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LIPPINCOTT MANUAL
of NURSING PRACTICE
Series
PATHOPHYSIOLOGY
◆
Philadelphia • Baltimore • New York • London
Buenos Aires • Hong Kong • Sydney • Tokyo
6636 FM.qxd 8/19/08 8:28 PM Page ii
STAFF The clinical treatments described and recom-
mended in this publication are based on re-
Executive Publisher search and consultation with nursing, medical,
Judith A. Schilling McCann, RN, MSN and legal authorities. To the best of our
knowledge, these procedures reflect currently
Editorial Director
accepted practice. Nevertheless, they can’t be
H. Nancy Holmes
considered absolute and universal recommen-
Clinical Director dations. For individual applications, all recom-
mendations must be considered in light of the
Joan M. Robinson, RN, MSN
patient’s clinical condition and, before admin-
Senior Art Director istration of new or infrequently used drugs, in
Arlene Putterman light of the latest package-insert information.
The authors and publisher disclaim any re-
Clinical Manager sponsibility for any adverse effects resulting
Eileen Cassin Gallen, RN, BSN from the suggested procedures, from any un-
detected errors, or from the reader’s misunder-
Editorial Project Manager
standing of the text.
Jennifer Lynn Kowalak
© 2007 by Lippincott Williams & Wilkins. All
Editor
rights reserved. This book is protected by
Julie Munden
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Includes bibliographical references and index.
BethJ.Welsh
1. Nursing—Handbooks, manuals, etc. 2.
Editorial Assistants Physiology, Pathological—Handbooks, manuals,
etc. I. Lippincott Williams & Wilkins. II. Title.
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III. Series.
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Design Assistant
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RT51.P32 2007
Indexer 616.07'5—dc22
ISBN13: 978-1-58255-663-5
Barbara Hodgson
ISBN10: 1-58255-663-6 (alk. paper) 2005030653
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CONTENTS
◆
Contributors and consultants v
1 Cardiovascular system 1
2 Respiratory system 84
3 Nervous system 129
4 Gastrointestinal system 189
5 Renal system 228
6 Endocrine system 262
7 Hematologic system 289
8 Immune system 308
9 Sensory system 336
10 Integumentary system 351
11 Musculoskeletal system 370
12 Reproductive system 402
13 Cancer 417
14 Fluids and electrolytes 447
15 Genetics 481
16 Infection 501
Selected references 523
Index 527
iii
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CONTRIBUTORS AND
CONSULTANTS
◆
Gary J. Arnold, MD Shirley Lyon Garcia, RN, BSN
Associate Professor Nursing Program Director, PNE
College of Nursing and Allied Health McDowell Technical Community College
Professions Marion, N.C.
University of Louisiana at Lafayette
Charla K. Hollin, RN, BSN
Cheryl A. Bean, APRN,BC, DSN, ANP, Nursing Program Director
AOCN Rich Mountain Community College
Associate Professor/Adult Nurse Practitioner Mena, Ark.
Indiana University School of Nursing
Indianapolis Shelley Yerger Huffstutler, RN, DSN,
CFNP, GNP
Mary Ann Boucher, APRN,BC, ND Associate Professor and Director, FNP Program
Assistant Professor of Nursing University of Alabama at Birmingham
University of Massachusetts Dartmouth School of Nursing
Peggy Bozarth, RN, MSN Mary T. Kowalski, RN, BA, MSN
Professor Director Vocational Nursing and Health Career
Hopkinsville (Ky.) Community College Programs
Cerro Coso Community College
Janie Choate, PA-C, MAT, BS, BA Ridgecrest, Calif.
Adjunct Faculty
University of the Sciences Grace G. Lewis, RN, MS, BC
Philadelphia Assistant Professor of Nursing
Georgia Baptist College of Nursing of
Laura M. Criddle, RN, MS, CCNS, CEN Mercer University
Doctoral Student Atlanta
Oregon Health & Science University
Portland Patricia J. McBride, RN, MSN, CIC
Infection Control Manager
Diane Dixon, PA-C, MA, MMSc Bryn Mawr (Pa.) Hospital
Assistant Professor and Academic Coordinator
University of South Alabama Cynthia A. Prows, RN, MSN, CNS
Department of Physician Assistant Studies Clinical Nurse Specialist
Mobile Children’s Hospital Medical Center
Cincinnati
v
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Betty E. Sims, RN, MSN
Nurse Consultant
Board of Nurse Examiners
Austin, Tex.
Adjunct Instructor
St. Philip’s College
San Antonio, Tex.
Sheryl Thomas, RN, MSN
Nurse Instructor
Wayne County Community College
Detroit
Dan Vetrosky, PA-C, MEd, PhD(c)
Assistant Professor
University of South Alabama
Mobile
Colleen R. Walsh, RN, MSN, ACNP-BC,
CS, ONC
Faculty, Graduate Nursing
University of Southern Indiana School of
Nursing & Health Professions
Evansville
vi CONTRIBUTORS AND CONSULTANTS
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1
CCAARRDDIIOOVVAASSCCUULLAARR
SSYYSSTTEEMM
Life-threatening
The cardiovascular system begins its
activity when the fetus is barely 1
Acute coronary
month old, and it’s the last system to
cease activity at the end of life. The syndromes
heart, arteries, veins, and lymphatics ◆
make up this system. These structures
transport life-supporting oxygen and Acute myocardial infarction (MI),
nutrients to cells, remove metabolic ST-segment elevation MI (STEMI),
waste products, and carry hormones non-ST-segment elevation MI (NSTE-
from one part of the body to another. MI), and unstable angina are now rec-
Circulation requires normal heart ognized as a part of a group of clinical
function, which propels blood disorders known as acute coronary
through the system by continuous syndromes (ACSs).
rhythmic contractions. In cardiovascular disease, death
Despite advances in disease detec- usually results from cardiac damage or
tion and treatment, cardiovascular dis- complications of MI—the leading
ease remains the leading cause of cause of death in the United States
death in the United States. The cardio- and Western Europe. Each year, ap-
vascular disorders covered in this proximately 900,000 people in the
chapter include acute coronary syn- United States experience MI. Mortali-
dromes, arterial occlusive disease, atri- ty is high when treatment is delayed,
al septal defect, cardiac arrhythmias, and almost one-half of sudden deaths
cardiac tamponade, cardiomyopathy, due to MI occur before hospitaliza-
coarctation of the aorta, endocarditis, tion, within 1 hour of the onset of
heart failure, hypertension, patent symptoms. The prognosis improves if
ductus arteriosus, pericarditis, Ray- vigorous treatment begins immediate-
naud’s disease, rheumatic fever and ly.
rheumatic heart disease, shock, tetral-
ogy of Fallot, transposition of the CAUSES
●
great arteries, valvular heart disease, Aging
●
and ventricular septal defect. Drug use, especially cocaine and
amphetamines
1
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●
Elevated serum triglyceride, total Three stages occur when a vessel is
cholesterol, and low-density lipopro- occluded: ischemia, injury, and infarct.
●
tein levels Ischemia occurs first. It indicates
●
Excessive intake of saturated fats that blood flow and oxygen demand
●
Gender (Men and postmenopausal are out of balance. Ischemia can be re-
women are more susceptible to MI solved by improving flow or reducing
than premenopausal women, al- oxygen needs. Electrocardiogram
though the incidence is increasing (ECG) changes indicate ST-segment
among women, especially those who depression or T-wave changes.
●
smoke and take hormonal contracep- Injury is the next stage. This occurs
tives.) when the ischemia is prolonged
●
Hypertension enough to damage the area of the
●
Obesity heart. ECG changes usually reveal
●
Positive family history ST-segment elevation (usually in two
●
Sedentary lifestyle or more contiguous leads).
● ●
Smoking In infarct, the third stage, actual
●
Stress or type A personality death of the myocardial cells has oc-
curred. ECG changes reveal abnormal
PATHOPHYSIOLOGY Q waves. The Q waves are considered
Rupture or erosion of plaque—an un- abnormal when they appear greater
stable and lipid-rich substance—initi- than or equal to 0.04 second wide and
ates all coronary syndromes. The rup- their height is greater than 25% of the
ture results in platelet adhesions, fib- R wave in height in that lead. Most
rin clot formation, and activation of patients with ST-segment elevation
thrombin. will develop Q-wave MI. (See Zones of
Early thrombus doesn’t necessarily myocardial infarction.)
block coronary blood flow. When the Although ischemia begins immedi-
thrombus progresses and occludes ately, the size of the infarct can be lim-
blood flow, an ACS results. The de- ited if circulation is restored within 6
gree of blockage and the time that the hours.
affected vessel remains occluded are Several changes occur after MI.
major determinants for the type of in- Cardiac enzymes and proteins are re-
farction that occurs. leased by the infarcted myocardial
For patients with unstable angina, cells, which are used in the diagnosis
a thrombus partially occludes a coro- of an MI. Within 24 hours, the infarct-
nary vessel. This thrombus is full of ed muscle becomes edematous and
platelets. The partially occluded vessel cyanotic. During the next several
may have distal microthrombi that days, leukocytes infiltrate the necrotic
cause necrosis in some myocytes. The area and begin to remove necrotic
smaller vessels infarct, and patients are cells, thinning the ventricular wall.
at higher risk for MI. These patients Scar formation begins by the third
may progress to an NSTEMI. week after MI, and by the sixth week,
If a thrombus fully occludes the scar tissue is well established.
vessel for a prolonged time, this is The scar tissue that forms on the
known as an STEMI. In this type of necrotic area inhibits contractility.
MI, there’s a greater concentration of When this occurs, the compensatory
thrombin and fibrin. mechanisms (vascular constriction, in-
2 CARDIOVASCULAR SYSTEM
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Focus in
ZONES OF
MYOCARDIAL INFARCTION
Myocardial infarction has a central area of necrosis surrounded by a zone of injury that may
recover if revascularization occurs.This zone of injury is surrounded by an outer ring of re-
versible ischemia.Characteristic electrocardiographic changes are associated with each
zone.
Myocardial
ischemia
◆T-wave
inversion
◆ST-segment
depression
Myocardial
injury
◆ST-segment
elevation
◆T-wave
inversion
Myocardial
infarction
◆Q waves
◆ST-segment
elevation
◆T-wave
inversion
creased heart rate, and renal retention CLINICAL FINDINGS
●
of sodium and water) try to maintain Persistent, crushing substernal
cardiac output. Ventricular dilation chest pain that may radiate to the left
may also occur in a process called re- arm, jaw, neck, or shoulder blades
modeling. Functionally, an MI may caused by reduced oxygen supply to
cause reduced contractility with ab- the myocardial cells (It may be de-
normal wall motion, altered left ven- scribed as heavy, squeezing, or crush-
tricular compliance, reduced stroke ing.)
volume, reduced ejection fraction, and Alert Women may experience typ-
elevated left ventricular end-diastolic ical chest pain with acute ischemia
pressure. and MI, but women and occasionally men,
elderly people, and patients with diabetes
may also experience atypical chest pain.
Atypical symptoms include upper back dis-
ACUTE CORONARY SYNDROMES 3
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by pain fibers or from vasovagal re-
PINPOINTING flexes
●
Shortness of breath and crackles re-
MYOCARDIAL
flecting heart failure
INFARCTION ●
Low-grade temperature in the days
Depending on the location,ischemia or following acute MI due to the inflam-
infarction causes changes in specific elec- matory response
trocardiographic leads. ●
Jugular vein distention reflecting
TYPESOF LEADS right ventricular dysfunction and pul-
monary congestion
MYOCARDIAL
●
INFARCTION S3and S4reflecting ventricular dys-
function
Inferior II,III,aV ● Loud holosystolic murmur in apex,
F
possibly caused by papillary muscle
Anterior V3,V4 rupture
●
Reduced urine output secondary to
Septal V,V
1 2 reduced renal perfusion and increased
Lateral I,aV V,V aldosterone and antidiuretic hormone
L 5 6
Anterolateral I,aVL,V3to V6 TEST RESULTS
●
Serial 12-lead ECG may reveal
Posterior V or V
1 2 characteristic changes, such as serial
Right ventricular V to V ST-segment depression in NSTEMI (a
1R 4R
more limited area of damage insuffi-
cient to cause changes in the pattern
of ventricular depolarization) and
comfort between the shoulder blades, palpi- ST-segment elevation in STEMI (a
tations, feeling of fullness in the neck, nau- larger area of damage, which causes
sea, abdominal discomfort, dizziness, unex- permanent change in the pattern of
plained fatigue, and exhaustion or shortness ventricular depolarization). An ECG
of breath. can also identify the location of MI,
●
Cool extremities, perspiration, anx- arrhythmias, hypertrophy, and peri-
iety, and restlessness due to the re- carditis. (See Pinpointing myocardial in-
lease of catecholamines farction.)
● ●
Blood pressure and pulse initially Serial cardiac enzymes and pro-
elevated resulting from sympathetic teins may show a characteristic rise
nervous system activation (If cardiac and fall, specifically CK-MB, the pro-
output is reduced, blood pressure may teins troponin T and I, and myoglo-
fall. Bradycardia may be associated bin, to confirm the diagnosis of MI.
●
with conduction disturbances, partic- Laboratory testing may reveal
ularly with damage to the inferior wall elevated white blood cell count,
of the left ventricle.) C-reactive protein level, and erythro-
●
Fatigue and weakness caused by cyte sedimentation rate due to inflam-
reduced perfusion to skeletal muscles mation, and increased glucose levels
●
Nausea and vomiting as a result of following the release of catechola-
reflex stimulation of vomiting centers mines.
4 CARDIOVASCULAR SYSTEM
