Đang tải... (xem toàn văn)
(BQ) Part 1 book Wilkins clinical assessment in respiratory care has contents: Preparing for the patient encounter, the medical history and the interview, cardiopulmonary symptoms, vital signs, fundamentals of physical examination,.... and other contents.
Contents PREPARING FOR THE PATIENT ENCOUNTER, THE MEDICAL HISTORY AND THE INTERVIEW, 15 CARDIOPULMONARY SYMPTOMS, 32 VITAL SIGNS, 56 FUNDAMENTALS OF PHYSICAL EXAMINATION, 73 NEUROLOGIC ASSESSMENT, 102 CLINICAL LABORATORY STUDIES, 126 INTERPRETATION OF BLOOD GASES, 152 PULMONARY FUNCTION TESTING, 178 10 CHEST IMAGING, 207 11 INTERPRETATION OF ELECTROCARDIOGRAM TRACINGS, 234 12 NEONATAL AND PEDIATRIC ASSESSMENT, 263 13 OLDER PATIENT ASSESSMENT, 296 14 RESPIRATORY MONITORING IN CRITICAL CARE, 314 15 VASCULAR PRESSURE MONITORING, 348 16 CARDIAC OUTPUT MEASUREMENT, 373 17 BRONCHOSCOPY, 396 18 NUTRITION ASSESSMENT, 410 19 SLEEP AND BREATHING ASSESSMENT, 436 20 HOME CARE PATIENT ASSESSMENT, 453 21 DOCUMENTATION, 468 GLOSSARY, 486 Albert J Heuer, PhD, MBA, RRT, RPFT Program Director, Masters in Health Care Management & Associate Professor, Respiratory Care Program-North School of Health Related Professions University of Medicine and Dentistry of New Jersey Newark, New Jersey Craig L Scanlan, EdD, RRT, FAARC Professor Emeritus School of Health Related Professions University of Medicine and Dentistry of New Jersey Newark, New Jersey 3251 Riverport Lane Maryland Heights, Missouri 63043 WILKINS’ CLINICAL ASSESSMENT IN RESPIRATORY CARE ISBN: 978-0-323-10029-8 Copyright © 2014 by Mosby, an imprint of Elsevier Inc Copyright © 2010, 2005, 2000, 1995, 1990, 1985 by Mosby Inc., an affiliate of Elsevier Inc All rights reserved No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher Notice Knowledge and best practice in this field are constantly changing As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications It is the responsibility of the practitioners, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions To the fullest extent of the law, neither the Publisher nor the Editors/Authors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book The Publisher Library of Congress Cataloging-in-Publication Data Wilkins’ clinical assessment in respiratory care / [edited by] Albert J Heuer, Craig L Scanlan – 7th ed p ; cm Clinical assessment in respiratory care Rev ed of: Clinical assessment in respiratory care / Robert L Wilkins, James R Dexter ; consulting editor, Albert J Heuer 6th ed c2010 Includes bibliographical references and index ISBN 978-0-323-10029-8 (pbk : alk paper) I Heuer, Albert J II Scanlan, Craig L., 1947- III Wilkins, Robert L Clinical assessment in respiratory care IV Title: Clinical assessment in respiratory care [DNLM: Diagnostic Techniques, Respiratory System Physical Examination Respiratory Therapy–methods WF 141] 617’.075—dc23 2012045666 Content Strategy Director: Jeanne Olson Content Manager: Billi Sharp Senior Content Development Specialist: Kathleen Sartori Publishing Services Manager: Gayle May Project Manager: Deepthi Unni Design Direction: Maggie Reid Printed in the United States of America Last digit is the print number: 9 8 7 6 5 4 3 2 Through the leadership and scholarly commitment of Dr. Robert L Wilkins, PhD, RRT, this text has become a cornerstone resource in respiratory patient assessment and is used by a majority of respiratory programs worldwide This accomplishment can be attributed directly to the significant and sustained efforts of Dr Wilkins, through the many editions of this text for which he has been senior editor Simply stated, this book is current, thorough, concise, and clearly written As a result of his untimely death, Dr Wilkins’ presence in preparing this edition was greatly missed, and maintaining his high standard was a challenge However, both editors for this seventh edition, Dr Craig Scanlan and I, had worked with Bob on other projects, including prior editions of this and other texts In addition, we assembled a team of returning and new contributors These factors, coupled with the appropriate retention of content written by Dr Wilkins for prior editions, have resulted in what we believe is worthy of the standard and style set by Dr Wilkins In recognition and appreciation of his contributions to this text and to respiratory therapy education, this text has been renamed Wilkins’ Clinical Assessment in Respiratory Care Dr Wilkins is deeply missed by me on a personal and professional level, and his absence from our profession will be felt for some time However, his legacy will live on in the memory of his family, friends, and colleagues, as well as the pages of this text Warmly, Al Heuer To Dr Robert L Wilkins and Dr Craig L Scanlan for their unwavering mentorship, to my lovely wife Laurel for her patience and support, and to the students, faculty, and my fellow respiratory therapists, who are constant sources of inspiration AJH To Mom and Dad who believed in me; to Barrie and Craig Patrick, in whom I believe CLS Sixth Edition Editors/Contributors Douglas D Deming, MD Professor of Pediatrics Loma Linda University Medical Director of Neonatal Respiratory Care Medical Director of ECMO Loma Linda University Children’s Hospital Loma Linda, California James A Peters, MD, DrPH, MPH, RD, RRT, FACPM Attending Physician, Preventive Medicine Department of Internal Medicine and Center for Health St Helena Hospital and Health Center; Physician and Owner Nutrition and Lifestyle Medical Clinic St Helena, California De De Gardner, MSHP, RRT, FAARC Associate Professor and Chair Department of Respiratory Care School of Health Professions University of Texas Health Science Center at San Antonio San Antonio, Texas Helen M Sorenson, MA, RRT, FAARC Assistant Professor Department of Respiratory Care School of Health Professions University of Texas Health Science Center at San Antonio San Antonio, Texas Susan L McInturff, RCP, RRT Clinical Director Farrell’s Home Health Bremerton, Washington Cheryl Thomas Peters, DCN, RD Clinical Manager St Helena Center for Health St Helena, California S Gregory Marshall, PhD, RRT, RPSGT, RST Associate Professor/Chair Department of Respiratory Care College of Health Professions Texas State University—San Marcos San Marcos, Texas vi Richard Wettstein, BS, RRT Assistant Professor Department of Respiratory Care School of Health Professions University of Texas Health Science Center at San Antonio San Antonio, Texas Contributors Robert F Allen, III, MA, RPSGT Manager, Sleep Wake Disorder Lab St Mary’s Medical Center Langhorne, Pennsylvania Zaza Cohen, MD, FCCP Assistant Professor Fellowship Program Director Division of Pulmonary and Critical Care Medicine University of Medicine and Dentistry of New Jersey Newark, New Jersey Cara DeNunzio, MPH, RRT, CTTS Adjunct Assistant Professor Respiratory Care Program—North School of Health Related Professions University of Medicine and Dentistry of New Jersey Newark, New Jersey Nadine A Fydryszewski, PhD, MLS Associate Professor School of Health Related Professions University of Medicine and Dentistry of New Jersey Newark, New Jersey David A Gourley, RRT, MHA, FAARC Executive Director of Regulatory Affairs Chilton Hospital Pompton Plains, New Jersey Elaine M Keohane, PhD, MLS Professor and Chairman Department of Clinical Laboratory Sciences University of Medicine and Dentistry of New Jersey Newark, New Jersey Kenneth Miller, MEd, RRT-NPS, AE-C Educational Coordinator, Dean of Wellness Respiratory Care Services Lehigh Valley Health Network Allentown, Pennsylvania Ruben D Restrepo, MD, RRT, FAARC Professor Director, Bachelor’s Completion Program School of Health Professions Department of Respiratory Care University of Texas Health Science Center San Antonio, Texas Narciso Rodriguez, BS, RRT-NPS, RPFT, AE-C Assistant Professor and Program Director Respiratory Care Program University of Medicine and Dentistry of New Jersey School of Health Related Professions Newark, New Jersey David L Vines, MHS, RRT, FAARC Chair and Program Director Department of Respiratory Care Rush University Chicago, Illinois Jane E Ziegler, MD, DCN, RD, LDN Assistant Professor Graduate Programs in Clinical Nutrition School of Health Related Professions University of Medicine and Dentistry of New Jersey Newark, New Jersey vii Reviewers Georgine Bills, MBA/HAS, RRT Program Director, Respiratory Therapy Dixie State College of Utah St George, Utah Craig P Black, PhD, RRT-NPS, FAARC Director, Respiratory Care Program The University of Toledo Toledo, Ohio Helen Schaar Corning, AS, RCP, RRT Shands Jacksonville Medical Center Jacksonville, Florida Erin Ellis Davis, MS, MEd, RRT-NPS, CPFT Director of Clinical Education-Clinical Coordinator Our Lady of Holy Cross College/Ochsner Health System New Orleans, Louisiana Dale Bruce Dearing, RCP, RRT, MSc Respiratory Therapy Program Assessment Coordinator San Joaquin Valley College Visalia, California Lindsay Fox, MEd, RRRT-NPS Respiratory Care Program Coordinator Southwestern Illinois College/St Elizabeth Hospital Belleville, Illinois Laurie A Freshwater, MA, RCP, RRT, RPFT Health Sciences Division Director Carteret Community College Morehead City, North Carolina Christine A Hamilton, DHSc, RRT, AE-C Assistant Professor, Director of Clinical Education Cardio-Respiratory Care Sciences Program Tennessee State University Nashville, Tennessee Sharon L Hatfield, PhD, RRT, RPFT, AE-C, COPD-C Chair of Community Health Sciences, Associate Professor of Respiratory Therapy and Healthcare Management Jefferson College of Health Sciences Roanoke, Virginia viii Robert L Joyner, PhD, RRT, FAARC Associate Dean and Director, Respiratory Therapy Program Henson School of Science & Technology Salisbury University Salisbury, Maryland Chris Kallus, MEd, RRT Professor and Program Director Victoria College Respiratory Care Program Victoria, Texas Kevin Shane Keene, DHSc, RRT-NPS, CPFT, RPSGT Program Director Respiratory Care University of Cincinnati Cincinnati, OH Tammy Kurszewski, MEd, RRT Director of Clinical Education, Respiratory Care Midwestern State University Wichita Falls, Texas J Kenneth LeJeune, MS, RRT, CPFT Program Director Respiratory Education University of Arkansas Community College at Hope Hope, Arkansas Stacy Lewis-Sells, EdM, RRT-NPS, CPFT, AE-C Program Director for Respiratory Care Southeastern Community College West Burlington, Iowa Cory E Martin, EdS, RRT Program Director, Associate Professor Volunteer State Community College Gallatin, Tennessee Michael McLeland, MEd, RPSGT, RST Program Director Sanford-Brown College Fenton, Missouri Harley R Metcalfe, BS, RRT Adjunct Professor Respiratory Care Program Johnson County Community College; Vice President PM Sleep Lab LLC Overland Park, Kansas REVIEWERS ix Michell Oki, MPAcc, RRT RPFT, RPSGT Assistant Professor Weber State University Respiratory Therapy Ogden, Utah Shawna L Strickland, PhD, RRT-NPS, AE-C, FAARC Clinical Associate Professor University of Missouri Columbia, Missouri Timothy Op’t Holt, EdD, RRT, AE-C, FAARC Professor University of South Alabama Mobile, Alabama Cam Twarog, RRT-NPS, BSRT, MBA Director of Clinical Education Respiratory Care Practitioner Program Wheeling Jesuit University Wheeling, West Virginia Sara Parker, BHS-RT, RRT-NPS, AE-C Clinical Instructor University of Missouri School of Health Professions Columbia, Missouri José D Rojas, PhD, RRT Associate Professor University of Texas Medical Branch Galveston, Texas Paula Denise Silver, BS Biology, PharmD Medical Instructor ECPI University Newport News, Virginia Helen M Sorenson, MA, RRT, FAARC Associate Professor Department of Respiratory Care UT Health Science Center San Antonio, Texas Michael D Werner, MS, RRT, CPFT Respiratory Therapy Program Director Concorde Career College North Hollywood Los Angeles, California Ancillary Authors Craig P Black, PhD, RRT-NPS, FAARC Director, Respiratory Care Program The University of Toledo Toledo, Ohio Jill H Sand, MEd, RRT Program Chair Respiratory Care Southeast Community College Lincoln, Nebraska 248 CHAPTER 11 • Interpretation of Electrocardiogram Tracings appears to be more than one P wave preceding a QRS complex, the rhythm may be the following: • Atrial flutter • Atrial fibrillation (no distinguishable P-waves with a fibrillatory baseline waveform) • Second-degree AV block • Third-degree AV block Measure the PR interval The normal PR interval is 0.12 to 0.20 second (120 to 200 msec) wide A PR interval that is wider than 0.20 second indicates a delay in conduction through the AV node, indicating the possibility of a block (Table 11-5) Measure the width of the QRS complex The normal QRS complex is less than 0.10 second (120 msec) wide Wide QRS complexes can occur with the following: • Bundle branch blocks • Ectopic beats originating in the ventricles (premature ventricular contractions) • Ventricular dysrhythmias such as ventricular tachycardia, idioventricular rhythm, or premature ventricular complexes • Third-degree AV block Inspect the ST segment in all leads ST segment elevation may indicate myocardial injury whereas ST segment depression may indicate myocardial ischemia The portion or wall of the heart that is ischemic can be determined by identifying the leads looking at that portion of the heart (see Table 11-3) The ST segment is measured from the J point: the junction between the QRS complex and the ST segment (see Fig 11-8) Identify the mean QRS axis Most 12-lead ECG tracings indicate the QRS axis Normal axis is to +90 degrees Left-axis deviation is −35 to −90 degrees, and rightaxis deviation is +90 to +180 degrees (see Fig 11-12 and Table 11-4) Box 11-2 lists causes of axis deviation Assess the waveform morphology Some QRS complexes may have additional deflections If there is a second deflection, the second portion is called prime (see Fig 11-6) For example, a second R wave would be labeled R′ Evaluate the Q wave A Q wave is considered normal (or physiologic) if it is less than 0.04 second (40 msec) wide and less than one-third the amplitude of the R wave Q waves that exceed either of these values are considered pathologic and indicate a new or possibly old infarction 10 Look for signs of chamber enlargement High-voltage R waves in the precordial leads indicate ventricular hypertrophy Large or abnormally shaped P waves indicate atrial enlargement (see review later in this chapter) SIMPLY STATED A systematic step-by-step evaluation of the ECG is needed to find all abnormalities Normal Sinus Rhythm Recognizing abnormal rhythms from an electrocardiographic strip is easier if you have an appreciation for the normal tracing (see Fig 11-5) The normal sinus rhythm begins with an upright P wave that is identical from one complex to the next As summarized in Table 11-5, the PR interval is consistent throughout the rhythm strip and is 0.12 to 0.20 second The QRS complexes are identical and no longer than 0.10 second The ST segment is flat The R-R interval is regular and does not vary more than 0.12 second between QRS complexes The heart rate is between 60 and 100 beats/min Identification of Common Dysrhythmias This section discusses the characteristics of some of the most commonly seen dysrhythmias It is always important to treat a symptomatic dysrhythmia, but it is just as important to determine the underlying cause Some of the most common causes of each dysrhythmia are also discussed TABLE 11-5 Summary of Normal Values for the Electrocardiogram Interpretation and Common Alterations Variable Normal Range Common Alterations Rate 60-100/min Rates > 100= tachycardia PR interval 0.12-0.20/sec QRS interval ST segment 0.20 = First-degree AV block >0.10 = Ectopic foci Elevated or depressed = myocardial ischemia Inverted with ischemia, tall and peaked with electrolyte imbalances Box 11-2 Causes of Axis Deviation RIGHT AXIS Left ventricular infarction Right ventricular hypertrophy Chronic obstructive lung disease Acute pulmonary embolism Infants up to year of age (normal) Biventricular hypertrophy Left posterior fascicular LEFT AXIS Right ventricular infarction Left ventricular hypertrophy Abdominal obesity Ascites or large abdominal tumors Third-trimester pregnancy Left anterior fascicular block Interpretation of Electrocardiogram Tracings • CHAPTER 11 Sinus Bradycardia Sinus bradycardia meets all the criteria for a normal sinus rhythm except for the heart rate, which is less than 60 beats/min It is important at this point to understand the difference between an absolute bradycardia and a relative bradycardia Absolute sinus bradycardia is simply a heart rate less than 60 beats/min and may be normal for a particular patient or tolerated well by the patient For example, a conditioned runner may present with a heart rate of 55 beats/min with no negative cardiopulmonary signs and symptoms By definition, this is an absolute bradycardia, but it is probably the patient’s normal heart rate On the other hand, a relative sinus bradycardia or a heart rate that is significantly below a patient’s baseline is generally not tolerated well because it often compromises cardiac performance Marked relative sinus bradycardia may result in hypotension, syncope, diminished cardiac output and shock Transient bradycardia may be caused by an increase in vagal tone as a result of direct carotid massage, manipulation of tracheostomy ties or tube, tracheal suctioning, or the Valsalva maneuver Damage to the SA node, as may occur with a myocardial infarction, can cause a long-term bradycardia Hypothyroidism, hypothermia, and hyperkalemia, and certain drugs may also result in bradycardia (Fig 11-14) Sinus Tachycardia Sinus tachycardia is present when the heart rate is 100 to 150 beats/min, the SA node is the pacemaker, and all the normal conduction pathways in the heart are followed Sinus tachycardia may be well-tolerated by the patient; however, it increases myocardial oxygen demand and decreases the diastolic period, both of which can lead to myocardial ischemia Sinus tachycardia results from sympathetic nervous system stimulation and may indicate a significant physiologic problem or be self-limiting and cease once the underlying cause is addressed Fever, pain, hypoxemia, hypovolemia, hypotension, sepsis, and heart failure are causes of sinus tachycardia It is especially important for the RT to note that tracheal suctioning, especially if it is performed without adequate oxygenation, can cause sinus tachycardia as a compensatory mechanism to hypoxemia In addition, many beta-agonist bronchodilators and excessive intake of caffeine often increase heart rate (Fig 11-15) Sinus Dysrhythmia Sinus dysrhythmia is a benign dysrhythmia that meets all the criteria for normal sinus rhythm except that the rhythm is irregular It usually does not produce symptoms in the patient and requires no treatment In most cases of sinus dysrhythmia, no abnormality of the heart is present Often the irregularities are related to the patient’s breathing pattern This suggests that the changes in intrathoracic pressure associated with breathing in and out are causing changes in the tone of the vagus nerve, which may produce mild alterations in regularity of the heart rate Systematic Evaluation Rate Rhythm P waves PR interval QRS complex 60 to 100 beats/min, may also present as a bradydysrhythmia (0.10 sec) PVCs occur in both the normal and the diseased heart PVCs commonly occur with anxiety or excessive use of caffeine, alcohol, or tobacco Certain medications, such as epinephrine and theophylline, FIGURE 11-19 Electrocardiogram tracing of a single premature ventricular contraction Systematic Evaluation Rate Rhythm P waves PR interval QRS complex That of the underlying rhythm Underlying rhythm is usually regular but irregular with a PVC None associated with the PVC Not measurable Generally more than 0.10 sec in width, abnormal configuration, and premature T wave after the PVC is deflected in a direction opposite to that of the QRS complex There is a full compensatory pause after the PVC confirmed by measuring the interval between the normal QRS complex immediately before the PVC and the normal QRS complex immediately after the PVC; it will be double the normal RR interval for that patient may also provoke PVCs in patients with normal hearts Myocardial ischemia is a common cause of PVCs in patients with heart disease Other causes may include acidosis, electrolyte imbalance, CHF, myocardial infarction, and hypoxia A single PVC poses no threat to the patient (Fig 11-19), but certain configurations of PVCs may signal a serious cardiac problem that may need immediate treatment Although the idea that PVCs are “warning” dysrhythmias has not been proved by clinical research, the following conditions warrant further investigation and indicate the need for close monitoring of the patient: • Increased frequency: Multiple PVCs occur in minute (Fig 11-20) • Multifocal PVCs: The QRS complexes of the PVCs have more than one configuration (Fig 11-21); this indicates that more than one area of the ventricles is irritated • Couplets: Two PVCs occur in a row • Salvos: Three or more PVCs occur in a row (sometimes called a short run of ventricular tachycardia) • R-on-T phenomenon: The PVC occurs during the downslope of the T wave of the preceding beat; this poses a real danger because it can precipitate ventricular tachycardia (Fig 11-22) Ventricular Tachycardia Ventricular tachycardia appears on the monitor as a series of broad QRS complexes, occurring at a rapid rate, each without an identifiable P wave This condition originates from an ectopic focus in the ventricles that may also be associated with enhanced automaticity or reentry By definition, ventricular tachycardia is a run of three or more consecutive PVCs It may be classified as sustained ventricular tachycardia, which lasts more than 30 seconds and requires immediate medical attention, or nonsustained ventricular tachycardia, which terminates spontaneously after FIGURE 11-20 Electrocardiogram tracing of frequent premature ventricular contractions FIGURE 11-21 Electrocardiogram tracing of multifocal premature ventricular contractions Interpretation of Electrocardiogram Tracings • CHAPTER 11 a short burst The rhythm is regular, and the rate is usually in the range of 140 to 300 beats/min The majority of patients deteriorate rapidly with this dysrhythmia; therefore it must be treated as an emergency Without appropriate treatment, sustained ventricular tachycardia may lead to ventricular fibrillation (described later) When ventricular tachycardia occurs, the patient may become hypotensive and be slow to respond If cardiac output deteriorates significantly, the patient usually becomes unresponsive In addition, such patients in ventricular tachycardia may not have a detectable carotid pulse, in which case the American Heart Association (AHA) Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS) rescue protocols should be immediately initiated Ventricular tachycardia is often caused by problems similar to those that cause PVCs When the heart is hypoxic, as occurs with severe myocardial ischemia, ventricular tachycardia is common and is a sign that the patient needs immediate care (Fig 11-23) Ventricular Fibrillation Ventricular fibrillation is the presence of chaotic, completely unorganized electrical activity in the ventricular myocardial fibers It produces a characteristic wavy, irregular pattern on the ECG monitor Depending on the amplitude of the electrical impulses, it can be mistaken for asystole or ventricular tachycardia Because the heart cannot pump blood when fibrillation is occurring, the cardiac output drops to zero and the patient becomes unconscious immediately This dysrhythmia is life threatening and must be treated immediately in accordance with the BLS and ACLS resuscitation protocols, including chest compressions between each defibrillation attempt Ventricular fibrillation often is caused by the same factors that precipitate ventricular tachycardia (Fig 11-24) Asystole Asystole is cardiac standstill and is invariably fatal unless an acceptable rhythm is rapidly restored In fact, asystole is one of the criteria used for the determination of clinical death Asystole is recognized on the ECG monitor as a straight or almost straight line In accordance with AHA resuscitation protocols, the RT or other clinician should quickly assess for a pulse and patient responsiveness early in any rescue effort because what may initially appears to be asystole on an ECG monitor, may simply be a disconnection of the ECG leads, which can resemble asystole In addition, the AHA guidelines call for the confirmation of asystole in more than one lead during resuscitation efforts to ensure it is not fine ventricular fibrillation Clinically, asystole is characterized by immediate pulselessness and loss of consciousness The ECG tracing shows a line that is flat or almost flat, without discernible electrical activity (Fig 11-25) FIGURE 11-22 Electrocardiogram tracing of R-on-T phenomenon FIGURE 11-23 Electrocardiogram tracing of ventricular tachycardia Systematic Evaluation Rate Rhythm P waves PR interval QRS complex 253 140 to 300 beats/min Regular None associated with the QRS complex They may occasionally occur because the sinoatrial node is still functioning Not measurable Abnormal and greater than 0.10 sec in width 254 CHAPTER 11 • Interpretation of Electrocardiogram Tracings SIMPLY STATED In an apparent case of asystole, the patient’s pulse and responsiveness should be quickly checked to confirm whether the patient is indeed pulseless or whether a lead has become disconnected or the equipment has otherwise malfunctioned Also, asystole should be confirmed in more than one lead during resuscitation efforts to ensure it is not fine ventricular fibrillation Pulseless Electrical Activity Pulseless electrical activity (PEA) is not a discrete dysrhythmia but rather an electromechanical condition that can be diagnosed clinically As the name implies, there is a dissociation of the electrical and the mechanical activity of the heart In other words, the pattern that appears on the ECG monitor does not generate a pulse Fortunately, PEA is rare and does not occur without a precipitating event Tension pneumothorax, cardiac trauma, hypothermia, and severe electrolyte or acid-base disturbances are among the most common causes of PEA PEA sometimes is seen as a terminal event in an unsuccessful cardiac resuscitation effort There is no relationship between the electrical pattern appearing on the ECG monitor or tracing and the mechanical activity of the heart PEA therefore is any rhythm that FIGURE 11-24 Electrocardiogram tracing of ventricular fibrillation Systematic Evaluation Rate Rhythm P waves PR interval QRS complex None Irregular, chaotic waves None None No waves appear with any regularity on the tracing There may be occasional lowamplitude waves that appear somewhat like ventricular-origin complexes, but they are sporadic in occurrence and totally irregular does not produce a pulse with the exception of ventricular tachycardia, ventricular fibrillation, and asystole Atrioventricular Heart Block AV heart block is a general term that refers to a disturbance in the conduction of impulses from the atria to the ventricles through the AV node However, the block may be at the level of the AV node or the bundle of His or in the bundle branches Classification of the AV blocks is based on the site of the block and the severity of the conduction disturbance Disturbances in AV conduction can occur as an adverse effect of medications, such as digitalis, or when damage to the conduction system occurs with myocardial infarction In some cases of complete heart block, the patient may develop symptoms associated with hypotension (fainting and weakness) if the ventricles are beating too slowly In milder forms of heart block, the patient often is asymptomatic First-Degree AV Block The mildest form of heart block is first-degree block, which is present when the PR interval is prolonged more than 0.2 second In first-degree block, all the atrial impulses pass through to the ventricles but are delayed at the AV node First-degree AV block may or may not compromise cardiac output It is important to assess the patient as discussed earlier in the section on Steps of ECG Interpretation Some potential causes of first-degree AV block include adverse effects of medications such as digitalis, increased vagal tone, hyperkalemia, myocarditis, and degenerative disease (Fig 11-26) Second-Degree AV Block Type I (Mobitz I) Second-degree AV block type I, also known as Wenckebach, is an intermediate form of heart block that presents with a PR interval that becomes progressively longer (changes in length) until the stimulus from the atria is blocked completely for a single cycle (dropped QRS complex) After the blocked beat, relative recovery of the AV junction occurs, and the progressive increasing of the PR interval starts all over again The ventricular rhythm is almost always irregular As with first-degree AV block, second-degree AV block type I may or may not compromise cardiac output; thus it is important to assess the patient in conjunction with rhythm interpretation Causes of second-degree AV block type I are similar to those of first-degree AV block (Fig 11-27A) FIGURE 11-25 Electrocardiogram tracing of asystole Interpretation of Electrocardiogram Tracings • CHAPTER 11 FIGURE 11-26 First-degree atrioventricular block with a PR interval of 0.30 Systematic Evaluation Rate Rhythm P waves PR interval QRS complex Underlying rhythm rate Regular Normal sinus configuration, each preceding a QRS complex Greater than 0.20 sec in length and constant Less than 0.10 sec in width A FIGURE 11-27 A, Second-degree atrioventricular block type I Systematic Evaluation Rate Rhythm Ventricular rhythm P waves PR interval QRS complex Varies, but ventricular rate is always less than the atrial rate Regular Irregular Normal sinus configuration, not always followed by QRS complex Varies, lengthens, and then drops a QRS complex Less than 0.10 sec in width B B, Second-degree atrioventricular block type II Systematic Evaluation Rate Atrial rhythm Ventricular rhythm P waves PR interval QRS complex Varies, but ventricular rate is always less than the atrial rate Regular May be regular if there is a constant conduction ratio or irregular if conduction is not constant Normal sinus configuration, not always followed by QRS complex Normal or prolonged but always constant Less than 0.10 sec in width 255 256 CHAPTER 11 • Interpretation of Electrocardiogram Tracings FIGURE 11-28 Third-degree heart block characterized by independent atrial (P wave) and ventricular activity The atrial rate is always faster than the ventricular rate Systematic Evaluation Rate Rhythm P waves PR interval QRS complex Usually less than 60 beats/min but may vary; ventricular rate is always less than the atrial rate Both atrial and ventricular rates are regular Normal sinus configuration, not always followed by QRS complex Varies, no relationship Usually greater than 0.10 sec but may also be less than 0.10 sec in width Second-Degree AV Block Type II (Mobitz II) Idioventricular Rhythm Second-degree AV block type II is a rarer but more serious form of second-degree AV block and is characterized by a series of nonconducted P waves followed by a P wave that is conducted to the ventricles It is important to note that each time the P wave is followed by a QRS complex, the PR interval is always fixed (not changing in length) This will help differentiate between the two types of second-degree AV block Sometimes the ratio of nonconducted to conducted P waves is fixed (at 3:1 or 4:1, for example) This block should be considered serious and treated promptly Common causes of second-degree AV block type II include extensive damage to the bundle branches after an acute anteroseptal myocardial infarction or degenerative disease (Fig 11-27B) Idioventricular rhythm occurs when the normal pacemaker does not set the pace for the ventricles In this case, an ectopic focus in one of the ventricles becomes the pacemaker for the ventricles The intrinsic rate of the ventricular tissue is usually less than 40 beats/min, so the ventricular rate is very slow (Fig 11-29) In idioventricular rhythm, the ECG pattern appears as a slow series of wide and bizarre QRS complexes The slower ventricular rate and the loss of assistance in ventricular filling provided by the atria decrease cardiac output significantly and can lead rapidly to heart failure and more severe dysrhythmias There is a variation of idioventricular rhythm called accelerated idioventricular rhythm In accelerated idioventricular rhythm, the rate is in the normal range (40 to 100 beats/min) Third-Degree AV Block Junctional Rhythm The most extreme form of heart block is third-degree AV block, which is caused by conduction disturbances below the AV node in the bundle of His (producing a narrow QRS complex) or bundle branches (producing a wide QRS complex) This block does not allow any conduction of stimuli from the atrium to the ventricles In this situation, the ventricles and atria beat independently of one another Thus there is no distinguishable pattern between the atria and ventricles Third-degree AV block may be transient or permanent but is always considered serious and should prompt immediate intervention Possible causes of transient third-degree AV block may include inferior myocardial infarction, increased vagal tone, myocarditis, and digitalis toxicity Permanent causes may include degenerative disease or acute anteroseptal myocardial infarction (Fig 11-28) In a junctional rhythm, an area in the AV junction assumes the pacemaking role and sends impulses down the normal conduction pathways in the ventricles Because the normal conduction pathways in the ventricles are being used, the QRS complexes appear normal The P wave may be present or absent If present, it may appear immediately after the QRS, plainly demonstrating retrograde conduction In this case, the P wave is typically inverted, indicating that depolarization of the atria followed a retrograde path The P wave may appear before the QRS, but when it does, the PR interval is less than normal duration (0.10 second) This indicates that there was not sufficient time for the P wave to be responsible for initiating the associated QRS complex Some potential causes of a junctional rhythm may include AV node damage, electrolyte disturbances, digitalis toxicity, heart failure, valvular disease, rheumatic fever, and myocarditis (Fig 11-30) Interpretation of Electrocardiogram Tracings • CHAPTER 11 257 FIGURE 11-29 Electrocardiogram tracing of idioventricular rhythm Systematic Evaluation Rate Rhythm P waves PR interval QRS complex 30 to 40 beats/min or slower, unless accelerated, then it may be between 40 and 100 beats/min Regular Absent None Greater than 0.10 sec FIGURE 11-30 Electrocardiogram tracing showing junctional tachycardia Systematic Evaluation Rate Rhythm P waves PR interval QRS complex Normal intrinsic junctional rate, 40 to 60 beats/min Accelerated junctional rate, 60 to 100 beats/min Junctional tachycardia, >100 beats/min Regular Absent or inverted Short if present Less than 0.10 sec FIGURE 11-31 Electrocardiogram tracing showing ST-segment depression Evidence of Cardiac Ischemia, Injury, or Infarction Normally, the ST segment is isoelectric, which means that it is in the same horizontal position as the baseline, or isoelectric line Significant deviations (1 mm) of the ST segment from baseline, either up or down, suggest an abnormality in myocardial perfusion and oxygenation Cardiac ischemia is often seen on the ECG as depression of the ST segment (Fig 11-31) or inversion of the T waves At this point, there is no permanent damage to the heart, and proper therapy usually reverses any ECG 258 CHAPTER 11 • Interpretation of Electrocardiogram Tracings FIGURE 11-32 Electrocardiogram tracing showing ST-segment elevation with a PVC I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 II FIGURE 11-33 Twelve-lead ECG tracing showing ST-segment elevation in leads V1, V2, V3, and V4 This pattern is indicative of acute anteroseptal myocardial injury abnormalities In many cases of myocardial infarction, however, this pattern of ischemia may not be seen because the event has already progressed to the injury phase When ischemia persists, the heart muscle can become permanently injured due to inadequate oxygen delivery for a sustained time period This is known as ST-elevation myocardial infarction (STEMI) In cases involving a STEMI, the typical manifestation on an ECG tracing is an ST elevation in the leads monitoring the electrical activity of the corresponding injured heart tissue (Fig 11-32) For example, an acute myocardial injury to the anteroseptal part of the heart will cause ST segment elevation in the leads that examine the anteroseptal portion of the heart (Fig 11-33; see Table 11-3) In general, the degree of damage to the heart caused by the ischemia determines the degree of ST segment elevation In addition, other symptoms It can be helpful to identify ST segment abnormalities by drawing a straight line over the imaginary isoelectric line This will reveal whether ST segment elevation or depression is present and to what degree If the deviation from the isoelectric line is greater than mm, significant changes have occurred and further investigation is appropriate The patient should be monitored closely when this abnormality is identified It should be noted that rapid identification and treatment of STEMI is critical in achieving favorable clinical outcomes As a result, the AHA has issued specific guidelines for identifying patients with suspected STEMI In addition to ECG changes, these include chest discomfort, shortness of breath, weakness, diaphoresis, nausea and lightheadedness, particularly in the presence of a prior cardiac history or other risk factors such as smoking and obesity In patients with STEMI, the ST segment abnormality often resolves when perfusion is restored However, it should be noted that at some point after myocardial infarction, significant Q waves (0.04 second in length) will be seen on the ECG in the corresponding leads Q waves may develop within hours of an infarction but may not evolve for several days in some patients They persist for the remainder of the patient’s life SIMPLY STATED T-wave inversion and ST-segment depression indicate myocardial ischemia ST-segment elevation indicates that an acute myocardial injury has occurred and indicates the presence of an ST-elevation myocardial infarction, or STEMI Interpretation of Electrocardiogram Tracings • CHAPTER 11 Assessing Chest Pain The significance of pain as a general clinical finding is discussed in Chapter Pain and distress are subjective to the patient’s perception of his or her condition and may be difficult to assess However, it is essential that signs and symptoms associated with cardiac events be accurately reported both verbally and on the patient’s chart The following sequence will provide you with a reference for assessing these signs and symptoms Ask the patient the following: O When and how abrupt was the onset of the symptoms? P What provoked the symptoms? (e.g., exercise, sleep, emotional upset) Q How would you describe the quality of the pain? (e.g., sharp, dull) Does the pain radiate anywhere? R Does anything provide relief from the pain? In what region is the pain located? Does the pain change with deep respiration? S Placing severity on a scale of to 10, how would you rate your pain? T What is the time frame of your symptoms? Is this chronic or acute? U What you think is wrong? Is this different from any previous episodes? The AHA recommends that for chest pain or associated symptoms not relieved by nitroglycerin, a myocardial infarction should be suspected until proven otherwise Remember that “time is muscle,” and treatment interventions, such as thrombolytic therapy or surgical intervention, should be implemented quickly to minimize damage to the myocardium The role of an RT in such cardiac events is to notify the patient’s physician, evaluate and optimize oxygen delivery, obtain a 12-lead ECG, and stand by to participate as a member of the cardiac arrest team if needed 259 with COPD and causes an enlargement of the right side of the heart Enlargement of the right atrium causes the following: • Rightward deviation of the P-wave axis • Enlarged positive P waves greater than 2.5 mm in leads II, III, and aVF • A prominent and negative P wave in lead I • This syndrome is called cor pulmonale Right ventricular enlargement may be associated with this syndrome and is recognized certain characteristics, including: • Right-axis deviation of the QRS complex • Increased R-wave voltage in leads V1, V2, and V3 • Reduced voltage in the limb leads (I, II, and III) is seen when severe pulmonary hyperinflation (emphysema) is present This is seen as QRS complexes that are less than mm tall in leads I, II, and III Reduced voltage in precordial leads V5 and V6 may also be present The reduced measured voltage appears to be caused by the following two factors: • Reduced transmission of electrical activity through hyperinflated lungs • A mean QRS axis directed posteriorly and perpendicular to the frontal plane of the limb leads, causing decreased voltage on the ECG Dysrhythmias often are seen in patients with COPD and acute lung disease Tachycardia, multifocal atrial tachycardia, and ventricular ectopic beats are some of the more common ECG abnormalities seen in COPD Such dysrhythmias occur as the result of hypoxemia from lung disease and from adverse effects of medications (e.g., bronchodilators) used to treat the obstructed airways Hypoxemia often worsens during sleep in patients with COPD and increases the prevalence of nighttime dysrhythmias SIMPLY STATED Patients with chronic hypoxemic lung disease often have evidence of right-axis deviation on the ECG This is seen as a negative QRS in lead I SIMPLY STATED For a patient with severe cardiac symptoms, the role of the RT is to quickly notify the physician, optimize oxygen delivery, obtain an ECG, and assist in resuscitation if the patient worsens Electrocardiogram Patterns with Chronic Lung Disease The majority of patients with COPD have ECG abnormalities Hyperinflation of the lungs and flattening of the diaphragm are associated with a more vertical position of the heart This causes a clockwise rotation and contributes to the right-axis deviation associated with COPD (For quick axis determination, see Table 11-4.) Additionally, chronic pulmonary hypertension is common in patients KEY POINTS w An ECG is an indirect measurement of the electrical activity of the heart w The normal electrical conducting pathway of the heart starts with the SA node, then travels through the AV junction, bundle of His, bundle branches, and Purkinje fibers and finally through the heart muscle known as the myocardium w The RT should recommend that an ECG be obtained whenever the patient has signs and symptoms (e.g., chest pain) of an acute cardiac disorder such as a myocardial infarction w Disturbances in the cardiac conduction system are called dysrhythmias, which can be detected with an ECG 260 CHAPTER 11 • Interpretation of Electrocardiogram Tracings KEY POINTS—cont’d w The RT should remember that dysrhythmias can occur for many reasons, including hypoxemia, myocardial ischemia, sympathetic nerve stimulation, and certain drugs w On an ECG, the initial wave of electrical activity or P wave signals atrial depolarization, the QRS complex represents ventricular depolarization, and the T wave occurs with ventricular repolarization w On ECG paper, time is measured on the horizontal axis, and voltage or amplitude is measured on the vertical axis w On ECG paper, each small square represents 0.04 second, and each large square is 0.2 second Therefore, if the interval between R waves (RR interval) is five large boxes (1 second) and the rhythm is regular, then the rate is 60 beats/minute w An ECG involves the placement of six leads on the extremities and another six chest leads across the chest to measure cardiac electrical activity from several different angles w There are several steps involved in ECG interpretation, including identifying the heart rate, evaluating the rhythm and presence of P waves, and measuring both the PR interval and the QRS complex w Sinus tachycardia in an adult is a common dysrhythmia characterized by a heart rate of 100 to 150 beats/minute, a regular rhythm, and normal P waves, PR interval, and QRS complex It may be caused by hypoxemia and selected respiratory medications such as certain β-agonist bronchodilators w Sinus bradycardia in an adult is characterized by a regular rhythm and heart rate less than 60 beats/minute as well as normal P waves, PR interval, and QRS complex This dysrhythmia can be caused by vagal stimulation associated with suctioning or tracheostomy tube manipulation w PVCs can occur in a normal heart as a result of causes such as hypoxemia, or they can signal a diseased heart PVCs can occur several times per minute, two or more in a row, as different shapes tend to be considered more serious w Dysrhythmias, such as ventricular fibrillation characterized by chaotic electrical activity or asystole (cardiac standstill), should be considered by the RT as medical emergencies that require immediate and aggressive intervention according to resuscitation protocols w In an apparent case of asystole, the RT should quickly assess for a pulse and patient responsiveness early in any rescue effort because what may initially appear to be asystole on an ECG monitor may simply be a disconnection of the ECG leads w The AHA guidelines indicate that during resuscitation efforts, asystole should be confirmed in more than one ECG lead to rule out fine ventricular fibrillation w Rapid identification and treatment of ST-elevation myocardial infarction (STEMI) is critical in achieving favorable clinical outcomes As a result, the AHA has issued specific guidelines for identifying patients with suspected STEMI In addition to ECG changes, these include chest discomfort, shortness of breath, weakness, diaphoresis, nausea, and lightheadedness w The role of the RT for a patient experiencing severe chest pain is to notify the physician, evaluate and optimize oxygen delivery, help ensure that a 12-lead ECG is quickly obtained, and be ready to participate as part of the cardiac resuscitation team ASSESSMENT QUESTIONS See Appendix for answers ECGs are useful to evaluate all of the following, except: a Impact of lung disease on the heart b Pumping ability of the heart c Severity of the myocardial infarction d Heart rhythm What clinical findings are most suggestive of the need for an ECG? a Headache and flulike symptoms b Orthopnea and chest pain c Fever and cough d Joint pain and swelling For an adult, what is the normal intrinsic rate of the heart’s primary pacemaker? a 90 to 110 beats/min b 60 to 100 beats/min c 40 to 80 beats/min d 40 to 60 beats/min What is the normal intrinsic rate of the heart’s secondary pacemaker? a 80 to 100 beats/min b 60 to 100 beats/min c 40 to 60 beats/min d 30 to 40 beats/min What does the P wave on the ECG recording represent? a Atrial depolarization b Atrial repolarization c Ventricular depolarization d Ventricular repolarization What does the QRS wave on the ECG recording represent? a Atrial depolarization b Atrial repolarization c Ventricular depolarization d Ventricular repolarization What does the T wave on the ECG recording represent? a Atrial depolarization b Atrial repolarization c Ventricular depolarization d Ventricular repolarization Which of the following is within the normal range for a PR interval? a 0.10 second b 0.20 second c 0.30 second d 0.40 second What is the upper limit of a normal QRS complex? a