ECG from Alpha to Omega

Course Objectives
• To recognize the normal rhythm of the
heart - “Normal Sinus Rhythm.”
• To recognize the 13 most common
rhythm disturbances.
• To recognize an acute myocardial
infarction on a 12-lead ECG.

Learning Modules
• ECG Basics
• How to Analyze a Rhythm
• Normal Sinus Rhythm
• Heart Arrhythmias
• Diagnosing a Myocardial Infarction
• Advanced 12-Lead Interpretation

Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

The “PQRST”
• P wave - Atrial
depolarization
• T wave - Ventricular
repolarization
• QRS - Ventricular
depolarization

The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for
the atria to contract
before the ventricles
contract)

Pacemakers of the Heart
• SA Node - Dominant pacemaker with
an intrinsic rate of 60 - 100
beats/minute.
• AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
• Ventricular cells - Back-up pacemaker
with an intrinsic rate of 20 - 45 bpm.

The ECG Paper
• Horizontally
– One small box - 0.04 s
– One large box - 0.20 s
• Vertically
– One large box - 0.5 mV

The ECG Paper (cont’d)
• Every 3 seconds (15 large boxes) is
marked by a vertical line.
• This helps when calculating the heart
rate.
NOTE: the following strips are not marked
but all are 6 seconds long.
3 sec 3 sec

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.

Step 1: Calculate Rate
• Option 1
– Count the # of R waves in a 6 second
rhythm strip, then multiply by 10.
– Reminder: all rhythm strips in the Modules
are 6 seconds in length.
Interpretation? 9 x 10 = 90 bpm
3 sec 3 sec

• 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)
R wave

• Option 2 (cont)
– Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50
Interpretation?
3
0
0
1
5
0
1
0
0
7
5
6
0
5
0
Approx. 1 box less than
100 = 95 bpm

Step 2: Determine regularity
• 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
R R

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

Normal Sinus Rhythm (NSR)
• 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.

NSR Parameters
• Rate 60 - 100 bpm
• Regularity regular
• P waves normal
• PR interval 0.12 - 0.20 s
• QRS duration 0.04 - 0.12 s
Any deviation from above is sinus
tachycardia, sinus bradycardia or an
arrhythmia

Arrhythmia Formation
Arrhythmias can arise from problems in
the:
• Sinus node
• Atrial cells
• AV junction
• Ventricular cells

SA Node Problems
The SA Node can:
• fire too slow
• fire too fast
Sinus Bradycardia
Sinus Tachycardia
Sinus Tachycardia may be an appropriate
response to stress.

Atrial Cell Problems
Atrial cells can:
• fire occasionally
from a focus
• fire continuously
due to a looping
re-entrant circuit
Premature Atrial
Contractions (PACs)
Atrial Flutter

Teaching Moment
• A re-entrant
pathway occurs
when an impulse
loops and results
in self-
perpetuating
impulse
formation.

Atrial Cell Problems
Atrial cells can also:
from multiple foci
or
fire continuously
due to multiple
micro re-entrant
“wavelets”
Atrial Fibrillation
Atrial Fibrillation

Teaching Moment
Multiple micro re-
entrant “wavelets”
refers to wandering
small areas of
activation which
generate fine chaotic
impulses. Colliding
wavelets can, in turn,
generate new foci of
activation.
Atrial tissue

AV Junctional Problems
The AV junction can:
due to a looping
re-entrant circuit
• block impulses
coming from the
SA Node
Paroxysmal
Supraventricular
Tachycardia
AV Junctional Blocks

Ventricular Cell Problems
Ventricular cells can:
• fire occasionally
from 1 or more foci
from multiple foci
due to a looping
re-entrant circuit
Premature Ventricular
Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia

Sinus Rhythms and
Premature Beats

Sinus Rhythms
• Sinus Bradycardia
• Sinus Tachycardia

Rhythm #1
30 bpm• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia

Sinus Bradycardia
• Deviation from NSR
- 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
130 bpm• Rate?
normal
0.08 s
• P waves?
• QRS duration?
Interpretation? Sinus Tachycardia

Sinus Tachycardia
- 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.

Premature Beats
• Premature Atrial Contractions
(PACs)
• Premature Ventricular Contractions
(PVCs)

Rhythm #3
70 bpm• Rate?
• Regularity? occasionally irreg.
2/7 different contour
0.08 s
• P waves?
• PR interval? 0.14 s (except 2/7)
• QRS duration?
Interpretation? NSR with Premature Atrial
Contractions

Premature Atrial Contractions
–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.

Premature Atrial Contractions
• Etiology: Excitation of an atrial cell
forms an impulse that is then conducted
normally through the AV node and
ventricles.

Teaching Moment
• When an impulse originates anywhere in
the atria (SA node, atrial cells, AV node,
Bundle of His) and then is conducted
normally through the ventricles, the QRS
will be narrow (0.04 - 0.12 s).

Rhythm #4
60 bpm• Rate?
• Regularity? occasionally irreg.
none for 7th QRS
0.08 s (7th wide)
• P waves?
• QRS duration?
Interpretation? Sinus Rhythm with 1 PVC

PVCs
– 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”.

PVCs
• Etiology: One or more ventricular cells
are depolarizing and the impulses are
abnormally conducting through the
ventricles.

Teaching Moment
• When an impulse originates in a
ventricle, conduction through the
ventricles will be inefficient and the
QRS will be wide and bizarre.

Ventricular Conduction
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles

Supraventricular &
Ventricular Arrhythmias

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

Rhythm #5
100 bpm• Rate?
• Regularity? irregularly irregular
none
0.06 s
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Atrial Fibrillation

Atrial Fibrillation
–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 Fibrillation
• Etiology: Recent theories suggest that it
is due to multiple re-entrant wavelets
conducted between the R & L atria.
Either way, impulses are formed in a
totally unpredictable fashion. The AV
node allows some of the impulses to
pass through at variable intervals (so
rhythm is irregularly irregular).

Rhythm #6
70 bpm• Rate?
flutter waves
0.06 s
• P waves?
• QRS duration?
Interpretation? Atrial Flutter

Atrial Flutter
–No P waves. Instead flutter waves
(note “sawtooth” pattern) are formed at
a rate of 250 - 350 bpm.
–Only some impulses conduct through
the AV node (usually every other
impulse).

Atrial Flutter
• Etiology: Reentrant pathway in the right
atrium with every 2nd, 3rd or 4th
impulse generating a QRS (others are
blocked in the AV node as the node
repolarizes).

Rhythm #7
74 148 bpm• Rate?
• Regularity? Regular 
regularNormal  none
0.08 s
• P waves?
• PR interval? 0.16 s  none
• QRS duration?
Interpretation? Paroxysmal Supraventricular
Tachycardia (PSVT)

PSVT
–The heart rate suddenly speeds up,
often triggered by a PAC (not seen
here) and the P waves are lost.

PSVT
• Etiology: There are several types of
PSVT but all originate above the
ventricles (therefore the QRS is narrow).
• Most common: abnormal conduction in
the AV node (reentrant circuit looping in
the AV node).

Ventricular Arrhythmias
• Ventricular Tachycardia
• Ventricular Fibrillation

Rhythm #8
160 bpm• Rate?
none
wide (> 0.12 sec)
• P waves?
• QRS duration?
Interpretation? Ventricular Tachycardia

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

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

–Completely abnormal.

• Etiology: The ventricular cells are
excitable and depolarizing randomly.
• Rapid drop in cardiac output and death
occurs if not quickly reversed

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
60 bpm• Rate?
normal
0.08 s
• P waves?
• QRS duration?
Interpretation? 1st Degree AV Block

1st Degree AV Block
–PR Interval > 0.20 s

1st Degree AV Block
• Etiology: Prolonged conduction delay in
the AV node or Bundle of His.

Rhythm #11
50 bpm• Rate?
• Regularity? regularly irregular
nl, but 4th no QRS
0.08 s
• P waves?
• PR interval? lengthens
• QRS duration?
Interpretation? 2nd Degree AV Block, Type I

2nd Degree AV Block, Type I
–PR interval progressively lengthens,
then the impulse is completely blocked
(P wave not followed by QRS).

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
40 bpm• Rate?
nl, 2 of 3 no QRS
0.08 s
• P waves?
• QRS duration?
Interpretation? 2nd Degree AV Block, Type II

2nd Degree AV Block, Type II
–Occasional P waves are completely
blocked (P wave not followed by QRS).

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
40 bpm• Rate?
no relation to QRS
wide (> 0.12 s)
• P waves?
• QRS duration?
Interpretation? 3rd Degree AV Block

3rd Degree AV Block
–The P waves are completely blocked in
the AV junction; QRS complexes
originate independently from below the
junction.

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.

Remember
• When an impulse originates in a ventricle,
conduction through the ventricles will be
inefficient and the QRS will be wide and
bizarre.

Diagnosing a MI
To diagnose a myocardial infarction you
need to go beyond looking at a rhythm
strip and obtain a 12-Lead ECG.
Rhythm
Strip
12-Lead
ECG

The 12-Lead ECG
• The 12-Lead ECG sees the heart
from 12 different views.
• Therefore, the 12-Lead ECG helps
you see what is happening in
different portions of the heart.
• The rhythm strip is only 1 of these 12
views.

The 12-Leads
The 12-leads include:
–3 Limb leads
(I, II, III)
–3 Augmented leads
(aVR, aVL, aVF)
–6 Precordial leads
(V1- V6)

Views of the Heart
Some leads get a
good view of the:
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart

ST Elevation
One way to
diagnose an
acute MI is to
look for
elevation of
the ST
segment.

ST Elevation (cont’d)
Elevation of the
ST segment
(greater than 1
small box) in 2
leads is
consistent with a
myocardial
infarction.

Anterior View of the Heart
The anterior portion of the heart is best
viewed using leads V1- V4.

Anterior Myocardial Infarction
If you see changes in leads V1 - V4
that are consistent with a myocardial
infarction, you can conclude that it is
an anterior wall myocardial infarction.

Putting it all Together
Do you think this person is having a
myocardial infarction. If so, where?

Interpretation
Yes, this person is having an acute anterior
wall myocardial infarction.

Other MI Locations
Now that you know where to look for an
anterior wall myocardial infarction let’s
look at how you would determine if the MI
involves the lateral wall or the inferior wall
of the heart.

Other MI Locations
First, take a look
again at this
picture of the heart.
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart

Other MI Locations
Second, remember that the 12-leads of the ECG look at
different portions of the heart. The limb and augmented
leads “see” electrical activity moving inferiorly (II, III and
aVF), to the left (I, aVL) and to the right (aVR). Whereas, the
precordial leads “see” electrical activity in the posterior to
anterior direction.
Limb Leads Augmented Leads Precordial Leads

Other MI Locations
Now, using these 3 diagrams let’s figure where
to look for a lateral wall and inferior wall MI.

Anterior MI
Remember the anterior portion of the heart is
best viewed using leads V1- V4.

Lateral MI
So what leads do you think
the lateral portion of the
heart is best viewed?
Leads I, aVL, and V5- V6

Inferior MI
Now how about the
inferior portion of the
heart?
Leads II, III and aVF

Now, where do you think this person is
having a myocardial infarction?

Inferior Wall MI
This is an inferior MI. Note the ST elevation
in leads II, III and aVF.

How about now?

Anterolateral MI
This person’s MI involves both the anterior wall
(V2-V4) and the lateral wall (V5-V6, I, and aVL)!

Advanced 12-Lead Interpretation

The 12-Lead ECG
The 12-Lead ECG contains a wealth of
information. In Module V you learned that
ST segment elevation in two leads is
suggestive of an acute myocardial
infarction. In this module we will cover:
–ST Elevation and non-ST Elevation MIs
–Left Ventricular Hypertrophy
–Bundle Branch Blocks

ST Elevation and
non-ST Elevation MIs

ST Elevation and non-ST Elevation MIs
• When myocardial blood supply is abruptly
reduced or cut off to a region of the heart, a
sequence of injurious events occur beginning
with ischemia (inadequate tissue perfusion),
followed by necrosis (infarction), and eventual
fibrosis (scarring) if the blood supply isn't
restored in an appropriate period of time.
• The ECG changes over time with each of
these events…

ECG Changes
Ways the ECG can change include:
Appearance
of pathologic
Q-waves
T-waves
peaked flattened
inverted
ST elevation &
depression

ECG Changes & the Evolving MI
There are two
distinct patterns
of ECG change
depending if the
infarction is:
–ST Elevation (Transmural or Q-wave), or
–Non-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation

ST Elevation Infarction
ST depression, peaked T-waves,
then T-wave inversion
The ECG changes seen with a ST elevation infarction are:
Before injury Normal ECG
ST elevation & appearance of
Q-waves
ST segments and T-waves return to
normal, but Q-waves persist
Ischemia
Infarction
Fibrosis

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

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?
ST elevation,
Q-waves and
T-wave
inversion

ST depression & T-wave inversion
The ECG changes seen with a non-ST elevation infarction are:
Before injury Normal ECG
ST depression & T-wave inversion
ST returns to baseline, but T-wave
inversion persists
Ischemia
Infarction
Fibrosis

Here’s an ECG of an evolving non-ST elevation MI:
Note the ST
depression
and T-wave
inversion in
leads V2-V6.
Question:
What area of
the heart is
infarcting?
Anterolateral

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)

Why is left ventricular hypertrophy characterized by tall
QRS complexes?
LVH ECHOcardiogram
Increased QRS voltage
As the heart muscle wall thickens there is an increase in
electrical forces moving through the myocardium resulting
in increased QRS voltage.

• Criteria exists to diagnose LVH using a 12-lead ECG.
– For example:
• The R wave in V5 or V6 plus the S wave in V1 or V2
exceeds 35 mm.
• However, for now, all
you need to know is
that the QRS voltage
increases with LVH.

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

So, 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 complex.
Right
BBB

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).

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?
V1
For RBBB the wide QRS complex assumes a
unique, virtually diagnostic shape in those
leads overlying the right ventricle (V1 and V2).
“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 S
waves
Normal

Summary
This Module introduced you to:
– ST Elevation and Non-ST Elevation MIs
– Left Ventricular Hypertrophy
– Bundle Branch Blocks
Don’t worry too much right now about trying to
remember all the details. You’ll focus more on
advanced ECG interpretation in your clinical
years!

Reading 12-Lead ECGs
• The 12-Lead ECG contains information that will assist
you in making diagnostic and treatment decisions in your
clinical practice. In previous modules you learned how to
read and interpret parts of the ECG. Now, we will bring all
that you have learned together so that you can
systematically read and interpret a 12-lead ECG.
• The information will be divided into two modules, VII a
and VII b.

The best way to read 12-lead ECGs is to develop a step-
by-step approach (just as we did for analyzing a rhythm
strip). In these modules we present a 6-step approach:
1. Calculate RATE
2. Determine RHYTHM
3. Determine QRS AXIS
4. Calculate INTERVALS
5. Assess for HYPERTROPHY
6. Look for evidence of INFARCTION

Rate Rhythm Axis Intervals Hypertrophy Infarct
• In Module II you learned how to calculate the
rate. If you need a refresher return to that module.
• There is one new thing to keep in mind when
determining the rate in a 12-lead ECG…

If you use the rhythm
strip portion of the
12-lead ECG the total
length of it is always
10 seconds long. So
you can count the
number of R waves
in the rhythm strip
and multiply by 6 to
determine the beats
per minute. Rate? 12 (R waves) x 6 = 72 bpm

• In Module II you learned how to systematically
analyze a rhythm by looking at the rate, regularity,
P waves, PR interval and QRS complexes.
• In Modules III, IV and V you learned how to
recognize Normal Sinus Rhythm and the 13 most
common rhythm disturbances.
• If you need a refresher return to these modules.

Tip: the rhythm strip portion of the 12-lead ECG is a good
place to look at when trying to determine the rhythm
because the 12 leads only capture a few beats.
Lead II
Rhythm?
Atrial
fibrillation
Rhythm
strip
1 of 12
leads

Axis refers to the mean QRS axis (or vector) during ventricular
depolarization. As you recall when the ventricles depolarize (in a
normal heart) the direction of current flows leftward and downward
because most of the ventricular mass is in the left ventricle. We like
to know the QRS axis because an abnormal axis can suggest
disease such as pulmonary hypertension from a pulmonary
embolism.

The QRS axis is determined by overlying a circle, in the frontal
plane. By convention, the degrees of the circle are as shown.
The normal QRS axis lies between -30o
and +90o
.
0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
A QRS axis that falls between -30o
and -90o
is
abnormal and called left axis deviation.
A QRS axis that falls between
+90o
and +150o
is abnormal and
called right axis deviation.
A QRS axis that falls
between +150o
and -90o
is
abnormal and called superior
right axis deviation.

• Causes of left axis deviation
include:
– Left ventricular hypertrophy
– Inferior wall MI
– Left bundle branch block
– Left anterior fascicular block
– Horizontal heart
0o
-90o
90o
180o
• Causes of right axis deviation
include:
– Right ventricular hypertrophy
– Lateral wall MI
– Right bundle branch block
– Pulmonary hypertension
– Vertical heart

We can quickly determine whether the QRS axis is
normal by looking at leads I and II.
If the QRS complex is
overall positive (R > Q+S)
in leads I and II, the QRS
axis is normal.
QRS negative (R < Q+S)
In this ECG what leads
have QRS complexes
that are negative?
equivocal?
QRS equivocal (R = Q+S)

How do we know the axis is normal when the QRS
complexes are positive in leads I and II?

The answer lies in the fact that each frontal lead
corresponds to a location on the circle.
0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
I
II
av
av
L
av
R
Limb leads
I = +0o
II = +60o
III = +120o
Augmented leads
avL = -30o
avF = +90o
avR = -150o
I
IIIII

0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
Since lead I is orientated at 0o
a wave of depolarization directed towards it
will result in a positive QRS axis. Therefore any mean QRS vector
between -90o
and +90o
will be positive.
I

0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
between -90o
and +90o
will be positive.
Similarly, since lead II is
orientated at 60o
a wave of
depolarization directed towards
it will result in a positive QRS
axis. Therefore any mean QRS
vector between -30o
and +150o
will be positive.
I
II

0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
between -90o
and +90o
will be positive.
Similarly, since lead II is orientated at 60o
a wave of depolarization directed towards
it will result in a positive QRS axis.
Therefore any mean QRS vector between
-30o
and +150o
will be positive.
Therefore, if the QRS complex is
positive in both leads I and II the
QRS axis must be between -30o
and
90o
(where leads I and II overlap)
and, as a result, the axis must be
normal.
I
II

0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
Now using what you just learned fill in the following table. For example, if
the QRS is positive in lead I and negative in lead II what is the QRS axis?
(normal, left, right or right superior axis deviation)
QRS Complexes
I
AxisI II
+ +
+ -
normal
left axis deviation
II

0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
… if the QRS is negative in lead I and positive in lead II what is the QRS
axis? (normal, left, right or right superior axis deviation)
QRS Complexes
I
AxisI II
+ +
+ -
- +
normal
left axis deviation
right axis deviation
II

0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
… if the QRS is negative in lead I and negative in lead II what is the
QRS axis? (normal, left, right or right superior axis deviation)
QRS Complexes
I
AxisI II
+ +
+ -
- +
- -
normal
left axis deviation
right superior
axis deviation
0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
II

Is the QRS axis normal in this ECG? No, there is left axis
deviation.
The QRS is
positive in I
and negative
in II.

To summarize:
– The normal QRS axis falls between -30o
and +90o
because ventricular
depolarization is leftward and downward.
– Left axis deviation occurs when the axis falls between -30o
and -90o
.
– Right axis deviation occurs when the axis falls between +90o
and +150o
.
– Right superior axis deviation occurs when the axis falls between between
+150o
and -90o
.
QRS Complexes
AxisI II
+ +
+ -
- +
- -
normal
left axis deviation
right superior
axis deviation
– A quick way to
determine
the QRS
axis is to look at the
QRS complexes in
leads I and II.

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct
To summarize VII a:
1. Calculate RATE
2. Determine RHYTHM
– Normal
– Left axis deviation
– Right axis deviation
– Right superior axis deviation

In VII b we will cover the next 3 steps:
1. Calculate RATE
2. Determine RHYTHM

In Module VII a we introduced a 6 step approach for
analyzing a 12-lead ECG and covered the first 3 steps. In
this module we will cover the last 3 steps.
1. Calculate RATE
2. Determine RHYTHM

• Intervals refers to the length of the PR and QT intervals
and the width of the QRS complexes. You should have
already determined the PR and QRS during the “rhythm”
step, but if not, do so in this step.
• In the following few slides we’ll review what is a normal
and abnormal PR, QRS and QT interval. Also listed are a
few common causes of abnormal intervals.

PR interval
< 0.12 s 0.12-0.20 s > 0.20 s
High catecholamine
states
Wolff-Parkinson-White
Normal AV nodal blocks
Wolff-Parkinson-White 1st Degree AV Block

QRS complex
< 0.10 s 0.10-0.12 s > 0.12 s
Normal
Incomplete bundle
branch block
Bundle branch block
PVC
Ventricular rhythm
Remember: If you have a BBB determine if it is a right or left
BBB. If you need a refresher see Module VI.
3rd
degree AV block with
ventricular escape rhythm
Incomplete bundle branch block

QT interval
The duration of the QT interval is
proportionate to the heart rate. The faster
the heart beats, the faster the ventricles
repolarize so the shorter the QT interval.
Therefore what is a “normal” QT varies
with the heart rate. For each heart rate you
need to calculate an adjusted QT interval,
called the “corrected QT” (QTc):
QTc = QT / square root of RR interval

QTc interval
< 0.44 s > 0.44 s
Normal Long QT
A prolonged QT can be very dangerous. It may predispose an individual to a type of
ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte
abnormalities, CNS disease, post-MI, and congenital heart disease.
Torsades de Pointes
Long QT

PR interval? QRS width? QTc interval?
0.08 seconds0.16 seconds 0.49 seconds
QT = 0.40 s
RR = 0.68 s
Square root of
RR = 0.82
QTc = 0.40/0.82
= 0.49 s
Interpretation of intervals? Normal PR and QRS, long QT

Tip: Instead of calculating the QTc, a quick way to estimate if the
QT interval long is to use the following rule:
A QT > half of the RR interval is probably long.
Normal QT Long QT
QT
RR
10 boxes
23 boxes 17 boxes
13 boxes

In this step of the 12-lead ECG analysis, we use the ECG
to determine if any of the 4 chambers of the heart are
enlarged or hypertrophied. We want to determine if there
are any of the following:
– Right atrial enlargement (RAE)
– Left atrial enlargement (LAE)
– Right ventricular hypertrophy (RVH)
– Left ventricular hypertrophy (LVH)

• In Module VI we introduced the concept of left ventricular
hypertrophy. As you remember the QRS voltage increases with LVH
and is characterized by tall QRS complexes in certain leads. Similarly
for right ventricular hypertrophy we look at the QRS complexes for
changes in voltage patterns.
• With right and left atrial enlargement we analyze the P wave (since
the P wave represents atrial depolarization). Here we also look for
changes in voltage patterns.
• Note: as mentioned in Module VI criteria exists to diagnose LVH,
the same goes for RAE, LAE and RVH. In the following slides we will
be presenting criteria you can use. However other criteria exists and
as a reference you might find it useful to carry a copy of Tom Evans’
ECG Interpretation Cribsheet.

Right atrial enlargement
– Take a look at this ECG. What do you notice about the P waves?
The P waves are tall, especially in leads II, III and avF.
Ouch! They would hurt to sit on!!

Right atrial enlargement
– To diagnose RAE you can use the following criteria:
• II P > 2.5 mm, or
• V1 or V2 P > 1.5 mm
Remember 1 small
box in height = 1 mm
A cause of RAE is RVH from pulmonary hypertension.
> 2 ½ boxes (in height)
> 1 ½ boxes (in height)

Left atrial enlargement
– Take a look at this ECG. What do you notice about the P waves?
The P waves in lead II are notched and in lead V1 they
have a deep and wide negative component.
Notched
Negative deflection

Left atrial enlargement
– To diagnose LAE you can use the following criteria:
• II > 0.04 s (1 box) between notched peaks, or
• V1 Neg. deflection > 1 box wide x 1 box deep
Normal LAE
A common cause of LAE is LVH from hypertension.

Right ventricular hypertrophy
– Take a look at this ECG. What do you notice about the axis and QRS
complexes over the right ventricle (V1, V2)?
There is right axis deviation (negative in I, positive in II) and
there are tall R waves in V1, V2.

– Compare the R waves in V1, V2 from a normal ECG and one from
a person with RVH.
– Notice the R wave is normally small in V1, V2 because the right
ventricle does not have a lot of muscle mass.
– But in the hypertrophied right ventricle the R wave is tall in V1, V2.
Normal RVH

– To diagnose RVH you can use the following criteria:
• Right axis deviation, and
• V1 R wave > 7mm tall
A common
cause of RVH
is left heart
failure.

Left ventricular hypertrophy
– Take a look at this ECG. What do you notice about the axis and QRS
complexes over the left ventricle (V5, V6) and right ventricle (V1, V2)?
There is left axis deviation (positive in I, negative in II) and there
are tall R waves in V5, V6 and deep S waves in V1, V2.
The deep S waves
seen in the leads over
the right ventricle are
created because the
heart is depolarizing
left, superior and
posterior (away from
leads V1, V2).

Left ventricular hypertrophy
– To diagnose LVH you can use the following criteria*:
• R in V5 (or V6) + S in V1 (or V2) > 35 mm, or
• avL R > 13 mm
A common cause of LVH
is hypertension.
* There are several
other criteria for the
diagnosis of LVH.
S = 13 mm
R = 25 mm

A 63 yo man has longstanding, uncontrolled hypertension. Is there evidence
of heart disease from his hypertension? (Hint: There a 3 abnormalities.)
Yes, there is left axis deviation (positive in I, negative in II), left atrial enlargement
(> 1 x 1 boxes in V1) and LVH (R in V5 = 27 + S in V2 = 10  > 35 mm).

• When analyzing a 12-lead ECG for evidence of an
infarction you want to look for the following:
– Abnormal Q waves
– ST elevation or depression
– Peaked, flat or inverted T waves
• These topics were covered in Modules V and VI where
you learned:
– ST elevation (or depression) of 1 mm in 2 or more
contiguous leads is consistent with an AMI
– There are ST elevation (Q-wave) and non-ST elevation
(non-Q wave) MIs

Tip: One way to determine if Q waves (and R waves) are abnormal is by
looking at the width and using the following mantra (read red downwards):
Any Any Q wave in V1
20 A Q wave > 20 msec in V4 (i.e. 0.02 sec or ½ width of a box)
30 A Q wave > 30 msec in V5
30 A Q wave > 30 msec in V6
30 A Q wave > 30 msec in I
30 A Q wave > 30 msec in avL
30 A Q wave > 30 msec in II
30 A Q wave > 30 msec in avF
R40 A R wave > 40 msec in V1
R50 A R wave > 50 msec in V2

This mantra corresponds to the ECG in the following way:
Any
Any
Any
20
30
30
30
3030
30
R40
R50

To summarize:
1. Calculate RATE
2. Determine RHYTHM
– Normal
– Left axis deviation
– Right axis deviation
– Right superior axis deviation

To summarize:
1. Calculate RATE
2. Determine RHYTHM
– PR
– QRS
– QT

To summarize:
1. Calculate RATE
2. Determine RHYTHM
– Right and left atrial enlargement
– Right and left ventricular hypertrophy

To summarize:
1. Calculate RATE
2. Determine RHYTHM
– Abnormal Q waves
– ST elevation or depression
– Peaked, flat or inverted T waves

To summarize:
1. Calculate RATE
2. Determine RHYTHM
Now to finish this module lets analyze a 12-lead ECG!

A 16 yo young man ran into a guardrail while riding a motorcycle.
In the ED he is comatose and dyspneic. This is his ECG.

What is the rate? Approx. 132 bpm (22 R waves x 6)

What is the rhythm? Sinus tachycardia

What is the QRS axis? Right axis deviation (- in I, + in II)

What are the PR, QRS
and QT intervals?
PR = 0.12 s, QRS = 0.08 s, QTc = 0.482 s

Is there evidence of
atrial enlargement?
No (no peaked, notched or negatively
deflected P waves)

Is there evidence of
ventricular hypertrophy?
No (no tall R waves in V1/V2 or V5/V6)

Infarct: Are there abnormal
Q waves?
Yes! In leads V1-V6 and I, avL
Any
Any
Any
20
30
30
30
3030
30
R40
R50

Infarct: Is the ST elevation
or depression?
Yes! Elevation in V2-V6, I and avL.
Depression in II, III and avF.

Infarct: Are there T wave
changes?
No

ECG analysis: Sinus tachycardia at 132 bpm, right axis deviation,
long QT, and evidence of ST elevation infarction in the
anterolateral leads (V1-V6, I, avL) with reciprocal changes (the
ST depression) in the inferior leads (II, III, avF).
This young man suffered an
acute myocardial infarction
after blunt trauma. An
echocardiogram showed
anteroseptal akinesia in the
left ventricle with severely
depressed LV function
(EF=28%). An angiogram
showed total occlusion in the
proximal LAD with collaterals
from the RCA and LCX.

ECG from Alpha to Omega

In this document