10.
Interpretation?

9 x 10 = 90 bpm
Step 2: Determine regularity
R R

• Look at the R-R distances (using a caliper or

markings on a pen or paper).
• Regular (are they equidistant apart)? Occasionally
irregular? Regularly irregular? Irregularly
irregular?
Interpretation? Regular
Step 3: Assess the P waves

• Are there P waves?

• Do the P waves all look alike?
• Do the P waves occur at a regular rate?
• Is there one P wave before each QRS?
Interpretation?
Normal P waves with 1 P wave for
every QRS
Step 4: Determine PR interval

• Normal: 0.12 - 0.20 seconds.

(3 - 5 boxes)

Interpretation? 0.12 seconds

Step 5: QRS duration

• Normal: 0.04 - 0.12 seconds.

(1 - 3 boxes)

Interpretation? 0.08 seconds

 Rhythm Summary

• Rate 90-95 bpm

• Regularity regular
• P waves normal
• PR interval 0.12 s
• QRS duration 0.08 s
Interpretation? Normal Sinus Rhythm
 Regular Sinus Rhythm (RSR)

• Etiology: the electrical impulse is formed in

the SA node and conducted normally.
• This is the normal rhythm of the heart;
other rhythms that do not conduct via the
typical pathway are called arrhythmias.
 RSR Parameters

• Rate 60 - 100 bpm

• Regularity regular
• P waves normal
• PR interval 0.12 - 0.20 s
• QRS duration 0.04 - 0.12 s
 Sinus Rhythms

• Sinus Bradycardia
• Sinus Tachycardia
 Rhythm #1

• Rate? 30 bpm
• Regularity? regular
• P waves? normal
• PR interval? 0.12 s
• QRS duration? 0.10 s
Interpretation? Sinus Bradycardia
 Sinus Bradycardia

• Deviation from RSR

- Rate < 60 bpm
 Sinus Bradycardia

• Etiology: SA node is depolarizing slower

than normal, impulse is conducted normally
(i.e. normal PR and QRS interval).
 Rhythm #2

• Rate? 130 bpm

• Regularity? regular
• P waves? normal
• PR interval? 0.16 s
• QRS duration? 0.08 s
Interpretation? Sinus Tachycardia
 Sinus Tachycardia

• Deviation from NSR

- Rate > 100 bpm
 Sinus Tachycardia

• Etiology: SA node is depolarizing faster

than normal, impulse is conducted
normally.
• Remember: sinus tachycardia is a response
to physical or psychological stress, not a
primary arrhythmia.
 SA Node Problems

The SA Node can:

• fire too slow Sinus Bradycardia
• fire too fast Sinus Tachycardia
 Premature Beats

• Premature Atrial Contractions

(PACs)
• Premature Ventricular Contractions
(PVCs)
 Rhythm #3

• Rate? 70 bpm
• Regularity? occasionally irreg.
• P waves? 2/7 different contour
• PR interval? 0.14 s (except 2/7)
• QRS duration? 0.08 s
Interpretation?
 Premature Atrial Contractions

• Etiology: Excitation of an atrial cell forms

an impulse that is then conducted normally
through the AV node and ventricles.
 Premature Atrial Contractions

• Deviation from NSR

• These ectopic beats originate in the atria
(but not in the SA node), therefore the
contour of the P wave, the PR interval,
and the timing are different than a
normally generated pulse from the SA
node.
 Rhythm #4

• Rate? 60 bpm
• Regularity? occasionally irreg.
• P waves? none for 7th QRS
• PR interval? 0.14 s
• QRS duration? 0.08 s (7th wide)
Interpretation? Sinus Rhythm with 1 PVC
 PVCs

• Etiology: One or more ventricular cells are

depolarizing and the impulses are
abnormally conducting through the
ventricles.
 PVCs

• Deviation from NSR

• Ectopic beats originate in the ventricles resulting
in wide and bizarre QRS complexes.
• When there are more than 1 premature beats and
look alike, they are called “uniform”. When they
look different, they are called “multiform”.
 Rhythm #5

• Rate? 100 bpm

• Regularity? irregularly irregular
• P waves? none
• PR interval? none
• QRS duration? 0.06 s
Interpretation? Atrial Fibrillation
 Rhythms

• Sinus Rhythms
• Premature Beats
• Supraventricular Arrhythmias
• Ventricular Arrhythmias
• AV Junctional Blocks
 Supraventricular Arrhythmias

• Atrial Fibrillation
• Atrial Flutter
• Paroxysmal Supraventricular
Tachycardia
 Atrial Fibrillation

• Deviation from NSR

• No organized atrial depolarization, so no
normal P waves (impulses are not
originating from the sinus node).
• Atrial activity is chaotic (resulting in an
irregularly irregular rate).
• Common, affects 2-4%, up to 5-10% if >
80 years old
 Atrial Flutter

• Regular rhythm in presence of fixed AV block.

• Ventricular rate ~150 bpm in presence of 2:1 AV block.
• Flutter waves / ‘saw-tooth pattern’ best seen in leads II,
III, aVF and V1.
 Ventricular Arrhythmias

• Ventricular Tachycardia
• Ventricular Fibrillation
 Rhythm #8

• Rate? 160 bpm

• Regularity? regular
• P waves? none
• PR interval? none
• QRS duration? wide (> 0.12 sec)
Interpretation? Ventricular Tachycardia
 Ventricular Tachycardia

• Deviation from NSR

• Impulse is originating in the ventricles (no
P waves, wide QRS).

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 Ventricular Tachycardia

• Etiology: There is a re-entrant pathway

looping in a ventricle (most common
cause).

• Ventricular tachycardia can sometimes

generate enough cardiac output to produce a
pulse; at other times no pulse can be felt.
 Rhythm #9

• Rate? none
• Regularity? irregularly irreg.
• P waves? none
• PR interval? none
• QRS duration? wide, if recognizable
Interpretation? Ventricular Fibrillation
 Ventricular Fibrillation

• Etiology: The ventricular cells are excitable

and depolarizing randomly.
Rate Rhythm Axis Hypertrophy Infarct Miscellaneous
The QRS axis is determined by overlying a circle, in the frontal plane. By
convention, the degrees of the circle are as shown.
aVF
III
II -90 o

-120o -60o
The normal QRS axis lies aVR aVL
between -30o and +100.
o
-150 -30 o

I 180o 0o I

A QRS axis that falls between - aVL

150o 30o
aVR
30o and -90o is abnormal and 120o 60o
o
90
called LEFT AXIS DEVIATION. III II
aVF
Rate Rhythm Axis Hypertrophy Infarct Miscellaneous
The QRS axis is determined by overlying a circle, in the frontal plane. By
convention, the degrees of the circle are as shown.
aVF
III
II o
-90
A QRS axis that falls between +90o -120o -60o

and +150o is abnormal and called aVR

-150 o
-30 o
aVL

RIGHT AXIS DEVIATION.

I 180o 0o I
A QRS axis that falls between
+150o and -90o is abnormal and aVL
150o 30o
aVR
called Undetermined or extreme 120o
60o
90o
right or EXTREME AXIS III II
aVF
DEVIATION.
Rate Rhythm Axis Hypertrophy Infarct Miscellaneous
• Long cut: 90 x aVF
│I │ + │ aVF │
• Short Cut:
Hypertrophy
 RIGHT ATRIAL ENLARGEMENT

•Tall (>2.5mm), pointed P

waves
 Right Atrial Enlargement

Criteria exists to diagnose RAE using a 12-lead ECG.

Any of the following:
In lead V1: Tall initial component of P wave
which is ≥ 2mm wide (0.08sec) and ≥2mm tall
(p pulmonale).
In any lead: P wave ≥ 2.5 mm tall
 Left Atrial Enlargement
Criteria exists to diagnose LAE
using a 12-lead ECG.
Any of the following:
In any lead: P wave wider than
0.12 sec (≥ 3 small squares) or
with a ≥ 1 mm notched in the
middle
 Right Ventricular
Hypertrophy
Criteria exists to diagnose RVH using a 12-
lead ECG.
Right axis deviation of +110 degrees
or more, with any of the following:
Lead V1: R wave > S wave
Deep S waves in leads V5 and V6
ST depression and T wave inversion
in V1-V3
 Left Ventricular Hypertrophy
Compare these two 12-lead ECGs. What stands out as
different with the second one?

Normal Left Ventricular Hypertrophy

Answer: The QRS complexes are very tall (increased voltage)

Left Ventricular
Hypertrophy
 Sokolow & Lyon Criteria
S in V1 + R in V5 or V6 > 35
R wave of 11 -13mm in lead aVL

Cornell criteria
SV3 + R avl > 28 in men
- SV3 + R avl > 20mm in women
 AV Nodal Blocks

• 1st Degree AV Block

• 2nd Degree AV Block, Type I
• 2nd Degree AV Block, Type II
• 3rd Degree AV Block
 Rhythm #10

regular
normal

PR interval = 0.36 s
1st Degree AV Block
 1st Degree AV Block

• Criteria
• There must be p waves
• One p wave to each QRS complex
• PR Interval > 0.20 s
• PR interval is constant

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 1st Degree AV Block

• Etiology: Prolonged conduction delay in the

AV node or Bundle of His.
Rhythm #11
 2nd Degree AV Block, Type I

• Criteria (Wenkebach)
• P waves and QRS complex present
• P waves
• morphology and axis usual for the subject
• Progressive prolongation of P-R interval with each succeeding beat
until there is a dropped beat
• Longest P-R interval is the one immediately before the dropped beat
• Shortest P-R interval is the one associated with the first conducted
beat after the dropped beat
 2nd Degree AV Block, Type I

• Etiology: Each successive atrial impulse

encounters a longer and longer delay in the
AV node until one impulse (usually the 3rd
or 4th) fails to make it through the AV node.
Rhythm #12
 2nd Degree AV Block, Type II

• Criteria (Mobitz)
• There must be P waves & QRS complexes
• P waves and QRS have morphology and axis usual
for the subject
• P-R interval of conducted beats may be normal or
long but fixed, then there is a dropped beat
• Constant P-R interval for all conducted beats
 2nd Degree AV Block, Type II

• Etiology: Conduction is all or nothing (no

prolongation of PR interval); typically
block occurs in the Bundle of His.
Rhythm #13
 3rd Degree AV Block

• Criteria
• No consistent or meaningful relationship
between atrial and ventricular activity.
Variable PR and RP intervals.
• QRS is usually constant and lies within the
range of 15-70 bpm
 3rd Degree AV Block

• Etiology: There is complete block of

conduction in the AV junction, so the atria
and ventricles form impulses independently
of each other. Without impulses from the
atria, the ventricles own intrinsic pacemaker
kicks in at around 30 - 45 beats/minute.
Bundle Branch Blocks

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 Bundle Branch Blocks
Turning our attention to bundle branch blocks…

Remember normal
impulse conduction is
SA node 
AV node 
Bundle of His 
Bundle Branches 
Purkinje fibers
 Normal Impulse Conduction
Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers
 Bundle Branch Blocks
Depolarization of the Bundle
Branches and Purkinje fibers are
seen as the QRS complex on the
ECG.

Therefore, a conduction block of

the Bundle Branches would be
reflected as a change in the QRS
Right
complex. BBB
 Bundle Branch Blocks
With Bundle Branch Blocks you will see two changes on the ECG.
1. QRS complex widens (> 0.12 sec).
2. QRS morphology changes (varies depending on ECG lead, and if it is
a right vs. left bundle branch block).
 Bundle Branch Blocks
Why does the QRS complex widen?

When the conduction

pathway is blocked it
will take longer for the
electrical signal to pass
throughout the
ventricles.
 Right Bundle Branch Blocks
What QRS morphology is characteristic?
For RBBB the wide QRS complex assumes a
unique, virtually diagnostic shape in those leads
overlying the right ventricle (V1 and V2).

V1

“Rabbit Ears”
 Left Bundle Branch Blocks
What QRS morphology is characteristic?
For LBBB the wide QRS complex assumes a
characteristic change in shape in those leads
opposite the left ventricle (right ventricular leads -
V1 and V2).

Broad, deep
Normal S waves
ISCHEMIA, INJURY
INFARCTION
 STAGES OF ISCHEMIC
CHANGES
• Ischemia
• Deficient O2 delivery for given O2 demand
• Symmetrical T wave inversion and ST depression
• Injury
• Lack of critical blood supply
• ST elevation in leads corresponding to involved area
• Infarction
• Irreversible cell necrosis and death
• Pathological Q waves (but may occur w/o Q waves)
 CRITERIA FOR
MYOCARDIAL INJURY
Depression of the origin of the ST segment at the J
point >1.0mm in at least 2 leads
• ST segment deviation typically either horizontal or
slope toward the direction of the T waves
• Symmetrical T wave inversion or flattening
• T waves are usually upright in I, II, V2-V6, inverted
aVR
 CRITERIA FOR
MYOCARDIAL INFARCTION
Elevation of the origin of the ST segment at it J point with
the QRS of:
>1.0mm (0.10mv) in >2 limb leads lasting >80msecs

Development of new Q waves on areas overlying the

infarct
• >0.04 sec duration
>25% of the height of associated R wave
 Rules regarding Q wave
• Not significant in aVR
• Ignored in V1 unless with abnormalities in other precordial leads
• Ignored in III unless with abnormalities in II, aVF
• More reliable if with ST-T segment changes
• Not significant if located in V1-3 in LBBB
• Significant in V1-2 in the presence of RBBB
• Pathologic if >0.04 sec and >25% of R wave amplitude
 ST Elevation

One way to diagnose an

acute MI is to look for
elevation of the ST
segment.
 ST Elevation (cont)

Elevation of the ST segment

(greater than 1 small box) in
2 leads is consistent with a
myocardial infarction.
 ANATOMY OF MYOCARDIAL
INFARCTION
Infarction Area ECG leads Coronary artery Branch

Extensive anterior aVL, V1-6 Left , LM LAD, LCx

Anteroseptal V1-V3 Left LAD

Anterolateral I, aVL, V4-6 Left LCx

Inferior II, III, aVF Right 80% PDA

True posterior V1-2 (reciprocal) Variable L/R LCx, PL

LAD = Left anterior descending artery

LCx = Left circumflex artery
LM = Left main artery
PDA = Posterior descending artery
PL = posterolateral branches
 ST Elevation Infarction
The ECG changes seen with a ST elevation infarction are:

Before injury Normal ECG

Ischemia ST depression, peaked T-waves, then

T-wave inversion
Infarction ST elevation & appearance of Q-waves

Fibrosis ST segments and T-waves return to

normal, but Q-waves persist
 ST Elevation Infarction
Here’s a diagram depicting an evolving infarction:

A. Normal ECG prior to MI

B. Ischemia from coronary artery occlusion results in ST depression

(not shown) and peaked T-waves

C. Infarction from ongoing ischemia results in marked ST elevation

D/E. Ongoing infarction with appearance of pathologic Q-waves and

T-wave inversion

F. Fibrosis (months later) with persistent Q- waves, but normal ST

segment and T- waves
 ST Elevation Infarction
Here’s an ECG of an inferior MI:

Look at the inferior leads (II,

III, aVF).

Question: What ECG

changes do you see?

ST elevation and
Q-waves
Extra credit: What is the
rhythm?
Atrial fibrillation (irregularly irregular with narrow QRS)!
 Non-ST Elevation Infarction
Here’s an ECG of an inferior MI later in time:

Now what do you see in the

inferior leads?

Q-waves and T-
wave inversion
 Non-ST Elevation Infarction
The ECG changes seen with a non-ST elevation infarction are:

Before injury Normal ECG

Ischemia ST depression & T-wave inversion

Infarction ST elevation & T-wave inversion

Fibrosis ST returns to baseline, but T-wave

inversion persists
 Non-ST Elevation Infarction
Here’s an ECG of an evolving non-ST elevation MI:

Note the ST depression and T-

wave inversion in leads V2-V6.
End