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Рассказывается о том, как получить и правильно интерпретировать ЭКГ. ECG Interpretation Made Incredibly Easy! Fifth Edition makes learning to read and interpret rhythm strips simple. This practical reference uses a unique, conversational writing style that breaks down complex concepts and information to make ECG interpretation easier to understand. Fully updated and now in full color, the book reviews fundamental cardiac anatomy and physiology, explains how to obtain and interpret a rhythm strip, and teaches the reader how to recognize and treat sinus, atrial, and ventricular arrhythmias as well as heart blocks. In addition, the book explains how to obtain and interpret 12-lead ECGs. Special elements found throughout the reference make it easy to remember key points. Each chapter features: A summary of key points clear, simple explanations of problems definitions of key terms illustrations that clearly explain key concepts bullets, ballot boxes, and checklists that make it easy to spot important points at a glance sidebars that highlights key facts about ECG interpretation and quick quizzes to test knowledge.
5th Edition
Lippincott Williams & Wilkins
ISBN 10:
ISBN 13:
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Chris Burghardt
Clinical Director
Joan M. Robinson, RN, MSN
Clinical Project Manager
Jennifer Meyering, RN, BSN, MS
Product Director
David Moreau
Product Manager
Jennifer K. Forestieri
Tracy S. Diehl
Art Director
Elaine Kasmer
Bot Roda
Design Assistant
Kate Zulak
Vendor Manager
Beth Martz
Associate Manufacturing Manager
Beth J. Welsh
Editorial Assistants
Karen J. Kirk, Jeri O’Shea, Linda K. Ruhf

The clinical treatments described and recommended
in this publication are based on research and consultation with nursing, medical, and legal authorities. To the
best of our knowledge, these procedures reflect currently accepted practice. Nevertheless, they can’t be
considered absolute and universal recommendations.
For individual applications, all recommendations must
be considered in light of the patient’s clinical condition
and, before administration of new or infrequently used
drugs, in light of the latest package-insert information.
The authors and publisher disclaim any responsibility
for any adverse effects resulting from the suggested
procedures, from any undetected errors, or from the
reader’s misunderstanding of the text.
© 2011 by Lippincott Williams & Wilkins. All rights
reserved. This book is protected by copyright. No part
of it may be reproduced, stored in a retrieval system, or
transmitted, in any form or by any means—electronic,
mechanical, photocopy, recording, or otherwise—
without prior written permission of the publisher, except
for brief quotations embodied in critical articles and
reviews and testing and evaluation materials provided by
publisher to instructors whose schools have adopted its
accompanying textbook. Printed in China. For information, write Lippincott Williams & Wilkins, 323 Norristown
Road, Suite 200, Ambler, PA 19002-2756.

Library of Congress Cataloging-in-Publication Data
ECG interpretation made incredi; bly easy!. —
5th ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-60831-289-4 (pbk. : alk. paper)
1. Electrocardiography. 2. Heart—Diseases—
Nursing. I. Lippincott Williams & Wilkins.
[DNLM: 1. Electrocardiography—Nurses’
Instruction. 2. Arrhythmias, Cardiac—Nurses’
Instruction. WG 140 E172 2011]
RC683.5.E5E256 2011
ISBN-13: 978-1-60831-289-4 (alk. paper)
ISBN-10: 1-60831-289-5 (alk. paper)


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Contributors and consultants
Not another boring foreword

Part I


ECG fundamentals
Cardiac anatomy and physiology
Obtaining a rhythm strip
Interpreting a rhythm strip


Part II Recognizing arrhythmias

Sinus node arrhythmias
Atrial arrhythmias
Junctional arrhythmias
Ventricular arrhythmias
Atrioventricular blocks


Part III Treating arrhythmias

Nonpharmacologic treatments
Pharmacologic treatments


Part IV The 12-lead ECG

Obtaining a 12-lead ECG
Interpreting a 12-lead ECG


Appendices and index
Practice makes perfect
ACLS algorithms
Brushing up on interpretation skills
Look-alike ECG challenge
Quick guide to arrhythmias
Selected references



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Contributors and consultants
Diane M. Allen, RN, MSN, ANP, BC, CLS
Nurse Practitioner
Womack Army Medical Center
Fort Bragg, N.C.

Karen Knight-Frank, RN, MS, CNS, CCRN, CCNS
Clinical Nurse Specialist, Critical Care
San Joaquin General Hospital
French Camp, Calif.

Nancy Bekken, RN, MS, CCRN
Nurse Educator, Adult Critical Care
Spectrum Health
Grand Rapids, Mich.

Marcella Ann Mikalaitis, RN, MSN, CCRN
Staff Nurse, Cardiovascular Intensive Care
Unit (CVICU)
Doylestown (Pa.) Hospital

Karen Crisfulla, RN, CNS, MSN, CCRN
Clinical Nurse Specialist
Hospital of the University of Pennsylvania

Cheryl Rader, RN, BSN, CCRN-CSC
Staff Nurse: RN IV
Saint Luke‘s Hospital of Kansas City (Mo.)

Maurice H. Espinoza, RN, MSN, CNS, CCRN
Clinical Nurse Specialist
University of California Irvine Medical Center
Kathleen M. Hill, RN, MSN, CCNS-CSC
Clinical Nurse Specialist, Surgical Intensive
Care Unit
Cleveland Clinic
Cheryl Kabeli, RN, MSN, FNP-BC, CNS-BC
Nurse Practitioner
Champlain Valley Cardiothoracic Surgeons
Plattsburgh, N.Y.

Leigh Ann Trujillo, RN, BSN
Clinical Educator
St. James Hospital and Health Center
Olympia Fields, Ill.
Rebecca Unruh, RN, MSN
Nurse Manager – Cardiac Intensive Care
Unit & Cardiac Rehabilitation
North Kansas City (Mo.) Hospital
Opal V. Wilson, RN, MA, BSN
RN Manager, PC Telemetry Unit
Louisiana State University Health Sciences


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Not another boring foreword
If you’re like me, you’re too busy to wade through a foreword that uses pretentious
terms and umpteen dull paragraphs to get to the point. So let’s cut right to the chase!
Here’s why this book is so terrific:
1. It will teach you all the important things you need to know about ECG interpretation.
(And it will leave out all the fluff that wastes your time.)
2. It will help you remember what you’ve learned.
3. It will make you smile as it enhances your knowledge and skills.
Don’t believe me? Try these recurring logos on for size:
Ages and stages identifies variations in ECGs related to patient age.

Now I get it offers crystal-clear explanations of complex procedures, such as how to
use an automated external defibrillator.

Don’t skip this strip identifies arrhythmias that have the most serious consequences.

Mixed signals provides tips on how to solve the most common problems in ECG
monitoring and interpretation.

I can’t waste time highlights key points you need to know about each arrhythmia for
quick reviews.
See? I told you! And that’s not all. Look for me and my
friends in the margins throughout this book. We’ll be there
to explain key concepts, provide important care reminders,
and offer reassurance. Oh, and if you don’t mind, we’ll be
spicing up the pages with a bit of humor along the way, to
teach and entertain in a way that no other resource can.
I hope you find this book helpful. Best of luck
throughout your career!


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Part I ECG fundamentals
1 Cardiac anatomy and physiology

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2 Obtaining a rhythm strip


3 Interpreting a rhythm strip


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Cardiac anatomy and physiology
Just the facts
In this chapter, you’ll learn:
 the location and structure of the heart
 the layers of the heart wall
 the flow of blood to and through the heart and the structures involved in this flow
 phases of the cardiac cycle
 properties of cardiac cells
 details of cardiac impulse conduction and their relationship to arrhythmias.

A look at cardiac anatomy
Cardiac anatomy includes the location of the heart; the structure
of the heart, heart wall, chambers, and valves; and the layout and
structure of coronary circulation.

The mediastinum
is home to the heart.

Outside the heart
The heart is a cone-shaped, muscular organ. It’s located in the
chest, behind the sternum in the mediastinal cavity (or mediastinum), between the lungs, and in front of the spine. The heart
lies tilted in this area like an upside-down triangle. The top of
the heart, or its base, lies just below the second rib; the bottom
of the heart, or its apex, tilts forward and down, toward the left
side of the body, and rests on the diaphragm. (See Location of the
pediatric heart, page 4.)

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The heart varies in size depending on the person’s body size,
but the organ is roughly 5⬙ (12.5 cm) long and 31/2⬙ (9 cm) wide, or
about the size of the person’s fist. The heart’s weight, typically 9
to 12 oz (255 to 340 g), varies depending on the person’s size, age,
sex, and athletic conditioning. An athlete’s heart usually weighs
more than that of the average person, and an elderly person’s
heart weighs less. (See The older adult heart.)

Layer upon layer
The heart’s wall is made up of three layers: the epicardium, myocardium, and endocardium. (See Layers of the heart wall.) The
epicardium, the outer layer (and the visceral layer of the serous
pericardium), is made up of squamous epithelial cells overlying
connective tissue. The myocardium, the middle layer, makes up
the largest portion of the heart’s wall. This layer of muscle tissue contracts with each heartbeat. The endocardium, the heart’s
innermost layer, contains endothelial tissue with small blood vessels and bundles of smooth muscle.
A layer of connective tissue called the pericardium surrounds
the heart and acts as a tough, protective sac. It consists of the
fibrous pericardium and the serous pericardium. The fibrous pericardium, composed of tough, white, fibrous tissue, fits loosely
around the heart, protecting it. The fibrous pericardium attaches
to the great vessels, diaphragm, and sternum. The serous pericardium, the thin, smooth, inner portion, has two layers:
• the parietal layer, which lines the inside of the fibrous pericardium
• the visceral layer, which adheres to the surface of the heart.

and stages

Location of the
pediatric heart
The heart of an infant is
positioned more horizontally in the chest cavity
than that of the adult. As
a result, the apex is at
the fourth left intercostal
space. Until age 4, the
apical impulse is to the
left of the midclavicular
line. By age 7, the heart
is located in the same
position as the adult

Between the layers
The pericardial space separates the visceral and parietal layers
and contains 10 to 20 ml of thin, clear pericardial fluid that lubricates the two surfaces and cushions the heart. Excess pericardial
fluid, a condition called pericardial effusion, compromises the
heart’s ability to pump blood.

I rest on the

Inside the heart
The heart contains four chambers—two atria and two ventricles.
(See Inside a normal heart, page 6.) The right and left atria serve
as volume reservoirs for blood being sent into the ventricles. The
right atrium receives deoxygenated blood returning from the body
through the inferior and superior vena cavae and from the heart
through the coronary sinus. The left atrium receives oxygenated
blood from the lungs through the four pulmonary veins. The interatrial septum divides the chambers and helps them contract. Contraction of the atria forces blood into the ventricles below.

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Layers of the heart wall


and stages

This cross section of the heart wall shows its various layers.

The older adult
Pericardial space

Fibrous pericardium

Parietal pericardium


Pump up the volume
The right and left ventricles serve as the pumping chambers of the
heart. The right ventricle receives blood from the right atrium and
pumps it through the pulmonary arteries to the lungs, where it picks
up oxygen and drops off carbon dioxide. The left ventricle receives
oxygenated blood from the left atrium and pumps it through the aorta
and then out to the rest of the body. The interventricular septum
separates the ventricles and also helps them to pump.
The thickness of a chamber’s walls depends on the amount of
high-pressure work the chamber does. Because the atria collect
blood for the ventricles and don’t pump it far, their walls are considerably thinner than the walls of the ventricles. Likewise, the left
ventricle has a much thicker wall than the right ventricle because
the left ventricle pumps blood against the higher pressures in
the body’s arterial circulation, whereas the right ventricle pumps
blood against the lower pressures in the lungs.

ECG_Chap01.indd 5

As a person ages, his
heart usually becomes
slightly smaller and loses
its contractile strength
and efficiency (although
exceptions occur in people with hypertension or
heart disease). By age
70, cardiac output at rest
has diminished by 30%
to 35% in many people.
Irritable with age
As the myocardium of
the aging heart becomes
more irritable, extra systoles may occur, along
with sinus arrhythmias
and sinus bradycardias.
In addition, increased
fibrous tissue infiltrates
the sinoatrial node and
internodal atrial tracts,
which may cause atrial
fibrillation and flutter.

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Inside a normal heart
This illustration shows the anatomy of a normal heart.

Branches of right
pulmonary artery
Superior vena cava
Pulmonary semilunar
Right atrium
Right pulmonary
Tricuspid valve
Chordae tendineae
Right ventricle
Papillary muscle

Aortic arch
Branches of left
pulmonary artery
Left atrium
Left pulmonary
Aortic semilunar
Mitral valve
Left ventricle

Inferior vena cava

Descending aorta

One-way valves
The heart contains four valves—two atrioventricular (AV) valves
(tricuspid and mitral) and two semilunar valves (aortic and pulmonic). The valves open and close in response to changes in pressure within the chambers they connect. They serve as one-way
doors that keep blood flowing through the heart in a forward
When the valves close, they prevent backflow, or regurgitation,
of blood from one chamber to another. The closing of the valves
creates the heart sounds that are heard through a stethoscope.
The two AV valves, located between the atria and ventricles,
are called the tricuspid and mitral valves. The tricuspid valve is
located between the right atrium and the right ventricle. The
mitral valve is located between the left atrium and the left ventricle.

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Cardiac cords
The mitral valve has two cusps, or leaflets, and the tricuspid valve
has three. The cusps are anchored to the papillary muscles in the
heart wall by fibers called chordae tendineae. These cords work
together to prevent the cusps from bulging backward into the atria
during ventricular contraction. If damage occurs, blood can flow
backward into a chamber, resulting in a heart murmur.


When valves
close, heart
sounds are

Under pressure
The semilunar valves are the pulmonic valve and the aortic valve.
These valves are called semilunar because the cusps resemble
three half-moons. Because of the high pressures exerted on the
valves, their structure is much simpler than that of the AV valves.
They open due to pressure within the ventricles and close
due to the back pressure of blood in the pulmonary arteries and
aorta, which pushes the cusps closed. The pulmonic valve, located
where the pulmonary artery meets the right ventricle, permits
blood to flow from the right ventricle to the pulmonary artery
and prevents blood backflow into that ventricle. The aortic valve,
located where the left ventricle meets the aorta, allows blood to
flow from the left ventricle to the aorta and prevents blood backflow into the left ventricle.

Blood flow through the heart
Understanding how blood flows through the heart is critical to
understanding the heart’s overall functions and how changes in
electrical activity affect peripheral blood flow. Deoxygenated
blood from the body returns to the heart through the inferior and
superior vena cavae and empties into the right atrium. From there,
blood flows through the tricuspid valve into the right ventricle.

Circuit city
The right ventricle pumps blood through the pulmonic valve into
the pulmonary arteries and then into the lungs. From the lungs,
blood flows through the pulmonary veins and empties into the left
atrium, which completes a circuit called pulmonary circulation.
When pressure rises to a critical point in the left atrium, the
mitral valve opens and blood flows into the left ventricle. The left
ventricle then contracts and pumps blood through the aortic valve
into the aorta, and then throughout the body. Blood returns to the
right atrium through the veins, completing a circuit called systemic circulation.

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Getting into circulation
Like the brain and all other organs, the heart needs an adequate
supply of blood to survive. The coronary arteries, which lie on
the surface of the heart, supply the heart muscle with blood and
oxygen. Understanding coronary blood flow can help you provide
better care for a patient with a myocardial infarction (MI) because
you’ll be able to predict which areas of the heart would be affected
by a blockage in a particular coronary artery.

Open that ostium
The coronary ostium, an opening in the aorta that feeds blood
to the coronary arteries, is located near the aortic valve. During
systole, when the left ventricle is pumping blood through the
aorta and the aortic valve is open, the coronary ostium is partially
covered. During diastole, when the left ventricle is filling with
blood, the aortic valve is closed and the coronary ostium is open,
enabling blood to fill the coronary arteries.
With a shortened diastole, which occurs during periods of
tachycardia, less blood flows through the ostium into the coronary
arteries. Tachycardia also impedes coronary blood flow because
contraction of the ventricles squeezes the arteries and lessens
blood flow through them.

That’s right, Coronary
The right coronary artery, as well as the left coronary artery (also
known as the left main artery), originates as a single branch off the
ascending aorta from the area known as the sinuses of Valsalva.
The right coronary artery supplies blood to the right atrium, the
right ventricle, and part of the inferior and posterior surfaces of the
left ventricle. In about 50% of the population, the artery also supplies blood to the sinoatrial (SA) node. The bundle of His and the AV
node also receive their blood supply from the right coronary artery.

Knowing about
coronary blood flow
can help me predict
which areas of the
heart would be
affected by a blockage
in a particular
coronary artery.

What’s left, Coronary?
The left coronary artery runs along the surface of the left atrium,
where it splits into two major branches, the left anterior descending and the left circumflex arteries. The left anterior descending
artery runs down the surface of the left ventricle toward the apex
and supplies blood to the anterior wall of the left ventricle, the
interventricular septum, the right bundle branch, and the left
anterior fasciculus of the left bundle branch. The branches of
the left anterior descending artery—the septal perforators and
the diagonal arteries—help supply blood to the walls of both

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Circling circumflex
The circumflex artery supplies oxygenated blood to the lateral
walls of the left ventricle, the left atrium and, in about half of
the population, the SA node. In addition, the circumflex artery
supplies blood to the left posterior fasciculus of the left bundle
branch. This artery circles the left ventricle and provides blood to
the ventricle’s posterior portion.

Circulation, guaranteed
When two or more arteries supply the same region, they usually
connect through anastomoses, junctions that provide alternative routes of blood flow. This network of smaller arteries, called
collateral circulation, provides blood to capillaries that directly
feed the heart muscle. Collateral circulation commonly becomes
so strong that even if major coronary arteries become clogged
with plaque, collateral circulation can continue to supply blood to
the heart.

Veins in the heart
The heart has veins just like other parts of the body. Cardiac veins
collect deoxygenated blood from the capillaries of the myocardium. The cardiac veins join to form an enlarged vessel called the
coronary sinus, which returns blood to the right atrium, where it
continues through the circulation.

A look at cardiac physiology
This discussion of cardiac physiology includes descriptions of
the cardiac cycle, how the cardiac muscle is innervated, how the
depolarization-repolarization cycle operates, how impulses are
conducted, and how abnormal impulses work. (See Events of the
cardiac cycle, page 10.)

Cardiac cycle dynamics
During one heartbeat, ventricular diastole (relaxation) and
ventricular systole (contraction) occur.
During diastole, the ventricles relax, the atria contract, and
blood is forced through the open tricuspid and mitral valves. The
aortic and pulmonic valves are closed.
During systole, the atria relax and fill with blood. The mitral
and tricuspid valves are closed. Ventricular pressure rises, which

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Events of the cardiac cycle
The cardiac cycle consists of the following five events.
1. Isovolumetric ventricular contraction:
In response to ventricular depolarization,
tension in the ventricles increases. The rise
in pressure within the ventricles leads to
1. Isovolumetric ventricular
closure of the mitral and tricuspid valves.
2. Ventricular ejection
The pulmonic and aortic valves stay closed
during the entire phase.
2. Ventricular ejection: When ventricular pressure exceeds aortic and pulmonary arterial
pressure, the aortic and pulmonic valves open
and the ventricles eject blood.
3. Isovolumetric relaxation: When ventricular pressure falls below pressure in the
aorta and pulmonary artery, the aortic and
pulmonic valves close. All valves are closed
during this phase. Atrial diastole occurs as
blood fills the atria.
4. Ventricular filling: Atrial pressure exceeds
3. Isovolumetric
ventricular pressure, which causes the mitral
5. Atrial
and tricuspid valves to open. Blood then flows
passively into the ventricles. About 70% of
ventricular filling takes place during this phase.
4. Ventricular filling
5. Atrial systole: Known as the atrial kick,
atrial systole (coinciding with late ventricular
diastole) supplies the ventricles with the remaining 30% of the blood for each heartbeat.

forces open the aortic and pulmonic valves. Then the ventricles
contract, and blood flows through the circulatory system.

Atrial kick
The atrial contraction, or atrial kick, contributes about 30% of the
cardiac output—the amount of blood pumped by the ventricles
in 1 minute. (See Quick facts about circulation.) Certain arrhythmias, such as atrial fibrillation, can cause a loss of atrial kick and a
subsequent drop in cardiac output. Tachycardia also affects cardiac
output by shortening diastole and allowing less time for the ventricles to fill. Less filling time means less blood will be ejected during
ventricular systole and less will be sent through the circulation.

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A balancing act
The cardiac cycle produces cardiac output, which is the amount
of blood the heart pumps in 1 minute. It’s measured by multiplying heart rate times stroke volume. (See Understanding preload,
afterload, and contractility, page 12.) The term stroke volume
refers to the amount of blood ejected with each ventricular
Normal cardiac output is 4 to 8 L/minute, depending on body
size. The heart pumps only as much blood as the body requires.
Three factors affect stroke volume—preload, afterload, and myocardial contractility. A balance of these three factors produces
optimal cardiac output.

Preload is the stretching of muscle fibers in the ventricles and is
determined by the pressure and amount of blood remaining in the
left ventricle at the end of diastole.


facts about
• It would take about 25
capillaries laid end-toend to fill 1⬙ (2.5 cm).
• The body contains
about 10 billion capillaries.
• On average, it takes
a red blood cell less than
1 minute to travel from
the heart to the capillaries and back again.

Afterload is the amount of pressure the left ventricle must work
against to pump blood into the circulation. The greater this resistance, the more the heart works to pump out blood.

Contractility is the ability of muscle cells to contract after depolarization. This ability depends on how much the muscle fibers are
stretched at the end of diastole. Overstretching or understretching
these fibers alters contractility and the amount of blood pumped
out of the ventricles. To better understand this concept, picture
trying to shoot a rubber band across the room. If you don’t stretch
the rubber band enough, it won’t go far. If you stretch it too much,
it will snap. However, if you stretch it just the right amount, it will
go as far as you want it to.

Contractility is
the heart’s ability
to stretch —
like a balloon!

Nerve supply to the heart
The heart is supplied by the two branches of the autonomic nervous system—the sympathetic, or adrenergic, and the parasympathetic, or cholinergic.
The sympathetic nervous system is basically the heart’s accelerator. Two sets of chemicals—norepinephrine and epinephrine—
are highly influenced by this system. These chemicals increase
heart rate, automaticity, AV conduction, and contractility.

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Understanding preload, afterload, and contractility
To better understand preload, afterload, and contractility, think of the heart as a balloon.
Preload is the passive stretching of muscle fibers in the ventricles. This stretching
results from blood volume in the ventricles
at end-diastole. According to Starling’s
law, the more the heart muscles stretch
during diastole, the more forcefully they
contract during systole. Think of preload
as the balloon stretching as air is blown
into it. The more air the greater the

Contractility refers to the inherent ability
of the myocardium to contract normally.
Contractility is influenced by preload.
The greater the stretch the more forceful the contraction—or, the more air in
the balloon, the greater the stretch, and
the farther the balloon will fly when air is
allowed to expel.
Afterload refers to the pressure that
the ventricular muscles must generate
to overcome the higher pressure in the
aorta to get the blood out of the heart.
Resistance is the knot on the end of the
balloon, which the balloon has to work
against to get the air out.

Braking the heart
The parasympathetic nervous system, on the other hand, serves
as the heart’s brakes. One of this system’s nerves, the vagus
nerve, carries impulses that slow heart rate and the conduction
of impulses through the AV node and ventricles. Stimulating this
system releases the chemical acetylcholine, slowing the heart rate.

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The vagus nerve is stimulated by baroreceptors, specialized nerve
cells in the aorta and the internal carotid arteries. Conditions that
stimulate the baroreceptors also stimulate the vagus nerve.
For example, a stretching of the baroreceptors, which can occur during periods of hypertension or when applying pressure to
the carotid artery, stimulates the receptors. In a maneuver called
carotid sinus massage, baroreceptors in the carotid arteries are
purposely activated in an effort to slow a rapid heart rate.

Transmission of electrical impulses
The heart can’t pump unless an electrical stimulus occurs first.
Generation and transmission of electrical impulses depend on
four characteristics of cardiac cells:
• Automaticity refers to a cell’s ability to spontaneously initiate
an impulse. Pacemaker cells possess this ability.
• Excitability results from ion shifts across the cell membrane
and indicates how well a cell responds to an electrical stimulus.
• Conductivity is the ability of a cell to transmit an electrical impulse to another cardiac cell.
• Contractility refers to how well the cell contracts after receiving a stimulus.


To help you
the difference between depolarization
and repolarization,
think of the R in
repolarization as
standing for REST.
Remember that repolarization is the
resting phase of the
cardiac cycle.

“De”-cycle and “re”-cycle
As impulses are transmitted, cardiac cells undergo cycles of
depolarization and repolarization. (See Depolarization-repolarization cycle, page 14.) Cardiac cells at rest are considered polarized, meaning that no electrical activity takes place. Cell membranes separate different concentrations of ions, such as sodium
and potassium, and create a more negative charge inside the cell.
This is called the resting potential. After a stimulus occurs, ions
cross the cell membrane and cause an action potential, or cell
When a cell is fully depolarized, it attempts to return to its resting state in a process called repolarization. Electrical charges in
the cell reverse and return to normal.
A cycle of depolarization-repolarization consists of five phases—0 through 4. The action potential is represented by a curve
that shows voltage changes during the five phases. (See Action
potential curve, page 15.)

Those impulses
really get around!

Many phases of the curve
During phase 0, the cell receives an impulse from a neighboring cell
and is depolarized. Phase 1 is marked by early, rapid repolarization.
Phase 2, the plateau phase, is a period of slow repolarization.
During phases 1 and 2 and at the beginning of phase 3, the
cardiac cell is said to be in its absolute refractory period. During

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Depolarization-repolarization cycle
The depolarization-repolarization cycle consists of the following phases:
Phase 0:
Rapid depolarization
• Sodium (Na+) moves rapidly into cell.
• Calcium (Ca++) moves slowly into cell.


Phase 1:
Early repolarization
• Sodium channels close.

Phase 4:
Resting phase
• Cell membrane is impermeable to
• Potassium moves out of the cell.



Phase 2:
Plateau phase
• Calcium continues to flow in.
• Potassium (K+) continues to flow out.
Phase 3:
Rapid repolarization
• Calcium channels close.
• Potassium flows out rapidly.
• Active transport via the sodiumpotassium pump begins restoring potassium to the inside of the cell and sodium to
the outside of the cell.







that period, no stimulus, no matter how strong, can excite the
Phase 3, the rapid repolarization phase, occurs as the cell returns to its original state. During the last half of this phase, when
the cell is in its relative refractory period, a very strong stimulus
can depolarize it.
Phase 4 is the resting phase of the action potential. By the end
of phase 4, the cell is ready for another stimulus.
All that electrical activity is represented on an electrocardiogram (ECG). Keep in mind that the ECG represents electrical activity only, not actual pumping of the heart.

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Action potential curve
An action potential curve shows the electrical changes in a myocardial cell during
the depolarization-repolarization cycle. This graph shows the changes in a nonpacemaker cell.




Relative refractory period


Pathway through the heart
After depolarization and repolarization occur, the resulting electrical impulse travels through the heart along a pathway called the
conduction system. (See The cardiac conduction system, page 16.)
Impulses travel out from the SA node and through the internodal tracts and Bachmann’s bundle to the AV node. From there,
they travel through the bundle of His, the bundle branches, and
lastly to the Purkinje fibers.

Setting the pace
The SA node is located in the upper right corner of the right
atrium, where the superior vena cava joins the atrial tissue mass.
It’s the heart’s main pacemaker, generating impulses 60 to 100
times per minute. When initiated, the impulses follow a specific
path through the heart. They usually can’t flow backward
because the cells can’t respond to a stimulus immediately after

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The cardiac conduction system
Specialized fibers propagate electrical impulses throughout the heart's cells, causing
the heart to contract. This illustration shows the elements of the cardiac conduction

Bachmann’s bundle
Sinoatrial node
Internodal tract
• Posterior (Thorel’s)
• Middle (Wenckebach’s)
• Anterior
Atrioventricular node
Bundle of His
Right bundle branch
Left bundle branch
Purkinje fibers

Bachmann’s bundle of nerves
Impulses from the SA node next travel through Bachmann’s bundle, tracts of tissue extending from the SA node to the left atrium.
Impulses are thought to be transmitted throughout the right atrium through the anterior, middle, and posterior internodal tracts.
Whether those tracts actually exist, however, is unclear. Impulse
transmission through the right and left atria occurs so rapidly that
the atria contract almost simultaneously.

AV: The slow node
The AV node, located in the inferior right atrium near the ostium
of the coronary sinus, is responsible for delaying the impulses that
reach it. Although the nodal tissue itself has no pacemaker cells,
the tissue surrounding it (called junctional tissue) contains pacemaker cells that can fire at a rate of 40 to 60 times per minute.

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The AV node’s main function is to delay impulses by 0.04 second to keep the ventricles from contracting too quickly. This delay
allows the ventricles to complete their filling phase as the atria
contract. It also allows the cardiac muscle to stretch to its fullest
for peak cardiac output.

Branch splitting


The bundle of His
eventually divides
into the right and left
bundle branches. This
branch works just fine
for me!

The bundle of His, a tract of tissue extending into the ventricles
next to the interventricular septum, resumes the rapid conduction
of the impulse through the ventricles. The bundle eventually divides into the right and left bundle branches.
The right bundle branch extends down the right side of the
interventricular septum and through the right ventricle. The left
bundle branch extends down the left side of the interventricular
septum and through the left ventricle.
The left bundle branch then splits into two branches, or fasciculi: the left anterior fasciculus, which extends through the anterior portion of the left ventricle, and the left posterior fasciculus,
which runs through the lateral and posterior portions of the left
ventricle. Impulses travel much faster down the left bundle branch
(which feeds the larger, thicker-walled left ventricle) than the
right bundle branch (which feeds the smaller, thinner-walled right
The difference in the conduction speed allows both ventricles
to contract simultaneously. The entire network of specialized
nervous tissue that extends through the ventricles is known as the
His-Purkinje system.

Those perky Purkinje fibers
Purkinje fibers extend from the bundle branches into the endocardium, deep into the myocardial tissue. These fibers conduct
impulses rapidly through the muscle to assist in its depolarization
and contraction.
Purkinje fibers can also serve as a pacemaker and are able
to discharge impulses at a rate of 20 to 40 times per minute,
sometimes even more slowly. (See Pacemakers of the heart,
page 18.) Purkinje fibers usually aren’t activated as a pacemaker
unless conduction through the bundle of His becomes blocked or
a higher pacemaker (SA or AV node) doesn’t generate an impulse.
(See Pediatric pacemaker rates, page 18.)

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and stages

Pacemakers of the heart
Pacemaker cells in lower areas,
such as the junctional tissue and the
Purkinje fibers, normally remain dormant because they receive impulses
from the sinoatrial (SA) node. They
initiate an impulse only when they
don’t receive one from above, such
as when the SA node is damaged
from a myocardial infarction.
Firing rates
This illustration shows intrinsic firing
rates of pacemaker cells located in
three critical areas of the heart.

SA node,
60 to 100/minute
Atrioventricular junction,
40 to 60/minute

Purkinje fibers,
20 to 40/minute

In children younger than
age 3, the atrioventricular node may discharge
impulses at a rate of 50
to 80 times per minute;
the Purkinje fibers may
discharge at a rate of 40
to 50 times per minute.

Abnormal impulses
Now that you understand how the heart generates a normal impulse, let’s look at some causes of abnormal impulse conduction,
including automaticity, backward conduction of impulses, reentry
abnormalities, and ectopy.

When the heart goes on “manual”
Automaticity is a special characteristic of pacemaker cells that
generates impulses automatically, without being stimulated to do
so. If a cell’s automaticity is increased or decreased, an arrhythmia can occur. Tachycardia, for example, is commonly caused by
an increase in the automaticity of pacemaker cells below the SA
node. Likewise, a decrease in automaticity of cells in the SA node
can cause the development of bradycardia or an escape rhythm
(a compensatory beat generated by a lower pacemaker site).

Out of synch
Impulses that begin below the AV node can be transmitted backward toward the atria. This backward, or retrograde, conduction
usually takes longer than normal conduction and can cause the
atria and ventricles to beat out of synch.

Coming back for more
Sometimes impulses cause depolarization twice in a row at a
faster-than-normal rate. Such events are referred to as reentry
events. In reentry, impulses are delayed long enough that cells

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have time to repolarize. In these cases, the active impulse reenters
the same area and produces another impulse.

Repeating itself
An injured pacemaker (or nonpacemaker) cell may partially depolarize, rather than fully depolarizing. Partial depolarization can
lead to spontaneous or secondary depolarization, which involves
repetitive ectopic firings called triggered activity.
The resultant depolarization is called afterdepolarization.
Early afterdepolarization occurs before the cell is fully repolarized
and can be caused by hypokalemia, slow pacing rates, or drug toxicity. If it occurs after the cell has been fully repolarized, it’s called
delayed afterdepolarization. These problems can be caused by
digoxin toxicity, hypercalcemia, or increased catecholamine release. Atrial or ventricular tachycardias may result. You’ll learn
more about these and other arrhythmias in later chapters.

That’s a wrap!

Cardiac anatomy and physiology review
The heart’s valves
• Tricuspid — AV valve between the
right atrium and right ventricle
• Mitral — AV valve between the left
atrium and left ventricle
• Aortic — semilunar valve between the
left ventricle and the aorta
• Pulmonic — semilunar valve between
the right ventricle and the pulmonary
Blood flow
• Deoxygenated blood from the body returns to the right atrium and then flows to
the right ventricle.
• The right ventricle pumps blood into the
lungs where it’s oxygenated. Then the
blood returns to the left atrium and flows
to the left ventricle.

• Oxygenated blood is pumped to the
aorta and the body by the left ventricle.
Coronary arteries and veins
• Right coronary artery — supplies blood
to the right atrium and ventricle and part
of the left ventricle
• Left anterior descending artery — supplies blood to the anterior wall of the left
ventricle, interventricular septum, right
bundle branch, and left anterior fasciculus of the left bundle branch
• Circumflex artery — supplies blood to
the lateral walls of the left ventricle, left
atrium, and left posterior fasciculus of
the left bundle branch
• Cardiac veins — collect blood from the
capillaries of the myocardium
• Coronary sinus — returns blood to the
right atrium

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Cardiac anatomy and physiology review (continued)
Cardiac cycle dynamics
• Atrial kick — atrial contraction, contributing about 30% of the cardiac output
• Cardiac output — the amount of blood
the heart pumps in 1 minute, calculated
by multiplying heart rate times stroke
• Stroke volume — the amount of blood
ejected with each ventricular contraction
(it’s affected by preload, afterload, and
• Preload — the passive stretching exerted by blood on the ventricular muscle
at the end of diastole
• Afterload — the amount of pressure
the left ventricle must work against to
pump blood into the aorta
• Contractility — the ability of the heart
muscle cells to contract after depolarization
Innervation of the heart
Two branches of the autonomic nervous
system supply the heart:
• Sympathetic nervous system —
increases heart rate, automaticity, AV conduction, and contractility
through release of norepinephrine and
• Parasympathetic nervous system —
vagus nerve stimulation reduces heart
rate and AV conduction through release
of acetylcholine.
Transmission of electrical impulses
Generation and transmission of electrical
impulses depend on these cell characteristics:
• Automaticity — a cell’s ability to spontaneously initiate an impulse, such as
found in pacemaker cells
• Excitability — how well a cell responds
to an electrical stimulus

ECG_Chap01.indd 20

• Conductivity — the ability of a cell to
transmit an electrical impulse to another
cardiac cell
• Contractility — how well the cell contracts after receiving a stimulus.
Depolarization-repolarization cycle
Cardiac cells undergo the following
cycles of depolarization and repolarization as impulses are transmitted:
• Phase 0: Rapid depolarization — the
cell receives an impulse from a nearby
cell and is depolarized
• Phase 1: Early repolarization — early
rapid repolarization occurs
• Phase 2: Plateau phase — a period of
slow repolarization occurs
• Phase 3: Rapid repolarization — the
cell returns to its original state
• Phase 4: Resting phase — the cell rests
and readies itself for another stimulus.
Cardiac conduction
• The electrical impulse begins in the
SA node and travels through the internodal tracts and Bachmann’s bundle to
the AV node.
• From the AV node, the impulse travels
down the bundle of His, along the bundle
branches, and through the Purkinje fibers.
Intrinsic firing rates
• SA node — 60 to 100/minute
• AV junction — 40 to 60/minute
• Purkinje fibers — 20 to 40/minute
Abnormal impulses
• Automaticity — the ability of a cardiac
cell to initiate an impulse on its own
• Retrograde conduction — impulses that
are transmitted backward toward the atria
• Reentry — when an impulse follows a
circular, rather than the normal, conduction path

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Quick quiz

The term automaticity refers to the ability of a cell to:
A. initiate an impulse on its own.
B. send impulses in all directions.
C. block impulses formed in areas other than the SA node.
D. generate an impulse when stimulated.

Answer: A. Automaticity, the ability of a cell to initiate an impulse on its own, is a unique characteristic of cardiac cells.

Parasympathetic stimulation of the heart results in:
A. increased heart rate and decreased contractility.
B. increased heart rate and faster AV conduction.
C. decreased heart rate and slower AV conduction.
D. decreased heart rate and increased contractility.

Answer: C. Parasympathetic stimulation of the vagus nerve
causes a decrease in heart rate and slowed AV conduction.

The normal pacemaker of the heart is the:
A. SA node.
B. AV node.
C. bundle of His.
D. Purkinje fibers.

Answer: A. The SA node is the normal pacemaker of the heart,
firing at an intrinsic rate of 60 to 100 times per minute.

The impulse delay produced by the AV node allows the atria

repolarize simultaneously.
contract before the ventricles.
send impulses to the bundle of His.
complete their filling.

Answer: B. The 0.04-second delay allows the atria to contract
and the ventricles to completely fill, which optimizes cardiac output.

The coronary arteries fill with blood during:
A. atrial systole.
B. atrial diastole.
C. ventricular systole.
D. ventricular diastole.

Answer: D. The coronary arteries fill with blood when the ventricles are in diastole and filling with blood. The aortic valve is
closed at that time, so it no longer blocks blood flow through the
coronary ostium into the coronary arteries.

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When stimulated, baroreceptors cause the heart rate to:
A. increase.
B. decrease.
C. stay the same.
D. become irregular.

Answer: B. Baroreceptors, when stimulated, cause the heart rate
to decrease.

The two valves called the semilunar valves are the:
A. pulmonic and tricuspid valves.
B. pulmonic and aortic valves.
C. aortic and mitral valves.
D. aortic and tricuspid valves.

Answer: B. The pulmonic and aortic valves are semilunar.
Passive stretching exerted by blood on the ventricular
muscle at the end of diastole is referred to as:
A. preload.
B. afterload.
C. the atrial kick.
D. cardiac output.
Answer: A. Preload is the passive stretching exerted by blood on
the ventricular muscle at the end of diastole. It increases with an
increase in venous return to the heart.
A patient admitted with an acute MI has a heart rate of 36
beats/minute. Based on this finding, which area of the heart is
most likely serving as the pacemaker?
A. SA node
B. AV node
C. Bachmann’s bundle
D. Purkinje fibers
Answer: D. If the SA node (which fires at a rate of 60 to 100 times
per minute) and the AV node (which takes over firing at 40 to 60
times per minute) are damaged, the Purkinje fibers take over firing at a rate of 20 to 40 times per minute.


ECG_Chap01.indd 22

If you answered all nine questions correctly, hooray! You’re a happenin’, heart-smart hipster.
If you answered six to eight questions correctly, way to go! You’re
clearly heart smart.
If you answered fewer than six questions correctly, take heart.
Just review this chapter and you’ll be up to speed.

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Obtaining a rhythm strip
Just the facts
In this chapter, you’ll learn:
 the importance of ECGs in providing effective patient care
 the functions of leads and planes
 types of ECG monitoring systems
 proper techniques for applying electrodes, selecting
leads, and obtaining rhythm strips
 solutions for cardiac-monitoring problems.

A look at ECG recordings
The heart’s electrical activity produces currents that radiate
through the surrounding tissue to the skin. When electrodes are
attached to the skin, they sense those electrical currents and
transmit them to an ECG monitor. The currents are then transformed into waveforms that represent the heart’s depolarizationrepolarization cycle.
You might remember that myocardial depolarization occurs
when a wave of stimulation passes through the heart and stimulates the heart muscle to contract. Repolarization is the return to
the resting state and results in relaxation.
An ECG shows the precise sequence of electrical events occurring in the cardiac cells throughout that process. It allows the
nurse to monitor phases of myocardial contraction and to identify
rhythm and conduction disturbances. A series of ECGs can be
used as a baseline comparison to assess cardiac function.

ECG_Chap02.indd 23

An ECG shows the
sequence of cardiac

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Leads and planes
To understand electrocardiography, you need to understand leads
and planes. Electrodes placed on the skin measure the direction
of electrical current discharged by the heart. That current is then
transformed into waveforms.
An ECG records information about those waveforms from different views or perspectives. Those perspectives are called leads
and planes.

Leads and planes
offer different views of
the heart’s electrical

Take the lead
A lead provides a view of the heart’s electrical activity between
one positive pole and one negative pole. Between the two poles
lies an imaginary line representing the lead’s axis, a term that
refers to the direction of the current moving through the heart.
The direction of the current affects the direction in which the
waveform points on an ECG. (See Current direction and wave
deflection.) When no electrical activity occurs or the activity is too
weak to measure, the waveform looks like a straight line, called
an isoelectric waveform.

Current direction and wave deflection
This illustration shows possible directions of electrical current, or depolarization, on a lead. The direction of the electrical current determines the upward or downward deflection of an electrocardiogram waveform.

As current travels
toward the negative pole,
the waveform deflects
mostly downward.

When current
flows perpendicular to
the lead, the waveform
may be small or go in
both directions

As current
travels toward the
positive pole, the
waveform deflects
mostly upward.

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Plane and simple
The term plane refers to a cross-sectional perspective of the
heart’s electrical activity. The frontal plane, a vertical cut through
the middle of the heart, provides an anterior-to-posterior view of
electrical activity. The horizontal plane, a transverse cut through
the middle of the heart, provides either a superior or an inferior

Types of ECGs
The two types of ECG recordings are the 12-lead ECG and a
rhythm strip. Both types give valuable information about heart

A dozen views
A 12-lead ECG records information from 12 different views of
the heart and provides a complete picture of electrical activity.
These 12 views are obtained by placing electrodes on the patient’s
limbs and chest. The limb leads and the chest, or precordial, leads
reflect information from the different planes of the heart.
Different leads provide different information. The six limb
leads—I, II, III, augmented vector right (aVR), augmented vector
left (aVL), and augmented vector foot (aVF)—provide information
about the heart’s frontal (vertical) plane. Leads I, II, and III require
a negative and positive electrode for monitoring, which makes
those leads bipolar. The augmented leads record information from
one lead and are called unipolar.
The six precordial or V leads—V1, V2, V3, V4, V5, and V6—provide information about the heart’s horizontal plane. Like the
augmented leads, the precordial leads are also unipolar, requiring
only a single electrode. The opposing pole of those leads is the
center of the heart as calculated by the ECG.

Just one view
A rhythm strip, which can be used to monitor cardiac status, provides information about the heart’s electrical activity from one or
more leads simultaneously. Chest electrodes pick up the heart’s
electrical activity for display on the monitor. The monitor also displays heart rate and other measurements and allows for printing
strips of cardiac rhythms.
Commonly monitored leads include the bipolar leads I, II, III,
V1, V6, MCL1, and MCL6. The initials MCL stand for modified chest
lead. These leads are similar to the unipolar leads V1 and V6 of the
12-lead ECG. MCL1 and MCL6, however, are bipolar leads.

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Monitoring ECGs
The type of ECG monitoring system you’ll use—hardwire monitoring or telemetry—depends on the patient’s condition and where
you work. Let’s look at each system.

Hardwire basics
With hardwire monitoring, the electrodes are connected directly
to the cardiac monitor. Most hardwire monitors are mounted permanently on a shelf or wall near the patient’s bed. Some monitors
are mounted on an I.V. pole for portability, and some may include
a defibrillator.
The monitor provides a continuous cardiac rhythm display and
transmits the ECG tracing to a console at the nurses’ station. Both
the monitor and the console have alarms and can print rhythm
strips. Hardwire monitors can also track pulse oximetry, blood
pressure, hemodynamic measurements, and other parameters
through various attachments to the patient.

There are pros and
cons with both ECG
monitoring systems.

Some drawbacks
Hardwire monitoring is generally used in intensive care units and
emergency departments because it permits continuous observation of one or more patients from more than one area in the unit.
However, this type of monitoring does have drawbacks, among
• limited patient mobility because the patient is tethered to a
monitor by a cable
• patient discomfort because the electrodes and cables are
attached to the chest
• possibility of lead disconnection and loss of cardiac monitoring
when the patient moves.

Portable points
Telemetry monitoring is generally used in step-down units and
medical-surgical units where patients are permitted more activity.
With telemetry monitoring, the patient carries a small, batterypowered transmitter that sends electrical signals to another location, where the signals are displayed on a monitor screen. This
type of ECG monitoring frees the patient from cumbersome wires
and cables associated with hardwire monitoring.
Telemetry monitoring still requires skin electrodes to be
placed on the patient’s chest. Each electrode is connected by
a thin wire to a small transmitter box carried in a pocket or
pouch. It’s especially useful for detecting arrhythmias that occur
with activity or stressful situations. Most systems, however, can
monitor heart rate and rhythm only.

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All about leads


Adjust the leads
according to the
patient’s condition.

Electrode placement is different for each lead, and different leads
provide different views of the heart. A lead may be chosen to highlight a particular part of the ECG complex or the electrical events
of a specific cardiac cycle.
Although leads II, V1, and V6 are among the most commonly
used leads for monitoring, you should adjust the leads according
to the patient’s condition. If your monitoring system has the capability, you may also monitor the patient in more than one lead.

Going to ground
All bipolar leads have a third electrode, known as the ground,
which is placed on the chest to prevent electrical interference
from appearing on the ECG recording.

Heeeere’s lead I
Lead I provides a view of the heart that shows current moving
from right to left. Because current flows from negative to positive,
the positive electrode for this lead is placed on the left arm or on
the left side of the chest; the negative electrode is placed on the
right arm. Lead I produces a positive deflection on ECG tracings
and is helpful in monitoring atrial rhythms and hemiblocks.

Introducing lead II
Lead II produces a positive deflection. Place the positive electrode on the patient’s left leg and the negative electrode on the
right arm. For continuous monitoring, place the electrodes on
the torso for convenience, with the positive electrode below the
lowest palpable rib at the left midclavicular line and the negative
electrode below the right clavicle. The current travels down and
to the left in this lead. Lead II tends to produce a positive, highvoltage deflection, resulting in tall P, R, and T waves. This lead is
commonly used for routine monitoring and is useful for detecting
sinus node and atrial arrhythmias.

Next up, lead III
Lead III produces a positive deflection. The positive electrode
is placed on the left leg; the negative electrode, on the left arm.
Along with lead II, this lead is useful for detecting changes associated with an inferior wall myocardial infarction.
The axes of the three bipolar limb leads—I, II, and III—form a
triangle around the heart and provide a frontal plane view of the
heart. (See Einthoven’s triangle, page 28.)

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Einthoven’s triangle
When setting up standard
limb leads, you’ll place electrodes in positions commonly
referred to as Einthoven’s
triangle, shown here. The
electrodes for leads I, II, and
III are about equidistant from
the heart and form an equilateral triangle.

Right arm

Left arm







Lead I
The axis of lead I extends
from shoulder to shoulder,
with the right-arm electrode being the negative
electrode and the left-arm
⫹ ⫹
electrode positive.
Left leg
The axis of lead II runs
from the negative right-arm
electrode to the positive left-leg electrode. The axis of lead III extends from the negative
left-arm electrode to the positive left-leg electrode.

The “a” leads
Leads aVR, aVL, and aVF are called augmented leads because the
small waveforms that normally would appear from these unipolar
leads are enhanced by the ECG. (See Augmented leads.) The “a”
stands for “augmented,” and “R, L, and F” stand for the positive
electrode position of the lead.
In lead aVR, the positive electrode is placed on the right arm
(hence, the R) and produces a negative deflection because the
heart’s electrical activity moves away from the lead. In lead aVL, the
positive electrode is on the left arm and produces a positive deflection on the ECG. In lead aVF, the positive electrode is on the left leg
(despite the name aVF) and produces a positive deflection. These
three limb leads also provide a view of the heart’s frontal plane.

Placed in sequence
across the chest,
precordial leads V1
through V6 provide
a view of the heart’s
horizontal plane.

The preeminent precordials
The six unipolar precordial leads are placed in sequence across
the chest and provide a view of the heart’s horizontal plane. (See
Precordial views, page 30.) These leads include:

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Augmented leads
Leads aVR, aVL, and aVF are
called augmented leads.
They measure electrical activity between one limb and
a single electrode. Lead aVR
provides no specific view of
the heart. Lead aVL shows
electrical activity coming
from the heart’s lateral wall.
Lead aVF shows electrical
activity coming from the
heart’s inferior wall.

Left arm

Right arm





Left leg

• Lead V1—The precordial lead V1 electrode is placed on the
right side of the sternum at the fourth intercostal rib space. This
lead corresponds to the modified chest lead MCL1 and shows the
P wave, QRS complex, and ST segment particularly well. It helps
to distinguish between right and left ventricular ectopic beats
that result from myocardial irritation or other cardiac stimulation outside the normal conduction system. Lead V1 is also useful
in monitoring ventricular arrhythmias, ST-segment changes, and
bundle-branch blocks.
• Lead V2—Lead V2 is placed at the left of the sternum at the
fourth intercostal rib space.
• Lead V3—Lead V3 goes between V2 and V4. Leads V1, V2, and V3
are biphasic, with both positive and negative deflections. Leads V2
and V3 can be used to detect ST-segment elevation.
• Lead V4—Lead V4 is placed at the fifth intercostal space at the
midclavicular line and produces a biphasic waveform.
• Lead V5—Lead V5 is placed at the fifth intercostal space at the
anterior axillary line. It produces a positive deflection on the
ECG and, along with V4, can show changes in the ST segment or
T wave.
• Lead V6—Lead V6, the last of the precordial leads, is placed
level with V4 at the midaxillary line. This lead produces a positive
deflection on the ECG.

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Precordial views
These illustrations show the different views of the heart obtained from
each precordial (chest) lead.

Center of the heart
(zero point)





The modest modified lead
MCL1 is similar to lead V1 on the 12-lead ECG and is created by
placing the negative electrode on the left upper chest, the positive
electrode on the right side of the sternum at the fourth intercostal
space, and the ground electrode usually on the right upper chest
below the clavicle.
When the positive electrode is on the right side of the heart
and the electrical current travels toward the left ventricle, the

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waveform has a negative deflection. As a result, ectopic or abnormal beats deflect in a positive direction.
You can use this lead to monitor premature ventricular contractions and to distinguish different types of tachycardia, such
as ventricular tachycardia and supraventricular tachycardia. Lead
MCL1 can also be used to assess bundle-branch defects and
P-wave changes and to confirm pacemaker wire placement.


A five-leadwire
system allows you
to monitor any six
modified chest leads
and the standard limb
leads. Yippee, Skippy!

A positive option
MCL6 may be used as an alternative to MCL1. Like MCL1 it monitors ventricular conduction changes. The positive lead in MCL6 is
placed in the same location as its equivalent, lead V6. The positive
electrode is placed at the fifth intercostal space at the midaxillary line, the negative electrode below the left shoulder, and the
ground below the right shoulder.

Electrode basics
A three- or five-electrode (or leadwire) system may be used for
cardiac monitoring. (See Leadwire systems, page 32.) Both systems use a ground electrode to prevent accidental electrical shock
to the patient.
A three-electrode system has one positive electrode, one negative electrode, and a ground.
The popular five-electrode system uses an exploratory chest
lead to monitor any six modified chest leads as well as the standard limb leads. (See Using a five-leadwire system, page 33.)
This system uses standardized chest placement. Wires that attach
to the electrodes are usually color-coded to help you to place
them correctly on the patient’s chest.
One newer application of bedside cardiac monitoring is a
reduced lead continuous 12-lead ECG system (EASI system),
which uses an advanced algorithm and only five electrodes
uniquely placed on the torso to derive a 12-lead ECG. The system
allows all 12 leads to be simultaneously displayed and recorded.
(See Understanding the EASI system, page 34.)

How to apply electrodes
Before you attach electrodes to your patient, make sure he knows
you’re monitoring his heart rate and rhythm, not controlling them.
Tell him not to become upset if he hears an alarm during the procedure; it probably just means a leadwire has come loose.
Explain the electrode placement procedure to the patient,
provide privacy, and wash your hands. Expose the patient’s chest
and select electrode sites for the chosen lead. Choose sites over
(Text continues on page 34.)

ECG_Chap02.indd 31

7/8/2010 4:16:51 PM



Leadwire systems
This chart shows the correct electrode
positions for some of the leads you’ll use
most often — the five-leadwire, threeleadwire, and telemetry systems. The
chart uses the abbreviations RA for the
right arm, LA for the left arm, RL for the
right leg, LL for the left leg, C for the chest,
and G for the ground.
Electrode positions
In the three- and the five-leadwire systems, electrode positions for one lead

Five-leadwire system

may be identical to those for another
lead. When that happens, change the
lead selector switch to the setting that
corresponds to the lead you want. In
some cases, you’ll need to reposition the

These are
the electrode
you’ll use
most often.

In a telemetry monitoring system, you
can create the same leads as the other
systems with just two electrodes and
a ground wire.

Three-leadwire system

Telemetry system

Lead I











Lead II











Lead III







ECG_Chap02.indd 32





7/8/2010 4:16:52 PM



Leadwire systems (continued)
Five-leadwire system

Three-leadwire system

Telemetry system

Lead MCL1








Lead MCL6









Using a five-leadwire system
This illustration shows the correct placement of the leadwires for a five-leadwire system. The chest electrode shown is located in the V1 position, but you can place it in any
of the chest-lead positions. The electrodes are color-coded as follows.
right arm (RA)


left arm (LA)

right leg (RL)

left leg (LL)

chest (C)




ECG_Chap02.indd 33


7/8/2010 4:16:55 PM



Understanding the EASI system
The five-lead EASI (reduced lead continuous 12-lead electrocardiogram [ECG]) configuration gives a three-dimensional view of the electrical activity of the heart from the frontal, horizontal, and sagittal planes. This provides 12 leads of information. A mathematical
calculation in the electronics of the monitoring system is applied to the information,
creating a derived 12-lead ECG.
Placement of the electrodes for the EASI system includes:
• E lead: lower part of the sternum at the level of the fifth intercostal space
• A lead: left midaxillary line at the level of the fifth intercostal space
• S lead: upper part of the sternum
• I lead: right midaxillary line at the level of the fifth intercostal space
• Ground: anywhere on the torso.





soft tissues or close to bone, not over bony prominences, thick
muscles, or skin folds. Those areas can produce ECG artifacts—
waveforms not produced by the heart’s electrical activity.

Prepare the skin
Next, prepare the patient’s skin. To begin, wash the patient’s chest
with soap and water and then dry it thoroughly. Because hair
may interfere with electrical contact, clip dense hair with clippers
or scissors. Then use the special rough patch on the back of the
electrode, a dry washcloth, or a gauze pad to briskly rub each site

ECG_Chap02.indd 34

To help
you remember where to
place electrodes
in a five-electrode
configuration, think
of the phrase “White
to the upper right.”
Then think of snow
over trees (white
electrode above
green electrode) and
smoke over fire (black
electrode above red
electrode). And of
course, chocolate
(brown electrode) lies
close to the heart.




7/8/2010 4:16:57 PM


until the skin reddens. Make sure that you don't damage or break
the skin. Brisk scrubbing helps to remove dead skin cells and
improves electrical contact.
If the patient has oily skin, clean each site with an alcohol pad
and let it air-dry. This ensures proper adhesion and prevents the
alcohol from becoming trapped beneath the electrode, which can
irritate the skin and cause skin breakdown.

Stick it to me
To apply the electrodes, remove the backing and make sure each
pregelled electrode is still moist. If an electrode has become dry,
discard it and select another. A dry electrode decreases electrical
contact and interferes with waveforms.
Apply one electrode to each prepared site using this method:
• Press one side of the electrode against the patient’s skin, pull
gently, and then press the opposite side of the electrode against
the skin.
• Using two fingers, press the adhesive edge around the outside
of the electrode to the patient’s chest. This fixes the gel and stabilizes the electrode.
• Repeat this procedure for each electrode.
• Every 24 hours, remove the electrodes, assess the patient’s skin,
and put new electrodes in place.

Clip, clip, snap, snap
You’ll also need to attach leadwires or cable connections to the
monitor and attach leadwires to the electrodes. Leadwires may
clip on or, more commonly, snap on. (See Clip-on and snap-on
leadwires.) If you’re using the snap-on type, attach the electrode
to the leadwire just before applying it to the patient’s chest. Keep
in mind that you may lose electrode contact if you press down to
apply the leadwire.
When you use a clip-on leadwire, apply it after the electrode
has been secured to the patient’s skin. That way, applying the clip
won’t interfere with the electrode’s contact with the skin.


Clip-on and
Several kinds of leadwires are available for
monitoring. A clip-on
leadwire should be attached to the electrode
after it has been placed
on the patient’s chest.
A snap-on leadwire
should be attached to
the electrode just before
it has been placed on
the patient’s chest. Doing so prevents patient
discomfort and disturbance of the contact
between the electrode
and the skin.
Clip-on leadwire


Snap-on leadwire

Observing the cardiac rhythm
After the electrodes are in proper position, the monitor is on, and
the necessary cables are attached, observe the screen. You should
see the patient’s ECG waveform. Although some monitoring systems
allow you to make adjustments by touching the screen, most require
you to manipulate buttons. If the waveform appears too large or too
small, change the size by adjusting the gain control. If the waveform
appears too high or too low on the screen, adjust the position.

ECG_Chap02.indd 35



7/8/2010 4:17:01 PM



Verify that the monitor detects each heartbeat by comparing
the patient’s apical rate with the rate displayed on the monitor.
Set the upper and lower limits of the heart rate according to your
facility’s policy and the patient’s condition. Heart rate alarms are
generally set 10 to 20 beats per minute higher and lower than the
patient’s heart rate.
Monitors with arrhythmia detectors generate a rhythm strip
automatically whenever the alarm goes off. You can obtain other
views of your patient’s cardiac rhythm by selecting different leads.
You can select leads with the lead selector button or switch.

Printing it out
To get a printout of the patient’s cardiac rhythm, press the record
control on the monitor. The ECG strip will be printed at the central console. Some systems print the rhythm from a recorder box
on the monitor itself.
Most monitor recording systems print the date, time, and the
patient’s name and identification number; however, if the monitor
you’re using can’t do this, label the rhythm strip with the date, time,
patient’s name, identification number and rhythm interpretation.
Add any appropriate clinical information to the ECG strip, such as
any medication administered, presence of chest pain, or patient
activity at the time of the recording. Be sure to place the rhythm
strip in the appropriate section of the patient’s medical record.

WOW! Did I really
do all of that?!

It’s all on paper
Waveforms produced by the heart’s electrical current are
recorded on graphed ECG paper by a stylus. ECG paper consists
of horizontal and vertical lines forming a grid. A piece of ECG
paper is called an ECG strip or tracing. (See ECG grid.)

ECG grid
This ECG grid shows the horizontal axis and vertical axis and their respective measurement values.

0.5 mV
(5 mm)

or voltage 1 mV

0.1 mV
(1 mm)

0.04 second
0.20 second

3 seconds
Time (in seconds)

ECG_Chap02.indd 36

7/8/2010 4:17:02 PM



The horizontal axis of the ECG strip represents time. Each
small block equals 0.04 second, and five small blocks form a large
block, which equals 0.2 second. This time increment is determined
by multiplying 0.04 second (for one small block) by 5, the number
of small blocks that compose a large block. Five large blocks equal
1 second (5 ✕ 0.2). When measuring or calculating a patient’s heart
rate, a 6-second strip consisting of 30 large blocks is usually used.
The ECG strip’s vertical axis measures amplitude in millimeters (mm) or electrical voltage in millivolts (mV). Each small
block represents 1 mm or 0.1 mV; each large block, 5 mm or 0.5
mV. To determine the amplitude of a wave, segment, or interval,
count the number of small blocks from the baseline to the highest
or lowest point of the wave, segment, or interval.

Monitor problems
For optimal cardiac monitoring, you need to recognize problems
that can interfere with obtaining a reliable ECG recording. (See
Troubleshooting monitor problems, pages 38 and 39.) Causes of
interference include artifact from patient movement and poorly
placed or poorly functioning equipment.

Artifact, also called waveform interference, may be seen with
excessive movement (somatic tremor). The baseline of the ECG
appears wavy, bumpy, or tremulous. Dry electrodes may also
cause this problem due to poor contact.

Electrical interference, also called 60-cycle interference, is caused
by electrical power leakage. It may also occur due to interference
from other room equipment or improperly grounded equipment.
As a result, the lost current pulses at a rate of 60 cycles per second. This interference appears on the ECG as a baseline that’s
thick and unreadable.

Wandering baseline
A wandering baseline undulates, meaning that all waveforms are
present but the baseline isn’t stationary. Movement of the chest
wall during respiration, poor electrode placement, or poor electrode contact usually causes this problem.

Faulty equipment
Faulty equipment, such as broken leadwires and cables, can
also cause monitoring problems. Excessively worn equipment

ECG_Chap02.indd 37

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Mixed signals

Troubleshooting monitor problems
This chart shows several ECG monitoring problems, along with their causes and possible solutions.

What you see

What might cause it

What to do about it

Artifact (waveform interference)

• Patient experiencing seizures,
chills, or anxiety

• If the patient is having a seizure, notify
the practitioner and intervene as ordered.
• Keep the patient warm and encourage
him to relax.
• Replace dirty or corroded wires.
• Check the electrodes and reapply them
if needed. Clean the patient’s skin well
because skin oils and dead skin cells
inhibit conduction.
• Check the electrode gel. If the gel is dry,
apply new electrodes.
• Replace broken equipment.

• Dirty or corroded connections
• Improper electrode application

• Short circuit in leadwires or
• Electrical interference from
other electrical equipment in the

• Static electricity interference
from inadequate room humidity

• Make sure all electrical equipment is
attached to a common ground. Check all
three-pronged plugs to ensure that none of
the prongs are loose. Notify the biomedical
• Regulate room humidity to 40% if possible.

False high-rate alarm

• Gain setting too high, particularly with MCL1 setting

• Assess the patient for signs and symptoms of hyperkalemia.
• Reset gain.

Weak signals

• Improper electrode application
• QRS complex too small to

• Reapply the electrodes.

• Wire or cable failure

ECG_Chap02.indd 38

• Reset gain so that the height of the complex is greater than 1 mV.
• Try monitoring the patient on another lead.
• Replace any faulty wires or cables.

7/8/2010 4:17:04 PM



Troubleshooting monitor problems (continued)
What you see

What might cause it

What to do about it

Wandering baseline

• Patient restless
• Chest wall movement during

• Encourage the patient to relax.
• Make sure that tension on the cable
isn’t pulling the electrode away from the
patient’s body.
• Reposition improperly placed electrodes.

• Improper electrode application;
electrode positioned over bone

Fuzzy baseline (electrical interference)

• Electrical interference from
other equipment in the room

• Improper grounding of the
patient’s bed
• Electrode malfunction
Baseline (no waveform)

• Ensure that all electrical equipment is attached to a common ground.
• Check all three-pronged plugs to make
sure none of the prongs are loose.
• Ensure that the bed ground is attached to
the room’s common ground.
• Replace the electrodes.

• Improper electrode placement
(perpendicular to axis of heart)

• Reposition improperly placed electrodes.

• Electrode disconnected

• Check if electrodes are disconnected.
Reapply them as necessary.
• Check electrode gel. If the gel is dry, apply new electrodes.
• Replace faulty wires or cables.

• Dry electrode gel
• Wire or cable failure

can cause improper grounding, putting the patient at risk for
accidental shock.
Be aware that some types of artifact resemble arrhythmias,
and the monitor will interpret them as such. For example, the
monitor may sense a small movement, such as the patient brushing his teeth, as a potentially lethal ventricular
tachycardia. So remember to treat the patient,
not the monitor. The more familiar you become
with your unit’s monitoring system—and with
your patient—the more quickly you can recognize
and interpret problems and act appropriately.

ECG_Chap02.indd 39

Worn equipment can
cause problems—
including a possible
shock for the patient.

7/8/2010 4:17:06 PM



That’s a wrap!

Obtaining a rhythm strip review
Leads and planes
• A lead provides a view of the heart’s electrical activity
between a positive and negative pole.
– When electrical current travels toward the negative
pole, the waveform deflects mostly downward.
– When the current flows toward the positive pole, the
waveform deflects mostly upward.
• A plane refers to a cross-section view of the electrical
activity of the heart.
– Frontal plane, a vertical cut through the middle of the
heart, provides an anterior-posterior view.
– Horizontal plane, a transverse cut through the middle
of the heart, provides a superior or inferior view.
Types of ECGs
• 12-lead ECG records electrical activity from 12 views of
the heart.
• Single-lead or dual-lead monitoring provides continuous
cardiac monitoring.
12-lead ECG
• Six limb leads provide information about the heart’s
frontal (vertical) plane.
• Bipolar (leads I, II, and III) require a negative and positive electrode for monitoring.
• Unipolar (leads aVR, aVL, and aVF) record information
from one lead and require only one electrode.
• The six precordial leads (leads V1 through V6) provide
information about the heart’s horizontal plane.
Leads I, II, and III
• Leads I, II, and III typically produce positive deflection
on ECG tracings.
• Lead I helps monitor atrial arrhythmias and hemiblocks.
• Lead II commonly aids in routine monitoring and detecting of sinus node and atrial arrhythmias.
• Lead III helps detect changes associated with inferior
wall myocardial infarction.

ECG_Chap02.indd 40

Precordial leads
• Lead V1
– Biphasic
– Distinguishes between right and left ventricular ectopic beats
– Monitors ventricular arrhythmias, ST-segment changes, and bundle-branch blocks
• Leads V2 and V3
– Biphasic
– Monitors ST-segment elevation
• Lead V4
– Produces a biphasic waveform
– Monitors ST-segment and T-wave changes
• Lead V5
– Produces a positive deflection on the ECG
– Monitors ST-segment or T-wave changes (when
used with lead V4)
• Lead V6
– Produces a positive deflection on the ECG
– Detects bundle-branch blocks
Modified leads
• Lead MCL1
– Similar to V1
– Assesses QRS-complex arrhythmias, P-wave
changes, and bundle-branch defects
– Monitors premature ventricular contractions
– Distinguishes different types of tachycardia
• Lead MCL6
– Similar to V6
– Monitors ventricular conduction changes
Electrode configurations
• Three-electrode system uses one positive electrode,
one negative electrode, and a ground.
• Five-electrode system uses an exploratory chest lead to
monitor modified chest or standard limb leads.

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Obtaining a rhythm strip review (continued)
ECG strip
• 1 small horizontal block ⫽ 0.04 second
• 5 small horizontal blocks ⫽ 1 large block ⫽ 0.2 second
• 5 large horizontal blocks ⫽ 1 second
• Normal strip ⫽ 30 large horizontal blocks ⫽ 6 seconds
• 1 small vertical block ⫽ 0.1 mV
• 1 large vertical block ⫽ 0.5 mV
• Amplitude (mV) ⫽ number of small blocks from baseline
to highest or lowest point

• Interference—electrical power leakage, interference
from other equipment, or improper equipment grounding
that produces a thick, unreadable baseline
• Wandering baseline—chest wall movement, poor electrode placement, or poor electrode contact that causes
an undulating baseline
• Faulty equipment—faulty and worn equipment that
causes monitoring problems and places the patient at
risk for shock

Monitoring problems
• Artifact—excessive movement or dry electrode that
causes baseline to appear wavy, bumpy, or tremulous

Quick quiz

On ECG graph paper, the horizontal axis measures:
A. time.
B. speed.
C. voltage.
D. amplitude.

Answer: A. The horizontal axis measures time and is recorded in
increments of 0.04 second for each small box.

On ECG graph paper, the vertical axis measures:
A. time.
B. speed.
C. voltage.
D. amplitude.

Answer: C. The vertical axis measures voltage by the height of a
A biphasic deflection will occur on an ECG if the electrical
current is traveling in a direction:
A. posterior to the positive electrode.
B. perpendicular to the positive electrode.
C. superior to the positive electrode.
D. anterior to the positive electrode.

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7/8/2010 4:17:11 PM



Answer: B. A current traveling in a route perpendicular to the
positive electrode will generate a biphasic wave, partially above
and below the isoelectric line.

If a lead comes off the patient’s chest, the waveform:
A. will appear much larger on the monitor.
B. will appear much smaller on the monitor.
C. will appear to wander on the monitor.
D. won’t be seen at all on the monitor.

Answer: D. Leadwire disconnection will stop the monitoring process, and the waveform won’t be seen on the monitor.

To monitor lead II, you would place the:
A. positive electrode below the lowest palpable rib at the
left midclavicular line and the negative electrode below
the right clavicle.
B. positive electrode below the right clavicle at the midline
and the negative electrode below the left clavicle at the
C. positive electrode below the left clavicle and the negative electrode below the right clavicle at the midclavicular line.
D. positive electrode below the lowest palpable rib at the
right midclavicular line and the negative electrode below the left clavicle.

Answer: A. This electrode position is the proper one for monitoring in lead II.


ECG_Chap02.indd 42

If you answered all five questions correctly, superb! We’re ready
to go out on a limb lead for you.
If you answered four questions correctly, great! We hardly need to
monitor your progress.
If you answered fewer than four questions correctly, keep at it!
A review of the chapter can get your current flowing in the
right direction.

7/8/2010 4:17:12 PM


Interpreting a rhythm strip
Just the facts
In this chapter, you’ll learn:
 the components of an ECG complex and their significance and variations
 techniques for calculating the rate and rhythm of an ECG
 the step-by-step approach to ECG interpretation
 properties of normal sinus rhythm.

A look at an ECG complex
An ECG complex represents the electrical events occurring in one
cardiac cycle. A complex consists of five waveforms labeled with
the letters P, Q, R, S, and T. The middle three letters —Q, R, and
S—are referred to as a unit, the QRS complex. ECG tracings represent the conduction of electrical impulses from the atria to the
ventricles. (See Normal ECG, page 44.)

The P wave
The P wave is the first component of a normal ECG waveform.
It represents atrial depolarization—conduction of an electrical
impulse through the atria. When evaluating a P wave, look closely
at its characteristics, especially its location, configuration, and deflection. A normal P wave has the following characteristics:
• location—precedes the QRS complex
• amplitude—2 to 3 mm high
• duration—0.06 to 0.12 second
• configuration—usually rounded and upright

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• deflection—positive or upright in leads I, II, aVF, and V2 to V6;
usually positive but variable in leads III and aVL; negative or inverted in lead aVR; biphasic or variable in lead V1.
If the deflection and configuration of a P wave are normal—
for example, if the P wave is upright in lead II and is rounded and
smooth—and if the P wave precedes each QRS complex, you can
assume that this electrical impulse originated in the sinoatrial
(SA) node. The atria start to contract partway through the P wave,
but you won’t see this on the ECG. Remember, the ECG records
electrical activity only, not mechanical activity or contraction.

Normal ECG
This strip shows the components of a normal ECG waveform.

ECG tracings
represent the
conduction of
electrical impulses
from the atria to the

ECG_Chap03.indd 44

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The odd Ps
Peaked, notched, or enlarged P waves may represent atrial hypertrophy or enlargement associated with chronic obstructive pulmonary disease, pulmonary emboli, valvular disease, or heart failure.
Inverted P waves may signify retrograde or reverse conduction
from the atrioventricular (AV) junction toward the atria. When an
upright sinus P wave becomes inverted, consider retrograde or
reverse conduction as possible conditions.
Varying P waves indicate that the impulse may be coming from
different sites, as with a wandering pacemaker rhythm, irritable
atrial tissue, or damage near the SA node. Absent P waves may
signify conduction by a route other than the SA node, as with a
junctional or atrial fibrillation rhythm.

The PR interval
The PR interval tracks the atrial impulse from the atria through
the AV node, bundle of His, and right and left bundle branches.
When evaluating a PR interval, look especially at its duration.
Changes in the PR interval indicate an altered impulse formation
or a conduction delay, as seen in AV block. A normal PR interval
has the following characteristics (amplitude, configuration, and
deflection aren’t measured):
• location—from the beginning of the P wave to the beginning of
the QRS complex
• duration—0.12 to 0.20 second.
These characteristics are different for pediatric patients. (See
Pediatric rates and intervals, page 46.)

The short and long of it
Short PR intervals (less than 0.12 second) indicate that the impulse originated somewhere other than the SA node. This variation is associated with junctional arrhythmias and preexcitation
syndromes. Prolonged PR intervals (greater than 0.20 second)
may represent a conduction delay through the atria or AV junction
due to digoxin toxicity or heart block—slowing related to ischemia or conduction tissue disease.

The QRS complex
The QRS complex follows the P wave and represents depolarization of the ventricles. Immediately after the ventricles depolarize,
as represented by the QRS complex, they contract. That contraction ejects blood from the ventricles and pumps it through the
arteries, creating a pulse.

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Ages and stages

Pediatric rates and intervals
The hearts of infants and children beat faster than those of adults because children have smaller ventricular size and
higher metabolic needs. The fast heart rate and small size produces short PR intervals and QRS intervals.


Heart rate (beats/minute)

PR interval (in seconds)

QRS interval (in seconds)

1 to 3 weeks

100 to 180

0.07 to 0.14

0.03 to 0.07

1 to 6 months

100 to 185

0.07 to 0.16

0.03 to 0.07

7 to 11 months

100 to 170

0.08 to 0.16

0.03 to 0.08

1 to 3 years

90 to 150

0.09 to 0.16

0.03 to 0.08

4 to 5 years

70 to 140

0.09 to 0.16

0.03 to 0.08

5 to 7 years

65 to 130

0.09 to 0.16

0.03 to 0.08

8 to 11 years

60 to 110

0.09 to 0.16

0.03 to 0.09

12 to 16 years

60 to 100

0.09 to 0.18

0.03 to 0.09

Not necessarily mechanical
Whenever you’re monitoring cardiac rhythm, remember that the
waveform you see represents the heart’s electrical activity only. It
doesn’t guarantee a mechanical contraction of the heart and a subsequent pulse. The contraction could be weak, as happens with
premature ventricular contractions, or absent, as happens with
pulseless electrical activity. So before you treat the strip, check
the patient.

It’s all normal
Pay special attention to the duration and configuration when
evaluating a QRS complex. A normal complex has the following
• location—follows the PR interval
• amplitude—5 to 30 mm high but differs for each lead used
• duration—0.06 to 0.10 second, or half of the PR interval. Duration is measured from the beginning of the Q wave to the end of

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QRS waveform variety
The illustrations below show the various configurations of QRS complexes. When documenting the QRS complex, use
uppercase letters to indicate a wave with a normal or high amplitude (greater than 5 mm) and lowercase letters to indicate a wave with a low amplitude (less than 5 mm). In some instances, a second R wave may appear in a QRS complex.
This is called R⬘.





the S wave or from the beginning of the R wave if the Q wave is
• configuration—consists of the Q wave (the first negative deflection after the P wave), the R wave (the first positive deflection
after the P wave or the Q wave), and the S wave (the first negative
deflection after the R wave). You may not always see all three
waves. The ventricles depolarize quickly, minimizing contact time
between the stylus and the ECG paper, so the QRS complex typically appears thinner than other ECG components. It may also
look different in each lead. (See QRS waveform variety.)
• deflection—positive in leads I, II, III, aVL, aVF, and V4 to V6 and
negative in leads aVR and V1 to V3.

Crucial I.D.
Remember that the QRS complex represents intraventricular conduction time. That’s why identifying and correctly interpreting it
is so crucial. If no P wave appears with the QRS complex, then the
impulse may have originated in the ventricles, indicating a ventricular arrhythmia. (See Older adult ECGs.)

Deep and wide
Deep, wide Q waves may represent myocardial infarction. In this
case, the Q-wave amplitude is 25% of the R-wave amplitude, or
the duration of the Q wave is 0.04 second or more. A notched R

ECG_Chap03.indd 47


and stages

Older adult
Always keep the
patient’s age in mind
when interpreting the
ECG. ECG changes in
the older adult include
increased PR, QRS, and
QT intervals, decreased
amplitude of the QRS
complex, and a shift of
the QRS axis to the left.

7/7/2010 5:51:00 PM



wave may signify a bundle-branch block. A widened QRS complex
(greater than 0.12 second) may signify a ventricular conduction
delay. A missing QRS complex may indicate AV block or ventricular standstill.

The ST segment
The ST segment represents the end of ventricular conduction or
depolarization and the beginning of ventricular recovery or repolarization. The point that marks the end of the QRS complex and
the beginning of the ST segment is known as the J point.

Normal ST
Pay special attention to the deflection of an ST segment. A normal
ST segment has the following characteristics (amplitude, duration,
and configuration aren’t observed):
• location—extends from the S wave to the beginning of the T wave
• deflection—usually isoelectric (neither positive nor negative);
may vary from –0.5 to +1 mm in some precordial leads.

Not so normal ST
A change in the ST segment may indicate myocardial damage.
An ST segment may become either elevated or depressed. (See
Changes in the ST segment.)

Changes in the ST segment
Closely monitoring the ST segment on a patient’s ECG can help you detect myocardial ischemia or injury before infarction develops.
ST-segment depression
An ST segment is considered depressed
when it’s 0.5 mm or more below the baseline. A depressed ST segment may indicate
myocardial ischemia or digoxin toxicity.

ECG_Chap03.indd 48

ST-segment elevation
An ST segment is considered elevated
when it’s 1 mm or more above the baseline. An elevated ST segment may indicate
myocardial injury.

7/7/2010 5:51:01 PM



The T wave
The T wave represents ventricular recovery or repolarization.
When evaluating a T wave, look at the amplitude, configuration,
and deflection. Normal T waves have the following characteristics
(duration isn’t measured):
• location—follows the S wave
• amplitude—0.5 mm in leads I, II, and III and up to 10 mm in the
precordial leads
• configuration—typically round and smooth
• deflection—usually upright in leads I, II, and V3 to V6; inverted
in lead aVR; variable in all other leads.

Heavily notched
or pointed T waves in
an adult may mean

Why is that T so bumpy?
The T wave’s peak represents the relative refractory period of ventricular repolarization, a period during which cells are especially
vulnerable to extra stimuli. Bumps in a T wave may indicate that a
P wave is hidden in it. If a P wave is hidden, atrial depolarization
has occurred, the impulse having originated at a site above the

Tall, inverted, or pointy Ts
Tall, peaked, or tented T waves indicate myocardial injury or hyperkalemia. Inverted T waves in leads I, II, or V3 through V6 may
represent myocardial ischemia. Heavily notched or pointed T
waves in an adult may mean pericarditis.

The QT interval
The QT interval measures ventricular depolarization and repolarization. The length of the QT interval varies according to heart
rate. The faster the heart rate, the shorter the QT interval. When
checking the QT interval, look closely at the duration.
A normal QT interval has the following characteristics (amplitude, configuration, and deflection aren’t observed):
• location—extends from the beginning of the QRS complex to the
end of the T wave
• duration—varies according to age, sex, and heart rate; usually
lasts from 0.36 to 0.44 second; shouldn’t be greater than half the
distance between consecutive R waves when the rhythm is regular.

The importance of QT
The QT interval shows the time needed for the ventricular
depolarization-repolarization cycle. An abnormality in duration
may indicate myocardial problems. Prolonged QT intervals indicate that the relative refractory period is longer. A prolonged QT

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Drugs that increase the QT interval
This chart lists drugs that have been shown to increase the QT interval, which increases the patient’s risk of developing
torsades de pointes.

Drug name

Drug class

Drug name

Drug class

amiodarone (Cordarone) or


haloperidol (Haldol)


ibutilide (Corvert)



ketoconazole (Nizoral)



levofloxacin (Levaquin)


clarithromycin (Biaxin)


methadone (Methadose or

opiate agonist

desipramine (Norpramin)
disopyramide (Norpace)




dofetilide (Tikosyn)




dolasetron (Anzemet)


sertraline (Zoloft)


droperidol (Inapsine)

sedative; antinauseant

sotalol (Betapace)


erythromycin (Erythrocin)

antibiotic; GI stimulant

sumatriptan (Imitrex)


fluoxetine (Prozac)




interval increases the risk of a life-threatening arrhythmia known
as torsades de pointes.
This variation is also associated with certain medications such
as Class IA antiarrhythmics. (See Drugs that increase the QT
interval.) Prolonged QT syndrome is a congenital conductionsystem defect present in certain families. Short QT intervals may
result from digoxin toxicity or hypercalcemia.

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The U wave
The U wave represents the recovery period of the Purkinje or ventricular conduction fibers. It isn’t present on every rhythm strip.
The configuration is the most important characteristic of the U
When present, a normal U wave has the following characteristics (amplitude and duration aren’t measured):
• location—follows the T wave
• configuration—typically upright and rounded
• deflection—upright.
The U wave may not appear on an ECG. A prominent U wave
may be due to hypercalcemia, hypokalemia, or digoxin toxicity.

What are the keys
for reading a rhythm
A sequential,
approach will
serve you best.

8-step method
Interpreting a rhythm strip is a skill developed through
practice. You can use several methods, as long as
you’re consistent. Rhythm strip analysis requires a
sequential and systematic approach such as that
which employs the eight steps outlined here.

Step 1: Determine the rhythm
To determine the heart’s atrial and ventricular
rhythms, use either the paper-and-pencil method
or the caliper method. (See Methods of measuring
rhythm, page 52.)
For atrial rhythm, measure the P-P intervals—the intervals
between consecutive P waves. These intervals should occur regularly with only small variations associated with respirations. Then
compare the P-P intervals in several cycles. Consistently similar
P-P intervals indicate regular atrial rhythm; dissimilar P-P intervals
indicate irregular atrial rhythm.
To determine
the ventricular
rhythm, measure
the intervals
between two consecutive R waves
in the QRS complexes. If an R wave isn’t present, use the Q wave
of consecutive QRS complexes. The R-R intervals should occur

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Methods of measuring rhythm
You can use the paper-and-pencil or caliper method to determine atrial or ventricular rhythm.
Paper-and-pencil method
Place the ECG
strip on a flat
surface. Then
position the
straight edge
of a piece of
paper along the
strip’s baseline.
Move the paper up slightly so the straight edge is near the
peak of the R wave. With a pencil, mark the paper at the
R waves of two consecutive QRS complexes, as shown
above. This is the R-R interval.
Next, move the paper across the strip, aligning the two
marks with succeeding R-R intervals. If the distance for
each R-R interval is the same, the ventricular rhythm is
regular. If the distance varies, the rhythm is irregular.
Use the same method to measure the distance between the P waves (the P-P interval) and determine
whether the atrial rhythm is regular or irregular.

Caliper method
With the ECG on
a flat surface,
place one point
of the caliper on
the peak of the
first R wave of
two consecutive
QRS complexes.
Then adjust the caliper legs so the other point is on the
peak of the next R wave, as shown above. This distance is
the R-R interval.
Now pivot the first point of the caliper toward the third
R wave and note whether it falls on the peak of that wave.
Check succeeding R-R intervals in the same way. If they’re
all the same, the ventricular rhythm is regular. If they vary,
the rhythm is irregular.
Use the same method to measure the P-P intervals to
determine whether the atrial rhythm is regular or irregular.

Then compare R-R intervals in several cycles. As with atrial
rhythms, consistently similar intervals mean a regular rhythm; dissimilar intervals point to an irregular rhythm.
Ask yourself: How irregular is the rhythm? Is it slightly irregular or markedly so? Does the irregularity occur in a pattern (a
regularly irregular pattern)? Keep in mind that variations of up to
0.04 second are considered normal.

Step 2: Determine the rate
You can use one of three methods to determine atrial and ventricular heart rate. Remember, don’t rely on these methods alone. Always check a pulse to correlate it with the heart rate on the ECG.

10-times method
The easiest way to calculate heart rate is the 10-times method,
especially if the rhythm is irregular. You’ll notice that ECG paper

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Calculating heart rate
This table can help make the sequencing method of determining heart rate more precise.
After counting the number of boxes between the R waves, use the table shown at right to
find the rate.
For example, if you count 20 small blocks or 4 large blocks, the rate would be 75 beats/
minute. To calculate the atrial rate, use the same method with P waves instead of R waves.
Rapid estimation
This rapid-rate calculation is also called the countdown method. Using the number of
large boxes between R waves or P waves as a guide, you can rapidly estimate ventricular or atrial rates by memorizing the sequence “300, 150, 100, 75, 60, 50.”

is marked in increments of 3 seconds, or 15 large boxes. To figure
the atrial rate, obtain a 6-second strip, count the number of P
waves, and multiply by 10. Ten 6-second strips represent 1 minute.
Calculate ventricular rate the same way, using the R waves.

1,500 method
If the heart rhythm is regular, use the 1,500 method — so named
because 1,500 small squares represent 1 minute. Count the small
squares between identical points on two consecutive P waves
and then divide 1,500 by that number to get the atrial rate. To
obtain the venV
tricular rate,
use the same
method with
two consecutive
R waves.

Sequence method

Number of
small blocks
5 (1 large block)
10 (2 large blocks)
15 (3 large blocks)
20 (4 large blocks)
25 (5 large blocks)
30 (6 large blocks)
35 (7 large blocks)
40 (8 large blocks)



The third method of estimating heart rate is the sequence method,
which requires that you memorize a sequence of numbers. (See
Calculating heart rate.) To get the atrial rate, find a P wave that
peaks on a heavy black line