ECGs Made Easy 6th Edition Aehlert

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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 mechani-
cal, including photocopying, .recording. or any in!ormali.on stDrap and Rtrieval. systmn. without permilaion in
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si.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 belt 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

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
Worktng together
to grow l!b-r.arLC'~ Li1
Printed in Canada
de•n:l oping: cnuntrm(:~

Last digit is the print number: 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 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
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 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:
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.
KEY TERMS
acute coronary syndrome (ACS): A term used to referto distinct
conditions caused by a similar sequence of pathologic events-
a 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, non-
ST-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.
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.
base of the heart: Posterior surface of the heart.
blood pressure: Force exerted by the blood against the walls of the arter-
ies 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 connec-
tive 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 pat-
tern; any cardiac rhythm other than a sinus rhythm.
ejection fraction: The percentage of blood pumped out of a heart cham-
ber 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 proxi-
mal 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 contrac-
tion), 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 bal-
anced 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 midcla-
vicular 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 sepa-
rated by a groove containing the posterior interventricu-
lar vessels. Because the inferior surface of the heart rests
on the diaphragm, it is also called the diaphragmatic sur-
face (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

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. 1.3 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~
The right and left phrenic nerves, which innervate the dia-
phragm, pass through the fibrous pericardium as they
descend to the diaphragm. Because these nerves sup-
ply 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 dia-
phragm, by means of ligaments. This helps prevent exces-
sive 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.
Chapter 1 Anatomy and Physiology
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. 1.4 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 pericar-
dium, 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 com-
presses 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 lon-
ger 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 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
Myocardium • Middle and thickest layer of the heart
• Muscular component of the heart;
responsible for the heart's pumping
action
Endocardium • 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
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 triphos-
phate (ATP) for energy. The mitochondria that are inter-
spersed 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 sarco-
plasm 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 chan-
nels are closed. As a result, calcium cannot pass through
the membrane of the SR. This results in a high concen-
tration 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 con-
ducted from the atrial syncytium into the ventricular syncy-
tium 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 ventri-
cles. 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
[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 extremi-
ties), 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 pul-
monary 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 encoun-
ter 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 ventri-
cles. The valves ofthe heart are discussed later in this chapter.
Q ECG Pearl _ _ _ _ _ _ _ _ __
Think of the atria as holding tanks or reservoirs for blood.
VENTRICLES
(Obiactive 5]
The heart's two lower chambers are the right and left ven-
tricles. 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).
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 api-
cal 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 Intel'" Trabeculae Marginal
ventricular mUICia Y811lrtcular camaae arl8ry
-11 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.
Fig. 1.12 Skeleton of the heart. This IX)Stel1or view shows part of the venll1cular
ATRIOVENTRICULAR VALVES myooardlum with 1he heart valves 81111 attached. The rim of each heart valve Is sup-
ported by a fibrous structure, called the sk8/stonofth6 h6art, which encircles all four
[Oblectlves 6, 7] valves. AV. Atrlovenll1cular. (From PatiDn KT, Thibodeau GA: Anatmny&ph~
Atrioventricular valves separate the atria from the ventricles. ed 9, St Louis, 201 6, Mosby.)
The two AV valves consist of tough. fibrous rings (annuli
:6.brosi); :flaps (lea11.ets or cusps) of endocardium; chordae
tendineae; and papillary muscles. left atrium and left ventricle (Fig. 1.14). The mitral valve is
1he tricuspid valve is the AV valve that lies between the so named because of its resemblance to a miter, which is a
right atrium and right ventricle. It consists of three separate double-cusp bishop's hat, when open.
cusps or flaps (Fig. 1.13). It is larger in diameter and thinner The AV valves open when a forward pressure gradi-
than the mitral valve. The mitral valve, which is also called ent forces blood in a forward direction. They close when
the bicuspid valve, has only two cusps and lies between the a ba.ck.ward pressure gradient pushes blood backward. The
 Chapter 1 Anatomy and Physiology

Superior vena

Right

TrtcuspldG Anterior cusp Septal papllluy miiiiCie

Septal cusp
valve Posterior cusp
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 ventri-
cle. 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 bulg-
ing 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 pre-
vent the bacldlow ofblood from the aorta and pulmonary arter-
ies 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, allow-
ing 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 dis-
ease 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 tendin-
eae 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 thick-
ens, 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 infarc-
tion), 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 con-
sidered abnormal An abnormal third heart sound is fre-
quently 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

Pulmonary velr1s..,::-----~...4
Superior vena
Left atrium7'9~L~
Aorta --r--ollil.l~
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 ven-
tricle 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 ventricu-
lar 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 pericar-
dium 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 myo-
cardium like a crown. or corona.
CORONARY ARTERIES
[Oblectlve 8]
lhe main coronary arteries lie on the outer (epicardial) sur-
face ofthe heart. Coronary arteries that run on the surface of
Chapter 1 Anatomy and Physiology
Aortic valve
cusps
Right
venlr1cle
lntervemrtcular
septum
the heart are called epicardial coronary arteries. They branch
into progressively smaller vessels, eventually becoming arte-
rioles, 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 supply-
ing the rest of the body. This freshly oxygenated blood is sup-
plied 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 ves-
sels lie just beyond the cusps of the aortic SL valve. When
the left ventricle contracts (systole), the force of the pres-
sure 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 arter-
ies) are compressed during ventricular contraction, reduc-
ing blood fl.ow to the tissues of the heart. Thus, the coronary
arteries fill when the aortic valve is closed and the left ven-
tricle 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 AuscultaUon position

for tr1cuspld valve 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 Separates the right atrium and Just to the left of the lower part of the ster-
right ventricle num near the fiHh intercostal space
Mitral (bicuspid) Atrioventricular Separates the left atrium and left Heart apex in the left fifth intercostal space
ventricle at the midclavicular line
Pulmonic (pulmonary) Semilunar Between the right ventricle and Left second intercostal space close to the
pulmonary artery sternum
Aortic Semilunar Between the left ventricle and Right second intercostal space close to the
aorta sternum

artery disease (CAD) if there is more than 5096 diameter nar-

rowing (i.e., stenosis) in one or more of these vessels. Right Coronary Artary
The RCA orlginates from the right side of the aorta (Fig.
(ill CLINICAL CORRELAT10NS 1.17). It travels along the groove between the right atrium
and right ventricle. A branch of the RCA supplies the follow-
Because a heart attack, which is also called a myocardial ing structures:
Infarction, Is usually caused by a blocked coronary artery, • Right atrium
it is worthwhile to become familiar with the arteries that • Right ventricle
supply the heart. When myocardial ischemia or infarction • Inferior surface of the left ventricle in about 85% of
is suspected, an understanding of coronary artery anatomy individuals
and the areas of the heart that each vessel supplies helps • Posterior surface of the left ventricle in 85%
you predict which coronary artery is blocked and anticipate • Sinoatrial (SA) node in about 60%
problems associated with blockage of that vessel.
• AV bundle in 8596 to 90%

Left Wiell
appendage
Ci-'lex lnncto of
laft main c;orvnuy ar1Bry
Luft enterlor d-ndlng
lnnch of Ifill
GOIIlllllry artery
Poalllllar diHicendng
~lar)
nncn of riGht
c:oranary artery
A B
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 sul-
cus) toward the heart's apex. In most patients. the LAD travels
around the apex ofthe left ventricle and ends along the left ven-
tricle'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%
Chapter 1 Anatomy and Physiology
flrachiDC&PMic
..,.,k
LGit pulmonery ~----·- Aot1lc arch
artery - >- ·- Superior-. cava
Left pulmonary
Right~-ry
vere artery
I.Mtalrtum
Right punnary
wins
Right atrtum
.,.___,.....~~ - Middle ean:llac
vein
"'-.,.~.._- Right ventrlde
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 descend-
ing 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 descend-
ing 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 right-
dominant system. If the Cx branches and ends at the poste-
rior 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 dis-
tinct 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 hard-
ening of the vessel walls. Atherosclerosis is a form of arterioscle-
rosis 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 pre-
vent infarction despite complete blockage ofthe primary artery.
Did You Know? _ _ _ _ _ __
Any artery in the body can develop atherosclerosis. If the coro-
nary 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 feel-
ing include "heaviness," "squeezing," "a band across my
chest," ·a weight in the center of my chest," and "a vise tight-
ening around my chest"

lfJ:!IJ!I Coronary Arteries

Coronary Artery Portion of Myocardium Supplied Portion of Conduction System Supplied
Right • Right atrium • Sinoatrial (SA) node (about 60%)*
• Right ventricle • Atrioventricular (AV) bundle (85% to 90%)*
• Inferior surface of left ventricle (about 85%)*
• Posterior surface of left ventricle (85%)*
Left anterior descending • Anterior surface of left ventricle • Most of right bundle branch
• Part of lateral surface of left ventricle • Part of left bundle branch
• Anterior two thirds of interventricular septum
Circumflex • Left atrium • SA node (about 40%)*
• Part of lateral surface of left ventricle • AV bundle (1 0% to 15%)*
• Inferior surface of left ventricle (about 15%)*
• Posterior surface of left ventricle (15%)*
*Of population.

Endothelium Intima
Chronic anc:lothallallnjury
• Hypertension Fattyatruk
• Tobacco use • Uplds accumulate and migrate
• Hypel11pldemla Into smooltl muscle cells
• Hyperhomocystelnemla
• Diabetes
• Infections
•Toxins
Damaged
endothelium

Fibrous plaqua Compllcat.d lesion

• Collagen covers the fatty streak • Plaque rupture
• Vessel lumen is narrowed • Thrombus formation
• Blood flow is reduced • Further narrowing or total
• FISSures can develop 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 discom-
fort is usually not sharp, is not worsened by deep inspira-
tion, 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 dis-
comfort 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 fea-
tures. 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 non-
cardiac surgery (Karve, Bossone, & Mehta. 2007). Older
adults may have atypical symptoms such as dyspnea, shoul-
der 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 shoul-
der 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 dilat-
ing 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 myocar-
dial 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 sub-
stances 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 pres-
ence 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
1he coronary (cardiac) veins travel alongside the arteries.
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 sepa-
rates 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
is benencial that both divisions of the autonomic nervous
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).
SYMPATHETIC ST1MULATION
Sympathetic (accelerator) nerves innervate specific areas of
the heart's electrical system, atrial muscle, and the ventricu-
lar 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 Projac:tlons of Parasympathe11c

nervous system sympathetic parasympathetic nervous system
nervous system nervous 8Y8tem

l...acl'lmal and
..
Eye

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.)

• Increased HR, force of contraction, conduction velocity,
blood pressure, and cardiac output (CO)
• Increased sweating
• Mobilization of stored energy to ensure an adequate sup-
ply 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 differ-
ent organs and have different physiologic actions when stim-
ulated. 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 periph-
eral 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 kid-
neys. 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 produc-
tion of angiotensin, a powerful vasoconstrictor. Beta2
receptor sites are found in the arterioles of the heart,
lungs, and skeletal muscle. Stimulation results in dila-
tion. Beta3 receptor sites are found in fat cells. When
Bllmulllllon
(may re~KJII in fast heart rate)
Excaaaiva accalaralion
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
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 mes-
senger (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 fol-
lowing 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)
 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

SympatheUc Division Parasympathedc Division
General effect Fght or flight Feed and breed; rest and digest
Primary neurotransmitter Norepinephrine, epinephrine Acetylcholine
Effects of stimulation
Abdominal blood vessels Constriction (alpha receptors) No effect
Adrenal medulla Increased secretion of epinephrine No effect
Bronchioles Dilation (beta receptors) Constriction
Blood vessels of skin Constriction (alpha receptors) No effect
Blood vessels of skeletal muscle Dilation (beta receptors) No effect
Cardiac muscle Increased rate and strength of Decreased rate; decreased strength of atrial contrac-
contraction (beta receptors) tion, little effect on strength of ventricular contraction
Coronary blood vessels Constriction (alpha receptors) Dilation
Dilation (beta receptors)

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 contrac-
tility, and speed of conduction through the AV node. 1hese
terms are explained in Box 1.2.

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 myo-
cardial contractility.
• A negative inotropic effect results in a decrease in myo-
cardial contractility.
Dromotropic Effect
• Refers to the speed of conduction through the atrio-
ventricular (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 ven-
tricles. 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
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
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 oxygen-
ated 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 con-
tract 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 cham-
ber: 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
 Chapter 1 Anatomy and Physiology
to fill. The myocardium receives its fresh supply of oxygen-
ated 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 con-
duction 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 extremi-
ties 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 sys-
temic 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'") contrac-
tion describes the brief period between the start of ventric-
ular systole and the opening of the SL valves. During this
period. the ventricular volume remains constant as the pres-
sure 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 capil-
laries. 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 ves-
sel 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 ven-
tricles are relaxed and begin to fill passively with blood. The
cardiac cycle begins again with atrial systole and the comple-
tion 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 ten-
sion in body tissues.
Blood pressure is affected by conditions or medica-
tiona that affect peripheral resistance or CO (Fig. 1.24).
For example, an increase in either CO or peripheral resis-
tance typically results in an increase in blood preasure.
Conversely, a decrease in either will result in a decrease in
blood pressure.
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KUUDESTOISTA LUKU.

Nuoren herra Andrzejn elinvoimainen henki ei halunnut jättää

maallista verhoaan eikä jättänytkään. Kuukauden kuluttua Lubicziin
paluun jälkeen hänen haavansa alkoivat parantua. Jo sitä ennen hän
oli tullut tajuihinsa ja silmäiltyään ympärilleen heti ymmärtänyt, että
hän oli Lubiczissa.

Hän kutsui luokseen uskollisen Sorokan.

— Soroka! — sanoi hän. — Jumala on armahtanut minua! Minä

tunnen, että en kuole!

— Kuten käskette! — vastasi vanha soturi pyyhkien kyynelen

nyrkillään.

Kmicic jatkoi aivan kuin itsekseen:

— Katumuksen aika on lopussa… minä huomaan sen selvästi.

Jumala armahtaa minua!

Sitten hän oli jonkin aikaa vaiti, mutta hänen huulensa liikkuivat,
sillä hän rukoili.

— Soroka! — sanoi hän taas hetkisen kuluttua.

 — Kuten teidän armonne käskee!

— Kuka nyt asuu Wodoktyssa?

— Neiti ja herra miekankantaja Billewicz.

— Kiitetty olkoon Herran nimi! Onko kukaan käynyt kysymässä

vointiani?

— Wodoktysta lähetettiin sitä kysymään siihen asti kun saatiin

tietää, että teidän armonne tervehtyy.

— Ja lakkasivatko he sitten kyselemästä?

— Sitten lakkasivat. Siihen sanoi Kmicic:

— He eivät vielä tiedä mitään, mutta saavat tietää kaiken minun

omasta suustani. Etkö ole sanonut kenellekään, että minä olen
sotinut täällä käyttäen nimeä Babinicz?

— Ei ole käsketty, — vastasi sotamies.

— Eikö herra Wolodyjowski laudalaisten kanssa vielä ole

palannut.

— Ei vielä, mutta heitä odotetaan tuleviksi minä päivänä hyvänsä.

Siihen päättyi heidän ensimmäinen keskustelunsa. Kaksi viikkoa

myöhemmin Kmicic jo oli jalkeilla ja käveli sauvojen varassa, ja
seuraavana sunnuntaina hän itsepintaisesti tahtoi lähteä kirkkoon.

— Mennään Upitaan, — sanoi hän Sorokalle, — sillä ensin on

kiitettävä
Jumalaa, ja sitten messun jälkeen menemme Wodoktyyn.
 Soroka ei uskaltanut väittää vastaan. Hän antoi vain levittää
paksulta heiniä rattaille. Herra Andrzej pukeutui juhlapukuun, ja he
lähtivät matkaan.

Kun he tulivat kirkkoon, oli siellä vielä vähän väkeä. Nojaten

Sorokan käsivarteen Kmicic astui pääalttarin luo ja polvistui
ensimmäiseen penkkiin. Ei kukaan tuntenut häntä, sillä hän oli kovin
muuttunut. Hänen kasvonsa olivat laihtuneet ja riutuneet, ja sitäpaitsi
hän oli sodan ja sairauden aikana parroittunut. Ne, jotka katsoivat
häneen, luulivat häntä joksikin matkustavaksi ylimykseksi, joka oli
poikennut kirkkoon. Seudulla vilisi nimittäin kaikkialla aatelismiehiä,
jotka palasivat sodasta maatiloilleen.

Vähitellen kirkko kuitenkin alkoi täyttyä rahvaasta ja lähiseudun

aatelista. Sitten alkoi tulla tilanomistajia kaukaisemmistakin
seuduista, sillä monessa paikassa oli kirkot poltettu, ja kuullakseen
messun täytyi tulla Upitaan saakka.

Kmicic oli niin syventynyt rukoilemaan, että hän ei nähnyt ketään.

Hurskaista ajatuksistaan hänet herätti vasta penkin narina, kun
siihen tuli ihmisiä.

Silloin hän nosti silmänsä, katsoi ja näki yllään Oleńkan armaat,

mutta surulliset kasvot.

Tyttökin näki hänet ja tunsi hänet heti, sillä hän hätkähti ja

peräytyi. Hänen kasvonsa punehtuivat ensin, mutta tulivat sitten
kalmankalpeiksi. Suurella tahdonponnistuksella hän kuitenkin voitti
liikutuksensa ja polvistui Kmicicin viereen. Kolmanneksi sijoittui
miekankantaja.
 Sekä Kmicic että tyttö painoivat alas päänsä ja peittivät kasvonsa
käsiinsä. Äänettöminä he olivat polvillaan vieretysten, mutta
kummankin sydän löi niin kiivaasti, että he kuulivat sen selvästi.
Viimein lausui herra Andrzej:

— Ylistetty olkoon Jeesus Kristus!

— Iankaikkisesta iankaikkiseen…, — vastasi Oleńka puoliääneen.

Sen jälkeen he eivät sanoneet enää mitään toisilleen.

Sillä välin oli pappi noussut saarnastuoliin. Kmicic koetti kuunnella

häntä, mutta ei ponnistuksistaan huolimatta ymmärtänyt mitään.
Hänen vierellään oli nyt tuo armas, jonka luo hän oli jo vuosikausia
ikävöinyt, joka aina oli ollut hänen ajatuksissaan ja sydämessään.
Hän tunsi hänet läheisyydessään, mutta ei uskaltanut kääntää
häneen silmiään, koska oltiin kirkossa. Sulkien silmänsä hän koetti
kuunnella hänen hengitystään…

— Oleńka! Oleńka on luonani! — sanoi hän itsekseen. — Jumala

antoi meidän yhtyä kirkossa…

Ja hänen sydämensä ja ajatuksensa toistelivat yhtämittaa tuota

nimeä:

— Oleńka! Oleńka! Oleńka!

Väliin hän oli purskahtaa itkuun ilosta, väliin taas hänet valtasi
sellainen kiitollisuuden tunne, että hän tuskin tiesi, mitä hänen
ympärillään tapahtui.

Oleńka oli edelleen polvillaan kasvot peitettyinä käsiin.

 Pappi lopetti saarnansa ja astui alas saarnastuolista.

Silloin kuului äkkiä kirkon edustalta aseitten kalinaa ja kavioitten

kapsetta. Joku huudahti kirkon ovella: "Laudalaiset tulevat!" — ja
sitten alkoi kirkossa kuulua äänten sorinaa, joka kohta muuttui
huudoksi:

— Lauda! Lauda!

Kansanjoukko alkoi liikkua, ja kaikkien päät kääntyivät oveen päin.

Ovessa näkyi ihmisvilinää, ja joukko aseellisia miehiä tuli kirkkoon.

Etunenässä kulkivat herra Wolodyjowski ja herra Zagloba kannukset
kilisten. Väkijoukko antoi heille tietä, ja he kulkivat läpi koko kirkon,
polvistuivat alttarin eteen ja rukoilivat lyhyen rukouksen, minkä
jälkeen molemmat menivät sakaristoon.

Laudalaiset jäivät kirkon keskelle. He olivat ääneti, ja paikan

pyhyys esti tervehtimästä ketään.

Mikä näky tuo olikaan! Tuimia kasvoja, jotka olivat ahavoittuneet

ulkoilmassa, riutuneet sodan vaivoissa ja saaneet merkkejä
ruotsalaisten, saksalaisten, unkarilaisten ja valakialaisten sapelien
iskuista. Koko sodan ja uskollisen Laudan historia oli niihin miekoin
kirjoitettu. Siinä oli juroja Butrymeja, Stakjaneja, Domaszewiczeja,
Gosciewiczeja, kaikki edustamassa useampia suvun jäseniä. Mutta
tuskin neljäs osa palasi niistä, jotka olivat aikoinaan lähteneet
Laudasta Wolodyjowskin johdolla.

Monet naiset etsivät joukosta turhaan miehiään, monet vanhukset

etsivät turhaan poikiaan. Itkua on kaikkialla, sillä nekin, jotka löytävät
omansa, itkevät, joskin ilosta. Koko kirkko kaikuu nyyhkytyksistä.
Silloin tällöin joku mainitsee ääneen jonkin rakkaan nimen, mutta
vaikenee sitten yht'äkkiä. Kotiin tulleet seisovat kunnian loisteessa,
miekkoihinsa nojaten, ja heidänkin tuimilla kasvoillaan vierii
kyyneleitä tuuheihin viiksiin.

Kellon kilinä sakariston ovelta sai nyyhkytykset ja äänten sorinan

vaikenemaan. Kaikki polvistuivat. Pappi astui esille messupuvussa ja
hänen mukanaan Wolodyjowski ja Zagloba, ja messu alkoi.

Mutta pappikin oli liikutettu, ja kun hän ensimmäisen kerran

kääntyi kansan puoleen lausuen: Dominus vobiscum! niin hänen
äänensä värähti. Mutta kun hän pääsi evankeliumiin saakka ja kaikki
sapelit yht'äkkiä paljastettiin merkiksi, että Lauda aina on valmis
puolustamaan uskoa, saattoi hän tuskin hillitä liikutustaan.

Mitä suurimman hartauden vallitessa sitten messu suoritettiin

loppuun. Mutta pantuaan sakramentin ciboriumiin pappi toimituksen
päätyttyä taas kääntyi seurakunnan puoleen ja teki merkin, että
hänellä oli vielä puhuttavaa.

Syntyi hiljaisuus. Pappi tervehti ensin sydämellisin sanoin kotiin

palanneita sotilaita ja ilmoitti lopuksi, että laudalaisen rykmentin
päällikön mukanaan tuoma kuninkaan kirje nyt luetaan.

Syntyi entistä syvempi hiljaisuus, ja hetken kuluttua kaikui alttarilta

yli koko kirkon kuuluva ääni:

"Me Jan Kasimir, Puolan kuningas, Liettuan, Masowian ja

Preussin
suuriruhtinas etc. etc. etc. Nimeen Isän, Pojan ja Pyhän Hengen,
amen.
 "Niinkuin pahain ihmisten rikolliset teot Majesteettia ja Isänmaata
vastaan jo täällä ajassa saavat rangaistuksensa, ennenkuin ne
joutuvat taivaallisen tuomioistuimen eteen, samoin on myös
kohtuullista, että hyve ei jää vaille palkintoa, joka kohottaa itse
hyveen kunniaan ja antaa jälkeentulevaisille intoa seurata hyviä
esimerkkejä.

"Tästä syystä Me teemme tiettäväksi koko ritaristolle ja

nimenomaan sotilas- ja siviilivirkojen haltijoille, cujusvis dignitatis et
praeeminentiae, samoinkuin kaikille Liettuan suuriruhtinaskunnan
ja Samogitian staarostakunnan asujamille, että ne gravamina, jotka
ovat haitanneet jalosukuisen, Meille rakkaan herra Andrzej Kmicicin
mainetta, nyt hänen myöhempien ansioittensa ja loistavien
tekojensa takia on ihmisten muistista poistettava, jotta hänen
kunniansa ja maineensa esiintyisi täysin vähentämättömänä."

Tässä pappi keskeytti lukemisensa ja katsahti penkkiin, jossa

Kmicic istui. Tämä nousi seisomaan, mutta istuutui taas samassa ja
nojasi päätään penkin laitaan aivan kuin olisi menemäisillään
tainnoksiin.

Kaikkien katseet kääntyivät häneen, kaikki alkoivat kuiskailla:

— Herra Kmicic! Kmicic! Kmicic! Tuolla, Billewiczien vieressä!

Mutta pappi antoi merkin kädellään ja jatkoi syvän äänettömyyden

vallitessa:

"Vaikka mainittu herra Andrzej Kmicic tosin onnettoman

ruotsalaisen sodan alussa oli ruhtinaan puolella, niin hän ei
kuitenkaan tehnyt sitä yksityisiä etuja tavoitellen, vaan
isänmaallisista vaikuttimista, sillä samainen ruhtinas oli johtanut
hänet harhaan vakuuttamalla hänelle vilpillisesti, että vain ruhtinaan
valitsemaa eikä mitään muuta tietä käyttäen salus reipublicae oli
saavutettavissa.

"Ruhtinas Boguslaw, luullen häntä palkatuksi kätyriksi, ilmaisi

hänelle kaikki Radziwillien häpeälliset suunnitelmat isänmaata
vastaan ja on sittemmin syyttänyt mainittua herra Kmiciciä siitä,
että tämä muka olisi tarjoutunut kohottamaan kätensä Meidän
persoonaamme vastaan. Mutta tämä syytös on valheellinen, ja
herra Kmicic päinvastoin asevoimin otti ruhtinaan itsensä kiinni
kostaakseen Meidän ja onnettoman isänmaan puolesta…"

— Jumala! Armahda minua syntistä! — huusi naisen ääni aivan

herra
Andrzejn vieressä, ja läpi kirkon kuului taas hämmästyksen sorina.

Pappi luki edelleen:

"Tämän saman ruhtinaan haavoittamana hän heti tervehdyttyään

meni Częstochowoon ja puolusti siellä oman henkensä uhalla
pyhää paikkaa ollen kaikille esimerkkinä sitkeydessä ja
rohkeudessa. Siellä hän mitä suurimpaan vaaraan antautuen
räjähdytti rikki vihollisen suurimman piiritystykin, jota uhkarohkeata
tekoa suorittaessaan hän joutui vangiksi ja tuomittiin julmaan
kuolemanrangaistukseen, minkä edellä häntä poltettiin tulella…"

Eri puolilta kirkkoa alkoi kuulua naisten itkua. Oleńka vapisi aivan
kuin kuumeessa.

"Mutta pelastuttuaan taivaallisen kuningattaren kautta näistäkin

suurista vaaroista hän tuli Meidän luoksemme Sleesiaan, ja kun
palatessamme rakkaaseen isänmaahamme petollinen vihollinen
yllättäen hyökkäsi Meidän kimppuumme, niin mainittu herra Kmicic
vain kolmen miehen kanssa hyökkäsi koko vihollisjoukon kimppuun
ja pelasti Meidän henkemme. Pahasti haavoittuneena ja
vertavuotavana hänet melkein hengettömänä tuotiin
taistelukentältä…"

Oleńka painoi molemmin käsin ohimoitaan, nosti päänsä ja

hengitti raskaasti. Hänen rinnastaan kohosi vaikerrus:

— Oi Jumala! Jumala! Jumala!

Ja taas kaikui papin ääni, sekin yhä suurempaa liikutusta

ilmaisten:

"Kun hän huolellisen hoidon avulla tervehtyi, niin hän ei

vieläkään suonut itselleen lepoa, vaan jatkoi sotimista hankkien
itselleen katoamattoman kunnian, niin että molempien
kansakuntien hetmanit mainitsivat häntä esikuvana ritareille. Näin
hän taisteli Varsovan valloitukseen asti, minkä jälkeen hän lähti
Preussiin käyttäen nimeä Babinicz."

Kun tämä nimi mainittiin, muuttui äänten sorina kirkossa myrskyn

pauhun kaltaiseksi. Hän siis oli Babinicz! Tuo ruotsalaisten kauhu,
Wolmontowiczin pelastaja, niin monen taistelun voittaja oli siis
Kmicic! Äänten sorina kasvoi yhä, ja väkijoukko alkoi painautua
alttaria kohti nähdäkseen hänet paremmin.

— Jumala siunatkoon häntä! Jumala siunatkoon häntä! —

kaikuivat sadat äänet.

Pappi kääntyi penkkiin päin ja tehden ristinmerkin siunasi

Kmiciciä, joka yhä edelleen nojasi penkin laitaa vastaan ja oli
enemmän kuolleen kuin elävän kaltainen, sillä onni riisti hänen
sielunsa irti ruumiista ja kohotti sen taivaaseen.

Sitten pappi luki vielä:

"Siellä hän hävitti vihollisen maata tulella ja miekalla, vaikutti

tehokkaasti voiton saamiseen Prostkin luona, voitti ja vangitsi omin
käsin ruhtinas Boguslawin. Lähetettynä senjälkeen Samogitiaan
hän teki meille verrattomia palveluksia. Miten monta kaupunkia ja
kylää hän on suojellut viholliselta, sen tietävät parhaiten sikäläiset
incolae."

— Tiedämme! Tiedämme! — kaikui kaikilta puolilta.

— Hiljaa! — sanoi pappi kohottaen ylös kuninkaan kirjeen. Ja hän

luki vielä:

"Tämän vuoksi Me ottaen huomioon hänen kaikki Meille ja

isänmaalle tekemänsä palvelukset, jotka ovat niin suuret, että poika
ei voisi tehdä isälleen ja äidilleen suurempia, olemme päättäneet
julistaa hänen ansionsa tässä kirjeessämme, jotta niin jalon ritarin
sekä uskon, Majesteetin ja valtakunnan puolustajan ei tarvitsisi
enää kärsiä ihmisten nurjamielisyyttä, vaan hän saisi nauttia
ansaitsemaansa kunnioitusta ja rakkautta. Ennenkuin valtiopäivät
tämän lausumamme tahdon mukaisesti vapauttavat hänet kaikesta
syyllisyydestä ja ennenkuin Me voimme palkita häntä Upitan
staarostan viralla, joka vacat, pyydämme kaikkia sydämellemme
rakkaita Samogitian asukkaita säilyttämään mielessään ja
sydämessään nämä sanamme, jotka justitia, fundamentum
regnorum on pakottanut Meidät tietoonne saattamaan."
 Pappi lopetti, kääntyi alttariin päin ja alkoi rukoilla. Kmicic tunsi
äkkiä, että pehmoinen pieni käsi tarttui hänen käteensä. Hän kohotti
katseensa. Oleńka oli, ennenkuin hän ennätti vetää kätensä pois,
kohottanut sen huulilleen kaikkien nähden.

— Oleńka! — huudahti Kmicic hämmästyneenä.

Mutta tyttö nousi, veti harson kasvojensa eteen ja sanoi

miekankantajalle:

— Setä! Menkäämme! Menkäämme heti!

He poistuivat sakariston oven kautta.

Herra Andrzej koetti nousta mennäkseen hänen jälkeensä, mutta

ei voinut. Hänen voimansa olivat aivan lopussa.

Neljännestuntia myöhemmin hän kuitenkin oli kirkon edessä

Wolodyjowskin ja Zagloban tukemana.

Sankat joukot aatelia ja rahvasta keräytyi heidän ympärilleen.

Naiset irtautuivat kotiinpalanneitten miestensä syleilystä ja juoksivat
sukupuolelleen ominaisella uteliaisuudella katselemaan tuota
aikoinaan niin peloittavaa Kmiciciä, joka nyt oli Laudan pelastaja ja
tuleva staarosta. Piiri tuli yhä sankemmaksi, niin että laudalaisten
lopulta täytyi asettua hänen ympärilleen ja suojella häntä
tunkeilijoilta.

— Herra Andrzej! — huusi Zagloba. — Emmekö tuoneetkin teille

hyviä tuomisia? Ette itsekään osannut sellaisia aavistaa! Mennäänpä
nyt Wodoktyyn! Wodoktyyn kihlajaisiin ja häihin!
 Zagloban puheen jatko hukkui voimakkaaseen eläköönhuutoon,
jonka kaikki laudalaiset Jozwa Jalattoman johdolla kohottivat:

— Eläköön herra Kmicic!

— Eläköön! — toisti väkijoukko. — Eläköön Upitan staarosta!

Eläköön!

— Wodoktyyn kaikki! — huusi taas Zagloba.

— Wodoktyyn! Wodoktyyn! — huusi tuhat ääntä. — Wodoktyyn

kosimaan yhdessä herra Kmicicin, pelastajamme kanssa! Neidin luo!
Wodoktyyn!

Syntyi vilkasta liikettä. Laudalaiset nousivat ratsujen selkään.

Väkijoukosta kaikki, kutka kynnelle kykenivät, asettuivat kaikkiin
mahdollisiin ajopeleinä. Jalkamiehet oikaisivat läpi metsien ja yli
peltojen. Kaikkialla kauppalassa kaikui huuto:

"Wodoktyyn!" Tiet täyttyivät kaikenkarvaisista ihmisistä.

Kmicic ajoi vaunuissa Wolodyjowskin ja Zagloban välissä ja syleili

heitä vuorotellen. Hän oli vielä liian liikutettu voidakseen puhua, ja
sitäpaitsi he ajoivat niin hurjaa vauhtia kuin tataarilaiset olisivat
hyökänneet Upitaan. Muut ajopelit seurasivat aivan heidän
jäljessään.

Zagloba lauleli iloissaan niin jyrisevällä bassoäänellä, että hevoset

pelkäsivät:

— Kaksi oli meitä, Kasienka, maailmassa,

mutta nyt tuntuu kuin ois kolmas saapumassa!
 Anusia ei ollut sinä sunnuntaina kirkossa, sillä hänen oli täytynyt
jäädä sairaan neiti Kulwiecin luo, jonka vuoteen ääressä hän ja
Oleńka vuorotellen valvoivat.

Koko aamu oli mennyt sairaan hoitelemiseen, ja varsin myöhään

Anusia ennätti ryhtyä lukemaan rukouksiaan.

Tuskin hän oli lausunut viimeisen amenen, kun portilta kuului

ratinaa ja Oleńka syöksyi huoneeseen.

— Jeesus! Maria! Mitä on tapahtunut? — huudahti Anusia

nähtyään hänet.

— Anusia! Tiedätkö, kuka Babinicz on?… Se on Kmicic!

Anusia hypähti pystyyn.

— Kuka on sinulle sanonut sen?

— Luettiin kuninkaan kirje… Herra Wolodyjowski toi sen…

Laudalaiset…

— Onko siis herra Wolodyjowski tullut takaisin? — huudahti

Anusia.

Ja hän heittäytyi äkkiä Oleńkan syliin.

Oleńka piti tätä tunteenpurkausta ystävyyden osoituksena

kohtaansa. Hän oli aivan kuin kuumeessa ja poissa suunniltaan.
Hänen kasvonsa hehkuivat ja rinta kohoili, kuin hän olisi juossut
pitkän matkan.

Hän alkoi kertoa sekavasti ja katkonaisella äänellä kaikesta, mitä

kirkossa oli tapahtunut, samalla kuin hän liikehti kuin hurjistunut
huoneessa ja toisteli vähän väliä: "Minä en ole hänen arvoisensa!"
Hän moitti itseään ankarasti siitä, että hän oli pahemmin kuin kukaan
muu tehnyt Kmicicille vääryyttä eikä edes ollut tahtonut rukoilla
hänen puolestaan silloin, kun Kmicic oli vuodattanut vertaan Pyhän
Neitsyen, isänmaan ja kuninkaan puolesta.

Turhaan koetti Anusia lohduttaa häntä. Oleńka toisteli yhä vain,

että hän ei ollut Kmicicin arvoinen ja että hän ei uskaltaisi katsoa tätä
silmiin. Sitten hän taas alkoi kertoa Babiniczin teoista, Boguslawin
kiinniottamisesta, tämän kostosta, kuninkaan hengen
pelastamisesta, Prostkista ja Wolmontowiczista ja Częstochowosta,
mutta lopuksi taas omasta syyllisyydestään ja kovuudestaan, jota
hänen oli kaduttava luostarissa.

Hänen itsesyyttelynsä keskeytti herra Tomasz, joka lensi kuin

pommi huoneeseen ja huudahti:

— Kautta Jumalan! Koko Upita on tulossa meille! He ovat jo

kylässä, ja
Babinicz on aivan varmaan mukana!

Hetken kuluttua ilmaisivat kauempaa kuuluvat huudot, että suuri

ihmisjoukko oli tulossa. Miekankantaja antoi Oleńkalle käsivartensa
ja vei hänet kuistille. Anusia seurasi heidän jäljessään.

Niin pitkälle kuin silmä kantoi oli tie mustanaan tulijoita. He

saapuivat viimein pihalle. Jalkamiehet ryntäsivät yli juoksuhaudan ja
aidan. Ajopelit kasaantuivat portin edustalle. Kaikki huusivat ja
heittelivät lakkejaan ilmaan.

Viimein saapui asestettu laudalaisten joukko keskellään vaunut,

joissa istui kolme miestä: herra Kmicic, herra Wolodyjowski ja herra
Zagloba.

Vaunut pysähtyivät hiukan syrjään, sillä oven edustalla tunkeili niin

paljon väkeä, että sinne ei voinut päästä. Zagloba ja Wolodyjowski
hyppäsivät ensin vaunuista ja auttoivat niistä sitten ulos Kmicicin,
ottaen hänet väliinsä.

— Väistykää! — huusi Zagloba.

— Väistykää! — toistivat laudalaiset.

Väki jakaantui heti kahteen joukkoon, niin että keskelle muodostui

kuja, jota pitkin molemmat ritarit taluttivat Kmicicin ovelle saakka.
Kmicic nojasi raskaasti kumpaankin saattajaansa ja oli hyvin kalpea,
mutta hänen päänsä oli pystyssä, ja hän oli samalla kertaa sekä
hämillään että onnellinen.

Oleńka seisoi nojaten ovea vastaan, ja hänen kätensä riippuivat

hervottomina. Mutta kun Kmicic oli jo lähellä ja kun tyttö katsoi hänen
kasvojaan, jotka olivat riutuneet ja kalpeat, alkoi hän nyyhkyttää.
Kmicic oli onnellinen, mutta samalla niin heikko ja hämmentynyt, että
hän ei tietänyt mitä sanoisi. Hän astui ovelle ja lausui vain
katkonaisella äänellä:

— No, Oleńka? Mitä?…

Tyttö lankesi äkkiä polvilleen hänen eteensä.

— Andrzej! Minä en ole kyllin arvokas suutelemaan sinun

haavojasi!

Mutta silloin ritari silmänräpäyksessä sai jälleen entisen voimansa.

Hän nosti tytön ilmaan kevyesti kuin höyhenen ja painoi hänet
rintaansa vastaan.

Niin voimakas huuto, että se sai talon seinät tärisemään ja

viimeisetkin lehdet varisemaan puista, kohosi ilmoille. Laudalaiset
alkoivat ammuskella musketeillaan, lakit lensivät ilmaan, ympärillä
näkyi vain iloa säteileviä kasvoja, säihkyviä silmiä ja avoimia suita,
jotka huutelivat:

— Vivat Kmicic! Vivat neiti Billewicz! Vivat nuori pari!

— Vivat kaksi nuorta paria! — huusi Zagloba. Mutta hänen

äänensä hukkui yleiseen meluun.

Wodokty muuttui kuin sotaleiriksi. Kaiken päivää teurastettiin

miekankantajan käskystä lampaita ja härkiä sekä kaivettiin maasta
esille olut- ja simatynnyreitä. Illalla alkoivat pidot. Vanhemmat ja
arvokkaimmat henkilöt istuivat sisällä huoneessa, nuoremmat
palvelusväen puolella, rahvas piti hauskaa nuotioitten ääressä
pihalla.

Pääpöydässä juotiin ahkerasti kahden onnellisen parin maljoja.

Viimein, kun innostus oli noussut korkeimmilleen, esitti herra
Zagloba vielä seuraavan maljan:

— Teidän puoleenne käännyn, jalo herra Andrzej, ja teidän

puoleenne, vanha ystäväni herra Michal! Ei riitä vielä se, että olette
panneet alttiiksi henkenne, vuodattaneet vertanne, voittaneet
vihollisen. Teidän tehtävänne ei ole vielä lopussa, sillä koska paljon
ihmisiä on tässä kauheassa sodassa kaatunut, täytyy teidän nyt
hankkia tälle rakkaalle valtakunnalle uusia kansalaisia, uusia
puolustajia, mihin toivoakseni teiltä ei puutu halua eikä rohkeutta!
Hyvät herrat! Noitten tulevien sukupolvien malja! Jumala siunatkoon
heitä ja sallikoon heidän säilyttää sen perinnön, jonka olemme
hankkineet työllämme, hiellämme ja verellämme ja jonka heille
jätämme. Muistakoot he meitä, kun vaikeat ajat tulevat, älköötkä
koskaan joutuko epätoivoon, vaan ymmärtäkööt, että ei ole sellaista
tilannetta, josta ei viribus unitis Jumalan avulla voisi selviytyä!

*****

Kohta häitten jälkeen herra Andrzej lähti uuteen sotaan, joka oli
syttynyt valtakunnan itärajalla. Mutta Czarnieckin ja Sapiehan
loistavat voitot Chowanskista ja Dolgorukista sekä hetmanien voitot
Szeremetistä lopettivat sodan lyhyeen. Silloin Kmicic niitettyään
uutta kunniaa palasi kotiin ja asettui pysyväisesti Wodoktyyn. Hän
sai palkinnoksi kuninkaalta Upitan staarostakunnan ja eli korkeaan
ikään hyvässä sovussa laudalaisten kanssa ja kaikkien
kunnioittamana. Panettelijat (ja kenelläpä ei niitä olisi?) väittivät
tosin, että hän kaikessa liiaksi totteli vaimoaan, mutta hän ei sitä
hävennyt, vaan tunnusti itse, että hän aina kaikissa tärkeissä
asioissa kysyi neuvoa vaimoltaan.
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