Exam (elaborations) Lippincott’s Fast Facts for NCLEX-RN By Lippincott Williams and Wilkins

Lippincott’s Fast Facts for NCLEX-RN By Lippincott Williams and Wilkins Lippincott’s Fast Facts for NCLEX-RN® Staff Publisher J. Christopher Burghardt Acquisitions Editor Bill Lamsback Clinical Director Joan M. Robinson, RN, MSN Clinical Project Manager Beverly Ann Tscheschlog, RN, MS Clinical Editors Joanne Bartelmo, RN, MSN Anita Lockhart, RN, MSN Leigh Ann Trujillo, RN, BSN Product Director David Moreau Senior Product Manager Diane Labus Editor Mary T. Durkin Copy Editors Heather Ditch Erika Kors Editorial Assistants Megan L. Aldinger, Karen J. Kirk, Jeri O’Shea, Linda K. Ruhf Art Director Elaine Kasmer Design Robert Dieters (cover) Vendor Manager Cynthia Rudy Manufacturing Manager Beth J. Welsh Production Services SPi Global The clinical treatments described and recommended in this publication are based on research and consultation with nursing, medical, and legal authorities. To the best of our knowledge, these procedures refl ect currently accepted practice. Nevertheless, they can’t be considered absolute and universal recommendations. For individual applications, all recommendations must be considered in light of the patient’s clinical condition and, before administration of new or infrequently used drugs, in light of the latest packageinsert information. The authors and publisher disclaim any responsibility for any adverse effects resulting from the suggested procedures, from any undetected errors, or from the reader’s misunderstanding of the text. © 2012 by Lippincott Williams & Wilkins. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means—electronic, mechanical, photocopy, recording, or otherwise—without prior written permission of the publisher, except for brief quotations embodied in critical articles and reviews, and testing and evaluation materials provided by the publisher to instructors whose schools have adopted its accompanying textbook. For information, write Lippincott Williams & Wilkins, 323 Norristown Road, Suite 200, Ambler, PA . Printed in China LFFNCLEXRN- Library of Congress Cataloging-in-Publication Data Lippincott’s fast facts for NCLEX-RN. p. ; cm. Fast facts for NCLEX-RN Includes bibliographical references. ISBN 978-1-4511-1327-3 1. Nursing—Examinations—Study guides. 2. Nursing—Examinations, questions, etc. I. Lippincott Williams & Wilkins. II. Title: Fast facts for NCLEX-RN. [DNLM: 1. Nursing Care—methods— Outlines. WY 18.2] RT55.L56 2012 610.73076—dc22 0 iii Contents Advisory board v Contributors and consultants vi How to use this book viii 1 Adult care 1 Cardiovascular system 1 Hematologic and immune systems 14 Respiratory system 19 Neurosensory system 29 Musculoskeletal system 47 Gastrointestinal system 57 Genitourinary system 68 Endocrine system 78 Integumentary system 85 2 Maternal-neonatal care 92 Antepartum 92 Intrapartum 100 Postpartum 105 Neonatal period 109 3 Pediatric care 117 Growth and development 117 Cardiovascular system 119 Hematologic and immune systems 126 Respiratory system 128 Neurosensory system 134 Musculoskeletal system 139 Gastrointestinal system 146 Genitourinary system 153 Endocrine system 159 Integumentary system 162 4 Psychiatric care 167 Essentials of psychiatric care 167 Anxiety and mood disorders 169 Cognitive disorders 172 Dissociative disorders 174 Eating disorders 174 iv Contents Personality disorders 175 Schizophrenic and delusional disorders 176 Sexual and gender identity disorders 178 Somatoform and sleep disorders 180 Substance abuse disorders 183 5 Pharmacology 185 Interactions 185 Adverse drug effects and adverse reactions 186 Contraindications 193 Blood and blood products 198 Central venous access devices 203 Dosage calculations 204 Expected actions and outcomes 206 Medication administration 219 Parenteral and intravenous therapies 222 Pharmacologic pain management 225 Total parenteral therapy 228 6 Management of care 231 Advance directives and client rights 231 Client advocacy 234 Case management 236 Collaboration with interdisciplinary team 238 Client confidentiality 239 Consultation and referrals 242 Continuity of care 243 Delegation, supervision, and prioritization 245 Ethical practice 248 Informed consent 252 Information technology 253 Legal rights and responsibilities 255 Performance and quality improvement 259 7 Patient safety 264 Accident and injury prevention and home safety 264 Emergency response plan 267 Error prevention 273 Handling hazardous materials 274 Infection control 277 Restraint use 284 Safe equipment use 288 Security 292 Appendices Understanding the question 295 Key strategies for answering correctly 301 Selected references 305 v Advisory board Susan Barnason, RN, PhD, CEN, CCRN, CS Associate Professor University of Nebraska Medical Center College of Nursing Lincoln Michael A. Carter, DNSc, FAAN, APRN-BC University Distinguished Professor University of Tennessee Health Science Center College of Nursing Memphis Caroline Dorsen, MSN, APRN-BC, FNP Clinical Instructor and Coordinator, Adult Nurse Practitioner Program New York University College of Nursing New York Stephen Gilliam, PhD, FNP, APRN-BC Assistant Professor Medical College of Georgia School of Nursing Athens Margaret Mary Hansen, RN, MSN, EdD, NI Certificate Associate Professor University of San Francisco San Francisco, Calif. Kathy Henley Haugh, RN, PhD Assistant Professor University of Virginia School of Nursing Charlottesville Janice J. Hoffman, RN, PhD Faculty/Course Coordinator Nursing in Adult Physical Health and Special Topics in Critical Care Nursing Johns Hopkins University School of Nursing Baltimore, Md. Linda Honan Pellico, MSN, PhD, APRN Assistant Professor Yale University School of Nursing New Haven, Conn. Susan L. Woods, RN, PhD, FAAN, FAHA Professor and Associate Dean for Academic Programs University of Washington Seattle vi Contributors and consultants Vicky H. Becherer, RN, MSN Assistant Teaching Professor College of Nursing at the University of Missouri St. Louis Julie Calvery Carman, APN, FNP-BC, MS Nurse Practitioner River Valley Musculoskeletal Fort Smith, Ark. Marsha L. Conroy, RN, MSN Nurse Educator Chamberlain College of Nursing Columbus, Ohio Maggie Thurmond Dorsey, RN, EdD Associate Professor of Nursing University of South Carolina—Aiken Aiken Sally E. Erdel, RN, MS, CNE Assistant Professor of Nursing Bethel College Mishawaka, Ind. Margaret Fried, RN, MA Instructional Faculty Pima Community College Tucson, Ariz. Kathy Henley Haugh, RN, PhD Assistant Professor University of Virginia School of Nursing Charlottesville Corlis Hayden, RN, MSN Assistant Professor Nebraska Methodist College Omaha Connie S. Hefl in, RN, MSN, CNE Professor of Nursing West Kentucky Community and Technical College Paducah Soosannamma Joseph, RN, MS Professor Cochran School of Nursing Yonkers, N.Y. Carolyn Kingston, RN, MSN Instructor/Coordinator Nursing Resource Center St. Francis Medical Center College of Nursing Peoria, Ill. Kathleen Lehmann, RN, BSN, BA, MEd Charge Nurse Edith Nourse Rogers VAMC Bedford, Mass. Marilyn Little, APRN, BS, MSN Professor Salt Lake Community College Salt Lake City, Utah Jennifer McWha, RN, MSN Associate Professor of Nursing Del Mar College Corpus Christi, Tex. Susan A. Moore, RN, BSN, MS, MSN Assistant Clinical Professor University of Memphis Memphis, Tenn. Contributors and consultants vii Noel C. Piano, RN, MS Instructor/Director Lafayette School of Practical Nursing Williamsburg, Va. Adjunct Faculty Thomas Nelson Community College Hampton, Va. Elizabeth R. Pratt, RNC-INP, BSN, MSN Assistant Professor of Nursing Southern Arkansas University Magnolia Nan C. Riedé, RN, MSN, CPN, PLNC Assistant Professor Baptist College of Health Sciences Memphis, Tenn. Ora V. Robinson, RN, PhD Assistant Professor of Nursing California State University San Bernardino Mary Frances Schneider, RN, BSN, MS Assistant Professor The Christ College of Nursing and Health Sciences Cincinnati, Ohio Lisa A. Seldomridge, RN, PhD Chair and Professor Salisbury University Salisbury, Md. Barbara Selvek, RN, MSN, CCRN Associate Professor Finger Lakes Community College Canandaigua, N.Y. Allison J. Terry, RN, MSN, PhD Director, Center for Nursing Alabama Board of Nursing Montgomery Mary L. Terwilliger, RN, MSN Associate Professor Clarion University of Pennsylvania Oil City Peggy Thweatt, RN, BSN, MSN Nursing Faculty Medical Careers Institute, LPN Program Newport News, Va. Sandra K. Voll, RNC, MS, WHNP, CNM, FNP Clinical Assistant Professor Virginia Commonwealth University School of Nursing Richmond Karen A. Wolf, APRN-BC, FNAP, PhD Associate Professor & Coordinator for Faculty Development Samuel Merritt University Oakland, Calif. Nurse Practitioner Lifelong Medical Berkeley, Calif. Michele Woodbeck, RN, MS Professor, Nursing Hudson Valley Community College Troy, N.Y. Patricia Zrelak, CNRN, CNAA-BC, PhD Administrative Nurse, Department of Neurology University of California at Davis Medical Center Davis viii How to use this book Lippincott’s Fast Facts for NCLEX-RN® is designed as a quick and easy review to use when studying for the NCLEX-RN. With over 5,000 bulleted facts, this book covers all aspects of nursing care, organized around the major subject areas tested on the exam: adult health, maternalneonatal nursing, pediatric nursing, psychiatric nursing, pharmacology, management of care, and patient safety. Within each chapter, you’ll fi nd hundreds of facts grouped according to key clinical topics that are specifi c to the subject area. For example, in Chapter 1, Adult Care, bullets are grouped by body system (such as cardiovascular system, respiratory system, musculoskeletal system, and integumentary system). In Chapter 2, Maternal-Neonatal Care, they’re arranged according to stages of pregnancy and delivery (antepartum, intrapartum, postpartum, neonatal). In Chapter 6, Management of Care, facts are organized according to client-focused concepts and nursing responsibilities, including advance directives, client rights, case management, and information technology. Each fact is accurate and up to date and has been thoroughly reviewed by nursing experts well versed in the NCLEX-RN test plan to ensure that the most likely content areas have been addressed. And each fact has been concisely worded to provide a kernel of valuable information that you’ll be able to easily understand and readily recall while taking the exam. A small open box precedes each stand-alone fact, serving to keep each point separate and distinct. You may use the box to check off the fact as “studied” when you feel you’ve suffi ciently learned or mastered the information, or leave it blank to return to later when you need a refresher or further review. Two appendices have been included to help prepare you for the types and style of questions found on the NCLEX and to teach you key strategies for how to answer questions correctly. Samples are also provided to graphically simulate how questions, including new alternate-format type questions (graphic option, chart/exhibit, drag-and-drop, hot spot, fi ll-inthe- blank, audio, and multiple-response/multiple choice) might appear on the actual exam. You’re busy, and fi nding the right time and place to study can sometimes be diffi cult. Because of its convenient size and portability, Lippincott’s Fast Facts for NCLEX-RN is the perfect tool to have on hand when studying alone or in group settings. Tuck it in your purse or backpack and carry it with you wherever you go to review facts—a few at a time, section by section, or whenever you have a few minutes—between classes, during lunch breaks, or even while waiting for a bus or train. You’ll be sure to make the most of your study time and increase your chance of success with this excellent review. How to use this book ix 1 Adult care Cardiovascular system A client’s electrocardiogram showing ST elevation in leads V2 , V3 , and V4 suggests an anterior-wall myocardial infarction. The left anterior descending artery is the primary source of blood for the anterior wall of the heart. The circumfl ex artery supplies the lateral wall of the heart. The internal mammary artery supplies the breast. The coronary arteries may receive a minute portion of blood during systole. Most of the blood fl ow to the coronary arteries is supplied during diastole. Breathing patterns are irrelevant to blood fl ow. Coronary artery disease accounts for 30% of all deaths in the United States. Atherosclerosis, or plaque formation, is the leading cause of coronary artery disease. A myocardial infarction is commonly a result of coronary artery disease. In atherosclerosis, hardened blood vessels can’t dilate properly; therefore, they constrict blood fl ow and block oxygen transport. As a result, oxygen can’t reach the heart muscle, resulting in angina. Diabetes mellitus is a risk factor for coronary artery disease that can be controlled with diet, exercise, and medication. Cholesterol levels above 240 mg/dL are considered excessive and are a risk factor for developing coronary artery disease. Total cholesterol levels below 240 mg/dL are considered below the nationally accepted levels and carry a lesser risk of coronary artery disease. A lipid panel tests the amount of total cholesterol, low-density l ipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. Sublingual nitroglycerin is administered to treat acute angina. Coronary artery bypass surgery and percutaneous transluminal coronary angioplasty are invasive, surgical treatments for coronary artery disease. An electrocardiogram showing ST elevation in leads II, III, and aVF suggests occlusion of the right coronary artery. The right coronary artery supplies the right ventricle, or the inferior portion of the heart. 2 Adult care Occlusion of the right coronary artery could produce an infarction in that area. The most common symptom of a myocardial infarction is chest pain, resulting from deprivation of oxygen to the heart. The correct landmark for obtaining an apical pulse is the left fi fth intercostal space in the midclavicular line. The apex of the heart is the point of maximal impulse where heart sounds are heard loudest. Rescuers of adult victims should begin compressions rather than opening the airway and delivering breaths. The sequence for cardiopulmonary resuscitation is CAB (compressions, airway, breathing) rather than ABC (airway, breathing, compressions). Chest compression depth on an adult should be at least 2 inches (5 cm). All rescuers, trained or not, should deliver high-quality chest compressions by pushing hard to a depth of at least 2 inches (5 cm), at a rate of at least 100 compressions per minute, allowing full chest recoil after each compression, and minimizing interruptions in chest compressions. Trained rescuers should also provide cardiopulmonary resuscitation with a compression to ventilation ratio of 30:2. The outermost layer of the heart is called the epicardium. The epicardium is made up of squamous epithelial cells overlying connective tissue. The myocardium is the middle layer of the heart and forms most of the heart wall. The myocardium has striated muscle fi bers that cause the heart to contract. The heart’s inner layer is called the endocardium. The endocardium consists of endothelial tissue with blood vessels and bundles of smooth muscle. The serous pericardium has two layers: the parietal and the visceral layer. The pericardium surrounds the heart and the roots of the great vessels. The pericardium has two layers: the fi brous and serous pericardium. Pulmonic sounds can be auscultated at the left second intercostal space in the midclavicular line. Abnormalities of the pulmonic valve are auscultated at the left second intercostal space along the left sternal border. Aortic valve abnormalities are heard at the second intercostal space to the right of the sternum. Cardiovascular system 3 Mitral valve abnormalities are heard at the fi fth intercostal space in the midclavicular line. Tricuspid valve abnormalities are heard at the third and fourth intercostal spaces along the sternal border. Troponin I levels rise rapidly and are detectable within 1 hour of myocardial injury. Lactate dehydrogenase isoenzymes may be useful in diagnosing cardiac injury. Because creatine kinase levels may rise with skeletal muscle injury, increased creatine kinase levels may help detect cardiac injury. Measuring for an increase in troponin I levels is the best indicator for determining myocardial injury. An aneurysm is an outpouching of a vessel. Systemic hypertension or increased atrial contraction can result in a fourth heart sound. Aortic valve malfunction is heard as a murmur. The left ventricle is responsible for most of the cardiac output. An anterior-wall myocardial infarction may result in a decrease in left ventricular function. When the left ventricle doesn’t function properly, resulting in left-sided heart failure, fl uid accumulates in the interstitial and alveolar spaces in the lungs and causes crackles. Pulmonic and tricuspid valve malfunction cause right-sided heart failure. Because the myocardium is deprived of oxygen during a myocardial infarction, additional oxygen is administered to assist in oxygenation and prevent further damage. Arrhythmias caused by oxygen deprivation to the myocardium are the most common complication of a myocardial infarction. Because the pumping function of the heart is compromised by a myocardial infarction (MI), heart failure is the second most common complication of MI. Pericarditis most commonly results from a bacterial or viral infection, but may also occur after a myocardial infarction. Jugular vein distention isn’t a symptom of abdominal aortic aneurysm or pneumothorax. A myocardial infarction, if severe enough, can progress to heart failure. Jugular venous pressure is measured with the head of the bed inclined between 15 and 30 degrees. A centimeter ruler is used to obtain the vertical distance between the sternal angle and the point of highest pulsation. 4 Adult care The apical pulse is the most accurate pulse point in the body. The radial pulse rate can be affected by cardiac and vascular disease; therefore, it won’t always accurately depict the heart rate. The heart contains four valves: two atrioventricular valves (mitral and tricuspid) and two semilunar valves (pulmonic and aortic). The aortic valve prevents backfl ow from the aorta into the left ventricle. The pulmonic valve prevents backfl ow from the pulmonary artery into the right ventricle. The tricuspid valve prevents backfl ow from the right ventricle into the right atrium. The mitral valve prevents backfl ow from the left ventricle into the left atrium. The mitral valve is also known as the bicuspid or left atrioventricular valve. Because the atria only have to pump blood into the ventricles, their walls are relatively thin. The walls of the left ventricle are the thickest of any of the chambers of the heart because the left ventricle pumps blood against the resistance of the systemic circulation. The walls of the right ventricle are thicker than those of the atria because the right ventricle pumps blood against the resistance of the pulmonary circulation. Crackles in the lungs are a classic sign of left-sided heart failure. The most accurate area on the body to assess dependent edema in a bedridden client is the sacral area. Sacral, or dependent, edema is secondary to right-sided heart failure. Inadequate deactivation of aldosterone by the liver after right-sided heart failure leads to fl uid retention, which causes oliguria. Adequate urine output, polyuria, and polydipsia aren’t associated with right-sided heart failure. The interatrial septum divides the atrial chambers, helping them to contract and force blood into the ventricles below. The right and left atria serve as volume reservoirs for blood being sent into the ventricles. Weight gain, nausea, and a decrease in urine output are secondary effects of right-sided heart failure. Cardiomyopathy is usually identifi ed as a symptom of left-sided heart failure. Left-sided heart failure causes primarily pulmonary symptoms rather than systemic ones. Cardiovascular system 5 Angina pectoris doesn’t cause weight gain, nausea, or a decrease in urine output. An increased PR interval is indicative of a fi rst-degree atrioventricular block. Normal sinus rhythm and sinus arrhythmia produce normal PR intervals. The PR interval (if present) is less than 0.12 second in accelerated junctional rhythm. The portion of the aorta distal to the renal arteries is more prone to an aneurysm because the vessel isn’t surrounded by stable structures, unlike the proximal portion of the aorta. Abdominal pain is the most common symptom in a client with an abdominal aortic aneurysm as a result of disruption of normal circulation in the abdominal region. An aortogram clearly delineates the vessels and any abnormalities. An abdominal aortic aneurysm will only be visible on an X-ray if it is calcifi ed. Computed tomography scan and ultrasound don’t give a direct view of the vessels and don’t yield as accurate a diagnosis as the aortogram. Rupture of an abdominal aortic aneurysm is a life-threatening emergency. Hypertension should be avoided or controlled in a client with an abdominal aortic aneurysm because it can cause the weakened vessel to rupture. Cardiac arrhythmias aren’t directly linked to an abdominal aortic aneurysm. The aorta lies directly left of the umbilicus. When assessing a client for an abdominal aortic aneurysm, the area of the abdomen that is most commonly palpated is the middle lower abdomen to the left of the midline. Continuous pressure on the vessel walls from hypertension causes the walls to weaken and an aneurysm to occur. Atherosclerotic changes can occur with peripheral vascular diseases and are linked to aneurysms, but the link isn’t as strong as it is with hypertension. Hypertension is linked to more than 50% of clients with abdominal aortic aneurysms. A bruit is a vascular sound that refl ects partial arterial occlusion. Severe lower back pain indicates an aneurysm rupture, secondary to pressure being applied within the abdominal cavity. Blood pressure decreases due to the loss of blood when an aneurysm ruptures. 6 Adult care After an abdominal aortic aneurysm ruptures, the vasculature is interrupted and blood volume is lost, so blood pressure doesn’t increase. The red blood cell count is decreased after the abdominal aortic aneurysm ruptures because the vasculature is interrupted and blood volume is lost. The white blood cell count increases after the abdominal aortic aneurysm ruptures as cells migrate to the site of injury. Symptoms of severe lower back pain, decreased blood pressure, decreased red blood cell count, and increased white blood cell count indicate a ruptured abdominal aortic aneurysm. Rupture of a repaired abdominal aortic aneurysm is most commonly caused by leakage at the repair site. Marfan syndrome results in degeneration of the elastic fi bers of the aortic media. In most cases of cardiomyopathy, the etiology is a viral or bacterial infection or cardiotoxic effects of drugs or alcohol. Although the cause isn’t entirely known, cardiac dilation and heart failure may develop in the mother during the last month of pregnancy or the fi rst few months after birth. In hypertrophic obstructive cardiomyopathy, hypertrophy of the ventricular septum is apparent. Heart failure most commonly occurs in clients with cardiomyopathy because the structure and function of the heart muscle is affected. Myocardial infarction results from prolonged myocardial ischemia due to reduced blood fl ow through one of the coronary arteries. Pericardial effusion is most predominant in clients with pericarditis. Atrial fi brillation is defi ned as chaotic, asynchronous, electrical activity in the atrial tissue. Ventricular fi brillation is a chaotic rhythm with no QRS complexes. In atrial fl utter there are fl utter waves that are “sawtooth” in appearance. P waves are present in sinus tachycardia. Dyspnea, cough, weight gain, weakness, and edema are classic symptoms of heart failure. Pericarditis is exhibited by a feeling of fullness in the chest and auscultation of a pericardial friction rub. Hypertension is usually exhibited by headaches, visual disturbances, and a fl ushed face. An S4 heart sound occurs as a result of increased resistance to ventricular fi lling after atrial contraction. Cardiovascular system 7 Increased resistance to ventricular fi lling is related to decreased compliance of the ventricle. A dilated aorta causes a murmur. An S4 heart sound isn’t heard in a normally functioning heart. The primary goals in the treatment of cardiomyopathy are to improve myocardial fi lling and cardiac output. The only defi nitive treatment for cardiomyopathy that can’t be controlled medically is a heart transplant because the damage to the heart muscle is irreversible. Coronary artery bypass grafting is a surgical intervention used for atherosclerotic vessels. Ischemic changes are represented on an electrocardiogram by T-wave inversion. An increased QRS complex duration suggests a bundle-branch block. A shortened PR interval indicates a junctional rhythm. Pathologic Q waves are present with myocardial infarction. Inadequate oxygen supply to the myocardium is responsible for the pain accompanying angina. Decreased afterload causes increased cardiac output. It is most important for the nurse to determine if the client has allergies to iodine or shellfi sh before cardiac catheterization because catheterization involves the injection of a radiopaque dye. Percutaneous transluminal coronary angioplasty can alleviate the blockage in the coronary arteries and restore blood fl ow and oxygenation. Cardiogenic shock is related to a reduced cardiac output and ineffective pumping of the heart. Distributive shock results from changes in the intravascular volume distribution and is usually associated with increased cardiac output. Of all clients with an acute myocardial infarction, 15% suffer cardiogenic shock secondary to the myocardial damage and decreased function. At least 40% of the heart muscle must be involved for cardiogenic shock to develop. The cardiac index is a fi gure derived by dividing the cardiac output by the client’s body surface area. The cardiac index is used for identifying whether the cardiac output is meeting a client’s needs. Heart rate, blood pressure, and decreased cerebral blood fl ow are less useful in detecting the risk of cardiogenic shock. The most useful factor in detecting a client’s risk of developing cardiogenic shock is the cardiac index. 8 Adult care Initially, the decrease in cardiac output results in a decrease in cerebral blood fl ow. A decrease in cerebral blood fl ow causes restlessness, agitation, or confusion. The diagnostic study that can determine when cellular metabolism becomes anaerobic and when pH decreases is arterial blood gas analysis. The fi rst treatment goal for cardiogenic shock is to increase myocardial oxygen supply. In a shock state, the myocardium requires more oxygen; if it doesn’t receive more oxygen, the shock worsens. Increasing the oxygen supply to the myocardium will play a large role in correcting metabolic acidosis and hypoxia. A systolic blood pressure of 140 to 159 mm Hg or a diastolic pressure of 90 to 99 mm Hg represents stage 1 hypertension. Systolic blood pressure greater than or equal to 160 mm Hg or diastolic pressure greater than or equal to 100 mm Hg represents stage 2 hypertension. A systolic blood pressure of 120 to 139 mm Hg or a diastolic pressure of 80 to 89 mm Hg represents prehypertension. A systolic blood pressure less than 120 mm Hg and a diastolic pressure less than 80 mm Hg are considered normal. Peripheral chemoreceptors in the aorta and carotid arteries are primarily stimulated by oxygen. Decreases in pulsatile pressure cause a refl ex increase in heart rate. Primary hypertension describes persistently elevated blood pressure with an unknown cause; it accounts for approximately 90% of hypertension cases. Primary hypertension is characterized by a progressive, usually asymptomatic blood pressure increase over several years. Malignant hypertension is rapidly progressive, uncontrollable, and causes a rapid onset of complications. Secondary hypertension occurs secondary to a known, correctable cause. An occipital headache is typical of hypertension secondary to continued increased pressure on the cerebral vasculature. The most common symptom of hypertension is headache. The brachial artery is most commonly used to measure blood pressure due to its easy accessibility and location. The radial and ulnar arteries can be used in extraordinary circumstances to obtain a blood pressure reading, but the measurement may not be as accurate. Primary varicose veins have a gradual onset and progressively worsen. Cardiovascular system 9 Fatigue and pressure are classic signs of varicose veins, secondary to increased blood volume and edema. Passive fi lling of the ventricles begins with diastole. The right atrium receives deoxygenated blood returning from the body through the inferior and superior venae cavae and from the heart through the coronary sinus. The left atrium receives oxygenated blood from the lungs through the four pulmonary veins. The right atrium receives deoxygenated blood returning from the body through the inferior and superior venae cavae and from the heart through the coronary sinus. The atria pump their blood through the two atrioventricular valves (mitral and tricuspid) directly into their respective ventricles. The right ventricle pumps blood through the pulmonic valve into the pulmonary arteries and then into the lungs. Oxygenated blood returns to the left atrium. The left ventricle pumps blood through the aortic valve into the aorta and then throughout the body. Deoxygenated blood returns to the right atrium. The fi ring of the sinoatrial node sets off a chain reaction in cardiac conduction. When an impulse leaves the sinoatrial node, it travels through the atria along Bachmann’s bundle and the internodal pathways on its way to the atrioventricular node. After the impulse passes through the atrioventricular node, it travels to the ventricles, fi rst down the bundle of His, then along the bundle branches and, fi nally, down the Purkinje fi bers. The sinoatrial node has a fi ring rate of 60 to 100 beats/minute. The atrioventricular node has a fi ring rate of 40 to 60 beats/minute. Purkinje fi bers have a fi ring rate of 20 to 40 beats/minute. Automaticity is the ability to spontaneously initiate an impulse (pacemaker cells have this ability). Excitability is a cell’s response to an electrical stimulus (results from ion shifts across the cell membrane). Conduction is the ability of a cell to transmit an electrical impulse to another cardiac cell. Contractility is the ability of a cell to contract after receiving a stimulus. Preload is the stretching of muscle fi bers in the ventricles as the ventricles fi ll with blood. 10 Adult care Contractility is infl uenced by preload. Afterload refers to the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta to get the blood out of the heart. Electrical stimulation causes troponin to expose actin-binding sites, which allows muscle contraction to occur in the heart. Valves in the veins prevent blood backfl ow, and most are located in smaller, more distal veins. The largest vein, the vena cava, has no valves. Arteries have thick, muscular walls to accommodate the high speed and pressure of blood fl ow. Arterioles have thinner walls than arteries and control blood fl ow to capillaries. Capillaries have microscopic walls composed of a single layer of endothelial cells. Conductive arteries typically have few branches and follow relatively straight lines. Distributive arteries typically have multiple branches and arise from the conductive arteries. The heart relies on the coronary arteries and their branches for its supply of oxygenated blood; it also depends on the cardiac veins to remove oxygen-depleted blood. During diastole, blood fl ows out of the heart and into the coronary arteries. The right coronary artery supplies blood to the right atrium, part of the left atrium, most of the right ventricle, and the inferior part of the left ventricle. The left coronary artery, which splits into the left anterior descending and circumfl ex arteries, supplies blood to the left atrium, most of the left ventricle, and most of the interventricular septum. Syncope is a brief loss of consciousness caused by a lack of blood to the brain; it usually occurs abruptly and can last for seconds to minutes. In the aortic area, sounds refl ect blood moving from the left ventricle d uring systole, crossing the aortic valve, and fl owing through the aortic arch. In the pulmonic area, sounds refl ect blood being ejected from the right ventricle during systole, crossing the pulmonic valve and fl owing through the main pulmonary artery. In the tricuspid area, sounds refl ect movement of blood from the right atrium across the tricuspid valve and right ventricular fi lling during diastole. In the mitral area, also called the apical area, sounds refl ect blood fl ow across the mitral valve and left ventricular fi lling during diastole. Cardiovascular system 11 Listen for heart murmurs over the same precordial areas used in auscultation for heart sounds. An S3 heart sound, also known as ventricular gallop, is commonly heard in children and may be normal in women during the last trimester of pregnancy; however, it may be a cardinal sign of heart failure in other adults. Also called an atrial gallop, an S4 heart sound is an adventitious heart sound that you’ll hear best over the tricuspid or mitral area when the client lies on his left side. A pericardial friction rub has a scratchy, rubbing quality. A weak pulse has decreased amplitude with a slower upstroke and downstroke. It may be a result of increased peripheral vascular resistance, as occurs in cold weather or with severe heart failure, or decreased stroke volume, as occurs with hypovolemia or aortic stenosis. A bounding pulse has a sharp upstroke and downstroke with a pointed peak and elevated amplitude and may result from increased stroke volume, as with aortic insuffi ciency, or arterial wall stiffness, which can occur with aging. Pulsus alternans is a regular, alternating pattern of weak and strong pulses and is associated with left-sided heart failure. Pulsus bigeminus is similar to pulsus alternans but occurs at irregular intervals and is caused by premature atrial or ventricular beats. Pulsus paradoxus has increases and decreases in amplitude associated with the respiratory cycle; marked decreases occur when the client inhales. Pulsus paradoxus is associated with pericardial tamponade, advanced heart failure, and constrictive pericarditis. Pulsus biferiens shows an initial upstroke, a subsequent downstroke, and then another upstroke during systole. Pulsus biferiens is caused by aortic stenosis and aortic insuffi ciency. Activated partial thromboplastin time, prothrombin time, bleeding time, and activated clotting time are tests that measure clotting time. Increased International Normalized Ratio (INR) values may indicate disseminated intravascular coagulation, cirrhosis, hepatitis, vitamin K defi ciency, salicylate intoxication, or uncontrolled oral anticoagulation. Electrophysiology studies are used to help determine the cause of an arrhythmia and the best treatment for it. In transesophageal echocardiography, ultrasonography is combined with endoscopy to provide a better view of the heart’s structures. Transesophageal echocardiography is used to evaluate valvular disease or repairs, but it’s also used to diagnose thoracic and aortic 12 Adult care disorders, endocarditis, congenital heart disease, intracardiac thrombi, and tumors. Cardiac blood pool imaging (also called multiple-gated acquisition, or MUGA, scanning) is used to evaluate regional and global ventricular performance. In arterial pressure–based cardiac output monitoring, a client’s existing arterial catheter is used to continuously calculate and display cardiac output. Arterial pressure-based cardiac output helps to determine a client’s fl uid status and potential response to a fl uid challenge before signifi cant changes in blood pressure occur. Endocarditis is an infl ammation of the endocardium, the heart valves, or a cardiac prosthesis; it typically results from bacterial invasion and therefore may also be referred to as infective endocarditis. Sharp pain and cool feet are symptoms of alteration in arterial blood fl ow. Varicose veins occur most commonly in the saphenous veins of the lower extremities. Edema and pigmentation are signs and symptoms of secondary varicose veins. Ligation and stripping of the vein can rid the vein of varicosity, but it won’t prevent other varicose veins from forming. Sitting and bed rest are contraindicated in the postoperative management of a client who has undergone ligation and stripping because both promote decreased blood return to the heart and venous stasis. Although ice packs would help reduce edema for a client who has undergone ligation and stripping, they would also cause vasoconstriction and impede blood fl ow. Pulmonary embolism is manifested by dyspnea, chest pain, and diminished breath sounds. A pulmonary embolism is a blood clot that forms in a vein, travels to the lungs, and lodges in the pulmonary vasculature. A hemothorax refers to blood in the pleural space. A pneumothorax is caused by an opening in the pleura. Pulmonary hypertension is an increase in pulmonary artery pressure, which increases the workload of the right ventricle. Hypercoagulability, along with venous stasis and venous wall injury, accounts for the formation of deep vein thrombosis. An embolus is a blood clot or fatty globule that forms in one area of the body and is carried through the bloodstream to another area. Deep vein thrombosis is associated with deep leg pain of sudden onset. Cardiovascular system 13 Production of pink, frothy sputum is a classic sign of acute pulmonary edema. Hypocapnia is a blood gas abnormality that is initially most suggestive of pulmonary edema. In an attempt to compensate for increased work of breathing due to hyperventilation, carbon dioxide decreases, causing hypocapnia. The left ventricle is responsible for the majority of force for cardiac output. If the left ventricle is damaged, the output decreases and fl uid accumulates in the interstitial and alveolar spaces, causing pulmonary edema. Damage to the left atrium would contribute to heart failure but wouldn’t affect cardiac output or the onset of pulmonary edema. If the right atrium and right ventricle were damaged, right-sided heart failure would result. Pulmonary edema is a life-threatening complication of heart failure. Pulmonary edema can develop in minutes, secondary to a sudden fl uid shift from the pulmonary vasculature into the interstitium and alveoli of the lung. The volume of blood in the ventricle at the end of diastole determines preload. Cardiac index is the individualized measurement of cardiac output, based on the client’s body surface area. Cardiac output is the amount of blood the heart expels per minute. Tachycardia, fi nger clubbing, and a loud S2 suggest transposition of the great arteries (a cyanotic congenital heart defect). Dyspnea, cough, and palpitations occur with mitral insuffi ciency. Dyspnea, fatigue, and syncope indicate aortic insuffi ciency. In a client with atrial fi brillation, warfarin reaches therapeutic levels when the International Normalized Ratio (INR) is 2 to 3. With atrial tachycardia, the rhythm is regular, the P wave is hidden in the preceding T wave, and the rate ranges from 140 to 250 beats/minute. A ventricular rate that varies with the degree of atrioventricular block, along with sawtooth P waves, characterizes atrial fl utter. Irregular ventricular response and absent P waves characterize atrial fi brillation. Regular and equal atrial and ventricular rhythms and a rate of 100 to 160 beats/minute characterize sinus tachycardia. Cardiac tamponade is associated with decreased cardiac output, which in turn reduces blood pressure. 14 Adult care Shortness of breath, tachypnea, low blood pressure, tachycardia, diffuse crackles, and a cough producing pink, frothy sputum are late signs of pulmonary edema. The murmur of aortic stenosis is low-pitched, rough, and rasping. The murmur of aortic stenosis is heard loudest in the second intercostal space to the right of the sternum. Atrial fi brillation occurs with irregular and rapid discharge from multiple ectopic atrial foci that cause quivering of the atria without atrial systole. Hematologic and immune systems For an adult client to be diagnosed with AIDS, he must test positive for human immunodefi ciency virus (HIV), have a CD4+ T-cell count below 200 cells/ml, and have one or more specifi c opportunistic infections or cancers along with the HIV infection. Human immunodefi ciency virus is most easily transmitted in blood, semen, and vaginal secretions and has also been found in urine, feces, saliva, tears, and breast milk. A gastrectomy can cause pernicious anemia due to the client’s inability to absorb vitamin B12. A client who has had a gastrectomy is at high risk for developing anemia. Antinuclear antibody titer is commonly used as a screening tool for rheumatoid arthritis (RA) but is not a diagnostic tool for RA. Complete blood count, erythrocyte sedimentation rate, and rheumatoid factor are all used as diagnostic tools for rheumatoid arthritis (RA) and are also used to monitor progress of RA or response to therapy. In adults, thrombocytopenia is indicated when the platelet count is less than 100,000/ml. Normal platelet count ranges from 140,000 to 400,000/ml. Thrombocytopathy is platelet dysfunction. Thrombocytosis is an excess number of platelets. The classic symptoms for thrombocytopenia are petechiae and bruising. Pancytopenia is a reduction in all blood cells. Idiopathic thrombocytopenic purpura and disseminated intravascular coagulation cause platelet aggregation and bleeding. Heparin-associated thrombosis and thrombocytopenia may be suspected when a decrease in platelet count from 230,000 ml to 5,000 ml is noted in a client who has had coronary artery bypass graft surgery. A xenogeneic transplant is a transplant between two different species. An allogeneic transplant is between two humans. A syngeneic transplant is between identical twins. Hematologic and immune systems 15 An autologous transplant is a transplant from the same individual. Systemic lupus erythematosus affects women eight times more often than men; usually strikes during childbearing age; is three times more common in black women than in white women; and is a chronic, infl ammatory, autoimmune disorder that primarily affects connective tissue. Systemic lupus erythematosus affects the skin and kidneys, and may also affect the respiratory, cardiac, neurologic, and renal systems. In stage I of Hodgkin’s disease, symptoms include a single enlarged lymph node (usually), unexplained fever, night sweats, malaise, and generalized pruritus. Kidney failure is the most common cause of death for clients with systemic lupus erythematosus. The classic sign of systemic lupus erythematosus (SLE) is the butterfl y rash (superfi cial lesions over the cheeks and nose). Other common signs of SLE include vomiting, weight loss, and diffi culty urinating. Pancytopenia and elevated antinuclear antibody titer support the diagnosis of systemic lupus erythematosus. Chronic lymphocytic leukemia shows a proliferation of small abnormal mature B cells and decreased antibody response. Thrombocytopenia is often present in chronic lymphocytic leukemia. Uncontrolled proliferation of granulocytes occurs in myelogenous leukemia. The initial phase of chemotherapy for acute lymphocytic leukemia, called the induction phase, is designed to put the client into remission by giving high doses of drugs and administering doses closer together than once each month. The hematologic system functions as an important part of the body’s defenses. Blood components play a vital role in transporting electrolytes and regulating acid-base balance. Lymphatic vessels prevent edema by moving fl uid and proteins from interstitial spaces to venous circulation; they also reabsorb fats from the small intestine. Lymph nodes are tissues that fi lter out bacteria and other foreign cells and are grouped by region. Lymph nodes are grouped by region: cervicofacial, supraclavicular, axillary, epitrochlear, inguinal, and femoral. The spleen destroys bacteria, fi lters blood, serves as a blood reservoir, forms lymphocytes and monocytes, and traps formed particles. Hematopoiesis occurs in the spleen and is the process by which red blood cells, white blood cells, and platelets are produced. 16 Adult care Bone marrow may be described as either red or yellow; red bone marrow is a source of lymphocytes and macrophages. Hematopoiesis is carried out by red bone marrow. Yellow bone marrow is red bone marrow that has changed to fat. Bone marrow contains stem cells, which may develop into several different cell types during hematopoiesis. Some stem cells evolve into lymphocytes; lymphocytes may become B cells or T cells; other stem cells evolve into phagocytes. Erythrocytes (also called red blood cells, or RBCs) are formed in the bone marrow and contain hemoglobin. Oxygen binds with hemoglobin to form oxyhemoglobin, which is then carried by red blood cells throughout the body. Thrombocytes (also called platelets) are formed in the bone marrow and function in the coagulation of blood. Leukocytes (also called white blood cells, or WBCs) are formed in the bone marrow and lymphatic tissue and include granulocytes and agranulocytes. White blood cells provide immunity and protection from infection by phagocytosis (engulfi ng, digesting, and destroying microorganisms). Plasma is the liquid portion of the blood; it is composed of water, protein (albumin and globulin), glucose, and electrolytes. A low-bacteria diet that excludes raw fruits and vegetables would be indicated for a neutropenic client with leukemia. Multiple myeloma is more common in middle-aged and older clients; mean age at diagnosis is 60 years. Multiple myeloma is twice as common in blacks as whites, and most often occurs in black men. Multiple myeloma is characterized by malignant plasma cells that produce an increased amount of immunoglobulin that isn’t functional. As more malignant plasma cells are produced in multiple myeloma, there’s less space in the bone marrow for red blood cell production. In late stages of multiple myeloma, platelets and white blood cell counts are reduced as the bone marrow is infi ltrated by malignant plasma cells. In cell-mediated immunity, T cells respond directly to antigens (foreign substances such as bacteria or toxins that induce antibody formation). Cell-mediated immunity involves destruction of target cells—such as virus-infected cells and cancer cells—through secretion of lymphokines (lymph proteins). Examples of cell-mediated immunity are rejection of transplanted organs and delayed immune responses that fi ght disease. Hematologic and immune systems 17 About 80% of blood cells are T cells. T cells probably originate from stem cells in the bone marrow; the t hymus gland controls their maturity and in the process, a large number of antigen-specifi c cells are produced. There are three main types of T cells: killer, helper, and suppressor T cells. Killer T cells bind to the surface of the invading cell, disrupt the membrane, and destroy it by altering its internal environment. Helper T cells stimulate B cells to mature into plasma cells, which begin to synthesize and secrete immunoglobulin (proteins with known antibody activity). Suppressor T cells reduce the humoral response. B cells act in a different way from T cells to recognize and destroy antigens. B cells are responsible for humoral or immunoglobulinmediated immunity. B cells originate in the bone marrow and mature into plasma cells that produce antibodies (immunoglobulin molecules that interact with a specifi c antigen). Antibodies destroy bacteria and viruses, thereby preventing them from entering host cells. Five major classes of immunoglobulin exist: immunoglobulin G, immunoglobulin M, immunoglobulin A, immunoglobulin D, and immunoglobulin E. Immunoglobulin G makes up about 80% of plasma antibodies, appears in all body fl uids, and is the major antibacterial and antiviral antibody. Immunoglobulin M is the fi rst immunoglobulin produced during an immune response, is too large to easily cross membranes, and is usually present only in the vascular system. Immunoglobulin A is found mainly in body secretions, such as saliva, sweat, tears, mucus, bile, and colostrums, and defends against pathogens on body surfaces, especially those that enter the respiratory and GI tracts. Immunoglobulin D is present in plasma, is easily broken down, is the predominant antibody on the surface of B cells, and is mainly an antigen receptor. Immunoglobulin E is the antibody involved in immediate hypersensitivity reactions, or allergic reactions that develop within minutes of exposure to an antigen. Immune function declines with age. Diminished immune function in the elderly can interfere with the ability to fi ght infection. Infl ammation and increased body temperature are normal immune responses to detected antigens. 18 Adult care Allergies are heightened responses to antigens. Autoimmune response is one in which the immune system forms antibodies against the body’s own tissues, resulting in disease. Antibodies are produced by B cells. Genetics and environment haven’t been shown to be factors in acquired immune defi ciency. A negative human immunodefi ciency virus (HIV) antibody test means that HIV antibodies weren’t in the client’s blood at the time the test was performed; if antibodies to HIV are present, the test result is positive. Antibodies to human immunodefi ciency virus (HIV) may take 3 weeks to 6 months or longer to develop. Incidence rate is the rapidity with which individuals without a disease contract it. Survival is the proportion of individuals affected by a disease who live for a particular length of time. Risk is the proportion of individuals without a disease who develop the disease within a particular time period. In community health and epidemiologic studies, the defi nition of disease prevalence is the number of individuals affected by a particular disease at a specifi c time. The American Association of Blood Banks recommends that blood or blood components should be transfused within 4 hours. Standard precautions stipulate that a health care worker who anticipates coming into contact with a client’s blood or body fl uids must wear gloves. In aplastic anemia, the diagnostic fi ndings are decreased levels of all the cellular elements of the blood (pancytopenia). Reed-Sternberg cells and lymph node enlargement occur with Hodgkin’s disease. Decreased levels of white blood cells, red blood cells, and platelets are consistent in the diagnosis of a client with aplastic anemia. Two people with the beta-thalassemia trait have a 25% chance of having a child with thalassemia major, a potentially life-threatening disease. Thalassemia occurs primarily in people of Italian, Greek, African, Asian, Middle Eastern, East Indian, and Caribbean descent. A client with severe abdominal pain and a history of sickle cell disease may be in a sickle cell crisis. Acute abdominal pain in sickle cell crisis is caused by sickling in the mesenteric circulation. Neutropenia occurs when the absolute neutrophil count falls below