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Understanding ECGs has never been easier than with ECGs Made Easy, 6th Edition! In compliance with the American Heart Association’s 2015 ECC resuscitation guidelines, Barbara Aehlert’s new edition offers clear explanations, a conversational tone, and a wealth of practice exercises to help students and professionals from a variety of medical fields learn how to accurately recognize and interpret basic dysrhythmias. Each heart rhythm covered in the book includes a sample ECG rhythm strip and a discussion of possible patient symptoms and general treatment guidelines. Other user-friendly features include: ECG Pearls with insights based on real-world experience, Drug Pearls highlighting the medications used to treat dysrhythmias, Clinical Correlation call-outs, Lead In applicatinos, Stop&Review questions, a comprehensive post-test with answers, and more. It’s everything you need to master ECG interpretation with ease!

Clear ECG discussions highlight what you need to know about ECG mechanisms, rhythms, and heart blocks, such as: How Do I Recognize It? What Causes It? What Do I Do About It?
Introduction to the 12-Lead ECG chapter provides all the basics for this advanced skill, including determining electrical axis, ECG changes associated with myocardial ischemia and infarction, bundle branch block, and other conditions.
A comprehensive post-test with answers at the end of the book measures your understanding.
ECG Pearl boxes offer useful hints for interpreting ECGs, such as the importance of the escape pacemaker.
Drug Pearl boxes highlight various medications used to treat dysrhythmias.
Chapter key terms focus your attention on the most important information.
Chapter objectives tied to chapter text enable you to quickly review content that satisfies specific learning objectives.
NEW! 38 New cardiac rhythm strips have been added to the book for a total of 260 practice strips.
NEW! AHA compliance ensures the book reflects the American Heart Association’s 2015 ECC resuscitation guidelines.
NEW! Lead In boxes cover ECG principles, practical applications, indications, techniques, and interpretation.
NEW! Expanded coverage of ambulatory monitoring provides more in-depth guidance in this critical area.
Κατηγορίες:
Έτος:
2017
Έκδοση:
6th Edition
Εκδότης:
Elsevier
Γλώσσα:
english
Σελίδες:
338
ISBN 13:
9780323415477
Σειρές:
Eğitim Tanrısı
Αρχείο:
PDF, 176,60 MB

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ELSEVIER
3251 lllverport Lane
St. Louis, Mbsouri 63043

ECGt MADE EASY, SIXTH EDITION

ISBN: 978-0-32340130-2

Copyright c 2018, lllsevier IDe. All r!pta raene4.
Prnloue e4itloall copyrlpted 2013,2011, 2006, 2002, uull995.
No part ofthil publication may be reproduced or transmitted in any form or by any mean1, electronk or mechanical, including photocopying, .recording. or any in!ormali.on stDrap and Rtrieval. systmn. without permilaion in
writing from the publiaher. Details on how to 1eek penniasion. further information about the Publither's permi.lsi.OIIJ policies and our arrangements with organi2al:ian.t such as the Copyright Clearance Center and the Copyright
Licenalng Agency, can be fuWld at our webalte: www.ellevier.com/permiaaiona.

This book and the lndlvldual contributl01111 contained In It are protected Wlder copyright by the Publilher (other
than u may be noted herein).

Notices
Knowledge and best practice in this field aR constantly changing. N new research and experience broaden
our undemanding, changes in research method.t, profesrional practices, or medical treatment may become

neceuary.
Practitioner~ and researchers must alwaya rely on their own aperlence and knowledge In evaluating and
uaing any Information, methods, compound&, or aperlmentl described herein. In usiDg tuc.h information or
method. they should be mindful of their own takty and the takty of others, including parties fur whom they
have a professional Rtpoll8ibility.
With respect. to any drug or pharmaceutical pmduct& ident:ified. reader• are adviled to check the mo1t
cun~nl information provided (i) on procedURS fealuRd or (ii) by the manufacturer of each product to be
administered. to verify the .recommended dose or formula, the method and duration of adminiltration, and
contnindlcatiOIIJ. It is the responsibility of practitioners, relying on their own experience and knowledge of
their patients, to make diagnose~, to determine doaget and the bel; t t.reatment for each individual patienl, and
to take all appropriate sarety precautionl.
To the fulli:st ment of the law, neither the Publisher nor the alrthon, contributors, or editor1, UNme
any liability fur any injury and/or damage to peraom or property u a matter of produculiabllity, nesJigence
or otherwile, or from any uae or operation of any method&, product., imtruction1, or ideu contained in the
m:rterial herein.

Name.: Aehlert, Barbara, author.
Title: ECGa made easy I Barbara Aehlert, MSEd, BSPA, RN.
Description: Sixth edition. I Phoenix, Arizona : Southwest EMS Education,
Inc., [2018liindudes blhllographical refuences and lnda. I
Identifiers: LCCN 2017015081 (print) I LCCN 2017026543 (ebook) I ISBN
9780323479059 () I ISBN 9780323401302 (pbk. : a1k. paper)
Subjecu: LCSH: Electrocardiography--Handboob. manuals. etc.
Cl.ulifi.c:ation: LCC RC683.5.F.5 (ebook) I LCC RC683.5.E5 A39 2018 (print) I
DDC 616.1/207547--dc23
LC record available at httpt:!/ka1loc.gov/2017015081

https://t.me/MBS_MedicalBooksStore
Executive Contel!t Stmteglst: Sandra Clark
Content Developmettt SpeclalUU: Laura SeltlrtiMelissa. Kinsey
Publishing Semcu Manager. Deepthi Unni
SenWr Project MaMpr. Umarani Na1arajan
~ Dirmton: Brian Saliabury

de•n:l oping: cnuntrm(:~

Printed in Canada
Last digit is the print number:

Worktng together
to grow l!b-r.arLC'~ Li1

9 8 7 6 5 4 3 2 1

Many ye.ars ago, as a green but enthusiastic nurse preparing to shift from medical-surgical nursing
to critical care, I signed up for a course in basic ECG recognition. It was an intimidating experience. My i.nst:ructor was extremely knowledgeable and kind. and I studied diligently throughout
the course, yet I struggled to crack the code of heart rhythm interpretation. To make matters
worse, I couldn't find any resources in which these complex concepts were presented in a practical, useful way. Although I passed the course. I decided to repeat it a few months later because I
simply coulchlt recall and apply the infonnation I needed to help my patients.
After successfully completing the second course, I promised myself that I would someday
present these concepts in a simpler way. 'Ihat promise became my life's work. Ever since then,
I have been looking for better ways in which to present the skill of basic ECG recognition to those
who will apply that knowledge every working day:
• Paramedics
• Nursing and medical students
• ECG monitor technicians
• Nurses and other allied health personnel world.ng in emergency departments, critical care
units, postanesthesia care units, operating rooms, and telemetry units
'!his book can be used alone or as part of a formal course of instruction in basic dysrhythmia recognition. 1he book'• content focuses on the essentials of ECG interpretation. Each ECG
rhythm is described and accompanied by a sample rhythm strip. 1hen the discussion turns to
possible signs and symptoms related to each rhythm and. where appropriate, current recommended treatment. At the end of each chapter, additional rhythm strips and their description.s are
provided for practice. (All rhythm strips shown in this text were recorded in lead n unless otherwise noted.) 1he Stop 8c Review exerci!es at the end of each chapter are self-usessment activities
that allow you to check your learning.
In addition, resources to aid the in.stru.ctor in teaching this content can be found on Evolve at
http://evolve.elsevier.com/Aehlert/ecgl. 1hese resources include:
• Image Collection
• PPTSlide.
• PPT Practice Slides

• TEACH2.4
• Test Bank
I have made every attempt to supply content consistent with current literature, including current resuscitation guidelines. However, medicine is a dynamic field. Recommendations change as
medical research evolves, technology improves, and new medications, procedures, and devices
are developed. As a result, be •ure to learn and follow local protocols as defined by your medical advisors. Neither I nor the publisher can assume responsibility or liability for loss or damage
resulting from the use of information contained within.
I genuinely hope this book is helpful to you, and I wish you success in your studies and clinical
practice.
Best regards,
Barbara Aehlert

iii

I would like to thank the manuscript reviewers foc their commenb and suggestiom. Areu of this
text were rewritten, reorganized, and clarified because of your effom.
I would also like to thank the following health care professionals, who provided many of the
rhythm strips used in this book: Andrew Baird, CEP; James Bratcher; Joanna Burgan, CEP; Holly
Button, CEP; Gretchen Chalmers, CEP; 'Ihomas Cole, CEP; Brent Haines, CEP; Paul Honeywell,
CEP; Timothy Klatt. RN; Bill Loughran. RN; Andrea Lowrey, RN; Joe Martinez, CEP; St.ephanos
Orphanidis, CEP; Jason Payne, CEP; Steve Ruehs, CEP; Patty Seneski, RN; David Stockton, CEP;
Jason Stodghill, CEP; Dionne Socie, CEP; Kristina Tellez, CEP; and Fran Wojculewicz, RN.
A special thanks to Melissa Kinsey for her humor, guidance, advice, and impeccable attention
to detail throughout this project.

iv

To
Deepak C. Patel, MD

whose knowledge, humor, and genuine compassion for his
patients are unparalleled.

Krlaten Bon:IWt, llN, MSN, PNP, Nll-P, CPN
Care Coordinator
Cincinnati Childrms Hospital Medical Center
Cincinnati, Ohio

BiB Miller
Paramedic Crew Chief
St. Louis Fire Department-HEMS
St. Louis, Missouri

Joshua BorkoU:.y, BS, pp.c

Mark.Nootena, MD, PACC

EMS Education Manager
University of Cincinnati College of Medicine
Cincinnati, Ohio

Cardiologist. Private Practice
Munster, Indiana

Ruth C. Tamulonis, MS, RN

Angela McConachie, DNP, MSN-PNP, RN
Assistant Professor
Goldfarb School ofNursing at Barnes-Jewish College
St Louis, Missouri

vi

Nursing Professor
Yuba College
Marysville, California

Barbara Aehlert, MSBd, BSPA, RN, has been a registered nurse for more than 40 years. with
clinical experience in medicallsurgical nursing. critical care nursing, prehotpital education, and
nursing education. Barbara i.s an active CPR and Advanced Cardiovascular Life Support (ACLS)
instructor with a special interest in teaching basic dysrhythmia recognition and ACLS to nurses
and paramedics.

vii

1 ANATOMY AND PHYSIOLOGY, 1
Location. SJu, and Shape of the Heart. 2
Surfaca of the Heart. 2
Coverinp of the Heart, 2
Structure of the Heart, 5
Layers of the Heart WalL 5
Heart Chambers, 6
Heart Valves, 8
The Heart's Blood Supply, 11
The Heart's Nerve Supply, 16

The Heart aa a Pump, 19
Cardiac Cycle, 19
Blood PreS3Ul't, 20
R£ferenca, '1.7

2 BASIC ELECTROPHYSIOLOGY, 28
Cardiac Cella, 30
Types of Cardiac Cells, 30
Propertia of Cardiac Cells, 30
Cardiac Action Potmtial, 30
Polarization, 31
Depolarization, 31
Repolarization, 32
Phases of the Cardiac Action Potential, 32
Refractory Periods, 34
Conduction Syatem, 35
Sinoatrial Node, 35
Atrioventricular Node and Bundle, 37
Right and Left Bundle Branches, 38
Purkinje Fibers, 38
Cauaea of Dyarhythmiaa, 39
Disorders of Impulse Formation, 39
Disorders of Impulse Conduction, 39
The Ela:trocardiogr, 41
Electrodes, 41
Leads, 42
Ambulatory Cardiac Monitoring, 46
Blectrocanliopaphy Paper, 47
Waveforms, 48
Segments, 53
Intervals, 55
Artifact. 56
Symmatic Rhythm J:nterpretation. 57
Asseas Regularity, 57
Asseas Rate, 58
Identify and Examine Waveforms, 60
Asseaslntervals and Examine Segments, 60
Interpret the Rhythm, 60
Re&renca, 74

viii

3 SINUS MECHANISMS, 78
Introdudlon. 76
Sinua Rhythm, 77
How Do I Recognize It? 77
Sinua Bradycardia. 78
How Do I Recognize It? 78
What Causes m 78
What Do I Do About It? 79
Sinua Tadlyardia, 80
How Do I Recognize It? 80
What Causes It? 80
What Do I Do About It? 81
Sinua Arrbytbmia, 81
How Do I Recognize It? 81
What Causes It! 81
What Do I Do About It? 82
Sinoatrial Block. 82
How Do I Recognize It? 82
What Causes It? 82
What Do I Do About It? 83
Sinua Arrest, 83
How Do I Recognize It? 83
What Causes It? 83
What Do I Do About It? 84

Referencea,IOI

4 ATRIAL RHYTHMS, 102
Introduction, 103
Atrial Dyar.bythmiaa: Mech.aDi~ms, 103
Abnormal Automaticity, 103
Tnggered Activity, 103
Reentry, 104
Premature Atrial Compleea, 104
How Do I Recognize It? 104
Noncompensatory versus Compensatory Pause, 105
Aberrantly Conducted Premature Atrial
Complexes, 106
Nonconducted Premature Atrial Complexes, 106
What Do I Do About Them? 107
Wuuleriq Atrial Pacemaker, 107
How Do I Recognize It? 107
What Causes It? 107
What Do I Do About It? 107
Mal.tifoc:al Atrial Tachycanlia, 108
How Do I Recognize It? 108
What Causes It? 108
What Do I Do About It? 108

Contents
Supraventricular 'Thchycardia, 108

Atrial Tachycardias, 109
Atrioventricular Nodal Reentrant Tachycardia, 113
Atrioventricular Reentrant Thchycardia, 114
Atrial Flutter, 117

How Do I Recognize It? 117
What Causes It? 118
What Do I Do About It? 118
Atrial Fibrillation, 119
How Do I Recognize It? 119
What Causes It? 121
What Do I Do About It? 121
References, 140

5

~UNCTIONAL

RHYTHMS, 141

Introduction, 141
Premature Juncticmal Compleus, 142
How Do I Recognize 1hem~ 142
What Causes 1hem? 143
What Do I Do About Them? 143
Junctional Escape Beau or Rhythm, 144
How Do I Recognize It? 144
What Causes It? 145
What Do I Do About It? 146
Accelerated Junctional Rhythm, 146
How Do I Recognize It? 146
What Causes It? 146
What Do I Do About It? 146
Junctional Tachyardia. 146
How Do I Recognize It? 146
What Causes It? 147
What Do I Do About It? 147
References, 164

What Causes It? 177
What Do I Do About It? 177
~(CanUa~S~).177

How Do I Recognize It? 177
What Causes It? 178
What Do I Do About It? 178
References, 193

7 ATRIOVENTRICULAR BLOCKS, 194
Introduction, 194
First-Degree Atrioventricalar Block, 195
How Do I Recognize It? 195
What Causes It? 196
What Do I Do About It? 197

Second-Degree Atrioventricular Blocks, 197
Second-Degree Atrioventricular Block Type I, 197
How Do I Recognize It? 197

What Causes It? 198
What Do I Do About It? 199
Second-Degree Atrioventricular Block Type ll, 199

How Do I Recognize It? 199
What Causes It? 200
What Do I Do About It? 200
2:1 Atriovmtricalar moa, 200
How Do I Recognize It? 200
Advanced Second-Degree Atriovent:rkular Block. 201
'Ihird-Degree Atrioventricu1ar Block, 202.
How Do I Recognize It? 202

What Causes It? 203
What Do I Do About It? 203
Reference8, 221

B PACEMAKER RHYTHMS, 222
6 VENTRICULAR RHYTHMS, 165
Introductlon,166
Premature Ventricular Complexes, 166
How Do I Recognize 1hem~ 166
What Causes 1hem? 170
What Do I Do About Them? 170
Ventricular .Escape Beats or Rhythm,170

How Do I Recognize It? 170
What Causes It? 172
What Do I Do About It? 172
Accelerated Idlovmtrl<:Ular :Rhythm. 172

How Do I Recognize It? 172
What Causes It? 172
What Do I Do About It? 173
Ventricnlar Tachycardia, 173
How Do I Recognize It? 173
Ventricular Fibrillation, 176

How Do I Recognize It? 176

Pacemaker Systema. 223

Permanent Pacemakers and hnplantable CardioverterDefibrillators, 223
Temporary Pacemakers, 224
Pacing Lead Symms, 225
Padng Chamben and Modes, 226

Single-Chamber Pacemakers, 226
Dual-Chamber Pacemakers, 227
Biventricular Pacemakers, 227
Fixed-Rate Pacemakers, 227
Demand Pacemakers, 227
Pacemaker Codes, 228
Pacemaker Malfunction.l28

Failure to Pace, 228
Failure to Capture, 229
Failure to Sense, 230
Analyzing Pacemaker Fund:ion on the ECG, 230
Reference., 240

Contents

9 INTRODUCTION TO THE 12-LEAD
ECG, 241
Introduction, 141
Layout of the 12-Lead Electrocardiogram, 242
Vedors,242
Axis,243
.Acute Coronary Syndromes, 244
Anatomic Location of a Myocardial Infarction, 246
Intraventricular Conduction Delays, 254
Structures of the Intraventricular Conduction
System,254
Bundle Branch Activation, 254
How Do I Recognize It? 254
What Causes It? 257
What Do I Do About It? 257
Chamber Enlargement, 257
Atrial .Abnormalities, 258
Ventricular Abnormalities. 259
Electrolyte Disturbances, 260
Sodium, 261
Potassium, 261
Calcium, 262
Magnesium, 263
ADalyzing the 12-Lead EledJ:ocanUogram, 263
References, 277

10 POSlTEST, 278

INDEX, 321

LEARNING OBJECTIVES
After reading this chapter, you should be able to:
1. Describe the location of the heart.
2. Identify the surfaces of the heart.
3. Describe the structure and function of the coverings of the heart.
4. Identify the three cardiac muscle layers.
5. Identify and describe the chambers of the heart and the vessels that
enter or leave each.
6. Identify and describe the location of the atrioventricular and semilunar
valves.
7. Explain atrial kick.
8. Name the primary branches and areas of the heart supplied by the
right and left coronary arteries.

9. Define and explain acute coronary syndromes.
10. Discuss myocardial ischemia, injury, and infarction, indicating which
conditions are reversible and which are not.
11. Compare and contrast the effects of sympathetic and parasympathetic
stimulation of the heart.
12. Identify and discuss each phase of the cardiac cycle.
13. Beginning with the right atrium, describe blood flow through the
normal heart and lungs to the systemic circulation.
14. Identify and explain the components of blood pressure and cardiac
output.

KEY TERMS
acute coronary syndrome (ACS): A term used to referto distinct
conditions caused by a similar sequence of pathologic eventsa temporary or permanent blockage of a coronar_y artery. These
conditions are characterized by an excessive dem nd or inadequate
supply of oxygen and nutrients to the heart muscle associated
with plaque disruption, thrombus formation, and vasoconstriction.
ACSs consist of three major syndromes: unstable angina, nonST-elevation myocardial infarction, and ST elevation myocardial
infarction.
afterload: The pressure or resistance against which the ventricles must
pump to eject blood.
angina pectoris: Chest discomfort or other related symptoms of sudden
onset that may occur because the increased oxygen demand of the
heart temporarily exceeds the blood supply.
apex of the heart: Lower portion of the heart that is formed by the tip of
the left ventricle.
atria: Two upper chambers of the heart (singular, atrium).
atrial kick: Blood pushed into the ventricles because of atrial contraction.
atrioventricular (AV) valve: The valve located between each atrium
and ventricle; the tricuspid separates the right atrium from the right
ventricle, and the mitral (bicuspid) separates the left atrium from the
left ventricle.
atypical presentation: Uncharacteristic signs and symptoms perceived
by some patients experiencing a medical condition, such as an ACS.

base of the heart: Posterior surface of the heart.
blood pressure: Force exerted by the blood against the walls of the arteries as the ventricles of the heart contract and relax.
cardiac output (CO): The amount of blood pumped into the aorta each
minute by the heart; defined as the stroke volume multiplied by the
heart rate.
chordae tendineae (tendinous cords): Thin strands of fibrous connective tissue that extend from the AV valves to the papillary muscles that
prevent the AV valves from bulging back into the atria during ventricular
systole (contraction).
chronotropy: A change in (heart) rate.
diastole: Phase of the cardiac cycle in which the atria and ventricles relax
between contractions and blood enters these chambers. When the term
is used without reference to a specific chamber of the heart, ventricular
diastole is implied.
dromotropy: Refers to the speed of conduction through the AV junction.
dysrhythmia: Any disturbance or abnormality in a normal rhythmic pattern; any cardiac rhythm other than a sinus rhythm.
ejection fraction: The percentage of blood pumped out of a heart chamber with each contraction.
endocardium: Innermost layer of the heart that lines the inside of the
myocardium and covers the heart valves.
epicardium: Also known as the visceral pericardium; the external layer of
the heart wall that covers the heart muscle.

1

Chapter 1 Anatomy and Physiology
hBart failure: Acondition In whlctl the heart Is unable tD pump enough
blood to meet the metabolic needs of the body; It may result from any
cond~ion that impairs preload, afterload, cardiac contractility, or heart

rare.

inDtropy: Refers to a change in myocardial contractility.
ischemia: Decreased supply of oxygena1ed blood tn a body part or organ.
mediastinum: Middle area of the thoracic cavity; contains the heart, great
vessels, trachea, and esophagus, among other structures; extends from
the sternum to the vertebral column.
mltochondrta: The energy-producing parts of a cell.
mvocardlallnfarctlon (M~: Death of some mass of the heart muscle
caused by an Inadequate blood supply.
mvocardlum: Middle and thickest layer of the heart; contains the cardiac
muscle fibers that cause contraction of the heart and contal ns the
conduction system and blood supply.
myofibril: Slender striated strand of muscle tissue.
papillary muscles: Muscles attached to the chordae mndineae of the AV
valves and the ventricular muscle of the heart that help prevent the AV
valves from bulging too far intn the abia.
pericardium: A double-walled sac thai erdoses the heart and helps
protect It from trauma and Infection.
peripheral resistance: Resistance to the flow of blood determined by
blood vessel diameter and the tone of the vascular musculature.
preload: Force exerted by the blood on the walls of the venb1cles at the
end of diastole.

LOCATION, SIZE, AND SHAPE

OFTHEHEART
[Oblectlve 1]
The heart is a hollow muscular organ that lies in the space
between the lungs (i.e., the mediastinum) in the middle of
the chest (Pig. 1.1). It sits behind the stemwn and just above
the diaphragm. About two thirds of the heart lies to the left
of the midline of the stemwn. The remaining third lies to the
right of the sternum.
The adult heart is about 5 inches ( 12 an) long, 3.5 inches
(9 em) wide, and 2.5 inches (6 em) thick (Fig_ 1.2). It typically
weighs between 250 and 350 g (about 11 oz) and is about
the size of its owner's fist The weight of the heart is about
0.4596 ofa man's body weight and about 0.40% ofa woman's,
A person's heart size and weight are influenced by his or her
age, body weight and build. frequency of physical exercise,
and heart disease.

SURFACES OF THE HEART
[Obiactiva 2]
The base, or posterior surface, of the heart is formed by the
left atrium, a small portion of the right atrium, and proximal portions of the superior and inferior venae cavae and
the pulmonary veins (Fig. 1.3). The front (anterior) surface
of the heart lies behind the sternum and costal cartilages. It is

pi'Oldmal: Location nearer to the midline of the body or the point of
attachment than something else Is.
sarcolemma: Membrane that covers smooth, striated, and cardiac
muscle fibers.
sarcomere: Smallest functional un~ of a myofibril.
sarcoplasm: SemWiuid cytnplasm of muscle cells.
sarcoplasmic reticulum: Network of tubules and sacs that plays an
important role in muscle contraction and relalration by releasing and
storing calcium Ions.
semilunar (SL) valves: Valves shaped like half-moons that separate the
ventricles from the aorta and pulmonary artery.
septum: An lntBmal wall of connective tissue.
stroke volume {SV): The amount of blood e]eclBd from a ventricle with
each heartbeat
sulcus: Groove.
systole: Contraction of the heart (usually refarri ng to ventricular contraction), during which blood is propelled intn the pulmonary artery and
aorta; when the tenn is used without reference to a specific chamber of
the heart, ventricular systole is implied.
tone: A term that may be used when referring to the normal state of balanced tension In body tissues.
venous return: Amount of blood flowing lntn the right atrium each minute
from the syslemlc c1rculatlon.
venb1cles: The two lower chambers of the heart

formed by portions of the right atrium and the left and right
vmtrides (Fig. 1.4). However, because the heart is tilted
slightly toward the left in the chest, the right ventricle is the
area of the heart that lies most directly behind the sternum.
The apa, or lower portion, of the heart is formed by the tip
of the left ventricle. The apex lies just above the diaphragm
at about the level of the fifth intercostal space in the midclavicular line.
The heart's left side (i.e., left lateral surface) faces the
left lung and is made up mostly of the left ventricle and a
portion of the left atrium. The right lateral surface faces
the right lung and consists of the right atrium. The heart's
bottom (i.e., inferior) surface is formed primarily by the
left ventricle, with small portions of the right ventricle
and right atrium. The right and left ventricles are separated by a groove containing the posterior interventricular vessels. Because the inferior surface of the heart rests
on the diaphragm, it is also called the diaphragmatic surface (Fig. 1.5).

COVERINGS OF THE HEART
[Obiactive 3)
The periQU'dium is a double-walled sac that encloses the
heart and helps protect it from trauma and infection. The
tough outer layer of the pericardia! sac is called the fibrous
parietal pericardium (Fig. 1.6). It anchors the heart to some

Chapter 1 Anatomy and Physiology

Mldclavlcular
line

Fig. 1.1 Antar1or v1aw of tha chest wall of a man lhM!rg skslalal structullls and
the surface projactlon of the heart (From Draka R, Vogl AW, Mlb:hall AWM: Gtay's
8II8JDmy for studsnts, ed 3, New York, 2015, Churchill LMngstooe.)

Fig. 1.2 Appean~nca of 1h& heart. This pho!Dgraph shows a living human heart
p111pered for transplan1al!on Into a paUent. NoiB liB slza llllaUveiD 1he hands that Rill
hading 1t. (From PaiiDn KT, Thlbolil&u GA: Anatomy& physiology. &d 9, St. Louis.
2016, Mosby.)

Anlartor
lntervent~wer

branch of left
coronary artery
Greal canlac vein

Fig. 1.3 The base af the heart. (Ffm1 Drake R, 'ql A.W, Milcrell A."WM: &ay's

Obtuee mergln

anaiDmy for stJJdents, ed 3, New York, 2015, Churchill Uvingslune~

The right and left phrenic nerves, which innervate the diaphragm, pass through the fibrous pericardium as they
descend to the diaphragm. Because these nerves supply sensory fibers to the fibrous pericardium, the parietal
serous pericardium, and the mediastinal pleura, discomfort
related to conditions affecting the pericardium may be felt
In the areas above the shoulders or lateral neck.

of the structures around it. such as the sternum and diaphragm, by means of ligaments. This helps prevent excessive movement of the heart in the chest with changes in
body position.

If the pericardium becomes Inflamed (pericarditis), excess
pericardia! fluid can be quickly generated in response to the
inflammation. Pericarditis can result from a bacterial or viral
infection, rheumatoid arthritis, tumors, destruction of the
heart muscle in a heart attack, among other causes.

Fig. 1.4 Th& ant:&r1or surface of the haart. (From Drake R, Vogl AW, Mitchell
AWM: Gray's anatomy frJr stJJd6nts, &d 3, Naw York, 2015, Churchill L.Mrgstona.)

The inner layer of the pericardium, the serous pericardium, consists of two layers: parietal and visceral (Fig. 1.7).
the parietal. layer lines the inside of the fibrous pericardium.
The visceral layer attaches to the large vessels that enter and
exit the heart and covers the outer surface ofthe heart muscle
(ie., the epicardium).
Between the visceral and parietal layers is a space (the
pericardia! space) that normally contains about 20 mL of
serous (pale yellow and transparent) fluid. This fluid acts as a
lubricant, preventing friction as the heart beats.

Heart surgery or trauma to the heart, such as a stab wound,
can cause a rapid buildup of blood in the pericardia! space. The
buildup of excess blood or fluid in the pericardia! space compresses the heart. This can affect the heart's abiily to relax and
fill with blood between heartbeats. Ifthe heart cannot adequately

Chapter 1 Anatomy and Physiology

fill with blood, the amount of blood the ventricles can pump out
to the body (cardi~ output) will be decreased. As a result, the
amount of blood returning to the heart is also decreased. These
changes can result in a life-threatening cond~ion called C8ldiac
temponade. The amount of blood or fluid in the pericardia!
space needed to impair the heart's ability to fill depends on the
rate at which the buildup of blood or fluid occurs and the ability
of the pericardium to stretch and accommodate the increased
volume of fluid.
The rapid buildup of as little as 100 to 150 ml of fluid or
blood can be enough to result in signs and symptoms of

shock. Conversely, 1000 mL of fluid may build up over a longer period without any significant effect on the heart's ability
to fill. This is because the pericardium accommodates the
increased fluid by stretching over time.
The symptoms of cardiac tamponade can be relieved
by removing the excess fluid from the pericardia! sac.
Pericardiocentesis is a procedure in which a needle is
inserted into the pericardia! space and the excess fluid
is sucked out (aspirated) through the needle. If scarring is
the cause of the tamponade, surgery may be necessary to
remove the affected area of the pericardium.

Right
ventricle

Rbrous
pericardium
{cut;)

Postertor
lnt8r-

ventrlcu lar
art8ly

Left verrtricla

and vein

Coronary

Right
atrium
Inferior

sulcus

vena cava

Fig. 1.15 The Inferior surface ot the heart The lnfe~or part ot the fibrous pe~card urn has been removed v.tlh the dlapluagm. (From Gosling JA: Human anaJDmy: color atlas and text. ad 4, L..ordcn, 2002, Mosby.)

Laft brachl~

oaphalil:
vein

Left

Aortic
arch

vagus
narve

Lung
roots

Left
phrenic

nerve

•.· ...

Cenlral

""""~- tendon of
diaphragm

Fig. 1 .& The fibrous pericanium and phrenic nerves revealed after reiTlCJ\Iill of the lungs. {From Gosling J&.: Human
anafDmy: color afias and text. ed 4, Lllndon, 2002, Mosby.)

Chapter 1 Anatomy and Physiology

Left and llgtrt
phrenic

Alcendng
aorta

Pulmonary
trunk

Fibrous

pertcardium
(cut)

V-.1
~--+-:ft-.,_;.;..- MI'OUS

pertcardium

Fig. 1.7 The fbrous pericardium has been opened to expose the visceral pericardium ~ring lhe anterior surface of the
heart. (From Gosling JA: HumaiJ anatomy: color atlas and tert; eel 4, London, 2002, Mosby.)

STRUCTURE OF THE HEART
Layers of the Heart Wall
[Oblactlve 4]
lhe walls of the heart are made up of three tissue layers: the
endocardium, myocardium, and epicardium (Fig. 1.8 and
Table 1.1). The heart's innennost layer, the endocardium, is
made up of a thin, smooth layer of epithelium and connective tissue and Unes the heart's inner chambers, valves, chordae tendineae (tendinous cords), and papillary muscles. The
terminal components of the heart's specialized conduction
system can be found within this layer (Anderson & Roden.
2010). The endocardium is continuous with the innennost
layer of the arteries, veins, and capillaries ofthe body, thereby
creating a continuous, closed circulatory system.
1he .myocarclium (middle layer) is a thick. muscular layer
that consists of cardiac muscle fibers (cells) responsible for the
pumping action of the heart The myocardium makes up about
30% ofthe total left. ventrkular mass (Anderson & Roden, 2010).
lhe innermost halfofthe myocardium is called the subendocar1&1 area. The outermost halfis called the subepicardial area. 1he
muscle fibers of the myocardium are separated by connective
tissues that have a rich supply ofcapillaries and nerve fibers.

Did You Know?- - - - - - The thickness of a heart chamber is related to the amount of
pressure or resistance that the muscle of the chamber must
overcome to eject blood.

Endocardium -~~=-~
Myocardium
VIsceral
pericardium
(epicardium)

Perlcardlal

apace

Abrous

layer
Flf. 1.8 The parlcardlal sac Is aJIIliOSIId af 1:\W layn separaiBd by a narrow
ftuld-fllled Sjlllllll. The v1scaral part:anllum (aplcmdklm) Is attached dlractly 1D 1ha
heart's surface, and the parlelal pertardlum fcnns the llJIEr layer af the sac. (from
~-l<lrlitx:Jm L, Blnlslk JL: PBthoplrys/rJ/o ad 5, PhiBde~hla, 2013, Elakr.)

The heart's outennost layer is called the epicardium. The
epicardium is continuous with the inner lining of the pericardium at the heart's apex. The epicardium contains blood
capillaries, lymph capillaries, nerve fibers, and fat. 1he main
coronary arteries lie on the epicardial surface of the heart.

Chapter 1 Anatomy and Physiology

lrJ:ll¥81 Layers of the Heart Wall
Heart Layer

Description

Epicardium

• External layer of 1he heart
• Coronary arteries, blood capillaries,
lymph capillaries, nerve fibers, and fat
are found in this layer
• Middle and thickest layer of the heart
• Muscular component of the heart;
responsible for the heart's pumping
action
• Innermost layer of the heart
• Lines heart's inner chambers, valves,
chordae tendineae, and papillary
muscles
• Continuous with the innermost layer
of arteries, veins. and capillaries of the
body

Myocardium

Endocardium

They feed this area first before entering the myocardium and
supplying the heart's inner layers with oxygenated blood.
Ischemia is a decreased supply of oxygenated blood to a
body part or organ. The heart's subendocardial area is at the
greatest risk ofischemia because this area has a high demand
for oxygen and it is fed by the most distal branches of the
coronary arteries.

CARDIAC MUSCLE
Cardiac muscle fibers make up the walls of the heart.
These fibers have striations, or stripes, similar to that of
skeletal muscle. Each muscle fiber is made up of many
muscle cells (Fig. 1.9). Each muscle cell is enclosed in
a membrane called a sarcolemma. Within each cell (as
with all cells) are mitocho.odria, the energy-producing
parts of a cell, and hundreds of long, tube-like structures
called myoflbrlls. Myofibrils are made up of many sar~o­
merea, the basic protein units responsible for contraction.
The process of contraction requires adenosine triphosphate (ATP) for energy. The mitochondria that are interspersed between the myofibrils are important sites of ATP
production.
The sarcolemma has holes in it that lead into tubes called
T (transverse) tubules. T tubules are extensions of the cell
membrane. Another system of tubules, the sarcoplasmic:
reticulum (SR), stores calcium. Muscle cells need calcium
in order to contract. Calcium is moved from the sarcoplasm of the muscle cell into the SR by means of "'pumps"
in the SR.
There are certain places in the cell membrane where
sodium (Na+), potassium (K+), and calcium (Ca++) can
pass. These openings are called pores or channels. There
are specific channels for sodium (sodium channels},

I

L------

lrrtercalallld dlskB

- Mltllchandrlon

Fig. 1.8 cardiac muscle filar. lklllke ather types a! muscle fibers, 1he cardiac
muscle flbar Is t)Pically branchoo and foiTI'IS junc1!oos, called lntaroalllled dis~. with
adjacent cardiac muscle fibers. (From PatiDn KT, Thltxxfeau GA: Anthony's IIJXtbook
of 8fi/J/Dmy & phys/okJgy, ad 20, St Louis, 2013, Mooby~

potassium (potassium channels), and calcium (calcium
channels). When the muscle is relaxed, the calcium channels are closed. As a result, calcium cannot pass through
the membrane of the SR. This results in a high concentration of calcium in the SR and a low concentration in
the sarcoplasm, where the muscle cells (sarcomeres) are
found. If the muscle cells do not have calcium available to
them, contraction is inhibited (the muscle stays relaxed).
The force of cardiac muscle contraction depends largely
on the concentration of calcium ions in the extracellular
fluid.

0

ECG Pear1 _ _ _ _ _ _ _ __

The heart consists of two syncytia: atrial and ventricular.
The atrial syncytium consists of the walls of the right and
left atria. The ventricular syncytium consists of the walls of
the right and left ventricles. Normally, impulses can be conducted from the atrial syncytium into the ventricular syncytium only by means of the atrioventricular (AV) junction. The
AV junction is a part of the heart's electrical system. This
allows the atria to contract a short time before ventricular
contraction.

Heart Chambers
The heart has four chambers, two atria and two ventricles. The outside surface of the heart has grooves called
sulci. The coronary arteries and their major branches lie
in these grooves. The coronary sulcus (groove) encircles
the outside of the heart and separates the atria from the
ventricles. It contains the coronary blood vessels and
epicardial fat.

Chapter 1 Anatomy and Physiology

,....,_-- Pulmonary tnlnk
Right atrium
·~~=---;;::::..:....:.-.- Openings to

coronary arteries
Aortic (SL) valve
Laftatrlum

F1g. 1.10 lntartor of the heart. This Illustration shows the heart as It would appear If It were a.Jt along a lronllll plane and
opened Ilks a book. The fnlnt portion of the heart lies ID 1hll reader's ~ght; the back portion of the heart lias ID the reader's
Iaft. ThB four chambers Ill 1hll heart-two a~a and two van~des--an~ easily seen. A~ Abtlvant~cular; st.. semilunar. [From
Patton KT, Thllodeau GA: Anatomy & physiology, ad 9, St. llluls, 2016, Mosby.)

ATRIA

VENTRICLES

[Obiactive 5]
The two upper chambers of the heart are the right and
left atria (singular, atrium) (Fig. 1.10). An earlike flap
called an auricle (meaning "little ear·) protrudes from
each atrium.
The purpose of the atria is to receive blood. The right
atrium receives blood low in oxygen from the superior vena
cava (which carries blood from the head and upper extremities), the inferior vena cava (which carries blood from the
lower body), and the coronary sinus (which is the largest
vein that drains the heart). The left atrium receives freshly
oxygenated blood from the lungs via the right and left pulmonary veins.
1he four chambers of the heart vary in muscular wall
thickness, reflecting the degree of pressure each chamber
must generate to pump blood. For example, the atria encounter little resistance when pumping blood to the ventricles. As
a result, the atria have a thin myocardial layer. The wall of
the right atrium is about 2 mm thick. and the wall of the left
atrium is about 3 m.m thick. Blood is pumped from the atria
through an atrioventricular (AV) valve and into the ventricles. The valves ofthe heart are discussed later in this chapter.

(Obiactive 5]
The heart's two lower chambers are the right and left ventricles. Their purpose is to pump blood. The right ventricle
pumps blood to the lungs. The left ventricle pumps blood
out to the body. Because the ventricles must pump blood
either to the lungs (the right ventricle) or to the rest of the
body (the left ventricle), the ventricles have a much thicker
myocardial layer than the atria. Because the right ventricle
moves blood only through the blood vessels of the lungs and
then into the left atrium, it has one sixth of the muscle mass
and one third of the wall thickness of the left ventricle, which
must propel blood to most vessels of the body (Hutchison &:
Rudakewich, 2009) (Fig. 1.11).

Q

ECG Pearl _ _ _ _ _ _ _ _ __

Think of the atria as holding tanks or reservoirs for blood.

When the left ventricle contracts, it normally produces an
impulse that can be felt at the apex of the heart (apical
impulse). This occurs because as the left ventricle con·
tracts, it rotates forward. In a normal heart, this causes the
apex of the left ventricle to hit the chest wall. You may be
able to sea the apical impulse in thin individuals. The apical impulse is also called the point of maximal impulse

because it is the site where the left ventricular contraction
is most strongly felt.

Chapter 1 Anatomy and Physiology

Antarlor lntarvenb1cuJar Right vantrk:ular

artery

wall

/
Left

Papillary

ventricular mUICia

-11

Intel'"

Trabeculae

Y811lrtcular

camaae

Marginal
arl8ry

saptum

Fig. 1.11 Section through the heart shi7Mng 1he &Peal porUn of the left and ~ghl venll1clas. (From Gosling JA: Human
anatumy: oo1or atlas and t8Xt, ed 4, London, 2002, Mosby.)

Heart Valves
The heart has a skeleton, which is made up of four rings
of thick connective tissue. This tissue surrounds the bases
of the pulmonary trunk, the aorta, and the heart valves.
The inside of the rings provides secure attachments for
the heart valves. The outside of the rings provides for the
attachment of the cardiac muscle of the myocardium (Fig.
1.12). The heart's skeleton also helps form the partitions
(septa) that separate the atria from the ventricles.
There are four one-way valves in the heart: two sets of AV
valves and two sets of&emilUIW' (SL) valves. The valves open
and close in a specific sequence and assist in producing the
pressure gradient needed between the chambers to ensure
a smooth :flow of blood through the heart and prevent the
bacldl.ow of blood.

ATRIOVENTRICULAR VALVES
[Oblectlves 6, 7]
Atrioventricular valves separate the atria from the ventricles.
The two AV valves consist of tough. fibrous rings (annuli
:6.brosi); :flaps (lea11.ets or cusps) of endocardium; chordae
tendineae; and papillary muscles.
1he tricuspid valve is the AV valve that lies between the
right atrium and right ventricle. It consists of three separate
cusps or flaps (Fig. 1.13). It is larger in diameter and thinner
than the mitral valve. The mitral valve, which is also called
the bicuspid valve, has only two cusps and lies between the

Fig. 1.12 Skeleton of the heart. This IX)Stel1or view shows part of the venll1cular
myooardlum with 1he heart valves 81111 attached. The rim of each heart valve Is supported by a fibrous structure, called the sk8/stonofth6 h6art, which encircles all four
valves. AV. Atrlovenll1cular. (From PatiDn KT, Thibodeau GA: Anatmny&ph~
ed 9, St Louis, 201 6, Mosby.)

left atrium and left ventricle (Fig. 1.14). The mitral valve is
so named because of its resemblance to a miter, which is a
double-cusp bishop's hat, when open.
The AV valves open when a forward pressure gradient forces blood in a forward direction. They close when
a ba.ck.ward pressure gradient pushes blood backward. The

Chapter 1 Anatomy and Physiology

Superior vena

Right

TrtcuspldG Anterior cusp
Septal cusp
valve Posterior cusp

Septal papllluy miiiiCie
Septom•rgln•l trabecul•

Fig. 1.13 Internal view of 1he right venll1cle. (From Drake R, Vogl AW, Mitchell AWM: Gmy~ snatrHny frJr si1Jdenls. ed 3,
New Yorll, 2015, Churchill Uvlngstone.)

MHral val¥8 antartor cuep
Pulmonary arteries

Pulmonary veins

Coronary sinus
valve poeterlor cuap

Fig. 1.14 Internal view of 1he left ventriCle. (From Drake R, Vcgl AW, MitChell AWM: !#a~ anatomy for students, ed 3, New
Ya'k, 2015, Chu I'Ch ill Livingstone.)

Chapter 1 Anatomy and Physiology
AV valves require almost no backflow to cause closure
(Hall, 2016).
The flow of blood from the superior and inferior venae
cavae into the atria is normally continuous. About 70%
of this blood flows directly through the atria and into the
ventricles before the atria contract; this is called passi'o'e
filling. & the atria fill with blood, the pressure within the
atrial chamber rises. This pressure forces the tricuspid
and mitral valves open, and the ventricles begin to fill,
gradually increasing the pressure within the ventricles.
When the atria contract, an additionallO% to 30% of the
returning blood is added to filling of the ventricles. This
additional contribution of blood resulting from atrial
contraction is called atrial kick. On the right side of the
heart, blood low in oxygen empties into the right ventricle. On the left side of the heart, freshly oxygenated blood
empties into the left ventricle. When the ventricles then
contract (i.e., systole), the pressure within the ventricles
rises sharply. The tricuspid and mitral valves completely
close when the pressure within the ventricles exceeds that
of the atria.
Chordae tendineae (tendlnoua cords) are thin strands
of connective tissue. On one end, they are attached to the
underside of the AV valves. On the other end, they are
attached to small mounds of myocardium called papillary
maades. Papillary muscles project inward from the lower
portion ofthe ventricular walls. When the ventricles contract
and relax, so do the papillary muscles. The papillary muscles
adjust their tension on the chordae tendineae, preventing
them from bulging too far into the atria. For example, when
the right ventricle contracts, the papillary muscles of the
right ventricle pull on the chordae tendineae. 1he chordae
tendineae prevent the flaps of the tricuspid valve from bulging too far into the right atrium. 1hus, the chordae tendineae
and papillary muscles serve as anchors. Because the chordae
tendineae are thin and string-like, they are sometimes called
"heart strings."

SEMILUNAR VALVES
[OIJiactlve B]
The pulmonic and aortic valves are SL valves. 1he SL valves prevent the bacldlow ofblood from the aorta and pulmonary arteries into the ventricles. 1he SL valves have three cusps shaped
like half-moons. 1he openings of the SL valves are smaller than
the openings of the AV valves, and the flaps of the SL valves are
smaller and thicker than the AV valves. Unlike the AV valves,
the SL valves are not attached to chordae tendineae.
When the ventricles contract, the SL valves open, allowing blood to flow out of the ventricles. When the right
ventricle contracts, blood low in oxygen flows through
the pulmonic valve into the pulmonary trunk. which
divides into the right and left pulmonary arteries. When
the left ventricle contracts, freshly oxygenated blood flows
through the aortic valve into the aorta and out to the body
(Fig. 1.15). The SL valves close as ventricular contraction

ends and the pressure in the pulmonary artery and aorta
exceeds that of the ventricles.

Improper valve function can hamper blood flow through the
heart. Valvular heart disease is the term used to describe
a malfunctioning heart valve. Types of valvular heart disease include the following:
• vaJvular prolapse. If a valve flap inverts, it is said to have
prolapsed. Prolapse can occur if one valve flap is larger
than the other. It can also occur if the chordae tendineae stretch markedly or rupture.
• vaJvutar regurgitation. Blood can flow backward, or
regurgitate, if one or more of the heart's valves does
not close properly. Valvular regurgitation Is also known
as valvular incompetence or valvular insufficiency.
• Valvular stenosis. If a valve narrows, stiffens, or thickens, it is said to be stenosed. The heart must work
harder to pump blood through a stenosed valve.
Papillary muscles receive their blood supply from the
coronary arteries. If a papillary muscle ruptures because
of an inadequate blood supply (as in myocardial infarction), the attached valve cusps will not completely
close and may result in a murmur. If a papillary muscle
in the left ventricle ruptures, the leaflets of the mitral
valve may invert Q.e., prolapse). This may result in blood
leaking from the left ventricle into the left atrium (e.g.,
regurgitation} during ventricular contraction. Blood flow
to the body o.e., cardiac output) could decrease as a
result.

HEART SOUNDS
Heart sounds occur because of vibrations in the tissues
of the heart caused by the closing of the heart's valves.
Vibrations are created as blood flow is suddenly increased
or slowed with the contraction and relaxation of the
heart chambers and with the opening and closing of the
valves.
Normal heart sounds are called Sl and S2. 1he first heart
sound ("lubb,.) occurs during ventricular contraction when
the tricuspid and mitral (AV) valves are closing. The second
heart sound ("dupp) occurs during ventricular relaxation
as the pulmonic and aortic (SL) valves close. A third heart
sound is produced by ventricular filling. In those younger
than 40 years ofage, the left ventricle normally permits rapid
filling. The more rapid the ventricular filling, the greater
the likelihood of hearing a third heart sound. A third heart
sound (S3) heard in people older than 40 years ofage is considered abnormal An abnormal third heart sound is frequently associated with heart failure. An Sl-S2-S3 sequence
is called a ventricular gallop or gallop rhythm. It sounds like
"Kentucky"-Ken (Sl) -tuck (S2) -y (S3). The location of the

Chapter 1 Anatomy and Physiology

Pulmonary velr1s..,::-----~...4
Superior vena

Aortic valve
cusps

Left atrium7'9~L~
Aorta --r--ollil.l~

Right
venlr1cle
lntervemrtcular
septum

Tricuspid

valve

Mitral valv&posterior cusp
Right ventricle

Fig. 1.1& Drawing of a heart split perpendicular to the interventriCular septum to illustrate the anatomic relationships of
the leaflets of the atroventricular and aortiC valveS. (From Koeppen BM, Stanton BA: Beme & LevyJJ/1YSiOlOgY. ed 6, St. L.Duis,
2010, Mosby.)

heart's AV and SL valves for auscultation is shown in Fig.
1.16. A summary ofthe heart's valves and auscultation points
for heart sounds appears in Table 1.2.

In people younger than 40 years of age, the left ventricle normally permits rapid filling. The more rapid the
ventricular filling, the greater the likelihood of hearing a
third heart sound. A third heart sound (S3) heard in those
older than 40 years of age is considered abnormal. An
abnormal third heart sound is frequently associated with
heart failure. An S 1-32-33 sequence Is called a ventricular gallop or gallop rhythm. It sounds like Ken (S1) -tuck
(S2) -y (S3).
Turbulent blood flow within the cardiac chambers and
vessels can produce heart murmurs. An inflamed pericardium can produce a peric8rdial friction rub, which sounds
like rough sandpaper.

The Heart's Blood Supply
lhe coronary circulation consists of coronary arteries and
veins. The right and left coronary arteries encircle the myocardium like a crown. or corona.

CORONARY ARTERIES
[Oblectlve 8]
lhe main coronary arteries lie on the outer (epicardial) surface ofthe heart. Coronary arteries that run on the surface of

the heart are called epicardial coronary arteries. They branch
into progressively smaller vessels, eventually becoming arterioles, and then capillaries. Thus, the epicardium has a rich
blood supply to draw from. Branches of the main coronary
arteries penetrate into the heart's muscle mass and supply the
subendocardium with blood. lhe diameter of these "feeder
branches" (i.e., collateral circulation) is much narrower. The
tissues supplied by these branches get enough blood and
oxygen to survive, but they do not have much extra blood

flow.
lhe work of the heart is important To ensure that it has
an adequate blood supply, the heart makes sure to provide
itself with a fresh supply of oxygenated blood before supplying the rest of the body. This freshly oxygenated blood is supplied mainly by the branches of two vessels: the right and left
coronary arteries.
lhe right and left coronary arteries are the very first
branches off the base of the aorta. The openings to these vessels lie just beyond the cusps of the aortic SL valve. When
the left ventricle contracts (systole), the force of the pressure within the left ventricle pushes blood into the arteries
that branch from the aorta. 'Ihis causes the arteries to fill
However, the heart's blood ~ssels (ie., the coronary arteries) are compressed during ventricular contraction, reducing blood fl.ow to the tissues of the heart. Thus, the coronary
arteries fill when the aortic valve is closed and the left ventricle is relaxed (i.e., diastole).
lhe three major epicardial coronary arteries include the left
anterior descending (LAD) artery, circumflex (Cx) artery, and
right coronary artery (RCA). A person is said to have coronary

Chapter 1 Anatomy and Physiology

Pulmonary valve

Auscultation position
for tr1cuspld valve

AuscultaUon position
for mitral valve

Fig. 1.18 An!Brlor view ot 1he chest r.owlng the heart, the looatlon of the heart's valves, and where to listen to heart
sounds. (From Drake R, Vogl AW, Mitchell AWM: Glay'unatomyfurstWents, ad 3, New York. 2015, Churchill LMngstone.)

if;1:Jii Q

Heart Valves and Auscultation Points

Yalve Name

Yalve 1W»e

IJicatlon

Auscultation Point

Tricuspid

Atrioventricular

Mitral (bicuspid)

Atrioventricular

Pulmonic (pulmonary)

Semilunar

Aortic

Semilunar

Separates the right atrium and
right ventricle
Separates the left atrium and left
ventricle
Between the right ventricle and
pulmonary artery
Between the left ventricle and
aorta

Just to the left of the lower part of the sternum near the fiHh intercostal space
Heart apex in the left fifth intercostal space
at the midclavicular line
Left second intercostal space close to the
sternum
Right second intercostal space close to the
sternum

artery disease (CAD) if there is more than 5096 diameter narrowing (i.e., stenosis) in one or more of these vessels.

(ill

CLINICAL CORRELAT10NS

Because a heart attack, which is also called a myocardial
Infarction, Is usually caused by a blocked coronary artery,
it is worthwhile to become familiar with the arteries that
supply the heart. When myocardial ischemia or infarction
is suspected, an understanding of coronary artery anatomy
and the areas of the heart that each vessel supplies helps
you predict which coronary artery is blocked and anticipate
problems associated with blockage of that vessel.

Right Coronary Artary
The RCA orlginates from the right side of the aorta (Fig.
1.17). It travels along the groove between the right atrium
and right ventricle. A branch of the RCA supplies the following structures:
• Right atrium

• Right ventricle
• Inferior surface of the left ventricle in about 85% of
individuals
• Posterior surface of the left ventricle in 85%
• Sinoatrial (SA) node in about 60%
• AV bundle in 8596 to 90%

Chapter 1 Anatomy and Physiology

flrachiDC&PMic

..,.,k

~----·- Aot1lc arch

LGit pulmonery
artery
Left Wiell
appendage

Ci-'lex lnncto of
laft main c;orvnuy ar1Bry

-

>-

·-

Left pulmonary

Superior-. cava
Right~-ry

vere

artery

I.Mtalrtum

Right punnary
wins

Luft enterlor d-ndlng

Right atrtum

lnnch of Ifill

GOIIlllllry artery
.,.___,.....~~ -

Middle ean:llac

vein

Poalllllar diHicendng
~lar)

"'-.,.~.._-

nncn of riGht

Right ventrlde

c:oranary artery

B

A

Fig. 1.17 Coronary artar18s s'-"~ylng the h881t. 1hEI ~ght ccronary artBry sup~les tha ~ght att1urn, vantJtde, BOO
postarlor aspect of tha left ventricle In most lndMiilals. The left coronary artery dlvldas IIIIo lha left antsr1or descending BOO
ciraJmllex artelies, which perfuse the left venllide. A, Anterior view. B, Posterior view. (Frnm Copstead-Ki ll<hom I., Banasik JL.:
Pathophysiology, ed 5, Philadelphia, 2013, Elsevier.)

Left Coronary Artery
lhe left coronary artery (LCA) originates from the left side
of the aorta (see Fig. 1.17). 1he 1irst segment of the LCA is
called the left main coronary artery. It is about the diameter
of a soda straw and less than 1 inch (2.5 em) long. ffioc.kage
of the proximal LAD coronary artery has been referred to as
the "widow maker" because of its association with sudden
cardiac arrest when it is blocked.
The left main coronary artery supplies oxygenated blood
to its two primary branches: the LAD, which is also called the
anterior interventricular artery, and the Cx.. 1hese vessels are
slightly smaller than the left main coronary artery.
1he LAD is on the outer (ie., epicardial) surface on the front
of the heart It travels along the groove that lies between the
right and left ventricles (i.e., the anterior interventricular sulcus) toward the heart's apex. In most patients. the LAD travels
around the apex ofthe left ventricle and ends along the left ventricle's inferior surface. In the remaining patients, the LAD does
not reach the inferior surface. Instead. it stops at or before the
heart's apex. 1he major branches of the LAD are the septal and
diagonal arteries. 1he LAD supplies blood to the fullowing:
• The anterior surface of the left ventricle
• Part of the lateral surface of the left ventricle
• The anterior two thirds of the interventricular septum
1he Cx coronary artery circles around the left side of the
heart in a groove on the back of the heart that separates the
left atrium from the left ventricle called the coronary sulcus
(see Fig. 1.17). 1he Cx supplies blood to the following:
• The left atrium
• Part of the lateral surface of the left ventricle
• 1he inferior surface of the left ventricle in about 1596 of
individuals
• The posterior surface of the left ventricle in 15%
• 1he SA node in about 40%
• TheAVbundle in 10% to 15%

A summary of the areas of the heart supplied by the three
major coronary arteries is shown in Table 1.3.

Coronary Artery Dominance
In about 8596 ofpeople the RCA forms the posterior descending artery, and in about 1096 of people the circumflex artery
forms the posterior descending artery (Lohr & Benjamin.
2016). The coronary artery that fonn.s the posterior descending artery is considered the dominant coronary artery. If a
branch of the RCA becomes the posterior descending artery,
the coronary artery arrangement is described as a rightdominant system. If the Cx branches and ends at the posterior descending artery, the coronary artery arrangement is
described as a left-dominant system. In some people, neither
coronary artery is dominant. If damage to the posterior wall
of the left ventricle is suspected, a cardiac catheterization
usually is necessary to determine which coronary artery is

involved.

ACUTE CORONARY SYNDROMES
[Obiactivas 9,10]
Aarte coronary syndrome (ACS) is a term that refers to distinct conditions caused by a similar sequence of pathologic
events involving abruptly reduced coronary artery blood flow.
This sequence of events results in conditions that range from
myocardial ischemia or injury to death (ie., necrosis) of the
heart muscle. 1he usual cause of an ACS is the rupture of an
atherosclerotic plaque. Arleriosderosis is a cb.ronic disease ofthe
arterial system characterized by abnormal thickening and hardening of the vessel walls. Atherosclerosis is a form of arteriosclerosis in which the thickening and hardening of the vessel walls
are caused by a buildup of fat-like deposits (e.g., plaque) in the
inner lining oflarge and middle-sized muscular arteries. As the
fatty deposits build up, the opening ofthe artery slowly narrows,
and blood flow to the muscle decreases (Fig. 1.18).

Chapter 1 Anatomy and Physiology
The complete blockage of a coronary artery may cause a
.myocardial.infardion (.MI). However, because a plaque usually
increases in size over months and years, other vascular pathways
may enlarge as portions of a coronary artery become blocked.
These vascular pathways (ie., collateral circulation) serve as an
alternative route for blood flow around the blocked artery to the
heart muscle; thus, the presence of collateral arteries may prevent infarction despite complete blockage ofthe primary artery.

Did You Know? _ _ _ _ _ __
Any artery in the body can develop atherosclerosis. If the coronary arteries are involved ~.e., coronary artery disease) and if
blood flow to the heart is decreased, angina pectoris or more
serious signs and symptoms may result. If the arteries in the
leg are involved (i.e., peripheral vascular disease), leg pain
Q.e., claudication) may result. If the arteries supplying the brain
are involved o.e., carotid artery disease), a stroke or transient
ischemic attack may result.

Angina pectoris is chest discomfort or other related
symptoms that occur suddenly when the increased oxygen
demand of the heart temporarily exceeds the blood supply.
Angina is a symptom of myocardial ischemia, and it most
often occurs in patients with CAD that involves at least one
coronary artery. However, it can be present in patients with
nonnal. coronary arteries. Angina also occurs in people with
uncontrolled high blood pressure or valvular heart disease.
Possible causes of myocardial ischemia are shown in Box l.l.
The term angina refers to squeezing or tightening rather
than pain. The discomfort that is associated with angina
occurs because of the stimulation of nerve endings by lactic
acid and carbon dioxide that builds up in ischemic tissue.
Examples of common words and phrases used by patients
experiencing angina to describe the sensation they are feeling include "heaviness," "squeezing," "a band across my
chest," ·a weight in the center of my chest," and "a vise tightening around my chest"

lfJ:!IJ!I Coronary Arteries
Coronary Artery

Portion of Myocardium Supplied

Portion of Conduction System Supplied

Right

•
•
•
•
•
•
•

• Sinoatrial (SA) node (about 60%)*
• Atrioventricular (AV) bundle (85% to 90%)*

Left anterior descending

Circumflex

•

•
•
•

Right atrium
Right ventricle
Inferior surface of left ventricle (about 85%)*
Posterior surface of left ventricle (85%)*
Anterior surface of left ventricle
Part of lateral surface of left ventricle
Anterior two thirds of interventricular septum
Left atrium
Part of lateral surface of left ventricle
Inferior surface of left ventricle (about 15%)*
Posterior surface of left ventricle (15%)*

• Most of right bundle branch
• Part of left bundle branch

• SA node (about 40%)*
• AV bundle (1 0% to 15%)*

*Of population.
Endothelium

Intima
Chronic anc:lothallallnjury
• Hypertension
• Tobacco use
• Hypel11pldemla
• Hyperhomocystelnemla

Fattyatruk
• Uplds accumulate and migrate
Into smooltl muscle cells

• Diabetes

• Infections
•Toxins
Damaged
endothelium

Fibrous plaqua
• Collagen covers the fatty streak
• Vessel lumen is narrowed
• Blood flow is reduced
• FISSures can develop

Compllcat.d lesion
• Plaque rupture
• Thrombus formation
• Further narrowing or total
occlusion of vessel

Fig. 1.18 Pathogenesis of atherosclerosis. A, Damaged en~llum. B, Fatty streak and lipid cae fonnatlon. C, Rbrous
plaque. Raised plaques are >Aslble: some are yellow; others are white. D, Conpllcated lesion: thromtxJs Is ltld, cdlagen Is blue.
Plaque Is compllcatad by rad tllrombus deposition. (From I..&Ws, Sl., aK:her L, Hellkemper MM, Perdlng MM: MedJcal-81.JfP}caJ
nurs/11g: 88888SI1I6i!t and manatJ6fT/6l1t ofcDnlcaJ problems, ad 10, St. Louis, 2017, Elsevier.)

Chapter 1 Anatomy and Physiology
Chest discomfort associated with myocardial ischemia
usually begins in the central or left chest and then radiates
to the arm (especially the little :finger [ulnar] side of the left
arm), the wrist, the jaw, the epigastrium, the left shoulder,
or between the shoulder blades. Ischemic chest discomfort is usually not sharp, is not worsened by deep inspiration, is not affected by moving muscles in the area where
the discomfort is localized. and is not positional in nature.
Other symptoms associated with ACSs include shortness
of breath, sweating, nausea. vomiting. dizziness, and discomfort in other areas of the upper body (O'Connor, et al.,
2010).
Not all patients experiencing an ACS present similarly.
Atypical preaentation refers to the uncharacteristic signs
and symptoms that are experienced by some patients.
Atypical chest discomfort is localized to the chest area
but may have musculoskeletal, positional or pleuritic features. Patients experiencing an ACS who are most likely
to present atypically include older adults, individuals with
diabetes, women, patients with prior cardiac surgery, and
patients in the immediate postoperative period after noncardiac surgery (Karve, Bossone, & Mehta. 2007). Older
adults may have atypical symptoms such as dyspnea, shoulder or back pain, weakness, fatigue, mental status changes,
syncope, wtexplained nausea, and abdominal or epigastric
discomfort. 1hey are also more likely than younger patients
to present with more severe preexisting conditions, such
as hypertension, heart failure, or a previous acute MI.
Individuals with diabetes may present atypically because
of autonomic dysfunction. Common signs and symptoms
include generalized weakness, syncope,lightheadedness, or
a change in mental status. Women who experience an ACS
report acute symptoms including chest discomfort, unusual
fatigue, sleep disturbances, dyspnea. nausea or vomiting,
indigestion, dizziness or fainting, sweating, arm or shoulder pain, and weakness. 1he location of the discomfort is

often in the back. arm, shoulder, or neck. Some women
have vague chest discomfort that tends to come and go with
no known aggravating factors.

0

ECO Pear1 _ _ _ _ _ _ _ __

The extent of arterial narrowing and the amount of reduction in
blood flow are critical determinants of coronary artery disease.

Ischemia can occur because of increased myocardial
oxygen demand (demand ischemia), reduced myocardial
oxygen supply (supply ischemia), or both. If the cause of
the ischemia is not reversed and blood flow restored to
the affected area of the heart muscle, ischemia may lead
to cellular injury and, ultimately, infarction. Ischemia can
quickly resolve by reducing the heart's oxygen demand.
resting or slowing the heart rate {HR) with medications
such as beta-blockers, or increasing blood flow by dilating the coronary arteries with drugs such as nitroglycerin
(NTG).
Ischemia prolonged by more than just a few minutes
causes myocardial injury. Myocardial injury refers to myocardial tissue that has been cut off from or experienced a severe
reduction in its blood and oxygen supply. Injured myocardial
cells are still alive but will die (i.e., infarct) if the ischemia is
not quickly corrected. An MI occurs when blood :flow to the
heart muscle stops or is suddenly decreased long enough to
cause cell death. 1he symptoms that accompany an MI are
often more intense than those associated with angina and
last more than 15 to 20 minutes.
Ifthe blocked coronary vessel is quickly opened to restore
blood flow and oxygen to the injured area. no tissue death
occurs. Methods of restoring blood flow may include giving
dot-busting drugs (i.e., fibrinolytics), performing coronary
angioplasty, or performing a coronary artery bypass graft
(CABG), among others.

l!illJ\.a.l 1 Possible Causes of Myocardial Ischemia
Inadequate Oxygen
lklpply
• Anemia
• Coronary artery narrowing
caused by a clot, vessel
spasm, or rapid prcgession
of atherosclerosis
• Hypoxemia

lncre8Md Myocardial Oxygen

Demand
•
•
•
•
•
•

Aortic stenosis
Cocaine, amphetamines
Eating a heavy meal
Emotional stress
Exercise
Exposure to cold weather

• Fever
•
•
•
•
•

Heart failure
Hypertension
Obstructive cardiomyopathy
Pheochromooytorna
Rapid heart rate

• Smoking
• Thyrotoxicosis

When myocardial cells die, such as during a myocardial
infarction, substances in intracardiac cells pass through
broken cell membranes and leak into the bloodstream.
These substances, which are called inflammatory markers,
cardiac biomarkers, or serum cardiac markers, include
creatine kinase myocardial band (CK-MB), myoglobin,
troponin I, and troponin T. To verify that an infarction has
occurred, blood tests can measure the levels of these substances in the blood. The diagnosis of an acute coronary
syndrome is made on the basis of the patient's assessment
findings and his or her symptoms and history, the presence of cardiovascular risk factors, serial electrocardiogram
results, blood test results ~.e., cardiac biomarkers), and
other diagnostic test results.

Chapter 1 Anatomy and Physiology
increase or decrease its HR and/or force of contraction, it

CORONARY VEINS

is benencial that both divisions of the autonomic nervous

1he coronary (cardiac) veins travel alongside the arteries.

system send fibers to the heart (Pig. 1.19). The sympathetic
division prepares the body to function under stress (i.e., the
'"fight-or-flight" response). The parasympathetic division
conserves and restores body resources (i.e., the •rest and
digest" response).

Blood that has passed through the myocardial capillaries is
drained by branches of the cardiac veins that join the coronary
sinus. The coronary sinus is the largest vein that drains the
heart (see Fig. 1.17). It lies in the groove (sulcus) that separates the atria from the ventricles. The coronary sinus receives
blood from the great, middle. and small cardiac veins; a vein
of the left atrium; and the posterior vein of the left ventricle.
The coronary sinus drains into the right atrium. The anterior
cardiac veins do not join the coronary sinus but empty directly
into the right atriwn.

The Heart's Nerve Supply
[Oblactlva 11]
The myocardium is able to produce its own electrical
impulses without signals from an outside source, such as
a nerve. Because there are times when the body needs to

SYMPATHETIC ST1MULATION
Sympathetic (accelerator) nerves innervate specific areas of
the heart's electrical system, atrial muscle, and the ventricular myocardium. When sympathetic nerves are stimulated,
the neurotransmitters norepinephrine and epinephrine are
released. Remember: The job of the sympathetic division is
to prepare the body for emergency or stressful situations.
Therefore, the release of norepinephrine and epinephrine
results in the following predictable actions:
• Dilation of pupils
• Dilation of smooth muscles of bronchi to improve
oxygenation

Sympathetic

Profacllons of

nervous system

sympathetic

Projac:tlons of
parasympathetic

nervous system

nervous 8Y8tem

Parasympathe11c

nervous system

..

Eye

l...acl'lmal and
salivary glands

-x . !.....

Cervical

111ontcic

L.umbar
L5

81
Sacntl

;4,

Iff=-

)L

Reproductive
organa

Paravertebral

chain
ganglia

Fig. 1.18 Schematk: showing the s,mpalhetlc and perasympatheUc pathwa~ Sympathetic pathways are Slawrl In red
and parasympathetic pathways in blue. {from Koeppen BM, Stanbln BA: Beme & LllfY physiology. ed 6, St. Louis, 201 o, Mosby.)

Chapter 1 Anatomy and Physiology
• Increased HR, force of contraction, conduction velocity,
blood pressure, and cardiac output (CO)
• Increased sweating
• Mobilization of stored energy to ensure an adequate supply of glucose for the brain and fatty acids for muscle
activity
• Shunting ofblood from skin and blood vessels ofinternal
organs to skeletal muscle
Sympathetic (adrenergic) receptors are located in different organs and have different physiologic actions when stimulated. There are :five main types of sympathetic receptors:
alpha1, alphaz, beta1, b~. and beta3•
• Alpha1 receptors are found in the eyes, blood vessels,
bladder, and male reproductive organs. Stimulation of
alpha1 receptor sites results in constriction.
• Alph~ receptor sites are found in parts of the digestive
system and on presynaptic nerve terminals in the peripheral nervous system. Stimulation results in decreased
secretions, peristalsis, and suppression of norepinephrine
release.
• Beta receptor sites are divided into beta1, beta2, and
beta3• Beta1 receptors are found in the heart and kidneys. Stimulation of beta1 receptor sites in the heart
results in increased HR, contractility, and, ultimately,
irritability of cardiac cells (Fig. 1.20). Stimulation of
beta1 receptor sites in the kidneys results in the release
of renin into the blood. Renin promotes the production of angiotensin, a powerful vasoconstrictor. Beta2
receptor sites are found in the arterioles of the heart,
lungs, and skeletal muscle. Stimulation results in dilation. Beta3 receptor sites are found in fat cells. When

Bllmulllllon
(may re~KJII in fast heart rate)

Excaaaiva accalaralion

stimulated, they are thought to promote the breakdown
of fats and other lipids.

0

ECG Peart _ _ _ _ _ _ _ __

Remember: Beta1 receptors affect the heart (you have one
heart); bel9..2 receptors affect the lungs (you have two lungs).

PARASYMPATHETIC STIMULATION
Parasympathetic (inhibitory) nerve fibers innervate the SA
node, the atrial muscle, and the AV bundle of the heart by
the vagus nerves. Acetylcholine (ACh) is a chemical messenger (neurotransmitter) released when parasympathetic
nerves are stimulated. ACh binds to parasympathetic
receptors. The two main types of cholinergic receptors are
nicotinic and muscarinic receptors. Nicotinic receptors are
located in skeletal muscle. Muscarinic receptors are located
in smooth muscle. Parasympathetic stimulation has the following actions:
• Slows the rate of discharge of the SA node (Fig. 1.21)
• Slows conduction through the AV node
• Decreases the strength of atrial contraction
• Can cause a small decrease in the force of ventricular
contraction

BARORECEPTORS AND
CHEMORECEPTOR&
Baroreceptors are specialized nerve tissue (sensors). They
are found in the internal carotid arteries and the aortic
arch. These sensory receptors detect changes in blood
pressure. When they are stimulated, they cause a reflex

Bladaula
(no dysrhythmia)

Normal auiaing IIIIa
(prevenm acx:eleration)

Fig. 1.20 Effacts Ill symp!llhatlc sUmulallon on the heart. (From Wledartmld R: E1fK:trrJcarrJJY: th8 monltDlfng 8IId
dJBgnostJc 188ds, ed 2, Phlladslphla, 1999, Saundsrs.)

Chapter 1 Anatomy and Physiology

Stlmuldan

Bloclcadll

(may result in Blow heart 11118 )

(no dysrhythmia}

55

Nonnal cruising 1'118
(pravarls braking)

Fig. 1.21 Effeclll of !Brasympalhstlc stlmulaUon on the heart. (Ff'liTl Wiederhold R: E1rK:trrx:BrrJ1 ths monltotlng
and dJagnostJc l8ads, ed 2, Philadelphia, 1999, SaundBIS.)

lfj:lij! I

Review of the Autonomic Nervous System

General effect
Primary neurotransmitter

SympatheUc Division

Parasympathedc Division

Fght or flight
Norepinephrine, epinephrine

Feed and breed; rest and digest
Acetylcholine

Constriction (alpha receptors)
Increased secretion of epinephrine
Dilation (beta receptors)
Constriction (alpha receptors)
Dilation (beta receptors)
Increased rate and strength of
contraction (beta receptors)
Constriction (alpha receptors)
Dilation (beta receptors)

No effect
No effect
Constriction
No effect
No effect
Decreased rate; decreased strength of atrial contraction, little effect on strength of ventricular contraction
Dilation

Effects of stimulation
Abdominal blood vessels
Adrenal medulla
Bronchioles
Blood vessels of skin
Blood vessels of skeletal muscle
Cardiac muscle
Coronary blood vessels

response in either the sympathetic or the parasympathetic
divisions of the autonomic nervous system. For example,
if the blood pressure decreases, the body wiD attempt to
compensate by:
• Constricting peripheral blood vessels
• Increasing the HR {chronotropy)
• Increasing the force of myocardial contraction (inotropy)
These compensatory responses occur because of a response
by the sympathetic division. This is called a sympathetic or
adrenergic response. If the blood pressure increases, the body
will decrease sympathetic stimulation and increase the response
by the parasympathetic division. This is called aparruympathetic

or cholinergic response. 1he baroreceptors will adjust to a new
normal after a few days ofexposure to a specific pressure.
Chemoreceptors in the internal carotid arteries and aortic
arch detect changes in the concentration of hydrogen ions
(pH), oxygen, and carbon dioxide in the blood. 1he response
to these changes by the autonomic nervous system can be
sympathetic or parasympathetic.
A review of the autonomic nervous system can be found
in Table 1.4. Chronotropy, inotropy, and dromotropy are
terms used to describe effects on HR. myocardial contractility, and speed of conduction through the AV node. 1hese
terms are explained in Box 1.2.

Chapter 1 Anatomy and Physiology
Tenninology
Chronotropic Effect
• Refers to a change in heart rate.
• A positive chronotropic effect refers to an increase in
heart rate.
• A negative chronotropic effect refers to a decrease in
heart rate.
Inotropic Etrect
• Refers to a change in myocardial contractility.
• A positive inotropic effect results in an increase in myocardial contractility.
• A negative inotropic effect results in a decrease in myocardial contractility.
Dromotropic Effect
• Refers to the speed of conduction through the atrioventricular (AV) junction.
• A positive dromotropic effect results in an increase in
AV conduction velocity.
• A negative dromotropic affect results In a decrease In
AV conduction velocity.

THE HEART AS A PUMP
The right and left sides of the heart are separated by an
internal wall of connective tissue called a aeptum. The
interatrial septum separates the right and left atria. The
int~rrventricular septum separates the right and left ventricles. The septa separate the heart into two functional
pumps. The right atrium and right ventricle make up one
pump. The left atrium and left ventricle make up the other
(Fig. 1.22).
The rJght side of the heart is a low-pressure system whose
job is to pump unoxygenated blood from the body to and
through the lungs to the left side of the heart. 'Ibis is called

the pulmonary circulation. The pressure within the right
atrium is nonnally between 2 and 6 mm Hg. The pressure
within the right ventricle is normally between 0 and 8 mm
Hg when the chamber is at rest (diastole) and between 15
and 25 nun Hg during contraction (systole).
The job of the left side of the heart is to receive oxygenated blood from the lungs and pump it out to the rest of
the body. This is called the systemic circulation. The left
side of the heart is a high-pressure pump. The pressure
within the left atrium is normally between 8 and 12 mm
Hg. Blood is carried from the heart to the organs of the
body through arteries, arterioles, and capillaries. Blood
is returned to the right side of the heart through venules
and veins.
The left ventricle is a high-pressure chamber. Its wall is
much thicker than the right ventricle (the right ventricle
is about 3 to 5 mm thick; the left ventricle is about 13 to
15 mm). This is because the left ventricle must overcome
a lot of pressure and resistance from the arteries and contract forcefully in order to pump blood out to the body.
The pressure within the left ventricle is normally between
8 and 12 mm Hg when the chamber is at rest (diastole) and
between 110 and 130 mm Hg during contraction (systole).
Because the wall of the left ventricle is much thicker than
the right, the interventricular septwn nonnally bulges to
the right.

cardiac Cycle
[Oblectlva812,13J
The cardiac cycle refers to a repetitive pumping process that
includes all of the events associated with blood flow through
the heart. The cycle has two phases for each heart chamber: systole and diastole. Systole is the period during which
the chamber contracts and blood is ejected. Diastole is the
period of relaxation during which the chambers are allowed

Fig. 1.22 Tha heart has two pumps. [From Dl'llkll R, Vogl AW, Mltmell AWM: Grsy's snatomy frJr sJJJd6ntB, ad 3, Naw YOOc,
2015, Churchill Uvlngslala.)

Chapter 1 Anatomy and Physiology
to fill. The myocardium receives its fresh supply of oxygenated blood from the coronary arteries during ventricular
diastole.
1he cardiac cycle depends on the ability of the cardiac
muscle to contract and on the condition of the heart's conduction system. The efficiency of the heart as a pump may be
affected by abnormalities of the cardiac muscle, the valves, or
the conduction system.
During the cardiac cycle, the pressure within each
chamber of the heart rises in systole and falls in diastole.
The heart's valves ensure that blood flows in the proper
direction. Blood flows from one heart chamber to another
from higher to lower pressure. These pressure relationships
depend on the careful timing of contractions. The heart's
conduction system (discussed in Chapter 2) provides the
necessary timing of events between atrial and ventricular
systole.

ATRIAL SYSTOLE AND DIASTOLE
Blood from the tissues of the head. neck, and upper extremities is emptied into the superior vena cava. Blood from the
lower body is returned to the inferior vena cava. During
atrial diastole, blood from the superior and inferior venae
cavae and the coronary sinus enters the right atrium. 1he
amount of blood :flowing into the right heart from the systemic circulation is called venous return. The right atrium
fills and distends. This pushes the tricuspid valve open, and
the right ventricle fills.
The left atrium receives oxygenated blood from the
four pulmonary veins (two from the right lung and two
from the left lung). The flaps of the mitral valve open u
the left atrium fills. This allows blood to flow into the left
ventricle.
The ventricles are 70% :filled before the atria contract.
Contraction of the atria forces additional blood (about 10%
to 30% of the ventricular capacity) into the ventricles (the
atrial kick). 1hus the ventricles fill completely with blood
during atrial systole. The atria then enter a period of atrial
diastole, which continues until the start of the next cardiac
cycle.

VENTRICULAR SYSTOLE
AND DIASTOLE
Ventricular systole occurs as atrial diastole begins. .M the
ventricles contract, blood is propelled through the systemic
and pulmonary circulation and toward the atria. The term
isovalumetric (meaning "having the same volume'") contraction describes the brief period between the start of ventricular systole and the opening of the SL valves. During this
period. the ventricular volume remains constant as the pressure within the chamber rises sharply.
When the right ventricle contracts, the tricuspid valve
closes. The right ventricle expels the blood through the
pulmonic valve into the pulmonary trunk. The pulmonary
trunk divides into a right and left pulmonary artery, each of
which carries blood to one lung (i.e., the pulmonary circuit).

Blood flows through the pulmonary arteries to the lungs.
Blood low in oxygen passes through the pulmonary capillaries. There it comes in direct contact with the al~lar­
capillary membrane, where oxygen and carbon dioxide are
exchanged Blood then flows into the pulmonary veins and
then to the left atrium.
When the left ventricle contracts, the mitral valve closes
to prevent bacldlow of blood. Blood leaves the left ventricle
through the aortic valve to the aorta. which is the main vessel of the systemic arterial circulation. Blood is distn'buted
throughout the body (ie., the systemic circuit) through
the aorta and its branches. Blood continues to move in one
direction because pressure pushes it from the high-pressure
(i.e., arterial) side, and valves in the veins prevent back.tlow
on the lower pressure (i.e., venous) side as blood returns to
the heart.

Did You Know?- - - - - - - The aorta is composed of four primary parts: the ascending
aorta, the aortic arch, the thoracic portion of the descending
aorta, and the abdominal portion of the descending aorta.

When the SL valves close, the heart begins a period of
ventricular diastole. During ventricular diastole, the ventricles are relaxed and begin to fill passively with blood. The
cardiac cycle begins again with atrial systole and the completion of ventricular filling. The cardiac cycle and blood flow
through the heart are shown in Fig. 1.23.

Did You Know?- - - - - - Both the atria and ventricles have a systolic and diastolic
phase. When the term systole or diastole is used but the area
of the heart is not specified, however, you can assume that the
term refers to ventricular systole or diastole.

Blood Pressure
[Oblectlve 14]
The mechanical activity of the heart is reflected by the pulse
and blood pressure. Blood pressure is the force exerted by
the circulating blood volume on the walls of the arteries. The
volume of blood in the arteries is directly related to arterial
blood pressure.
Blood pressure is equal to CO x peripheral resistance. CO
is discussed later. Peripheral resistance is the resistance to
the flow of blood determined by blood vessel diameter and
the tone ofthe vucular musculature. Tone is a term that may
be used when referring to the normal state of balanced tension in body tissues.
Blood pressure is affected by conditions or medicationa that affect peripheral resistance or CO (Fig. 1.24).
For example, an increase in either CO or peripheral resistance typically results in an increase in blood preasure.
Conversely, a decrease in either will result in a decrease in
blood pressure.

Chapter 1 Anatomy and Physiology
Semilunar valves

Pulmonary artery

Right atrium

~~---w~~~~

0

Atltal aystole: Atria
contract, pushing
blood through the open
tricuspid and mitral valves
intn the ventriclee.

Heart

sound

Semilunar valve8 are
closed.
Beginning of ventricular
systole. Ventricles
contract, increasing
preasure within the
ventricles. The tricuspid
and mitral valves close,
causing the first heart
sound.

Period of falling pressure:
Blood flows from veina intn
the relaxed atria. Tricuspid
and mitral valves open
when pressul'9 in the
ventricles falls below that

in the ab1a.

'

/

Heart
sound

Beginning of ventricular
diastole: Pressure In the
relaxing ventr1clee drops
below that In the arteries.
Semilunar valves snap
shut, causing the second
heart sound.

Period olllslng preuure:
Semilunar valves open
when preaeure In the
ventricle exceeds that In
the arteries. Blood spurts

Into the aorta and
pulmomuy arteries.

Fig. 1.23 Blood flow 1hrough 1he heart during 1he cardiac ~le. (From SolOmon E: lntrOduclicn ID human analooly and
PhysiOlOgy, ed 4, StLouis, 2016, Saunders.)

f Slroka volume

t Blood vlacoelty

I...... t

cardiac OU!pUI permii'IUIII ......J

'

L.

t Volume of blood antertng

'Volume o1 blood leavtng arte~es

par mlnuta, the 'artariole rul'lllll"

arta~BB par rr*luta

I

~ Dlamalllr of arllllloiBB

, t

Arterial blood VOlume

I

Fig. 1 ..24 Relationship between artet1al blood volume and blood PI'888UI'EI. Arterial blood PI'888UI'EIIs directly proportlcm
1D artarlal bbod volume. cardiac outp.Jt (CO) and per1pharalraslstarce (PR) are directly pr~aiiD artarlal blood volume
but for opposiiB ~= CO affects blood aniBring the artarles, and PR attects blood laavlng the artarles. If cardiac ootput
lnCI'EIBSBS, the amount af blood en!Br1ng the artar1es Increases and 18nds 1D Increase the volume af blood In the artartes. If
per1pheralrEtsi81Bnoe Increases, It decreases 1he amount d blood leaving the artarles, which tends 1D Increase the amount d
blood left In them .Thus, en lncr&IISB In either CO or PR results In an Increase In artar1al blood volume, whk:h lnCrEteses arterial
blood pressul'l!. (From Pai!Dn KT, lhllxldeau GA: Analomy& (Jhys/ology. ed 9, St. Louis, 2016, Mosby.)

Chapter 1 Anatomy and Physiology

CARDIAC OUTPUT
[Obiective 14]
Each ventricle holds about 150 mL of blood when it i8 full.
They normally eject about half this volume (70-80 mL) with
each contraction. CanlJac output (CO) is the amount of
blood pumped into the aorta each minute by the heart. It
is defined as the ltrob wiume (SV), which is the amount
of blood ejected from a ventricle with each heartbeat, multiplied by the HR. In a healthy averase adult, the CO at rest
is about 5 IJmin (an SV of 70 mL multiplied by an HR of
70 beats/min). Becaue the cardiovascular system is a closed
system, the volume of blood leaving one part of the system
must equal that entering another part. For example, if the
left ventricle normally pumps 5 Umin, the volume flowing
through the arteries, capillaries, and veins must equal 5 U
min. Thta, the CO of the right ventricle (pulmonary blood
:8ow) is normally equal to that of the left ventricle on a minute-to-minute basis.
1he percentage of blood pumped out of a ventricle with
each contraction i8 called the ejcdion fraaion. Ejection
fraction is used as a measure of ventricular function. A normal ejection fraction is between 5096 and 6596. A person is
said to have impaired ventricular function when the ejection
fraction is less than 4096.

Stroke Volume
Cardiac output may be increased by an increase in SV or HR.
SV is determined by the following:
• 'Ihe degree of ventricular :filling when the heart is relaxed
(preload)
• 1he pressure against which the ventricle must pump
(afterload)
• 1he myocardium's contractile state (contracting or
reluing)

Preload, which is also called the end-diastolic volume, is the force exerted on the walls of the ventricles at
the end of diastole. 1he volume of blood returning to the
heart influences preload. More blood returning to the right
atrium (e.g., increased venous return) increases preload.
Less blood returning decreases preload. According to the
Prank-Starling law of the heart, the greater the stretch of
the cardiac muscle (within limits), the greater the resulting
contraction. Heart mucle fibers stretch in response to the
.increased volume (preload) before contracting. Stretching
of the mucle fibers allows the heart to eject the additional
volume with increased force, thereby increasing SV. So in a
normal heart, the greater the preload, the greater the force
of ventricular contraction and the greater the SV, resulting
in increased CO.
1bh ability to adjtat iJ important so that the heart can
alter its pumping capacity in response to changes in venous
return. For example, during exercise, the heart muscle fibers
stretch in response to increased volume (preload) before
contracting. If. however. the ventricle is stretched beyond
its physiologic limit, CO may fall because of volume overload and overstretching of the muscle fibers. Heart failure

iJ a condition in which the heart is unable to pump enough
blood to meet the metabolic needs of the body. It may result

from any condition that impairs preload, afterloa.d, cardiac
contractility, or HR.
Afterload is the pressure or resistance against which the
ventricles must pump to eject blood. Afterloa.d is influenced

Abnormal heart rhythms (dyvhythmias), such as atrial
flutter and atrial fibrillation (discussed in Chapter 4), impede
normal atrial contraction. Ineffectual atrial contraction can
result In a loss of atrial kick, decreased stroke volume, and
a subsequent decrease in cardiac output.

by the following:
• Arterial blood pressure
• The ability of the arteries to become stretched (arterial
distensibility)
• Arterial resistance
The lower the resistance (lower afterload), the more euUy blood can be ejected. Increased afterload (increased
resistance) increases the heart's workload. Conditions that
contribute to increased afterload include increased thickness
of the blood (viscosity) and high blood pressure.

Heart Rata
Remember that CO may be increased byan increase in SV or
HR. Increases in HR shorten all phases of the cardiac cycle.
1he moat important is that the time the heart spends relaxing
is less. If the length of'time for ventricular relaxation is shortened, there is less time for them to fill adequately with blood.
If the ventricles do not have time to fill the following occur:
• The amount of blood sent to the coronary arteries is
reduced.
• The amount of blood pumped out of the ventricles will
decrease (i.e., CO).
• Signs of myocardial ischemia may be seen.
The concentrations of extracellular ions also affect HR.
mess potassium (i.e., hyperkalemia) causes the heart to
become dUated and flaccid (limp), slows the HR, and can
dramatically alter conduction. An increase in calcium (ie.,
hypercalcemia) has an effect almost exactly opposite that
of potassium, cauing the heart to go into spastic contraction. Decreased caldum levels (i.e.. hypocalcemia) make
the heart flaccid, similar to the effect of increased potassium levels.
Other factors that influence HR include hormone levels (e.g., epinephrine, norepinephrine), medications, stress,
amiety, fear, and body temperature. HR increases when
body temperature increases and decreases when body temperature decreases.
An increase in the force of the heart's contractions (and,
subsequently, SV) may occur because of many conditions,
including norepinephrine and epinephrine release from

Chapter 1 Anatomy and Physiology
•:fil':ti ~ ~ Signs and Symptoms of Decreased

cardiac"'
•
•
•
•
•
•
•
•
•
•

Acute changes in blood pressure
Acute changes in mental status
Cold, clammy skin
Color changes In the skin and mucous membranes
Crackles (rales)
Dyspnea
Dysrhythmias
Fatigue
Orthopnea
Restlessness

the adrenal medulla. insulin and glucagon release from the
pancreas, and medications (e.g., calcium, digitalis, dopamine, dobutamine). A decrease in the force of contraction
may result from many conditions, including severe hypoxia,
decreased pH, elevated carbon dioxide levels (hypercapnia), and medications (e.g., calcium channel blockers,
beta-blockers).
Cardiac output varies depending on hormone balance, an
individual's activity level and body size, and the bodys metabolic needs. Factors that increase CO include increased body
metabolism, exercise, and the age and size ofthe body. Factors
that may decrease CO include shock, hypovolemia. and heart
failure. Signs and symptoms of decreased CO appear in Box
1.3. Heart failure may result from any condition that impairs

preload, afterload, cardiac contractility, or HR. As the heart
begins to fail. the bodys compensatory mechanisms attempt
to improve CO by manipulating one or more of these factors.
Now that we have discussed CO, SV, and HR, let us
review an important point. Remember that CO may be
increased by an increase in HR or SV. Consider the following
examples:
1. A patient has an SV of 80 mL/beat. His HR is 70 beats/
min. Is his CO normal, decreased, or increased? Substitute
numbers into the formula you already learned: CO "' SV
x HR. 5600 mUmin = 80 mLibeat x 70 beats/min. CO
is normally between 4 and 8 IJmin. This patient's CO is
within normal limits.
2. Now, let us see what an increase in HR will do. If the
patient's HR increases to 180 beats/min and his SV
remains at 80 mUbeat, what happens to his CO? Using
our formula again (CO = SV x HR) and substituting
numbers, we end up with 14,400 miJmin = 80 mUbeat x
180 beats/min. This patient's CO is increased.
3. What happens to CO if the patient's HR is 70 beats/min
but his SV drops to 50 mUbeatr Using our formula one
more time (CO= SV x HR) and substituting numbers,
we end up with 3500 mL/min = 50 miJbeat x 70 beats/
min. This patient's CO is decreased. If the patient's HR
increased to 90 beats/min to try to compensate for his failing pump, what would happen to his CO? (4500 mL/min
= 50 mUbeat x 90 beats/min). According to our example,
the patient's CO would increase-at least temporarily.

Chapter 1 Anatomy and Physiology

STOP & REVIEW
Multiple Choice
Identify the choice that best completes the statement or
answers the question.
__ 1. The area in the middle ofthe thoracic cavity in which
the heart lies is the
a. mediastinum.
b. pleural cavity.
c. parietal cavity.
d. visceral cavity.
_ _ 2. The inferior surface of the heart is formed by the
a. right and left atria.
b. right and left ventricles.
c. left atrium and left ventricle.
d. right atrium and right ventricle.
__ 3. Which of the following statements is correct?
a. The circumflex artery is a branch of the right
coronary artery.
b. A branch of the right coronary artery supplies the
right atrium and right ventricle.
c. The major branches ofthe right coronary artery
are the septal and diagonal arteries.
d. The left main coronary artery is another name for
the left anterior descending artery.
_ _ 4. The right atrium
a. pumps blood to the lungs.
b. pumps blood to the systemic circulation.
c. receives blood from the right and left pulmonary
veins.
d. receives blood from the superior and inferior
vena cavae and the coronary sinus.
__ 5. Although about 70% of ventricular filling occurs
passively, _ contributes an additional 1096 to 3096
of blood flow to ventricular tilling.
a. atrial kick
b. sv

c. CO
d. ventricular systole
_ _ 8. Which of the following is the innermost layer of the

heart that lines its inner chambers and valves and is
continuous with the innermost layer of the arteries,
veins, and capillaries of the body?
a. Epicardium
b. Myocardium
c. Pericardium
d. Endocardium
_ _ 7. When a ventricle relaxes in the normal heart, blood
is prevented from flowing back into it by
a. the mitral valve.
b. an SL valve.
c. the tricuspid valve.
d. an AV valve.

_ _ 8. The right ventricle

a. pumps oxygenated blood into the systemic
circulation.
b. pumps unoxygenated blood into the pulmonary

circulation.
c. receives unoxygenated blood from the systemic
circulation.
d. receives oxygenated blood from the pulmonary
circulation.
_ _ 9. The_ pericardium is the inner layer of the pericardium, which is also the outer layer of the heart wall
called the _,.
a.parietal,myocardium
b. visceral. epicardium
c.parietal,endocardi~

d. visceral. endocardium
_ _ 10. Which of the following conditions are potentially

reversible?
a. Myocardial ischemia and myocardial injury
b. Myocardial injury and MI
c. Myocardial ischemia and MI
_ _ 11. Which of the following statements is true regarding
CO?
a. 1he higher the afterload, the more easily blood
is ejected from a ventricle.
b. SV is the percentage of blood p~ped out of a
ventricle with each contraction.
c. An inverse relationship exists between venous
return and preload; increased venous return
decreases preload.
d. Within limits, the more blood that is returned
to the heart, the greater the volume of blood
pumped during the next contraction.
Questions 12 tllrough 14 pertain 1D tile following scenario.
A 65-year-old man presents with a sudden onset ofsubsternal
chest pain that radiates to his left arm and jaw and nausea. He
stares that his symptoms began while at rest The patient has a
history ofcoronary artery disease and had a three-vessel co~
nary artery bypass graft last year. His medications include diltiazem. (Cardizem) and nitroglycerin. He has no .known allergies.
_ _ 12. On the basis of the information presented, this
patient is most likely experiencing a(n)
a. stroke.
b. cardiac arrest.
c. valvular prolapse.
d.ACS.

Chapter 1 Anatomy and Physiology
__ 13. Your assessment reveals that the patient is anxious,
his skin is pale and sweaty, and his heart rate is
faster than nonnal for his age. 1he patient's assel!iSment findings are most likely
a. the result of a blocked cerebral blood vessel
b. the result of the improper closure ofone or
more heart valves.
c. caused by sympathetic stimulation and the
release of norepinephrine.
d. caused by parasympathetic stimulation and the
release of acetylcholine.

_

14. 1his patient's heart rate is faster than normal for his
age. Why might this finding be a cause for concern?
a. Rapid heart rates predispose the patient to valvular heart disease.
b. Rapid heart rates shorten diastole and can result
in decreased CO.
c. Rapid heart rates lengthen systole but decrease
myocardial contractility, which can lead to
shock.
d. Rapid heart rates are usually accompanied by pulmonary congestion. which leads to heart fuilure.

Matching
Match the terms below with their descriptions by placing the letter ofeach correct answer in the space provided
a. Right coronary artery
I. SV
b. Arteriosclerosis
J. Aortic
c. Septum
k. Ventricles
d. Atria
I. Pericardium
a. Endocardium
m. Ischemia
I. Atrioventricular
n. Angina pectoris
g. Contracts
o. Ejection fraction
h. Halfmoon
15. A double-walled sac that encloses the heart
__ 16. An SL valve is shaped like a_.
_17. Decreased supply of oxygenated blood to a body part or organ

_18. Innermost layer of the heart
19. Lower heart chambers
_
_

20. 1his type of heart valve separates an atrium and ventricle.
21. Chest discomfort or other related symptoms of sudden onset that may occur because the increased oxygen demand of

the heart temporarily exceeds the blood supply
_22. Coronary artery that supplies the SA node and AV node in most of the population

_23. 1he amount ofblood ejected from a ventricle with each heartbeat
_24. Upper chambers of the heart
25. One of the SL valves
_
26. 1he percentage of blood pumped out of a heart chamber with each contraction
27. An internal wall of connective tissue
_
28. When actin and myosin filaments slide together, the cardiac muscle cell_.
_
29. A chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls

Chapter 1 Anatomy and Physiology

STOP & REVIEW I ANSWERS
1. A. The heart lies in the space between the lungs (i.e.,
the mediastinum) in the middle of the chest. The mediastinum contains the heart, great vessels, truhea, and
esophagus, among other structures; it extends from the
sternum to the vertebral column.
OBJ: Describe the location of the heart
2. B. The heart's bottom (inferior) surface is formed by
both the right and left ventricles, but mostly the left. The
inferior surface of the heart is also called the diaphragmatic surface.
OBJ: Identify the surfaces of the heart.
3. B. A branch of the right coronary artery supplies the
right atrium and right ventricle. 1he left main coronary
artery supplies oxygenated blood to its two primary
branches: the left anterior descending (LAD) artery and
the circumflex artery. The major branches of the LAD
are the septal and diagonal arteries.
OBJ: Name the primary branches and areas of the heart supplied by the right and left coronary arteries.
4. D. The right atrium receives blood low in oxygen from
the superior vena cava (which carries blood from the
head and upper extremities), the inferior vena cava
(which carries blood from the lower body), and the
coronary sinus (which is the largest vein that drains the
heart). The left atrium receives freshly oxygenated blood
from the lungs via the right and left pulmonary veins.
The right ventricle pumps blood to the lungs. The left
ventricle pumps blood to the systemic circulation.
OBJ: Identify and describe the chambers of the heart and the
vessels that enter or leave each.
5. A. Although about 70% of ventricular 6lling ocam passively, atrial contraction (also known as the atrial kick)
contributes an additionaliO% to 30% of blood flow to
ventricular £illing.
OBJ: Explain atrial kick.
6. D. The endocardium is the heart's innermost layer. It
lines the hearts inner chambers, valves, chordae tendineae (tendinous cords), and papillary muscles and is continuous with the innermost layer of the arteries, veins,
and capillaries of the body, thereby creating a continuous, closed circulatory system.
OBJ: Identify the three cardiac muscle layers.
7. B. The SL valves prevent backflow of blood from the
aorta and pulmonary arteries into the ventricles. When
the right ventricle relu:es, blood is prevented from flowing back into it by the pulmonic valve. When the left
ventricle relaxes, blood is prevented from flowing back
into it by the aortic valve.
OBJ: Identify and describe the location of the atrioventricular and semilunar valves.

a.

B. The right side of the heart is a low-pressure system
whose job is to pump unoxygenated blood from the
body to and through the lungs to the left side of the
heart The right ventricle receives blood low in oxygen
from the right atrium and pumps the blood through
the pulmonic valve into the pulmonary trunk, which
divides into the right and left pulmonary arteries.
OBJ: Beginning with the right atrium, describe blood ft.ow
through the normal heart and lungs to the systemic circulation.
9. B. The visceral pericardium is the inner layer of the pericardiwn, which also attaches to the large vessels that
enter and exit the heart and covers the outer surface of
the heart muscle (i.e., the epicardium).
OBJ: Describe the structure and function of the coverings of
the heart.
10. A. The sequence of events that occurs during an ACS
results in conditions that range from myocardial
ischemia or injury to death (i.e., necrosis) of heart muscle. Ischemia prolonged more than just a few minutes
results in myocardial injury. Myocardial injury refers to
myocardial tissue that has been cut off from or experienced a severe reduction in its blood and oxygen supply.
Injured myocardial cells are still alive but will die (i.e.,
infarct) if the ischemia is not qui.ckly corrected. An MI
occurs when blood :flow to the heart muscle stops or is
suddenly decreased long enough to cause cell death.
OBJ: Discuss myocardial ischemia. injury, and infarction,
indicating which conditions are reversible and which are not
11. D. According to the Frank-Starling law of the heart, the
greater the stretch of the cardiac muscle (within limits),
the greater the resulting contraction. Preload (end-diastolic volume) is the force exerted on the walls of the ventricles at the end ofdiastole. In a normal heart, the greater
the preload, the greater the force of ventricular contraction and the greater the SV. resulting in increased CO.
Afterload is the pressure or resistance against which the
ventricles must pump to eject blood. The lower the resistance (lower afterload), the more easily blood is ejected.
The percentage of blood pumped out of a ventricle with
each contraction is called the ejection.{r'Qction.
OBJ: Identify and explain the components ofblood pressure
and cardiac output
12. D. On the buis of the information presented, this
patient is most likely experiencing an ACS