Introduction to Electrocardiogram (ECG) Basics

 To recognize the normal rhythm of the heart -
“Normal Sinus Rhythm.”
 To recognize the 17 most common rhythm
disturbances (3-Lead)
 To be shown an acute myocardial infarction
on a 12-Lead ECG.
2

 ECG Basics
 How to Analyze a Rhythm
 Normal Sinus Rhythm
 Heart Arrhythmias
 Diagnosing a Myocardial Infarction
 Advanced 12-Lead Interpretation
3

Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
4

Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
5

 In the heart, this electrical
activity is referred to
as depolarisation.The
contraction causes the blood to
be pumped around the body.
Contracted chambers within the
heart are termed systolic.
 Relaxation of the heart muscle is
caused by
electrical repolarisation.
Relaxed chambers within the
heart are termed diastolic.
6

 The normal resting rate
of self-excitation of
the sinus node is about 75
times per minute in
adults.
 Since this rate is faster
than that of other cardiac
muscle fibres, the sinus
node is called
the pacemaker.
7

Atrial Depolarisation
 The conduction continues to
travel in a wave both
downwards and leftwards,
through both atria,
depolarising each cell in turn
and causing the atria to
contract. It is this
depolarisation that can be
seen as the P wave on the ECG.
8

Atrioventricular Nodal Depolarisation
 Eventually this conduction of
depolarisation meets the atrioventricular
node near the centre of the heart. It is
the atrioventricular node that is the main
cause of delay in conducting the impulse
from the atria to the ventricles.
 This delay allows the atria to fill
the ventricles with blood before they
contract.
 As the atrioventricular node is small, no
depolarisation voltage is recorded and an
isoelectric PR segment is seen on the ECG.
9

Septal Depolarisation
 The depolarisation travels down the
septum and along the bundle of His, before
splitting to follow the left and right bundle
branches. It continues onward to the
conduction myofibres which distribute the
action potential and thus depolarise the
muscle cells of the ventricles.
 As the left bundle branch is activated first,
the depolarisation proceeds from left to
right and may give rise to a small negative
deflection within the ECG, referred to as
the Q wave. At the same time
the atria and sinus node start to repolarise
and relax.
10

EarlyVentricular Depolarisation
 The wave of depolarisation continues
down the septum and into the
ventricular wall. Since the mass of the
left ventricular wall is significantly
greater than the right, the mean vector
of depolarisation of the ventricular wall
is to the left.
 The depolarisation takes place quickly,
causing ventricular contraction, and is
seen as the R wave on the
ECG. Atrial, atrioventricular nodal, and
bundle of His relaxation continues.
11

LateVentricular Depolarisation
 The rim of the ventricular
muscle is the last to contract.
The direction of depolarisation
leads to the S wave on the ECG.
12

Ventricular Systole
 After the contraction
of the ventricles,
there is an
isoelectric ST
segment on the ECG
that corresponds to
the plateau of the
action potential of all
fibres.
13

Ventricular Repolarisation
 Repolarisation is the
return of the membrane
potential to the baseline
and relaxation of the
muscle.This gives a
deflection on the ECG in
the same direction as
depolarisation because
both polarity and direction
are negated — theT wave.
14

Atrial andVentricular Relaxation
 When the heart has completely
repolarised, the chambers are
relaxed and there is no electrical
activity until the sinus
node triggers the start of the next
heartbeat.
15

 P wave - Atrial
depolarization
17
• T wave - Ventricular
repolarization
• QRS - Ventricular
depolarization

Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for
the atria to contract
before the ventricles
contract)
18

 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.
20

 Horizontally
 One small box - 0.04 s
 One large box - 0.20 s
 Vertically
 One large box - 0.5 mV
27

ReallyVery Easy
How to Analyze a Rhythm

 Step 1: Calculate rate.
 Step 2: Determine regularity.
 Step 3: Assess the P waves.
 Step 4: Determine PR interval.
 Step 5: DetermineQRS duration.
29

 Option 1
 Count the # of R waves in a 6 second rhythm strip,
then multiply by 10.
Interpretation?
30
9 x 10 = 90 bpm
3 sec 3 sec

 Option 2
 Find a R wave that lands on a bold line.
 Count the number 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)
31
R wave

 Option 2 (cont)
 Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50
Interpretation?
32
3
0
0
1
5
0
1
0
0
7
5
6
0
5
0
Approx. 1 box less than
100 = 95 bpm

 COUNTTHE NUMBER OF BOXES BETWEEN
2 COSECUTIVE RWAVES AND DIVIDE 300 BY
THAT NUMBER
 WHATTO DO IF ITS IRREGULAR?
33

 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?
38
Regular
R R

Rhythm Irregular
Rate
Very fast (> 350 bpm) for Atrial, but ventricular
rate may be slow, normal or fast
P Wave Absent - erratic waves are present
PR Interval Absent
QRS
Normal but may be widened if there are
conduction delays
42
•EKG Quick Reference Guide

 Only one fast conducting foci compared to
atrial fibrillation
 Rough looking (saw tooth)waves
43

 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?
45
Normal P waves with 1 P
wave for every QRS

 Normal: 0.12 - 0.20 seconds.
(3 - 5 boxes)
Interpretation?
46
0.12 seconds

 Normal: 0.04 - 0.12 seconds.
(1 - 3 boxes)
Interpretation?
47
0.08 seconds

 Rate 90-95 bpm
 Regularity regular
 P waves normal
 PR interval 0.12 s
 QRS duration 0.08 s
Interpretation?
48
Normal Sinus Rhythm

 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
49

Arrhythmias can arise from problems in
the:
• Sinus node
• Atrial cells
• AV junction
• Ventricular cells
50

The SA Node can:
 fire too slow
 fire too fast
Sinus Bradycardia
SinusTachycardia*
51
*Sinus Tachycardia may be an appropriate response to stress.

Atrial cells can:
 fire occasionally
from a focus
 fire continuously
due to a looping re-
entrant circuit
Premature Atrial
Contractions (PACs)
Atrial Flutter
52

53
Atrial cells can also:
• fire continuously
from multiple foci
or
fire continuously
due to multiple
micro re-entrant
“wavelets”
Atrial Fibrillation
Atrial Fibrillation

54
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

The AV junction can:
 fire continuously due
to a looping re-
entrant circuit
 block impulses
coming from the SA
Node
Paroxysmal
Supraventricular
Tachycardia
AV Junctional Blocks
55

Ventricular cells can:
 fire occasionally from
1 or more foci
 fire continuously
from multiple foci
 fire continuously due
to a looping re-
entrant circuit
PrematureVentricular
Contractions (PVCs)
Ventricular Fibrillation
VentricularTachycardia
56

 Sinus Rhythms
 Premature Beats
 Supraventricular Arrhythmias
 Ventricular Arrhythmias
 AV Junctional Blocks
57

 Sinus Bradycardia
 SinusTachycardia
 Sinus Arrest
 Normal Sinus Rhythm
58

59
30 bpm• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia

 Deviation from NSR
- Rate < 60 bpm
60

 Etiology: SA node is depolarizing slower
than normal, impulse is conducted
normally (i.e. normal PR and QRS
interval).
61

62
130 bpm• Rate?
normal
0.08 s
• P waves?
• QRS duration?
Interpretation? Sinus Tachycardia

- Rate > 100 bpm
63

 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.
64

 Etiology: SA node fails to depolarize and no
compensatory mechanisms take over
 Sinus arrest is usually a transient pause in sinus node
activity
65

 Premature Atrial Contractions
(PACs)
 PrematureVentricular Contractions (PVCs)
66

67
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

 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.
68

 Etiology: Excitation of an atrial cell
forms an impulse that is then conducted
normally through the AV node and
ventricles.
69

 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).
70

71
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

 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”.
72

 Etiology: One or more ventricular cells
are depolarizing and the impulses are
abnormally conducting through the
ventricles.
73

 When an impulse originates in a
ventricle, conduction through the
ventricles will be inefficient and the QRS
will be wide and bizarre.
74

75
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles

 Atrial Fibrillation
 Atrial Flutter
 Paroxysmal SupraVentricularTachycardia
(PSVT)
76

77
100 bpm• Rate?
• Regularity? irregularly irregular
none
0.06 s
• P waves?
• PR interval? none
• QRS duration?
Interpretation? 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
78

 Etiology: due to multiple re-entrant wavelets
conducted between the R & L atria and the
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).
79

80
70 bpm• Rate?
flutter waves
0.06 s
• P waves?
• QRS duration?
Interpretation? 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).
81

 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).
82

83
74 148 bpm• Rate?
• Regularity? Regular  regular
Normal  none
0.08 s
• P waves?
• PR interval? 0.16 s  none
• QRS duration?
Interpretation?
Paroxysmal Supraventricular Tachycardia
(PSVT)

 The heart rate suddenly speeds up, often
triggered by a PAC (not seen here) and the P
waves are lost.
84

 NORMALAXIS : BETWEEN -30TO +90
 LEFTAXIS DEVIATION: LESSTHAN 30
 RIGHT AXIS DEVIATION: MORETHAN 90
86

LEAD I LEADAVF QUADRANT AXIS
Positive Positive Left lower quadrant Normal (0 to +90 degrees)
Positive Negative Left upper quadrant Possible LAD (0 to -90 degrees)
Negative Positive Right lower quadrant RAD (+90 to 180 degrees)
Negative Negative Right upper quadrant ExtremeAxis Deviation (-90 to 180 degrees)
87

 1st Degree AV Block
 2nd Degree AV Block,Type I
 2nd Degree AV Block,Type II
 3rd Degree AV Block
91

 The electrical impulses are slowed as they pass through the conduction
system, but they all successfully reach the ventricles. First-degree heart
block rarely causes symptoms or problems.Well-trained athletes may
have first-degree heart block. Medications can also cause this condition.
No treatment is generally needed for first-degree heart block.
 PR interval greater than 0.20sec.
93

 The electrical impulses are delayed further and further with
each heartbeat until a beat fails to reach to the ventricles
entirely. It sometimes causes dizziness and/or other
symptoms. People with normal conduction systems may
sometimes have type 1 second degree heart block when they
sleep.
 Type 1 (aka Mobitz 1,Wenckebach): Progressive
prolongation of PR interval with dropped beats (the PR
interval gets longer and longer; finally one beat drops) .
96

PR interval remains unchanged prior to the P wave which
suddenly fails to conduct to the ventricles.
97

 Usually see complete AV dissociation because the
atria and ventricles are each controlled by separate
pacemakers.
 none of the electrical impulses from the atria reach the ventricles.
When the ventricles (lower chambers) do not receive electrical impulses
from the atria (upper chambers), they may generate some impulses on
their own, called junctional or ventricular escape beats.Ventricular
escape beats, the heart’s naturally occurring backups, are usually very
slow. Patients frequently feel poorly in complete heart block, with light
headedness and fatigue
100

103
60 bpm• Rate?
normal
0.08 s
• P waves?
• QRS duration?
Interpretation? 1st Degree AV Block

 PR Interval > 0.20 s
104

 Etiology: Prolonged conduction delay in
the AV node or Bundle of His.
105

106
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

 PR interval progressively lengthens, then the
impulse is completely blocked (P wave not
followed by QRS).
107

 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.
108

109
40 bpm• Rate?
nl, 2 of 3 no QRS
0.08 s
• P waves?
• QRS duration?
Interpretation? 2nd Degree AV Block, Type II

 Occasional P waves are completely blocked (P
wave not followed by QRS).
110

111
40 bpm• Rate?
no relation to QRS
wide (> 0.12 s)
• P waves?
• QRS duration?
Interpretation? 3rd Degree AV Block

 The P waves are completely blocked in theAV
junction; QRS complexes originate
independently from below the junction.
112

 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.
113

 In RBBB, activation of the right ventricle is delayed as depolarisation has to
spread across the septum from the left ventricle.
 The left ventricle is activated normally, meaning that the early part of the QRS
complex is unchanged.
 The delayed right ventricular activation produces a secondary R wave (R’) in the
right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads.
 Delayed activation of the right ventricle also gives rise to secondary
repolarization abnormalities, with ST depression andT wave inversion in the right
precordial leads.
 In isolated RBBB the cardiac axis is unchanged, as left ventricular activation
proceeds normally via the left bundle branch.
114

ECG CRITERIA
 Broad QRS > 120 ms
 RSR’ pattern inV1-3 (‘M-shaped’QRS
complex)
 Wide, slurred S wave in the lateral leads (I,
aVL,V5-6)
115

 Normally the septum is activated from left to right, producing small Q waves in
the lateral leads.
 In LBBB, the normal direction of septal depolarisation is reversed (becomes right
to left), as the impulse spreads first to the RV via the right bundle branch and
then to the LV via the septum.
 This sequence of activation extends the QRS duration to > 120 ms and eliminates
the normal septal Q waves in the lateral leads.
 The overall direction of depolarisation (from right to left) produces tall R waves in
the lateral leads (I,V5-6) and deep S waves in the right precordial leads (V1-3),
and usually leads to left axis deviation.
 As the ventricles are activated sequentially (right, then left) rather than
simultaneously, this produces a broad or notched (‘M’-shaped) R wave in the
lateral leads.
117

 QRS duration of > 120 ms
 Dominant S wave inV1
 Broad monophasic R wave in lateral leads (I,
aVL,V5-V6)
 Absence of Q waves in lateral leads (I,V5-V6;
small Q waves are still allowed in aVL)
 Prolonged R wave peak time > 60ms in left
precordial leads (V5-6)
118

 Rhythm: irregular-coarse or fine, wave form varies in size and shape
 Fires continuously from multiple foci
 No organized electrical activity
 No cardiac output
 Causes: MI, ischemia, untreatedVT, underlying CAD, acid base
imbalance, electrolyte imbalance, hypothermia,
121

 Ventricular cells fire continuously due to a looping re-entrant circuit
 Rate usually regular, 100 - 250 bpm
 P wave: may be absent, inverted or retrograde
 QRS: complexes bizarre, > .12
 Rhythm: usually regular
123

 Ventricular standstill, no electrical activity, no cardiac output – no pulse!
 Cardiac arrest, may followVF or PEA
 Remember! No defibrillation with Asystole
 Rate: absent due to absence of ventricular activity. Occasional P wave
may be identified.
125

 Escape rhythm (safety mechanism) to prevent ventricular standstill
 HIS/purkinje system takes over as the heart’s pacemaker
 Treatment: pacing
 Rhythm: regular
 Rate: 20-40 bpm
 P wave: absent
 QRS: > .12 seconds (wide and bizarre)
126

To diagnose a myocardial infarction you need
to go beyond looking at a rhythm strip and
obtain a 12-Lead ECG.
130
Rhythm
Strip

 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.
131

The 12-leads include:
132
–3 Limb leads
(I, II, III)
–3 Augmented leads
(aVR, aVL, aVF)
–6 Precordial leads
(V1- V6)

Some leads get a
good view of the:
133
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart

One way to
diagnose an
acute MI is to
look for
elevation of
the ST
segment.
134

Elevation of the ST
segment (greater
than 1 small box) in
2 leads is
consistent with a
myocardial
infarction.
135

The anterior portion of the heart is best
viewed using leadsV1-V4.
136

If you see changes in leadsV1 -V4 that are
consistent with a myocardial infarction, you
can conclude that it is an anterior wall
myocardial infarction.
137

Do you think this person is having a myocardial
infarction. If so, where?
138

Yes, this person is having an acute anterior wall
myocardial infarction.
139

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.
140

Some leads get a
good view of the:
141
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart

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.
142
Limb Leads Augmented Leads Precordial Leads

Now, using these 3 diagrams let’s figure where to look for a
lateral wall and inferior wall MI.
143

Remember the anterior portion of the heart is best viewed
using leadsV1-V4.
144

So what leads do you think the
lateral portion of the heart is best
viewed?
145
Leads I, aVL, and V5- V6

Now how about the inferior
portion of the heart?
146
Leads II, III and aVF

Now, where do you think this person is having
a myocardial infarction?
147

This is an inferior MI. Note the ST elevation in
leads II, III and aVF.
148

This person’s MI involves both the anterior wall (V2-V4) and
the lateral wall (V5-V6, I, and aVL)!
150

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). 5-step approach:
1. Calculate RATE
2. Determine RHYTHM
3. Determine p wave, QRS AXIS, t wave
4. Calculate INTERVALS
5. Look for evidence of INFARCTION
151

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152

Good Luck with your education
153

Introduction to Electrocardiogram (ECG) Basics

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