6636 FM.qxd 8/19/08 8:28 PM Page i 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 copyright. No part of it may be reproduced, Clinical Editors stored in a retrieval system, or transmitted, in Joanne M. 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Dorshaw (director), 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. Megan L. Aldinger, Karen J. Kirk, III. Series. LindaK. Ruhf [DNLM: 1. Disease—Handbooks. 2. Nursing Care—Handbooks. 3. Pathology—Handbooks. Design Assistant WY 49 P2962 2007] Georg Purvis 4th RT51.P32 2007 Indexer 616.07'5—dc22 ISBN13: 978-1-58255-663-5 Barbara Hodgson ISBN10: 1-58255-663-6 (alk. paper) 2005030653 6636 FM.qxd 8/19/08 8:28 PM Page iii 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 6636 FM.qxd 8/19/08 8:28 PM Page iv 6636 FM.qxd 8/19/08 8:28 PM Page v 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 6636 FM.qxd 8/19/08 8:28 PM Page vi 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 663601.qxd 8/19/08 8:29 PM Page 1 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 663601.qxd 8/19/08 8:29 PM Page 2 ● 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 663601.qxd 8/19/08 8:29 PM Page 3 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 663601.qxd 8/19/08 8:29 PM Page 4 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