ECG Basics Lecture 1

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‫ِ‬ ‫بسمك‬
Step 1: Calculate Rate
R wave
– 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
– Memorize the sequence:

300 - 150 - 100 - 75 - 60 - 50
Interpretation?
Approx. 1 box less than
100 = 95 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 – 2.5 boxes)
Interpretation? 0.08 seconds

Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50
• QRS 1-2.5
•P >2.5×2.5
• PR 3-5
Arrhythmia Formation
Arrhythmias can arise from problems in

the:
• Sinus node
• Atrial cells
• AV junction
• Ventricular cells
QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

SA Node Problems
The SA Node can:

• fire too slow Sinus Bradycardia
• fire too fast Sinus Tachycardia
Sinus Tachycardia may be an appropriate

response to stress.
QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

Atrial Cell Problems
Atrial cells can:

• fire occasionally Premature Atrial
from a focus Contractions (PACs)
• fire continuously Atrial Flutter

due to a looping
re-entrant circuit
QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

Rhythm #1
• Rate? 30 bpm
• Regularity? regular
• P waves? normal
• PR interval? 0.12 s
• QRS duration? 0.10 s
Interpretation? Sinus Bradycardia
QRS 1-2.5 P > 2.5 ×2.5 PR 3-5
Rhythm #2
• Rate? 130 bpm

• P waves? normal
Interpretation? Sinus Tachycardia
Rhythm #3
• Rate? 70 bpm
• Regularity? occasionally irreg.
• P waves? 2/7 different contour
• PR interval? 0.14 s (except 2/7)
Interpretation? NSR with Premature Atrial
Contractions
PJCs (Premature Junctional
Contractions)
The underlying rhythm is interrupted
by an early beat arising from the AV
node or junction.
Most often the impulse is conducted
with a narrow QRS complex.
The P wave in lead II is negative or
absent
• Although most premature
supraventricular beats (PACs or
PJCs) are conducted to the
ventricles normally (i.e., with a
narrow QRS complex), this is not
always the case
• Instead, PACs or PJCs may
sometimes occur so early in the
cycle as to be "blocked" (i.e., non-
conducted), because the
conduction system is still in an
absolute refractory state. They will
be found if looked for, they'll often
be hiding (notching) a part of the
preceding T wave (see subtle T
wave notching in the figure right).
• Other times, premature beats may
occur during the relative refractory
period,in which case aberrant
conduction (with a widened QRS)
occurs. Practically speaking, aberrant
conduction is most likely to take the
form of some type of bundle branch
block/hemiblock pattern (most
commonly RBBB). Attention to QRS
morphology may help to distinguish
between aberrancy and ventricular
beats.
Rhythm #4
• Rate? 60 bpm
• Regularity? occasionally irreg.
• P waves? none for 7th QRS
• QRS duration? 0.08 s (7th wide)
Interpretation? Sinus Rhythm with 1 PVC
Ventricular Conduction
Normal Abnormal
Signal moves rapidly Signal moves slowly
through the ventricles through the ventricles
Bigeminy
Every other beat is ventricular
Rhythm #5
• Rate? 100 bpm

• Regularity? irregularly irregular
• P waves? none
• PR interval? none
Interpretation? Atrial Fibrillation
Rhythm #6
• Rate? 70 bpm
• P waves? flutter waves
Interpretation? Atrial Flutter
Rhythm #7
• Rate? 74 148 bpm

• Regularity? Regular  regular
• P waves? Normal  none
• PR interval? 0.16 s  none
Interpretation? Paroxysmal Supraventricular
Tachycardia (PSVT)
Accessory pathways
• Abnormal, congenital extra pathways

between the atria and ventricles are
common, and can perforate the
electrically insulating fibrous ring that
normally separates the atrial `chamber'
and the ventricular one.
QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

• Because depolarisation moves `antegrade'
from atria to ventricles, part of the ventricle
depolarises prematurely, and this is
responsible for the slurred, initial delta wave.
It should be clear that the PR interval will therefore be

short, and the QRS duration should be prolonged.
Rhythm #8
• Rate? 160 bpm

• P waves? none
• QRS duration? wide (> 0.12 sec)
Interpretation? Ventricular Tachycardia
Rhythm #9
• Rate? none
• Regularity? irregularly irreg.
• P waves? none
• QRS duration? wide, if recognizable
Interpretation? Ventricular Fibrillation
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
• Rate? 60 bpm
• P waves? normal
Interpretation? 1st Degree AV Block
Rhythm #11
• Rate? 50 bpm
• Regularity? regularly irregular
• P waves? nl, but 4th no QRS
• PR interval? lengthens
Interpretation? 2nd Degree AV Block, Type I
Rhythm #12
• Rate? 40 bpm
• P waves? nl, 2 of 3 no QRS
Interpretation? 2nd Degree AV Block, Type II
Rhythm #13
• Rate? 40 bpm
• P waves? no relation to QRS
• QRS duration? wide (> 0.12 s)
Interpretation? 3rd Degree AV Block
Remember
• When an impulse originates in a ventricle,
conduction through the ventricles will be
inefficient and the QRS will be wide and
bizarre.
300 - 150 - 100 - 75 - 60 - 50
• QRS 1-2.5
•P > 2.5×2.5
• PR 3-5
300 - 150 - 100 - 75 - 60 - 50
QRS 1-2.5 QRS Complexes
I II Axis
P> 2.5×2.5 + + normal
PR 3-5 + - left axis deviation

- + right axis deviation
Rate Rhythm Axis Intervals Hypertrophy Infarct
PR interval 3-5 Boxes
< 0.12 s 0.12-0.20 s > 0.20 s
High catecholamine
states Normal AV nodal blocks
Wolff-Parkinson-White
Wolff-Parkinson-White 1st Degree AV Block

QRS complex
< 0.10 s 0.10-0.12 s > 0.12 s
Bundle branch block

Incomplete bundle
Normal PVC
branch block
Ventricular rhythm
Incomplete bundle branch block 3rd degree AV block with

ventricular escape rhythm
300 - 150 - 100 - 75 - 60 - 50
QRS 1-2.5 QRS Complexes
I II Axis
P > 2.5×2.5 + + normal
PR 3-5 + - left axis deviation
A QT > half of the RR - + right axis deviation
interval
Right ventricular hypertrophy

– 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
– 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
S = 13 mm
* There are several
other criteria for the
diagnosis of LVH.
R = 25 mm
A common cause of LVH
is hypertension.
e s t
A R
ke
Ta
Memorize 300 - 150 - 100 - 75 - 60 - 50
• QRS 1-2.5 QRS Complexes

• P > 2.5×2.5 I II Axis
• PR 3-5 + + normal
• A QT > half of the RR + - left axis deviation
interval - + right axis deviation
RVH RAD, and V1 R wave > 7mm tall

LVH R in V5 (or V6) + S in V1 (or V2)
> 35, or
avL R > 13 mm
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
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 Right
reflected as a change in BBB
the QRS complex.
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.
If the QRS Complex is Wide
If the rhythm is supraventricular and QRS
winding is not due to WPW
there are only 3 possibilities:
1. There may be typical RBBB
2. There may be typical LBBB
3. IVCD (IntraVentricular Conduction
Delay).
Note: The 3 key leads
(and the only 3 leads
needed) to determine the
type of conduction defect
(RBBB, LBBB, or IVCD)
are leads I, V1, and V6.
ECG Diagnosis of Bundle Branch Block
QRS > 0.12sec

Look at V1:
Terminal R = RBBB
as excitation spreading from left to right
Terminal S = LBBB
as excitation spreading away from right
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”
RBBB and the "r's" -- rSR' complex
with the taller right rabbit ear (the R') in
a right-sided lead (i.e., V1).
• Confirm LI & V6
Terminal wide S = RBBB as excitation
going away from left side
ECG Diagnosis of Bundle Branch Block
QRS > 0.12sec

Look at V1:
Terminal R = RBBB
as excitation spreading from left to right
Terminal S = LBBB
as excitation spreading away from right
• Confirm LI & V6
• Terminal R = LBBB as excitation
heading towards left
Left Bundle Branch Blocks
What QRS morphology is characteristic?
For LBBB the wide QRS complex assumes a
characteristic change in shape in V1 and V2).
Broad,
Normal deep S
waves
Memorize 300 - 150 - 100 - 75 - 60 - 50
• QRS 1-2.5 QRS Complexes

• P > 2.5×2.5 I II Axis
• PR 3-5 + + normal
• A QT > half of the RR + - left axis deviation
QRS > 0.12sec

LVH R in V5 (or V6) + S in V1 (or V2) Look at V1:
> 35, or Terminal R = RBBB
avL R > 13 mm
Terminal S = LBBB
ST Elevation and
non-ST Elevation MIs
Ischaemic Changes
• S-T segment elevation

• S-T segment depression
• Hyper-acute T-waves
• T-wave inversion
• Pathological Q-waves
• Left bundle branch block
ST Segment
• The ST segment represents period between
ventricular depolarisation and repolarisation.
• The ventricles are unable to receive any further
stimulation
• The ST segment normally lies on the isoelectric line.
ST Segment Elevation
The ST segment lies above the isoelectric
line:
• Represents myocardial injury

• It is the hallmark of Myocardial Infarction
• The injured myocardium is slow to repolarise
and remains more positively charged than the
surrounding areas
• Other causes to be ruled out include
pericarditis and ventricular aneurysm
ST-Segment Elevation
Myocardial Infarction
• A medical emergency!!!
• ST segment curves upwards in the
leads looking at the threatened
myocardium.
• Presents within a few hours of the
infarct.
• Reciprocal ST depression may be
present
ST Segment Depression
Can be characterised as:-
• Downsloping
• Upsloping
• Horizontal
Horizontal ST Segment Depression
Myocardial Ischaemia:
• Stable angina - occurs on exertion, resolves
with rest and/or GTN
• Unstable angina - can develop during rest.
• Non ST elevation MI - usually quite deep,
can be associated with deep T wave
inversion.
• Reciprocal horizontal depression can occur
during AMI.
Horizontal ST depression
ST Segment Depression
Downsloping ST segment depression:-

• Can be caused by digoxin.
Upward sloping ST segment depression:-

• Normal during exercise.
T waves
• The T wave represents ventricular
repolarisation
• Should be in the same direction as and
smaller than the QRS complex
• Hyperacute T waves occur with S-T
segment elevation in acute MI
• T wave inversion occurs during
ischaemia and shortly after an MI
T waves
Other causes of T wave inversion include:
• Normal in some leads
• Cardiomyopathy
• Pericarditis
• Bundle Branch Block (BBB)
• Sub-arachnoid haemorrhage
• Peaked T waves indicate hyperkalaemia

Hyperacute T waves
Wide QRS (LBBB)
Reciprocal Changes
Reciprocal Changes
• Changes occurring on the opposite side

of the myocardium that is infarcting
Reciprocal Changes
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
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 depression & T-wave inversion
Fibrosis ST returns to baseline, but T-wave

inversion persists
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:
30 Any R40 20
30 30 Any R50 30
30 Any 30
Any Q wave in V1
V2
V3
• Pathological Q waves refer to Q

waves that have a height of 25% or
more than that of the partner R wave
and/or have a width of greater than
0.04 seconds.
Memorize 300 - 150 - 100 - 75 - 60 - 50
QRS Complexes
• QRS 1-2.5 Axis
I II
• P > 2.5×2.5
+ + normal
• PR 3-5
+ - left axis deviation
• A QT > half of the RR

> 35, or
avL R > 13 mm
QRS > 0.12sec
Look at V1:
Pathological Q waves Terminal R = RBBB
(1)any Q wave in V1&V2&V3
(2) have a height of <25% partner R Terminal S = LBBB
(3) <0.04 seconds.
• Normal Q waves, when present,
represent depolarization of the
interventricular septum.
• For this reason, they are referred to as

septal Q waves, and can be
appreciated in the lateral leads I, aVL,
V5 and V6.
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
Lateral portion
Some leads get a of the heart
good view of the:
Anterior portion
of the heart
Inferior portion
of the heart
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 Lateral portion
again at this of the heart
picture of the heart.
Anterior 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 Leads I, aVL, and V5- V6
heart is best viewed?

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

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)!
Memorize 300 - 150 - 100 - 75 - 60 - 50
QRS Complexes
• QRS 1-2.5 Axis
I II
• P > 2.5×2.5
+ + normal
• PR 3-5

> 35, or
avL R > 13 mm
QRS > 0.12sec
Look at V1:
(3) <0.04 seconds.
Sinus Tachycardia
RATE**RHYTHM**AXIS**INTERVALS P
waves-
•Atrial Fibrillation
waves-
•Atrial Flutter
waves-
3rd Degree (Complete)
Heart Block
waves-
2nd Degree heart block
mobitz type I
waves-
2nd degree heart block
mobitz type II
waves-
Supra Ventricular Tachycardia
waves-
1st degree heart
block
waves-
Memorize 300 - 150 - 100 - 75 - 60 - 50
QRS Complexes
• QRS 1-2.5 Axis
I II
• P > 2.5×2.5
+ + normal
• PR 3-5

> 35, or
avL R > 13 mm
QRS > 0.12sec
Look at V1:
(3) <0.04 seconds.

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‫اللهم‬

– Find a R wave that lands on a bold line.

– Memorize the sequence:

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

• Are there P waves?

• Normal: 0.12 - 0.20 seconds.

Interpretation? 0.12 seconds

• Normal: 0.04 - 0.12 seconds.

Interpretation? 0.08 seconds

Arrhythmias can arise from problems in

QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

The SA Node can:

Sinus Tachycardia may be an appropriate

QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

Atrial cells can:

• fire continuously Atrial Flutter

QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

• Rate? 130 bpm

• Rate? 100 bpm

• Rate? 74 148 bpm

• Abnormal, congenital extra pathways

QRS 1-2.5 P > 2.5 ×2.5 PR 3-5

It should be clear that the PR interval will therefore be

• Rate? 160 bpm

• 1st Degree AV Block

QRS 1-2.5 QRS Complexes

PR 3-5 + - left axis deviation

PR interval 3-5 Boxes

< 0.12 s 0.12-0.20 s > 0.20 s

Wolff-Parkinson-White 1st Degree AV Block

Bundle branch block

Incomplete bundle branch block 3rd degree AV block with

QRS 1-2.5 QRS Complexes

Right ventricular hypertrophy

• QRS 1-2.5 QRS Complexes

RVH RAD, and V1 R wave > 7mm tall

When the conduction

QRS > 0.12sec

QRS > 0.12sec

• QRS 1-2.5 QRS Complexes

QRS > 0.12sec

• S-T segment elevation

• Represents myocardial injury

Downsloping ST segment depression:-

Upward sloping ST segment depression:-

• Peaked T waves indicate hyperkalaemia

• Changes occurring on the opposite side

Before injury Normal ECG

Ischemia ST depression, peaked T-waves,

B. Ischemia from coronary artery occlusion

C. Infarction from ongoing ischemia results in

D/E. Ongoing infarction with appearance of

F. Fibrosis (months later) with persistent Q-

Before injury Normal ECG

Ischemia ST depression & T-wave inversion

Infarction ST depression & T-wave inversion

Fibrosis ST returns to baseline, but T-wave

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 I

R40 A R wave > 40 msec in V1