ECGs Made Easy, 6th Edition

Visit the link below to download the full version of this book:

https://medipdf.com/product/ecgs-made-easy-6th-edition/

Click Download Now

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 experi-
ence. 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 practi-
cal, 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 dysrhyth-
mia 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 recom-
mended 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 other-
wise 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 cur-
rent 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 medi-
cal 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 BiB Miller
Care Coordinator Paramedic Crew Chief
Cincinnati Childrms Hospital Medical Center St. Louis Fire Department-HEMS
Cincinnati, Ohio St. Louis, Missouri

Joshua BorkoU:.y, BS, pp.c Mark.Nootena, MD, PACC

EMS Education Manager Cardiologist. Private Practice
University of Cincinnati College of Medicine Munster, Indiana
Cincinnati, Ohio
Ruth C. Tamulonis, MS, RN
Angela McConachie, DNP, MSN-PNP, RN Nursing Professor
Assistant Professor Yuba College
Goldfarb School ofNursing at Barnes-Jewish College Marysville, California
St Louis, Missouri

vi
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 3 SINUS MECHANISMS, 78

Location. SJu, and Shape of the Heart. 2 Introdudlon. 76

Surfaca of the Heart. 2 Sinua Rhythm, 77
Coverinp of the Heart, 2 How Do I Recognize It? 77
Structure of the Heart, 5 Sinua Bradycardia. 78
Layers of the Heart WalL 5 How Do I Recognize It? 78
Heart Chambers, 6 What Causes m 78
Heart Valves, 8 What Do I Do About It? 79
The Heart's Blood Supply, 11 Sinua Tadlyardia, 80
The Heart's Nerve Supply, 16 How Do I Recognize It? 80
The Heart aa a Pump, 19 What Causes It? 80
Cardiac Cycle, 19 What Do I Do About It? 81
Blood PreS3Ul't, 20 Sinua Arrbytbmia, 81
R£ferenca, '1.7 How Do I Recognize It? 81
What Causes It! 81
What Do I Do About It? 82
2 BASIC ELECTROPHYSIOLOGY, 28 Sinoatrial Block. 82
How Do I Recognize It? 82
Cardiac Cella, 30 What Causes It? 82
Types of Cardiac Cells, 30 What Do I Do About It? 83
Propertia of Cardiac Cells, 30 Sinua Arrest, 83
Cardiac Action Potmtial, 30 How Do I Recognize It? 83
Polarization, 31 What Causes It? 83
Depolarization, 31 What Do I Do About It? 84
Repolarization, 32 Referencea,IOI
Phases of the Cardiac Action Potential, 32
Refractory Periods, 34
Conduction Syatem, 35 4 ATRIAL RHYTHMS, 102
Sinoatrial Node, 35
Atrioventricular Node and Bundle, 37 Introduction, 103
Right and Left Bundle Branches, 38 Atrial Dyar.bythmiaa: Mech.aDi~ms, 103
Purkinje Fibers, 38 Abnormal Automaticity, 103
Cauaea of Dyarhythmiaa, 39 Tnggered Activity, 103
Disorders of Impulse Formation, 39 Reentry, 104
Disorders of Impulse Conduction, 39 Premature Atrial Compleea, 104
The Ela:trocardiogr, 41 How Do I Recognize It? 104
Electrodes, 41 Noncompensatory versus Compensatory Pause, 105
Leads, 42 Aberrantly Conducted Premature Atrial
Ambulatory Cardiac Monitoring, 46 Complexes, 106
Blectrocanliopaphy Paper, 47 Nonconducted Premature Atrial Complexes, 106
Waveforms, 48 What Do I Do About Them? 107
Segments, 53 Wuuleriq Atrial Pacemaker, 107
Intervals, 55 How Do I Recognize It? 107
Artifact. 56 What Causes It? 107
Symmatic Rhythm J:nterpretation. 57 What Do I Do About It? 107
Asseas Regularity, 57 Mal.tifoc:al Atrial Tachycanlia, 108
Asseas Rate, 58 How Do I Recognize It? 108
Identify and Examine Waveforms, 60 What Causes It? 108
Asseaslntervals and Examine Segments, 60 What Do I Do About It? 108
Interpret the Rhythm, 60
Re&renca, 74

viii
 Contents

Supraventricular 'Thchycardia, 108 What Causes It? 177

Atrial Tachycardias, 109 What Do I Do About It? 177
Atrioventricular Nodal Reentrant Tachycardia, 113 ~(CanUa~S~).177
Atrioventricular Reentrant Thchycardia, 114 How Do I Recognize It? 177
Atrial Flutter, 117 What Causes It? 178
How Do I Recognize It? 117 What Do I Do About It? 178
What Causes It? 118 References, 193
What Do I Do About It? 118
Atrial Fibrillation, 119
How Do I Recognize It? 119 7 ATRIOVENTRICULAR BLOCKS, 194
What Causes It? 121
What Do I Do About It? 121 Introduction, 194
References, 140 First-Degree Atrioventricalar Block, 195
How Do I Recognize It? 195
What Causes It? 196
5 ~UNCTIONAL RHYTHMS, 141 What Do I Do About It? 197
Second-Degree Atrioventricular Blocks, 197
Introduction, 141 Second-Degree Atrioventricular Block Type I, 197
Premature Juncticmal Compleus, 142 How Do I Recognize It? 197
How Do I Recognize 1hem~ 142 What Causes It? 198
What Causes 1hem? 143 What Do I Do About It? 199
What Do I Do About Them? 143 Second-Degree Atrioventricular Block Type ll, 199
Junctional Escape Beau or Rhythm, 144 How Do I Recognize It? 199
How Do I Recognize It? 144 What Causes It? 200
What Causes It? 145 What Do I Do About It? 200
What Do I Do About It? 146 2:1 Atriovmtricalar moa, 200
Accelerated Junctional Rhythm, 146 How Do I Recognize It? 200
How Do I Recognize It? 146 Advanced Second-Degree Atriovent:rkular Block. 201
What Causes It? 146 'Ihird-Degree Atrioventricu1ar Block, 202.
What Do I Do About It? 146 How Do I Recognize It? 202
Junctional Tachyardia. 146 What Causes It? 203
How Do I Recognize It? 146 What Do I Do About It? 203
What Causes It? 147 Reference8, 221
What Do I Do About It? 147
References, 164
B PACEMAKER RHYTHMS, 222

6 VENTRICULAR RHYTHMS, 165 Pacemaker Systema. 223

Permanent Pacemakers and hnplantable Cardioverter-
Introductlon,166 Defibrillators, 223
Premature Ventricular Complexes, 166 Temporary Pacemakers, 224
How Do I Recognize 1hem~ 166 Pacing Lead Symms, 225
What Causes 1hem? 170 Padng Chamben and Modes, 226
What Do I Do About Them? 170 Single-Chamber Pacemakers, 226
Ventricular .Escape Beats or Rhythm,170 Dual-Chamber Pacemakers, 227
How Do I Recognize It? 170 Biventricular Pacemakers, 227
What Causes It? 172 Fixed-Rate Pacemakers, 227
What Do I Do About It? 172 Demand Pacemakers, 227
Accelerated Idlovmtrl<:Ular :Rhythm. 172 Pacemaker Codes, 228
How Do I Recognize It? 172 Pacemaker Malfunction.l28
What Causes It? 172 Failure to Pace, 228
What Do I Do About It? 173 Failure to Capture, 229
Ventricnlar Tachycardia, 173 Failure to Sense, 230
How Do I Recognize It? 173 Analyzing Pacemaker Fund:ion on the ECG, 230
Ventricular Fibrillation, 176 Reference., 240
How Do I Recognize It? 176
 Contents

9 INTRODUCTION TO THE 12-LEAD 10 POSlTEST, 278

ECG, 241
Introduction, 141
Layout of the 12-Lead Electrocardiogram, 242 INDEX, 321
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
LEARNING OBJECTIVES
After reading this chapter, you should be able to: 9. Define and explain acute coronary syndromes.
1. Describe the location of the heart. 10. Discuss myocardial ischemia, injury, and infarction, indicating which
2. Identify the surfaces of the heart. conditions are reversible and which are not.
3. Describe the structure and function of the coverings of the heart. 11. Compare and contrast the effects of sympathetic and parasympathetic
4. Identify the three cardiac muscle layers. stimulation of the heart.
5. Identify and describe the chambers of the heart and the vessels that 12. Identify and discuss each phase of the cardiac cycle.
enter or leave each. 13. Beginning with the right atrium, describe blood flow through the
6. Identify and describe the location of the atrioventricular and semilunar normal heart and lungs to the systemic circulation.
valves. 14. Identify and explain the components of blood pressure and cardiac
7. Explain atrial kick. output.
8. Name the primary branches and areas of the heart supplied by the
right and left coronary arteries.

KEY TERMS
acute coronary syndrome (ACS): A term used to referto distinct base of the heart: Posterior surface of the heart.
conditions caused by a similar sequence of pathologic events- blood pressure: Force exerted by the blood against the walls of the arter-
a temporary or permanent blockage of a coronar_y artery. These ies as the ventricles of the heart contract and relax.
conditions are characterized by an excessive dem nd or inadequate cardiac output (CO): The amount of blood pumped into the aorta each
supply of oxygen and nutrients to the heart muscle associated minute by the heart; defined as the stroke volume multiplied by the
with plaque disruption, thrombus formation, and vasoconstriction. heart rate.
ACSs consist of three major syndromes: unstable angina, non- chordae tendineae (tendinous cords): Thin strands of fibrous connec-
ST-elevation myocardial infarction, and ST elevation myocardial tive tissue that extend from the AV valves to the papillary muscles that
infarction. prevent the AV valves from bulging back into the atria during ventricular
afterload: The pressure or resistance against which the ventricles must systole (contraction).
pump to eject blood. chronotropy: A change in (heart) rate.
angina pectoris: Chest discomfort or other related symptoms of sudden diastole: Phase of the cardiac cycle in which the atria and ventricles relax
onset that may occur because the increased oxygen demand of the between contractions and blood enters these chambers. When the term
heart temporarily exceeds the blood supply. is used without reference to a specific chamber of the heart, ventricular
apex of the heart: Lower portion of the heart that is formed by the tip of diastole is implied.
the left ventricle. dromotropy: Refers to the speed of conduction through the AV junction.
atria: Two upper chambers of the heart (singular, atrium). dysrhythmia: Any disturbance or abnormality in a normal rhythmic pat-
atrial kick: Blood pushed into the ventricles because of atrial contraction. tern; any cardiac rhythm other than a sinus rhythm.
atrioventricular (AV) valve: The valve located between each atrium ejection fraction: The percentage of blood pumped out of a heart cham-
and ventricle; the tricuspid separates the right atrium from the right ber with each contraction.
ventricle, and the mitral (bicuspid) separates the left atrium from the endocardium: Innermost layer of the heart that lines the inside of the
left ventricle. myocardium and covers the heart valves.
atypical presentation: Uncharacteristic signs and symptoms perceived epicardium: Also known as the visceral pericardium; the external layer of
by some patients experiencing a medical condition, such as an ACS. 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 pi'Oldmal: Location nearer to the midline of the body or the point of
blood to meet the metabolic needs of the body; It may result from any attachment than something else Is.
cond~ion that impairs preload, afterload, cardiac contractility, or heart sarcolemma: Membrane that covers smooth, striated, and cardiac
rare. muscle fibers.
inDtropy: Refers to a change in myocardial contractility. sarcomere: Smallest functional un~ of a myofibril.
ischemia: Decreased supply of oxygena1ed blood tn a body part or organ. sarcoplasm: SemWiuid cytnplasm of muscle cells.
mediastinum: Middle area of the thoracic cavity; contains the heart, great sarcoplasmic reticulum: Network of tubules and sacs that plays an
vessels, trachea, and esophagus, among other structures; extends from important role in muscle contraction and relalration by releasing and
the sternum to the vertebral column. storing calcium Ions.
mltochondrta: The energy-producing parts of a cell. semilunar (SL) valves: Valves shaped like half-moons that separate the
mvocardlallnfarctlon (M~: Death of some mass of the heart muscle ventricles from the aorta and pulmonary artery.
caused by an Inadequate blood supply. septum: An lntBmal wall of connective tissue.
mvocardlum: Middle and thickest layer of the heart; contains the cardiac stroke volume {SV): The amount of blood e]eclBd from a ventricle with
muscle fibers that cause contraction of the heart and contal ns the each heartbeat
conduction system and blood supply. sulcus: Groove.
myofibril: Slender striated strand of muscle tissue. systole: Contraction of the heart (usually refarri ng to ventricular contrac-
papillary muscles: Muscles attached to the chordae mndineae of the AV tion), during which blood is propelled intn the pulmonary artery and
valves and the ventricular muscle of the heart that help prevent the AV aorta; when the tenn is used without reference to a specific chamber of
valves from bulging too far intn the abia. the heart, ventricular systole is implied.
pericardium: A double-walled sac thai erdoses the heart and helps tone: A term that may be used when referring to the normal state of bal-
protect It from trauma and Infection. anced tension In body tissues.
peripheral resistance: Resistance to the flow of blood determined by venous return: Amount of blood flowing lntn the right atrium each minute
blood vessel diameter and the tone of the vascular musculature. from the syslemlc c1rculatlon.
preload: Force exerted by the blood on the walls of the venb1cles at the venb1cles: The two lower chambers of the heart
end of diastole.

LOCATION, SIZE, AND SHAPE formed by portions of the right atrium and the left and right
vmtrides (Fig. 1.4). However, because the heart is tilted
OFTHEHEART slightly toward the left in the chest, the right ventricle is the
[Oblectlve 1] area of the heart that lies most directly behind the sternum.
The heart is a hollow muscular organ that lies in the space The apa, or lower portion, of the heart is formed by the tip
between the lungs (i.e., the mediastinum) in the middle of of the left ventricle. The apex lies just above the diaphragm
the chest (Pig. 1.1). It sits behind the stemwn and just above at about the level of the fifth intercostal space in the midcla-
the diaphragm. About two thirds of the heart lies to the left vicular line.
of the midline of the stemwn. The remaining third lies to the The heart's left side (i.e., left lateral surface) faces the
right of the sternum. left lung and is made up mostly of the left ventricle and a
The adult heart is about 5 inches ( 12 an) long, 3.5 inches portion of the left atrium. The right lateral surface faces
(9 em) wide, and 2.5 inches (6 em) thick (Fig_ 1.2). It typically the right lung and consists of the right atrium. The heart's
weighs between 250 and 350 g (about 11 oz) and is about bottom (i.e., inferior) surface is formed primarily by the
the size of its owner's fist The weight of the heart is about left ventricle, with small portions of the right ventricle
0.4596 ofa man's body weight and about 0.40% ofa woman's, and right atrium. The right and left ventricles are sepa-
A person's heart size and weight are influenced by his or her rated by a groove containing the posterior interventricu-
age, body weight and build. frequency of physical exercise, lar vessels. Because the inferior surface of the heart rests
and heart disease. on the diaphragm, it is also called the diaphragmatic sur-
face (Fig. 1.5).

SURFACES OF THE HEART

COVERINGS OF THE HEART
[Obiactiva 2]
The base, or posterior surface, of the heart is formed by the [Obiactive 3)
left atrium, a small portion of the right atrium, and proxi- The periQU'dium is a double-walled sac that encloses the
mal portions of the superior and inferior venae cavae and heart and helps protect it from trauma and infection. The
the pulmonary veins (Fig. 1.3). The front (anterior) surface tough outer layer of the pericardia! sac is called the fibrous
of the heart lies behind the sternum and costal cartilages. It is 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

Obtuee mergln
Fig. 1.3 The base af the heart. (Ffm1 Drake R, 'ql A.W, Milcrell A."WM: &ay's
anaiDmy for stJJdents, ed 3, New York, 2015, Churchill Uvingslune~

Fig. 1.4 Th& ant:&r1or surface of the haart. (From Drake R, Vogl AW, Mitchell
The right and left phrenic nerves, which innervate the dia- AWM: Gray's anatomy frJr stJJd6nts, &d 3, Naw York, 2015, Churchill L.Mrgstona.)
phragm, pass through the fibrous pericardium as they
descend to the diaphragm. Because these nerves sup- The inner layer of the pericardium, the serous pericar-
ply sensory fibers to the fibrous pericardium, the parietal dium, consists of two layers: parietal and visceral (Fig. 1.7).
serous pericardium, and the mediastinal pleura, discomfort the parietal. layer lines the inside of the fibrous pericardium.
related to conditions affecting the pericardium may be felt
The visceral layer attaches to the large vessels that enter and
In the areas above the shoulders or lateral neck.
exit the heart and covers the outer surface ofthe heart muscle
(ie., the epicardium).
of the structures around it. such as the sternum and dia- Between the visceral and parietal layers is a space (the
phragm, by means of ligaments. This helps prevent exces- pericardia! space) that normally contains about 20 mL of
sive movement of the heart in the chest with changes in serous (pale yellow and transparent) fluid. This fluid acts as a
body position. lubricant, preventing friction as the heart beats.

If the pericardium becomes Inflamed (pericarditis), excess Heart surgery or trauma to the heart, such as a stab wound,
pericardia! fluid can be quickly generated in response to the can cause a rapid buildup of blood in the pericardia! space. The
inflammation. Pericarditis can result from a bacterial or viral buildup of excess blood or fluid in the pericardia! space com-
infection, rheumatoid arthritis, tumors, destruction of the presses the heart. This can affect the heart's abiily to relax and
heart muscle in a heart attack, among other causes. 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 shock. Conversely, 1000 mL of fluid may build up over a lon-
to the body (cardi~ output) will be decreased. As a result, the ger period without any significant effect on the heart's ability
amount of blood returning to the heart is also decreased. These to fill. This is because the pericardium accommodates the
changes can result in a life-threatening cond~ion called C8ldiac increased fluid by stretching over time.
temponade. The amount of blood or fluid in the pericardia! The symptoms of cardiac tamponade can be relieved
space needed to impair the heart's ability to fill depends on the by removing the excess fluid from the pericardia! sac.
rate at which the buildup of blood or fluid occurs and the ability Pericardiocentesis is a procedure in which a needle is
of the pericardium to stretch and accommodate the increased inserted into the pericardia! space and the excess fluid
volume of fluid. is sucked out (aspirated) through the needle. If scarring is
The rapid buildup of as little as 100 to 150 ml of fluid or the cause of the tamponade, surgery may be necessary to
blood can be enough to result in signs and symptoms of remove the affected area of the pericardium.

Right Rbrous
ventricle pericardium
{cut;)
Postertor
lnt8r-
ventrlcu lar
art8ly Left verrtricla
and vein
Right Coronary
sulcus
atrium
Inferior
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 dla-
pluagm. (From Gosling JA: Human anaJDmy: color atlas and text. ad 4, L..ordcn, 2002, Mosby.)

Laft brachl~ Left

oaphalil: Aortic vagus
vein arch 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
pert-
cardium
(cut)

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

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 Endocardium -~~=-~
made up of a thin, smooth layer of epithelium and connec-
Myocardium
tive tissue and Unes the heart's inner chambers, valves, chor-
dae tendineae (tendinous cords), and papillary muscles. The VIsceral
terminal components of the heart's specialized conduction pericardium
(epicardium)
system can be found within this layer (Anderson & Roden.
2010). The endocardium is continuous with the innennost Perlcardlal
apace
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
Abrous
that consists of cardiac muscle fibers (cells) responsible for the layer
pumping action of the heart The myocardium makes up about
Flf. 1.8 The parlcardlal sac Is aJIIliOSIId af 1:\W layn separaiBd by a narrow
30% ofthe total left. ventrkular mass (Anderson & Roden, 2010). ftuld-fllled Sjlllllll. The v1scaral part:anllum (aplcmdklm) Is attached dlractly 1D 1ha
lhe innermost halfofthe myocardium is called the subendocar- heart's surface, and the parlelal pertardlum fcnns the llJIEr layer af the sac. (from
1&1 area. The outermost halfis called the subepicardial area. 1he ~-l<lrlitx:Jm L, Blnlslk JL: PBthoplrys/rJ/o ad 5, PhiBde~hla, 2013, Elakr.)
muscle fibers of the myocardium are separated by connective
tissues that have a rich supply ofcapillaries and nerve fibers.
The heart's outennost layer is called the epicardium. The
Did You Know?- - - - - - - epicardium is continuous with the inner lining of the peri-
cardium at the heart's apex. The epicardium contains blood
The thickness of a heart chamber is related to the amount of
pressure or resistance that the muscle of the chamber must capillaries, lymph capillaries, nerve fibers, and fat. 1he main
overcome to eject blood. 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 I
Myocardium • Middle and thickest layer of the heart L------
lrrtercalallld dlskB
• Muscular component of the heart;
responsible for the heart's pumping
action
Endocardium • Innermost layer of the heart
• Lines heart's inner chambers, valves,
- Mltllchandrlon
chordae tendineae, and papillary
muscles
• Continuous with the innermost layer Fig. 1.8 cardiac muscle filar. lklllke ather types a! muscle fibers, 1he cardiac
of arteries, veins. and capillaries of the muscle flbar Is t)Pically branchoo and foiTI'IS junc1!oos, called lntaroalllled dis~. with
body adjacent cardiac muscle fibers. (From PatiDn KT, Thltxxfeau GA: Anthony's IIJXtbook
of 8fi/J/Dmy & phys/okJgy, ad 20, St Louis, 2013, Mooby~

They feed this area first before entering the myocardium and potassium (potassium channels), and calcium (calcium
supplying the heart's inner layers with oxygenated blood. channels). When the muscle is relaxed, the calcium chan-
Ischemia is a decreased supply of oxygenated blood to a nels are closed. As a result, calcium cannot pass through
body part or organ. The heart's subendocardial area is at the the membrane of the SR. This results in a high concen-
greatest risk ofischemia because this area has a high demand tration of calcium in the SR and a low concentration in
for oxygen and it is fed by the most distal branches of the the sarcoplasm, where the muscle cells (sarcomeres) are
coronary arteries. found. If the muscle cells do not have calcium available to
them, contraction is inhibited (the muscle stays relaxed).
CARDIAC MUSCLE The force of cardiac muscle contraction depends largely
Cardiac muscle fibers make up the walls of the heart. on the concentration of calcium ions in the extracellular
These fibers have striations, or stripes, similar to that of fluid.
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
0 ECG Pear1 _ _ _ _ _ _ _ __
The heart consists of two syncytia: atrial and ventricular.
with all cells) are mitocho.odria, the energy-producing The atrial syncytium consists of the walls of the right and
parts of a cell, and hundreds of long, tube-like structures left atria. The ventricular syncytium consists of the walls of
called myoflbrlls. Myofibrils are made up of many sar~o­ the right and left ventricles. Normally, impulses can be con-
merea, the basic protein units responsible for contraction. ducted from the atrial syncytium into the ventricular syncy-
The process of contraction requires adenosine triphos- tium only by means of the atrioventricular (AV) junction. The
phate (ATP) for energy. The mitochondria that are inter- AV junction is a part of the heart's electrical system. This
spersed between the myofibrils are important sites of ATP allows the atria to contract a short time before ventricular
production. contraction.
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
Heart Chambers
in order to contract. Calcium is moved from the sarco- The heart has four chambers, two atria and two ventri-
plasm of the muscle cell into the SR by means of "'pumps" cles. The outside surface of the heart has grooves called
in the SR. sulci. The coronary arteries and their major branches lie
There are certain places in the cell membrane where in these grooves. The coronary sulcus (groove) encircles
sodium (Na+), potassium (K+), and calcium (Ca++) can the outside of the heart and separates the atria from the
pass. These openings are called pores or channels. There ventricles. It contains the coronary blood vessels and
are specific channels for sodium (sodium channels}, 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] (Obiactive 5]
The two upper chambers of the heart are the right and The heart's two lower chambers are the right and left ven-
left atria (singular, atrium) (Fig. 1.10). An earlike flap tricles. Their purpose is to pump blood. The right ventricle
called an auricle (meaning "little ear·) protrudes from pumps blood to the lungs. The left ventricle pumps blood
each atrium. out to the body. Because the ventricles must pump blood
The purpose of the atria is to receive blood. The right either to the lungs (the right ventricle) or to the rest of the
atrium receives blood low in oxygen from the superior vena body (the left ventricle), the ventricles have a much thicker
cava (which carries blood from the head and upper extremi- myocardial layer than the atria. Because the right ventricle
ties), the inferior vena cava (which carries blood from the moves blood only through the blood vessels of the lungs and
lower body), and the coronary sinus (which is the largest then into the left atrium, it has one sixth of the muscle mass
vein that drains the heart). The left atrium receives freshly and one third of the wall thickness of the left ventricle, which
oxygenated blood from the lungs via the right and left pul- must propel blood to most vessels of the body (Hutchison &:
monary veins. Rudakewich, 2009) (Fig. 1.11).
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 encoun-
ter little resistance when pumping blood to the ventricles. As
a result, the atria have a thin myocardial layer. The wall of When the left ventricle contracts, it normally produces an
the right atrium is about 2 mm thick. and the wall of the left impulse that can be felt at the apex of the heart (apical
atrium is about 3 m.m thick. Blood is pumped from the atria impulse). This occurs because as the left ventricle con·
through an atrioventricular (AV) valve and into the ventri- tracts, it rotates forward. In a normal heart, this causes the
cles. The valves ofthe heart are discussed later in this chapter. apex of the left ventricle to hit the chest wall. You may be
able to sea the apical impulse in thin individuals. The api-
Q ECG Pearl _ _ _ _ _ _ _ _ __ cal impulse is also called the point of maximal impulse
because it is the site where the left ventricular contraction
Think of the atria as holding tanks or reservoirs for blood. is most strongly felt.