Pocket ECG.pdf

Most beautiful book

2. Pocket ECGs
Bruce Shade, EMT-P, EMS-I, AAS
A Quick Information Guide
Boston Burr Ridge, IL Dubuque, IA New York San Francisco St. Louis
Bangkok Bogotá Caracas Kuala Lumpur Lisbon London Madrid Mexico City
Milan Montreal New Delhi Santiago Seoul Singapore Sydney Taipei Toronto
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3. POCKET ECGS: A QUICK INFORMATION GUIDE
Published by McGraw-Hill, a business unit of The McGraw-Hill Companies, Inc., 1221 Avenue of the Americas, New York, NY 10020. Copyright
© 2008 by The McGraw-Hill Companies, Inc. All rights reserved. No part of this publication may be reproduced or distributed in any form or by
any means, or stored in a database or retrieval system, without the prior written consent of The McGraw-Hill Companies, Inc., including, but not
limited to, in any network or other electronic storage or transmission, or broadcast for distance learning.
Some ancillaries, including electronic and print components, may not be available to customers outside the United States.
This book is printed on acid-free paper. 1 2 3 4 5 6 7 8 9 0 EUS/EUS 0 9 8 7 6 ISBN 978–0–07–351976–0
MHID 0–07–351976–6
Library of Congress Control Number: 2006931518
www.mhhe.com
Publisher, Career Education: David T. Culverwell
Senior Sponsoring Editor: Claire Merrick
Director of Development: Kristine Tibbetts
Developmental Editor: Michelle L. Zeal
Senior Marketing Manager: Lisa Nicks
Senior Project Manager: Sheila M. Frank
Senior Production Supervisor: Kara Kudronowicz
Senior Coordinator of Freelance Design: Michelle D. Whitaker
(USE) Cover Image: © Tarhill Photos, Inc./CORBIS
Compositor: Electronic Publishing Services Inc., NYC
Ty peface: 11.5/12 Minion
Printer: Quebecor World Eusey, MA
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4. iii
This book is dedicated to my wife Cheri, my daughter Katherine, and my son Christopher. Their love
and support gave me the strength to carry this good idea from concept to a handy pocket guide.
Bruce Shade
Dedication
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5. Preface
This book, as its title implies, is meant to serve as a
portable, easy to view, quick reference pocket guide. At
your fingertips you have immediate access to the key
characteristics associated with the various dysrhyth-
mias and cardiac conditions. Essential (what you need
to know) information is laid out in visually attractive
color-coded pages making it easy to find the informa-
tion for which you are looking. This allows you to
quickly identify ECG tracings you see in the field or the
clinical setting. It is also a useful tool in the classroom
for quickly looking up key information. Small and
compact, it can be easily carried in a pocket.
Chapter 1 provides a short introduction regard-
ing the location of the heart and lead placement.
Chapter 2 briefly describes the nine-step process for
interpreting the various waveforms and normal and
abnormal features found on ECG tracings. It visually
demonstrates how to calculate the heart rate, identify
irregularities, and identify and measure the various
waveforms, intervals and segments. Key values for each
waveform, interval, and segment are listed. Chapters 3
through 7 lead you through dysrhythmias of the sinus
node, the atria, the AV junction, the ventricles, and
AV heart block. Characteristics for each dysrhythmia
are listed in simple to view tables. Sample tracings
include figures of the heart that illustrate where each
dysrhythmia originates and how it occurs. This helps
you understand the ECG dysrhythmia rather than just
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6. v
memorize strips. Chapter 8 introduces the concept of
electrical axis. Chapters 9 and 10 introduce concepts
important to 12-lead ECG interpretation and recog-
nizing hypertrophy, bundle branch block, preexcita-
tion and myocardial injury, ischemia, and infarction.
Finally, Chapter 11 discusses other cardiac conditions
and their effects on the ECG.
We hope this learning program is beneficial to
both students and instructors. Greater understanding
of ECG interpretation can only lead to better patient
care everywhere.
Acknowledgments
I would first like to thank Lisa Nicks, Senior Marketing
Manager, and the sales force at McGraw-Hill who
came to Claire Merrick, our Sponsoring Editor and
said the readers were clamoring for a simple to use tool
to go along with our Fast & Easy ECGs textbook. Claire
was quick to put the book on the front burner and
get the project underway. I would like to thank Dave
Culverwell, Publisher at McGraw-Hill. Dave embraced
the idea of this book with great enthusiasm and lent his
support and guidance. I would like to thank Michelle
Zeal, the project’s Developmental Editor. Michelle
did a great job keeping things on track but yet did it
in such a way that she didn’t add a lot of stress to an
already stressful process. Her hard work on the book
shaped its wonderful look and style as well as helped
ensure the accuracy of the content. This book, because
of its dynamic, simplistic, visual approach, required
significant expertise on the part of our production
project manager, Sheila Frank. She helped condense a
wealth of text and figures into a small compact pocket
guide that maintains the warm, stimulating tapestry of
its parent textbook, Fast & Easy ECGs.
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7. Publisher’s Acknowledgments
Rosana Darang, MD
Medical Professional Institute, Malden, MA
Carol J. Lundrigan, PhD, APRN, BC
North Carolina A&T State University, Greensboro, NC
Rita F. Waller
Augusta Technical College, Augusta, GA
Robert W. Emery
Philadelphia University, Philadelphia, PA
Gary R. Sharp, PA-C, M.P.H.
University of Oklahoma, Oklahoma City, OK
Lyndal M. Curry, MA, NREMT-P
University of South Alabama, Mobile, AL
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8. The Electrocardiogram
1
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9. Chapter 1 The Electrocardiogram 2
What is in this chapter
The ECG
∞
The normal ECG
The heart
Conduction system
∞
Waveform direction
ECG paper
ECG leads—I, II, III
Augmented limb leads—aV
R,
aV
L, and aV
F
Precordial (chest) leads—V
1, V
2,
V
3, V
4, V
5, and V
6
Modified chest leads (MCL)
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10. Chapter 1 The Electrocardiogram 3
The ECG
Identifies irregularities in heart
rhythm.
Reveals injury, death, or other
physical changes in heart
muscle.
Used as an assessment and
diagnostic tool in prehospital,
hospital, and other clinical
settings.
Can provide continuous
monitoring of heart’s electrical
activity.
Figure 1-1
The electrocardiograph is the device that detects, measures, and records the ECG.
ECG tracing
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11. Chapter 1 The Electrocardiogram 4
Figure 1-2
The electrocardiogram is the tracing or graphic representation of the heart’s electrical activity.
The normal ECG
Upright, round P waves occurring at regular intervals at a rate of 60 to 100 beats per minute.
PR interval of normal duration (0.12 to 0.20 seconds) followed by a QRS complex of normal upright
contour, duration (0.06 to 0.12 seconds), and configuration.
Flat ST segment followed by an upright, slightly asymmetrical T wave.
T T T
QRS QRS QRS
PPP
QRS
T T
T T
QRS
QRS QRS
PP PP
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12. Chapter 1 The Electrocardiogram 5
The heart
About the same size as its
owner’s closed fist.
Located between the two
lungs in mediastinum behind
the sternum.
Lies on the diaphragm in front
of the trachea, esophagus, and
thoracic vertebrae.
About two thirds of it is situ-
ated in the left side of the chest
cavity.
2nd rib
Sternum
Base of the
heart
Diaphragm
5th rib
Apex of the
heart
A
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13. Chapter 1 The Electrocardiogram 6
Has a front-to-back (anterior-
posterior) orientation.
∞
Its base is directed posteriorly
and slightly superiorly at the
level of the second intercostal
space.
∞
Its apex is directed anteriorly
and slightly inferiorly at the level
of the fifth intercostal space in
the left midclavicular line.
∞
In this position the right ven-
tricle is closer to the front of the
left chest, while the left ventricle
is closer to the left side of the
chest. Knowing the position and orientation of the heart will help you to
understand why certain ECG waveforms appear as they do when the
electrical impulse moves toward a positive or negative electrode.
Left ventricle
Lungs
Base of
the heart
Thoracic
vertebra
Sternum Right ventricle
Apex of
the heart
Posterior
AnteriorB
Figure 1-3
(a) Position of the heart in the chest.
(b) Cross section of the thorax at the level of the heart.
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14. Chapter 1 The Electrocardiogram 7
Conduction
system
Sinoatrial (SA) node initiates the
heartbeat.
Impulse then spreads across the right
and left atrium.
Atrioventricular (AV) node carries the
impulse from the atria to the ventricles.
From the AV node the impulse is carried
through the bundle of His, which then
divides into the right and left bundle
branches.
The right and left bundle branches
spread across the ventricles and even-
tually terminate in the Purkinje fibers.
1
2
4
3
Left atrium
Left ventricle
Apex
Bundle
of His
Atrioventricular
node
Sinoatrial
node
Left and right
bundle branches
Purkinje
fibers
Inherent rate 20–40 beats per minute
Inherent rate 40–60 beats per minute
Inherent rate 60–100 beats per minute
Figure 1-4
Electrical conductive system of the heart.
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15. Chapter 1 The Electrocardiogram 8
Waveform
direction
Direction an ECG
waveform takes
depends on whether
electrical currents are
traveling toward or
away from a positive
electrode.
Impulses traveling
perpendicular to the
positive electrode
may produce a
biphasic waveform
(one that has both a
positive and negative
deflection).
Positive
electrode
Negative
electrode
–+
Impulses traveling toward a positive electrode produce upward deflections.
Impulses traveling away from a positive electrode and/or toward a negative
electrode will
produce
downward
deflections.
Figure 1-5
Direction of electrical impulses and waveforms.
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16. Chapter 1 The Electrocardiogram 9
ECG paper
Grid layout on ECG paper con-
sists of horizontal and vertical
lines.
Allows quick determination
of duration and amplitude of
waveforms, intervals, and seg-
ments.
Vertical lines represent ampli-
tude in electrical voltage (mV)
or millimeters.
Horizontal lines represent time.
Horizontal
Vertical
Voltage
Time
Heated
writing tip
Moving
stylus
Figure 1-6
Recording the ECG.
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17. Chapter 1 The Electrocardiogram 10
Each small square= 0.04
sec in duration and 0.1 mV in
amplitude.
Five small squares= one
large box and 0.20 seconds
in duration.
Horizontal measurements
determine heart rate.
15 large boxes= 3 seconds.
30 large boxes= 6 seconds.
On the top or bottom of the
printout there are often vertical
markings to represent 1-, 3-, or
6-second intervals.
Voltage
Time
3 seconds
0.5 mV
(5 mm)
0.2
seconds
0.04
seconds
0.1 mV
(1 mm)
Figure 1-7
ECG paper values.
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18. Chapter 1 The Electrocardiogram 11
ECG leads–
I, II, III
Bipolar leads
Lead I
Positive electrode—left arm (or
under left clavicle).
Negative electrode—right arm
(or below right clavicle).
Ground electrode—left leg (or
left side of chest in midclavicu-
lar line just beneath last rib).
Waveforms are positive.
RA
LL
+
+–
–
G
LA
Impulses
moving
toward
the
positive
lead
A Lead I
vie
w view
or
=
= Upright
wa
veforms
To properly position the electrodes, use the lettering located on the
top of the lead wire connector for each lead; LL stands for left leg,
LA stands for left arm, and RA stands for right arm.
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19. Chapter 1 The Electrocardiogram 12
Lead II
Positive electrode—left leg (or on
left side of chest in midclavicular
line just beneath last rib).
Negative electrode—right arm (or
below right clavicle).
Ground electrode—left arm (or
below left clavicle).
Waveforms are positive.
Lead III
Positive electrode—left leg (or left
side of the chest in midclavicular
line just beneath last rib).
Negative electrode—left arm (or
below left clavicle).
Ground electrode—right arm (or
below right clavicle).
Waveforms are positive or
biphasic.
LA
+
–
RA LA
LL
+
–
+
–
+
–G
GRA
LL
= Upright
waveforms
= Upright or
biphasic
waveforms
Impulses
moving
toward
the
positive
lead
Impulses
intersect
with
negative
to positive
layout of
ECG
leads
B
C Lead III
Lead II
view
view
view
view
or
or
=
=
Figure 1-8 (a) Lead I. (b) Lead II. (c) Lead III.
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20. Chapter 1 The Electrocardiogram 13
Augmented limb
leads—aV
R, aV
L,
and aV
F
Unipolar leads.
Enhanced by ECG machine because wave-
forms produced by these leads are nor-
mally small.
Lead aV
R
Positive electrode placed on right arm.
Waveforms have negative deflection.
Views base of the heart, primarily the atria.
= Downward
waveforms
Impulses
moving
away
from the
positive
lead
+
A Lead aV
R
view
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21. Chapter 1 The Electrocardiogram 14
Lead aV
L
Positive electrode placed on
left arm.
Waveforms have positive
deflection.
Views the lateral wall of the
left ventricle.
Lead aV
F
Positive electrode located on
left leg.
Waveforms have a positive
deflection.
Views the inferior wall of the
left ventricle.
view
Impulses
moving
toward
the
positive
lead
+
B Lead aV
L
Impulses
moving
toward
the
positive
lead
+
C Lead aV
F
= Upright
waveforms
view
= Upright or
biphasic
waveforms
Figure 1-9 (a) Lead aV
R. (b) Lead aV
L. (c) Lead aV
F.
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22. Chapter 1 The Electrocardiogram 15
Precordial (chest)
leads—V
1, V
2, V
3, V
4,
V
5, and V
6
Lead V
1 electrode is placed on the right side of
the sternum in the fourth intercostal space.
Lead V
2 is positioned on the left side of the
sternum in the fourth intercostal space.
Lead V
3 is located between leads V
2 and V
4.
Lead V
4 is positioned at the fifth intercostal
space at the midclavicular line.
Lead V
5 is placed in the fifth intercostal space
at the anterior axillary line.
Lead V
6 is located level with V
4 at the
midaxillary line.
V
1
V
1
V
2
V
3
V
4
V
5
V
6
V
2
V
3
V
4
V
5
V
6
Figure 1-10 Precordial leads.
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23. Chapter 1 The Electrocardiogram 16
Modified chest leads (MCL)
MCL
1 and MCL
6 provide continuous
cardiac monitoring.
For MCL
1, place the positive electrode
in same position as precordial lead V
1
(fourth intercostal space to the right
of the sternum).
For MCL
6, place the positive electrode
in same position as precordial lead V
6
(fifth intercostal space at the midaxil-
lary line).
Impulses
moving
away
from the
positive
lead
Impulses
moving
toward
the
positive
lead
= Downward
waveforms
= Upright
waveforms
MCL
1
MCL
6
RA
LL
+
–
A
LA
B
LA
+
–
RA
LL
G
G
Figure 1-11 MCL leads. (a) MCL
1 and (b) MCL
6.
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24. Analyzing the ECG
2
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25. Chapter 2 Analyzing the ECG 18
What is in this chapter
Five-step (and nine-step)
process
Methods for determining the
heart rate
Dysrhythmias by heart rate
Determining regularity
Methods used to determine
regularity
ECG waveforms
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26. Chapter 2 Analyzing the ECG 19
Five-step (and nine-step) process
The five-step process (and nine-step) is a logical and systematic process for analyzing
ECG tracings
1. Determine the rate. (Is it normal, fast, or slow?)
2. Determine the regularity. (Is it regular or irregular?)
3. Assess the P waves. (Is there a uniform P wave preceding each QRS complex?)
4. Assess the QRS complexes. (Are the QRS complexes within normal limits? Do they
appear normal?)
5. Assess the PR intervals. (Are the PR intervals identifiable? Within normal limits?
Constant in duration?)
Four more steps can be added to the five-step process making it a nine-step process.
6. Assess the ST segment. (Is it a flat line? Is it elevated or depressed?)
7. Assess the T waves. (Is it slightly asymmetrical? Is it of normal height? Is it oriented in
the same direction as the preceding QRS complex?)
8. Look for U waves. (Are they present?)
9. Assess the QT interval. (Is it within normal limits?)
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27. Chapter 2 Analyzing the ECG 20
Figure 2-1 (a) The five-step process. (b) Nine-step process.
Rate Regularity P waves
Fiv
e-step process
QRS complexes PR intervals
Assess
Rate Regularity P waves
Nine-step process
QRS
comple
xes
PR
intervals
Assess
A
ST
segments
U
waves
T
waves
QT
intervals
B
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28. Chapter 2 Analyzing the ECG 21
Methods for determining the heart rate
Using the 6-second! 10 method
Multiply by 10 the number of QRS complexes (for the ventricular rate) and the P waves (for the atrial
rate) found in a 6-second portion of ECG tracing. The rate in the ECG below is approximately 70
beats per minute.
3-second interval 3-second interval
Multiply the number of QRS complexes or P waves by 10
6-second interval
3-second
marks
12 3 4 567
Figure 2-2 6-second interval!10 method.
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29. Chapter 2 Analyzing the ECG 22
Using the 300, 150, 100, 75, 60, 50 method
Figure 2-3 300, 150, 100, 75, 60, 50 method.
300
150
100
75
60
50
R
wave
End
point
Start
point
The heart rate in the ECG below is
approximately 100 beats per minute.
Begin by finding an
R wave (or P wave)
located on a bold line
(the start point).
Then find the next
consecutive R wave.
The bold line it falls
on (or is closest to) is
the end point and
represents the
heart rate.
If the second R wave
does not fall on a bold
line the heart rate must
be approximated.
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30. Chapter 2 Analyzing the ECG 23
Using the thin lines to determine the heart rate
Figure 2-4 Identified values shown for each of the thin lines.
To more precisely determine the heart rate when the second R wave falls between
two bold lines, you can use the identified values for each thin line.
300 150 100 75 60 50 43 38 33
250
214
188
167
136
125
115
107
94
88
84
79
72
68
65
63
58
56
54
52
48
47
45
44
42
41
40
39
37
36
35
34
Star
t
point
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31. Chapter 2 Analyzing the ECG 24
Using the 1500 method
Begin by counting number of small squares between two consecutive R waves and divide 1500 by
that number. Remember, this method cannot be used with irregular rhythms.
End
point
Start
point
38 small
boxes
1500 divided by 38 small boxes = 40 beats per minute
Figure 2-5 The 1500 method.
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32. Chapter 2 Analyzing the ECG 25
Dysrhythmias by heart rate
Average adult has a heart rate of 60-100 beats per minute (BPM).
Rates above 100 BPM or below 60 BPM are considered abnormal.
A heart rate less than 60 BPM is called bradycardia.
∞ It may or may not have an adverse affect on cardiac output.
∞
In the extreme it can lead to severe reductions in cardiac output and eventually deteriorate into
asystole (an absence of heart rhythm).
A heart rate greater than 100 BPM is called tachycardia.
∞
It has many causes and leads to increased myocardial oxygen consumption, which can
adversely affect patients with coronary artery disease and other medical conditions.
∞
Extremely fast rates can have an adverse affect on cardiac output.
∞
Also, tachycardia that arises from the ventricles may lead to a chaotic quivering of the ventricles
called ventricular fibrillation.
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33. Chapter 2 Analyzing the ECG 26
Figure 2-6 Heart rate algorithm.
Heart rate
Slow FastNormal
Sinus bradycardia
Sinus arrest*
Junctional escape
Idioventricular rhythm
AV heart block
Atrial flutter or
fibrillation with slow
ventricular response
Normal sinus rhythm
Sinus dysrhythmia
Wandering atrial
pacemaker
Accelerated junctional
rhythm
Atrial flutter or
fibrillation with normal
ventricular response
Sinus tachycardia
Junctional tachycardia
Atrial tachycardia, SVT,
PSVT
Multifocal atrial
tachycardia (MAT)
Ventricular tachycardia
Atrial flutter or
fibrillation with fast
ventricular response
*Heart rate can also be normal
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34. Chapter 2 Analyzing the ECG 27
Determining regularity
Equal R-R and P-P intervals
Normally the heart beats in a regular, rhythmic fashion. If the distance of the R-R intervals
and P-P intervals is the same, the rhythm is regular.
Figure 2-7 This rhythm is regular as each R-R and P-P interval is 21 small boxes apart.
212121212121
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35. Chapter 2 Analyzing the ECG 28
Unequal R-R and P-P intervals
If the distance differs, the rhythm is irregular.
Irregular rhythms are considered abnormal.
Use the R wave to measure the distance between QRS complexes as it is typically the tallest
waveform of the QRS complex.
Remember, an irregular rhythm is considered abnormal. A variety of conditions can produce
irregularities of the heartbeat.
Figure 2-8 In this rhythm, the number of small boxes differs between some of the R-R and P-P intervals.
For this reason it is considered irregular.
21 25 22 21
1
/2 21
1
/215
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36. Chapter 2 Analyzing the ECG 29
Methods used to determine regularity
Using calipers
Place ECG tracing on a flat surface.
Place one point of the caliper on a
starting point, either the peak of an
R wave or P wave.
Open the calipers by pulling the
other leg until the point is positioned
on the next R wave or P wave.
With the calipers open in that
position, and keeping the point
positioned over the second P wave
or R wave, rotate the calipers across
to the peak of the next consecutive
(the third) P wave or R wave.
Figure 2-9 Use of calipers to identify regularity.
Peak of
first R or
P wave
Peak of
second R or
P wave
Peak of
third R or
P wave
Peak of
fourth R or
P wave
Peak of
fifth R or
P wave
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37. Chapter 2 Analyzing the ECG 30
Using paper and pen
Place the ECG tracing on a flat
surface.
Position the straight edge of a piece
of paper above the ECG tracing so
that the intervals are still visible.
Identify a starting point, the peak of an
R wave or P wave, and place a mark
on the paper in the corresponding
position above it.
Find the peak of the next consecutive
R wave or P wave, and place a mark
on the paper in the corresponding
position above it.
Move the paper across the ECG trac-
ing, aligning the two marks with suc-
ceeding R-R intervals or P-P intervals.
Figure 2-10 Use of paper and pen to identify regularity.
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38. Chapter 2 Analyzing the ECG 31
Counting the small squares between each R-R interval
Count the number of small squares between the peaks of two consecutive R waves (or P waves)
and then compare that to the other R-R (or P-P) intervals to reveal regularity.
Figure 2-11 Counting the number of small squares to identify regularity.
1+ 5 + 5 + 5 + 5 = 21
This R-R interval is 21
small boxes in duration.
21
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39. Chapter 2 Analyzing the ECG 32
Regular Irregular
Occasional
or very
Slightly
Sudden
acceleration
in heart rate
Patterned Totally
Variable
conduction
ratio
Evaluating regularity
Types of irregularity
Irregularity can be categorized as:
∞
occasionally irregular or very irregular.
∞
slightly irregular.
∞
sudden acceleration in the heart rate.
∞
patterned irregularly.
∞
irregularly (totally) irregular.
∞
variable conduction ratio.
Figure 2-12 Algorithm for regular and irregular rhythms.
Each type of irregularity is
associated with certain dys-
rhythmias. Knowing which
irregularity is associated
with which dysrhythmias
makes it easier to later inter-
pret a given ECG tracing.
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40. Chapter 2 Analyzing the ECG 33
Occasionally irregular
The dysrhythmia is mostly regular but from time to time you see an area of irregularity.
Figure 2-13 An occasionally irregular rhythm.
21 25 21 21 2115
Area where
it is irregular
Area where
it is regular
Shorter
R-R interval
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41. Chapter 2 Analyzing the ECG 34
Frequently irregular
A very irregular dysrhythmia has many areas of irregularity.
Figure 2-14 A frequently irregular rhythm.
Shorter
R-R interval
Shorter
R-R interval
Area where
it is irregular
Area where
it is regular
Underlying rhythm against
which the regularity of the
rest of rhythm is measured.
Area where
it is irregular
Shorter
R-R interval
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42. Chapter 2 Analyzing the ECG 35
Slightly irregular
Rhythm appears to change only slightly with the P-P intervals and R-R intervals
varying somewhat.
Figure 2-15 A slightly irregular rhythm.
Area where it is
regular
Area where it is
slightly irregular
Area where it is
regular
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43. Chapter 2 Analyzing the ECG 36
Paroxsymally irregular
A normal rate suddenly accelerates to a rapid rate producing an irregularity
in the rhythm.
Figure 2-16 A paroxsymally irregular rhythm.
Area where it is
regular
Area where the heart rate
suddenly accelerates
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44. Chapter 2 Analyzing the ECG 37
Patterned irregularity
The irregularity repeats in a cyclic fashion.
Figure 2-17 A patterned irregular rhythm.
Area where it is
patterned irregular
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45. Chapter 2 Analyzing the ECG 38
Irregular irregularity
No consistency to the irregularity.
Figure 2-18 An irregularly irregular rhythm.
Entire tracing is
irregular
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46. Chapter 2 Analyzing the ECG 39
Areas where
the conduction
ratio changes
Variable irregularity
The number of impulses reaching the ventricles changes, producing
an irregularity.
Figure 2-19 Variably irregular rhythm.
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47. Chapter 2 Analyzing the ECG 40
Regularity
Normal sinus rhythm
Sinus bradycardia
Sinus tachycardia
Atrial tachycardia
Junctional escape
Accelerated junctional
Junctional tachycardia
Idioventricular rhythm
Ventricular tachycardia
Atrial flutter/constant
1
st
& 3
rd
degree AV block
2
nd
(Type II)
Regular Irregular
Occasionally or
very
Slightly
Sudden
acceleration in
heart rate
Patterned Totally
Variable
conduction
ratio
Sinus arrest
Premature
beats (PACs,
PJCs, PVCs)
Wandering
atrial
pacemaker PSVT,
PAT, P J T Sinus
dysrhythmia
Premature
beats—
(bigeminy,
trigeminy,
quadrigeminy
2
nd
degree AV
block, Type I
Atrial
fibrillation Atrial flutter
2
nd
degree AV
heart block,
Type II
Irregularity algorithm
Figure 2-20 Algorithm showing which
dysrhythmias display which type of irregularity.
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48. Chapter 2 Analyzing the ECG 41
ECG waveforms
P wave
Begins with its movement away from the base-
line and ends in its return to the baseline.
Characteristically round and slightly asymmetrical.
There should be one P wave preceding each
QRS complex.
In leads I, II, aV
F, and V
2 through V
6, its deflection
is characteristically upright or positive.
In leads III, aV
L, and V
1, the P wave is usually
upright but may be negative or biphasic (both
positive and negative).
In lead aV
R, the P wave is negative or inverted.
Figure 2-21 P wave.
Duration is 0.06
to 0.10 seconds
Amplitude is
0.5 to 2.5 mm
P
Usually rounded
and upright
One P wave
precedes
each QRS
Time (duration, rate)
Height/amplitude (energy)
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49. Chapter 2 Analyzing the ECG 42
QRS complex
Follows PR segment and consists of:
∞
Q wave—first negative deflection fol-
lowing PR segment. It is always negative.
In some cases it is absent. The amplitude
is normally less than 25% of the ampli-
tude of the R wave in that lead.
∞
R wave—first positive triangular deflec-
tion following Q wave or PR segment.
∞
S wave—first negative deflection that
extends below the baseline in the QRS
complex following the R wave.
In leads I, II, III, aV
L, aV
F, and V
4 to V
6, the deflection
of the QRS complex is characteristically positive or upright.
In leads aV
R and V
1 to V
3, the QRS complex is usually
negative or inverted.
In leads III and V
2 to V
4 the QRS complex may also be biphasic.
Figure 2-22 QRS complex.
Duration is 0.06 to
0.12 seconds
QRS
complex
R
QS
Time (duration, rate)
Height/amplitude (energy)
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50. Chapter 2 Analyzing the ECG 43
Differing forms of QRS complexes
QRS complexes can consist of positive (upright) deflections called R waves and negative
(inverted) deflections called Q and S waves: all three waves are not always seen.
If the R wave is absent, complex is called a QS complex. Likewise, if the Q wave is absent,
complex is called an RS complex.
Waveforms of
normal or greater
than normal
amplitude are
denoted with a
large case letter,
whereas wave-
forms less than 5
mm amplitude are
denoted with a
small case letter
(e.g., “q,” “r,” “s”).
Figure 2-23 Common QRS complexes.
R
Q
QS
R
q
R
S
q
R
S
R
S
r
S
rr
R
S
r
Q
r
S
r
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51. Chapter 2 Analyzing the ECG 44
A
0.10 seconds
in duration
0.12 seconds
in duration
S
S
Q
J pointJ point
R
R
B
0.08 seconds
in duration
0.08 seconds
in duration
0.14 seconds
in duration
0.22 seconds
in duration
0.18
seconds
in duration
S
S
S
Q
J pointJ point
J point
J point
J point
R
R
R
S
S
R
R
Measuring the QRS complex
First identify the QRS complex with the longest duration and
most distinct beginning and ending.
Start by finding the beginning of the QRS complex.
∞
This is the point where the first wave of the complex (where
either the Q or R wave) begins to deviate from the baseline.
Then measure to the point where the last
wave of the complex transitions into the
ST segment (referred to as the J point).
∞
Typically, it is where the S wave or R
wave (in the absence of an S wave)
begins to level out (flatten) at,
above, or below the baseline.
∞
This is considered the end of the
QRS complex.
Figure 2-24 Measuring the QRS complex. (a) These two QRS complexes have easy to see J points. (b) These QRS complexes have
less defined transitions making measurement of the QRS complex more challenging.
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52. Chapter 2 Analyzing the ECG 45
PR interval
Extends from the beginning of the
P wave to the beginning of the
Q wave or R wave.
Consists of a P wave and a flat
(isoelectric) line.
It is normally constant for each
impulse conducted from the atria
to the ventricles.
The PR segment is the isoelectric
line that extends from the end of the
P wave to the beginning of the Q
wave or R wave.
Figure 2-25 PR interval.
Time (duration, rate)
PR interval
Duration is 0.12
to 0.20 seconds
PR segment
Height/amplitude (energy)
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53. Chapter 2 Analyzing the ECG 46
Measuring the PR interval
To measure the width (duration) of a
PR interval, first identify the interval
with the longest duration and the most
distinct beginning and ending.
Start by finding the beginning of the
interval. This is the point where the
P wave begins to transition from the
isoelectric line.
Then measure to the point where the
isoelectric line (following the P wave)
transitions into the Q or R wave (in the
absence of an S wave).
This is considered the end of the
PR interval.
Figure 2-26 Measuring PR intervals.
Time (duration, rate)
This PR interval 0.16 seconds in duration
Height/amplitude (energy)
Start
measurement
here
End
measurement
here
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54. Chapter 2 Analyzing the ECG 47
ST segment
The line that follows the QRS complex and
connects it to the T wave.
Begins at the isoelectric line extending from the
S wave until it gradually curves upward to the
T wave.
Under normal circumstances, it appears as a flat
line (neither positive nor negative), although it may
vary by 0.5 to 1.0 mm in some precordial leads.
The point that marks the end of the QRS and
the beginning of the ST segment is known as
the J point.
The PR segment is used as the baseline from
which to evaluate the degree of displacement
of the ST segment from the isoelectric line.
Measure at a point 0.04 seconds (one small box) after the J point. The ST segment is considered
elevated if it is above the baseline and considered depressed if it is below it.
Figure 2-27 ST segment, T wave, and QT interval.
J point
ST
segment
T wave
QT interval
Time (duration, rate)
Height/amplitude (energy)
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55. Chapter 2 Analyzing the ECG 48
T wave
Larger, slightly asymmetrical waveform that follows the ST segment.
Peak is closer to the end than the beginning, and the first half has a more gradual slope than
the second half.
Normally not more than 5 mm in height in the limb leads or 10 mm in any precordial lead.
Normally oriented in the same direction as the preceding QRS complex.
Normally positive in leads I, II, and V
2 to V
6 and negative in lead aV
R. They are also positive in
aV
L and aV
F but may be negative if the QRS complex is less that 6 mm in height. In leads III and
V
1, the T wave may be positive or negative.
QT interval
Distance from onset of QRS complex until end of T wave.
Measures time of ventricular depolarization and repolarization.
Normal duration of 0.36 to 0.44 seconds.
U wave
Small upright (except in lead aV
L) waveform sometimes seen fol-
lowing the T wave, but before the next P wave.
Figure 2-28 U waves.
QRS
PP
TT
QRS
U
wave
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56. Chapter 2 Analyzing the ECG 49
One for
every
QRS
More P
waves than
QRS
Absent
Normal,
round
Unusual
looking
Inverted
Peaked,
notched,
enlarged
Differing
morphology
Sawtooth
Chaotic
baseline
Evaluate P waves
Present
Abnormal P waves
P waves seen with impulses that originate in the SA node but travel
through altered or damaged atria (or atrial conduction pathways) appear
tall and rounded or peaked, notched, wide and notched or biphasic.
Figure 2-29 Algorithm for normal and abnormal
P waves.
P waves appear different than sinus P waves when
the impulse arises from the atria instead of the sinus
node.
Sawtooth appearing waveforms (flutter waves) occur
when an ectopic site in the atria fires rapidly.
A chaotic-looking baseline (no discernible P waves)
occurs when many ectopic atrial sites rapidly fire.
P waves are inverted, absent, or follow the QRS com-
plex when the impulse arises from the left atria, low
in the right atria, or in the AV junction.
More P waves than QRS complexes occur when
impulses arise from the SA node, but do not all reach
the ventricles due to a blockage.
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57. Chapter 2 Analyzing the ECG 50
Figure 2-30 Types of waveforms: (a) abnormal sinus P waves, (b) atrial P wave associated with a PAC, (c) flutter waves,
(d) no discernible P waves, (e) inverted P wave, (f) absent P wave, (g) P wave that follows QRS, and (h) P waves that are
not all followed by a QRS complex.
P
P
P
Tall, rounded Tall, peaked Notched Wide, notched Biphasic
PPPP
P
P
A B C
E
“f ”
waves
“F”
waves
more P waves than
QRS complexes
F G HD
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58. Chapter 2 Analyzing the ECG 51
Abnormal QRS complexes
Abnormally tall due to ventricular hypertrophy
or abnormally small due to obesity, hyperthy-
roidism, or pleural effusion.
Slurred (delta wave) due to ventricular
preexcitation.
Vary from being only slightly abnormal to
extremely wide and notched due to bundle
branch block, intraventricular conduction distur-
bance, or aberrant ventricular conduction.
Wide due to ventricular pacing by a cardiac
pacemaker.
Wide and bizarre looking due to electrical
impulses originating from an ectopic or escape
pacemaker site in the ventricles.
Follow
each
P wave
More P
waves than
QRS
complexes
Present Absent
Normal
0.06–0.12
seconds
Unusual
looking
Inverted
Tall, low
voltage
Notched
Wide (greater
than 0.12
seconds),
bizarre
appearance
Chaotic
Evaluate QRS
complexes
Figure 2-31 Algorithm
for normal and abnor-
mal QRS complexes.
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59. Delta
wave
A B C D E F G
H
P„
Figure 2-32 Types of QRS complexes: (a) tall, (b) low amplitude, (c) slurred, (d) wide due to intraventricular conduction defect,
(e) wide due to aberrant conduction, (f) wide due to bundle branch block, (g) wide due to ventricular cardiac pacemaker, and
(h) various wide and bizarre complexes due to ventricular origin.
Chapter 2 Analyzing the ECG
52
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60. Chapter 2 Analyzing the ECG 53
Abnormal PR intervals
Abnormally short or absent due to impulse arising
from low in the atria or in the AV junction.
Abnormally short due to ventricular preexcitation.
Absent due to ectopic site in the atria firing rap-
idly or many sites in the atria firing chaotically.
Absent due to impulse arising from the ventricles.
Longer than normal due to a delay in AV
conduction.
Vary due to changing atrial pacemaker site.
Progressively longer due to a weakened AV node
that fatigues more and more with each conduct-
ed impulse until finally it is so tired that it fails to
conduct an impulse through to the ventricles.
Absent due to the P waves having no relationship
to the QRS complexes.
Figure 2-33 Algorithm for normal and abnormal PR
intervals.
Normal
0.12–0.20
seconds
Abnormal
Present Absent
Shorter
than 0.12
seconds
Longer
than 0.20
seconds
Absent
Vary in
duration
Evaluate PR
intervals
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61. Chapter 2 Analyzing the ECG 54
Figure 2-34 Types of PR intervals: (a) shortened, (b) absent, (c) longer than normal, (d) progressively longer in a cyclical
manner, (e) varying, and (f) absent due to an absence in the relationship between the atrial impulses and ventricular impulses.
0.18 0.10
Premature
atrial
complex
P P
0.30
0.35 0.42 absent 0.19
PPPP
0.20
P

0.16
P

0.12
P

0.14
P

PPPPP PP
A B C D
E F
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62. Sinus Dysrhythmias
3
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63. Chapter 3 Sinus Dysrhythmias 56
What is in this chapter
Normal sinus rhythm
characteristics
Sinus bradycardia
characteristics
Sinus tachycardia
characteristics
Sinus dysrhythmia
characteristics
Sinus arrest characteristics
Characteristics common to sinus dysrhythmias
Arise from SA node.
Normal P wave precedes each QRS complex.
PR intervals are normal at 0.12 to 0.20 seconds in duration.
QRS complexes are normal.
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64. Chapter 3 Sinus Dysrhythmias 57
Figure 3-1
Summary of characteristics of normal sinus rhythm.
Normal sinus rhythm characteristics
Rate: 60 to 100 beats per minute
Regularity: It is regular
P waves: Present and normal; all the P waves are followed by a QRS complex
QRS complexes: Normal
PR interval: Within normal range (0.12 to 0.20 seconds)
QT interval: Within normal range (0.36 to 0.44 seconds)
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65. Chapter 3 Sinus Dysrhythmias 58
Normal sinus rhythm arises from the SA node. Each impulse travels down through the conduction system
in a normal manner.
Figure 3-2
Normal sinus rhythm.
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66. Chapter 3 Sinus Dysrhythmias 59
Sinus bradycardia characteristics
Rate: Less than 60 beats per minute
Regularity: It is regular
P waves: Present and normal; all the P waves are followed by a QRS
complex
QRS complexes: Normal
PR interval: Within normal range (0.12 to 0.20 seconds)
QT interval: Within normal range (0.36 to 0.44 seconds) but may be
prolonged
Figure 3-3
Summary of characteristics of sinus bradycardia.
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67. Chapter 3 Sinus Dysrhythmias 60
Sinus bradycardia arises from the SA node. Each impulse travels down through the conduction system in
a normal manner.
Figure 3-4
Sinus bradycardia.
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68. Chapter 3 Sinus Dysrhythmias 61
Sinus tachycardia characteristics
Rate: 100 to 160 beats per minute
Regularity: It is regular
P waves: Present and normal; all the P waves are followed by a QRS
complex
QRS complexes: Normal
PR interval: Within normal range (0.12 to 0.20 seconds)
QT interval: Within normal range (0.36 to 0.44 seconds) but commonly
shortened
Figure 3-5
Summary of characteristics of sinus tachycardia.
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69. Chapter 3 Sinus Dysrhythmias 62
Sinus tachycardia arises from the SA node. Each impulse travels down through the conduction system
in a normal manner.
Figure 3-6
Sinus tachycardia.
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70. Chapter 3 Sinus Dysrhythmias 63
Sinus dysrhythmia characteristics
Rate: Typically 60 to 100 beats per minute
Regularity: It is regularly irregular (patterned irregularity); seems to speed
up, slow down, and speed up in a cyclical fashion
P waves: Present and normal; all the P waves are followed by a QRS
complex
QRS complexes: Normal
PR interval: Within normal range (0.12 to 0.20 seconds)
QT interval: May vary slightly but usually within normal range (0.36 to 0.44
seconds)
Figure 3-7
Summary of characteristics of sinus dysrhythmia.
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71. Chapter 3 Sinus Dysrhythmias 64
Sinus dysrhythmia arises from the SA node. Each impulse travels down through the conduction system in
a normal manner.
Figure 3-8
Sinus dysrhythmia.
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72. Chapter 3 Sinus Dysrhythmias 65
Sinus arrest characteristics
Rate: Typically 60 to 100 beats per minute, but may be slower
depending on frequency and length of arrest
Regularity: It is irregular where there is a pause in the rhythm (the SA node
fails to initiate a beat)
P waves: Present and normal; all the P waves are followed by a QRS
complex
QRS complexes: Normal
PR interval: Within normal range (0.12 to 0.20 seconds)
QT interval: Within normal range (0.36 to 0.44 seconds); unmeasurable
during a pause
Figure 3-9
Summary of characteristics of sinus arrest.
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73. Chapter 3 Sinus Dysrhythmias 66
Sinus arrest occurs when the SA node fails to initiate an impulse.
Figure 3-10
Summary of characteristics of sinus arrest.
SA node fails to
initiate impulse
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74. Atrial Dysrhythmias
4
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75. Chapter 4 Atrial Dysrhythmias 68
What is in this chapter
Premature atrial complexes
(PACs) characteristics
Wandering atrial pacemaker
characteristics
Atrial tachycardia characteristics
Multifocal atrial tachycardia
characteristics
Atrial flutter characteristics
Atrial fibrillatrion characteristics
Characteristics common to atrial dysrhythmias
Arise from atrial tissue or internodal pathways. P’ waves (if present) that differ in appearance from normal sinus P waves
precede each QRS complex.
P’R intervals may be normal, shortened, or prolonged. QRS complexes are normal (unless there is also an interventricular
conduction defect or aberrancy).
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76. Chapter 4 Atrial Dysrhythmias 69
Wandering atrial pacemaker characteristics
Rate: Usually within normal limits
Regularity: Slightly irregular
P waves: Continuously change in appearance
QRS complexes: Normal
PR interval: Varies
QT interval: Usually within normal limits but may vary
Figure 4-1
Summary of characteristics of wandering atrial pacemaker.
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77. Chapter 4 Atrial Dysrhythmias 70
Wandering atrial pacemaker arises from different sites in the atria.
Figure 4-2
Wandering atrial pacemaker.
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78. Chapter 4 Atrial Dysrhythmias 71
Premature atrial complexes (PAC) characteristics
Rate: Depends on the underlying rhythm
Regularity: May be occasionally irregular or frequently irregular (depends
on the number of PACs present). It may also be seen as pat-
terned irregularity if bigeminal, trigeminal, or quadrigeminal
PACs are seen.
P waves: May be upright or inverted, will appear different than those of
the underlying rhythm
QRS complexes: Normal
PR interval: Will be normal duration if ectopic beat arises from the upper- or
middle-right atrium. It is shorter than 0.12 seconds in duration
if the ectopic impulse arises from the lower right atrium or in
the upper part of the AV junction. In some cases it can also be
prolonged
QT interval: Usually within normal limits but may vary
Figure 4-3
Summary of characteristics of premature atrial complexes.
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79. Chapter 4 Atrial Dysrhythmias 72
Premature atrial complexes arise from somewhere in the atrium.
Figure 4-4
Premature atrial complexes.
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80. Chapter 4 Atrial Dysrhythmias 73
The pause that follows a
premature beat is called
a noncompensatory pause
if the space between the
complex before and after
the premature beat is less
than the sum of two R-R
intervals.
Non-compensatory
pauses are typically seen
with premature atrial
and junctional complexes
(PACs, PJCs).
When the tip of the
right caliper leg
fails to line up with
the next R wave it
is considered a
noncompensatory
pause
Measure first
R-R interval
that precedes
the early beat
Rotate or slide
the calipers
over until
the left leg is
lined up with
the second
R wave —
mark the point
where the tip
of the right
leg falls
Rotate or slide
the calipers
over until the
left leg is lined
up with your
first mark
Figure 4-5
Premature beats with a noncompensatory pause.
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81. Chapter 4 Atrial Dysrhythmias 74
When the tip of the
right caliper leg lines up
with the next R wave it
is considered a
compensatory pauseMeasure first R-R
interval that precedes
the early beat
Compensatory pauses are typically
associated with premature ventricular
complexes (PVCs)
Rotate or slide the calipers over until the left leg is lined up with the second R wave —mark the point where the tip of the right leg falls
Rotate or slide the calipers over until the left leg is lined up with your first mark
Figure 4-6
Premature beats with a compensatory pause.
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82. Chapter 4 Atrial Dysrhythmias 75
Premature beats occurring in a pattern
One way to describe PACs is how they are intermingled among the normal beats. When every other beat
is a PAC, it is called bigeminal PACs, or atrial bigeminy. If every third beat is a PAC, it is called trigeminal
PACs, or atrial trigeminy. Likewise, if a PAC occurs every fourth beat, it is called quadrigeminal PACs, or
atrial quadrigeminy. Regular PACs at greater intervals than every fourth beat have no special name.
Figure 4-7
Premature atrial complexes: (a) bigeminal PACs, (b) trigeminal PACs, and (c) quadrigeminal
PACs.
Normal
a)
Normal Normal Normal PACPACPACPAC
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83. Chapter 4 Atrial Dysrhythmias 76
Normal
Normal
b)
c)
Normal Normal Normal Normal PACPACPAC
Normal Normal Normal Normal PACPAC
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84. Chapter 4 Atrial Dysrhythmias 77
Narrow complex
tachycardia that
has a sudden,
witnessed onset
and abrupt
termination is
called paroxys-
mal tachycardia.Atrial tachycardia characteristics
Rate: 150 to 250 beats per minute
Regularity: Regular unless the onset is witnessed (thereby
producing paroxysmal irregularity)
P waves: May be upright or inverted, will appear differ-
ent than those of the underlying rhythm
QRS complexes:Normal
PR interval: Will be normal duration if ectopic beat arises
from the upper- or middle-right atrium. It is
shorter than 0.12 seconds in duration if the
ectopic impulse arises from the lower-right
atrium or in the upper part of the AV junc-
tion
QT interval: Usually within normal limits but may be
shorter due to the rapid rate
Narrow com-
plex tachycardia
that cannot be
clearly identi-
fied as atrial
or junctional
tachycardia is
referred to as
supraventricular
tachycardia.
Figure 4-8
Summary of characteristics of atrial tachycardia.
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85. Chapter 4 Atrial Dysrhythmias 78
Atrial tachycardia arises from a single focus in the atria.
Figure 4-9
Atrial tachycardia.
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86. Chapter 4 Atrial Dysrhythmias 79
Multifocal atrial tachycardia characteristics
Rate: 120 to 150 beats per minute
Regularity: Irregular
P waves: P„ waves change in morphology (appearance) from beat to beat
(at least three different shapes)
QRS complexes: Normal
PR interval: Varies
QT interval: Usually within normal limits but may vary
Figure 4-10
Summary of characteristics of multifocal atrial tachycardia.
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87. Chapter 4 Atrial Dysrhythmias 80
In multifocal atrial tachycardia, the pacemaker site shifts between the SA node, atria, and/or
the AV junction.
Figure 4-11
Multifocal atrial tachycardia.
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88. Chapter 4 Atrial Dysrhythmias 81
Atrial flutter characteristics
Rate: Ventricular rate may be slow, normal, or fast; atrial rate is
between 250 and 350 beats per minute
Regularity: May be regular or irregular (depending on whether the
conduction ratio stays the same or varies)
P waves: Absent, instead there are flutter waves; the ratio of atrial
waveforms to QRS complexes may be 2:1, 3:1, or 4:1. An
atrial-to-ventricular conduction ratio of 1:1 is rare
QRS complexes: Normal
PR interval: Not measurable
QT interval: Not measurable
Figure 4-12
Summary of characteristics of atrial flutter.
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89. Chapter 4 Atrial Dysrhythmias 82
Atrial flutter arises from rapid depolarization of a single focus in the atria.
Figure 4-13
Atrial flutter.
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90. Chapter 4 Atrial Dysrhythmias 83
Atrial fibrillation characteristics
Rate: Ventricular rate may be slow, normal, or fast; atrial rate is
greater than 350 beats per minute
Regularity: Totally (chaotically) irregular
P waves: Absent; instead there is a chaotic-looking baseline
QRS complexes: Normal
PR interval: Absent
QT interval: Unmeasurable
Figure 4-14
Summary of characteristics of atrial fibrillation.
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91. Chapter 4 Atrial Dysrhythmias 84
Atrial fibrillation arises from many different sites in the atria.
Figure 4-15
Atrial fibrillation.
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92. Junctional
Dysrhythmias
5
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93. Chapter 5 Junctional Dysrhythmias 86
What is in this chapter
Premature junctional complexes (PJCs)
characteristics
Junctional escape rhythm characteristics
Accelerated junctional rhythm
characteristics
Junctional tachycardia characteristics
Characteristics common to junctional dysrhythmias
Arise from the AV junction, the area around the AV node, or the bundle of His.
P’ wave may be inverted (when they would otherwise be upright) with a short P’R interval
(less than 0.12 seconds in duration).
Alternatively, the P’ wave may be absent (as it is buried by the QRS complex), or it may
follow the QRS complex. If the P’ wave is buried in the QRS complex it can change the
morphology of the QRS complex.
If present, P’R intervals are shortened.
QRS complexes are normal (unless there is an interventricular conduction defect or
aberrancy).
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94. Chapter 5 Junctional Dysrhythmias 87
Premature junctional complexes (PJCs) characteristics
Rate: Depends on the underlying rhythm
Regularity: May be occasionally irregular or frequently irregular (depends
on the number of PJCs present). It may also be seen as patterned
irregularity if bigeminal, trigeminal, or quadrigeminal PJCs are
seen.
P waves: Inverted—may immediately precede, occur during (absent), or
follow the QRS complex
QRS complexes: Normal
PR interval: Will be shorter than normal if the P„ wave precedes the QRS
complex and absent if the P„ wave is buried in the QRS; referred
to as the RP„ interval if the P„ wave follows the QRS complex
QT interval: Usually within normal limits
Figure 5-1
Summary of characteristics of premature junctional complexes (PJCs).
PJCs are typically followed by a non-compensatory pause.
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95. Chapter 5 Junctional Dysrhythmias 88
Premature junctional complex arises from somewhere in the AV junction.
Figure 5-2
Summary of characteristics of premature junctional complexes (PJCs).
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96. Chapter 5 Junctional Dysrhythmias 89
Junctional escape rhythm characteristics
Rate: 40 to 60 beats per minute
Regularity: Regular
P waves: Inverted—may immediately precede, occur during (absent), or
follow the QRS complex
QRS complexes: Normal
PR interval: Will be shorter than normal if the P„wave precedes the QRS
complex and absent if the P„ wave is buried in the QRS; referred
to as the RP„ interval if the P„ wave follows the QRS complex
QT interval: Usually within normal limits
Figure 5-3
Summary of characteristics of junctional escape rhythm.
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97. Chapter 5 Junctional Dysrhythmias 90
Junctional escape rhythm arises from a single site in the AV junction.
Figure 5-4
Junctional escape rhythm.
Junctional escape rhythm
40 to 60 beats per minute
Accelerated junctional rhythm
60 to 100 beats per min
ute
Junctional tachycardia
100 to 180 beats per minute
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98. Chapter 5 Junctional Dysrhythmias 91
Accelerated junctional rhythm characteristics
Rate: 60 to 100 beats per minute
Regularity: Regular
P waves: Inverted—may immediately precede, occur during (absent), or
follow the QRS complex
QRS complexes: Normal
PR interval: Will be shorter than normal if the P„ wave precedes the QRS
complex and absent if the P„ wave is buried in the QRS; referred
to as the RP„ interval if the P„ wave follows the QRS complex
QT interval: Usually within normal limits
Figure 5-5
Summary of characteristics of accelerated junctional rhythm.
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99. Chapter 5 Junctional Dysrhythmias 92
Accelerated junctional rhythm arises from a single site in the AV junction.
Figure 5-6
Accelerated junctional rhythm.
Junctional escape rhythm
40 to 60 beats per minute
Accelerated junctional rhythm
60 to 100 beats per minute
Junctional tachycardia
100 to 180 beats per minute
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100. Chapter 5 Junctional Dysrhythmias 93
Junctional tachycardia characteristics
Rate: 100 to 180 beats per minute
Regularity: Regular
P waves: Inverted—may immediately precede, occur during (absent), or
follow the QRS complex
QRS complexes: Normal
PR interval: Will be shorter than normal if the P„ wave precedes the QRS
complex and absent if the P„ wave is buried in the QRS; referred
to as the RP„ interval if the P„ wave follows the QRS complex
QT interval: Usually within normal limits
Figure 5-7
Summary of characteristics of junctional tachycardia.
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101. Chapter 5 Junctional Dysrhythmias 94
Junctional tachycardia arises from a single focus in the AV junction.
Figure 5-8
Junctional tachycardia.
Junctional escape rhythm
40 to 60 beats per minute
Accelerated junctional rhythm
60 to 100 beats per minute
Junctional tachycardia
100 to 180 beats per min
ute
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102. Ventricular
Dysrhythmias
6
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103. Chapter 6 Ventricular Dysrhythmias 96
What is in this chapter
Premature ventricular complexes (PVCs)
characteristics
Idioventricular rhythm characteristics
Accelerated idioventricular rhythm
characteristics
Ventricular tachycardia characteristics
Characteristics common to ventricular dysrhythmias
Arise from the ventricles below the bundle of His.
QRS complexes are wide (greater than 0.12 seconds in duration) and bizarre looking.
Ventricular beats have T waves in the opposite direction of the R wave.
P waves are not visible as they are hidden in the QRS complexes.
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104. Chapter 6 Ventricular Dysrhythmias 97
Premature ventricular complexes (PVCs) characteristics
Rate: Depends on the underlying rhythm
Regularity: May be occasionally irregular or frequently irregular (depends
on the number of PVCs present). It may also be seen as pat-
terned irregularity if bigeminal, trigeminal, or quadrigeminal
PVCs are seen.
P waves: Not preceded by a P wave (if seen, they are dissociated)
QRS complexes: Wide, large, and bizarre looking
PR interval: Not measurable
QT interval: Usually prolonged with the PVC
Figure 6-1
Summary of characteristics of premature ventricular complexes.
PVCs are followed by a compensatory pause.
Sometimes, PVCs originate from only one location in the ventricle. These beats look the same and are called
uniform (also referred to as unifocal) PVCs. Other times, PVCs arise from different sites in the ventricles. These
beats tend to look different from each other and are called multiformed (multifocal) PVCs.
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105. Chapter 6 Ventricular Dysrhythmias 98
Premature ventricular complexes arise from somewhere in the ventricle(s).
Figure 6-2
Premature ventricular complexes (PVCs).
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106. Chapter 6 Ventricular Dysrhythmias 99
PVCs that occur one
after the other (two
PVCs in a row) are
called a couplet, or
pair.
Three or more PVCs
in a row at a ventricu-
lar rate of at least 100
BPM is called ven-
tricular tachycardia. It
may be called a salvo,
run, or burst of ven-
tricular tachycardia.
Figure 6-4
Run of PVCs.
Figure 6-3
Couplet of PVCs.
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107. Chapter 6 Ventricular Dysrhythmias 100
Figure 6-6 R-on-T PVC.
An interpolated PVC
occurs when a PVC
does not disrupt the
normal cardiac cycle.
It appears as a PVC
squeezed between two
regular complexes.
A PVC occurring on
or near the previous
T wave is called an
R-on-T PVC.
PVC that occurs on or near the T wave can
precipitate ventricular tachycardia or fibrillation
Figure 6-5 Interpolated PVC.
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108. Chapter 6 Ventricular Dysrhythmias 101
Idioventricular rhythm characteristics
Rate: 20 to 40 beats per minute (may be slower)
Regularity: Regular
P waves: Not preceded by a P wave (if seen, they are dissociated and
would therefore be a 3rd-degree heart block with an idioven-
tricular escape)
QRS complexes: Wide, large, and bizarre looking
PR interval: Not measurable
QT interval: Usually prolonged
Figure 6-7
Summary of characteristics of idioventricular rhythm.
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109. Chapter 6 Ventricular Dysrhythmias 102
Idioventricular rhythm arises from a single site in the ventricles(s).
Figure 6-8
Idioventricular rhythm.
Idioventricular rhythm arises from a single site in the ventricles.
Rate is 20 to
40 beats per
minute
Rhythm is
regular
P waves are not visible as
they are hidden in the QRS
complexes
QRS complexes are
wide and bizarre in
appearance, have T
waves in the
opposite direction of
the R wave
PR intervals
are absent
Idioventricular rhythm
20 to 40 beats per min
ute
Accelerated idioventricular rhythm
40 to 100 beats per min
ute
Ventricular tachycardia
100 to 250 beats per minute
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110. Chapter 6 Ventricular Dysrhythmias 103
Accelerated idioventricular rhythm characteristics
Rate: 40 to 100 beats per minute
Regularity: Regular
P waves: Not preceded by a P wave
QRS complexes: Wide, large, and bizarre looking
PR interval: Not measurable
QT interval: Usually prolonged
Figure 6-9
Summary of characteristics of accelerated idioventricular rhythm.
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111. Chapter 6 Ventricular Dysrhythmias 104
Accelerated idioventricular rhythm arises from a single site in the ventricles(s).
Figure 6-10
Accelerated idioventricular rhythm.
Idioventricular rhythm
20 to 40 beats per minute
Accelerated idioventricular rhythm
40 to 100 beats per min
ute
Ventricular tachycardia
100 to 250 beats per minute
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112. Chapter 6 Ventricular Dysrhythmias 105
Ventricular tachycardia characteristics
Rate: 100 to 250 beats per minute
Regularity: Regular
P waves: Not preceded by a P wave (if seen, they are dissociated)
QRS complexes: Wide, large, and bizarre looking
PR interval: Not measurable
QT interval: Not measurable
Ventricular tachycardia may be monomorphic, where the appearance of each QRS complex is similar, or
polymorphic, where the appearance varies considerably from complex to complex.
Figure 6-11
Summary of characteristics of ventricular tachycardia.
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113. Chapter 6 Ventricular Dysrhythmias 106
Ventricular tachycardia arises from a single site in the ventricles(s).
Idioventricular rhythm
20 to 40 beats per minute
Accelerated idioventricular rhythm
40 to 100 beats per minute
Ventricular tachycardia
100 to 250 beats per min
ute
Two other conditions to be familiar with:
Ventricular fibrillation (VF)—results from chaotic firing of multiple sites in the ventricles. This causes the
heart muscle to quiver, much like a handful of worms, rather than contracting efficiently. On the ECG monitor
it appears like a wavy line, totally chaotic, without any logic.
Asystole—is the absense of any cardiac activity. It appears as a flat (or nearly flat) line on the monitor screen.
Figure 6-12
Ventricular tachycardia.
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114. AV Heart Blocks
7
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115. Chapter 7 AV Heart Blocks 108
What is in this chapter
1st-degree AV heart block characteristics
2nd-degree AV heart block, Type I
(Wenckebach) characteristics
2nd-degree AV heart block, Type II
characteristics
3rd-degree AV heart block characteristics
Characteristics common to AV heart blocks
P waves are upright and round. In 1st-degree AV block all the P waves are followed
by a QRS complex. In 2nd-degree AV block not all the P waves are followed by a QRS
complex, and in 3rd-degree block there is no relationship between the P waves and
QRS complexes.
In 1st-degree AV block PR interval is longer than normal and constant. In 2nd-degree
AV block, Type I, in a cyclical manner the PR interval is progressively longer until a
QRS complex is dropped. In 2nd-degree AV block, Type II, the PR interval of the con-
ducted beats is constant. In 3rd-degree block there is no PR interval.
QRS complexes may be normal or wide.
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116. Chapter 7 AV Heart Blocks 109
1st-degree AV heart block characteristics
Rate: Underlying rate may be slow, normal, or fast
Regularity: Underlying rhythm is usually regular
P waves: Present and normal and all are followed by a QRS complex
QRS complexes: Should be normal
PR interval: Longer than 0.20 seconds and is constant (the same each time)
QT interval: Usually within normal limits
Figure 7-1
Summary of characteristics of 1st-degree AV block.
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117. Chapter 7 AV Heart Blocks 110
In 1st-degree AV heart block impulses arise from the SA node but their passage through the AV node is
delayed.
Figure 7-2
1st-degree AV block.
Delay
Delay
Delay
Delay
Delay
Delay
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118. Chapter 7 AV Heart Blocks 111
2nd-degree AV heart block, Type I (Wenckebach) characteristics
Rate: Ventricular rate may be slow, normal, or fast; atrial rate is within
normal range
Regularity: Patterned irregularity
P waves: Present and normal; not all the P waves are followed by a QRS
complex
QRS complexes: Should be normal
PR interval: Progressively longer until a QRS complex is dropped; the cycle
then begins again
QT interval: Usually within normal limits
Figure 7-3
Summary of characteristics of 2nd-degree AV block, Type I.
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119. Chapter 7 AV Heart Blocks 112
In 2nd-degree AV heart block, Type I (Wenckebach), impulses arise from the SA node but their passage
through the AV node is progressively delayed until the impulse is blocked.
Figure 7-4
2nd-degree AV block, Type I.
Delay
More delayEven more delay
Impulse is blocked
Blocked
Delay
More delay
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120. Chapter 7 AV Heart Blocks 113
2nd-degree AV heart block, Type II characteristics
Rate: Ventricular rate may be slow, normal, or fast; atrial rate is within
normal range
Regularity: May be regular or irregular (depends on whether conduction
ratio remains the same)
P waves: Present and normal; not all the P waves are followed by a QRS
complex
QRS complexes: Should be normal
PR interval: Constant for all conducted beats
QT interval: Usually within normal limits
Figure 7-5
Summary of characteristics of 2nd-degree AV block, Type II.
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121. Chapter 7 AV Heart Blocks 114
In 2nd-degree AV heart block, Type II, impulses arise from the SA node but some are blocked
in the bundle of His or bundle branches.
Figure 7-6
2nd-degree AV block, Type II.
Blocked
Blocked
Blocked
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122. Chapter 7 AV Heart Blocks 115
3rd-degree AV heart block characteristics
Rate: Ventricular rate may be slow, normal, or fast; atrial rate is within
normal range
Regularity: Atrial rhythm and ventricular rhythms are regular but not relat-
ed to one another
P waves: Present and normal; not related to the QRS complexes; appear to
march through the QRS complexes
QRS complexes: Normal if escape focus is junctional and widened if escape focus
is ventricular
PR interval: Not measurable
QT interval: May or may not be within normal limits
Figure 7-7
Summary of characteristics of 3rd-degree AV block.
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123. Chapter 7 AV Heart Blocks 116
In 3rd-degree AV heart block there is a complete block at the AV node resulting in the atria being
depolarized by an impulse that arises from the SA node and the ventricles being depolarized by an
escape pacemaker that arises somewhere below the AV node.
Figure 7-8
3rd-degree AV block.
Blocked
B l o cke d
Blocked
Blocked
Blocked
Blocked
Blocked
Blocked
Escape Escape
Escape
Escape
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124. Electrical Axis
8
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125. Chapter 8 Electrical Axis 118
What is in this chapter
Direction of ECG waveforms
Mean QRS Vector
Methods for Determining
QRS axis
Lead I
Lead aV
F
Axis Deviation
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126. Chapter 8 Electrical Axis 119
Direction of ECG waveforms
Depolarization and repolarization of
the cardiac cells produce many small
electrical currents called instanta-
neous vectors.
The mean, or average, of all the
instantaneous vectors is called the
mean vector.
When an impulse is traveling toward
a positive electrode, the ECG machine
records it as a positive or upward
deflection.
When the impulse is traveling away
from a positive electrode and toward
a negative electrode, the ECG
machine records it as a negative or
downward deflection.
Negative
electrode
Positive
electrode
–
+
Impulses traveling
toward a positive
electrode produce
an upward
deflection
Impulses traveling away from a positive electrode and/or toward a negative electrode produce downward deflections
Figure 8-1
Direction of ECG waveforms when the electrical cur-
rent is traveling toward a positive ECG electrode or
away from it.
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127. Chapter 8 Electrical Axis 120
Mean QRS Vector
The sum of all the small vectors of ventricular
depolarization is called the mean QRS vector.
Because the depolarization vectors of the
thicker left ventricle are larger, the mean QRS
axis points downward and toward the patient’s
left side.
Changes in the size or condition of the heart
muscle and/or conduction system can affect
the direction of the mean QRS vector.
If an area of the heart is enlarged or damaged,
specific ECG leads can provide a view of that
portion of the heart.
While there are several methods used to
determine the direction of the patient’s elec-
trical axis, the easiest is the four-quadrant
method.
Figure 8-2
Direction of of the mean QRS axis.
AV node
Mean QRS axis
Impulse originates in SA
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128. Chapter 8 Electrical Axis 121
+180°
+150°
+120°
+90°
+60°
+30°
0°
–30°
–60°
–90°
–120°
–150°
Mean QRS axis
Lead aV
F
Lead I
AV node
Method for determining QRS axis
The four-quadrant method works in the following
manner:
∞
An imaginary circle is drawn over the patient’s
chest; it represents the frontal plane.
∞
Within the circle are six bisecting lines, each
representing one of the six limb leads.
∞
The intersection of all lines divides the circle
into equal, 30-degree segments.
The mean QRS axis normally remains
between 0 and +90° degrees.
∞
As long as it stays in this range it is
considered normal.
∞
If it is outside this range, it is considered
abnormal.
∞
Leads I and aV
F can be used to determine
if the mean QRS is in its normal position.
Figure 8-3
Normal direction of the mean QRS axis.
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129. Chapter 8 Electrical Axis 122
Lead I
Lead I is oriented at 0° (located at
the three o’clock position).
A positive QRS complex indicates
the mean QRS axis is moving from
right to left in a normal manner and
directed somewhere between –90°
and +90° (the right half of the circle).
If the QRS complex points down
(negative), then the impulses are
moving from left to right; this is
considered abnormal.
Figure 8-4
A positive QRS complex is seen in lead I if the mean QRS axis is
directed anywhere between –90 and +90.
+
+
+
+
+
+
+++
+
+
+
+++
+
+
–
–
–
–
–
–
–
–
– –
–
–
+
Right
+90°
Left
–90°
Lead I
–+
QRS
in lead I
AV node
Mean QRS axis
Left arm electrode
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130. Chapter 8 Electrical Axis 123
+
+
+
+
+
+
++
++
+
+
+
+
+
+
+
–
–
–
–
––
–
–
–
–
–
–
–
–
+
+180° 0°
To p
+
AV node
Bottom
Lead aV
F
QRS
in lead
aV
F
Mean QRS axis
Lead aV
F
Lead aV
F is oriented at +90° and is
located at the six o’clock position.
If the mean QRS axis is directed any-
where between 0° and –180° (the
bottom half of the circle), you can
expect aV
F lead to record a positive
QRS complex.
If the mean QRS is directed toward the
top half of the circle, the QRS complex
points downward.
Figure 8-5
A positive QRS complex is seen in lead aV
F if the mean QRS
axis is directed anywhere between 0 and 180 degrees.
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131. Chapter 8 Electrical Axis 124
Axis deviation
Positive QRS complexes in lead I and aV
F indi-
cate a normal QRS axis.
A negative QRS complex in lead I and an upright
QRS complex in lead aV
F indicates right axis
deviation.
An upright QRS complex in lead I and a nega-
tive QRS complex in lead aV
F indicates left axis
deviation.
Negative QRS complexes in both lead I and lead
aV
F indicates extreme axis deviation.
Persons who are thin, obese, or pregnant can
have axis deviation due to a shift in the position
of the apex of the heart.
Myocardial infarction, enlargement, or hypertro-
phy of one or both of the heart’s chambers, and
hemiblock can also cause axis deviation.
Figure 8-6
Direction of QRS complexes in lead I and aV
F indicate
changes in size or condition of the heart muscle and/or
conduction system.
+180°
+150°
+120°
+90°
+60°
+30°
0°
–30°
–60°
–90°
–120°
–150°
Lead I
+
+
I
I
aV
F aV
F
I
I
aV
F
aV
F
Lead aV
F
Extreme
axis
deviation
Left axis
deviation
Right axis
deviation
Normal
axis
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132. Hypertrophy, Bundle
Branch Block, and
Preexcitation
9
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133. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 126
What is in this chapter
Right atrial enlargement
Right ventricular hypertrophy
Right bundle branch block
Left atrial enlargement
Left ventricular hypertrophy
Left bundle branch block
Left anterior hemiblock
Left posterior hemiblock
Wolff-Parkinson-White (WPW)
syndrome
Lown-Ganong-Levine (LGL) syndrome
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134. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 127
Right atrial enlargement
Leads II and V
1 provide the necessary infor-
mation to assess atrial enlargement.
Indicators of right atrial enlargement
include:
∞
An increase in the amplitude of the first
part of the P wave.
∞
The P wave is taller than 2.5 mm.
∞
If the P wave is biphasic, the initial
component is taller than the terminal
component.
The width of the P wave, however, stays
within normal limits because its terminal
part originates from the left atria, which
depolarizes normally if left atrial enlarge-
ment is absent.
+
+
Right atrial
enlargement
Lead II
Lead
V
1
P pulmonale
II, III, and aV
F
Biphasic P wave
V
1
Figure 9-1
Right atrial enlargement leads to an increase in the
amplitude of the first part of the P wave.
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135. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 128
Left atrial enlargement
Indicators of left atrial enlargement include:
∞
The amplitude of the terminal portion of the
P wave may increase in V
1.
∞
The terminal (left atrial) portion of the P
wave drops at least 1 mm below the iso-
electric line (in lead V
1).
∞
There is an increase in the duration or
width of the terminal portion of the P wave
of at least one small square (0.04 seconds).
Often the presence of ECG evidence of left
atrial enlargement only reflects a nonspecific
conduction irregularity. However, it may also
be the result of mitral valve stenosis causing
the left atria to enlarge to force blood across
the stenotic (tight) mitral valve.
Figure 9-2
Left atrial enlargement leads to an increase in the amplitude
and width of the terminal part of the P wave.
+
+
Left atrial
enlargement
P wave
Lead II
Lead V
1
Broad
P w
ave
Biphasic
P wave
V
1
–V
2
Notched P wave
(P mitrale)
I, II, and V
4
–V
6
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136. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 129
Right ventricular hypertrophy
Key indicators of right ventricular hyper-
trophy include:
∞
The presence of right axis deviation
(with the QRS axis exceeding +100°).
The R wave larger than the S wave in lead
V
1, whereas the S wave is larger than the
R wave in lead V
6.
Left ventricular hypertrophy
Key ECG indicators of left ventricular
hypertrophy include:
∞
Increased R wave amplitude in those
leads overlying the left ventricle.
∞
The S waves are smaller in leads over-
lying the left ventricle, but larger in
leads overlying the right ventricle.
Figure 9-3
In right ventricular hypertrophy the QRS axis moves to
between +90 and +180 degrees. The QRS complexes in right
ventricular hypertrophy are slightly more negative in lead I
and positive in lead aV
F.
+
+
+180° 0°
+90°
–90°
Lead I
Lead aV
F
Right ventricular
hypertrophy
aV
F
Mean QRS axis
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137. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 130
Right ventricular
hypertrophy
Starting with V
1
, the waveforms take an
upward deflection but then moving toward
V
6
the waveforms take a downward
deflection
V
1
V
2
V
3
V
4
S
R
Figure 9-4
The thick wall of the enlarged right ventricle causes
the R waves to be more positive in the leads that lie
closer to lead V
1.
Mean QRS axis
+180° 0°
–90°
The mean QRS axis moves
farther leftward resulting in
left axis deviation
R
S
V
1
V
2
V
3
V
4
V
5
V
6
+90°
Left ventricular
hypertrophy
Figure 9-5
The thick wall of the enlarged left ventricle causes the R waves to be
more positive in the leads that lie closer to lead V
6 and the S waves to
be larger in the leads closer to V
1.
V
1 V
2 V
3 V
4 V
5 V
6
S
R
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138. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 131
Right bundle branch block
The best leads for identifying right bundle
branch are V
1 and V
2.
Right bundle block causes the QRS com-
plex to have a unique shape — its appear-
ance has been likened to rabbit ears or the
letter “M.”
∞
As the left ventricle depolarizes, it pro-
duces the initial R and S waves, but as
the right ventricle begins its delayed
depolarization, it produces a tall R wave
(called the R„ ).
In the left lateral leads overlying the left
ventricle (I, aV
L, V
5, and V
6), late right ven-
tricular depolarization causes reciprocal
late broad S waves to be generated.Figure 9-6
In right bundle branch block, conduction through the
right bundle is blocked causing depolarization of the
right ventricle to be delayed; it does not start until the
left ventricle is almost fully depolarized.
+
+
+
+
V
1 V
2
V
5V
6
R
R
R
S
S
S
R∞ R∞
r∞
Block
QRS
configuration
in V
5,
V
6
, I, aV
L
QRS
configuration
in V
1,
V
2
Late broad S waves
Different M-shaped configurations
that may be seen
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139. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 132
Left bundle branch block
Leads V
5 and V
6 are best for identifying left
bundle branch block.
∞
QRS complexes in these leads normally
have tall R waves, whereas delayed
left ventricular depolarization leads to a
marked prolongation in the rise of those
tall R waves, which will either be flat-
tened on top or notched (with two tiny
points), referred to as an R, R„ wave.
∞
True rabbit ears are less likely to be seen
than in right bundle branch block.
Leads V
1 and V
2 (leads overlying the right
ventricle) will show reciprocal, broad, deep
S waves.
V
1 V
2
V
5
V
6
R∞
+
+
+
+
Block
R
R
R∞ R∞
R∞
R
R R
QRS
configuration
in V
1, V
2
QRS
configuration
in V
5
, V
6
Different configurations
that may be seen
QS Deep S
Figure 9-7
In left bundle branch block, conduction through the left bundle is
blocked causing depolarization of the left ventricle to be delayed; it
does not start until the right ventricle is almost fully depolarized.
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140. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 133
Left anterior hemiblock
With left anterior hemiblock, depolar-
ization of the left ventricle occurs pro-
gressing in an inferior-to-superior and
right-to-left direction.
∞
This causes the axis of ventricu-
lar depolarization to be redirected
upward and slightly to the left, pro-
ducing tall positive R waves in the
left lateral leads and deep S waves
inferiorly.
∞
This results in left axis deviation with
an upright QRS complex in lead I and
a negative QRS in lead aV
F.
+
+
Block
Left axis
deviation
Deep S
Small R
QRS
configuration
in lead III
Small Q
QRS
configuration
in lead I
+180° 0°
+90°
–90°
Lead aV
F
Lead ITall R
Figure 9-8
With left anterior hemiblock, conduction down the left anterior fas-
cicle is blocked resulting in all the current rushing down the left poste-
rior fascicle to the inferior surface of the heart.
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141. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 134
Left posterior hemiblock
In left posterior hemiblock, ventricular
myocardial depolarization occurs in
a superior-to-inferior and left-to-right
direction.
∞
This causes the main electrical axis
to be directed downward and to the
right, producing tall R waves infe-
riorly and deep S waves in the left
lateral leads.
∞
This results in right axis deviation.
With a negative QRS in lead I and a
positive QRS in lead aV
F.
In contrast to complete left and right
bundle branch block, in hemiblocks,
the QRS complex is not prolonged.
+
+
Block
Right axis
deviation
Small Q
Tall R
QRS
configuration
in lead III
Deep S
Small
R
QRS
configuration
in lead I
Lead aVF
Figure 9-9
With left posterior hemiblock, conduction down the left
posterior fascicle is blocked resulting in all the current
rushing down the left anterior fascicle to the myocardium.
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142. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 135
Wolff-Parkinson-White
(WPW) syndrome
WPW is identified through the
following ECG features:
∞
Rhythm is regular.
∞
P waves are normal.
∞
QRS complexes are wid-
ened due to a characteristic
slurred initial upstroke,
called the delta wave.
∞
PR interval is usually short-
ened (less than 0.12 sec-
onds).
WPW can predispose the
patient to various tachydys-
rhythmias; the most common
is PSVT.
Figure 9-10
In WPW, the bundle of Kent, an accessory pathway, connects the atrium to the
ventricles, bypassing the AV node. The QRS complex is widened due to premature
activation of the ventricles.
Instead of the
impulse traveling
through the AV node,
it travels down an
accessory pathway
to the ventricles
Bundle of Kent
Delta
wave
Delta
wave
Delta
wave
Delta
wave
Delta
wave
Delta
wave
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143. Chapter 9 Hypertrophy, Bundle Branch Block, and Preexcitation 136
Instead of traveling
through the AV node,
the impulse is carried
to the ventricles by
way of an intranodal
accessory pathway
James fibers
Impulse travels
down through
the atria
Lown-Ganong-Levine
(LGL) syndrome
LGL is identified through the
following ECG features:
Rhythm is regular.
∞
P waves are normal.
∞
The PR interval is less than
0.12 seconds.
∞
The QRS complex is not
widened.
∞
There is no delta wave.
WPW and LGL are called
preexcitation syndromes and
are the result of accessory
conduction pathways between
the atria and ventricles.
Figure 9-11
In LGL, the impulse travels through an intranodal accessory pathway, referred
to as the James fibers, bypassing the normal delay within the AV node. This pro-
duces a shortening of the PR interval but no widening of the QRS complex.
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144. Myocardial Ischemia
and Infarction
10
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145. Chapter 10 Myocardial Ischemia and Infarction 138
What is in this chapter
ECG changes associated with
ischemia, injury, and infarction
Identifying the location of myo-
cardial ischemia, injury, and
infarction
∞
Anterior
∞
Septal
∞
Lateral
∞
Inferior
∞
Posterior
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146. Chapter 10 Myocardial Ischemia and Infarction 139
ECG changes associated with ischemia,
injury, and infarction
The ECG can help identify the presence of ischemia,
injury, and/or infarction of the heart muscle.
The three key ECG indicators are:
∞
Changes in the T wave (peaking or inversion).
∞
Changes in the ST segment (depression or
elevation).
∞
Enlarged Q waves or appearance of new Q waves.
ST segment elevation is the earliest reliable sign that
myocardial infarction has occurred and tells us the
myocardial infarction is acute.
Pathologic Q waves indicate the presence of irrevers-
ible myocardial damage or past myocardial infarction.
Myocardial infarction can occur without the develop-
ment of Q waves.
Ischemia
ST segment
changes
Inverted
T wave
Ta l l ,
peaked
T wave
Depressed
ST segment
Elevated
ST
segment
T wave
changes
Q wave
changes
Injury
Infarction
Figure 10-1
Key ECG changes with ischemia, injury, or
infarction
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147. Chapter 10 Myocardial Ischemia and Infarction 140
Figure 10-2
Leads V
1, V
2, V
3, and V
4 are used to identify ante-
rior myocardial infarction.
+
+
+
V1
V2
V3
V4
+
Anterior infarction
V
1
V
2
V
3
V
4
Identifying the location of myocardial
ischemia, injury, and infarction
Leads V
1, V
2, V
3, and V
4 provide the best view for identi-
fying anterior myocardial infarction.
Leads V
1, V
2, and V
3 overlie the ventricular septum, so
ischemic changes seen in these leads, and possibly in
the adjacent precordial leads, are often considered to
be septal infarctions.
Lateral infarction is identified by ECG changes such as ST
segment elevation; T wave inversion; and the develop-
ment of significant Q waves in leads I, aV
L, V
5, and V
6.
Inferior infarction is determined by ECG changes such as
ST segment elevation; T wave inversion; and the develop-
ment of significant Q waves in leads II, III, and aV
F.
Posterior infarctions can be diagnosed by looking for
reciprocal changes in leads V
1 and V
2.
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148. Chapter 10 Myocardial Ischemia and Infarction 141
Figure 10-3
Leads V
1, V
2, and V
3 are used to identify septal
myocardial infarction.
+
+
+
V
1
V
2
V
3
V
1
V
2
V
3
Septal infarction
+
+
+
+
aV
L
V
5
I
V
6
aV
L
V
5
V
6
I
Lateral infarction
Figure 10-4 Leads I, aV
L, V
5, and V
6 are used to iden-
tify lateral myocardial infarction.
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149. Chapter 10 Myocardial Ischemia and Infarction 142
Figure 10-5
Leads II, III, and aV
F are used to identify infe-
rior myocardial infarction.
Figure 10-6
Leads V
1 and V
2 are used to identify posterior myocardial infarction.
+ + +
Inferior infarction
II III aV
F
II III aV F
+
+
V
1
V
2
V
3
Posterior infarction
Posterior view of heart
+
V
1
V
2
V
3
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150. Other Cardiac
Conditions
11
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151. Chapter 11 Other Cardiac Conditions 144
What is in this chapter
Pericarditis
Pericardial effusion with low-
voltage QRS complexes
Pericardial effusion with electri-
cal alternans
Pulmonary embolism
Pacemakers
Electrolyte imbalances
Digoxin effects seen on the ECG
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152. Chapter 11 Other Cardiac Conditions 145
Pericarditis
Initially with pericarditis the T wave is upright
and may be elevated. During the recovery
phase it inverts.
The ST segment is elevated and usually flat or
concave.
While the signs and symptoms of pericarditis
and myocardial infarction are similar, certain
features of the ECG can be helpful in differenti-
ating between the two:
∞
The ST segment and T wave changes in
pericarditis are diffuse resulting in ECG
changes being present in all leads.
∞
In pericarditis, T wave inversion usually
occurs only after the ST segments have
returned to base line. In myocardial infarc-
tion, T wave inversion is usually seen before
ST segment normalization.
(continued)
Effects on ECG
Effects of pericarditis on the heart
Normal
pericardium
Enlarged view
Inflamed
pericardium
ST segments and T waves are off the baseline,
gradually angling back down to the next QRS complex
Elevated ST segment is flat or concave
Figure 11-1
Pericarditis and ST segment elevation.
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153. Chapter 11 Other Cardiac Conditions 146
∞
In pericarditis, Q wave development does not
occur.
Pericardial effusion with low-voltage
QRS complexes
Pericardial effusion is a buildup of an abnormal
amount of fluid and/or a change in the character of
the fluid in the pericardial space.
∞
The pericardial space is the space between the
heart and the pericardial sac.
Formation of a substantial pericardial effusion damp-
ens the electrical output of the heart, resulting in
low-voltage QRS complex in all leads.
However, the ST segment and T wave changes of
pericarditis may still be seen.
I
aV
R
aV
L
aV
F
II
III
Pericardial
sac
Collection
of fluid
Nor
mal pericardium Pericardial effusion
Dampened
electrical
output
Figure 11-2
Pericardial effusion with low-voltage QRS complexes.
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154. Chapter 11 Other Cardiac Conditions 147
Pericardial effusion with
electrical alternans
If a pericardial effusion is large
enough, the heart may rotate freely
within the fluid-filled sac.
This can cause electrical alternans, a
condition in which the electrical axis
of the heart varies with each beat.
A varying axis is most easily recog-
nized on the ECG by the presence of
QRS complexes that change in height
with each successive beat.
This condition can also affect the
P and T waves.
Figure 11-3 Pericardial effusion with electrical alternans.
Pericardial effusion
Hear t
rotates
freely
Pericardial
sac
Collection of
fluid
II
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155. Chapter 11 Other Cardiac Conditions 148
Pulmonary embolism
ECG changes that suggest the development of a
massive pulmonary embolus include:
∞
Tall, symmetrically peaked P waves in leads
II, III, and aV
F and sharply peaked biphasic
P waves in leads V
1 and V
2.
∞
A large S wave in lead I, a deep Q wave in
lead III, and an inverted T wave in lead III.
This is called the S
1 Q
3 T
3 pattern.
∞
ST segment depression in lead II.
∞
Right bundle branch block (usually subsides
after the patient improves).
∞
The QRS axis is greater than
+90° (right axis deviation).
∞
The T waves are inverted in leads V
1–V
4.
∞
Q waves are generally limited to lead III.
Embolus S
1
Q
3
T
3
Large S wave
in lead I
ST segment
depression
in lead II
Large Q wave
in lead III with
T wave inversion
Right bundle branch
block in leads V
1
–V
4
T wave inversion
in leads V
1
–V
4
V
1
V
2
V
3
V
4
Figure 11-4
ECG changes seen with pulmonary embolism.
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156. Chapter 11 Other Cardiac Conditions 149
Pacemakers
A pacemaker is an artificial device
that produces an impulse from a
power source and conveys it to the
myocardium.
It provides an electrical stimulus
for hearts whose intrinsic ability to
generate an impulse or whose abil-
ity to conduct electrical current is
impaired.
The power source is generally
positioned subcutaneously, and the
electrodes are threaded to the right
atrium and right ventricle through
veins that drain to the heart.
The impulse flows throughout the
heart causing the muscle to depolar-
ize and initiate a contraction.
Figure 11-5
Pacemakers are used to provide electrical stimuli for hearts with an
impaired ability to conduct an electrical impulse.
Impulses initiated
by the SA node do
not reach the ventricles
BLOCKED
Pacemaker initiates
impulses that stimulate
the ventricles to contract
Pacemaker
spike
Pacemaker
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157. Chapter 11 Other Cardiac Conditions 150
An atrial pacemaker will produce a spike trailed by a P wave and a normal QRS complex.
With an AV sequential pacemaker, two spikes are seen, one that precedes a P wave and one
that precedes a wide, bizarre QRS complex.
With a ventricular pacemaker, the resulting QRS complex is wide and bizarre. Because the
electrodes are positioned in the right ventricle, the right ventricle will contract first, then the
left ventricle. This produces a pattern identical to left bundle branch block, with delayed left
ventricular depolarization.
Figure 11-6
Location of pacemaker
spikes on the ECG tracing
with each type of pacemaker.
Atrial pacing
Pacemaker impulses
Ventricular pacing
Pacemaker spikes
Atrial and ventricular pacing
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158. Electrolyte
imbalances
Hypokalemia
ECG changes seen
with serious hypoka-
lemia include:
∞
ST segment
depression.
∞
Flattening of the
T wave.
∞
Appearance of
U waves.
∞
Prolongation of
the QT interval.
Figure 11-7
ECG effects seen with hypokalemia.
T wave flattens
(or is inverted)
and U wave appears
U wave becomes more
prominent
Depressed
ST segmentU w
ave
U wave
Depressed
ST segment
Peaked, narrow T waves in
all leads
T wave peaking increases, P
waves flatten and QRS
complexes widen
Widened QRS complexes and
peaked T waves become almost
indistinguishable, forming what are
described as a “sine-wave pattern”
Hyperkalemia
ECG changes seen with
hyperkalemia include:
∞
Peaked T waves (tenting).
∞
Flattened P waves.
∞
Prolonged PR interval (1st-
degree AV heart block).
∞
Widened QRS complex.
∞
Deepened S waves and
merging of S and T waves.
∞
Concave up and down
slope of the T wave.
∞
Sine-wave pattern.
Figure 11-8 ECG effects seen with hyperkalemia.
Chapter 11 Other Cardiac Conditions
151
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159. Chapter 11 Other Cardiac Conditions 152
Hypercalcemia/
Hypocalcemia
Alterations in serum
calcium levels mainly
affect the QT interval.
Hypocalcemia pro-
longs the QT interval
while hypercalcemia
shortens it.
Torsades de pointes, a
variant of ventricular
tachycardia, is seen
in patients with pro-
longed QT intervals.
Figure 11-9
ECG effects seen with hypocalcemia
and hypercalcemia.
Short QT interval
Prolonged QT interval
Gradual downward curve of the ST segment
Digoxin effects seen on the ECG
Digoxin produces a characteristic gradual downward
curve of the ST segment (it looks like a ladle).
∞
The R wave slurs into the ST segment.
∞
Sometimes the T wave is lost in this scooping effect.
The lowest portion of the ST segment is depressed
below the baseline.
When seen, the T waves have shorter amplitude and
can be biphasic.
The QT interval is usually shorter than anticipated,
and the U
waves are
more visible.
Also, the PR
interval may
be prolonged.
Figure 11-10
Effects of digoxin on the ECG.
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160. Index
Accelerated idioventricular rhythm,
103–104
Accelerated junctional rhythm, 91–92
Atrial dysrhythmias, 68
Atrial fibrillation, 83–84
Atrial flutter, 81–82
Atrial tachycardia, 77–78
Augmented limb leads, 13–14
AV heart blocks, 108–116

Bipolar leads, 11
Bradycardia, 25, 26

Caliper method, 29
Conduction system, heart’s, 7
Counting the small squares method, 31
Digoxin, 152–153
Dysrhythmias, by heart rate, 25–26

ECG (electrocardiogram), 3–4
ECG leads
augmented limb leads (aV
R
, aV
L
,
aV
F
), 13–14, 123
Leads I, II, III, 11–12, 122
modified chest leads, 16
precordial leads (Leads

V
1
–V
6
),
15–16
ECG paper, 9–10
ECG tracings, 3, 4, 19–20
Electrical axis, 119–124
Electrical conductive system, 4, 7
Electrolyte imbalances, 151–152
1500 method, heart rate using, 24
1st-degree AV heart block,
109–110

Heart, 5–7
Heart rate, determining, 21–24
Hypercalcemia/hypocalcemia, 152
Hypokalemia/hyperkalemia, 151

Idioventricular rhythm, 101–102
Irregularity, types of, 32, 40
frequently irregular, 34
irregular irregularity, 38
occasionally irregular, 33
paroxysmally irregular, 36
patterned irregularity, 37
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161. Index
slightly irregular, 35
variable irregularity, 39

Junctional dysrhythmias, 86
Junctional escape rhythm, 89–90
Junctional tachycardia, 93–94

Left anterior hemiblock, 133
Left atrial enlargement, 128
Left bundle branch block, 132
Left posterior hemiblock, 134
Left ventricular hypertrophy, 129, 130
Lown-Ganong-Levine syndrome, 136

Mean QRS axis, 120–123
Multifocal atrial tachycardia, 79–80
Myocardial ischemia and infarction,
139–142

P wave, 41, 49–50
Pacemakers, 149–150
Paper and pen method, 30
Pericardial effusion, 146–147
Pericarditis, 145–146
P–P interval, 27–28
PR interval, 45–46, 53–54
Premature atrial complexes (PACs),
71–76
Premature junctional complexes
(PJCs), 87–88
Premature ventricular complexes
(PVCs), 97–100
Pulmonary embolism, 148

Q wave, 42
QRS complex, 42–44, 51–52, 124
QT interval, 48

R wave, 42
Regularity, determining, 27–40
Right atrial enlargement, 127
Right bundle branch block, 131
Right ventricular hypertrophy, 129, 130
R–R interval, 27–28, 31
S wave, 42
2nd-degree AV heart block, 111–114
Sinus arrest, 65–66
Sinus bradycardia, 59–60
Sinus dysrhythmias, 56, 63–64
Sinus rhythm, 57–58
Sinus tachycardia, 61–62
6-second X 10 method, heart rate
using, 21
ST segment, 47

T wave, 48
Tachycardia, 25, 26
Thin lines, to determine heart
rate, 23
3rd-degree AV heart block, 115–116
300, 150, 100, 75, 60, 50 method, heart
rate using, 22

U waves, 48

Ventricular dysrhythmias, 96
Ventricular tachycardia, 105–106

Wandering atrial pacemaker, 69–70
Waveforms, ECG, 8, 41–54, 119
Wenckebach, 111–112
Wolff-Parkinson-White syndrome, 135
154
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