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Electrocardiography

John Fowler, PhD


john.fowler@ttuhsc.edu
DOME and CPMB
School of Medicine
TTUHSC

Learning objectives
1. Describe the electrode conventions used to standardize ECG measurements.
Know the electrode placements and polarities for the 12-lead ECG and the
standard values for pen amplitude calibration and paper speed.
2. Name the parts of a typical bipolar (Lead II) ECG tracing and explain the
relationship between each of the waves, intervals, and segments in relation to
the electrical state of the heart.
3. Explain why the ECG record looks different in each of the 12 leads.
4. Define mean electrical axis of the heart and give the normal range. Determine
the mean electrical axis from knowledge of the magnitude of the QRS complex
in the standard frontal limb leads.
5. Describe the roles of altered automaticity, conduction block, and reentry in
arrhythmias. Explain the role of refractory period in preventing reentry.
6. Describe electrocardiographic changes associated respectively with myocardial
ischemia, injury and necrosis.

Fowler, ECG

Suggested Reading
ECG Interpretation made Incredibly Easy,
Lippincott
Dale Dubin, Rapid Interpretation of EKGs
Website:
http://www.themdsite.com
Costanzo, Physiology, 3rd ed., Ch. 4:
Cardiovascular Physiology, pp. 136-137.
Boron and Boulpaep, Medical Physiology, 2nd
ed., Ch. 21: Cardiac Electrophysiology and the
Electrocardiogram
Boron & Boulpaep: Medical Physiology, 2nd ed.
3

ECG Resources
ECG Learning Center
The Alan E. Lindsay ECG Learning Center
University of Utah School of Medicine:
http://ecg.utah.edu
An internet ECG library in the United Kingdom:
http://www.ecglibrary.com/ecghome.html
London Ambulance Service (unofficial)
Understanding the ECG (EKG):
http://www.lond.ambulance.freeuk.com/ecg/ECG.htm

Fowler, ECG

Electrocardiogram 12 lead ECG


The electrocardiogram (ECG or
EKG) measures bio-potentials that
originate from electrical activity in
cardiac muscle (myocardium).
Electric potentials consist of a
repeated sequence of characteristic
waveforms which correspond to a
heart beat.
+

12 Lead
ECG

II

aVR

V1

V4

aVL

V2

V5

The amplitudes of ECG potentials


depend on the amplitude and
orientation of electrical activity in
cardiac muscle with respect to each
recording electrode.

Fowler, ECG
III

aVF

6 frontal leads

V3

V6

6 precordial leads
5

Kinds of information provided by the ECG


The ECG:
Does NOT provide information on the actual mechanical
functioning of the heart.
CANNOT be used to assess cardiac output, blood pressure or
tissue perfusion.
The ECG DOES provide information on:
1. Rate
2. Disturbances of Rhythm and Conduction
3. Mean electrical axis (MEA)
e.g., the anatomical orientation of cardiac chambers.
e.g., the relative sizes of its chambers such as with
hypertrophy.
4. Infarction
The extent, location, and progression of ischemic damage to
myocardium.

Dubins Rapid Interpretation of EKGs, http://www.themdsite.com/

Lead II
use this lead for Rate and Rhythm

Fowler, ECG

How depolarization travels through the heart


(or, Where do ECG waves, intervals, segments and complex come from?)
normally, the QRS
is dominated by left
ventricular muscle
mass

Lead II

+
Right side

Left side

ST
segment
T wave

isoelectric
line

Q-T interval

ventricular muscle
action potential

~200 msec

Fowler, ECG

Waves, intervals, segments and complex


0.2 sec
10 mv
10 mv

Lead II

5 mm

complex

Range (s)

Events

PR interval

0.12 0.20

Atrial depolarization and conduction through AV node, Beginning of


P wave to beginning of QRS, useful for diagnosing heart blocks

PR segment

0.05 - 0.120

Flat baseline indicating transit through AV node, from end of P wave


to beginning of ventricular depolarization

J point

N/A

J point indicates end of QRS and beginning of ST segment, used to


measure the degree of ST elevation or depression

QRS complex

0.08 - 0.10

Ventricular depolarization and atrial repolarization

QT interval

0.40 - 0.43

Ventricular depolarization plus ventricular repolarization

ST segment

0.08 - 0.12

Represents the period when the ventricles are depolarized in


plateau phase
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Rate
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10

Calculating heart rate

each big box = 0.2 s


each small box = 0.04 s
start

Lead II

300
150
100
75
60

between 75 and
60 bpm

P P interval

1 second

R R interval

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Rhythms
12

Rhythms
Arrhythmic complications of acute
myocardial infarction (AMI):
About 90% of patients who have an AMI
develop some form of cardiac arrhythmia.
The clinician must be aware of these
arrhythmias and must treat those that
require intervention to avoid exacerbation
of ischemia and subsequent
hemodynamic compromise.

medicine.medscape.com/article/164924-overview#aw2aab6b3

13

ECG strips to recognize


Sinus rhythms
Sinus Arrhythmia
Sinus Bradycardia
Sinus Tachycardia
Sinus arrest or pause
Nonsinus atrial rhythm
Premature atrial contraction (PAC)
Wandering pacemaker
Atrial tachycardia
Atrial flutter
Atrial fibrillation
Junctional arrhythmia
Wolff-Parkinson-White syndrome (WPW)
Premature junctional contraction (PJC)
Junctional escape rhythm
Ventricular arrhythmias
Premature ventricular contraction (PVC)
Idioventricular rhythm
Ventricular tachycardia

Fowler, ECG

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Sinus rhythms

Sinus Rhythm: origin in SA node

Sinus rhythm

300 150 100 75 60 50

300 150 100 75 60 50

http://www.bem.fi/book/Fowler, ECG

60 to 100 bpm

Sinus tachycardia

> 100 bpm

Sinus bradycardia

< 60 bpm

occurs with increased vagal


tone

physiological response to
physical exercise or stress, but
may also result from congestive
heart failure
15

Sinus arrhythmia

This arrhythmia is so common


in young people that it is not
considered heart disease.
One origin for the sinus
arrhythmia may be the vagus
nerve which mediates
respiration as well as heart
rhythm.
The nerve is active during
respiration and, through its
effect on the sinus node,
causes an increase in heart
rate during inspiration and a
decrease during expiration.

http://www.bem.fi/book/19/19.htm

The effect is particularly


pronounced in children.
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Nonsinus atrial rhythm wandering pacemaker


Occurs when multiple
areas (ectopic foci)
within the atrium generate
consecutive action
potentials that are all
conducted to the
ventricles.
Irregular rhythm
Rate < 100bpm
If Rate > 100 bpm then it
is called Multifocal Atrial
Tachycardia (MAT)
The origin of the atrial
contraction may also vary
or wander. Consequently,
the P-waves will vary in
polarity, and the PRinterval will also vary.

http://www.bem.fi/book/19/19.htm

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Nonsinus atrial rhythm


Paroxysmal atrial tachycardia (PAT)
Circus movement reentry - when the Pwaves are a result of a reentrant activation in
the atria.
Abnormal P-waves difficult to see.
Rate between 160 and 220/min.
The P-wave is regularly followed by a normal
QRS-complex.
The isoelectric baseline is apparent between
T and next P-wave.
Atrial flutter
The isoelectric interval between the end of T
and beginning of P disappears.
Origin is circus reentrant atrial pathway.
Rate between 220 and 300/min.
The AV-node and, thereafter, the ventricles
are generally activated by every second or
every third atrial impulse (2:1 or 3:1 heart
block).

http://www.bem.fi/book/19/19.htm

Fowler, ECG

Atrial fibrillation
Activation in the atria is fully irregular and
chaotic, producing irregular fluctuations in
the baseline.
A consequence is that the ventricular rate is
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rapid and irregular, though the QRS contour

Junctional arrhythmia

inverted P wave

narrow QRS

Arising from the atrioventricular (AV) junction as an automatic


tachycardia or as an escape mechanism during periods of significant
bradycardia with rates slower than the intrinsic junctional pacemaker.
Rate: 40-60 bpm (intrinsic junctional pacemaker)
Rhythm: Regular
P Wave: Inverted, absent or after QRS
PR interval <.12 seconds
QRS <.12 seconds
19

Ventricular arrhythmias
Ventricular tachycardia
Activation of the ventricular muscle at a
high rate (over 120/min)
AV dissociation
Bizarre and wide QRS-complexes
Ventricular automaticity limit overcome
by multiple foci.
Often a consequence of ischemia and
myocardial infarction.

Ventricular fibrillation
Coarse irregular undulations without
QRS-complexes.
Cause of fibrillation is the establishment
of multiple reentry loops usually
involving diseased heart muscle.
The contraction of the ventricular muscle
is irregular and is ineffective at pumping
blood. The lack of blood circulation
leads to almost immediate loss of
consciousness and death within
minutes.
Fibrillation progresses to Asystole
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Ventricular arrhythmias Torsade de pointes

Polymorphic ventricular
tachycardia with a
characteristic illusion of
a twisting of the QRS
complex around the
isoelectric baseline.
Hemodynamically
unstable and causes a
sudden drop in arterial
blood pressure, leading
to dizziness and
syncope.

Fowler, ECG

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Premature ventricular contraction (PVC)

Caused by an ectopic cardiac pacemaker located in the ventricle


Also called ventricular premature beat (VPB) or extrasystole
QRS-complex has a very abnormal form and lasts longer than 0.1 s.

Fowler, ECG

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Disorders of activation sequence

Coming up:
Conduction block and Reentrant excitation
Sinus Arrest (aka sinus pause) resulting in Escape rhythms
Atrioventricular (AV) conduction blocks
Wolf-Parkinson-White syndrome (WPW)

Fowler, ECG

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Reentry
Reentry (bottom panel) can occur if branch 2,
for example, has a unidirectional block.
In such a block, impulses can travel
retrograde (from branch 3 into branch 2) but
not orthograde.
An action potential will travel down the branch
1, into the common distal path (branch 3),
and then travel retrograde through the
unidirectional block in branch 2 (blue line).
Within the block (gray area), the conduction
velocity is reduced because of depolarization.
When the action potential exits the block, if it
finds the tissue excitable, then the action
potential will continue by traveling down (i.e.,
reenter) the branch 1

http://cvphysiology.com/Arrhythmias/A008c.htm
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Sinus Arrest (aka sinus pause) resulting in Escape rhythms

Escape rhythm is determined


by automaticity of ectopic
focus.
Atrial escape rhythm
rate: 60-100 bpm

Junctional escape rhythm


rate: 40-60 bpm

Ventricular escape rhythm


rate: 15-40 bpm

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Atrioventricular (AV) conduction blocks


10 AV block
When the P-wave always
precedes the QRS-complex and
PR-interval > 0.2 s.
20 AV block
Mobitz Type I (Wenckebach) PR interval progressively
increases until failure of
conduction occurs.
Mobitz Type II PR interval
remains fairly constant until
conduction fails.
30 AV block or complete hear
block
No relationship between the Pwave and the QRS-complex.
Note there are two rates.

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Wolff-Parkinson-White (WPW) syndrome

The accessory
pathway, Kent bundle,
is an abnormal "bridge"
of tissue that allows the
heart's electrical
impulse to bypass the
AV node and to travel
in a circular pattern
from the ventricles to
the atria.
Delta wave is a
slurring and slow rise of
the initial upstroke of
QRS complex.

http://www.mayoclinic.org/wolff-parkinson-white/enlargeimage2572.html

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Q&A

What does strip show?


a) sinus arrhythmia
b) sinus bradycardia
c) sinus tachycardia
d) atrial fibrillation
e) atrial flutter
Fowler, ECG
http://afib.utorontoeit.com/clinicalevaluation.html

28

Mean Electrical Axis


(MEA)

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Mean Electrical Axis (MEA)


The MEA tells us the net direction the
depolarization or repolarization is
heading.
When the atria (or ventricles) undergo
depolarization, the wave of
depolarization that spreads across the
muscle mass occurs in many different
directions simultaneously.
If a snapshot of electrical activity could
be taken at a given instant, each
individual wave of depolarization can
be represented as a vector.
The mean electrical axis (MEA)
represents the sum of all of the
individual vectors at a given instant in
time.
Einthovens triangle is an equilateral
triangle, with heart at the center, used
to determine the MEA.
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http://www.cvphysiology.com/Arrhythmias/A015.htm

Mean Electrical Axis (MEA)

Calculation of the MEA requires some


additional background associated with
the leads of the electrocardiogram:
Rules of the ECG
Frontal hexaxial reference system
(6 lead ECG)
Four-quadrant method of
determining MEA

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Rules of the ECG

Wave of depolarization traveling towards


a positive electrode = an upward
deflection on the ECG.
direction depolarization

Wave of depolarization traveling away


from a positive electrode = a downward
deflection on the ECG
Wave of depolarization traveling
perpendicular to a positive electrode line
= biphasic wave.

direction repolarization

repolarization wave

Wave of repolarization traveling away


from a positive electrode = an upward
deflection on the ECG
Wave of repolarization traveling towards
a positive electrode = a downward
deflection.

depolarization wave

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Frontal hexaxial reference system (6 lead ECG)


Lead II

Lead I

Lead III

R
major direction of
ventricular
depolarization
Right
aVR

+
Left
aVL

aVF

+
+
+
Leads I, II, III are bipolar limb leads
aVR, aVL and aVF are augmented unipolar limb leads

33

Frontal hexaxial reference system (6 lead ECG)

+
+

+
+

The hexaxial reference system is diagram based on the first six (frontal) leads of
the 12 lead ECG.
It is used to help determine the heart's mean electrical axis in the frontal plane.

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Four-quadrant method of determining MEA using Lead I and aVF

+
Normal range ~ -30 to +90
0

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Ventricular hypertrophy
LVH = Left axis deviation

RVH = Right axis deviation

Right

Left

+I
+ aVF

LVH

RVH
36

12 lead ECG - adding the 6 precordial leads


Interventricular
septum

Anterior surface of heart: V1 - V4

V6

RV

LV

V1

V3

V2

V4

V5

Lateral surface of heart: V5 - V6


Right anterior

12 lead ECG adds 6


precordial chest leads.
The six precordial leads
record the bio-electric
potentials in a cross sectional
plane.
Left lateral

Note R wave
progression through V1
- V6
37

Fowler, ECG

Bundle Branch Blocks

rabbit
ears of
RBBB

Delay in right ventricle activation


A helpful hint for recalling an RBBB
is rabbit ears. The QRS complex
can resemble rabbit ears in V1 and
V2. There are two peaks of the R

Delay in left ventricle


activation
38

Summary of QRS amplitudes in 12 lead ECG


Lead I

aVR

V1

V4

Lead 2

aVL

V2

V5

Lead 3

aVF

V3

V6

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Myocardial Infarction
Myocardial infarction (MI) or acute
myocardial infarction (AMI), commonly
known as a heart attack, results from the
partial interruption of blood supply to a
part of the heart.
Most commonly due to occlusion
(blockage) of a coronary artery following
the rupture of a vulnerable
atherosclerotic plaque.

Fowler, ECG

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An heart attack evolves over time and


space
Tombstone
ST elevation

Classic ECG signs are:


1. T-wave inversion
occurs at onset
indicates myocardial ischemia
reversible
2. Elevated ST segment
indicates myocardial injury
reversible
3 Large Q wave
occurs after hours to days
indicates irreversible death (necrosis)

Fowler, ECG

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Typically, ECG changes are confined to the leads that 'face'


the infarction

Major cardiac territories and their


corresponding coronary artery supply
Location

ECG changes

Coronary artery

Anterior

V2-V4

Left main coronary


artery or LAD (widow
maker)

Inferior

II, III, aVF

Right coronary,
circumflex

Lateral

I, aVL, V5-V6

Circumflex, diagonal

Blueprints Clinical Cases in Emergency Medicine

Later
al
wall

Anterio
r wall

Inferi
or
wall
http://www.madsci.com/manu/ekg_mi.htm

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http://www.med.umich.edu/lrc/baliga/case01/03A-T.html

Electrocardiography - Key concepts


1. The 12 lead ECG is composed of I, II, III, avR, aVL, aVF and precordial leads V 1 V6.
2. Each of these leads has a different view of cardiac bio-potentials as described by the
Rules of the ECG.
3. The ECG is a repeated sequence of waves, segments and intervals that reflect the
myocardial electrical state during each heart beat.
4. The mean electrical axis (MEA) tells us the net direction of depolarization or
repolarization through myocardium. A mean electrical axis can be calculated from
any ECG waveform but is most often done with the QRS where shifts in the axis can
indicate pathological changes in the relative thickness of ventricular muscle masses.
5. In general, arrhythmias can arise from one of 4 mechanisms: abnormal SA
pacemaker function, ectopic focus (originating from some point other than the SA
node), conduction system blocks, and abnormal conduction pathways.
6. Classic ECG signs of a heart attack are: inverted T wave indicating myocardial
ischemia and occurring at onset; elevated ST segment indicating myocardial injury,
and a large Q wave indicating irreversible death (necrosis), occurring within hours to
days.

Fowler, ECG

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THE
END
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