(BQ) Part 2 book Wilkins clinical assessment in respiratory care has contents: Pulmonary function testing, chest imaging, interpretation of electrocardiogram tracings, neonatal and pediatric assessment, older patient assessment,.... 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 Interpretation of Electrocardiogram Tracings • CHAPTER 11 241 ϭ Electrical impulse Fully repolarized and resting cell Onset of depolarization Partially depolarized and contracted Depolarization Repolarization Fully depolarized and contracted Fully repolarized and relaxed cell Partially repolarized and relaxed Onset of repolarization FIGURE 11-4 Depolarization and repolarization of a cardiac cell (From Huszar RH: Basic dysrhythmias: interpretation and management, ed St Louis, 2007, Mosby.) QRS P PR Interval PR Segment T ST U ST Segment QT Interval FIGURE 11-5 Normal configuration of electrocardiogram waves, segments, and intervals repolarization In most cases the U wave is not seen The clinical significance of its presence or absence is not known QRS complexes usually consist of several distinct waves, each of which has a letter assigned to it as a label This labeling system is needed because the precise configuration of the QRS complex can vary from one lead to the next and from one patient to the next To establish a standardized labeling system, several guidelines have been developed If the first deflection of the QRS complex is downward (negative in lead II), it is labeled a Q wave The initial upward (positive) deflection is called an R wave The first negative deflection following an R wave is called an S wave (Fig 11-6) If the QRS complex has a second positive deflection, it is labeled R′ (R prime), and if a second S wave is also present it is called S′ (S prime) A negative deflection can be called a Q wave only if it is the first wave of the complex In clinical practice, each ventricular depolarization complex is called a QRS complex whether it has all three waves or not SIMPLY STATED The QRS complex is important in evaluating the ECG because it reflects the electrical activity of the ventricles CHAPTER 11 • Interpretation of Electrocardiogram Tracings 242 Electrocardiogram Paper and Measurements The electrical activity of the heart is recorded on paper that has gridlike boxes with light and dark lines running horizontally and vertically (Fig 11-7) The light lines circumscribe small boxes (1 × mm) and the dark lines circumscribe larger boxes (5 × mm) Time is measured on the horizontal axis of the ECG paper The ECG paper moves through the electrocardiograph at a speed of 25 mm/sec Therefore each small square (1 mm) represents 0.04 second and each larger square (5 mm) represents 0.2 second Five large boxes represent 1.0 second On the vertical axis, voltage, or amplitude, of the ECG waves is measured The exact voltage of any ECG wave can R R R S Q Q S R1 R R R S S S1 FIGURE 11-6 QRS nomenclature See text for explanation be measured because the electrocardiograph is standardized so that mV produces a deflection 10 mm in amplitude Therefore, the standard for most ECG recordings is 1 mV = 10 mm Each small square represents mm To measure the amplitude of a specific wave, the isoelectric baseline must be identified This is the flat line seen just before the P wave or right after the T or U wave (Fig 11-8) Any movement of the ECG stylus above this line is considered positive; any downward movement is considered negative To measure the degree of positive or negative amplitude of a specific wave, the isoelectric line is used as a reference point marking zero voltage R waves are measured from the isoelectric line to the top of the R wave Q and S waves are measured from the isoelectric line to the bottom of the wave (see Fig 11-6) P waves can be either positive or negative and are also measured from the isoelectric line to the top (if positive) or bottom (if negative) of the wave In addition to the amplitude of any wave, the duration of waves, intervals, and segments can be measured A segment is a straight line between two waves An interval encompasses at least one wave plus the connecting straight line The normal P wave is less than 2.5 mm in height and not more than 0.11 second in length The PR interval is an important measurement that provides information regarding conduction time This interval is measured from the beginning of the P wave, where the P wave lifts off the isoelectric line, to the beginning of the QRS complex (see Fig 11-5) The PR interval represents the time it takes for the electrical stimulus to spread through the atria and to pass through the AV junction to the ventricles The normal PR interval is between 0.12 and 0.20 second (3 to small boxes) If conduction of the impulse through the AV junction is abnormally delayed, the PR interval will exceed 0.2 second A prolonged PR interval is called first-degree AV block and is discussed later in this chapter The duration of ventricular depolarization is determined by measuring the QRS interval This interval is measured from the first wave of the QRS complex to the end of the last wave of the QRS complex Normally the QRS interval does QRS 0.04 sec mm Isoelectric P ST Baseline T mm 0.20 sec FIGURE 11-7 Gridlike boxes of electrocardiogram paper illustrating the 1-mm and 5-mm boxes FIGURE 11-8 Isoelectric baseline used for measuring voltage of electrocardiogram waves (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed St Louis, 2006, Mosby.) Interpretation of Electrocardiogram Tracings • CHAPTER 11 not exceed 0.10 seconds (2 1/2 small boxes) The amplitude of the QRS complex may range from to 15 mm, depending on the lead and the size of the ventricular mass A very important segment to evaluate is the ST segment This segment is the portion of the ECG cycle from the end of the QRS complex (even if no S wave is present) to the beginning of the T wave (see Fig 11-5) It measures the time from the end of ventricular depolarization to the start of ventricular repolarization The normal ST segment is isoelectric (no positive or negative voltage) or at least does not move more than mm above or below baseline Certain pathologic abnormalities, such as myocardial ischemia or injury, cause the ST segment to be elevated or depressed (Fig 11-9) The duration of the ST segment is not as important as its configuration 243 to the next indicates that the heartbeat is irregular and may be a sign of sinus dysrhythmia, which is described in more detail in the section on dysrhythmia identification The QT interval is measured from the beginning of the QRS complex to the end of the T wave (see Fig 11-5) This interval represents the time from the beginning of ventricular depolarization to the end of ventricular repolarization The normal values for the QT interval depend on the heart rate As the heart rate increases, the QT interval normally shortens; as the heart rate decreases, the QT interval increases As a general rule, the QT interval that exceeds one half of the RR interval is prolonged if the heart rate is 80 beats/min or less Common causes of an abnormally prolonged QT interval include hypokalemia (low potassium), hypocalcemia (low calcium), and the side effects of certain medications such as quinidine SIMPLY STATED Evaluating Heart Rate In patients suspected of having acute myocardial ischemia, the ST segment is important to evaluate Significant elevation or depression of the ST segment must be recognized and responded to immediately If the heart rate is regular, one of the easiest ways of determining the heart rate is to count the number of large (0.2 second) boxes between successive QRS complexes and divide this number into 300 For example, if there is one large box between successive R waves, then each R wave is separated by 0.2 second Over the course of 1.0 second there will be QRS complexes and 300 QRS complexes in 60 seconds Therefore the heart rate is 300 beats/min Following this logic: large boxes = rate of 150 beats/min (300/2=150) large boxes = rate of 100 beats/min (300/3=100) large boxes = rate of 75 beats/min (300/4=75) large boxes = rate of 60 beats/min (300/5=60) large boxes = rate of 50 beats/min (300/6=50) If the heart rate is irregular, this method will not be accurate because the spacing between QRS complexes will vary from beat to beat In such cases, the average rate can be determined by counting the number of QRS complexes in a 6-second interval (30 large boxes) and multiplying the number by 10 Because the top of the ECG paper is marked with small vertical dashes every seconds, 6-second intervals are easy to identify An increase or decrease in heart rate by more than 20% of the baseline value is generally regarded as a significant change and should be evaluated further An abnormally slow heart rate may reduce cardiac performance to the point of compromised perfusion Recall that cardiac output is a product of stroke volume and heart rate A heart rate below 60 beats/min is referred to as an absolute bradycardia However, bradycardia that may require intervention is relative to the individual patient For example, a well-conditioned runner may present with a heart rate of 50 beats/min with no signs of inadequate cardiac output On the other hand, a person with poor myocardial contractility that presents with a heart rate of 50 beats/min is likely to show signs of compromised perfusion or even cardiogenic shock in severe cases At the other extreme, an adult heart rate greater than 100 beats/min is known as tachycardia An increase in heart The RR interval is useful in identifying the rate and regularity of ventricular contraction The distance in millimeters is determined from one R wave to the next in successive QRS complexes This is done for several different RR intervals ECG calipers can be helpful in making this measurement The average of the measurements is determined and converted to time Remember that each large box is equal to 0.2 second and large boxes equal 1.0 second If the RR interval is 1.5 seconds, the heart rate is 40 beats/min (60 seconds divided by 1.5 = 40) If the RR interval is 1.0 second, the heart rate is 60 beats/min If the RR interval is 0.5 second, the heart rate is 120 beats/min This method for determining the heart rate is easy to apply if the RR interval falls conveniently on one of the numbers just described Unfortunately, this is not usually the case Other methods for calculating the heart rate are described later Marked variation in the RR interval from one interval A B C FIGURE 11-9 ST segments A, Normal B, Abnormal elevation C, Abnormal depression 244 CHAPTER 11 • Interpretation of Electrocardiogram Tracings rate above 130-140 beats/min may compromise cardiac performance This is because an abnormally rapid heart rate will increase myocardial oxygen demand, possibly to the point of inducing ischemia if the demand exceeds the supply Additionally, significant tachycardia may further induce ischemia because it shortens the diastolic period, which is the period when most coronary perfusion occurs In instances of extreme tachycardia where the heart rate exceeds 160 beats/minute, the ventricular filling time may be too short to permit adequate refilling, thus reducing cardiac output In severe tachycardia, the combined effects of increased oxygen demand and decreased cardiac output is potentially dangerous, especially for those patients with pre-existing cardiac conditions Such patients should be monitored carefully and the attending physician notified immediately Superior aVR aVL I Left Right III aVF II Electrocardiogram Leads Because the heart is a three-dimensional organ, a more complete picture of the electrical activity in the heart will be obtained if it is viewed from several different angles The standard ECG uses 12 different leads to provide 12 different views from different angles of the heart Interpretation of the 12 leads is a little more difficult, but the information obtained is more complete and abnormalities are not likely to be missed The 12 leads can be subdivided into two groups: extremity (limb) leads and chest leads To obtain the six limb leads, two electrodes are placed on the patient’s wrists and two on the patient’s ankles The ECG machine can vary the orientation of these four electrodes to one another to create the six limb leads The chest leads are created by attaching six electrodes across the patient’s chest The chest leads are discussed after the limb leads are reviewed Limb Leads The six limb leads are called leads I, II, III, aVR, aVL, and aVF Leads I, II, and III are bipolar Each lead is created by comparing the difference in electrical voltage between two electrodes For lead I, the ECG machine temporarily designates the electrode on the left arm as a positive lead and the electrode on the right arm as negative The measured difference in voltage between these two leads results in lead I For lead II, the right arm electrode remains negative and the left leg electrode is positive Lead III is created by making the left arm negative and the left leg positive The other three limb leads (aVR, aVL, and aVF) are called augmented leads because the ECG machine must amplify the tracings to get an adequate recording The augmented leads are created by measuring the electrical voltage at one limb lead, with all other limb leads made negative For the augmented leads, the ECG machine must augment the recorded voltages by about 50% to get an adequate recording Lead aVR is created by making the right arm positive Inferior FIGURE 11-10 Frontal plane showing spatial relationships of six extremity leads (Modified from Goldberger AL: Clinical electrocardiography: a simplified approach, ed St Louis, 2006, Mosby.) and all the others negative Lead aVL calls for the left arm to be positive, and lead aVF is created by making the left leg positive The six limb leads view the heart in a vertical plane called a frontal plane Any electrical activity that is directed up, down, left, or right is recorded by the limb leads (Fig 11-10) The frontal plane can be envisioned as a giant circle that surrounds the patient and lies in the same plane as the patient This circle can be marked off in 360 degrees, as shown in Figure 11-10 The angle of orientation for each of the bipolar limb leads can be determined by drawing a line from the designated negative lead to the designated positive lead For lead I, the angle of orientation is degrees; for lead II, +60 degrees; and for lead III, +120 degrees For the augmented leads, the angle of orientation can be determined by drawing a line from the average of the other three limb leads to the one that is designated as the positive lead The angle of orientation is −150 degrees for lead aVR, −30 degrees for lead aVL, and 90 degrees for lead aVF In review, the limb leads consist of three bipolar leads and three unipolar leads The three bipolar leads are called Interpretation of Electrocardiogram Tracings • CHAPTER 11 TABLE 11-3 The 12 Leads of an Electrocardiogram and the Myocardial Wall that Each Set Views Lead View I, aVL, V5, V6 II, III, aVF V1, V2 V3, V4 Lateral Inferior Septal Anterior Cells and Function Pacemaker cells Conducting cells Myocardial cells Specialized cells that have a high degree of automaticity and provide the electrical power for the heart Cells that conduct the electrical impulse throughout the heart Cells that contract in response to electrical stimuli and pump the blood 245 limb leads, each chest lead has its own view or angle of orientation Leads V1 through V4 often are called the anterior leads because they view the anterior portion of the heart Leads V5 and V6 view the left lateral portion of the heart and are therefore called the left lateral leads (see Table 11-3) More specifically, leads V1 and V2 are positioned next to the sternum and normally view the interventricular septum, leads V3 and V4 are placed on the left anterior chest to view the anterior wall of the left ventricle, and V5 and V6 are positioned on the axillary area of the left chest and therefore view the lateral wall of the left ventricle SIMPLY STATED The normal ECG has six limb leads that examine the heart in the vertical plane and six chest leads that examine the heart in the horizontal plane Evaluating the Mean QRS Axis Angle of Louis V1 V2 V3 V4 V5 V6 FIGURE 11-11 Position of the six chest leads V1 is located in the fourth intercostal space right of the sternum V2 is located in the fourth intercostal space left of the sternum V3 is placed between V2 and V4 V4 is placed in the fifth intercostal space in the midclavicular line V5 is placed between V4 and V6 V6 is placed in the fifth intercostal space in the midaxillary line (Modified from Goldberger AL: Clinical electrocardiography: a simplified approach, ed St Louis, 2006, Mosby.) leads I, II, and III The three unipolar leads are called aVR, aVL, and aVF The abbreviation a refers to augmented, V to voltage, and R, L, and F to right arm, left arm, and left leg (foot), respectively The limb leads measure the electrical activity in the heart that occurs in the frontal plane, and each lead has its own specific view or angle of orientation to the heart (Table 11-3) Chest Leads The six chest leads, or precordial leads, are called leads V1, V2, V3, V4, V5, and V6 The chest leads are unipolar leads that are placed across the chest in a horizontal plane Figure 11-11 shows the correct placment of the six chest leads The chest leads define a horizontal or transverse plane and view electrical voltages that move anteriorly and posteriorly Like the The QRS axis represents the general direction of current flow during ventricular depolarization Although depolarization spreads through the ventricles in different directions, an average or mean direction can be determined Normally, the mean QRS axis (vector) points leftward (patient’s left) and downward, somewhere between and 90 degrees in the frontal plane previously described (Fig 11-12) The ECG records a positive (upward) QRS complex when the mean QRS axis is moving toward a positive electrode When the mean QRS axis is moving toward a negative lead, the QRS complex is negative (downward) Because each of the six limb leads has its own angle of orientation as defined in the hexaxial reference system, a review of the recorded limb leads should identify the mean QRS axis in the frontal plane To identify the mean QRS axis, begin by sketching the hexaxial reference system, including labels for the points where the limb leads are located on the circle Next, identify which limb lead has the QRS complex with the most voltage (positive or negative) This is accomplished by identifying the QRS complex with the largest deflection from baseline If the largest deflection is positive (R wave), the mean QRS axis points toward the lead with the tallest QRS If the most voltage is negative (Q or S wave), the mean axis points away from that lead For example, if the most voltage is found to be in lead II and it is positive, then the mean QRS axis must be about +60 degrees because this is where lead II is located on the hexaxial reference system (see Fig 11-12) This would be considered a normal axis because it falls between and +90 degrees If the most voltage is found in lead I and is negative, then the QRS axis is approximately 180 degrees because lead I is located at degrees This would be consistent with rightaxis deviation In some situations, the most voltage may be equally present in two leads If two leads exhibit equal positive voltage, 246 CHAPTER 11 • Interpretation of Electrocardiogram Tracings I II III aVR aVL Ϫ150° aVR aVF Ϫ30° aVL I 0° III ϩ120° II ϩ60° aVF FIGURE 11-12 Normal mean QRS axis of 60 degrees (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed St Louis, 2013, Mosby.) I II III aVR aVL aVF FIGURE 11-13 Sample electrocardiogram showing right-axis deviation Note the positive QRS complex (R wave) in leads II and III and the negative QRS complex (S wave) in lead I (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed St Louis, 2013, Mosby.) the mean axis must fall midway between the two leads If the most voltage is equally negative in two leads, the mean axis is opposite the midpoint between the two leads As mentioned, a normal QRS axis is approximately −35 to +90 degrees If the axis is found to be between +90 and 180 degrees, right-axis deviation is present Right-axis deviation is common in patients with cor pulmonale (right ventricular enlargement due to chronic lung disease) In such cases, the QRS complex will be negative in lead I but positive in lead aVF Leads II and III are both positive in most cases of right-axis deviation; however, lead III will be taller than lead II (Fig 11-13 and Table 11-4) Right-axis deviation is important to recognize early in the care of the patient since it often indicates significant chronic pulmonary TABLE 11-4 Quick Axis Determination Lead Axis I is positive II is positive I is positive II is negative I is negative II is positive I is negative II is negative Normal Left deviation Right deviation Extreme right deviation Interpretation of Electrocardiogram Tracings • CHAPTER 11 hypertension This is most often related to chronic hypoxemia from chronic obstructive pulmonary disease (COPD) Left-axis deviation is present when the mean axis is found to be between -35 and -90 degrees Left-axis deviation can occur in several different conditions, including left ventricular hypertrophy and blocks of the left bundle branch In such cases, the QRS complex is positive in lead I and negative in lead aVF In addition, the QRS complex in lead III will demonstrate negative voltage with left-axis deviation If the mean QRS axis is found to be between −90 and −180 degrees, extreme left or right-axis deviation is present This condition is not common When the ECG recording indicates that it may be present, the extremity leads should be checked to make sure they are attached properly The same principles of axis evaluation can be applied to the P wave as to the QRS complex When normal sinus rhythm is present and the atria are normal in size, the P wave is positive in lead II and negative in lead aVR Therefore the normal P wave is directed toward lead II and away from lead aVR, making the normal mean P wave axis about +60 degrees In cor pulmonale, right atrial enlargement is common The ECG will show tall, narrow P waves in leads II, III, and aVF in such cases SIMPLY STATED The normal mean axis is somewhere between −35 and +90 degrees Right-axis deviation indicates that the right ventricle is enlarged; left-axis deviation suggests that the left ventricle is enlarged Steps of Electrocardiogram Interpretation First and most importantly, the patient’s condition must be evaluated All dysrhythmias should be interpreted and evaluated in accordance with the patient’s clinical presentation and medical history Important signs and symptoms that may be associated with dysrhythmias may include the following: • Chest pain • Dyspnea • Fine, inspiratory crackles in the lower lobes • Palpitations • Nausea • Pale, cool, clammy skin • Dizziness or syncope • Sense of impending doom • Hypotension • Altered level of consciousness Interpretation of dysrhythmias can be accomplished on three levels The first level is simply identifying ventricular response The contraction of the ventricles determines the majority of the cardiac output and perfusion of blood to the tissues The ventricular response is determined by 247 evaluating the QRS complexes and subsequent pulse strength Second, dysrhythmias can be placed into categories based on the origin of the impulse formation, which may include the following: • Atrial • Junctional • Ventricular Third, dysrhythmias can be evaluated based on the electrophysiology (or pathway) of the conduction disturbance These can be categorized as follows: • Ectopic beats or rhythms • Escape beats or rhythms • AV blocks • Bundle branch blocks To make sure that all components of the ECG tracing are reviewed by the RT or other member of the patient care team, a systematic method should be used It is important to avoid assumptions resulting from quickly glancing at an ECG strip, because they may lead to misinterpretation Every strip should be read from left to right and the step-by-step process described here should be followed, generally in the order they are listed The steps are as follows: Identify the heart rate Most modern ECG monitors provide a display of the heart rate Always take the patient’s pulse to verify that the monitor is calculating the heart rate correctly Note that the monitor may not provide an accurate rate if the rhythm is irregular If this is the case, a strip should be printed and calculation should be done as mentioned in the section on Evaluating Heart Rate Rhythms are called bradycardia if the rate is below 60 beats/min and tachycardia if the heart rate is over 100 beats/min (see Table 11-4) Evaluate the rhythm Note whether the spacing between the QRS complexes is equal Small variations of 0.04 second (40 msec) are considered normal If the spaces are greater than 0.04 second, the rhythm is irregular Irregularity may occur randomly or in patterns (e.g., occur every other beat or change with respirations) Irregular rhythms are present with the following dysrhythmias: • Ectopic beats • Escape beats • Second-degree AV blocks • Atrial fibrillation • Sinus dysrhythmia Note the presence of P waves A normal P wave generally is positive, depending on the lead, and has a rounded shape Normal P waves are less than 0.11 second (110 msec) wide and less than 2.5 mm (21/2 small boxes) tall Oddly shaped P waves may indicate atrial enlargement Normal rhythms will only have one P wave preceding each QRS complex, and each P wave should have the same configuration as the others If there 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 ... 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... Radiograph, 21 2 Clinical and Radiographic Findings in Lung Diseases, 21 4 Postprocedural Chest Radiograph Evaluation, 22 2 Computed Tomography, 22 5 Magnetic Resonance Imaging, 22 7 Radionuclide Lung Scanning,... and index ISBN 978-0- 323 -10 029 -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