Egan's Fundamentals of Respiratory Care [12 ed.] 0323811213, 9780323811217

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EGAN’S

FUNDAMENTALS OF RESPIRATORY CARE

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EDITION

EGAN’S

12

FUNDAMENTALS OF RESPIRATORY CARE Robert M. Kacmarek, PhD, RRT, FAARC, FCCP, FCCM Professor of Anesthesiology Department of Anesthesia, Critical Care and Pain Medicine Harvard Medical School; Director of Respiratory Care Respiratory Care Services Massachusetts General Hospital Boston, Massachusetts

James K. Stoller, MD, MS, FAARC, FCCP Professor and Chairman, Education Institute, Cleveland Clinic Jean Wall Bennett Professor of Medicine Samson Global Leadership Academy Endowed Chair Cleveland Clinic Cleveland, Ohio

Albert J. Heuer, PhD, MBA, RRT-ACCS, RPFT, FAARC Professor Department of Interdisciplinary Studies Rutgers, School of Health Professions Newark, New Jersey; Lead Respiratory Therapist Adult Intensive Care Morristown Medical center Morristown, New Jersey; Co-Owner and Associate Course Director RT Board Review.net Strategic Learning Associates, LLC Belleville, New Jersey

Consulting Editors

Robert L. Chatburn, MHHS, RRT-NPS, FAARC

Richard H. Kallet, MS, RRT, FAARC

Professor of Medicine Lerner College of Medicine of Case Western Reserve University, Director Simulation Fellowship, Education Institute Program Manager Enterprise Respiratory Care Research Respiratory Institute Cleveland Clinic Cleveland, Ohio

Formerly, Director of Clinical Research and Quality Assurance (Retired) Department of Anesthesia Respiratory Care Division University of California, San Francisco; San Francisco General Hospital and Trauma Center San Francisco, California

3251 Riverport Lane St. Louis, Missouri 63043 EGAN’S FUNDAMENTALS OF RESPIRATORY CARE, TWELFTH EDITION Copyright © 2021 by Elsevier, Inc. All rights reserved.

ISBN: 978-0-323-51112-4

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. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notice Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2017, 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, and 1969. Library of Congress Control Number: 2019940232

Director, Traditional Nursing Program: Tamara Myers Senior Content Strategist: Yvonne Alexopoulos Content Development Manager: Luke Held Senior Content Development Specialist: Maria Broeker Publishing Services Manager: Julie Eddy Senior Project Manager: Rachel E. McMullen Design Direction: Amy Buxton Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

For my wonderful children, Darla, Robert, Julia, Katie, and Callie, some gone too early from my life, who all make it worthwhile, and for Cristina, the love of my life, who has made me whole again. RMK I dedicate this work to the memory of my parents, Norma and Alfred Stoller, who instilled the values of rigor and commitment that inform this book; to my wife, Terry Stoller, whose love and support have been the foundation upon which my contribution to this book is possible; to our son, Jake Fox Stoller, whose shining promise gives purpose and illuminates the world; and to generations of Respiratory Therapists, whose daily activities and commitment better our health and give hope. JKS To my mother, who is long gone from this earth but continues to be the most dominant, positive influence in my life. Mom taught me many lessons, including that failure is to be expected on the way to success, and excellence can only be achieved through hard work, sacrifice, and perseverance. These lessons have proven invaluable. Hence, my work on this text is dedicated to my mother, Edith; as well as my lovely wife, Laurel; my faculty colleagues and students; fellow respiratory therapists; and the patients we tirelessly serve. AJH

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CONTRIBUTORS Loutfi S. Aboussouan, MD, FCCP

Will Beachey, PhD, RRT, FAARC

Associate Professor of Medicine Cleveland Clinic Lerner College of Medicine Director Neuromuscular program Respiratory Institute Cleveland Clinic Cleveland, Ohio

Professor Emeritus Department of Respiratory Care School of Health Sciences University of Mary Bismarck, North Dakota

Adam Alter, MD Pulmonary & Critical Care Medicine Maine Medical Center Portland, Maine

Arzu Ari, PhD, RRT, PT, CPFT, FAARC Professor Department of Respiratory Care Cleveland Clinic Lerner College of Medicine of Texas State University San Marcos, Texas

Edwin L. Coombs, Jr. MA, RRT, NPS, ACCS, CPFT, FAARC Director of Marketing-Intensive Care Marketing Department Draeger, Inc. Telford, Pennsylvania

Lorenzo Berra, MD

M. Cornelia Cremens, MD, MPH

Anesthesiologist and Critical Care Physician Massachusetts General Hospital; Reginald Jenney Associate Professor of Anesthesia Harvard Medical School Boston, Massachusetts

Geriatric Psychiatrist Co-chair of the Optimum Care Committee Assistant in Psychiatry at Harvard Medical School Massachusetts General Hospital Boston, Massachusetts

Jason Bordelon, MHA, RRT

Anthony L. DeWitt, RRT, CRT, JD, FAARC

Director Respiratory Care Services Houston Methodist -The Medical Center Houston, Texas

Attorney at Law Bartimus, Frickleton, Robertson, Rader, PC Leawood, Kansas

Rendall W. Ashton, MD, FACP, FCCP Associate Professor of Medicine Cleveland Clinic Lerner College of Medicine of the Case Western Reserve University Associate Director of Graduate Medical Education, Education Institute Program Director, Pulmonary and Critical Care Medicine Fellowship, Respiratory Institute Cleveland, Ohio

Amy Attaway, MD Assistant Professor of Medicine, Lerner College of Medicine Departments of Pulmonary and Critical Care Medicine/Respiratory Institute Cleveland Clinic Cleveland, Ohio

Joseph Thomas Azok, MD Staff Radiologist Imaging Institute Radiology Lerner College of Medicine of Case Western Reserve University Cleveland Clinic Cleveland, Ohio

Thomas A. Barnes, EdD, RRT, FAARC Lead Faculty MSRC Program College of Professional Studies, Professor Emeritus of Cardiopulmonary Sciences Department of Health Sciences Bouve College of Health Sciences Boston, Massachusetts

Jeffrey T. Chapman, MD Chair Respiratory Institute and Quality & Patient Safety Institute at Cleveland Clinic Abu Dhabi Abu Dhabi, United Arab Emirates

Robert L. Chatburn, MHHS, RRT-NPS, FAARC Professor of Medicine Lerner College of Medicine of Case Western Reserve University; Director Simulation Fellowship, Education Institute, Program Manager Enterprise Respiratory Care Research, Respiratory Institute Cleveland Clinic Lerner College of Medicine Cleveland, Ohio

Robert M. DiBlasi, BSRT, RRT-NPS, FAARC Research Manager, Principal Investigator Respiratory Therapy Department Seattle Children’s Hospital and Research Institute Seattle, Washington

Raed A. Dweik, MD, MBA, FACP, FRCP(C), FCCP, FCCM, FAHA, ATSF Professor and Chairman, Respiratory Institute Cleveland Clinic Lerner College of Medicine Cleveland, Ohio

Matthew C. Exline, MD MPH

Assistant Director of Respiratory Care Massachusetts General Hospital Boston, Massachusetts

Associate Professor Medical Director, Medical Intensive Care Unit Division of Pulmonary, Critical Care, and Sleep Medicine Department of Internal Medicine The Ohio State University Columbus, Ohio

Joseph Cicenia, MD, MBA, FCCP

James B. Fink, PhD, RRT, FAARC, FCCP

Staff Respiratory Institute Cleveland Clinic Cleveland, Ohio

Adjunct Faculty Graduate College Division of Health Sciences Rush University Graduate College; Chicago, Illinois; Chief Science Officer Aerogen Pharma Corp San Mateo, California

Daniel W. Chipman BS, RRT

Zaza Cohen, MD ICU Director Department of Medicine Hackensack University Medical Center at Mountainside Montclair, New Jersey

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CONTRIBUTORS

Daniel F. Fisher, MS, RRT

Anne Marie Hilse, RRT-ACCS

Sarah A. Longworth, MD

Director Respiratory Care Boston Medical Center Boston, Massachusetts

Lead Respiratory Therapist Atlantic Health System Morristown Medical Center Morristown, New Jersey

Assistant Professor of Clinical Medicine Department of Medicine Hospital of the University of Pennsylvania Philadelphia, Pennsylvania

Thomas G. Fraser, MD

Robert Duncan Hite, MD, FCCP, FACP

Scott P. Marlow, RRT, BA

Staff Physician, Medical Director for Infection Prevention Infectious Disease Cleveland Clinic Lerner College of Medicine of Case Western Reserve University Cleveland, Ohio

Professor, Mark A. and Alice W. Brown Chair Director of Medical Intensive Care Division of Pulmonary, Critical Care and Sleep Medicine University of Cincinnati College of Medicine Cincinnati, Ohio

Pulmonary Rehabilitation Coordinator Respiratory Institute Cleveland Clinic Cleveland, Ohio

Jacopo Fumagalli, MD Staff Anesthesiologist Anesthesia, Critical Care and Pain Medicine Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico di Milano Milan, Italy

Douglas S. Gardenhire, EdD, RRT-NPS, FAARC Chair Department of Respiratory Therapy Georgia State University Atlanta, Georgia

Robert M. Kacmarek, PhD, RRT, FAARC, FCCP, FCCM Professor of Anesthesiology Department of Anesthesia, Critical Care and Pain Medicine Harvard Medical School; Director of Respiratory Care Respiratory Care Services Massachusetts General Hospital Boston, Massachusetts

Richard H. Kallet, MS, RRT FAARC Donna D. Gardner, MSHP, RRT-NPS, FAARC, FCCP Associate Professor Respiratory Care Texas State University San Marcos, Texas

Umur Hatipoğlu, MD Enterprise Medical Director of Respiratory Therapy and the Section Head of Respiratory Therapy Department of Critical Care Medicine, Director, COPD Center Associate Professor of Medicine Pulmonary and Critical Care Medicine Cleveland Clinic Lerner College of Medicine of Case Western Reserve University; Respiratory Institute Cleveland Clinic Lerner College of Medicine Cleveland, Ohio

Albert J. Heuer, PhD, MBA, RRT-ACCS, RPFT, FAARC Professor Department of Interdisciplinary Studies Rutgers, School of Health Professions Newark, New Jersey; Lead Respiratory Therapist Adult Intensive Care Morristown Medical center Morristown, New Jersey; Co-Owner and Associate Course Director RT Board Review.net Strategic Learning Associates, LLC Belleville, New Jersey

Director of Clinical Research and Quality Assurance (Retired) Department of Anesthesia Respiratory Care Division University of California, San Francisco; San Francisco General Hospital and Trauma Center San Francisco, California

Danai Khemasuwan, MD, MBA Assistant Professor Pulmonary, Critical Care and Sleep Medicine St. Elizabeth Medical Center/Tufts University School of Medicine Boston, Massachusetts

Peter J. Mazzone, MD, MPH, FCCP Director of Lung Cancer Program Respiratory Institute Cleveland Clinic Cleveland, Ohio

Atul C. Mehta, MD, FACP, FCCP Professor of Medicine Lerner College of Medicine, Buoncore Family Endowed Chair in Lung Transplantation, Staff Department of Pulmonary Medicine Respiratory Institute Cleveland Clinic Lerner College of Medicine Cleveland, Ohio

Michele Messam, BSMT (ASCP), CIC Infection Preventionist Infection Prevention Department Cleveland Clinic Cleveland, Ohio

Eduardo Mireles-Cabodevila, MD Director, Medical Intensive Care Unit Medical Director, Simulation and Advanced Skills Center Assistant Professor of Medicine Cleveland Clinic Lerner College of Medicine of Case Western Reserve University Respiratory Institute Cleveland Clinic Cleveland, Ohio

Carolyn J. La Vita, MHA, RRT Assistant Director Respiratory Care Massachusetts General Hospital Boston, Massachusetts

Alex George LeGassey, BS Associate of Science; Respiratory Care Bachelor of Science; Applied Science with Minor in Biology, ECMO Program Coordinator Department of Respiratory Care Massachusetts General Hospital Boston, Massachusetts

Andres Osorio, MSHM, RRT Master of Science in Healthcare Management, Bachelor of Science in Health Science, Associate in Applied Science in Respiratory Care, Respiratory Therapist, Director of Project Implementation & Safety Officer Respiratory Care The PromptCare Companies, Inc New Providence, New Jersey

CONTRIBUTORS

Hilary Petersen, MPAS, PA-C

Daryl Rogers, MAS, RRT

Assistant Professor School of Medicine, Physician Assistant Program Case Western Reserve University; Physician Assistant Respiratory Institute Cleveland Clinic Cleveland Ohio

Director of Professional Services AtHome Medical Atlantic Health System Morris Plains, New Jersey

Thomas Piraino, RRT, FCSRT, FAARC Clinical Specialist, Mechanical Ventilation Department of Respiratory Care Center of Excellence in Mechanical Ventilation St. Michael’s Hospital Toronto, Ontario, Canada; Lecture (Adjunct) Department of Anesthesia Division of Critical Care McMaster University Hamilton, Ontario, Canada

Massimiliano Pirrone, MD Anaesthesiologist Dipartimento di Anestesia-Rianimazione e Emergenza Urgenza Fondazione IRCCS Ca’ Granda - Ospedale Maggiore Policlinico Milan, Italy

Janet Reid-Hector, EdD RDN Asst. Professor, Director Masters in Healthcare Management Program Department of Interdisciplinary Studies, Rutgers University, Biomedical & Health Sciences, School of Health Professions Newark, New Jersey

Frederic Romain, RRT, BA, MDiv, DMin Reverend Doctor Massachusetts General Hospital Respiratory Care Services Massachusetts General Hospital Optimum Care Committee (Ethics) Boston, Massachusetts

Steven K. Schmitt, M.D., FIDSA, FACP Associate Professor of Medicine Department of Infectious Disease Cleveland Clinic Lerner College of Medicine of Case Western Reserve University; Head, Section of Bone and Joint Infections Associate Professor of Medicine Department of Infectious Disease Cleveland Clinic Cleveland, Ohio

Brian K. Siegel, MD, MS, FACS Clinical Assistant Professor of Surgery Sidney Kimmel Medical College of Thomas Jefferson University Attending Physician, Trauma and Surgery Morristown Medical Center Morristown, New Jersey

Siddharta D. Silva, RRT Assistant Manager Respiratory Care Department Morristown Medical Center Atlantic Health System Morristown, New Jersey

Robert C. Stansbury Ellen M. Robinson, RN, PhD, HECC Massachusetts Memorial Hospital Nurse Ethicist and Co-Leader of MGH Optimal Care Committee Boston, Massachusetts

Narciso E. Rodriguez, BS, RRT, RRTNPS, RRT-ACCS, RPFT Co-Owner and Course Director RT Board Review.net Strategic Learning Associates, LLC Belleville, New Jersey; Staff Therapist Saint Barnabas Medical Center Livingston, New Jersey

James K. Stoller, MD, MS, FAARC, FCCP Professor and Chairman, Education Institute, Cleveland Clinic Jean Wall Bennett Professor of Medicine Samson Global Leadership Academy Endowed Chair Cleveland Clinic Cleveland, Ohio

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Patrick J. Strollo, Jr., MD, FACP, FCCP, FAASM Vice Chair of Medicine for Veterans Affairs, Professor of Medicine and Clinical and Translational Science Division of Pulmonary, Allergy, and Critical Care Medicine University of Pittsburgh Montefiore University Hospital Pittsburgh, Pennsylvania

Clorinda B. Suarez, RRT-NPS, BS Quality and Safety Officer Respiratory Care Department Massachusetts General Hospital Boston, Massachusetts

Adriano R. Tonelli, MD, MSc Staff Respiratory Institute Cleveland Clinic Cleveland, Ohio

David L. Vines, PhD, RRT, FAARC, FCCP Chairperson and Respiratory Care Program Director Department of Cardiopulmonary Sciences Rush University Medical Center Chicago, Illinois

Teresa A. Volsko, MBA, MHHS, RRT, CMT-E, FAARC Instructor, Director, Respiratory Care, Transport, the Communication Center Akron Children’s Hospital Akron, Ohio

Brian K. Walsh, PhD, RRT, RRT-NPS, RRT-ACCS, FAARC Professor and Director of Respiratory Therapy Allied Health Professions Liberty University Lynchburg, Virgina

Purris F. Williams, BS RRT Respiratory Therapist Senior Clinician Respiratory Care Department ALS Multidisciplinary Clinic Massachusetts General Hospital Boston, Massachusetts

REVIEWERS Suellen Carmody-Menzer MBA, RRT, RRT-NPS, AE-C Director Clinical Education/Instructor Respiratory Care Program Health Department Southeastern Community College West Burlington, Iowa Diana Day, MBA/GM, RRT, RCP Program Director Allied Health Fresno City College Fresno, California Lindsay Fox, MEd, RRT-NPS Program Director Respiratory Care Program St. Louis Community College St. Louis, Missouri Jennifer L. Keely, RCP, MEd, RRT-ACCS Assistant Clinical Professor Department of Clinical and Diagnostic Sciences University of Missouri Columbia, Missouri

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Jennifer Riggs, RRT, MSCTE Respiratory Care Muskegon Community College Muskegon, Michigan Beth A. Zickefoose, B.S., RRT-ACCS, NPS, RPFT, Licensed as an RCP in the State of Ohio Retired Professor and Director of Respiratory Care Program Respiratory Care Sinclair Community College Dayton, Ohio Emily L. Zyla, MS, LRT, RRT Clinical Coordinator, Asst. Professor Department of Clinical Laboratory Sciences, Respiratory Care and Health Care Administration College of Health Profession Ferris State University Big Rapids, Michigan

P R E FA C E Donald F. Egan, MD, the original author of Egan’s Fundamentals of Respiratory Care, sought to provide a foundation of knowledge for respiratory therapy students learning the practice in 1969. However, the scope of the respiratory care profession is ever-expanding, and the skills and information needed to be an effective respiratory therapist have expanded with it. With improved technology and vast scientific and medical advances, the body of knowledge required for respiratory therapists has increased greatly since the first edition of the text was published. Now in its twelfth edition, Egan’s Fundamentals of Respiratory Care encompasses the most relevant information to date and has provided a comprehensive knowledge base for students and professionals for more than 45 years. While these updated editions of Egan’s Fundamentals of Respiratory Care still accomplish Dr. Egan’s original goal—“to present what is felt to be the minimum knowledge for the safe and effective administration of inhalation therapy”—this text also goes far beyond the minimum, delving into important concepts and providing detailed information and resources to enhance student comprehension. Every editor, guest editor, and contributor to the book is a leading figure in respiratory care, and the vast experience of these individuals ensures that critical content is covered accurately. Using the combined knowledge of these individuals, Egan’s Fundamentals of Respiratory Care covers the role of respiratory therapists, the scientific bases for treatment, and clinical application skills. With 58 detailed chapters all focused on a unique aspect of respiratory care, Egan’s Fundamentals of Respiratory Care is without equal in providing the prerequisite information required of a respiratory therapist today.

ORGANIZATION This edition of the text is organized in a logical sequence of sections and chapters that build on each other to facilitate comprehension of the material. The earlier sections provide a basis for the profession and cover the physical, anatomic, and physiologic principles necessary to understand succeeding chapters. The later chapters address specific cardiopulmonary diseases and the diagnostic and therapeutic techniques that accompany them. Details on preventive and long-term care, as well as Ethics and End of Life, are also provided in the later chapters. In order of presentation, the seven sections are: I. Foundations of Respiratory Care II. Applied Anatomy and Physiology III. Assessment of Respiratory Disorders IV. Review of Cardiopulmonary Disease V. Basic Therapeutics VI. Acute and Critical Care VII. Patient Education and Long-Term Care

FEATURES There are many characteristic features throughout the book designed with the student in mind, making Egan’s Fundamentals of Respiratory Care unique and engaging as a primary textbook. Each chapter begins in a similar manner, outlining the content and drawing attention to what should be mastered through the use of: • Chapter Objectives • Chapter Outlines • Key Terms The most important features within each chapter are accented by the ample use of figures, boxes, and tables containing key information and by the use of: • “Rules of Thumb”—“pearls” of information highlighting rules, formulas, and key points necessary to the study of respiratory therapy and to future clinical practice • “Mini-Clinis”—critical thinking case studies illustrating potential problems that may be encountered during patient care • Therapist-Driven Protocols—examples of decision trees developed by hospitals and used by respiratory therapists to assess patients, initiate care, and evaluate outcomes Also, each chapter concludes with: • A “Summary Checklist” of key points that the student should have mastered on completion of the chapter • A complete list of references

NEW TO THIS EDITION This edition has been updated to reflect the most current information in the National Board for Respiratory Care (NBRC) Therapist Exam Content Outline. Also featured is an expanded role for the NBRC Exam Matrix Correlation chart within all of the student and instructor offerings. Several chapters have been added, including Heart Failure; and ethics and end-of-life. Many other chapters have been substantially revised or completely rewritten to reflect the dynamic and expanding field of respiratory care. Furthermore, the content of the entire text has been refined and simplified to be more easily understood and relevant to our key audiences: respiratory therapy students, faculty, and therapists throughout the world.

LEARNING AIDS Workbook and Evolve Resources The Workbook for Egan’s Fundamentals of Respiratory Care is an exceptional resource for students. Offering a wide range of activities, it allows students to apply the knowledge they have gained using the core text. Presented in an engaging format, the workbook breaks down the more difficult concepts and guides students through the most important information. Beyond the many NBRC-style multiple-choice questions in the workbook, students xi

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PREFACE

have access to animations, English/Spanish glossary, student lecture notes, and Body Spectrum, an anatomy coloring book. Answers to the Workbook are available on the Evolve site. Evolve also includes animations, English/Spanish Glossary, Student Lecture Notes, and Body Spectrum Anatomy Coloring Book.

FOR THE INSTRUCTOR Evolve Resources Evolve is an interactive learning environment designed to work in coordination with this text. Instructors may use Evolve to provide an Internet-based course component that expands the concepts presented in class. Evolve can be used to publish the class syllabus, outlines, and lecture notes; set up “virtual

office hours” and email communication; and encourage student participation through chatrooms and discussion boards. Evolve also allows instructors to post exams and manage their grade books. The intuitive and comprehensive Evolve Learning Resources associated with this text provide instructors with valuable resources to use as they teach, including: • More than 3000 test bank questions available in ExamView • Comprehensive PowerPoint presentations for each chapter • An image collection of the figures in the book • Workbook answer key • TMC/CSE Correlation Guide For more information, visit http://evolve.elsevier.com/Egans or contact an Elsevier sales representative.

CONTENTS SECTION I

Foundations of Respiratory Care

1 Early History of Respiratory Care, 1 Robert M. Kacmarek, Albert J. Heuer, and James K. Stoller

2 The Profession of Respiratory Therapy, 15

SECTION IV Review of Cardiopulmonary Disease 24 Pulmonary Infections, 490 Sarah A. Longworth and Steven K. Schmitt

Scott P. Marlow and Umur Hatipoğlu

25 Obstructive Lung Disease: Chronic Obstructive Pulmonary Disease (COPD), Asthma, and Related Diseases, 510

Michele Messam and Thomas G. Fraser

26 Interstitial Lung Disease, 538

Brian K. Walsh

3 Quality, Patient Safety, and Communication, 28 4 Principles of Infection Prevention and Control, 47 5 Ethical and Legal Implications of Practice, 68 Anthony L. DeWitt

6 Physical Principles of Respiratory Care, 87 Daniel F. Fisher

7 E-Medicine in Respiratory Care, 112 Narciso E. Rodriguez and Albert J. Heuer

8 Fundamentals of Respiratory Care Research, 134 Robert L. Chatburn

SECTION II

Applied Anatomy and Physiology

9 The Respiratory System, 150 Narciso E. Rodriguez and Siddharta Silva

10 The Cardiovascular System, 206 Narciso E. Rodriguez

11 Ventilation, 225 Eduardo Mireles-Cabodevila

12 Gas Exchange and Transport, 246 Zaza Cohen

13 Solutions, Body Fluids, and Electrolytes, 268 Daniel F. Fisher

14 Acid–Base Balance, 285 Will Beachey

15 Regulation of Breathing, 308 Will Beachey

SECTION III Assessment of Respiratory Disorders 16 Bedside Assessment of the Patient, 317 Richard H. Kallet

17 Interpreting Clinical and Laboratory Data, 342 Richard H. Kallet

18 Interpreting the Electrocardiogram, 353 Albert J. Heuer

19 Analysis and Monitoring of Gas Exchange, 368 Brian K. Siegel, Albert J. Heuer, and Richard H. Kallet

20 Pulmonary Function Testing, 395 Zaza Cohen

21 Review of Thoracic Imaging, 419 Joseph Thomas Azok and James K. Stoller

22 Flexible Bronchoscopy and the Respiratory Therapist, 447 Danai Khemasuwan and Atul C. Mehta

23 Nutrition Assessment, 468 Janet Reid-Hector

Amy Attaway, Umur Hatipoğlu, and James K. Stoller Jeffrey T. Chapman and Jason Bordelon

27 Pleural Diseases, 552 Joseph Cicenia

28 Pulmonary Vascular Disease, 569 Adriano R. Tonelli and Raed A. Dweik

29 Acute Respiratory Distress Syndrome, 587 Matthew C. Exline, Eduardo Mireles-Cabodevila, and Robert Duncan Hite

30 Respiratory Management of Trauma, Obesity, Near Drowning, and Burns, 612 Massimiliano Pirrone and Lorenzo Berra

31 Acute Heart Failure, 630 Jacopo Fumagalli and Lorenzo Berra

32 Lung Cancer, 647 Peter J. Mazzone and Hilary Petersen

33 Neuromuscular and Other Diseases of the Chest Wall, 663 Adam Alter, Eduardo Mireles-Cabodevila, and Rendell W. Ashton

34 Disorders of Sleep, 682 Robert C. Stansbury and Patrick J. Strollo, Jr.

35 Neonatal and Pediatric Respiratory Disorders, 699 Robert M. DiBlasi and Edwin L. Coombs, Jr.

SECTION V Basic Therapeutics 36 Airway Pharmacology, 725 Douglas S. Gardenhire

37 Airway Management, 748 Carolyn J. La Vita

38 Emergency Cardiovascular Life Support, 788 Thomas A. Barnes

39 Humidity and Bland Aerosol Therapy, 817 James B. Fink and Arzu Ari

40 Aerosol Drug Therapy, 842 James B. Fink and Arzu Ari

41 Storage and Delivery of Medical Gases, 884 David L. Vines

42 Medical Gas Therapy, 906 Albert J. Heuer and Anne Marie Hilse

43 Lung Expansion Therapy, 936 Daniel F. Fisher

44 Airway Clearance Therapy, 952 David L. Vines and Donna D. Gardner

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CONTENTS

SECTION VI Acute and Critical Care

53 Discontinuing Ventilatory Support, 1184

45 Respiratory Failure and the Need for Ventilatory Support, 972

54 Neonatal and Pediatric Respiratory Care, 1212

Loutfi S. Aboussouan

46 Mechanical Ventilators, 987 Robert L. Chatburn and Teresa A. Volsko

47 Physiology of Ventilatory Support, 1013 Robert M. Kacmarek

48 Patient–Ventilator Interactions, 1053 Robert M. Kacmarek

49 Initiating and Adjusting Invasive Ventilatory Support, 1072 Robert M. Kacmarek

50 Noninvasive Ventilation, 1105 Purris F. Williams

51 Extracorporeal Life Support, 1128

Robert M. Kacmarek Daniel W. Chipman

SECTION VII Patient Education and Long-Term Care 55 Patient Education and Health Promotion, 1243 Donna D. Gardner

56 Cardiopulmonary Rehabilitation, 1260 Andres Osorio and Albert J. Heuer

57 Respiratory Care in Alternative Settings, 1279 Albert J. Heuer and Daryl Rogers

58 Ethics and the End of Life, 1299 Ellen M. Robinson, Frederic Romain, and M. Cornelia Cremens

Clorinda B. Suarez and Alex George LeGassey

52 Monitoring the Patient in the Intensive Care Unit, 1146 Thomas Piraino

Glossary, 1318

SECTION I  Foundations of Respiratory Care

1  Early History of Respiratory Care Robert M. Kacmarek, Albert J. Heuer, and James K. Stoller

CHAPTER OBJECTIVES After reading this chapter you will be able to: • Define respiratory care • Summarize some of the major events in the history of science and medicine that have directly affected respiratory care • Explain how the respiratory care profession began • Describe the historical development of the major clinical areas of respiratory care

• Name some of the important historical figures in respiratory care • Describe the major respiratory care educational, credentialing, and professional associations • Explain how the important respiratory care organizations began • Describe the development of respiratory care education

CHAPTER OUTLINE Definitions, 2 History of Respiratory Medicine and Science, 2 Ancient Times, 2 The Middle Ages, Renaissance, and Enlightenment Period, 2 Nineteenth and Early Twentieth Centuries, 4

Development of the Respiratory Care Profession, 4 Clinical Advances in Respiratory Care, 4 Professional Organizations and Events, 9 American Association for Respiratory Care, 9 Respiratory Care Week, 10 Board of Medical Advisors, 10

American Respiratory Care Foundation, 10 International Council for Respiratory Care, 10 National Board for Respiratory Care, 11 Committee on Accreditation for Respiratory Care, 11 Respiratory Care Education, 11

Fellow of the American Association for Respiratory Care (FAARC) International Council for Respiratory Care (ICRC) National Board for Respiratory Care (NBRC)

physician assistant respiratory care respiratory care practitioner respiratory therapist (RT) respiratory therapy

KEY TERMS American Association for Respiratory Care (AARC) American Respiratory Care Foundation (ARCF) Board of Medical Advisors (BOMA) Committee on Accreditation for Respiratory Care (CoARC)

The history of science and medicine is a fascinating topic, which begins in ancient times and progresses to the 21st century. Although respiratory care is a newer discipline, its roots go back to the dawn of civilization. The first written account of positivepressure ventilation using mouth-to-mouth resuscitation is

thought to have been recorded more than 28 centuries ago.1 Air was thought to be one of the four basic elements by the ancients, and the practice of medicine dates back to ancient Babylonia and Egypt. The progression of science and medicine continued through the centuries, and the development of the modern 1

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SECTION I  Foundations of Respiratory Care

disciplines of anesthesiology, pulmonary medicine, and respiratory care during the 20th century depended on the work of many earlier scientists and physicians. This chapter describes the early development of respiratory medicine and the history and development of the field of respiratory care. Specifically, after a historical overview, the birth of respiratory care as a profession is discussed, followed by a discussion of specific therapies (e.g., supplemental oxygen, mechanical ventilation) and a description of various respiratory care organizations (e.g., the American Association for Respiratory Care, the American Respiratory Care Foundation).

DEFINITIONS Respiratory care, also known as respiratory therapy, has been defined as the health care discipline that specializes in the promotion of optimal cardiopulmonary function and health.2 Respiratory therapists (RTs) apply scientific principles to prevent, identify, and treat acute or chronic dysfunction of the cardiopulmonary system.2 Respiratory care includes the assessment, treatment, management, control, diagnostic evaluation, education, and care of patients with deficiencies and abnormalities of the cardiopulmonary system.2 Respiratory care is increasingly involved in preventing respiratory disease, managing patients with chronic respiratory disease, and promoting health and wellness.2 RTs, also known as respiratory care practitioners, are health care professionals who are educated and trained to provide respiratory care to patients. Approximately 75% of all RTs work in hospitals or other acute care settings.3 However, many RTs are employed in clinics, physicians’ offices, skilled nursing facilities, and cardiopulmonary diagnostic laboratories. Others work in research, disease management programs, home care, and industry. RTs are also employed by colleges and universities to teach students the skills they need to become RTs. A human resources survey conducted in 2014 by the American Association for Respiratory Care (AARC) revealed that there were approximately 172,000 RTs practicing in the United States3; this represented a 19% increase over a similar study conducted 4 years earlier in 2009. As the incidence of chronic respiratory diseases continues to increase, the demand for RTs is expected to be even greater in the years ahead. Although the RT as a distinct health care provider was originally a uniquely North American phenomenon, since the 1990s there has been a steady increase in specially trained professionals providing respiratory care worldwide. This trend is referred to as the globalization of respiratory care. RULE OF THUMB  Respiratory care has been defined as the health care discipline that specializes in promoting optimal cardiopulmonary function and health.2 RTs apply scientific principles to prevent, identify, and treat acute or chronic dysfunction of the cardiopulmonary system.

HISTORY OF RESPIRATORY MEDICINE AND SCIENCE Several excellent reviews of the history of respiratory care have been written; the reader is encouraged to review these

publications.1,4-6 A summary of notable historical events in respiratory care is provided in Tables 1.1. A brief description of the history of science and medicine follows.

Ancient Times Humans have been concerned about the common problems of sickness, disease, old age, and death since primitive times. Early cultures developed herbal treatments for many diseases, and surgery may have been performed in Neolithic times. Physicians practiced medicine in ancient Mesopotamia, Egypt, India, and China.1,4,7 However, the foundation of modern western medicine was laid in ancient Greece, with the development of the Hippocratic corpus.1,4,7,8 This ancient collection of medical treatises is attributed to the “father of medicine,” Hippocrates, a Greek physician who lived during the fifth and fourth centuries bc.1,7,8 Hippocratic medicine was based on four essential fluids, or “humors”—phlegm, blood, yellow bile, and black bile—and the four elements—earth (cold, dry), fire (hot, dry), water (cold, moist), and air (hot, moist). Diseases were thought to be humoral disorders caused by imbalances in these essential substances. Hippocrates believed that an essential substance in air was distributed to the body by the heart.1 The Hippocratic oath, which admonishes physicians to follow certain ethical principles, is given in a modern form to medical students at graduation.1,8 Aristotle (384 to 322 bc), a Greek philosopher and perhaps the first great biologist, believed that knowledge could be gained through careful observation.1,8 He made many scientific observations, including some obtained by performing experiments on animals. Erasistratus (~330 to 240 bc), regarded by some as the founder of the science of physiology, developed a pneumatic theory of respiration in Alexandria, Egypt, in which air (pneuma) entered the lungs and was transferred to the heart.1,7 Galen (130 to 199 ad) was an anatomist in Asia Minor whose comprehensive work dominated medical thinking for centuries.1,6,7 Galen also believed that inspired air contained a vital substance that somehow charged the blood through the heart.1

The Middle Ages, Renaissance, and Enlightenment Period The Romans carried on the Greek traditions in philosophy, science, and medicine. With the fall of the Western Roman Empire in 476 ad, many Greek and Roman texts were lost and Europe entered a period during which few advances were made in science or medicine. In the seventh century ad, the Arabians conquered Persia, where they found and preserved many of the works of the ancient Greeks, including the works of Hippocrates, Aristotle, and Galen.1,7 A golden age of Arabian medicine (850 to 1050 ad) followed. An intellectual rebirth in Europe began in the 12th century.1,7 Medieval universities were formed, and contact with the Arabs in Spain and Sicily reintroduced ancient Greek and Roman texts. Magnus (1192 to 1280) studied the works of Aristotle and made many observations related to astronomy, botany, chemistry, zoology, and physiology. The Renaissance (1450 to 1600) ushered in a period of scientific, artistic, and medical advances. Leonardo da Vinci (1452 to 1519) studied human anatomy, determined that subatmospheric intrapleural pressures inflated the lungs,

CHAPTER 1  Early History of Respiratory Care

3

TABLE 1.1  Major Historical Events in Respiratory Care in the 20th Century 1909 1910 1911 1913 1918 1926 1928 1938 1945 1947 1948 1952 1954 1958 1960 1961 1963 1964 1967 1967 1968 1969 1970 1971 1972 1973 1974 1974 1975 1977 1978 1979 1982 1983 1983 1984 1984 1991 1992, 1993 1994 1998

Melltzer (1851–1920; United States) introduces oral endotracheal intubation. Oxygen tents are in use, and the clinical use of aerosolized epinephrine is introduced. Drager (1847–1917; Germany) develops the Pulmotor ventilator for use in resuscitation. Jackson develops a laryngoscope to insert endotracheal tubes. Oxygen mask is used to treat combat-induced pulmonary edema. Barach develops an oxygen tent with cooling and carbon dioxide removal. Drinker develops his “iron lung” negative-pressure ventilator. Barach develops the meter mask for administering dilute oxygen. Boothby, Lovelace, and Bulbulian devise the BLB mask at the Mayo Clinic for delivering high concentrations of oxygen. Motley, Cournand, and Werko use intermittent positive-pressure ventilation to treat various respiratory disorders. The ITA is formed in Chicago, Illinois. The ITA later becomes the AARC. Bennett introduces the TV-2P positive-pressure ventilator. Mørch introduces the piston ventilator. The ITA becomes the AITA. Bird introduces the Bird Mark 7 positive-pressure ventilator. The Campbell Ventimask for delivering dilute concentrations of oxygen is introduced. Jenn becomes the first registered respiratory therapist. Also, metaproterenol, a preferential β-2 bronchodilator, is introduced. The Board of Schools is formed to accredit inhalation therapy educational programs. The Emerson Postoperative Ventilator (3-PV) positive-pressure volume ventilator is introduced. The Bennett MA-1 volume ventilator is introduced, ushering in the modern age of mechanical ventilatory support for routine use in critical care units. The combined pH-Clark-Severinghaus electrode is developed for rapid blood gas analysis. The fiberoptic bronchoscope becomes available for clinical use. The Engström 300 and Ohio 560 positive-pressure volume ventilators are introduced. ARDS and PEEP are described by Petty, Ashbaugh, and Bigelow. The Swan-Ganz catheter, developed for the measurement of pulmonary artery pressures, is introduced. The ARCF is incorporated. The JRCITE is incorporated to accredit respiratory therapy educational programs. CPAP is introduced by Gregory. The Respiratory Care journal is introduced. The Siemens Servo 900 ventilator is introduced. IMV is described by Kirby and Downs. The AAIT becomes the AART. The IMV Emerson ventilator is introduced. The National Board for Respiratory Therapy (NBRT) is formed. The Bourns Bear I ventilator is introduced. The JRCITE becomes the JRCRTE. Puritan Bennett introduces the MA-2 volume ventilator. The AAR Times magazine is introduced. AIDS is recognized by the Centers for Disease Control (CDC [later, Centers for Disease Control and Prevention]). Siemens Servo 900C and Bourns Bear II ventilators are introduced. The NBRT becomes the National Board for Respiratory Care (NBRC). President Reagan signs a proclamation declaring National Respiratory Care Week. Bennett 7200 microprocessor-controlled ventilator is introduced. The AART is renamed the AARC. The Servo 300 ventilator is introduced. The AARC holds national respiratory care education consensus conferences. The CDC publishes the first guidelines for the prevention of ventilator-associated pneumonia. The CoARC is formed, replacing the JRCRTE.

AAIT, American Association for Inhalation Therapist; AARC, American Association for Respiratory Care; ARCF, American Respiratory Care Foundation; ARDS, acute respiratory distress syndrome; BLB, Boothby, Lovelace, and Bulbulian; CoARC, Committee on Accreditation for Respiratory Care; CPAP, continuous positive-airway pressure; IMV, intermittent mandatory ventilation; ITA, Inhalational Therapy Association; JRCITE, Joint Review Committee for Inhalation Therapy Education; JRCRTE, Joint Review Committee for Respiratory Therapy Education; NBRC, National Board for Respiratory Care; NBRT, National Board for Respiratory Therapy; PEEP, positive end-expiratory pressure. Data from references 1, 3–9, 11–14, and 17.

and observed that fire consumed a vital substance in air without which animals could not live.1,4 Vesalius (1514 to 1564), considered to be the founder of the modern field of human anatomy, performed human dissections and experimented with resuscitation.1 In 1543, the date commonly given as the birth modern science, Copernicus observed that the planet Earth orbited the

sun.8 Before this time, it had been accepted that Earth was the center of the universe. The 17th century was a time of great advances in science. Accomplished scientists from this period include Kepler, Bacon, Galileo, Pascal, Hooke, and Newton. In 1628, Harvey fully described the circulatory system.4,8 In 1662, the chemist Boyle

4

SECTION I  Foundations of Respiratory Care

published what is now known as Boyle’s law, governing the relationship between the volume and pressure of a gas.8 Torricelli invented the barometer in 1650, and Pascal showed that atmospheric pressure decreases with altitude.1,4 van Leeuwenhoek (1632 to 1723), known as the “father of microbiology,” improved the microscope and was the first to observe and describe singlecelled organisms, which he called “animalcules.”7 The 18th-century Enlightenment period brought further advances in the sciences. In 1754, Black described the properties of carbon dioxide, although the discovery of carbon dioxide should be credited to van Helmont, whose work occurred approximately 100 years earlier.1 In 1774, Priestley described oxygen, which he called “dephlogisticated air.”1,4 Before 1773, Scheele performed the laboratory synthesis of oxygen, which he called “fire air”; a general description of his discovery appeared in 1774, and a more thorough description in 1777.1,4 Shortly after the discovery of oxygen, Spallanzani worked out the relationship between the consumption of oxygen and tissue respiration.1 In 1787, Charles described the relationship between gas temperature and volume, now known as Charles’ law.8 In experiments performed between 1775 and 1794, Lavoisier showed that oxygen was absorbed by the lungs and that carbon dioxide and water were exhaled.1,4 In 1798, Beddoes began using oxygen to treat various conditions at his Pneumatic Institute in Bristol.1,4 RULE OF THUMB In 1662, the chemist Boyle published what is now known as Boyle’s law, governing the relationship between gas volume and pressure.

Nineteenth and Early Twentieth Centuries During the 19th century, important advances were made in physics and chemistry related to respiratory physiology. Dalton described his law of partial pressures for a gas mixture in 1801 and his atomic theory in 1808.8 Young in 1805 and de LaPlace in 1806 described the relationship between pressure and surface tension in fluid droplets.8 Gay-Lussac described the relationship between gas pressure and temperature in 1808; in 1811, Avogadro determined that equal volumes of gases at the same temperature and pressure contain the same number of molecules.1,8 In 1831, Graham described his law of diffusion for gases (Graham’s law).8 In 1865, Pasteur advanced his “germ theory” of disease, which held that many diseases are caused by microorganisms.8 Medical advances during this time included the invention of the spirometer and ether anesthesia in 1846, antiseptic techniques in 1865, and vaccines in the 1880s.1,4,7 Koch, a pioneer in bacteriology, discovered the tubercle bacillus, which causes tuberculosis, in 1882, and the vibrio bacterium, which causes cholera, in 1883.7 He also developed Koch’s postulates, which are criteria designed to establish a causative relationship between a microbe and a disease. Respiratory physiology also progressed with the measurement in 1837 of blood oxygen and carbon dioxide content, description around 1880 of the respiratory quotient, demonstration in 1885 that carbon dioxide is the major stimulant for breathing, and demonstration in 1878 that oxygen partial pressure and blood oxygen content were related.1,4,9 In 1895, Roentgen

discovered the x-ray, and the modern field of radiologic imaging sciences was born.8 Pioneering respiratory physiologists of the early 20th century described oxygen diffusion, oxygen and carbon dioxide transport, the oxyhemoglobin dissociation curve, acidbase balance, and the mechanics of breathing and made other important advances in respiratory physiology. RULE OF THUMB In experiments performed between 1775 and 1794, Lavoisier showed that oxygen was absorbed by the lungs and that carbon dioxide and water were exhaled.

DEVELOPMENT OF THE RESPIRATORY CARE PROFESSION Clinical Advances in Respiratory Care The evolution of the respiratory care profession depended in many ways on developments in the various treatment techniques that matured in the 20th century. As the scientific basis for oxygen therapy, mechanical ventilatory support, and administration of medical aerosols became well established, the need for a health care practitioner to provide these services became apparent. Concurrent with this need was the continuing development of specialized cardiopulmonary diagnostic tests and monitoring procedures, which also required health care specialists to perform. The first health care specialists in the field were oxygen technicians in the 1940s.1,4,5 The development of positive-pressure breathing during World War II for breathing support of highaltitude pilots led to its use as a method to treat pulmonary patients and deliver aerosol medications during the 1950s, expanding the role of the oxygen technicians. Inhalation therapists began to be trained in the 1950s, and formal education programs began in the 1960s.1,4,5 By the end of the 1960s, respiratory care personnel were all referred to as inhalation therapists; they provided oxygen therapy via H cylinders and oxygen tents, masks, and nasal catheters. In addition, these inhalation therapists delivered aerosolized medications and performed intermittent positive-pressure breathing (IPPB) treatments. The development of sophisticated mechanical ventilators in the 1960s and beyond naturally led to a further expansion in the role of RTs, who soon also found themselves responsible for arterial blood gas and pulmonary function laboratories. In 1974, the designation respiratory therapist became standard, and the RT became the allied health professional primarily concerned with the assessment, diagnostic testing, treatment, education, and care of patients with deficiencies and abnormalities of the cardiopulmonary system. RULE OF THUMB  When information about the respiratory care profession is being sought, the best place to look is the AARC (see www.AARC.org). The AARC’s Virtual Museum can be accessed through the AARC website.

Oxygen Therapy The therapeutic administration of oxygen first occurred in 1798; in 1878, Bert showed that lack of oxygen caused hyperventilation. However, the physiologic basis and indications for oxygen therapy were not well understood until the 20th century.1,4 Large-scale

CHAPTER 1  Early History of Respiratory Care

5

in conjunction with a pressure booster to allow for the transfilling of small portable oxygen cylinders in the home. Smaller, lightweight portable oxygen concentrators were also introduced. Both of these advances have greatly enhanced the ability of patients receiving long-term oxygen therapy to ambulate beyond the confines of their homes. Furthermore, the National Institutes of Health launched the Long-Term Oxygen Treatment Trial (LOTT), a randomized controlled trial to explore the benefits of supplemental oxygen in patients with chronic obstructive pulmonary disease (COPD) and mild resting hypoxemia (SpO2 89% to 93%) or with exercise desaturation.10 In contrast to the case of COPD patients with severe hypoxemia (i.e., resting SpO2 100 milliamps [mA]) that pass through the chest can cause ventricular fibrillation, diaphragm dysfunction (owing to severe, persistent contraction), and death. Because current is most important, you should be familiar with the equation used to calculate it: Current (A) = Voltage (V) Resistance (Ω) For example, as long as a person is insulated by normal clothing and shoes and is in a dry environment, a 120 V shock may hardly be felt because the resistance is high in this situation (10,000 Ω). Current can be calculated as: Current (A) = 120 V 10, 000 Ω = 0.012 A or 12 mA Currents of 12 mA would cause a tingling sensation but no physical damage. However, if the same person is standing without shoes on a wet floor, a much higher current occurs because the resistance is much lower (1000 Ω). The current is then calculated as: Current (A) = 120 V 1000 Ω = 0.12 A or 120 mA Because the heart is susceptible to any current level greater than 100 mA, 120 mA represents a potentially fatal shock; this is in sharp contrast to the first example, in which the same voltage caused only a tingling sensation. A shock hazard exists only if the electrical “circuit” through the body is complete, meaning that two electrical connections to the body are required for a shock to occur. In the previous example, the person standing in water with no shoes has “grounded” himself. The finger touching the hot wire provides the input source while the feet standing in water provide the exit to ground. If the same person is wearing rubber boots, the connection to ground does not exist and the current cannot flow through the individual. In electrical devices, these two connections typically consist of a “hot” wire and a “neutral” wire. The neutral wire completes the circuit by taking the electrical current to a ground. A ground is simply a low-resistance pathway to a point of zero voltage, such as the earth (hence the term ground). Fig. 3.11 shows how current can flow through the body. In this case a piece of electrical equipment is connected to an AC

Hot Practitioner Neutral

Grounded

Broken ground wire

37

Instrument case

Damp floor

Fig. 3.11  Hazard created by broken ground wire.

38

SECTION I  Foundations of Respiratory Care

Hot

Broken ground wire

Transducer Saline-filled tube or catheter

Ground

Fig. 3.12  Possible microshock hazard caused by patient grounding.

Practitioner

Pacer wire to heart

Patient Instrument with defective ground or other undergrounded metal surface

Pacemaker

Monitor that grounds right leg of patient

Ground Fig. 3.13  Possible hazard through use of certain cardiac monitors and a pacemaker.

line power via a standard three-prong plug. However, unknown to the practitioner, the cord has a broken ground wire. Normally, current leakage from the equipment would flow back to the ground through the ground wire. However, this pathway is unavailable. Instead, the leakage current finds a path of low resistance through the practitioner to the damp floor (an ideal ground). Current can readily flow into the body, causing damage to vital organs when the skin is bypassed via conductors such as pacemaker wires or saline-filled intravascular catheters (Figs. 3.12 and 3.13). Even urinary catheters can provide a path for current flow. The heart is particularly sensitive to electrical shock. Ventricular fibrillation can occur when currents of 20 µA (20 microamperes, or 20 millionths of 1 ampere) are applied directly to the heart. Electrical shocks are classified into two types: macroshock and microshock. A macroshock exists when a high current (usually >1 mA) is applied externally to the skin. A microshock exists when a small, usually imperceptible current (6000 >6,000,000

0.1–3

100–3000

100,000

0.050

50

50,000

0.016

16

16,000

0.001

1

1,000

Applied to Myocardium (Microshock) 0.001 0.1 100

Effects Sustained myocardial contraction followed by normal rhythm; temporary respiratory paralysis; burns, if small area of contact Ventricular fibrillation; respiratory center intact Pain; fainting; exhaustion; mechanical injury; heart and respiratory function intact “Let go” current; muscle contraction Threshold of perception; tingling Ventricular fibrillation

Duration of exposure and current pathway are major determinants of human response to electrical shock. Physiologic effects of AC shocks applied for 1 second to the trunk or directly to the myocardium.

the ground wire is simply a protection device and not part of the main circuit, equipment continues to operate normally even if the ground wire is broken. All electrical equipment must be checked for appropriate grounding on a regular basis by a qualified electrical expert. Patients may wish to use their own continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) in the hospital setting. It is important to know your hospital’s policy regarding the use of this equipment. If allowed, this equipment should first be checked by the hospital’s qualified electrical expert. Life support devices should be connected to outlets that may function in case of a power failure. These outlets may be denoted by being “red” in color.

Fire Hazards In 1980, approximately 12,000 healthcare facility fires were officially reported in the United States.18 During the period of 2011 to 2015, the average annual number of fires in healthcare facilities was 5750.18 These healthcare facilities include hospitals, hospice facilities, nursing homes, mental health facilities, and doctors’ offices or clinics. This significant reduction in healthcare facility fires is primarily due to education and enforcement of strict fire codes. Hospital fires can be very serious, especially when they occur in patient care areas and when supplemental O2 is in use. Fires in O2-enriched atmospheres (OEAs) are larger, more intense, faster burning, and more difficult to extinguish. In addition,

39

some material that would not burn in room air would burn in O2-enriched air. Hospital fires are also more serious because evacuation of critically ill patients is difficult and slow. For these reasons, hospital fires often cause more injuries and deaths per fire than do residential fires. For a fire to start, three conditions must exist: (1) flammable material must be present, (2) O2 must be present, and (3) the flammable material must be heated to or above its ignition temperature. When all three conditions are present, a fire starts. Conversely, removing any one of the conditions can stop a fire from starting or extinguish it after it has begun. Fire is a serious hazard around respiratory care patients using supplemental O2. Although O2 is nonflammable, it greatly accelerates the rate of combustion. Burning speed increases with an increase in either the concentration or the partial pressure of O2. Flammable material should be removed from the vicinity of O2 use to minimize fire hazards. Flammable materials include cotton, wool, polyester fabrics, bed clothing, paper materials, plastics, and certain lotions or salves such as petroleum jelly. Removal of flammable material is particularly important whenever O2 enclosures, such as O2 tents or croupettes, are used. Hyperbaric oxygen chambers are another potential hazard because they supply high concentration of O2 in a pressurized enclosed environment. These chambers are designed with internal fire suppressants, but steps should be taken to reduce all flammable material. Ignition sources, such as cigarette lighters, should not be allowed in rooms where O2 is in use. In addition, the use of electrical equipment capable of generating high-energy sparks, such as exposed switches, must be avoided. All appliances that transmit house current should be kept out of O2 enclosures. Children should not play with toys that may create a spark when O2 is in use. RTs must be diligent in educating patients and visitors about the dangers associated with spark-producing items, open flames, and burning cigarettes in the hospital environment, especially in areas with O2-enriched air. A frequent source of concern is the presence of static electrical sparks generated by friction. Even in the presence of high O2 concentrations, the overall hazard from static sparks with the materials in common use is very low. Solitary static sparks generally do not have sufficient heat energy to raise common materials to their flash points. The minimal risk that may be present can be reduced further by maintaining high relative humidity (>60%). If you identify a fire in a patient care area, you must know what to do. Each hospital must have a core fire plan that identifies the responsibilities of hospital personnel. The plan should be taught to all hospital personnel and practiced with fire drills to reinforce the education. Requirements may include routinely walking the fire exits and reviewing proper fire extinguisher training. Fire extinguisher training includes following the acronym PASS: Pull the pin. There may be an inspection tag attached. Aim the nozzle. Aim low at the bottom of the fire. Squeeze the handle. The extinguisher has less than 30 seconds of spray time. Sweep the nozzle across the base of the fire. The core fire plan follows the acronym RACE:

40

SECTION I  Foundations of Respiratory Care

Rescue patients in the immediate area of the fire. The person discovering the fire should perform the rescue. Alert other personnel about the fire so they can assist in the rescue and can relay the location of the fire to officials. This step also involves pulling the fire alarm. Contain the fire. After rescuing patients, shut doors to prevent the spread of the fire and the smoke. In patient care areas, follow your hospital policy regarding turning off O2 zone valves. Evacuate other patients and personnel in the areas around the fire who may be in danger if the fire spreads. RTs are frequently key participants in successful handling of hospital fires. First, they know where the O2 zone valves are located and how to shut them off. Second, they have the knowledge and skills needed to evacuate patients receiving mechanical ventilation or supplemental O2 to sustain life. Third, they know how to treat and resuscitate victims of smoke inhalation. For these reasons, RTs should be included in all hospital evacuation planning and practices.

General Safety Concerns In addition to electrical and fire safety, RTs need to be aware of general safety concerns, including the direct patient environment, disaster preparedness, magnetic resonance imaging (MRI) safety, and medical gas safety. Medical gas safety is discussed in more detail in Chapter 41.

Direct Patient Environment The immediate environment around the patient can create risk for patient safety. Because RTs use medical equipment and participate in direct patient care, it is necessary for RTs to be cognizant of the patient’s immediate environment. To reduce the risk for patient falls and allow easy access to care, the patient care environment should be as free of impediments to care as possible. Use of respiratory supplies and medical equipment by the RT creates an environment that could impede access to care and create a fall risk. It is the responsibility of the RT to position equipment, tubing, and treatments in a way that does not impede access to care and that reduces risk for falls. In addition, when care is completed, the RT should ensure that the patient has easy access to the patient call system.

Magnetic Resonance Imaging Safety MRI exposes the body to powerful magnetic fields and a small amount of radiofrequency. This powerful magnetic field can create a risk to patients, healthcare workers, and equipment if metal objects containing ferrous-based material, stainless steel or nickel alloys are brought within specified proximity to the field. There are safe proximity areas referred to as safety zones or Gauss lines. Metal objects can be so forcefully attracted to the magnet of the MRI that they can mimic a missile, causing physical harm. Reports of accidents associated with MRI have involved O2 cylinders, stethoscopes, scissors, and IV poles. Deaths have been described when O2 cylinders were pulled into the magnetic area where a patient was lying to undergo an MRI examination. RTs need to become familiar with MRI-compatible ventilators, O2 supplies, and ancillary equipment. Each radiology department has specific rules and safety precautions that need to be communicated to all patients, caregivers, and healthcare personnel. Medical Gas Cylinders Use of compressed gas cylinders by RTs requires special handling. The physical hazards resulting from improper storage or handling of cylinders include increased risk for fire, explosive release of high-pressure cylinders, and the toxic effect of some gases. It is important to store and transport cylinders in appropriate racks or chained containers. Compressed gas cylinders should never be stored without support. Additional information regarding the storage and delivery of medical gases can be found in Chapter 41.

COMMUNICATION Because the delivery of safe, high-quality healthcare requires interactions among many contributors from different disciplines (e.g., physicians, RTs, nurses), communication is essential to the quality mission of a healthcare organization. Strategies to enhance communication are critical to organizational success. Communication is a dynamic human process involving sharing of information, meanings, and rules. Communication has five basic components: sender, message, channel, receiver, and feedback (Fig. 3.14). The sender is the individual or group who transmits the message. The message is the information or attitude that is

Feedback

Sender • Communication skills • Attitudes • Experience • Culture • Self-concept

Message • Elements • Structure • Content • Treatment • Coding

Channel • Seeing • Hearing • Touching • Smelling • Tasting

Fig. 3.14  Elements of human communication.

Receiver • Communication skills • Attitudes • Experience • Culture • Self-concept

CHAPTER 3  Quality, Patient Safety, and Communication

communicated by the sender. Messages may be verbal or nonverbal. Verbal messages are voiced or written. Examples of different kinds of messages are lectures, letters, text messages, and e-mail memos. Nonverbal communication is any communication that is not voiced or written. Nonverbal communication includes gestures, facial expressions, eye movements and contact, voice tone, space, and touch. The channel of communication is the method used to transmit messages. The most common channels involve sight and hearing, such as written and oral messages. However, other sensory input, such as touch, may be used with visual or auditory communication. In addition, communication channels may be formal (memos or letters) or informal (conversation). The receiver is the target of the communication and can be an individual or a group. One-on-one communication is often more effective because both parties can respond to each other. Communication with a group can be more challenging but is a more efficient way to get information to numerous individuals. The last essential part of communication is feedback. Human communication is a two-way process in which the receiver serves an active role. Feedback from the receiver allows the sender to measure communication success and provide additional information when needed.

Communication in Healthcare Effective communication is the most important aspect of providing safe patient care. The first two 2018 National Patient Safety Goals of TJC are to improve accuracy of patient identification and effectiveness of communicating critical test values among caregivers.19 All healthcare personnel must correctly identify patients before initiating care using a two–patient identifier system. The patient identifiers can include any two of the following: name, birth date, and medical record number. Effectively communicating critical test values should include a “read back” scenario verifying the reporter and the receiver of the information and accurate reporting and recording of test values. Each institution may have specific values as critical test values; for example, RTs may be expected to report blood gas values of a pH less than 7.20 or a PaO2 less than 50 mm Hg. The process of the read back scenario is described in Box 3.4.

BOX 3.4  “Read Back” Process to Ensure

Accurate Communication of Information

Prescriber/Reporter • Orders or critical test results are read and clearly enunciated, using two patient identifiers. • Avoid abbreviations. • Ask receiver to “read back” the information if this is not done voluntarily. • Verify with the receiver that the information is correct. Receiver • Record the order or value. • Ask “prescriber/reporter” to repeat if information is not understood. • “Read back” the information, including two patient identifiers. • Receive confirmation from the “prescriber/reporter” that the information is correct; if incorrect, repeat the process.

41

Another setting for improving communication between RTs regards transitions of care or “hand-off” of care; that is, when one RT is telling a colleague about the care of a patient who will be passed to the incoming RT for care. An effective communication tool in this instance may be an SBAR (Situation, Background, Assessment, and Recommendation).20 An example of this would be an RT discussing a patient’s intolerance to noninvasive ventilation. The situation (S) is that the patient was admitted to the intensive care and prescribed noninvasive ventilation but is not tolerating the device. The background (B) is that the patient has COPD and was admitted with a high PaCO2 and would benefit from the noninvasive ventilation. The assessment (A) is the patient feels “claustrophobic” in the current full-face mask. Finally, the recommendation (R) would be to try a smaller, less-confining mask to improve patient comfort. A second transition of care communication tool is known as I-PASS, which stands for Illness severity, Patient summary, Action list, Situation awareness and contingency plans and Synthesis by receiver.21 Considering the same situation as the previous paragraph, the illness severity (I) is severe and the patient summary (P) is the patient has COPD and was admitted with a high PaCO2. The action list (A) is to try to stabilize the patient with noninvasive ventilation. The situation (S) awareness and contingency plan are that the patient is not tolerating the noninvasive ventilation and feels claustrophobic. The RT forming the contingency plan of trying a smaller, less-confining mask. Finally, the synthesis by the receiver (S) is that during the “hand off ” the next shift RT would summarize what has been discussed, ask questions, and restate the actions to take place and attempt to use a smaller more comfortable noninvasive ventilation mask. As an RT, you will have many opportunities to communicate with patients, other RTs, nurses, physicians, and other members of the healthcare team. Success as an RT depends on your ability to communicate with these key people. Poor communication skills can limit your ability to treat patients, work well with others, and find satisfaction in your employment.

Factors Affecting Communication Many factors affect communication in the healthcare setting (Fig. 3.15). The uniquely human or “internal” qualities of sender and receiver (including their prior experiences, attitudes, values, cultural backgrounds, and self-concepts and feelings) play a large role in the communication process. In general, the verbal and nonverbal components of communication should enhance and reinforce each other. Other factors that can affect communication include the patient’s direct healthcare environment and their sensory or emotional state. The RT who considers all of these factors will become a better communicator. One example of this is the RT who combines a compassionatetoned verbal message such as, “You’re going to be all right now,” with a confirming touch of the hand. This communication is sending a much stronger message to an anxious patient than the message provided by either component alone. Several key purposes of communication are summarized in Box 3.5.

Improving Communication Skills To enhance your ability to communicate effectively, focus on improving sending, receiving, and feedback skills. In

42

SECTION I  Foundations of Respiratory Care SENSORY/EMOTIONAL FACTORS INTERNAL FACTORS Previous experiences Attitudes, values Cultural heritage Religious beliefs Self-concept Listening habits Preoccupations, feelings

Fear Stress, anxiety Pain Mental acuity, brain damage, hypoxemia Sight, hearing, speech impairment ENVIRONMENTAL FACTORS Lighting Noise Privacy Distance Temperature VERBAL EXPRESSION

NONVERBAL EXPRESSION

Language barrier Jargon Choice of words/questions Feedback, voice tone

Body movement Facial expression Dress, professionalism Warmth, interest

INTERNAL FACTORS Previous experiences Attitudes, values Cultural heritage Religious beliefs Self-concept Listening habits Preoccupations, feelings Illnes

Fig, 3.15  Factors Influencing Communication. (Modified from Wilkins RL, Sheldon RL, Krider SJ: Clinical assessment in respiratory care, 6th ed., St. Louis, 2010, Mosby.)

BOX 3.5  Purposes of Communication in

MINI CLINI

the Healthcare Setting

Patient Communication

• To establish rapport with another individual, such as a colleague, a patient, or a member of the patient’s family • To comfort an anxious patient by explaining the unknown • To obtain information, such as during a patient interview • To relay pertinent information, as when charting the results of a patient’s treatment • To give instructions, as when teaching a patient how to perform a lung function test • To persuade others to take action, as when attempting to convince a patient to quit smoking • To educate and confirm understanding as in a “teach back” scenario

Problem A 73-year-old man with COPD is admitted to the emergency department for acute shortness of breath that is not relieved with rest. The patient has been admitted more than eight times during the past year for various respiratory problems. The patient’s physician thinks that this episode may reflect a worsening of his disease process and orders an inhaled bronchodilator via an MDI. After the RT enters the room and introduces herself, the patient becomes quite defensive, stating that he does not need any assistance with treatments and that she should just leave the medication in the room. The RT has not treated the patient in the past and has to decide how to respond to the patient’s request.

addition, identify and overcome common barriers to effective communication.

Practitioner as Sender Your effectiveness as a sender of messages can be improved in several ways. These suggestions may be applied to the clinical setting as follows: • Share information rather than telling. Health professionals often provide information in an authoritative manner by telling colleagues or patients what to do or say. This approach can cause defensiveness and lead to uncooperative behavior. Conversely, sharing information creates an atmosphere of cooperation and trust. • Seek to relate to people rather than control them. This is of particular significance during communication with patients. Healthcare professionals often attempt to control patients. Few people like to be controlled. Patients feel much more important if they are treated as an equal partner in the

Discussion Although this patient exhibited reluctance in allowing the RT to administer the therapy, enough verbal and perhaps nonverbal communication (message) was expressed by the patient (sender) for the RT (receiver) to determine a plan of action. Because human communication is a two-way process, the RT serves an active role for further messages and interaction. This is a key concept for RTs to master because it helps in identifying a patient’s problems, evaluating progress, and recommending further respiratory care. The RT must recognize that when an individual verbalizes disagreement with a treatment order and exhibits defensive behavior, the RT must attempt to understand what the patient is saying and must not overreact. The RT could try to put the patient at ease by making eye contact, gesturing effectively, and maintaining a safe distance from the patient when talking. The RT should seek feedback from the patient to ensure that the message was understood as it was intended. In this situation, it may be appropriate for the RT to review and demonstrate MDI use, ask the patient to “teach back” proper inhaler use, and observe the patient self-administering the medication. This process (message) can be repeated until the patient can demonstrate proper technique. Allowing the patient to participate actively in medical care when possible may serve to help him maintain a sense of control over his disease process.

CHAPTER 3  Quality, Patient Safety, and Communication

relationship. Explaining procedures to patients and asking their permission to proceed is a way to make them feel part of the decision-making regarding their care. • Value disagreement as much as agreement. When individuals express disagreement, make an attempt to understand what they are saying and do not become defensive. Be prepared for disagreement and be open to the input of others. • Use effective nonverbal communication techniques. The nonverbal communication that you use is just as important as what you say. Nonverbal techniques may include eye contact, effective gesturing, facial expressions, and voice tone. It is important that your nonverbal communication matches what you are saying. It is also important to be aware of cultural differences in nonverbal contact. Some cultures may view direct eye contact as inappropriate, whereas in the United States, most find it an effective communication tool.

Practitioner as Receiver and Listener Receiver skills are just as important as sender skills. Messages sent are of no value unless they are received as intended. Active listening on the part of the receiver is required. Learning to listen requires a strong commitment and great effort. A few simple principles can help improve your listening skills, as follows: • Work at listening. Listening is often a difficult process. It takes effort to hear what others are saying. Focus your attention on the speaker and on the message. • Stop talking. Practice silent listening and avoid interrupting the speaker during an interaction. Interrupting the patient is a sure way to diminish effective communication. • Resist distractions. It is easy to be distracted by surrounding noises and conversations. This is particularly true in a busy environment such as a hospital. When you are listening, try to tune out other distractions and give your full attention to the person who is speaking. • Keep your mind open; be objective. Being open-minded is often difficult. All people have their own opinions that may influence what they hear. Try to be objective in your listening so that you treat everyone fairly. • Hear the speaker out completely before making an evaluation. Listen to the complete communication, not just the first few words of the speaker. Often, listeners hear the first sentence and tune out the rest, assuming they know what is being said. It is important to listen to the entire message; otherwise, you may miss important information. • Maintain composure; control emotions. Listen authentically to understand. Allowing emotions, such as anger or anxiety, to distort your understanding or drawing conclusions before a speaker completes his or her thoughts or arguments is a common error in listening that is best avoided. • Active listening is a key component in healthcare communication. Part of active listening is paraphrasing, or repeating back to the patient what you understood the patient to say. This confirms to the patient that you were listening and also allows them to correct any errors you may have made in understanding. Active listening is very important to prevent losing information, which could jeopardize the care you are providing.

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Providing Feedback To enhance communication with others, effective feedback needs to be provided. Examples of effective feedback mechanisms in oral communication with patients include attending, paraphrasing, requesting clarification, perception checking, and reflecting feelings: • Attending. Attending involves the use of gestures and posture that communicates one’s attentiveness. Attending also involves confirming remarks, such as, “I see what you mean.” • Paraphrasing. Paraphrasing, or repeating the other’s response in one’s own words, is a technique that is useful in confirming that understanding is occurring between the parties involved in the interaction. Note that overuse of paraphrasing can be irritating. • Requesting clarification. Requesting clarification begins admitting that you may have misunderstood, with the goal of better understanding through restating or using alternative examples or illustrations. Overuse of this technique can impair effective communication, especially if it is used in a condescending or patronizing manner. Requests for clarification should be used only when truly necessary and always should be nonjudgmental in nature. • Perception checking. Perception checking involves confirming or disproving the more subtle components of a communication interaction, such as messages that are implied but not stated. For example, the RT might sense that a patient is unsure of the need for a treatment. In this case, the RT might check this perception by saying, “You don’t seem to be sure that you need this treatment. Is that correct?” By verifying or disproving this perception, both the healthcare professional and the patient understand each other better. • Reflecting feelings. Reflecting feelings involves the use of statements to determine better the emotions of the other party. Nonjudgmental statements, such as, “You seem to be anxious about (this situation),” provide the opportunity for patients to express and reflect on their emotions and can help them confirm or deny their true feelings. Minimizing Barriers to Communication There are many potential barriers to effective communication. A skillful communicator tries to identify and eliminate or minimize the influence of these barriers in all interactions. By minimizing the influence of these barriers, the sender can help ensure that the message will be received as intended. Key barriers to effective communication are the following: • Use of symbols or words that have different meanings. Words and symbols (including nonverbal communication) can mean different things to different people. These differences in meaning derive from differences in the background or culture between the sender and receiver and the context of the communication. For example, RTs often use the letters COPD to refer to patients with COPD caused by long-term smoking. Patients may hear COPD used in reference to them and be confused about the meaning and interpret COPD to mean a fatal lung disease. Never assume that the patient has the same understanding as you do about interpreting commonly used symbols or phrases.

44

SECTION I  Foundations of Respiratory Care

• Different value systems. Everyone has his or her own value system, and many people do not recognize the values held by others. A large difference among the values held by individuals can interfere with communication. A clinical supervisor may inform students of the penalties for being late with clinical assignments. If a student does not value timeliness, he or she may not take seriously what is being said. • Emphasis on status. A hierarchy of positions and power exists in most healthcare organizations. If superiority is emphasized by individuals of higher status, communication can be stifled. Everyone has experienced interactions with professionals who make it clear who is in charge. Emphasis on status can be a barrier to communication not only among healthcare professionals but also between healthcare professionals and patients. • Conflict of interest. Many people are affected by decisions made in healthcare organizations. If people are afraid that a decision will take away their advantage or “invade their territory,” they may try to block communication. An example might be a staff member who is unwilling to share expertise with students. This person may unfortunately feel that a student is somehow a threat. Lack of acceptance of differences in points of view, feelings, values, or purposes. Most of us are aware that people have different opinions, feelings, and values. These differences can interfere with effective communication. To overcome this barrier, an effective communicator allows others to express their differences. Encouraging individuals to communicate their feelings and points of view benefits everyone. Not uncommonly, people may think they are always correct. Accepting input from others promotes growth and cooperation. Feelings of personal insecurity. It is difficult for people to admit feelings of inadequacy. Individuals who are insecure do not offer information for fear they appear ignorant or they may be defensive when criticized, blocking clear communication. To become an effective communicator, identify the purpose of each communication interaction and your role in it. Use specific sending, receiving, and feedback skills in each interaction. Finally, minimize any identified barriers to communication with patients or peers, to ensure that messages are received as intended.

CONFLICT AND CONFLICT RESOLUTION Conflict is sharp disagreement or opposition among people over interests, ideas, or values. Because no two people are exactly alike in their backgrounds or attitudes, conflict can be found in every organization. Healthcare professionals may experience a great deal of conflict in their jobs. Rapid changes occurring in healthcare have made everyone’s jobs more complex and often more stressful. Because conflict is inevitable, all healthcare professionals must be able to recognize its sources and help resolve or manage its effect on people and on the organization.

Sources of Conflict The first step in conflict management is to identify its potential sources. The four primary sources of conflict in organizations are: (1) ineffective communication, (2) structural problems, (3) personal behavior, and (4) role conflict.

Ineffective Communication Ineffective communication is the primary source of conflict in organizations. The previously discussed barriers to communication all are potential sources of conflict. If a supervisor is unwilling to accept different points of view for dealing with a difficult patient, an argument may occur. The importance of good communication cannot be overemphasized. Structural Problems The structure of the organization itself can increase the likelihood of conflict. Conflict tends to grow as the size of an organization increases. Conflict is also greater in organizations whose employees are given less control over their work and in organizations in which certain individuals or groups have excessive power. Structural sources of conflict are the most rigid and are often difficult to control. Personal Behavior Personal behavior factors are a major source of conflict in organizations. Different personalities, attitudes, and behavioral traits create the possibility of great disagreement among healthcare professionals and between healthcare professionals and patients. Role Conflict Role conflict is the experience of being pulled in several directions by individuals who have different expectations of a person’s job functions. A clinical supervisor is often expected to function both as a staff member and as a student supervisor. Trying to fill both roles simultaneously can cause stress and create interpersonal conflict.

Conflict Resolution Conflict resolution or management is the process by which people control and channel disagreements within an organization. The following are five basic styles of handling conflict: 1. Competing 2. Accommodating 3. Avoiding 4. Collaborating 5. Compromising

Competing Competing is an assertive and uncooperative conflict resolution strategy. Competing is a power-oriented method of resolving conflict. A supervisor who uses rank or other forces to attempt to win is using the competing strategy. This strategy may be useful when an unpopular decision must be made or when one must stand up for his or her rights. However, because it often causes others to be quiet and feel inferior, competing should be used cautiously. Accommodating Accommodating is the opposite of competing. Accommodating is being unassertive and cooperative. When people accommodate others involved in conflict, they neglect their own needs to meet

CHAPTER 3  Quality, Patient Safety, and Communication

the needs of the other party. Accommodation is a useful strategy when it is essential to maintain harmony in the environment. Accommodation is also appropriate when an issue is much more important to one party or the other in a dispute.

Avoiding Avoiding is both an unassertive and an uncooperative conflict resolution strategy. In avoiding conflict, one or both parties decide not to pursue their concerns. Avoidance may be appropriate if there is no possibility of meeting one’s goals. In addition, if one or both of the parties are hostile, avoidance may be a good strategy, at least initially. However, too much avoidance can leave important issues unattended or unresolved. Collaborating As a conflict resolution strategy, collaborating is the opposite of avoiding. Collaborating is both assertive and cooperative and often offers the best chance of reaching a mutually beneficial solution. In collaboration, the involved parties try to find mutually satisfying solutions to their conflict. Collaboration usually takes more time than other methods of conflict management and is harder when the involved parties harbor strong negative feelings about each other. Compromising Compromising is a middle-ground strategy that combines assertiveness and cooperation. People who compromise give up more than individuals who compete but give up less than individuals who accommodate. Compromise is best used when a quick resolution is needed that both parties can accept. However, because both parties often feel they are losing something with a compromise, compromise should not be used exclusively. Deciding which type of conflict resolution strategy to use requires knowledge of the context, the specific underlying problem, and the desires of the involved parties.

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• Hospital accreditation by TJC is based on satisfying specific standards established by professional and technical advisory committees. • Good posture is needed when lifting patients or heavy equipment to avoid injury. • Electrical current (flow) is the dangerous element of electricity. Current is directly related to voltage and inversely related to resistance. • A microshock is a small, imperceptible current ( va). According to the Bernoulli theorem, the higher velocity at point b should result in a lower lateral pressure at that point (Pb < Pa). As a fluid flows through the constriction, its velocity increases and its lateral pressure decreases. This equation also helps demonstrate how heliox therapy works. The equation implies that the lower the density, the higher is the velocity (and hence flow) for the same inspiratory effort (driving pressure) or the lower is the pressure for the same velocity—either way lowering the effort for someone struggling to breathe. A special application of the Bernoulli prinicple is the Venturi effect. The Venturi effect describes the flow of a gas through a constriction and the subsequent drop in pressure at the constriction. As the gas passes from a larger bore through a constriction, the flow increases and the pressure perpendicular to the constriction decreases. The Venturi effect can be used for measuring gas flow in ventilators.

Larger ports

Increased flow

C Smaller jet Fig. 6.25  Air Injector. (A) Basic design. (B) Greater entrainment and total flow occurs with larger entrainment ports. (C) Alternatively, a smaller jet increases source gas velocity and entrains more air.

Fluid Entrainment Jet entrainment is the design principle used in simple O2 masks with variable FiO2 settings, although they are often mistakenly called Venturi masks. In this case, a pressurized gas, usually O2, serves as the primary flow source. This pressurized gas passes through a nozzle or jet, beyond which is an air entrainment port (Fig. 6.25A). In this case, air entrainment occurs as a consequence of fluid viscosity. The viscous shearing force that exists between moving and static layers of gas causes the non-moving gas (room air) to be dragged into the moving stream of O2.15 The amount of air entrained depends on both the diameter of the jet orifice and the size of the air entrainment ports. For a fixed jet size, the larger the entrainment ports, the greater is the volume of air entrained, the higher is the total flow, and the lower is the FiO2 (see Fig. 6.25B). The entrained volume can still be altered, with fixed entrainment ports, by changing the jet diameter (see Fig. 6.25C). A large jet results in a lower gas velocity and less entrainment, whereas a small jet boosts velocity, entrained volume, and total flow.

Fluidics and the Coanda Effect Fluidics is a branch of engineering that applies hydrodynamic principles in flow circuits for purposes such as switching, pressure and flow sensing, and amplification. Because fluidic devices have no moving parts, they are very dependable and require little maintenance. The primary principle underlying most fluidic circuitry is a phenomenon called wall attachment, or the Coanda effect. This effect is observed mainly when a fluid flows through a small orifice with properly contoured downstream surfaces.16 We know that a jet or nozzle entrains any surrounding fluid, such as air,

110

SECTION I  Foundations of Respiratory Care Ambient pressure

Negative pressure region Entrained air, lowered pressure B Fig. 6.26  Coanda Wall Effect. (A) Entrainment into the fluid stream. (B) Wall attachment initiated by negative pressure near wall.

A

into the primary flow stream (Fig. 6.26A). If a carefully contoured curved wall is added to one side of the jet (see Fig. 6.26B), the pressure near the wall becomes negative relative to atmospheric pressure. The atmospheric pressure on the other side of the gas stream pushes it against the wall, where it remains “locked” until interrupted by some counterforce. By carefully extending the wall contour, we can deflect the fluid stream through a full 180-degree turn. Various fluidic devices can be designed using this principle, including on/off switches, pressure and flow sensors, and flow amplifiers. These individual components can be combined into integrated fluidic logic circuits, which function much like electronic circuit boards but without the need for electrical power.

SUMMARY CHECKLIST • Gases have no inherent boundary, are readily compressed and expanded, and can flow. • Three temperature scales are in common use: Kelvin (SI), Celsius (cgs), and Fahrenheit (fps); conversion among these scale units can be done by using simple formulas. • Transfer of heat energy can occur by conduction, convection, radiation, and evaporation. • Liquids exert pressure and exhibit the properties of flow, buoyant force, viscosity, capillary action, and surface tension. • The pressure exerted by a liquid depends on both its height (depth) and weight density. • Surface tension forces increase the pressure inside a liquid drop or bubble; this pressure varies directly with the surface tension of the liquid and varies inversely with the radius. • A liquid can vaporize by either boiling or evaporation; in evaporation, the required heat energy is taken from the air surrounding the liquid, cooling the air. • Vaporization causing cooling and condensation causes warming of the surroundings. • The capacity of air to hold water vapor increases with temperature. • Relative humidity (RH) is the ratio of water vapor content (absolute humidity) to saturated water vapor capacity; for a constant content, cooling increases RH and warming decreases RH. • The rate of diffusion of a gas is inversely proportional to its molecular weight. • The total pressure of a mixture of gases must equal the sum of the partial pressures of all component gases.

• The volume of a gas that dissolves in a liquid equals its solubility coefficient times its partial pressure; high temperatures decrease gas solubility, and low temperatures increase gas solubility. • Volume and pressure of a gas vary directly with temperature; however, with constant temperature, gas volume and pressure vary inversely. • The critical temperature of a substance is the highest temperature at which it can exist as a liquid; gases with critical temperatures higher than room temperature can be stored under pressure as liquids without cooling. • Under conditions of laminar flow, the difference in pressure required to produce a given flow is defined by Poiseuille’s law. • Boyle’s law explains the relationship between pressure and volume of a gas. • Charles’ law explains the relationship between volume and temperature of a gas. • Gay-Luccac’s law explains the relationship between temperature and pressure of a gas. • When the flow of gas increases, the pressure downstream will decrease, this is called the Bernoulli principle. • The Venturi effect is an application of Bernoulli’s principle using gases.

REFERENCES 1. McNaught AD, Wilkinson A: Compendium of chemical terminology. In IUPAC Gold Book, Oxford, 2010, Blackwell Scientific. 2. Debenedetti PG, Stillinger FH: Supercooled liquids and the glass transition, Nature 410:259–267, 2001. 3. Ojovan MI: Configurons: thermodynamic parameters and symmetry changes at glass transition, Entropy 10:334–364, 2008. 4. Masanes L, Oppenheim J: A general derivation and quantification of the third law of thermodynamics, Nat Commun 8:2017. Article number 14538. 5. International System of Units (SI): Bureau International des Poids et Mesures (BIPM), 2006. 6. Cohen ER, Cvitas T, Frey JG, et al: Quantities, units and symbols in physical chemistry. In IUPAC Green Book, ed 3, Cambridge, 2008, IUPAC & RSC. 7. Mohr PJ, Taylor BN, Newell DB: CODATA recommended values of the fundamental physical constants, Rev Mod Phys 84:1527– 1605, 2012.

CHAPTER 6  Physical Principles of Respiratory Care 8. Park M, Vitale-Mendes P, Viera Costa EL, et al: Factors associated with blood oxygen partial pressure and carbon dioxide partial pressure regulation during respiratory extracorporeal membrane oxygenation, Rev Bras Ter Intensiva 28(1):11–18, 2016. 9. Thom SR: Hyperbaric oxygen: its mechanisms and efficacy, Plast Reconstr Surg 127:131S–141S, 2011. 10. West JB: Robert Boyle’s landmark book of 1660 with the first experiments on rarified air, J Appl Physiol 98:31–39, 2004. 11. Eastlake CN: An aerodynamicist’s view of lift, Bernoulli, and Newton, Phys Teach 40:166–176, 2002. 12. Nakamura Y, Awa S: Radius exponent in elastic and rigid arterial models optimized by the least energy principle, Physiol Rep 2:1–18, 2014.

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13. Gamsjäger E, Wiessner M: Low temperature heat capacities and thermodynamic functions described by Debye-Einstein integrals, Monatsh Chem 149:357–368, 2018. 14. Rembold CM, Suratt PM: Airway turbulence and changes in upper airway hydraulic diameter can be estimated from the intensity of high frequency inspiratory sounds in sleeping adults, J Physiol 592:3831–3839, 2014. 15. Wagstaff TAJ, Soni N: Performance of six types of oxygen delivery devices at varying respiratory rates, Anaesthesia 62:492–503, 2007. 16. Ginghina C: The Coanda effect in cardiology, J Cardiovasc Med 8:411–413, 2007.

7  E-Medicine in Respiratory Care Narciso E. Rodriguez and Albert J. Heuer CHAPTER OBJECTIVES After reading this chapter you will be able to: • Define electronic health records (EHR) and their major uses in medicine and respiratory care. • State the differences between the EHR and the electronic medical record (EMR). • Describe the role of telehealth in healthcare in the delivery of healthcare services • Identify the value of E-medicine applications in informatics and clinical decision support. • Describe E-medicine applications in clinical care and management.

• Evaluate the trustworthiness and accuracy of health information sources. • Describe major uses of E-medicine applications in healthcare administration. • Outline steps necessary to maintain security and confidentiality of EHR. • Describe major E-medicine applications in respiratory care education and training. • Discuss the future of E-medicine.

CHAPTER OUTLINE The Electronic Health Record and the Electronic Medical Record, 113 Computerized Physician Order Entry, 113 Enterprise Software Packages, 114 Applications for Patient Care, 115 Applications in Diagnostics, 115 Applications in Treatment, 116 Applications in Disease and Infection Prevention, 118 Informatics and Clinical Decision Support, 119 Business Intelligence, 120 Clinical Decision Support, 120

American Association for Respiratory Care Benchmarking System, 120 Research, 121 Telehealth and Telemonitoring, 121 Sources of Health Information, 122 Health Information Sources for Respiratory Therapists and Other Clinicians, 122 Health Information Sources for Consumers, 122 Applications in Healthcare Administration, 122 Documentation, Workload, Staffing, and Scheduling, 123 Financial Management, 123

Quality Assurance, 125 Regulatory Compliance, 125 Web Analytics, 125 Human Resources, 125 Privacy and Confidentiality, 125 Applications in Training and Education, 126 Clinical Simulations, 126 Full-Scale Physiologic Clinical Simulators, 127 Clinical Education Applications, 127 National Board for Respiratory Care Credentialing, 127 Learning Management Systems, 128 Future of E-Medicine, 128

electronic health record (EHR) electronic medical record (EMR) enterprise software packages E-medicine health informatics Health Information Technology for Economic and Clinical Health (HITECH) Act information retrieval key performance indicators (KPIs) learning management systems

Merit-based Incentive Payment System (MIPS) m-health picture archiving and communication systems (PACS) point-of-care testing root-cause analysis telehealth telemedicine telemonitoring value-based purchasing

KEY TERMS benchmarking business intelligence central line-associated blood stream infection (CLABSI) clinical decision support clinical simulation closed-loop ventilation computerized physician order entry (CPOE) continuing respiratory care education continuous quality improvement 112

CHAPTER 7  E-Medicine in Respiratory Care

E-Medicine is the term that relates to the use of computerized or digital technology to enhance efficiency and effectiveness of healthcare in general and more specifically in patient care. E-Medicine was initially used to describe the use of basic computer applications in clinical care, recordkeeping, and healthcare education. However, because of significant and widespread technologic advancements, the term E-medicine now refers to a wide array of hardware and software applications used in essentially every facet of healthcare delivery and services. As a vital part of the patient care team, respiratory therapists (RTs) need to understand, and be proficient in, many aspects of E-medicine. This chapter describes digital applications related to electronic health records, direct clinical care, disease management, healthcare administration, health information sources, healthcare delivery, and healthcare training and education.

THE ELECTRONIC HEALTH RECORD AND THE ELECTRONIC MEDICAL RECORD A transformation has taken place in the recent past whereby medical records formerly maintained primarily in paper form are now almost exclusively computerized and are maintained as part of the patient’s electronic health record (EHR). A closely related but different term is the electronic medical record (EMR), which represents the computerized record produced every time the patient (or consumer) uses healthcare services. The EHR is the sum of all EMRs produced by a patient during the different encounters with various healthcare entities throughout a lifetime. Unlike the EHR, which is owned by the patient, the EMR (the “chart”) is owned by the hospital or healthcare delivery organization.1 The terms EHR and EMR are so closely related that for simplicity we will use the term EHR to describe both concepts for the rest of this chapter. RULE OF THUMB  The record for a patient admission or healthcare event can be found in the electronic medical records, or EMR. The sum of all EMRs of a patient can be found in the patient’s electronic health records, or EHR.

Nonclinical information such as patient demographics (e.g., age, gender, religion), health insurance, and financial records are also now electronic. Likewise, clinical information, including the patient’s history and physical examination information, progress notes, physician orders, laboratory and other testing results, vital signs trending, and other information formerly found only in the hard-copy chart are now in electronic form. This information is now readily available to authorized clinicians and the patient via secured personal computers and mobile devices. In addition to being able to access existing medical information, new records can be more readily entered and updated, making most EHRs more current than paper records. Medical imaging and laboratory tests generally become a part of the EHR immediately as the results are finalized. The net impact of these factors is that the EHR has helped make disease diagnosis quicker and more accurate by facilitating the efficient access of medical records.2,3 EHRs are also proving to be a significant asset in the realm of patient treatment. When coupled with other computerized

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BOX 7.1  Core Functions of Electronic

Health Records

• Medical records • Results reporting • Computerized physician order entry • Clinical decision support • Electronic communication • Channels between healthcare providers and patients • Patient-entered data

tools such as clinical decision support (CDS) applications, EHRs have enhanced treatment and disease management, as discussed in more detail later. The core functions of EHRs are shown in Box 7.1. EHRs are more than a repository for medical records and patient-related information. EHRs are also a rich source of information that can be used in a variety of applications, including quality improvement and regulatory compliance, as detailed later in this chapter. EHRs also can serve as a vital source of data for conducting research, as discussed in Chapter 8 of this text.

Computerized Physician Order Entry A subset of EHRs is the computerized physician order entry (CPOE) system. CPOE systems is a required feature for hospitals seeking to demonstrate meaningful use of EMR systems and qualify for federal financial incentives.4 CPOEs allow new orders to be electronically transmitted to the EHR and ancillary departments such as the pharmacy, physical therapy, respiratory department, and so on, saving time and reducing transcription errors resulting from handwriting clarity issues. Built-in stopgaps and prescribing templates alert physicians about potential problems such as incorrect dose, formulary issues, potential side effects, and drug interaction concerns. The interfacing of CPOE systems with other hospital computer systems also alerts RTs and other clinicians of new, expired, or changed orders. CPOE systems have a substantial impact on patient care in areas where the potential for medical error is high, and the clinical workflow is complex such as intensive care units (ICUs), emergency rooms (ERs), and operating rooms (ORs).5 Thus CPOE has helped facilitate patient care and reduce medical errors.6 All of these factors combined to make EHR and CPOE systems value-added features for healthcare organizations, clinicians, and patients alike. Indeed, EHRs and other computerized applications are helping transform medicine and enhancing both efficiency and effectiveness in essentially all aspects of healthcare and respiratory care.7

RULE OF THUMB CPOE systems are the standard of care for large, complex healthcare institutions to meet national required guidelines to prevent and eliminate preventable medical errors. CPOE improves accuracy and communication of physician orders and therapies among the institution and healthcare providers.

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SECTION I  Foundations of Respiratory Care

Enterprise Software Packages An issue that had plagued healthcare organizations and our healthcare system involves the use of separate software packages for individual organizational functions, including but not limited to EHRs. In the past, the need for one such system to interface or “communicate” to another was dealt with on an as-needed basis through software “patches” and upgrades. Over time these separate software packages, which were originally designed to stand alone or provide a specific or limited number of functions, became inefficient and much less able to meet the increasingly sophisticated and numerous requirements of healthcare organizations, including hospitals and departments within them. At about the same time that this problem was reaching critical proportions, the US government (as part of a larger legislative initiative) passed the Health Information Technology for Economic and Clinical Health Act of 2009, or the HITECH Act, as part of a national strategy for building a national health information infrastructure (Fig. 7.1). The HITECH Act provided the Health and Human Services (HHS) Department with the authority to establish programs to improve healthcare quality, safety, and

efficiency through the promotion of health IT, including EHRs and private and secure electronic health information (EHI) exchange.8 Among other things, HITECH provided financial incentives to hospitals, physicians, and other health service providers who demonstrated that they are meaningfully using their EHRs by meeting predefined standards for a number of objectives. These objectives related to the submission of patient data to authorized third-party surveillance registries, making clinical data including lab values, vital signs, and office visit summaries more easily available to patients via secure internet sources, as well as interfacing multiple functions together, such as EHRs with CPOE.9-11 In October 2016, the Centers for Medicare and Medicaid Services (CMS) Merit-based Incentive Payment System (MIPS) replaced the Medicare EHR Incentive Program for eligible clinicians (also known as meaningful use) originally found in the HITECH Act. MIPS now replaces meaningful use, but it still aims to achieve the same objectives, including but not limited to improving quality, safety, and efficiency, and reducing health disparities, engaging patients and family, improving care coordination, and maintaining privacy and security of patient health

• Patient ID • Health industry

Health care provider dimension

• Health insurance

Personal health dimension

• Consent forms • Medication alerts

• Provider notes

• Nonshared personal information

• Clinical orders

• Self-care trackers

• Practice guidelines

• Audit logs

• Decision-support programs

• Personal library • De-identified information • Mandatory reporting • Community directories • Public health services • Survey data

• Vital statistics

• Inspection reports • Public education materials

• Population health risks • Communicable diseases

• Neighborhood environmental hazards

• Socioeconomic conditions • Registries

Population health dimension • Infrastructure data • Planning and policy documents • Surveillance systems • Health disparities data

Fig. 7.1  Electronic health records: dimensions of the national health information structure. (From U.S. Department of Health and Human Services. Information for health: a strategy for building the national health information infrastructure. http://aspe.hhs.gov/sp/NHII/Documents/NHIIReport2001/default.htm. [Accessed 25.09.2006].)

CHAPTER 7  E-Medicine in Respiratory Care

TABLE 7.1  Top Vendors of Enterprise

Electronic Health Record Systems (October 2011 to October 2012) Vendor

Location

Website

Allscripts Cerner Corp. CPSI Eclipsys Epic Systems Corp Healthcare Management Systems Healthland McKesson Provider Technologies Meditech Siemens Healthcare

Chicago, IL Kansas City, MO Mobile, AL Atlanta, GA Verona, WI Nashville, TN

http://www.allscrips.com http://www.cerner.com http://www.cpsinet.com http://www.allscripts.com http://www.epic.com http://www.wns.com

Minneapolis, MN Alpharetta, GA

http://www.healthland.com http://www.mckesson.com

Westwood, MA Malvern, PA

http://ehr.meditech.com http://www.healthcare .siemens.com

Modified from Top vendors of enterprise EMR systems. Modern Healthcare 2012.

information. Additional information about HITECH and additional regulatory guidelines regarding the use of information technology can be found at www.healthit.gov. To address these regulatory demands, hospitals and other healthcare providers increasingly use a single comprehensive software system or enterprise software package designed to provide integrated functionality to enhance both efficiency and effectiveness, as well as comply with current CMS and HHS information technology (IT) regulations. A variety of such software packages are available to healthcare organizations (Table 7.1). Enterprise EHR vendors such as Meditech, Epic, and Cerner continue to dominate the industry year after year, but small and specialty vendors can still hold their own.10 In addition to serving as a secure repository for EHRs, these software packages provide integrated functionality for a multitude of purposes, such as CPOE sytems, RT documentation of therapy given, test results, patient education resources, and so on. Other purposes are for the retrieval, review, and interpretation of existing records, such as those used to provide direct patient care, or for nondirect care functions, such as billing, process improvement, regulatory reporting, or other similar functions discussed later in this chapter.6 Nowadays, enterprise software systems that interface the EHRs with functions relevant to respiratory care and other clinical departments are the standard of care.

APPLICATIONS FOR PATIENT CARE Applications in Diagnostics Because the EHR contains an abundance of important clinical information, the RT needs to be able to promptly access and interpret key elements of it to assist the patient care team in accurately diagnosing, managing, and treating the patient’s condition. This may involve hemodynamic monitoring, blood gas, and point-of-care testing (POCT), medical imaging applications, and pulmonary function testing (PFT), among others.

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MINI CLINI Central Line–Associated Blood Stream Infection Problem An ARDS patient is being hemodynamically monitored using a PAC. The catheter was inserted 5 days ago. The patient has developed a fever of 101.9°F, tachycardia, and tachypnea (HR 110 beats/min, RR 28 breaths/min) with decreased urine output. Sepsis caused by a Central Line-associated Blood Stream Infection (CLABSI) is suspected. Discussion The PAC was introduced in 1971 for the assessment of heart function at the bedside. Since its introduction, its use has generated controversy regarding the benefits and potential harms caused by this invasive form of hemodynamic monitoring.12

Hemodynamic Monitoring In hemodynamic monitoring, bedside monitors and stand-alone devices can calculate cardiac output (CO), monitor intravascular fluid volume, and provide cardiac parameters and indices using both invasive and noninvasive applications. However, invasive methods using a pulmonary artery catheter or PAC (see Chapter 52) have a multitude of complications, including the risk for infection and death. As a result, the rapid evolution of E-medicine technologies has allowed for the development of safer noninvasive hemodynamic monitoring applications in perioperative and intensive care medicine. According to clinical studies, these technologies can provide CO readings noninvasively and continuously with minimal complications. Like most new technologies, their performance and accuracy need further validation. These new applications might prove to be innovative tools for the assessment of advanced hemodynamic monitoring without the drawbacks of invasive techniques.11 Pulmonary arterial catheterization is an invasive procedure. Inflation of the catheter once in a PA may cause rupture of that vessel with disastrous consequences. Furthermore, the continual presence of a PAC (more than 72 hours) increases the likelihood of CLABSI and endocarditis.12 If sepsis-related symptoms are noticed, removal and culture of the catheter must be done without delay. If advanced monitoring of hemodynamic parameter is still necessary, a non-invasive method must be used to avoid further complications and increased morbidity. General strategies for prevention of catheter-related infections in adult and pediatric patients include (1) education of healthcare personnel regarding the indications for PAC use and proper procedures for insertion and maintenance; (2) periodically assessing knowledge of and adherence to guidelines for all personnel involved in the insertion and maintenance of a PAC; and (3) allowing only trained personnel to maintain and manage PACs.13 Blood Gas Laboratories and Point-of-Care Applications The accuracy and precision of blood gas data influence clinical decisions and patient safety. Computerized blood gas analyzers and computer-assisted quality assurance measures in a blood

116

SECTION I  Foundations of Respiratory Care

gas laboratory are crucial functions in a respiratory care department. Quality assurance data are necessary for accreditation of blood gas laboratories by the College of American Pathologists (CAP), the Clinical Laboratory Improvement Amendments (CLIA), and the Joint Commission (TJC). Blood gas laboratory applications interface analyzers with the patient’s EHR to make blood gas results immediately available at the point of care and alert the clinician of critical results. In addition, this interfacing enables the storage, maintenance, retrieval, billing, and quality assurance of the blood gas analyzer data. Point-of-care testing (POCT) refers to blood gas analysis performed at or near the site of a patient, in a setting that is different from a normal hospital clinical laboratory. POCT testing reduces the time required to produce blood gas test results (turnaround time) and thus improves clinical care and decision-making for the clinician. POCT applications integrate seamlessly with the HER, allowing for immediate reporting of results and flagging of critical values. POCT applications can be used in a variety of clinical settings, including the OR, critical care unit, emergency department (ED), maternity unit, and outpatient clinic.14

Medical Imaging and Picture Archiving and Communication Systems Remote access to a patient’s imaging studies (see Chapter 21) has become an essential element in the delivery of care. Clinical integration of all these imaging modalities with the EHR is critical to help in the diagnosis of the pulmonary patient and to improve patient care and patient safety. A picture archiving and communication system (PACS) is an application that allows for imaging storage, portability, communication, and clinical integration of all imaging modalities with the EHR.15 Advances in technology and computer applications have allowed for PACS enterprise systems to flourish. In addition to the advantages mentioned earlier, current PACS applications have enhanced medical treatment and research by providing a variety of digital tools for the manipulation and interpretation of radiologic images, including three-dimensional imaging and three-dimensional printing technology. Pulmonary Function Testing and Interpretation Essentially the older volume displacement and spirograph PFT systems have been replaced by those that use different technology methods and computer interfaces to measure, display, and interpret the results. Similarly, most hospitals interface their PFT systems with the EHR, which allows clinicians to access reports and graphics from multiple workstations and remote devices. Interpretation of Pulmonary Function Tests Computer algorithms use standard reference-predicted values and formulas to aid in the interpretation of PFTs, including spirometry, lung volume, diffusing capacity, and bronchodilator response. The algorithms compare the patterns of the patient’s measured values with reference values based on age, height, gender, and race. These algorithms are used by computers to classify the patterns of the patient’s measured values as either normal or abnormal with degrees of severity. However, qualified interpreters must consider the effect of patient effort and other

MINI CLINI Computer-Assisted Interpretations of Pulmonary Function Tests in an Individual Patient Problem A patient with alpha1-antitrypsin deficiency has repeat PFTs, including a diffusing capacity of the lung for carbon monoxide (DLCO). Based on a computerassisted interpretation, there appears to be a remarkable decrease in the percent-of-predicted value for DLCO. It was previously normal; now it is 68% of predicted, indicative of emphysema. An effective therapy, pooled human plasma alpha-1 antitrypsin, is available but expensive. What additional information should the clinician evaluate? Discussion The clinician should determine (1) the actual observed DLCO values of the previous and repeat test and (2) whether the computer-assisted interpretations are based on different reference values among the tests. If the computerassisted percent-of-predicted values for each test were based on different sets of reference values, it could account for the change in DLCO. Further investigation of the results is warranted before final diagnosis and treatment.

factors on the computer-assisted interpretation of PFTs. Physician review and confirmation of computer-generated PFT results is always required.

Applications in Treatment Many current devices, therapies, and protocols developed in the last decade rely on technologic advances generated by E-medicine applications. These applications can be used in acute or nonacute settings by RTs to provide support and care for the pulmonary patient.

Applications in the Acute Care Setting Mechanical ventilators. Most mechanical ventilators use microprocessors with complex software applications to deliver, monitor, and in some cases independently manage (closed-loop ventilation) ventilator modes.16 A “mode” of ventilation is defined as a predetermined pattern of patient-ventilator interaction. Modes can be quite complex, as explained in detail in Chapter 46. Some modes, such as neurally adjusted ventilatory assist (NAVA), aim to enhance the patient-ventilator synchrony via automation that is highly responsive to the patient’s respiratory needs.17 Microprocessors also provide for graphic outputs and touch screens and interfaces, control ventilator alarms, data trending, and archive the history of set and measured values and settings, which can be downloaded and used later for review. Current conventional ventilators allow for updating and adding new modes of ventilation via software updates by their manufacturer. It is worth mentioning that all data taken or physically downloaded from any medical device in use is consider protected health information (PHI) and, hence, subjected to all HIPPA and other regulatory guidelines. Protocols for ventilator weaning and management of certain respiratory conditions (e.g., acute respiratory distress syndrome) coupled with the trending capabilities of today’s microprocessor

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CHAPTER 7  E-Medicine in Respiratory Care

ADULT VENTILATOR MONITOR Time of Tx: 06/07/05.16.02

Patient Data

Settings VT: 600 Rate: 26 PK Flow: 90 Trig: P - - 2.0 Sens: O2% Set: 60 PEEP: 10 Waveform:

ml bpm L/m F/P cmH2O % cmH2O

Ins Paus: 0.0

sec

Alarm Settings Hi Pres: 0 Low Pres: 0 Low PEEP: 0 Low VT: 0 Low VE: 0.0 Hi Rate: 0 Apnea Time: 0

Ventilator: PB840

cmH2O cmH2O cmH2O ml L/m bpm sec

Airway Management

Ppeak: Pplat: PEEP: Int PEEP: Pmean: I:E 1: Tot Rate: Tot Cor VE:

cmH2O cmH2O cmH2O cmH2O cmH2O bpm L/m

%O2 Meas: SpO2: ETCO2: Positn: Condtn: Breath sounds: N Suctioned: N

% % mmHg

Y/N Y/N

Last Value: F4-Save

Mode: ASSIST/CONTR Lavage: N Sputum: N Airway Care: N

Calculated Values ml ml Y/N

Tube Data Type: Desc: Size: 0.0 Pos: 0.0 Cuff Prs: 0

cmH2O

Circuit Data Set temp: 0.0 Meas temp: 0.0 Bag and Mask: Y Circ change: N Suct change: N HME change: N Ctube: 0.0

F10-Exit w/o saving

C C Y/N Y/N U/N Y/N ml/cmH2O

M Cor VTe:

ml

Comp: VT/Kg: 9.0

ml/cmH2O ml/kgBWP

Notes Advs Reaction: N SVC: Y/N SCD: HOB Pa>PV

PA Pa Arterial

in excessive fluid leaks and the formation of pulmonary edema. The third function is non-respiratory, involving the production, processing, and clearance of various chemicals and blood clots. Table 9.8 compares the hemodynamic parameters of the systemic and pulmonary circulatory systems.49 Although the entire cardiac output passes through both pulmonary and systemic circuits, the pulmonary circulation offers much lower resistance and consequently has much lower blood pressure. The low vascular pressures within the pulmonary circuit are essential in the maintenance of fluid balance at the alveolar-capillary interface. The pulmonary capillaries are exposed to vascular pressures of approximately 7 to 10 mm Hg. Increased pressure in the pulmonary circulation can occur with mitral valve disease or congestive (left) heart failure, disrupting fluid balance and leading to excessive fluid leakage, fluid accumulation, and alveolar congestion, which can impair gas exchange and lead to hypoxia. The low vascular pressures of the pulmonary circulation result in regional blood flow within the lungs that is highly influenced by gravity (dependent areas), airway pressure, and gas exchange.48 In the upright lung, blood pressure in the pulmonary arteries increases approximately 1 cm H2O for each 1 cm traversed downward from the apex to the base. Pulmonary blood flow distribution is highly dependent on gravitational effects. In the normal upright human lung, pulmonary blood flow decreases approximately linearly with distance up the lung, reaching very low values at the apex. Blood flow distribution in the lungs is divided into three zones according to the relative magnitudes of the pulmonary arterial, alveolar, and venous pressures (Fig. 9.34).16 Zone 1 is that region of the lung above the level at which pulmonary arterial pressures are lower than alveolar pressures; in other words, in this region, alveolar pressure exceeds arterial pressure and the collapsible capillaries close because the pressure inside exceeds the pressure outside. In Zone 2 the blood flow is determined by the difference between arterial and alveolar pressures, rather than by the expected arterial-venous pressure difference. Zone 3 is that part of the lung in which venous pressure exceeds alveolar pressure. Blood flow increases as one moves vertically down this zone due to the progressive distention from the increasing transmural pressure (intravascular pressure increasing down the zone while alveolar pressure is constant). Areas of regional lung hypoxia, because of reduced ventilation, congestion, or airway obstruction, can result in local pulmonary arterial vasoconstriction and cause blood flow to shift from these areas toward areas of higher O2 content and pulmonary vasodilation.16

Alveolar

Zone 2 Pa>PA>PV

PV Distance

Venous

Zone 3 Pa>PV>PA

Blood flow

Fig. 9.34  Three-zone model designed to account for the uneven topographic distribution of blood flow in the lung. Pa, Pulmonary arterial pressure; PA, pulmonary alveolar pressure; Pv, pulmonary venous pressure. From Broaddus: Murray & Nadel’s Textbook of Respiratory Medicine, 6th Edition, ed 6, St. Louis, 2013, Mosby.)

RULE OF THUMB As a consequence of having low blood pressure in some areas of the pulmonary circulation and being susceptible to gravity, the blood flow is much higher in the lung bases in resting upright subjects than in the lung apices. Gravity-related effects also occur in supine or recumbent positions but are less pronounced.

Non-respiratory Function of the Pulmonary Circulation The pulmonary circulation also serves as a blood reservoir for the left ventricle.16,48 This reservoir maintains stable left ventricular volumes despite small changes in cardiac output. The pulmonary blood volume (approximately 600 mL) is sufficient to maintain normal left ventricle filling for several cardiac cycles. This reservoir is important if filling of the right heart is momentarily decreased or interrupted. The pulmonary circulation also acts as a filter for the systemic circulation. The capillaries have an inner diameter of approximately 7 to 10 µm and theoretically trap particles (e.g., blood clots) down to this size before they enter the systemic circulation, where blockages could be life-threatening. The lungs also play an active role in the clearance, activation, and release of various biochemical factors.48 They are responsible for the synthesis, activation, inactivation, and detoxification of many bioactive substances. Angiotensin I is converted to its active form (angiotensin II) as it circulates through the lung. Various proinflammatory cytokines are also released from the lung when it is injured or repetitively overinflated during mechanical ventilation.50

Bronchial Circulation A separate arterial supply system called the bronchial circulation supplies blood to the airways from the trachea to the bronchioles and most of the visceral pleurae.51 The metabolic needs of the lung are comparatively low, and much of the lung parenchyma

CHAPTER 9  The Respiratory System

is oxygenated by direct contact with the inhaled gas. The bronchial circulation is a branch of the systemic circuit and is supplied with blood from the aorta via minor thoracic branches. Blood flow through the bronchial circulation constitutes approximately 1% to 2% of the total cardiac output. A single right bronchial artery supplying the right lung arises from the upper intercostal artery, the right subclavian artery, or an internal mammary artery. Two bronchial arteries supply the left lung and branch directly from the upper thoracic aorta. Bronchial arteries follow their respective bronchi. The bronchial arterial circulation terminates in a plexus of capillaries joining the alveolar-capillary bed. Bronchial venous blood drains through the azygos, hemiazygos, and intercostal veins to the right atrium. Some drain through the pulmonary capillaries to the pulmonary veins and into the left atrium. Fig. 9.33 shows the interrelationship and comingling of the pulmonary and bronchial circulatory systems. The bronchial and pulmonary circulations share an important compensatory relationship.51 Decreased pulmonary arterial blood pressure tends to cause an increase in bronchial artery blood flow to the affected area. This compensation minimizes the danger of pulmonary infarction, as sometimes occurs when a blood clot (pulmonary embolus) enters the lung. Similarly, loss of bronchial circulation can be partially offset by increases in pulmonary arterial perfusion. The adult lung does not require the bronchial circulation to remain viable, as evidenced by the success of lung transplantation, which does not preserve the bronchial circulation. However, this circulation plays a more important role in lung development, helps to preserve gas exchange during various congenital cardiac conditions, and appears to compensate in certain pulmonary diseases.

Lymphatics The lymphatic system of the lungs is an extensive system of lymphatic vessels, lymph nodes, the tonsils, and the thymus gland.28 The primary function of the lymphatic system is to clear fluid from the interstitial and pleural spaces to help maintain the fluid balance in the lungs. The lymphatic system also plays an important role in the specific defenses of the immune system. It removes bacteria, foreign material, and cell debris via the lymph fluid and through the action of various phagocytic cells (e.g., macrophages), providing defense against foreign material and cells that can penetrate deep into the lung. It also produces various lymphocytes and plasma cells to aid in defense. Both roles are essential for maintaining the normal function of the respiratory system. Most of the pulmonary lymphatic system consists of superficial and deep vessels—the superficial (pleural) vessels that drain the lung surface and the deep (peri-bronchovascular) conduitlike vessels that travel through the connective tissue tracts.28 Both drain the lymphatic capillaries in the respective regions. The deeper lymph vessels are closely associated with the small airways but do not extend into the walls of the alveolar-capillary membranes. The lymphatic vessels are thin-walled vessels that contain little connective and muscle tissue in their walls. Lymph fluid is collected by the loosely formed lymphatic capillaries and drains through the lymph vessels toward the hilum.

179

Paratracheal nodes Superior tracheobronchial nodes Inferior tracheobronchial nodes

Fig. 9.35  Mediastinal and paratracheal pulmonary lymph nodes. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

The fluid is propelled through the lymphatic system by the collective actions of valves that direct flow toward the hilum. The combined milking actions of smooth muscle contractions in the deeper conduit-like vessels and the cycle of ventilation act as a pump and squeeze the lymphatic vessels. Lymph fluid flow from the lungs can be increased after an injury to the pulmonary capillaries that results in increased leakage (e.g., acute ARDS) or from pulmonary capillary hypertension secondary to heart disease (e.g., left-sided heart failure). The lymph vessels emerge from the hilum of each lung and drain lymph fluid through a series of lymph nodes clustered around each hilum and the mediastinum. From there, lymph fluid travels through various lymph nodes within the mediastinum (Fig. 9.35). The lymph fluid rejoins the general circulation after passing through the right lymphatic or thoracic duct, draining into the jugular, subclavian, or innominate veins. The lymph fluid mixes with blood and returns to the heart. Lymphatic channels are not usually visible on chest radiographs. They may be detected if distended or thickened by disease. The “butterfly” pattern that radiates from the hilar region of both lungs during the acute development of pulmonary edema is thought to be the result of interstitial and lymph vessel distention with fluid. In this situation, the lymphatic drainage system has been overwhelmed by a sudden and excessive surge of fluid from the circulation. The development of a pleural effusion suggests that the lymphatic system is unable to remove excess fluid in the lung.

Neural Control of the Lungs All of the major structures of the respiratory system are innervated by branches of the peripheral nervous system: the autonomic and somatic branches (Fig. 9.36).52 Their primary functions are to (1) maintain homeostasis by regulating the depth and rate of breathing, bronchomotor tone, airway secretion, and other

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SECTION II  Applied Anatomy and Physiology

Pons Jugular ganglion Medulla

Nodose ganglion Superior cervical ganglion

Phrenic nerve Intercostal nerves Ribs

Intercostal muscles

Diaphragm

C1 2 3 4 5 6 7 8 T1 2 3 4 5 6 7 8 9 10 11 12

Vagus nerve Pulmonary plexus

Sympathetic chain Parasympathetic Sympathetic Motor (to skeletal muscle) Fig. 9.36  Schematic of the autonomic innervation (motor and sensory) of the lung and the somatic (motor) nerve supply to the intercostal muscles and diaphragm. (Modified from Murray JF: The normal lung, ed 2, Philadelphia, 1986, WB Saunders.)

TABLE 9.9  Summary of Important Airway Reflex Responses That Contribute to the Neural

Control of the Lung Regulation of respiratory system

Breathing pattern

Airway smooth muscle

Regulation of cardiovascular system

Airway secretion Cough reflex Cardiac function Vascular resistance Bronchial circulation

Inflation reflex (Hering-Breuer) Head’s reflex

Suppresses inspiration to initiate expiration Controls the depth of breathing Stimulates a deeper breath rather than inhibiting further inspiration It may prevent alveolar collapse by producing occasional deep breaths or gasps It also may be responsible for gasping in newborn infants as they progressively inflate their lungs Parasympathetic-bronchospasm Sympathetic-bronchodilation Activation of C-fibers reflexively stimulates submucosal gland secretion in the trachea A full-fledged cough action may come from activation of multiple types of airway sensors Lung inflation at low pressure causes reflex tachycardia, whereas inflation at higher pressure causes bradycardia Activation of C-fibers causes significant systemic hypotension, which results from vasodilation in addition to bradycardia and decreased stroke volume Stimulation of C-fibers produces bronchial vasodilation

cardiopulmonary functions under both healthy and disease conditions; and (2) initiate important defense reflexes that protect the lung and body from potential health-hazardous effects of air-borne particulates and chemical irritants (Table 9.9).53,54 The somatic system provides voluntary and automatic motor control and sensory innervation to the chest wall and respiratory muscles. Most of the major motor nerves that carry nervous signaling to the respiratory muscles are summarized in Tables 9.6 and 9.7. The autonomic nervous system signaling to and from the lungs is carried through afferent (summarized in Table 9.10 and Box 9.2) and efferent pathways. These pathways carry

unconscious autonomic nervous system motor signals to and from smooth muscles, airway lumen, and glands, and various sensory signals to and from the brain. Autonomic innervation of the lungs is carried from the brainstem through branches of the right and left vagus nerves (cranial nerve X) and from the spinal cord to four or five thoracic sympathetic ganglia that lie just laterally to the spinal cord.55 Both contribute fibers to the anterior and posterior pulmonary plexus at the root of each lung. From these plexuses, sympathetic and parasympathetic fibers enter the lung through the hilum and innervate various structures.

CHAPTER 9  The Respiratory System

181

TABLE 9.10  Summary of Vagal Afferent Pathways That Contribute to the Neural Control of

the Lung Laryngeal afferents

Recurrent laryngeal nerves Superior laryngeal nerve (internal and external branches) Myelinated and unmyelinated afferents

• Cold receptors • Drive receptors (contraction) • Pressure receptor

Reflex responses to prevent upper airway collapsing and preserve its patency in wakefulness and sleep

• Sensitive to chemical and mechanical stimulation and are responsible for eliciting the protective reflex responses (e.g., apnea, cough, etc.) against inhaled irritants • Can be activated by high concentration (>8%) of CO2 • Stimulated by solution lacking permanent anions (e.g., chloride ion) administered topically or by aerosol Bronchopulmonary Slowly adapting receptors • Found along the airways with the density being highest in the trachea and gradually decreasing along the afferents (SARs) or pulmonary airways to the lung periphery stretch receptors • They are mechanoreceptors and insensitive to chemical stimulation • During eupneic breathing, they discharge regularly, characterized by increased response during lung expansion and decreased response during lung deflation • They adapt very slowly to maintain lung inflation, and their stimulation can be sustained for as long as an hour Rapidly adapting receptors • Distributed along the airways with a high density in the large airways and the carina (RARs) • Classified as mechanoreceptors • Sense changes in lung volume and mechanics • Stimulated mainly by the rate of change in the amplitude of stimulation. In quiet breathing, many RARs are inactive and others discharge irregularly • Most activity occurs during the lung inflation phase • RARs respond to changes in lung volume, flow rate, airway pressure, the rate of change of airway pressure, and lung stiffness Deflation-activated • Found along the airways but their exact location (in muscle or mucosal layers) has not been defined receptors (DARs) • Possibly activated by mechanical forces in the lung High-threshold Aδ • Found in the large airways and in lung periphery, often located near the hilum receptors (HTARs) • Stimulated by hypertonic saline, hydrogen peroxide, bradykinin • Many afferent properties and reflex functions attributed to RARs may belong to HTARs C-fiber afferents (also • Stimulated by chemical stimulants delivered intravenously or by aerosol called juxtacapillary or • Distributed from the trachea to the lung periphery J receptors) • Represent ∼80% of the vagal bronchopulmonary afferents • Activated by a variety of endogenous and exogenous agents, such as hydrogen ions, adenosine, reactive oxygen species (ROS), capsaicin, and phenyldiguanide • Also activated by changes in osmolarity and temperature Pulmonary C-fibers • Receive blood supply from pulmonary circulation and are often located in the lung periphery • Respond to a stimulant with short latency Bronchial C-fibers • Perfused by systemic circulation via the bronchial artery • Often located in large airways and superficially in the lumen Nonadrenergic, noncholinergic (NANC) • Travels within the vagus nerve to each lung system • Releases a neurotransmitter that promotes the production of nitric oxide • Causes the relaxation of airway smooth muscle and dilation • Capable of bronchoconstriction through the local reflex release of substance P (a peptide protein) and neurokinin A Cough receptors • Initiate the cough reflex • Located mainly in different regions of the respiratory tract, including larynx, tracheobronchial tree, and alveoli

Efferent Pathways The parasympathetic nervous preganglionic fibers exit the brainstem via the two vagus nerves. On entry into the chest, the vagus nerve branches to the larynx. This branch is called the recurrent laryngeal nerve. Each vagus nerve also develops a branch called the superior laryngeal nerve. The external branch of this nerve supplies the cricothyroid muscle. The internal branch provides sensory fibers to the larynx. The recurrent laryngeal nerves provide the primary motor innervation to the larynx. Damage to laryngeal nerves can cause unilateral or bilateral vocal cord paralysis,

depending on which branches are involved. Hoarseness, loss of voice, and an ineffective cough may result. After forming ganglia and postganglionic nerve fibers, parasympathetic and sympathetic nerve fibers enter the lung through the hilum and run parallel to the airways as they branch (Fig. 9.37). Parasympathetic fibers form their ganglia much closer to the target tissues (e.g., bronchioles, glands, and blood vessels) and have much shorter postganglionic nerve fibers. Most of the sympathetic fibers form their ganglia along the spinal cord and then form longer postganglionic fibers that penetrate the lungs and end on the airway smooth muscle and glands. Both

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SECTION II  Applied Anatomy and Physiology

sympathetic and parasympathetic postganglionic efferent fibers innervate the smooth muscle and glands of the airways and the smooth muscles of the pulmonary arterioles. They influence the diameter of the airway by causing more or less tension in the smooth muscles that wrap around the airway, and they also influence glandular secretion. The smooth muscles in the medial wall of the pulmonary arterioles cause constriction when tensed and dilation when relaxed. The combined effects of the parasympathetic and sympathetic nervous activity, which generally oppose each other’s action, result in a balanced control of airway tone, vessel diameter, and glandular secretion.55 The parasympathetic postganglionic fibers generally secrete acetylcholine as their primary neurotransmitter when they receive BOX 9.2  Summary of Sympathetic

Afferent Pathways’ Roles in the Neural Control of the Lung • Sympathetic afferents travel with their efferent counterpart • Their cell bodies reside in the dorsal root ganglion (DRG) and fibers travel through the white ramus communicans to the paravertebral ganglia as well as the prevertebral ganglia • Have much more diffused sensory territory than the vagal afferent system • Stimulation of pulmonary sympathetic afferents fibers alters breathing pattern • They are believed to mediate the pain sensation, especially when pain arising from the pleural region is involved • Respiratory sensations, such as dyspnea, air hunger, tightness of chest, airway irritation, and urge to cough, are generated by sensory signals related to breathing or arising from the respiratory structures • These sensations involve multiple sensors located in different parts of the respiratory systems and neural pathways, and complex signal processing in specific neural structures and regions in the central nervous system (CNS)

signals from the brainstem. Acetylcholine binds to M3 muscarinic cholinergic receptors, causing airway smooth muscle constriction, blood vessel dilation, and glandular secretion. The sympathetic postganglionic fibers are much less developed in comparison. The sympathetic postganglionic fibers in the lung primarily secrete norepinephrine. The adrenal glands release epinephrine into the circulation when they receive sympathetic signals from the spinal cord. Epinephrine and norepinephrine bind to α-adrenergic and β-adrenergic receptors of blood vessels. This binding causes dilation and relaxation in the β-adrenergic receptors of the bronchial airway and vessel smooth muscles. The airways are provided with a third autonomic pathway that is neither parasympathetic nor sympathetic in action. The nonadrenergic, noncholinergic (NANC) system nerve fibers travel within the vagus nerve to each lung. For additional description of this system’s roles in lung innervation refer to Table 9.10.56 Box 9.3 lists the most common effects of the parasympathetic system stimulation that affect the lungs and other organs by using the pneumonic SLUG BAM (the first initial for all of its manifestations). BOX 9.3  Effects of the Parasympathetic

Nervous System (SLUG BAM Pneumonic) • • • • • • •

Salivation/↑ secretions/sweating Lacrimation Urination Gastrointestinal upset Bradycardia/bronchoconstriction/bowel movement Abdominal cramps/anorexia Miosis (pupils become constricted)

Ganglia Brain

Postganglionic parasympathetic and NANC fibers

Vagus nerve (cranial nerve X) preganglionic parasympathetic fiber

Brainstem Spinal cord

Airway

Ganglia Preganglionic sympathetic fibers

Postganglionic sympathetic fibers

Blood vessel

Fig. 9.37  Schematic of sympathetic, parasympathetic, and nonadrenergic, noncholinergic (NANC) neural fiber connections to the airways and blood vessels of the lungs.

CHAPTER 9  The Respiratory System

Afferent Pathways Most afferent fibers follow pathways from the lungs to the central nervous system in the vagus nerve. The vagus afferent pathways are activated by a variety of different receptors within the lung that are sensitive to inflation, deflation, and chemical stimulation.57 Slow-adapting receptors (SARs) are concentrated in the small and medium-sized airways and are closely associated with the airway smooth muscle. SARs, also known as pulmonary stretch receptors, are activated by an increase in tension in the walls of airways, thereby providing information about increases in lung volume. In the mucosal layer of the airway, rapid-adapting receptors (RARs) sense changes in tidal volume, respiratory rate, and lung compliance, responding to a wide variety of mechanical and chemical irritants. Also, a variety of other chemical and congestion sensors, when active, seem to modify the sensation of breathing and modify the breathing pattern (e.g., cough reflex and response to alveolar congestion). Additional receptors are located outside the lungs; they include respiratory muscle proprioceptors that sense the stretch state of the muscles and peripheral chemoreceptors that sense the chemical condition of blood (e.g., O2, CO2, and hydrogen ion concentration) that are involved in the control of ventilation (see Table 9.10). Pulmonary stretch slow-adapting and RAR progressively discharge during lung inflation and are linked to inhibition of further inflation. This is a type of negative feedback known as the inflation reflex. It was originally described by Hering and Breuer and continues to bear their names (the Hering-Breuer reflex). The inflation reflex is thought to be actively involved with controlling the depth of breathing and may affect the duration of the expiratory pause between breaths. The inflation reflex is probably very weak or absent during quiet breathing in healthy adults, but there appears to be evidence of its activity in newborns (see Table 9.9).53 Irritant or mechanical rapid adapting receptors are found mainly in the posterior wall of the trachea and at bifurcations of the larger bronchi. These receptors respond to various mechanical, chemical, and physiologic stimuli, such as physical manipulation or irritation, inhalation of noxious gases, histamine-induced bronchoconstriction, asphyxia, and microembolization of the pulmonary arteries. Stimulation of the irritant RARs can result in bronchoconstriction, hyperpnea, glottic closure, cough, and sneeze.58 Stimulation of these receptors also can cause a reflex slowing of the heart rate (bradycardia). This response is referred to as the vasovagal reflex. It may occur during tracheobronchial suctioning, intubation of the airway, or bronchoscopy. Unmyelinated slow-conducting C-fiber endings (also known as juxtacapillary or J receptors), are present in the walls of the bronchial and terminal airway region and have been linked to a breathing reflex pattern associated with mechanical stretch, pulmonary congestion, and exposure to various chemicals.59 When C-fibers become activated, signals are sent back to the brainstem via the vagus nerve, resulting in rapid, shallow breathing. C-fiber activation also has been shown to cause bradycardia, hypotension, bronchoconstriction, mucus production, and apnea in experimental animals.60 Stimulation of these receptors may contribute to the sensation of dyspnea and, in severe cases, the

183

vasovagal reflex, which can accompany pulmonary edema, pulmonary embolism, and pneumonia (see Table 9.10).

ANATOMY OF THE RESPIRATORY TRACT Upper Respiratory Tract The upper respiratory tract is defined as the airways that start at the nose and mouth and extend down to the trachea (Fig. 9.38).55 The upper airway is open to the outside environment through the external nares, or nostrils, and the mouth opening of the oral cavity. Most of the air moved through the respiratory tract during resting breathing enters through the nares and nasal cavity. Mouth breathing is used during exercise to reduce the resistance to gas flow at higher ventilation rates. The functions of the upper airway are summarized in Box 9.4.

Nasal Cavity and Sinuses There are two flared openings called alae that form the external nares. The alae enclose a space on each side called the vestibule. The vestibules have hairs that act as a gross filter. Located posterior to the vestibules are the openings to the internal nose or the anterior nares. The left and right nasal cavities are formed by cartilage and numerous skull bones. The roof is formed by the nasal, frontal, sphenoid, and ethmoid bones. The septum separating the two cavities is formed by cartilage and the ethmoid and vomer bones (Fig. 9.39). The lateral walls are created by the maxilla, lacrimal, and palatine bones. The floor of the cavity, or palate, is primarily formed by the maxilla. Three shelf-like bones protrude into the cavity from the lateral walls. These bony shelves are called the superior, middle, and inferior conchae, or turbinates. The role of the conchae is to increase the surface area and complexity of the nasal cavity, enabling the nasal cavity to work as a passageway, filter, humidifier, and heater of the inhaled gas. The posterior openings of the nasal cavity are called the internal or posterior nares and are formed in part by the flexible soft palate. The surface of the nasal cavity is covered with epithelia. The anterior portion is covered with stratified squamous cells and possesses hair follicles and hair. This is the same type of tissue that forms the epidermis of the skin. The middle portion of the cavity is covered with a mucous membrane composed of ciliated pseudostratified epithelia and goblet cells. The mucous membrane functions to secrete mucus, humidify the inhaled air, and trap inhaled particles. Just below the mucous membrane is an extensive network of veins forming a venous plexus. Inflammation of this mucous membrane is caused by irritation or infection and leads to vasodilation and increased vessel leakage. The consequence BOX 9.4  Functions of the Upper Airway • Passageway for gas flow • Filter • Heater • Humidification • Sense of smell and taste • Phonation • Protection of the lower airways

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SECTION II  Applied Anatomy and Physiology Cribriform plate of ethmoid bone Frontal bone Frontal sinus Nasal bone

Posterior ethmoid sinus

Nasal cartilage Superior nasal concha Middle nasal concha

Sphenoid sinus Opening of eustachian tube Pharyngeal tonsil Soft palate Uvula

External nares Inferior nasal concha Hard palate Valecula

Palatine tonsil

Mandible

Esophagus

Hyoid bone Epiglottis Vocal cord Thyroid cartilage Cricoid cartilage Thyroid gland Trachea

Fig. 9.38  Midsagittal section through the upper airway. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

Frontal sinus Cribriform plate of ethmoid bone

Nasal bone Perpendicular plate of ethmoid

Sphenoid sinus Pharyngeal tonsil

Septal cartilage Vomer

Vomeronasal cartilage

S

Maxilla Palatine bone

A

P I

Incisive foramen Fig. 9.39  The bony nasal septum. (From Patton KT, Thibodeau GA: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby.)

of nasal cavity inflammation is a partial or complete blockage of the air passages. The vessels of the venous plexus can rupture as a result of breathing dry air or the passage of foreign bodies through the nose. Rupture of these vessels can cause considerable nasal bleeding (epistaxis). The posterior portion of the nasal cavity is covered with stratified squamous epithelium similar to the tissue covering of the nearby oral cavity.

Within the skull bones and around the nasal cavity are the sinuses (Fig. 9.40). These hollow spaces are named for the bones in which they are found.61 The sinuses are lined with a mucous membrane and drain into the nasal cavity through numerous ducts. They function to reduce the weight of the skull, strengthen the skull, and modify the voice during phonation. The nasal cavity conducts air to and from the respiratory tract, conditions inhaled gas, acts as the sinus and eye fluid drain, and contains olfactory sensors for the sensation of smell. Conditioning inhaled gas helps defend the respiratory tract and involves filtering, heating, and humidifying the air (see Chapter 39). Filtration of inhaled air is carried out by the hair in the anterior portion of the cavity and the sticky mucous membrane that covers the complex surface of the cavity. Filtration is enhanced by the flow pattern through the nasal cavity. Inhaled gas is accelerated to a high velocity through the anterior nares. It changes direction sharply as it enters the internal nasal cavity. This pattern causes particles larger than 10 µm in diameter to impact on the nasal mucosa. Ciliary action or nose blowing clear these particles. Past the external nares, the cross-sectional area increases resulting in a decrease in gas velocity. Turbulence increases because of the narrow convolutions of the passages and the turbinates. Low velocity and turbulence combine to remove any remaining particles. Filtration is based on impaction, sedimentation, and diffusion of various-sized particles.

CHAPTER 9  The Respiratory System

185

MINI CLINI Exercise-Induced Asthma (EIA)

Frontal sinuses

Ethmoid sinuses Sphenoid sinuses Maxillary sinuses

The upper airway, along with the trachea and mainstem bronchi, plays crucial roles in conditioning the air being breathed. These airways not only conduct gas from the atmosphere to the lower airways but also warm, humidify, and filter it. Problem Some asthmatics develop shortness of breath, wheezing, and coughing when they exercise outdoors. What could be causing their asthma attack? Is there an alternative form of exercise that could reduce the symptoms and allow them to receive an aerobic workout? Discussion In many cases, exercise-induced asthma (EIA) or exercise-induced bronchospasm (EIB) appears to be triggered by reflexes from the large airways (upper airway, trachea, bronchi). These airways warm and humidify inspired gas. Water vapor is absorbed from the fluid lining of the airways and replenished from the cells lining the airways. As gas is exhaled, it cools, and some of the water vapor is reabsorbed. Only a small amount of water is lost from the body via this mechanism. Exercise (with its increased ventilatory demands) causes an increase in heat and water loss from the airways. The airways in some individuals are especially sensitive (hyperresponsive) to a wide variety of triggering agents. When these individuals exercise and increase their ventilation, the loss of heat or water from the large airways can trigger an asthmatic reaction (i.e., coughing, wheezing, and shortness of breath).

A

exhalation, the heated and moist exhaled gas passes over the concha and is cooled. The excess moisture deposits on the concha as condensation to help retain and recycle humidity. These defense/conditioning mechanisms help ensure inspired gas is free from particulate and bacterial contamination and is heated and humidified to 37°C and 100% relative humidity by the time it reaches the trachea (see Chapter 39). In addition, the mucous membrane contains chemoreceptors that send signals to the olfactory nerve for the sensation of smell.

B

C Fig. 9.40  (A) Positions of the frontal, maxillary, sphenoid, and ethmoid sinuses; the nasal sinuses are named for the bones in which they occur. (B) Axial computed tomography (CT) scan at the approximate level of the inferior turbinates (IT) and maxillary sinuses (MS). The nasal septum (NS) is also well defined. (C) Coronal CT scan showing the anterior ethmoid sinuses (AE) and the middle turbinates (MT) in addition to the structures seen in (B).

Surface fluids originate from the goblet cells and submucosal glands. This fluid lining has mild antibacterial properties. Ciliary activity in the nasal mucous membranes helps transport the mucus produced so it can be cleared. Foreign matter is typically cleared from the nasal cavity by sniffing and swallowing. During

Oral Cavity Air also can enter and exit from the respiratory tract through the oral cavity (Fig. 9.41). The oral cavity is defined as the space from the lips to the end of the hard palate. The anterior roof of the oral cavity is the hard palate and is formed by the maxillary bone. The posterior portion is known as the soft palate. Its soft tissue composition has the ability to move upward and seal off the nasal cavity. The end of the soft palate hangs down into the posterior portion of the oral cavity. This part of the soft palate is called the uvula. The walls of the oral cavity are formed by the cheeks, and the floor is dominated by the tongue. The uvula and the surrounding walls control the flow of air, fluid, and food during eating, drinking, sneezing, coughing, and vomiting. The tongue is involved in mechanical digestion, taste, and phonation. The posterior surface of the tongue is supplied with many sensory nerve endings. These nerves produce a vagal gag reflex when stimulated, protecting the lungs from aspiration. This reflex must be considered when passing tubes or instruments through the mouth in conscious or semiconscious patients.62

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SECTION II  Applied Anatomy and Physiology

Philtrum Oral cavity Oropharynx Hypopharynx

Lip

Hard palate Soft palate Uvula Epiglottis

Palatine tonsil

Laryngeal inlet Esophageal inlet

Tongue

Cricopharyngeal muscle Larynx

Esophagus

Lip

Fig. 9.41  Frontal view into the open mouth showing the major structures within. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

The mucosal surfaces of the oral cavity also provide humidification and warming of the inspired air. These surfaces are much less efficient than the nose. Saliva is produced by major and minor salivary glands. Saliva functions primarily as a wetting and digestive agent for food but provides some humidification of inspired gas. The oral cavity ends at a double web on each side, called the palatine folds. The palatine tonsils sit between these folds on each side (see Fig. 9.41). The palatine tonsils are vascularized lymphoid tissues that play an immunologic role, especially in childhood. Reflexes of the mouth, pharynx, and larynx help protect the lower respiratory tract during swallowing.63 These protective functions can be severely compromised during anesthesia or unconsciousness. Loss or compromise of these important reflexes can result in aspiration of bacteria-colonized saliva or food causing pulmonary infection and asphyxiation in severe cases.

Pharynx The posterior portion of the nasal and oral cavities opens into a region called the pharynx. The entire pharynx is lined with stratified squamous epithelium. The pharynx is subdivided into the nasopharynx, oropharynx, and hypopharynx, or laryngopharynx. The nasopharynx lies at the posterior end of the nasal cavity and extends to the tip of the uvula. Numerous foreign particles impact the surface of the nasopharynx. Located in this region are two pharyngeal tonsils (also called the adenoids) on either side of the lateral and posterior walls of the pharynx. They monitor and interact with the particles inhaled through the actions of the lymphoid cells located there. In the same region are two openings into the left and right eustachian tubes that link the upper airway with the middle ear (see Fig. 9.38). The

Fig. 9.42  Schematic of the oral cavity (green), oropharynx (yellow), and hypopharynx (blue) along with the esophageal inlet, cricopharyngeal muscle, and upper esophageal sphincter. (From Broaddus VC: Murray & Nadel’s Textbook of Respiratory Medicine, ed 6, St. Louis, 2013, Mosby.)

eustachian tubes drain fluid out of the middle ear and allow gas to move in or out, equalizing pressure on either side of the tympanic membrane (eardrum). The oropharynx is located in the posterior region of the oral cavity that spans the space between the uvula and the upper rim of the epiglottis. This region is also equipped with a pair of palatine tonsils that are located on the lateral walls of the oropharynx. These tonsils can become chronically swollen causing partial airway obstruction. If the swelling is excessive and the individual has numerous repeat throat and ear infections, the tonsils can be surgically removed via a tonsillectomy.64 The region below the oropharynx is known as the hypopharynx or laryngopharynx. It extends from the upper rim of the epiglottis to the opening between the vocal cords. The tissues of the nasopharynx and hypopharynx can move and undergo large changes of shape during speech and swallowing. Immediately below the hypopharynx the digestive and respiratory tracts separate (Fig. 9.42). During unconsciousness, the muscles of the tongue and hypopharynx can relax and allow the tongue and other soft tissues to collapse and occlude the opening of the hypopharynx. This condition can result in partial to complete blockage of the upper airway and limit air movement to and from the respiratory tract. This condition is a primary cause of obstructive sleep apnea (OSA), discussed later in this text.

Larynx The larynx lies below the hypopharynx and is formed by a complex arrangement of nine cartilages and numerous muscles (Fig. 9.43).65 It protects the respiratory tract during eating and drinking and in phonation. The thyroid cartilage forms most

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CHAPTER 9  The Respiratory System

Tongue Epiglottis Hyoid bone Hyoid bone Thyroid membrane

Thyroid membrane

Thyroid cartilage

Thyroid cartilage Corniculate cartilage Arytenoid cartilage

Cricothyroid ligament

Cricoid cartilage

Cricoid cartilage Cricotracheal ligament Tracheal C-shaped cartilages

Tracheal C-shaped cartilages

Fig. 9.43  Anterior and lateral views of the larynx. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

of the upper portion of the larynx and is generally referred to as Adam’s apple. This cartilage is named for the thyroid gland that lies over its outer surface. Just below the thyroid cartilage is the cricoid cartilage. It is the only laryngeal structure that forms a complete ring of cartilage around the airway and is the narrowest region of the upper airway in infants. A membrane of connective tissue called the cricothyroid ligament spans the space between the thyroid and cricoid cartilage. This membrane is occasionally used as the location for placement of an emergency artificial airway in patients who have a life-threatening blockage of the upper airway (cricothyrotomy). The cartilaginous and leaf-shaped epiglottis lies within and is attached to the thyroid cartilage by a flexible joint. In adults, it is 2 to 4 cm long, 2 to 3 cm wide, and 2 to 5 mm deep. It is not easily visualized in adults, but it can be seen in small children and crying infants because of its higher position. During breathing, the thyroid cartilage slides down and remains apart from the epiglottis, allowing air to move in and out of the respiratory tract. The epiglottis helps prevent liquids and food from entering the respiratory tract by forming a tight seal with the thyroid cartilage during swallowing. The act of swallowing is a complex series of muscular contractions. It results in early closure of the vocal cords, upward motion of the thyroid cartilage, and movement of the epiglottis down and back to form a tight seal as food is propelled to the back of the mouth and toward the esophagus.66 The inlet to the larynx lies below and behind the base of the tongue. Fig. 9.44 shows the inlet as it appears when viewed with a laryngoscope. The base of the tongue is attached to the epiglottis by three folds. These folds form a space between the tongue and the epiglottis called the vallecula, which is a key landmark in oral intubation (see Fig. 9.38).

Base of tongue Epiglottis

Vestibular fold (false vocal cord)

Vocal folds (true vocal cords)

Arytenoid cartilage

A Rima glottidis A L

Cuneiform cartilage Corniculate cartilage

R P

B Fig. 9.44  (A) Superior view of true vocal cords, glottis (rima glottidis), epiglottis, and other structures within the larynx. (B) An endoscopic photograph showing vocal cords in the open position. (From Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St Louis, 2011, Mosby.)

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SECTION II  Applied Anatomy and Physiology

Within the thyroid cartilage and just above the cricoid cartilage are the arytenoid cartilages. The vocal ligaments or true cords span the opening in the larynx by attachments to the thyroid and movable arytenoid cartilages that lie posteriorly. Above and laterally are the vestibular folds or false cords. The true vocal cords are composed of connective tissue and muscle and covered with a mucous membrane. They have poor lymphatic drainage and are susceptible to inflammation, which can result in airway obstruction. In the same region are the corniculate and cuneiform cartilages that function to support the soft tissue on either side of the vocal cords. The opening formed between the vocal cords is called the glottis (Rima glottidis). During swallowing, the vocal cords close to help protect the lower airways. Damage to the cricoarytenoid joint, which allows the arytenoid cartilages to rotate, can result in an inability to open the vocal cords properly and cause difficulties in speaking and breathing. Laryngeal spasm and resultant partial or total temporary airway closure are brought about by laryngeal stimulation and reflex spasm of various laryngeal muscles that cause closure of the false and true vocal cords. The muscles of the larynx are innervated by the inferior laryngeal nerve, also known as the recurrent laryngeal nerve. It is a motor nerve that branches from the vagus nerve.53 Impulses carried by this nerve are important in phonation and swallowing. Injuries to this nerve can cause partial or complete paralysis of the vocal cords and inability to swallow correctly. This nerve injury results in difficulty with speech and in severe cases can cause airway obstruction as a result of vocal cord closure. Speech.  The laryngeal component of speech is called phonation. It requires the adjustment of vocal cord tension and position relative to one another.67 The action of the posterior cricoarytenoid muscles causes the arytenoid cartilages to rotate and opens the vocal cords. Closure of the vocal cords is accomplished by rotating the arytenoids in the opposite direction through the action of the lateral cricoarytenoid and oblique arytenoid muscles. On closure of the vocal cords, the expiratory muscles of breathing (e.g., abdominal wall muscle group) compress the thoracic cavity and can increase intrapulmonary pressures to 35 cm H2O during forceful speech. To form sound, the cricothyroid muscles tilt the cricoid and arytenoid cartilages posteriorly with respect to the thyroid cartilage, elongating and tensing the vocal cords. Simultaneously, this action is opposed by the thyroarytenoid muscles, which pull the arytenoid cartilages anteriorly and relax vocal cord tension. The release of pressurized airflow through the tensed vocal cords causes vocal cord vibration and the production of audible sound waves, which resonate in the upper airway and sinuses. By careful adjustment of thyroarytenoid muscle tension and mandible and tongue position, fine control over sound production or speaking is achieved. Swelling of the vocal cords or the adjacent tissues increases their mass and disturbs their ability to vibrate; this can result in hoarseness and the inability to speak. Breath hold, effort closure, and cough.  Tight closure of the larynx and the buildup of intrapulmonary pressure through muscular effort are called effort closure. Effort closure of the larynx is necessary to generate loud sounds and for effective coughing and sneezing. It is generated by closure of the false and true vocal cords of the larynx. This action effectively “clamps”

the airway closed and enables the intra-airway pressures to increase to more than 100 cm H2O when the various expiratory muscles compress the thorax. The sudden opening of the larynx results in the immediate release of high-flow gas that is necessary for coughing and sneezing.68 Patients who have artificial airways have difficulty producing an effective cough because the artificial airway prevents the closure of the larynx (see Chapter 44).

Patent Upper Airway The relative positions of the oral cavity, pharynx, and larynx are crucial to the patency of the upper airway in an unconscious patient. In upright subjects, the head and neck form a 90-degree angle with the axis of the pharynx and larynx (Fig. 9.45B). With the loss of consciousness, the head flexes forward and decreases this angle (see Fig. 9.45A). This positional change can partially or completely obstruct the upper airway. Extension of the head and lower jaw into the “sniff” position alleviates this obstruction (see Fig. 9.45C). Extension of the head moves the tongue away from the rear of the pharynx. This technique is used to maintain the airway in unconscious patients and facilitates placement of artificial airways. RULE OF THUMB  When a cervical spinal injury is suspected, the airway must be opened by using the jaw-thrust maneuver. This maneuver is performed by placing the index and middle fingers behind the jaw angle to physically push the posterior aspects of the mandible upwards while the thumbs push down on the chin to open the mouth. This movement will move the tongue forward relieving the obstruction.

Lower Respiratory Tract The airways of the tracheobronchial tree extend from the larynx down to the airways participating in the gas exchange. Each branching of an airway produces subsequent generations of smaller airways. The first 15 generations are known as conducting airways because they transport gas from the upper airway to the structures that participate in the gas exchange with the blood. The microscopic airways beyond the conducting airways that carry out gas exchange with blood are classified as the respiratory airways.

Trachea and Bronchi The trachea extends from its connection to the cricoid cartilage down through the neck and into the thorax to the articulation point between the manubrium and body of the sternum (angle of Louis). At this point, it divides into two main stem bronchi (Fig. 9.46). The adult trachea is approximately 12 cm long and has an inner diameter of about 2 cm.55 Fig. 9.47 shows the different layers of tissue that form the trachea. The outermost layer is a thin connective tissue sheath. Below this sheath are numerous C-shaped cartilaginous rings that provide support and maintain the trachea as an open tube. The typical adult trachea has 16 to 20 of these rings. The inner surface of the trachea is covered with a mucous membrane. In the posterior wall of the trachea is a thin band of tissue called the trachealis muscle that supports the open ends of the tracheal rings. The esophagus lies just behind the trachea.

CHAPTER 9  The Respiratory System

A

B

189

Flexed

Normal

C

Extended

Fig. 9.45  The Position of the Head Affects the Patency of the Airway. (A) With the head flexed, the airway may be kinked, making breathing or intubation difficult. (B) The normal upright relationship of the head and neck to the chest. (C) Extension of the head straightens the airway, making breathing, clearance of material, or intubation easier.

The cartilaginous rings support the trachea so it does not collapse during exhalation. Some compression occurs when the pressure around the trachea becomes positive. During a strong cough, the trachea is capable of some compression and even collapse. The negative pressure generated around the trachea during inhalation causes it to expand and lengthen slightly. The trachea is positioned midline in the upper mediastinum and branches into right and left main stem bronchi (see Fig. 9.46). As mentioned before, at the base of the trachea, the last cartilaginous ring that forms the bifurcation for the two bronchi is called the carina. The carina is an important landmark used to identify the level where the two mainstem bronchi branch off from the trachea; this is normally at the base of the aortic arch. The right bronchus branches off from the trachea at an angle of approximately 20 to 30 degrees, and the left bronchus branches with an angle of about 45 to 55 degrees (Fig. 9.48). The lower angle branching (closer to mid-line) of the right

bronchus results in a greater frequency of right-mainstem intubation and the foreign body aspiration into the right lung because of the more direct pathway. Each bronchus carries gas to and from one lung. It enters the lung with the pulmonary vessels, lymph vessels, and nerves through the hilum. The bronchus repeatedly branches within each lung to supply gas to separate regions of each lung.

Lobar and Segmental Pulmonary Anatomy The lungs have an apex and a base and are subdivided by fissures into lobes.44 The lobes are divided further into bronchopulmonary segments (Table 9.11 and Fig. 9.49). Each segment is supplied with gas from a single segmental bronchus. Controversy exists over the exact number of segments; some anatomists accept that each lung has ten segments, whereas others maintain that the right has 10 and the left has 8. Knowledge of segmental anatomy is important in the physical examination of a patient

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Thyroid cartilage Cricothyroid ligament Cricoid cartilage Cricotracheal ligament Trachea

Right bronchus

Left bronchus

Upper lobe bronchus Upper lobe bronchus Lingular bronchus

Carina Middle lobe bronchus

Lower lobe bronchus

Lower lobe bronchus

Fig. 9.46  Major airways of the tracheobronchial tree. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

Mucosa

Anterior Epithelia Lamina propria Submucosal glands Hyaline cartilage Adventitia Trachealis muscle

Esophagus

Posterior Fig. 9.47  Cross-sectional view through the trachea and esophagus. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

MINI CLINI Right Mainstem Intubation The placement of an endotracheal tube (ET) through the upper airway and into the trachea is a common airway management technique to facilitate artificial airway placement. Problem After placement of an ET in a patient with a 70-kg predicted body weight (PBW), it is noted that breath sounds are heard in the right chest only, it is somewhat difficult to ventilate, and the oxygenation is deteriorating. Is the airway placement the cause of the problem? How can this problem be avoided? Discussion An ET of proper diameter should be placed in the trachea, so the tip is 3 to 5 cm above the carina. If the ET is advanced too far, it often enters the right mainstem bronchus because of the straighter path this bronchus offers. Right mainstem intubation results in right lung ventilation only. The left lung continues to receive pulmonary blood flow but does not ventilate and oxygenate adequately and eventually collapses. Neck movement (flexion and extension) can also displace the ET into a mainstem bronchus. To help avoid this problem, the ET tube generally should not be advanced more than 24 cm past the lips in an average 70-kg PBW patient. At this point, auscultation is done with a stethoscope to confirm bilateral breath sounds. Symmetrical chest rising should also be checked. A chest radiograph should always be taken shortly after the ET tube is inserted to confirm proper position inside the trachea.

CHAPTER 9  The Respiratory System

Right

20°–30°

191

Left

45°–55°

Fig. 9.48  Course of trachea and right and left main stem bronchi, superimposed on a standard chest radiograph. The right mainstem bronchus has a straighter course from midline than the left main stem bronchus.

TABLE 9.11  Bronchopulmonary Segments Segment

Segment

Number

Right Upper Lobe Apical 1 Posterior 2 Anterior 3

Left Upper Lobe Upper division Apical-posterior Anterior

1 and 2a 3

Right Middle Lobe Lateral 4 Medial 5

Lower Division (Lingula) Superior lingula 4 Inferior lingula 5

Right Lower Lobe Superior 6 Medial basal 7

Left Lower Lobe Superior Anterior basal or antero-medial Lateral basal Posterior basal

Anterior basal Lateral basal Posterior basal

Number

8 9 10

6 7 and 8 9 10

The subdivisions of the lung and bronchial tree are fairly constant. Slight variations between right and left sides are noted by combined names and numbers. a Some authors believe that the left lung should be numbered so that there are eight segments, where the apical-posterior is numbered 1, and the anteromedial is numbered 6.

to identify the location of a defect such as an infection site or a tumor mass in the lungs. RULE OF THUMB: The 60-to-40 Rule  The right lung is slightly larger than the left lung because of the location of the heart. The right lung has a sizable middle lobe, and the left lung has a smaller lingular segment in the left upper lobe. For purposes of estimating the contribution of the right and left lungs to ventilation and gas exchange, the 60-to-40 rule is sometimes used. The right lung is assumed to provide 60% of the ventilation/gas–exchange capacity, and the left lung is assumed to provide the remaining 40%. If a patient requires removal of the entire left lung (pneumonectomy), a 40% decrease in lung volume would be expected and vice-versa.

The airways continue to divide as they penetrate deeper into the lungs. The segmental bronchi bifurcate into approximately 40 subsegmental bronchi, and these divide into hundreds of smaller bronchi. Thousands of bronchioles branch from the smaller bronchi. Bronchioles do not possess cartilage in their walls. Tens of thousands of terminal bronchioles arise from the bronchioles. Terminal bronchioles are the smallest conducting airways and function to supply gas to the respiratory zone of the lung. With further divisions, the number of airways increases tremendously. The cross-sectional area of the conducting system increases exponentially to facilitate and enhance gas exchange

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SECTION II  Applied Anatomy and Physiology Right

Left 1

Left

Right

1 and 2

1

1 and 2 3

3

2

3

4

4 5

4

2 6

6

8

5

9

8

9

10

10

8

8 Anterior view

Posterior view

1 1 and 2 2

3

6 10

4

1 2

5

1 and 2 3

8

9

3

3 6

6

6

4

4

5 8

4

Right lateral view

5

5

2

Left lateral view

8

9

10

6

3

10

7 7

1

9

8

1 and 2

10 9 Hilum

3 6

4 5

5

7

10

10

7 and 8

Left mediastinal view Right mediastinal view Fig. 9.49  Bronchopulmonary segmental divisions of the lungs (see Table 9.11). (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

as explained later. At the level of the terminal bronchioles, the cross-sectional area is approximately 20 times greater than at the level of the trachea (Fig. 9.50). Gas flow in these airways conforms to the laws of fluid physics. Increased cross-sectional area reduces the velocity of gas flow during inspiration. When inspired gas reaches the level of the terminal bronchiole, its average velocity has fallen to about the same rate as the speed of diffusing gas molecules.69 Low-velocity gas movement at the level of the terminal bronchiole and beyond is physiologically important for two reasons. First, laminar flow develops minimizing resistance in the small airways and decreases the work associated with inspiration. Second, low gas velocity facilitates rapid mixing of alveolar gases. This mixing provides a stable partial pressure of O2 and CO2 in the alveolar environment that supports stable diffusion and gas exchange.70

Histology of the Airway Wall All of the conducting airways, from the trachea to the bronchioles, have walls that are constructed of three layers: an inner

layer, a submucosa middle layer, and outer layer. The inner layer forms a mucous membrane called the mucosa, which is primarily composed of epithelia. The submucosa middle layer is composed of connective tissue, bronchial glands, and smooth fibers that wrap around the airway. The outer covering of connective tissue is called the adventitia (Figs. 9.51 and 9.52).71 The cartilaginous rings and plates found in larger airways are located in the adventitia. The mucosa is composed of many different types of specialized epithelial cells that sit on top of a basement membrane. The most common type of epithelia are the numerous pseudostratified, ciliated, columnar epithelia.71 The pseudostratified epithelial cells are held together toward their surface, or apical end through three types of junctions—tight apical junctions, zonal adherens junctions, and desmosome-type junctions—and they are anchored in place to the basement membrane.72 The junctions, especially the tight junctions, play an important role in the maintenance of fluid and electrolyte (e.g., chloride ions) transport across the mucous membrane. These junctions prevent

CHAPTER 9  The Respiratory System

193

Total cross-sectional area (cm2)

500

400

300 Submucosal gland Smooth muscle 200

Conducting zone

Resp. zone

Goblet cell Epithelium Basement membrane

100

Fig. 9.51  Cross-sectional view through a bronchiole. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

Terminal bronchioles 0 0

5

10

15

20

23

Airway generation Fig. 9.50  Diagram showing the extremely rapid increase in total crosssectional area of the airways in the respiratory zone. (From Broaddus: Murray & Nadel’s Textbook of Respiratory Medicine, 6th Edition, ed 6, St. Louis, 2013, Mosby.)

Serous cell Mucus blanket

Goblet cell

Gel layer Sol layer

Ciliated pseudostratified columnar epithelia Mucosa

Basement membrane

Lamina propria

Bronchial gland Submucosa

Smooth muscle

Cartilage

Adventitia

Connective tissue

Fig. 9.52  Microscopic view of the mucous membrane. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

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the movement of fluids and electrolytes between the apical surface and basal surfaces of the airway. Disturbances in this transport (e.g., Cl− transport malfunction in cystic fibrosis) lead to mucus and mucus transport abnormalities. Near the base of the pseudostratified cells are large numbers of basal cells. The basal cells contribute to the appearance of a “pseudostratified” cellular layer. Basal cells mature into pseudostratified cells and are thought to play an important role in the repair of the mucous membrane after diseases and injury. Dispersed between the pseudostratified epithelia are mucusproducing goblet cells and serous cells (in newborns) and the openings of submucosal bronchial glands. The bronchial glands are exocrine glands formed by secretory epithelial cells that sit on the basement membrane, extending down into the lamina propria and the submucosa. In this region are also neuroendocrine cells (also known as Kulchitsky cells), which often are organized into small clusters called neuroepithelial bodies.73 Neuroendocrine cells are connected to the vagus nerve and are thought to function during lung development, are hypoxia and stress-strain sensors, and secrete various bioactive chemicals (e.g., serotonin, calcitonin, and gastrin-releasing peptide). Lymphocytes are found intermixed with these cells, and it is thought they may be migratory. Below the epithelial and basement membrane of the mucosa is the lamina propria.72 It is composed of loose fibro-elastic connective tissue, lymphoid tissue, and a dense layer of elastic fibers. Below the lamina propria lies the submucosa. The submucosa of large airways contains bronchial glands, a capillary network, smooth muscle, some elastic tissue, and cartilage in larger airways. Bronchial glands vary in size up to 1 mm in length and connect to the bronchial surface via long, narrow ducts. The number of these glands increases significantly in diseases such as chronic bronchitis. Mast cells are also found in the submucosa and release numerous and potent vasoactive and bronchoactive substances such as histamine.74 Histamine causes vasodilation and bronchoconstriction, acting directly on smooth muscle. The triggering of mast cell release of its various substances and the resultant inflammation and bronchospasm of the airway are characteristic of asthma. The various secretory cells (primarily goblet cells) of the mucosa and bronchial glands of the submucosa contribute to the production of mucus.75 Normally, the respiratory tract produces approximately 100 mL of mucus per day. Most of the mucus formed in the larger airways is produced by the bronchial glands. Goblet cells contribute more in the smaller airways. The amount and composition of mucus produced can increase and change with airway irritation and diseases such as chronic bronchitis and asthma.76 Mucus is spread over the surface of the mucus membrane to a depth of approximately 7 µm and is propelled by the ciliated epithelia toward the pharynx. The outer layer of mucus is more gelatinous and is called the gel layer. The inner layer is much more fluid-like and is referred to as the sol layer. The mucus normally produced is a nearly clear fluid with greater viscosity than water. It is a mixture of 97% water and 3% solute.75 The solute portion is produced primarily by goblet cells and bronchial glands; it is called mucin and is composed of protein and minerals. The glycoprotein, lipid, and water content of mucus provide its viscoelastic gel properties.

Viscoelastic refers to the ability of mucus to deform and spread when force is applied. Mucus functions to protect the underlying tissue. It helps prevent excessive amounts of water moving into and out of the epithelia.75 It shields the epithelia from direct contact with potentially toxic materials and microorganisms. It acts like sticky flypaper to trap particles. This makes mucus an important part of the pulmonary defenses. The production of mucus is stimulated by local mechanical and chemical irritation, the release of proinflammatory mediators (e.g., cytokines), and parasympathetic (vagal) stimulation. The ciliated pseudostratified epithelia play a crucial role in the defense of the respiratory tract by propelling mucus toward the pharynx (the mucociliary escalator). Ciliated cells are found in the nasal cavity and all the airways from the larynx to the terminal bronchioles. Each of the pseudostratified cells possesses approximately 200 cilia on its luminal surface.72 Under the electron microscope, the surface of the mucous membrane looks like a “shag carpet” of cilia with approximately 1 to 2 billion cilia per cm2. Each cilium is an extension of the cell with an average length of about 6 µm and a diameter of about 0.2 µm. A crosssectional view through the cilium reveals it to be constructed of one inner and nine outer pairs of microtubules that are encased in the cell membrane (Fig. 9.53). The outer pairs of microtubules are interlinked by a filamentous protein called nexin. From each of the outer pairs of microtubules, protein filaments called dynein extend toward the adjacent pair of microtubules. Each of the outer pairs also extends a protein spoke toward the central pair of microtubules. The presence of magnesium ions and adenosine triphosphate within the cilium causes the dynein arms and spokes to attach and slide along the outer and inner microtubules, similar to the action of actin and myosin. This action results in rapid bending of the cilium resembling a whipping motion (Fig. 9.54). The cilia “stroke” at a rate of approximately 15 times per second, producing a sequential motion of the cilia called a metachronal wave.77 The metachronal “wavelength” is approximately 20 µm and propels surface material in a specific direction. In the nose, this motion propels material back to the pharynx. From the bronchioles up to the larynx, it moves material toward the pharynx. The stroking action of millions of cilia propels the surrounding mucus at a speed of approximately 2 cm/min. This action is commonly referred to as the mucociliary escalator. In healthy lungs, this mechanism allows inhaled particles to be removed within 24 hours. The control and coordination of ciliary motion are not fully understood and represent some of the many fascinating properties of the pulmonary epithelium. The production of mucus and the rate of ciliary beating are sensitive to various conditions and chemicals. Mucus production increases when the respiratory tract is irritated by particles and by various chemicals and during increased parasympathetic nervous stimulation.76 Ciliary beating can be effectively slowed or stopped if the viscosity of the sol layer is increased by exposure to dry gas. Ciliary motion is also slowed or stopped after exposure to smoke, high concentrations of inhaled O2, and drugs such as atropine. The smooth muscle of the airways varies in location and structure. In the large airways (e.g., the trachea), smooth muscle

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Ciliary ultrastructure Membrane Microtubule doublets Nexin links

Two central single microtubules

Radial spokes Orientation of central microtubules defines axis of beating cilia

Axis

Inner Dynein arm Outer Dynein arm

Membrane-encased axoneme Fig. 9.53  The Structure and Function of Cilia are Elegant and Complex. Each ciliated epithelial cell possesses approximately 200 cilia. The direction of ciliary beating is determined by the orientation of the central pair of microtubules. Dysfunction of the ciliary apparatus may involve a variety of structural abnormalities in the cilia or disorganization of the ciliary axes. The cilia beat in a relatively fluidic periciliary medium; above that, adherent by a thin physicochemical junction, is a gelatinous layer of mucus (not shown). (From Broaddus VC: Murray & Nadel’s Textbook of Respiratory Medicine, ed 6, St. Louis, 2013, Mosby.)

is bundled in sheets. In smaller airways, smooth muscle forms a helical pattern that wraps the airway in bundles in decreasing quantities as the airways branch and become smaller. Muscle fibers crisscross and spiral around the airway walls. This placement reduces the diameter of the airway and shortens it when the muscle contracts. This pattern of smooth muscle continues but thins out on reaching the smallest bronchioles. The tone of the smooth muscle is increased and results in bronchospasm by the activity of the parasympathetic nervous system (release of acetylcholine) and proinflammatory mediator release from mast and other cells. The adventitia is a sheath of connective tissue that surrounds the airways. It is interspersed with bronchial arteries, veins, nerves, lymph vessels, and adipose tissue. Between the submucosa and adventitia of the large airways are incomplete rings or plates of hyaline cartilage, providing structural support for the larger airways. However, the small airways depend on transmural pressure gradients and the “traction” of surrounding elastic tissues to remain open. During a forced exhalation, pressures across the walls of the small airways exceed the supporting forces of the elastic tissues. As a result, the small airways can collapse. The

cartilage in the larger airways prevents their collapse during such maneuvers. The type of cell of the respiratory mucosa changes toward the smaller airways (Fig. 9.55). As the thickness of the airway walls decreases, bronchial glands become fewer in number. At the bronchiolar level, the number of ciliated cells decreases. Simple columnar and cuboidal epithelial cells begin to predominate and are interspersed with goblet cells. In this region, large numbers of Clara cells, non-ciliated cuboidal cells with apical granules, are found. It is thought that these cells play a role in degrading various oxidants, contribute proteins for surfactant production, synthesize various lipids, and play a role in lung repair by being able to differentiate into other important epithelial cells in the mucosa after injury.78

Respiratory Zone Airways The terminal bronchioles begin about 12 to 15 generations beyond the trachea (Fig. 9.56).79 There are about 16,000 terminal bronchioles with airway opening diameters of approximately 700 µm. This yields a combined cross-sectional area opening that is almost 100 times that of the mainstem bronchi. All the

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airways down to and including the terminal bronchioles carry or conduct gas flow to and from the airways participating in gas exchange with the blood. As described before, the airways from the nares to and including the terminal bronchioles constitute the conducting zone airways, which do not participate in gas exchange (Fig. 9.57). These airways constitute the anatomic deadspace (VD) of the respiratory system, which is rebreathed Mucus movement

Gel layer

with each breath. In an adult human, the volume filling the airways of the VD is approximately 2.2 mL/kg (1 mL/lb) of PBW, or about 150 mL in an average adult. Unless the patient has a tracheostomy (which lowers VD), VD will range between 30% to 45% of the tidal volume.80 Branching of the terminal bronchioles gives rise to unique airways called respiratory bronchioles. Respiratory bronchioles are approximately 0.4 mm in diameter and have walls formed largely from flattened squamous epithelia and a thin outer layer of connective tissue. They have some ciliated cells at the

MINI CLINI Deadspace to Tidal Volume Ratio The deadspace (VD)/tidal volume (VT) ratio is an indirect indicator of ventilation/ perfusion matching. Therefore, it can be used in patients with congestive heart failure to detect the organ system limiting the exercise tolerance (lung or heart) by using it to calculate the actual deadspace.

Sol layer

Problem A 5-foot tall, 105-lb patient has a deadspace to tidal volume ratio of 0.40 and a tidal volume of 500 mL. What is her deadspace volume? Discussion VD = VD VT VT VD = 0.40 × 500 mL VD = 200 mL

Cilia Epithelial cell surface Fig. 9.54  Whipping action of the cilium within the sol layer of mucus produces a metachronal wave motion (mucociliary escalator). (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

Segmental bronchus

Small bronchus

Bronchiole

In healthy subjects, the VD/VT ratio ranges between 0.33 and 0.45. Ventilation is efficient when the VD/VT falls within this range. However, since positive pressure ventilation increases deadspace, this normal range will seldom be observed in patients receiving ventilatory support. For this reason, VD/VT ratios in the 0.4 to 0.6 range are clinically acceptable. VD/VT ratios above 0.6 indicate grossly inefficient ventilation that may impair a patient’s ability to maintain normal CO2 levels.

Terminal bronchiole

Respiratory bronchiole

Alveolar duct

Alveoli (squamous epithelium) Pulmonary vein Pulmonary artery Fig. 9.55  Histologic diagram of airways from the segmental bronchus to the alveolus. (Modified from Freeman WH, Bracegridle B: An atlas of histology, London, 1966, Heinemann Educational.)

CHAPTER 9  The Respiratory System

T

0 1

B

Conducting zone

LB

2 3

SB 4 5 BR 6

TB

16 17

RBL

18

Respiratory zone

19 20 21 AD 22

23

AS Alveolus

Fig. 9.56  Airways of the conducting (generation 0 through 16) and respiratory (generation 17 through 23) zones: T, trachea; B, right and left bronchi; LB, lobar bronchi; SB, segmental and subsegmental bronchi; BR, bronchioles; TB, terminal bronchioles; RBL, respiratory bronchioles; AD, alveolar ducts; and AS, alveolar sacs. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

connection with the terminal bronchiole, generally lack mucusproducing cells, and have rings of smooth muscles where they branch to form alveolar ducts. Respiratory bronchioles have a dual function. Similar to conducting airways, they not only conduct gas flow but also have small outpouchings known as alveoli in their walls. The alveoli and their pulmonary capillary bed enable the respiratory bronchioles to carry out gas exchange. The respiratory bronchioles constitute a transitional zone type of airway. A single terminal bronchiole supplies a cluster of respiratory bronchioles. Collectively, this unit is referred to as the acinus, or primary lobule. Each acinus comprises numerous respiratory bronchioles, alveolar ducts, and approximately 10,000 alveoli (Fig. 9.58). The adult lung is thought to contain more than 30,000 acini. Each acinus is supplied with pulmonary blood flow from a pulmonary arteriole, and blood is drained away from several acini through a pulmonary venule. In addition, each

197

acinus is equipped with a lymphatic drainage vessel and nerve fibers. These features make the primary lobule the functional unit of the lungs.72 Gas molecule movement in this region is mainly via diffusion rather than by convective flow, which occurs in larger airways. Millions of alveolar ducts branch off the respiratory bronchioles (Fig. 9.59). Alveolar ducts are tiny airways only 0.3 mm in diameter, and their walls are composed entirely of alveoli. Each alveolar duct ends in a cluster of alveoli, which is frequently referred to as an alveolar sac. Each alveolar sac opens into about 16 or 17 alveoli, and about one-half the total number of alveoli are found in this region.

Alveoli More recent estimates suggest the number of alveoli in adult lungs range from 270 to 790 million, with an average of about 480 million.25 The number of alveoli increases with an individual’s height. Fig. 9.60 shows alveoli in a normal rat lung at different states of inflation and how their shapes change. When inflated at and beyond the functional residual volume (see Fig. 9.60A to C), alveoli have a polyhedral shape resulting from numerous flat walls rather than a curved spherical structure. Alveoli found in the apical regions of the vertical lung have greater diameters than alveoli in the basal regions as a result of the gravitational effects. Alveoli in the basal regions are partially collapsed because of the weight of the organ. The alveolar walls, or septa, are formed by various cell types that are arranged to provide a thin surface for gas exchange and strength.81 The alveolar septa are covered with the extremely flat squamous epithelia of the type I pneumocytes (Fig. 9.61). Although they represent only approximately 8% of all the cells found in the alveolar region, type I cells cover about 93% of the alveolar surface.82 These cells form a “patchwork”-like surface that covers the alveolar capillaries and forms the gas-exchange surface of the alveolus. At the edges where they meet one another, they form tight junctions. These tight junctions help to limit the movement of material into the alveolar airspace from the interstitial space. They are held in place and supported from below by a network of collagen and elastin fibers. They are susceptible to injury and apoptosis (programmed cell death) from inhaled particles (e.g., cigarette smoke), bacterial infection, and high concentrations of inhaled O2. Interspersed on the alveolar surface and concentrated in the corners of the alveolar septa are type II pneumocytes, which are cuboidal epithelia with apical microvilli (Fig. 9.62). These cells are twice as numerous as the type I cells, but they occupy only 7% of the alveolar surface.82 As indicated earlier in this chapter, Type II cells do not function as gas-exchange membranes as the type I cells do. They (along with the Clara cells) manufacture surfactant, store it in vesicles called lamellated bodies, and secrete it onto the alveolar surface.83 As mentioned earlier in the chapter, surfactant reduces the surface tension of the alveolus, sheds water from the alveolar surface, helps prevent alveolar surface tensiondriven collapse, improves lung compliance, reduces the work of breathing, and protects the alveolar surface. Normally, the surfactant is removed from the alveolar space continuously by type II cells and macrophages. The type II cells recycle approximately

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Smooth muscle Terminal bronchiole

Respiratory bronchioles

Pores of Kohn

Alveolar duct

Acinus (respiratory zone) Alveolus

Alveolar sac

Fig. 9.57  Gas Exchange Portion of the Lungs. These subdivisions of the terminal bronchioles form the acinus. (From Beachey W: Respiratory care anatomy and physiology foundations for clinical practice, ed 3, St. Louis, 2013)

Alveolar sac Alveolar atrium Alveolus Capillary network Alveolar duct Respiratory bronchiole

Terminal bronchiole Pulmonary vein Pulmonary artery Fig. 9.58  The acinus (primary lobule) of the lung is composed of a single terminal bronchiole, numerous respiratory bronchioles, alveolar ducts, sacs of alveoli, and about 10,000 alveoli. Pulmonary blood flow is delivered to the acinus by a pulmonary arteriole and drained from it by a pulmonary venule. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

CHAPTER 9  The Respiratory System

199

Respiratory bronchiole Alveolar duct Atrium

Pore

Alveolar sac

Atrium

Alveolus

Fig. 9.59  Microscopic view of respiratory zone airways. (Modified from Sorokin SP: The respiratory system. In Greep RO, Weiss L, editors: Histology, New York, 1973, McGraw-Hill.)

50% of it, whereas the macrophages primarily remove it through catabolism.84 Although the lungs do not have stem cells in the classic sense, the type II cells do have a “stem cell”—like action. They can proliferate and differentiate into type I cells to repopulate and repair the alveolar surface after injury.85 They are also involved in alveolar defense through surfactant production and the release of some cytokines that trigger inflammation. Macrophages are another common cell found in the alveolar region.82 They can move from the pulmonary capillary circulation by squeezing through openings in the alveolar septa and then move out onto the alveolar surface. They are defensive cells that patrol the alveolar region and phagocytize foreign particles and cells (e.g., bacteria). They can present portions of the foreign particles and bacteria to lymphocytes as part of the immune response and contain various digestive enzymes (e.g., trypsin) that break down the material they engulf. Within the inter-alveolar septum is an interstitial space that contains matrix material and the pulmonary capillaries. Also found in the interstitial space are bands of elastin fibers and a collagen fiber matrix.47 These fibers support the alveolar cells and the shape of the alveolus. Small openings are found in the alveolar septa. Some of the openings allow gas to move from one alveolus to another. These are called the pores of Kohn. Other openings connect alveoli with secondary respiratory bronchioles. These passageways are called the canals of Lambert. All of these alveolar openings and passageways facilitate the collateral movement of gas (called “collateral ventilation”) and help maintain alveolar volume.81

Blood-Gas Barrier Gas exchange between alveolar gas and pulmonary capillary blood occurs across the alveolar-capillary membrane. In a typical adult, this blood-gas barrier stretches over a surface area of approximately 140 m2 and is less than 1 µm thick.86 This makes the membrane more than 50 times larger than the area covered by skin and more than 2000 times thinner. The blood-gas barrier is composed of many different layers through which O2 and CO2 diffuse (Fig. 9.63). The outermost layer is a very thin film of a fluid composed primarily of surfactant that forms into a tubular myelin matrix. Below the surfactant fluid layer is the thinly stretched type I cell. The delicate structure of type I cells makes them highly susceptible to injury from toxins carried to them by either airborne or blood-borne routes. The interstitial space and its contents lie below. Within this space are basement membranes, matrix material connective tissue fibers, and the alveolar capillary.47 The capillary wall is formed from thin, flat squamous epithelia called endothelial cells that form a thin tube by connecting at their edges with tight junctions. Within the capillary lie the plasma and, finally, the erythrocytes. Both O2 and CO2 cross through the membrane via partial pressure-driven diffusion. The blood-gas barrier is not equal in thickness and chemical content from side to side (see Fig. 9.63). On one side of the alveolar wall, the type I cells and capillary endothelial cells lie close together, with a thin interstitial space. This part of the blood-gas barrier is, on average, 0.2 to 0.3 µm thick, and it is where the alveolar capillary bulges into the alveolar space.86 On

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AI

AI

20 µm

A

20 µm

B

AI

AI

C

20 µm

D

20 µm

Fig. 9.60  Scanning electron photomicrographs at the same magnification of perfusion-fixed normal rat lung at different degrees of inflation pressure. (A) 30 cm H2O (total lung capacity [TLC]). (B) 8 cm H2O (approximately 50% TLC). (C) 4 cm H2O (near resting inflation or functional residual capacity [FRC]). (D) 0 cm H2O (minimum volume). Pulmonary artery pressure was held constant at 25 cm H2O, and left atrial pressure was held at 6 cm H2O. Intrinsic shape of alveoli (Al) is maintained from FRC to TLC (A–C). Alveolar walls are flat with sharp corners where the adjacent walls meet. Note the flat shape of the alveolar capillaries (arrow) at TLC (A, lung zone 1 conditions, air pressure > blood pressure) compared with their round shape (arrow) at FRC (C, lung zone 3 conditions, blood pressure > air pressure). The alveolar walls are folded, and the alveolar shape is distorted at the minimum lung volume (D). The arrow in B identifies a type II pneumocyte at an alveolar corner. The arrowhead in B identifies a pore of Kohn through an alveolar wall. (From Mason RJ, Broaddus VC, Martin T, et al., editors: Murray and Nadel’s textbook of respiratory medicine, ed 4, Philadelphia, 2011, WB Saunders.)

the other side, where there is a thicker interstitial space with greater fiber, matrix, and nuclear material content, the barrier can be more than 3 to 10 times thicker. This difference between the two sides functionally results in “faster-weaker” and “slowerstronger” diffusion sides of the blood-gas barrier. The interstitial space within the alveolar septum contains a network of fibers that form a kind of connective tissue skeleton holding the alveolar structures in place and together.87 These fibers within the alveolar septum are part of the continuum of connective tissue fibers found in the pleural surface and in the airway walls. They extend all the way to the root of the lung in the hilar region. Fibroblasts from elastin and collagen fiber bands form into a network within the interstitial space into which the capillaries are woven. Also, around the fibers and capillaries is a non-living matrix of fluid and solutes. The weaving path taken

by the capillaries passes them from the thick to the thin sides of the blood-gas barrier as they extend through the septum. On the thin side, the basement membranes of the endothelial and type I cells fuse into a structure called the lamina densa, which is formed from collagen.86 On the thick side, bands of collagen and elastin are found. The collagen and endothelial cells are attached to either side of the lamina densa by a series of protein fibers collectively known as laminins. Laminins effectively bind together the blood-gas barrier into a three-part laminate that results in a relatively strong and thin structure that can normally, with the additional support offered by the capillary network, withstand the everyday stress of alveolar and capillary stretch.88 However, conditions of pulmonary hypertension, excessive tidal volume, and high airway pressures during positive pressure ventilation (e.g., tidal volume > 6 to 8 mL/kg and airway plateau

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Connective tissue entrance ring Interstitial space Erythrocyte Type I cell

Fig. 9.61  Highly magnified crosssectional sketch of the cells and organization of the alveolar septa. (From Hicks GH: Cardiopulmonary anatomy and physiology, Philadelphia, 2000, WB Saunders.)

Endothelial cell

Capillary

Alveolar space

Macrophage Pore of Kohn Type II cell

Connective tissue fibers Interstitial cell

II AS Mv

LB

G

Nu I

Fig. 9.62  Transmission Electron Photomicrograph of Human Lungs at High Magnification. (A) Type II pneumocytes are cuboidal epithelial cells that contain characteristic lamellar bodies (LB) in their cytoplasm and have stubby microvilli (Mv) that extend from their apical surface into the alveolar airspace (AS). Other prominent organelles within the type II cells are mitochondria (Mi), a single nucleus (Nu), and a Golgi apparatus (G), which forms the lamellar bodies. Adjacent to the type II cell is a portion of a type I pneumocyte (I). The abluminal side of the epithelial cells of the alveolus rests on a continuous basal lamina (arrowhead). (B) Apical region of a type II cell contains two lamellar bodies (LB), one of which has been fixed in the process of secreting its contents (arrows). The lamellar bodies are believed to be the source of surfactant. Type II cells are more often found in the corners of the alveolar walls. (From Mason RJ, Broaddus VC, Martin, T, et al., editors: Murray and Nadel’s textbook of respiratory medicine, ed 4, Philadelphia, 2011, WB Saunders.)

Mi

A

1.0 µm

LB

B

LB

0.5 µm

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I

I

A

E

* COL

Nu

R

E

C

I EL A

I

1.0 µm

Fig. 9.63  High-magnification transmission electron photomicrograph of a human lung showing a cross-section of an alveolar wall through which O2 and CO2 diffuse. Air (A) in the alveolar space is seen on either side of the wall. The thin side of the alveolar-capillary membrane (short double arrow) consists of type I pneumocytes (I), interstitium (*) formed by the fused basement membranes of the type I cell and the endothelial cells (E), and its nucleus (Nu) that forms the pulmonary capillary wall. Within the capillary (C) is the erythrocyte (R). The thick side of the membrane (long double arrows) has an accumulation of elastin (EL), collagen (COL), and matrix material that jointly separates the type I cell from the capillary endothelial cell. Greater diffusion occurs across the thin side. (From Mason RJ, Broaddus VC, Martin T, et al., editors: Murray and Nadel’s textbook of respiratory medicine, ed 4, Philadelphia, 2011, WB Saunders.)

pressures > 30 cm H2O) can result in stress failure of the bloodgas membrane. Stress failure results in endothelial or type I cell stretching and shearing injuries.

SUMMARY CHECKLIST • Gas exchange between the atmosphere and blood is termed external respiration. This process supports the internal respiration, which is the exchange of gases between blood and tissues. • The respiratory system humidifies and warms inspired air while removing inhaled contaminants and filtering out chemicals and small blood clots deposited or formed in the blood. • Many different genes regulate the development of the respiratory system from conception through adult life. Many pulmonary diseases are caused by genetic abnormalities. • Injury to the embryo or genetic damage during the embryonic phase of development can lead to many congenital anomalies, including tracheoesophageal fistulas, esophageal atresia, choanal atresia, pulmonary hypoplasia, and complex heart and vascular anomalies. • The development of the respiratory system follows a welldefined schedule; interruptions or insults during development can result in respiratory disease at birth and in adulthood. • Premature infants younger than 32 weeks are at greater risk for developing respiratory distress due, among other reasons, to the lack of mature alveoli in their lungs.

• Human pulmonary surfactant, which promotes lung inflation and protects the alveolar surface, begins to be produced around 24 to 25 weeks of development by type II pneumocytes. • The maternal placenta is the actual gas-exchange organ for the fetus. • Three important bypass pathways (shunts) function in the developing fetus to enhance the flow of blood to the developing organs: ductus venosus, ductus arteriosus, and foramen ovale. • Before birth, 90% of the fetal blood bypasses the pulmonary circulation through the foramen ovale and the ductus arteriosus (right-to-left shunting). Any additional shunting after birth is considered an anomaly. • Fetal circulation and respiration differ markedly from circulation and respiration in the postnatal period. • The transition from intrauterine to extra-uterine life involves a non-aerated, fluid-filled lung converting to an efficient airfilled organ of gas exchange. • Closure of the foramen ovale and ductus arteriosus are important events in the transition to extra-uterine life. • During neonatal or infant resuscitation, the baby’s head and neck should be neutral or slightly extended in the sniffing position to avoid airway obstruction and collapse and provide effective ventilation. • Most infants breathe preferentially through the nose. However, most term newborn infants can shift to oral breathing in response to nasal occlusion and hypoxia.

CHAPTER 9  The Respiratory System

• Despite the presence of cartilage in the central airways of an infant, the trachea and larger bronchi of a neonate lack the rigidity of adult central airways. The compliant nature of these airways makes them prone to collapse and airway obstruction. • Chest retractions, evident by the use of accessory muscles in the neck, rib cage, sternum, or abdomen, occur when lung compliance is poor, or airway resistance is high in a neonate or infant. • Visceral control of the smooth muscle of the respiratory system is carried out by branches of the sympathetic and parasympathetic nervous systems and mediators transported to the lungs via the pulmonary circulation. • The lymphatic circulation plays a central role in the control of fluid and protein balance within the lung and houses various defensive cells. • Grunting is an expiratory sound caused by the sudden closure of the glottis during exhalation to maintain FRC and prevent alveolar atelectasis. • Because lung compliance is worse at very low or very high FRC, achieving and maintaining physiologic FRC is essential in the management of respiratory disorders with poor compliance in neonates and infants, such as RDS or TTN. • The thorax houses and protects the lungs; it is also a movable shell that makes ventilation possible. • The diaphragm is the primary muscle of ventilation; together with the accessory muscles and thoracic structures, it provides the ability to move large volumes of gas into and out of the lungs. • Because exhalation is passive, the diaphragm normally does not actively participate in exhalation. • The accessory muscles of respiration assist the diaphragm and intercostal muscles when ventilatory demand increases. • The scalene, sternocleidomastoid, pectoral, and abdominal wall muscles are the predominant accessory muscles. • Patients with advanced COPD often use accessory muscles to assist the flattened diaphragm, helping relieve their work of breathing. • Abnormal excess of fluids between the visceral and parietal pleura tend to pool in the costophrenic angle in an upright individual. This pooling of fluid causes the angle to appear blunted or flattened to 90 degrees when viewed in the chest radiograph. • The lungs receive blood flow from the pulmonary circulation for gas exchange and the bronchial circulation to support the airway and pleural tissue metabolism. • The pulmonary circulation is capable of acting as a reservoir, removing blood clots and numerous mediators, as well as activating important vasoactive agents. • The low vascular pressures of the pulmonary circulation result in regional blood flow within the lungs that is highly influenced by gravity, airway pressure, and gas exchange. • The bronchial circulation is a branch of the systemic circuit and is supplied with blood from the aorta via minor thoracic branches. Blood flow through the bronchial circulation constitutes approximately 1% to 2% of the total cardiac output. • The primary function of the lymphatic system in the lungs is to clear fluid from the interstitial and pleural spaces to help

•

•

• •

•

•

•

• •

•

•

•

•

•

203

maintain the fluid balance in the lungs. The lymphatic system also plays an important role in the specific defenses of the immune system. All of the major structures of the respiratory system are innervated by branches of the peripheral nervous system: the autonomic and somatic branches. The somatic system provides voluntary and automatic motor control and sensory innervation to the chest wall and respiratory muscles. Autonomic neurons conduct motor and sensory signaling to control various tissues and sense various activities. The upper respiratory tract heats and humidifies inspired air. Its various structures also protect the lungs against foreign substances. Reflexes of the mouth, pharynx, and larynx help protect the lower respiratory tract during swallowing. These protective functions can be severely compromised during anesthesia or unconsciousness. The lower respiratory tract conducts inhaled gases from the upper airway to the respiratory zones of the lung. It contains many structures that help clear and defend the lung. During unconsciousness, the muscles of the tongue and hypopharynx can relax and allow the tongue and other soft tissues to collapse and occlude the opening of the hypopharynx. The airways branch into lobes in both the right and the left lungs; these lobes consist of various segments. The right bronchus branches off from the trachea at an angle of approximately 20 to 30 degrees, and the left bronchus branches with an angle of about 45 to 55 degrees. The lower angle branching (closer to mid-line) of the right bronchus results in a greater frequency of right-mainstem intubation and the foreign body aspiration into the right lung because of the more direct pathway. The right lung is assumed to provide 60% of the ventilation/ gas–exchange capacity, and the left lung is assumed to provide the remaining 40%. In an adult human, the volume filling the airways of the anatomic deadspace is approximately 2.2 mL/kg (1 mL/lb) of PBW, or about 150 mL in an average adult. Gas exchange between alveolar gas and pulmonary capillary blood occurs across the alveolar-capillary membrane. In a typical adult, this blood-gas barrier stretches over a surface area of approximately 140 m2 and is less than 1 µm thick. The respiratory bronchioles, alveolar ducts, and alveoli provide a large, yet extremely thin, membrane for the exchange of O2 and CO2 between air and blood. Disruption of the blood-gas barrier can occur from excessive capillary pressures, lung inflation, and exposure to various toxins (e.g., 100% O2).

REFERENCES 1. Marieb EN, Hoehn KN: The respiratory system. In Marieb EN, Hoehn KN, editors: Human anatomy and physiology, ed 11, San Francisco, 2018, Pearson Benjamin Cummings. 2. Schnapf BM, Kirley SM: Fetal lung development. In Walsh BK, Czervinske MP, DiBlasi RM, editors: Perinatal and pediatric respiratory care, ed 3, St Louis, 2010, Elsevier.

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3. Shannon JM, Kathryn WB, Greenberg JM: Lung growth and development. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 4. Zenzes MT: Smoking and reproduction: gene damage to human gametes and embryos, Hum Reprod Update 6:122, 2000. 5. Joshi S, Kotecha S: Lung growth and development, Early Hum Dev 83:789, 2007. 6. Perez-Gil J, Weaver TE: Pulmonary surfactant pathophysiology: current models and open questions, Physiology (Bethesda) 25:132, 2010. 7. Mason RJ, Dobbs LG: Alveolar epithelium and pulmonary surfactant. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 8. Yarbrough ML, Grenache DG, Grownosky AM: Fetal lung maturity testing: the end of an era, Biomark Med 8:509, 2014. 9. Morrisey EE, Hogan BLM: Preparing for the first breath: genetic and cellular mechanisms in lung development, Dev Cell 18:8, 2010. 10. Czervinske MP: Fetal gas exchange and circulation. In Walsh BK, Czervinske MP, DiBlasi RM, editors: Perinatal and pediatric respiratory care, ed 3, St Louis, 2010, Elsevier. 11. Blackburn S: Fetal assessment. In Mattson S, Smith JE, editors: Maternal, fetal, and neonatal physiology: a clinical perspective, ed 4, Philadelphia, 2013, WB Saunders. 12. Victory R, Penava D, Da Silva O, et al: Umbilical cord pH and base excess values in relation to adverse outcome events for infants delivering at term, Am J Obstet Gynecol 191:2021, 2004. 13. Malin GL, Morris RK, Khan KS: Strength of association between umbilical cord pH and perinatal and long-term outcomes: systematic review and meta-analysis, BMJ 340:c1471, 2010. 14. American College of Obstetricians and Gynecologists (ACOG) and American Academy of Pediatrics (AAP): Neonatal encephalopathy and neurologic outcome, 2nd ed, Washington, DC, 2014, ACOG. 15. Davis L: Placental respiratory gas exchange. In Ginosar Y, Reynolds F, Halpern S, et al, editors: Anesthesia and the fetus, Oxford, UK, 2013, Wiley-Blackwell. 16. Powell FL, Wagner PD, West JB: Ventilation, blood flow, and gas exchange. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 17. Burri PH: Development and growth of the human lung, Compr Physiol Supplement 10:1–46, 2011. Handbook of Physiology, The Respiratory System, Circulation and Nonrespiratory Functions. 18. Katz C, Bentur L, Elias N: Clinical implication of lung fluid balance in the perinatal period, J Perinatol 31:230, 2011. 19. Shovlin CL, Jackson JE: Pulmonary vascular abnormalities. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 20. Stack CG, Dobbs P: Differences between the child, the neonate and the adults: essentials of pediatric intensive care, ed 4, New York, 2006, Cambridge University Press. 21. Cozzi F, Morini F, Tozzi C, et al: Effect of pacifier use on oral breathing in healthy newborn infants, Pediatr Pulmonol 33:36, 2002. 22. Bradley T, Thach MD: Maturation and transformation of reflexes that protect the laryngeal airway from liquid aspiration from fetal to adult life, Am J Med 111:69, 2001.

23. Praud JP, Reix P: Upper airways and neonatal respiration, Respir Physiol Neurobiol 149:131, 2005. 24. Gaultier C, Denjean A: Developmental anatomy and physiology of the respiratory system. In Taussig LM, Landau LI, editors: Pediatric respiratory medicine, ed 2, St Louis, 2008, Mosby. 25. Ochs M, Nyengaard JR, Jung L, et al: The number of alveoli in the human lung, Am J Respir Crit Care Med 169:120, 2004. 26. Moore KL, Persaud TVN, Torchia MG: The respiratory system. In Moore KL, Persaud TVN, editors: The developing human: clinically oriented embryology, ed 9, Philadelphia, 2011, Elsevier. 27. Burri PH: Structural aspects of postnatal lung development: alveolar formation and growth, Biol Neonate 89:313, 2006. 28. Garcia JG: Pulmonary circulation and regulation of fluid balance. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 29. Hsia CC: Signals and mechanisms of compensatory lung growth, J Appl Physiol 97:1992, 2004. 30. Schellhaese DE: Examination and assessment of the pediatric patient. In Walsh BK, Czervinske MP, DiBlasi RM, editors: Perinatal and pediatric respiratory care, ed 3, St Louis, 2010, Elsevier. 31. Hepper PG, Dornan JC, Lynch C: Sex differences in fetal habituation, Dev Sci 15:373, 2012. 32. Gatzoulis M, Tsiridis E: Chest wall and breast. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier. 33. Marieb EN, Hoehn KN: The thoracic cage is the bony structure of the chest. In Marieb EN, Hoehn KN, editors: Human anatomy and physiology, ed 11, San Francisco, 2018, Pearson Benjamin Cummings. 34. Henderson W, Paré PA, Ayas NT: Respiratory system mechanics and energetics. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 35. Benditt JO, McCool FD: The respiratory system and neuromuscular diseases. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 36. Gatzoulis M, Pepper J: Diaphragm and phrenic nerve. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier. 37. Ratnovsky A, Elad D, Halpern P: Mechanics of respiratory muscles, Respir Physiol Neurobiol 163(1–3):82, 2008. 38. DeTroyer A, Boriek AM: Mechanics of respiratory muscles, Compr Physiol 1:1273, 2011. 39. Bhatt SP, Guleria R, Luqman-Arafath TK, et al: Effect of tripod position on objective parameters of respiratory function in stable chronic obstructive pulmonary disease, Indian J Chest Dis Allied Sci 51(2):83, 2009. 40. Borley NR: Anterior abdominal wall. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier. 41. Ishida H, Hirose R, Watanabe S: Comparison of changes in the contraction of the lateral abdominal muscles between the abdominal drawing-in maneuver and breathe held at the maximum expiratory level, Man Ther 17:427, 2012. 42. Urquhart DM, Hodges PW, Story IH: Postural activity of the abdominal muscles varies between regions of these muscles and between body positions, Gait Posture 22(4):295–301, 2005. 43. Gatzoulis M, Padley S, Shah P, et al: Mediastinum. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier.

CHAPTER 9  The Respiratory System 44. Gatzoulis M, Padley S, Shah P, et al: Pleura, lungs and bronchi. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier. 45. Agostoni E, Zocchi L: Pleural liquid and its exchanges, Respir Physiol Neurobiol 159:311, 2007. 46. Noppen M: Normal volume and cellular contents of pleural fluid, Curr Opin Pulm Med 7:180, 2001. 47. Weibel ER: What makes a good lung?, Swiss Med Wkly 139:375, 2009. 48. Lumb AB: The pulmonary circulation. In Lumb AB, editor: Nunn’s applied respiratory physiology, ed 7, Philadelphia, 2010, Elsevier. 49. Berne RM, Mathew LN: Cardiovascular physiology, ed 8, St Louis, 2001, Mosby. 50. Halbertsma FJ, Vaneker M, Scheffer GJ, et al: Cytokines and biotrauma in ventilator-induced lung injury: a critical review of the literature, Neth J Med 63:382, 2005. 51. McCullagh A, Rosenthal M, Wanner A, et al: The bronchial circulation: worth a closer look—a review of the relationship between the bronchial vasculature and airway inflammation, Pediatr Pulmonol 45:1, 2010. 52. Jordan D: Central nervous pathways and control of the airways, Respir Physiol 125:67, 2001. 53. Lee LY, Yu J: Sensory Nerves in Lung and Airways, Compr Physiol 4:287–324, 2014. 54. Canning BJ, Fischer A: Neural regulation of airway smooth muscle tone, Respir Physiol 125:113, 2001. 55. Albertine KH: Anatomy of the lungs. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 56. Lin CJ, Chen WN, Chen CJ, et al: An antinociceptive role for substance P in acid-induced chronic muscle pain, Proc Natl Acad Sci USA 109(2):E76–E83, 2012. 57. Widdicombe J: Airway receptors, Respir Physiol 125:3, 2001. 58. Canning BJ: Functional implications of the multiple afferent pathways regulating cough, Pulm Pharmacol Ther 24:295, 2011. 59. Kubin L, Alheid GF, Zuperku EJ, et al: Central pathways of pulmonary and lower airway vagal afferents, J Appl Physiol 101:618, 2006. 60. Carr MJ, Undem BJ: Bronchopulmonary afferent nerves, Respirology 8:291, 2003. 61. Jafeck B, Jones N: Nose, nasal cavity, and paranasal sinuses. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier. 62. Miller AJ: Oral and pharyngeal reflexes in the mammalian nervous system: their diverse range in complexity and the pivotal role of the tongue, Crit Rev Oral Biol Med 13(5):409–425, 2002. 63. Strohl KP, Butler JP: Mechanical properties of the upper airway, Compr Physiol 2:1853, 2012. 64. Courey MS, Pletcher SD: Upper airway disorders. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 65. Standring S: Larynx. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier. 66. Martin-Harris B, Michel Y, Castell DO: Physiologic model of oropharyngeal swallowing revisited, Otolaryngol Head Neck Surg 133(2):234–240, 2005.

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67. Hickok G: Functional anatomy of speech perception and speech production: psycholinguistic implications, J Psycholinguist Res 30(3):225–235, 2001. 68. Chung KF, Mazzone SB: Cough. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 69. Fisher S, Dubois AE: The lung: physiologic basis of pulmonary function tests, ed 3, St Louis, 2000, Mosby. 70. Tsuda A, Henry FS, Butler JP: Gas and aerosol mixing in the acinus, Respir Physiol Neurobiol 163(1–3):139–149, 2008. 71. Knight DA, Holgate ST: The airway epithelium: structural and functional properties in health and disease, Respirology 8(4):432–446, 2003. 72. Albertine KH, Williams MC, Hyde DM: Anatomy of the lungs. In Broaddus VC, Mason RJ, Ernst JD, editors: Murray and Nadel’s textbook of respiratory medicine, ed 6, Philadelphia, 2016, Elsevier-Saunders. 73. Cutz E, Yeger H, Pan J, et al: Pulmonary neuroendocrine cell system in health and disease, Curr Respir Med Rev 4:174, 2008. 74. Amin K: The role of mast cells in allergic inflammation, Respir Med 106(1):9–14, 2012. 75. Fahy JV, Dickey BF: Airway mucus function and dysfunction, N Engl J Med 363:2233, 2010. 76. Rogers DF: Physiology of airway mucus secretion and pathophysiology of hypersecretion, Respir Care 52:1134, 2007. 77. Salathe M: Regulation of mammalian ciliary beating, Annu Rev Physiol 69:401, 2007. [76]. 78. Reynolds SD, Malkinson AM: Clara cell: progenitor for the bronchiolar epithelium, Int J Biochem Cell Biol 42:1, 2010. 79. Hajari AJ, Yablonskiy DA, Sukstanskii AL, et al: Morphometric changes in the human pulmonary acinus during inflation, J Appl Physiol 112(6):937–943, 2011. 80. Vines DL: Respiratory monitoring in critical care. In Heuer AJ, Scanlan CL, editors: Wilkin’s clinical assessment in respiratory care, ed 7, St Louis, 2014, Elsevier-Mosby. 81. Johnson D, section editor: Microstructure of trachea, bronchi and lungs. In Standring S, editor: Gray’s anatomy: the anatomic basis of clinical practice, ed 40, St Louis, 2009, Elsevier. 82. Tomashefski JF, Farver CF: Anatomy and histology of the lung. In Dail and hammar’s pulmonary pathology, New York, NY, 2008, Springer. 83. Tzortzaki EG, Vlachaki E, Siafakas NM: Pulmonary surfactant, Pneumon 4:364, 2007. 84. Ikegami M: Surfactant catabolism, Respirology 11:S24, 2006. 85. Crowther JA, Vijay KK, et al: Pulmonary surfactant protein a inhibits macrophage reactive intermediate production in response to stimuli by reducing NADPH oxidase activity, J Immunol 172:6866, 2004. 86. West JB: Thoughts on the pulmonary blood-gas barrier, Am J Physiol Lung Cell Mol Physiol 285:L501, 2003. 87. Dudek SM, Garcia JGN: Cytoskeletal regulation of pulmonary vascular permeability, J Appl Physiol 91:1487, 2001. 88. Maina JN, West JB: Thin and strong! The bioengineering dilemma in the structural and functional design of the blood-gas barrier, Physiol Rev 85:811, 2005.

10  The Cardiovascular System Narciso E. Rodriguez

CHAPTER OBJECTIVES After reading this chapter you will be able to: • Describe the anatomy of the heart and vascular systems. • State the key characteristics of the cardiac tissue. • Describe the local and central control mechanisms of the heart and vascular systems. • Describe how the cardiovascular system functions under normal and abnormal conditions.

• Calculate cardiac output given stroke volume and heart rate. • Calculate ejection fraction given stroke volume and end-diastolic volume. • Identify the electrical and mechanical events related to the normal cardiac cycle.

CHAPTER OUTLINE Functional Anatomy, 207 Heart, 207 Vascular System, 211

Control of the Cardiovascular System, 214 Regulation of Peripheral Vasculature, 215

Regulation of Cardiac Output, 215 Cardiovascular Control Mechanisms, 218 Events of the Cardiac Cycle, 221

ejection fraction (EF) end-diastolic volume (EDV) end-systolic volume (ESV) epicardium excitability fibrous pericardium Frank-Starling law foramen ovale (FO) heart failure heart rate (HR) interatrial septum interventricular septum ischemia left ventricular aid negative feedback loop negative inotropism Non-ST segment elevation myocardial infarction (NSTEMI) mitral valve myocardial infarction (MI) myogenic control pericardial effusion pericardial fluid pericarditis

pericardium positive inotropism preload pulmonary vascular resistance (PVR) pulseless electrical activity (PEA) P wave refractory period regurgitation semilunar valves serous pericardium ST-segment elevation myocardial infarction (STEMI) stenosis stroke volume (SV) sulci systemic vascular resistance (SVR) thebesian veins thoracic pump tricuspid valve T wave vasoconstriction vasodilation v wave

KEY TERMS acute coronary syndrome (ACS) afterload angina pectoris arteriovenous anastomosis atria atrial kick atrioventricular (AV) rings atrioventricular (AV) valves automaticity a waves baroreceptors cardiac output (CO) cardiac tamponade central venous pressure (CVP) chemoreceptors chordae tendineae cordis conductivity congestive heart failure (CHF) contractility coronary artery diseases (CAD) coronary circulation coronary sinus c wave dicrotic notch 206

CHAPTER 10  The Cardiovascular System

207

PULMONIC VALVE

Second right intercostal space AORTIC VALVE

Second left intercostal space

Third left intercostal space

MITRAL VALVE Fourth left intercostal space TRICUSPID VALVE

Fifth left intercostal space (mitral apical)

Fig. 10.1  Anterior view of the thorax showing the position of the heart in relation to the ribs, sternum, diaphragm and position of the heart valves. (From Seidel HM, Ball JW, Dains JE, et al: Mosby’s guide to physical examination, ed 2, St Louis, 1991, Mosby.)

FUNCTIONAL ANATOMY Heart Anatomy of the Heart The heart is a four-chambered muscular organ approximately the size of a fist. It is positioned in the mid-mediastinum of the chest, behind the sternum (Fig. 10.1). Approximately two-thirds of the heart lies to the left of the midline of the sternum between the 2nd and the 6th ribs. The apex of the heart is formed by the tip of the left ventricle and lies above the diaphragm at the level of the 5th intercostal space to the left. The base of the heart is formed by the atria and projects to the right, lying below the 2nd rib. Posteriorly, the heart rests at the level of the 5th to the 8th thoracic vertebrae.1 As a result of its position between the sternum and the spine, compression of the heart maintains blood flow during cardiopulmonary resuscitation (CPR).2 RULE OF THUMB  High-quality chest compressions improve survival from cardiac arrest. High-quality compressions include ensuring adequate rate, adequate depth, allowing full-chest recoil between compressions and minimizing interruptions.

RULE OF THUMB  During cardiopulmonary resuscitation, the heel of one hand should be placed on the center of the chest on the lower half of the sternum while performing chest compressions. Compressions must be done at a depth of at least 2 inches (5 cm) for an average adult, avoiding excessive chest-compression depths.

Externally, surface grooves called sulci mark the boundaries of the heart chambers. The heart is enclosed in a sac called the pericardium.3 The structure of the pericardium can be summarized as follows:

1. Fibrous pericardium: Tough, loose-fitting and inelastic sac surrounding the heart 2. Serous pericardium: Consisting of two layers: a. Parietal layer: Inner lining of the fibrous pericardium b. Visceral layer or epicardium: Covering the outer surface of the heart and great vessels A thin layer of fluid called the pericardial fluid separates the two layers of the serous pericardium. Inflammation of the pericardium results in a clinical condition called pericarditis. An abnormal amount of fluid can accumulate between the layers, resulting in a pericardial effusion. A large pericardial effusion may lessen the pumping function of the heart, resulting in a cardiac tamponade, which compresses the heart muscle, leading to a serious decrease in blood flow to the body. This, ultimately, may lead to shock and death.1,4 RULE OF THUMB  A cardiac tamponade should be suspected in patients presenting with hypotension, jugular venous distension, pulsus paradoxus, tachycardia, tachypnea, narrowing pulse pressures and/or severe dyspnea.

The heart wall consists of three layers: (1) outer epicardium, (2) middle myocardium, and (3) inner endocardium. The myocardium composes the bulk of the heart muscle and consists of bands of involuntary striated muscle fibers. The contraction of these muscle fibers creates the pump-like action needed to move blood throughout the body. Support for the four interior chambers and valves of the heart is provided by four atrioventricular (AV) rings, which form a fibrous “skeleton.” Each ring is composed of dense connective tissue termed annulus fibrosus cordis, which encircles the bases of the pulmonary trunk, aorta and heart valves and electrically isolates the atria from the ventricles. No electrical impulses can

208

SECTION II  Applied Anatomy and Physiology Pulmonary artery Left atrium Left auricular appendage

Aorta Orifices of coronary arteries Right auricular appendage

Mitral valve—anterior cusp Pulmonary veins Superior vena cava

Aortic valve cusps Right ventricle

Left atrium

Interventricular septum

Aorta Right atrium

Papillary muscles

Membranous septum Tricuspid valve

Medial cusp Left ventricle

Posterior cusp Anterior cusp Mitral valve— posterior cusp Right ventricle

Papillary muscle Left ventricle

Fig. 10.2  Drawing of the heart split perpendicular to the interventricular septum to illustrate anatomic relationships of the heart. (From Berne RM, Levy MN, editors: Physiology, ed 5, St Louis, 2004, Mosby.)

be transmitted through the heart muscle and connective tissue from the atria to the ventricles.1,3 The two atrial chambers are thin-walled “cups” of myocardial tissue that contribute little to the total pumping activity of the heart. They are separated by an interatrial wall or septum. On the right side of the interatrial septum is an oval depression called the fossa ovalis cordis, the remnant of the fetal foramen ovale (FO). Each atrium has an appendage, or auricle, the function of which is unknown. In the presence of cardiac dysrhythmias (e.g., atrial fibrillation), blood flow can pool on these appendages, leading to the formation of thrombi. The two lower-heart chambers, or ventricles, make up the bulk of the heart’s muscle mass and do most of the pumping that circulates the blood (Fig. 10.2). The mass of the left ventricle is approximately two-thirds larger than the mass of the right ventricle and has a spherical appearance when viewed across anteriorly.5 The right ventricle has a thinner wall than the left and forms a pocket-like attachment to the left ventricle. Because of this relationship, the left ventricle pulls in and pushes the right ventricular wall, aiding to its filling and contraction. This effect, termed left ventricular aid, explains why some forms of right ventricular failure are less harmful than might be expected. The right and left ventricles are separated by a muscle wall termed the interventricular septum (see Fig. 10.2).5 The valves of the heart are flaps of fibrous tissue firmly anchored to the annulus fibrosus cordis (Fig. 10.3) and because they are located between the atria and ventricles, they are called atrioventricular (AV) valves or AV valves. The valve on the right side is called the tricuspid valve and the valve on the left is called the bicuspid or mitral valve. The AV valves close during systole (contraction of the ventricles), preventing backflow of blood into the atria. The free ends of the AV valves are anchored to papillary muscles of the endocardium by the chordae tendineae

cordis (see Fig. 10.2). During systole, papillary muscle contraction prevents the AV valves from swinging upward into the atria. Damage to either the chordae tendineae cordis or the papillary muscles can impair the function of the AV valves and cause leakage upward into the atria.1 Common valve problems include regurgitation and stenosis. Regurgitation is the backflow of blood through a malfunctioning leaky valve and stenosis is a pathologic narrowing or constriction of a valve outlet, which causes blood to back up and increased pressure in the proximal chamber and vessels. Both conditions can affect cardiac performance. In mitral stenosis, high pressures in the left atrium back up into the pulmonary circulation and these high pressures can cause pulmonary edema and a diastolic murmur (see Chapter 16).4,6 A set of semilunar valves separates the ventricles from their arterial outflow tracts, the pulmonary artery (in the right) and the aorta (in the left) (Fig. 10.3). Consisting of three half-moonshaped cusps attached to the arterial wall, these valves prevent backflow of blood into the ventricles during diastole (or when the chambers of the heart fill with blood). Like the AV valves, the semilunar valves can leak (regurgitation) or become partially obstructed (stenosis).1 Similar to the lungs, the heart has its own circulatory system, which is called the coronary circulation; however, in contrast to the lungs, the heart has a high metabolic rate that requires more blood flow per gram of tissue weight than any other organ except the kidneys. To meet these needs, the coronary circulation provides an extensive network of branches to all myocardial tissue (Fig. 10.4). Two main coronary arteries, one in the left and one in the right, arise from the root of the aorta right underneath the semilunar valves. Blood flows through the coronary arteries only during diastole when the semilunar valves are closed. Partial

CHAPTER 10  The Cardiovascular System

209

Anterior cusp Pulmonic valve

Right cusp Left cusp Left cusp

Aortic valve

Right cusp Posterior cusp

Anterior cusp Medial cusp

Tricuspid valve

Posterior cusp Mitral valve

Anterior cusp Posterior cusp Annulus fibrosus

Annulus fibrosus

Fig. 10.3  Four Cardiac Valves as Viewed from the Base of the Heart. Note how the leaflets overlap in the closed valves.

MINI CLINI Mitral Stenosis, Poor Oxygenation, and Increased Work of Breathing The mitral valve lies between the left atrium and left ventricle. Mitral stenosis causes high resistance to the blood flow into the left ventricle from the left atrium. This increased resistance causes a backflow into the pulmonary circulation, leading to pulmonary edema with fluid collecting in the alveoli and interstitial spaces in the lungs, impairing oxygenation and breathing. Problem Why does a patient with mitral stenosis have poor oxygenation of the blood and increased work of breathing? Discussion Blood flows from the lungs into the left atrium, where it may encounter high resistance through a narrowed, stenotic mitral valve; this causes high pressure to build in the left atrium. The pressure in the pulmonary veins and, eventually, in the pulmonary capillaries also increases. This high pressure within the capillaries engorges them and forces fluid components of the blood plasma out of the vessels and into the interstitial spaces of the lungs and inside the alveoli, creating pulmonary edema. This collection of fluid interferes with oxygen diffusion from the lung into the blood. Engorged capillaries surrounding the alveoli create a stiff “web” around each alveolus, which makes expanding the lungs difficult; thus, mitral stenosis, a cardiac problem, often has significant pulmonary consequences.

obstruction of a coronary artery may lead to tissue ischemia (decreased oxygen supply). Complete obstruction of a coronary artery may cause tissue death or infarct, a condition called myocardial infarction (MI).4 Acute Coronary Syndrome (ACS) is the name given to three types of coronary artery diseases (CAD) that are associated with gradual and/or sudden obstruction of the coronary arteries. These are (1) unstable angina or angina pectoris, (2) Non-ST segment

elevation myocardial infarction (NSTEMI) and (3) ST-segment elevation myocardial infarction (STEMI). Although heart disease mortality rates have declined over the past four decades in western countries, this condition remains responsible for approximately one third of all deaths in individuals over the age of 35.7 Nearly one-half of all middle-aged men and one-third of middle-aged women in the USA will develop some manifestation of a coronary heart disease (CHD). The 2016 Heart Disease and Stroke Statistics update of the American Heart Association (AHA) reported that 15.5 million people in the USA have CHD. The reported prevalence increases with age for both women and men. In the US the lifetime risk of developing CHD with ≥2 major risk factors is 37.5% for men and 18.3% for women.8 RULE OF THUMB  Classic signs of tissue ischemia (decreased oxygen supply) are chest pain and shortness of breath resulting in a clinical condition called angina pectoris. Symptoms of a myocardial infarction include tightness or pain in the chest, neck, back or arms, as well as fatigue, lightheadedness, abnormal heartbeat and anxiety. Women are more likely to have atypical symptoms than men.

After passing through the capillary beds of the myocardium, the venous blood is collected by the coronary veins that closely parallel the arteries (see Fig. 10.4). These veins gather together into a large vessel called the coronary sinus, which passes left to right across the posterior surface of the heart. The coronary sinus empties into the right atrium between the opening of the inferior vena cava (IVC) and the tricuspid valve.1 In addition, some coronary venous blood flows back into the heart through the thebesian veins.1 The thebesian veins empty directly into all the heart chambers. Any deoxygenated blood coming from the thebesian veins that enters the left atrium or ventricle lowers

210

SECTION II  Applied Anatomy and Physiology Pulmonary veins

Superior vena cava

Circumflex branch of left coronary artery Area of sinus node Great cardiac vein Inferior vena cava

Coronary sinus Right coronary artery Posterior descending branch of right coronary artery

Posterior View

Superior vena cava Aorta Right atrial appendage Right coronary artery

Anterior coronary veins

Left atrium Left coronary artery Circumflex branch Descending branch

Great cardiac vein

Pulmonary artery Anterior View Fig. 10.4  Coronary circulation as seen on anterior and posterior surfaces of the heart, illustrating the location and distribution of the principal coronary vessels.

the overall oxygen content of the systemic circulation. Because the thebesian veins bypass or shunt around the pulmonary circulation as part of the normal anatomy, this phenomenon is called an anatomic shunt. When combined with a similar bypass in the bronchial circulation (see Chapter 9), these normal anatomic shunts account for approximately 2% to 3% of the total cardiac output.1,5

Properties of the Heart Muscle The performance of the heart as a pump depends on its ability to (1) initiate and conduct electrical impulses and to (2) synchronously contract the heart’s muscle quickly and efficiently.5 These actions are only possible because myocardial tissue possesses the following four key properties: • Excitability • Inherent rhythmicity or automaticity • Conductivity • Contractility

Excitability is the ability of cells to respond to electrical, chemical or mechanical stimulation. Electrolyte imbalances, congenital cardiac anomalies and certain drugs can increase myocardial excitability and produce abnormalities in electrical conduction that may lead to cardiac arrhythmias. Inherent rhythmicity, or automaticity, is the unique ability of the cardiac muscle to initiate a spontaneous electrical impulse (depolarization and repolarization). Although such impulses can arise from anywhere in the cardiac tissue. This ability is highly developed in specialized areas called the heart pacemaker or nodal tissues. The sinoatrial (SA) node and the atrioventricular (AV) node are the heart’s primary pacemakers. An electrical impulse from any source other than a normal heart pacemaker is considered abnormal (or ectopic) and represents one of the many causes of abnormal heart rhythms or cardiac arrhythmias (see Chapter 18). Conductivity is the ability of the myocardial tissue to spread and conduct electrical impulses. This property allows the myocardium to contract without direct neural innervation (as required

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MINI CLINI Heart Rate and Coronary Perfusion Problem Why might an extremely high heart rate decrease blood flow through the coronary arteries? Discussion Blood flow through the coronary arteries occurs only during ventricular diastole when the aortic semilunar valves close and the heart relaxes. During systole, the myocardium contracts with such force that coronary artery pressures increase to values greater than aortic pressures. As the heart rate (HR) increases, both systolic and diastolic times must decrease. As diastolic time decreases, increasingly less time is available for coronary artery perfusion that occurs during diastole and, therefore, coronary blood flow is significantly reduced. This reduction in flow is critically important for an individual who already has reduced coronary circulation caused by arteriosclerotic heart disease. Not only is coronary artery perfusion decreased with severe tachycardia but also the shortened ventricular filling time causes decreased stroke volume (SV) and decreased cardiac output (CO) leading to decreased systemic and coronary perfusion.

MINI CLINI Pulseless Electrical Activity and Cardiopulmonary Resuscitation Problem Why should pulmonary resuscitation should continue even in the presence of a normal sinus rhythm (NSR) in the monitor during a resuscitation attempt? Discussion Pulseless electrical activity (PEA), also known as electromechanical dissociation, refers to cardiac arrest in which the electrocardiogram (ECG) shows a heart rhythm that should produce a pulse, but does not.9 In this case there is an ‘electrical’ signal but the heart muscle does not respond accordingly to generate a palpable pulse. In the absence of a pulse (non-perfusion state), even in the presence of a “normal” ECG cardiac rhythm, chest compressions must continue to guarantee adequate perfusion to central organs during the arrest. Troubleshooting of the possible causes of PEA must ensue immediately (see Chapter 18).

by skeletal muscle). When the electrical signals of a depolarization wave reach the contractile cells they contract (systole). When the repolarization signals reach the myocardial cells they relax (diastole) and thus the electrical signals cause the mechanical pumping action of the heart; mechanical events always follow the electrical events. The rate at which electrical impulses spread throughout the myocardium is variable. These differences in conduction rates are needed to ensure synchronous contraction of the cardiac chambers. Abnormal conductivity can affect the timing of chamber contractions and decrease cardiac efficiency. Contractility, in response to an electrical impulse, is the primary function of the myocardium. Contrary to the contractions of other muscle tissues, cardiac contractions cannot be sustained or tetanized because myocardial tissue exhibits a prolonged period of inexcitability after contraction. The period during which the myocardium cannot be stimulated is called the refractory period and lasts approximately 250 ms, nearly as long as the heart contraction or systole.

T tubule Nucleus

Intercalated disc Mitochondrion Sarcomere T tubule Sarcoplasmic reticulum Sarcolemma

Fig. 10.5  Major Structural Features of Cardiac Muscle Fibers. Note the presence of intercalated discs connecting successive sarcomeres. (Modified from Moffett DF, Moffett SB, Schauf CL: Human physiology: foundations and frontiers, ed 2, St Louis, 1993, Mosby.)

Microanatomy of the Heart Muscle Understanding how cardiac muscle contracts requires knowledge of the microanatomy of the heart. Cardiac cells are short, fat, branched and interconnected. Individual cardiac fibers are enclosed in a membrane called the sarcolemma, which is surrounded by a rich capillary network (Fig. 10.5). Cardiac fibers are separated by irregular transverse thickenings of the sarcolemma called intercalated discs. These discs provide structural support and aid in electrical conduction between fibers. Each fiber consists of many smaller units called myofibrils, which contain repeated structures approximately 2 µm in size termed sarcomeres. Within the sarcomeres are contractile protein filaments responsible for shortening the myocardium during systole. These proteins are of two types: thick filaments composed mainly of myosin and thin filaments composed mostly of actin. Myocardial cells contract when actin and myosin combine to form reversible bridges between these thick and thin filaments.3,6 The tensions developed during myocardial contraction are directly proportional to the number of cross-bridges between the actin and myosin filaments. This principle underlies Starling’s law of the heart, also known as the Frank-Starling law, which is discussed later in this chapter. According to this law, the more a cardiac fiber is stretched (up to a point), the greater the tension it generates when contracted. This relationship is extremely important and is explored later in the discussion of the heart as a pump.10

Vascular System The vascular system has two major subdivisions: the systemic circulation and the pulmonary circulation. The systemic circulation begins with the aorta on the left ventricle and ends in the right atrium. The pulmonary circulation begins with the pulmonary artery out of the right ventricle and ends in the left atrium. The blood flow to and from the heart is shown in Fig. 10.6.3

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Systemic capillaries

O2 Circulation to tissues of head and upper body Lung

Lung

CO2 CO2 O2

O2

Pulmonary capillaries Pulmonary circulation

CO2

O2

Circulation to tissues of lower body

Systemic circulation Fig. 10.6  Generalized circulatory and gas exchange pathways between the heart, lung, and systemic circulation.

Venous, or deoxygenated, blood from the head and upper extremities enters the right atrium from the superior vena cava (SVC), and venous blood from the abdomen and lower body enters from the inferior vena cava (IVC). From the right atrium, blood flows into the right ventricle. The right ventricle pumps the blood into the pulmonary arteries, which are the only arteries in the body that carry deoxygenated or venous blood. From there, this venous blood participates in gas exchange in the lungs, picking up oxygen and eliminating carbon dioxide through the alveolar-capillary membrane of the lungs. RULE OF THUMB  When performing hemodynamic calculations requiring the use of mixed-venous blood samples, these blood samples must always be drawn slowly from a line inserted in the pulmonary artery vessel. This is commonly called a Swan-Ganz catheter or Pulmonary Artery catheter (PAC). A PAC can also help determine whether any hemodynamic, or blood-flowrelated, abnormalities exist in the heart and lungs.10

Arterial, or oxygenated, blood returns to the left atrium through the pulmonary veins. The left atrium pumps blood into the left ventricle and the blood is then pumped to the body through the aorta. After gas exchange at the tissue level, from

the capillary network of the various body tissues, the deoxygenated venous blood returns to the right ventricle through the SVC and IVC.1

Systemic Circulation The systemic circulation has three major components: (1) the arterial system, (2) the capillary system, and (3) the venous system. These vessels regulate not only the amount of blood flow per minute (CO) but also the distribution of blood to organs and tissues (perfusion). To achieve these functions, each component has a unique structure and plays a different role in the circulatory system as a whole.3 The arterial system consists of large, highly elastic, lowresistance arteries and small, muscular arterioles of varying resistance. With their elasticity, the large arteries help transmit and maintain the head of pressure generated by the heart. Together, the large arteries are called conductance vessels. Just as faucets control the flow of water into a sink, the smaller arterioles control blood flow into the capillaries. Arterioles provide this control by varying their flow resistance; they play a major role in the distribution and regulation of blood pressure and are referred to as resistance vessels.

CHAPTER 10  The Cardiovascular System

Capillary network

Arteriole

Venule

Arteriovenous anastomosis

Fig. 10.7  Components of a Microcirculatory Network. Blood flows from arteriolar to venular vessels through a network of capillaries. The opening of the arteriovenous anastomosis directs blood flow out of the capillary network. (Modified from Stevens A, Lowe J: Human histology, ed 2, St Louis, 1997, Mosby.)

The vast capillary system, or microcirculation, maintains a constant exchange of nutrients and waste products for the cells and tissues of the body. For this reason, the capillaries are commonly referred to as exchange vessels. Fig. 10.7 shows the structure of a typical capillary network. Blood flows into the network by an arteriole and out through a venule. Direct communication between these vessels is called an arteriovenous anastomosis. When open, these anastomoses allow arterial blood to shunt around the capillary bed and flow directly into the venules. Downstream, the arteriole divides into terminal arterioles, which branch further into thoroughfare channels and true capillaries. Capillaries have smooth muscle rings at their proximal ends, called precapillary sphincters. Contraction of these sphincters decreases blood flow locally, whereas relaxation increases local perfusion. In combination, these various channels, sphincters and bypasses allow precise control over the direction and amount of blood flow to a given organ or area of tissue. The venous system consists of small, expandable venules and veins and larger, more elastic veins. Besides conducting blood back to the heart, these vessels act as a reservoir for the circulatory system. At any given time, the veins and venules hold approximately three-quarters of the body’s total blood volume. The volume of blood held in this reservoir can be rapidly changed as needed simply by altering the tone of these vessels. By quickly changing its holding capacity, the venous system can match the

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volume of circulating blood to that needed to maintain adequate tissue perfusion. The components of the venous system, especially the small, expandable venules and veins, are termed capacitance vessels. The venous system must overcome gravity to return blood to the heart. The following four mechanisms aid the venous return to the heart: (1) sympathetic venous tone; (2) skeletal muscle pumping or “milking” (combined with one-way venous valves); (3) cardiac suction; and (4) thoracic pressure differences caused by respiratory efforts.5 The last mechanism is often called the thoracic pump. This is particularly important to respiratory therapists (RTs) because artificial ventilation with positive pressure reverses normal thoracic pressure gradients. Positive pressure ventilation (PPV) impedes, rather than assists, venous return. As long as blood volume, cardiac function and vasomotor tone are adequate, PPV generally has a minimal effect on venous return; however, patients who are hypovolemic or in cardiac failure are vulnerable to a reduction in cardiac output when PPV is applied to the lungs.10 Although the heart is a single organ, it functions as two separate pumps. The right side of the heart generates a systolic pressure of approximately 25 mm Hg to drive blood through the low-resistance, low-pressure pulmonary circulation. The left side of the heart generates systolic pressures of approximately 120 mm Hg to propel blood through the higher pressure, high-resistance systemic circulation. This pressure gradient helps the cardiac suction effect in returning the venous blood to the right side of the heart.

Vascular Resistance Similar to the movement of any fluid through tubes, blood flow through the vascular system is opposed by frictional forces. The sum of all frictional forces opposing blood flow through the systemic circulation is called systemic vascular resistance (SVR). SVR must equal the difference in pressure between the beginning and the end of the circuit, divided by the flow. The beginning pressure for the systemic circulation is the mean aortic pressure; ending pressure equals right atrial pressure or central venous pressure (CVP). Flow for the system in its entirety equals the cardiac output (CO). SVR can be calculated by the following formula: SVR =

Mean aortic pressure − Right atrial pressure Cardiac output

Given a normal mean aortic pressure of 90 mm Hg, a mean right atrial pressure of approximately 4 mm Hg and a normal CO of 5 L/min, normal SVR is computed as follows: 90 mm Hg − 4 mm Hg 5 L min = 17.2 mm Hg L min

SVR =

The same concepts can be used to compute resistance in the pulmonary circulation. Beginning pressure for the pulmonary circulation is the mean PA pressure; ending pressure equals left atrial pressure. Flow for the pulmonary circulation is the same as it is for the systemic system, which equals the CO; hence,

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RULE OF THUMB  Changes in resistance are the primary means by which blood flow is regulated within organs because control mechanisms in the body generally maintain arterial and venous blood pressures within a narrow range. When applying Ohm’s law for the flow of blood in a blood vessel (Blood Flow = ΔP/Resistance or MAP = CO/SVR), the ΔP is the pressure difference between any two points along a given length of the vessel. When describing the flow of blood for an organ, the pressure difference is generally expressed as the difference between the arterial pressure (PA) and venous pressure (PV). For example, the blood flow for the kidney is determined by the renal artery pressure, renal vein pressure, and renal vascular resistance.

pulmonary vascular resistance (PVR) can be calculated by using the following formula: PVR =

Mean PA pressure − Left atrial pressure Cardiac output

Given a normal mean PA pressure of approximately 16 mm Hg and a normal mean left atrial pressure of 8 mm Hg, normal PVR is computed as follows: 16 mm Hg − 8 mm Hg 5 L min = 1.6 mm Hg L min

PVR =

Resistance to blood flow in the pulmonary circulation is approximately one-tenth of that of the systemic circulation. The pulmonary circulation is characterized as a low-pressure, lowresistance system and the systemic circulation as a high-pressure, high-resistance system.

Determinants of Blood Pressure A healthy cardiovascular system maintains sufficient pressure to propel blood throughout the body.6 The priority of the cardiovascular system is to maintain perfusion pressures to tissues and organs at functional levels, even under changing conditions. If the equation for computing SVR is rearranged by deleting the normally low atrial pressure, the average blood pressure in the circulation is directly related to both CO and flow resistance, as follows: Mean arterial pressure (MAP) = (CO × SVR) + CVP Some MAP formulas disregard the CVP contribution because the CVP levels are generally negligible under normal circumstances (0 to 6 mm Hg). It is important to note that under many conditions, vascular resistance tends to vary inversely with the size of the blood vessels (i.e., the capacity of the vascular system). All else being constant, MAP is directly related to the volume of blood in the vascular system and inversely related to its capacity: MAP =

Volume Capacity

Based on this relationship, MAP is regulated by either changing the volume of circulating blood, changing the capacity of

the vascular system or changing both. Volume changes can reflect absolute changes in total blood volume, such as changes resulting from hemorrhagic shock or blood transfusion. Alternatively, changes in “relative” volume can occur when vascular space increases or decreases. Vascular space decreases when vasoconstriction (constriction of the smooth muscles in the peripheral blood vessels) occurs, which causes blood pressure to increase even though blood volume is the same. Vascular space increases when vasodilation (relaxation of the smooth muscles in the arterioles) occurs, which causes blood pressure to decrease even though blood volume has not changed (e.g., during septic shock). In a normal adult, MAP ranges from 80 to 100 mm Hg. When MAP decreases below 60 mm Hg, which may accompany some forms of untreated shock, perfusion to the brain and the kidney is severely compromised and organ failure may occur in minutes.4 The blood pressure value that should be targeted during the management of septic shock is an important clinical issue. The MAP is one of the first variables that is monitored in septic patients.11 Prolonged hypotension, defined as a MAP of less than 60 to 65 mm Hg, is associated with poor outcome in general. RULE OF THUMB  The results of the SEPSISPAM (Sepsis and Mean Arterial Pressure) study suggest that a MAP target of 65 to 75 mm Hg is usually sufficient in patients with septic shock, but a higher MAP (around 75 to 85 mm Hg) may be preferable in patients with chronic arterial hypertension.12

To avoid organ and tissue damage and maintain adequate perfusion pressures under changing conditions, the cardiovascular system attempts to balance relative volume and resistance. When a person exercises, the circulating blood volume undergoes a relative increase, but blood pressure remains near normal, because the skeletal muscle vascular beds dilate, causing a large increase in system capacity; however, when blood loss occurs, as with hemorrhage, the system capacity is decreased by constriction of the peripheral vessels. Perfusion pressures may be kept near normal unless the volume loss is extreme. Regulation of blood flow and pressure is much more complex than is suggested by these simplified equations. Cardiovascular control is achieved by a complex array of integrated functions, some of which are explained subsequently.

CONTROL OF THE CARDIOVASCULAR SYSTEM The cardiovascular system is responsible for transporting metabolites to and from the tissues under various conditions and demands. It must act in a highly coordinated fashion achieved by integrating the functions of the heart and vascular system. The goal is to maintain adequate perfusion to all tissues according to their needs.10 The cardiovascular system regulates blood flow mainly by altering the capacity of the vasculature and the volume of blood it holds. The heart plays only a secondary role in regulating blood flow; the vascular system tells the heart how much blood it needs, rather than the heart dictating what volume of blood the vascular system will receive.

CHAPTER 10  The Cardiovascular System

These integrated functions involve local and central neural control mechanisms. Local, or intrinsic, controls operate independently without central nervous system control. Intrinsic control alters perfusion under normal conditions to meet metabolic needs. Central or extrinsic control involves both the central nervous system and circulating humoral agents. Extrinsic control mechanisms maintain a normal level of vascular tone; however, central control mechanisms take over when the competing needs of local vascular beds must be coordinated. Basic knowledge of vascular regulatory mechanisms and factors controlling CO is essential to understand how the cardiovascular system responds under both normal and abnormal conditions.3

Regulation of Peripheral Vasculature A normal level of vascular muscle tone is normally maintained throughout the vascular system at all times. Normal vascular muscle tone must be present to allow for effective regulation. If blood vessels remained completely relaxed, further dilation would be impossible and local increases in perfusion could not occur. Local vascular tone is maintained by the smooth muscle of the precapillary sphincters of the microcirculation and can function independently of neural control at the local tissue level according to metabolic needs. Central control of vasomotor tone involves either direct central nervous system innervation or circulation hormones. Central control mainly affects the highresistance arterioles and capacitance veins.

Local Control Local regulation of tissue blood flow includes both myogenic and metabolic control mechanisms. Myogenic control involves the relationship between vascular, smooth-muscle tone and perfusion pressure. Myogenic control ensures relatively constant flows to the capillary beds despite changes in perfusion pressures. Metabolic control involves the relationship between vascular, smooth-muscle tone and the level of local cellular metabolites. High amounts of carbon dioxide (CO2) or lactic acid, low pH levels, low partial pressures of O2 levels, histamines (released during an inflammatory response), endothelium-derived relaxing factor, and some prostaglandins all cause relaxation of the smooth muscle and vasodilation, increasing blood flow to the affected area. The influence of myogenic and metabolic control mechanisms varies in different organ systems, with the brain being the most sensitive to changes in the local metabolite levels, particularly CO2 and pH.3 Central Control Central control of blood flow is primarily achieved by the sympathetic division of the autonomic nervous system. Smoothmuscle contraction and increased flow resistance are mostly caused by adrenergic stimulation and the release of norepinephrine. Smooth-muscle relaxation and vessel dilation is caused by stimulation of either cholinergic or specialized β-adrenergic receptors. Although the contractile response is distributed throughout the entire vascular system, the dilation response appears to be limited to the precapillary vessels. In addition to the sympathetic control, blood flow through the large veins can also be affected by abdominal and intrathoracic pressure changes.

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MINI CLINI Calculating Cardiac Output Problem How to calculate the CO of a patient with a resting HR of 70 beats/min and a measured stroke volume (SV) of 75 mL/beat? Discussion A normal resting CO of approximately 5 L/min can be calculated by substituting a normal HR (70 beats/min) and SV (75 mL, or 0.075 L, per contraction): CO = 70 beats min × 0.075 L beat = 5.25 L min This calculation is a hypothetical average because actual CO normally varies according to a person’s gender, height and weight, as well as being impacted by various diseases.

Regulation of Cardiac Output The heart, similar to the vascular system, is regulated by both intrinsic and extrinsic factors. These mechanisms act together, along with vascular control, to ensure that the output of the heart matches the different needs of the tissues. As previously discussed, the total amount of blood pumped by the heart per minute is called the cardiac output (CO). CO is simply the product of the HR and the volume ejected by the left ventricle on each contraction, or stroke volume (SV): CO = HR × SV Regardless of an individual’s state of health or illness, a change in CO must involve a change in SV, a change in HR or both. SV is affected primarily by intrinsic control of three factors: (1) preload, (2) afterload, and (3) contractility (all three factors are discussed subsequently). HR is affected primarily by extrinsic or central control mechanisms.4,10

Changes in Stroke Volume The heart does not eject all of the blood it contains during systole. Instead, a small volume, called the end-systolic volume (ESV), remains inside the ventricles. During the resting phase or diastole, the ventricles fill to a volume called the end-diastolic volume (EDV). SV equals the difference between the EDV and the ESV, as follows: SV = EDV − ESV In a healthy person at rest, the EDV ranges from 110 to 120 mL. Given a normal SV of approximately 70 mL, a normal ejection fraction (EF), or proportion of the EDV ejected on each stroke, can be calculated as follows: SV × 100 EDV 70 mL = × 100 110 mL = 64%

EF =

As shown in Fig. 10.8, an increase in SV occurs when either the EDV increases or the ESV decreases. Conversely, a decrease

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Normal

Increased SV EDV

Decreased SV ESV

EDV

ESV

Diastolic reserve Normal EDV

A Normal ESV

Stroke volume

B

C

D

E

Systolic reserve

Fig. 10.8  Relationship between stroke volume (SV), end-diastolic volume (EDV), and end-systolic volume (ESV). (A) Normal relationship between EDV, ESV and SV; (B) increased SV resulting from increased EDV; (C) increased SV resulting from decreased ESV; (D) decreased SV resulting from decreased EDV (hypovolemia); and (E) decreased SV resulting from increased ESV (poor contractility).

MINI CLINI

TABLE 10.1  Factors Affecting Preload

Heart Failure and Cardiomyopathy

Factor

Affect

On each contraction, a healthy heart ejects approximately two-thirds of its stored volume (60% to 66%). Decreases in EF are normally associated with a weakened myocardium (heart failure), decreased contractility or both. When the EF decreases below 30%, a person’s exercise tolerance becomes severely limited.10

End-diastolic filling pressure

Problem Why does a patient with heart failure and low EF develop generalized weakness and difficulty breathing?

End-diastolic stretch

Total blood volume Blood volume distribution Atrial contraction Venous compliance Total peripheral resistance Venous return End-diastolic filling pressure Compliance of ventricle and pericardium Normal physiology Compensatory hypertrophy

Discussion A healthy heart beats about 60 to 100 times per minute to pump oxygenated blood throughout the body. Heart failure, also known as congestive heart failure (CHF), occurs when a person’s heart is weakened and not able to pump blood the way it should, therefore the EF falls below normal, healthy levels. As a result, the body does not get enough blood—and the oxygen that blood cells carry—to maintain the body and its normal functions. Low EF can be caused by many cardiac and vascular conditions such as cardiomyopathy, CAD, MI, heart valve disease and systolic heart failure (see Chapter 31).

in SV occurs when either the EDV decreases or the ESV increases. This relationship is key to understanding regulation of CO. The heart’s ability to change SV solely according to the EDV is an intrinsic regulatory mechanism. As mentioned before, according to the Frank-Starling law, the force the ventricle can generate results from the length (or stretch) of the myocardial fibers just before contraction. As the ventricle fills with blood, the myocardial fibers are stretched and as the stretch increases, the tension (force) within the walls of the heart increases (analogous to stretching a rubber band).10 The concepts of tension or force and filling volume are often described in terms of preload and afterload and as with many

Myocardial wall thickness

Data from Chiumello D, Carlesso E, Cadringher P, et al: Lung stress and strain during mechanical ventilation for acute respiratory distress syndrome, Am J Respir Crit Care Med 15;178:346, 2008.

terms in medicine, the definitions of preload and afterload vary considerably in the literature.13 This variability seems to be related to the term load, which in general means “a force against which something that causes motion (a pump or motor) acts.” In the context of the cardiovascular system, the heart is analogous to a pump and force, in this sense, is related to stretch of the cardiac muscle according to the Frank-Starling Law. Using this description of load and preload therefore represents the combined force of all the factors that contribute to ventricular wall stretch at the end of diastole. Preload may be calculated in a manner that recognizes the forces that stretch the resting cardiac muscle to a given length before contraction. Many factors determine preload, including venous return, total blood volume and distribution and atrial activity. These and the other factors that influence preload are summarized in Table 10.1.13 In a similar fashion, afterload can be described as the combined force of all the factors that the left ventricle encounters and must overcome when stimulated to contract and achieve the end of systole. Several factors determine afterload, most

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notably peripheral vascular resistance and the physical characteristics of arterial blood. These and the other factors that determine afterload are shown in Fig. 10.9.13 It should be noted that an increased preload or afterload caused by an abnormal increased downstream resistance over time can be “normalized” (up to a point) by increasing the wall thickness of the heart, which the body attempts to do by increasing muscle mass (hypertrophy), leading to cardiomyopathy and heart failure.13

Stroke volume

Fig. 10.9  Factors determining afterload within the cardiovascular system during systole. (From Norton JM: Toward consistent definitions for preload and afterload, Adv Physiol Educ 25:53, 2001.)

RULE OF THUMB  Increases in preload (EDV) and decreases in ESV result in increased SV in the healthy heart.

All else being constant, the greater the afterload on the ventricles the harder it is for the ventricles to eject their volume. For a given EDV, an increase in afterload means the ESV increased. If the EDV remains constant while the ESV increases, the SV (EDV-ESV) decreases (see Fig. 10.8). Normally, however, the healthy heart muscle responds to increased afterload by altering its contractility. RULE OF THUMB  Increases in afterload can decrease SV, especially in the failing heart by increasing the ESV.

Contractility represents the amount of systolic force exerted by the heart muscle at any given preload. At a given preload (or EDV), an increase in contractility results in an increased EF, a decreased ESV and an increased SV. Conversely, a decrease in contractility results in a decreased EF, an increased ESV and a decreased SV. Changes in contractility affect the slope of the ventricular function curve (Figs. 10.10 and 10.11). A higher SV for a given preload (increased slope) indicates a state of increased contractility, often

Stretch Fig. 10.10  The Frank-Starling law: stroke volume (SV) as a function of ventricular end-diastolic stretch. An increase in the stretch of the ventricles immediately before contraction (end-diastole) results in an increase in end-diastolic volume and SV. Ventricular end-diastolic stretch is synonymous with the concept of preload.

referred to as positive inotropism. The opposite is also true. A lower SV for a given preload indicates decreased contractility, referred to as negative inotropism. Drugs that increase contractility of the heart muscle are called positive inotropes and drugs that decrease contractility are negative inotropes.10 In addition to local mechanisms, cardiac contractility is influenced by neural control, circulating hormonal factors, and certain medications. Typically, neural or drug-mediated sympathetic stimulation has a positive inotropic effect. Conversely, parasympathetic stimulation exerts a negative inotropic effect. Profound hypoxia and acidosis impair myocardial function and decrease cardiac contractility.

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MINI CLINI

Cardiac output

↓Afterload ↑Contractility ↑Heart rate

Effect of Increased Afterload on Cardiac Output in a Normal Heart

↑Afterload ↓Contractility ↓Heart rate

Preload Fig. 10.11  Effects of preload, afterload, contractility and heart rate on cardiac output function curve. (Modified from Green JF: Fundamental cardiovascular and pulmonary physiology, ed 2, Philadelphia, 1987, Lea & Febiger.)

RULE OF THUMB  Hypoxia and acidosis decrease cardiac contractility and output.

Changes in Heart Rate The last factor influencing CO is HR. In contrast to the factors controlling SV, the factors affecting HR are mainly of central origin (i.e., neural or hormonal). Factors that increase HR are called positive chronotropic factors. Likewise, factors that decrease HR are called negative chronotropic factors. RULE OF THUMB  Increase in HR increases CO in a healthy heart up to a rate of 160 to 180 beats/min.

The combined effects of preload, afterload, contractility and HR on cardiac performance are graphically portrayed in Fig. 10.11. The middle curve represents the normal state and the upper, steeper curve represents a hyperdynamic heart. In the hyperdynamic heart, a given preload results in a greater than normal CO. Factors contributing to this state include decreased afterload, increased contractility (decreased ESV), and increased HR. The bottom curve has a lower slope than normal, indicating a hypodynamic heart. Factors contributing to this state include increased afterload, decreased contractility (increased ESV), and decreased rate. When the pumping efficiency of the heart is so low that CO is inadequate to meet tissues needs, the heart is said to be in CHF as discussed before.4,10

Cardiovascular Control Mechanisms Cardiovascular control is achieved by integrating local and central regulatory mechanisms that affect both the heart and the vasculature. The goal is to ensure that all tissues receive sufficient blood flow to meet their metabolic needs; however, when demands are increased or abnormal, such as during exercise or massive bleeding, central mechanisms take over primary control.

Afterload is the resistance the ventricle must overcome or the forces that oppose ejection of blood pressure generated as the heart works to eject its SV. As afterload increases, the SV ejected by the ventricle decreases, assuming that the contractility of the heart (force with which the heart contracts) remains constant. Problem During exercise, a healthy person’s blood pressure increases considerably, indicating that the afterload has increased. Yet the SV and CO in a healthy heart do not decrease. Why is this so? Discussion When afterload increases, the initial ventricular contractions that experience the increased afterload produce smaller SVs, which causes more blood to remain in the ventricle at the end of systole (i.e., ESV is increased). During the subsequent diastole, blood rushes in from the atria to fill the ventricles, and because of the higher-than-normal ESV, the ventricles become more distended and stretched. Healthy heart muscle responds to increased stretch in a way described by the Frank-Starling law; that is, the heart now contracts with greater force than before, ejecting a greater SV. By increasing contractility in this fashion, SV and CO are not compromised by increased afterload in a healthy heart. As expected, CO increases and decreases with similar changes in HR; however, this relationship is only maintained up to approximately 160 to 180 beats/min in a healthy heart. At higher HRs, there is not enough time for the ventricles to fill completely between each heartbeat, causing a decrease in EDV, SV, and CO. Even worse, as the HR exceeds this level, oxygen consumption of the heart increases and coronary perfusion decreases, further comprising the patient. This phenomenon often occurs at significantly less than 160 beats/min in the failing heart.

RULE OF THUMB  Under normal conditions, blood flow to a specific vascular bed is primarily regulated by local mechanisms.

Central control of cardiovascular function occurs by the interaction between the brainstem and selected peripheral receptors (Fig. 10.12). The brainstem constantly receives feedback from these receptors about the pressure, volume and chemical status of the blood. The brainstem also receives input from higher brain centers, such as the hypothalamus and cerebral cortex. These inputs are integrated with the inputs coming from the heart and blood vessels to maintain adequate blood flow and pressure in all but the most abnormal conditions.4

Cardiovascular Control Centers Fig. 10.12 is a simplified diagram of the cardiovascular regulatory centers. Areas in the medulla receive input from higher brain centers, peripheral pressure and chemical receptors. Stimulation of the vasoconstrictor area within the medulla causes vasoconstriction and increased vascular resistance. Closely associated with the vasoconstrictor center is a cardioaccelerator area. Stimulation of this center increases HR by increasing sympathetic discharge to the SA and AV nodes of the heart. A cardioinhibitory area plays the opposite role. Stimulation

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3. Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit cardioacceleratory center) and inhibit vasomotor center. 4a. ↓Sympathetic impulses to heart cause ↓HR, ↓contractility, and ↓CO. 2. Baroreceptors in carotid sinuses and aortic arch are stimulated.

1. Stimulus: ↑Blood pressure (arterial blood pressure rises above normal range).

Imb alan ce

4b. ↓Rate of vasomotor inpulses allows vasodilation, causing ↓R.

5. ↓CO and ↓R return blood pressure to homeostatic range.

Homeostatis: Blood pressure in normal range

5. ↑CO and ↑R return blood pressure to homeostatic range.

Imb alan ce 4b. Vasomotor fibers stimulate vasoconstriction, causing ↑R.

1. Stimulus: ↓Blood pressure (arterial blood pressure falls below normal range).

2. Baroreceptors in carotid sinuses and aortic arch are inhibited. 4a. ↑Sympathetic impulses to heart cause ↑HR, ↑contractility, and ↑CO.

3. Impulses from baroreceptors stimulate cardioacceleratory center (and inhibit cardioinhibitory center) and stimulate vasomotor center. Fig. 10.12  Simplified diagram of cardiovascular regulatory centers. CO, Cardiac output; HR, heart rate; R, resistance. (Modified from Marieb EN, Hoehn KN: Anatomy and physiology, ed 4, San Francisco, 2011, Pearson Benjamin Cummings.)

MINI CLINI Heart Rate and the Administration of Bronchodilator Drugs Problem You are giving a bronchodilator-aerosolized drug to a patient and you notice a significant increase in the patient’s HR. Would you expect increased HR to be a common side effect of pulmonary bronchodilators? Discussion The discharge rate of the sinus node and the HR are increased by sympathetic nervous stimulation and decreased by parasympathetic nervous stimulation. The airways of the lung are dilated by sympathetic nervous stimulation and constricted by parasympathetic stimulation. Drugs that cause bronchodilation either mimic sympathetic stimulation (sympathomimetic) or block parasympathetic stimulation (parasympatholytic). Both of these drug actions can also cause the HR to increase (see Chapter 36).

of this center decreases HR by increasing vagal (parasympathetic) stimulation to the heart. Higher brain centers also influence the cardiovascular system, both directly and through the medulla. Signals coming from the cerebral cortex in response to exercise, pain or anxiety pass directly through the cholinergic fibers to the vascular smooth muscle, causing vasodilation. Signals from the hypothalamus, in particular its heat-regulating areas, indirectly affect HR and vasomotor tone through the cardiovascular centers. The cardiovascular centers are also affected by local chemical changes in the surrounding blood and cerebrospinal fluid. Decreased levels of CO2 tend to inhibit the medullary centers and general inhibition of these centers causes a decrease in vascular tone and a decrease in blood pressure. A local decrease in O2 tension has the opposite effect. Mild hypoxia in this area increases sympathetic discharge rates, which tends to elevate both HR and blood pressure; however, severe hypoxia has a depressant effect.

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Peripheral Receptors In addition to high-level and local input, the cardiovascular centers receive signals from peripheral receptors (see Fig. 10.12). There are two types of peripheral cardiovascular receptors: baroreceptors, or stretch receptors, and chemoreceptors. Baroreceptors respond to pressure changes, whereas chemoreceptors respond to changes in blood chemistry.4 The cardiovascular system has two different sets of baroreceptors. The first set is located in the aortic arch and carotid sinuses and these receptors monitor arterial pressures generated by the left ventricle. The second set is located in the walls of the atria and the large thoracic and pulmonary veins and these low-pressure sensors respond mainly to changes in vascular volumes. Baroreceptor output is directly proportional to the stretch on the vessel wall. The greater the blood pressure, the greater is the stretch and the higher the rate of neural discharge to the medulla. Together with the cardiovascular regulatory centers, these receptors form a negative feedback loop, where stimulation of a receptor causes an opposite response by the effector. In the case of the arterial receptors, an increase in blood pressure increases aortic and carotid receptor stretch and their neuronal discharge rates. The increased discharge rates cause an opposite response by the medullary centers (i.e., depressor response decreasing blood pressure). Decreased blood pressure (decreased baroreceptor output) has the opposite effect, causing peripheral vessel constriction and increased HR and contractility. This mechanism usually restores blood pressure to normal (see Fig. 10.12).3,4

Although the high-pressure arterial receptors constantly control blood pressure, the low-pressure sensors are responsible for longterm regulation of plasma volume. The low-pressure atrial and venous baroreceptors regulate plasma volume mainly by activating several chemical and hormonal mechanisms. Table 10.2 provides a detailed description of some of these mechanisms. The major pathways for plasma-volume control are outlined in Fig. 10.13. Combined with a central nervous system-mediated increase in renal filtration, these humoral mechanisms decrease the overall plasma volume. A decrease in blood volume has the TABLE 10.2  Hormonal Control

Mechanisms Affecting Blood Pressure Hormone

Place of Action

Effect

Angiotensin II Antidiuretic hormone

Arterioles Kidneys

↑ SVR (vasoconstriction) ↑ Blood volume (↑water retention) ↑ SVR (vasoconstriction) ↓ SVR (vasodilation)

Atrial natriuretic peptide Aldosterone

Arterioles Arterioles Kidneys

Cortisol

Kidneys

Norepinephrine

Heart (β-1 receptors) Arterioles (α receptors)

↑ Blood volume (↑water and salt retention) ↑ Blood volume (↑water and salt retention) ↑ Cardiac output (HR and contractility) ↑ SVR (vasoconstriction)

HR, Heart rate; SVR, systemic vascular resistance.

↑Intrathoracic blood volume Cardiovascular receptors Central nervous system ↓Vasopressin release

↑Natriuretic hormone

↓Sympathetic activity ↓Renin

↓Thirst

↓Angiotensin II ↓Aldosterone

↑Renal perfusion

↑Glomerular filtration rate ↑Sodium and water excretion ↓Plasma volume

Fig. 10.13  Major Pathways for Plasma Volume Control. See text for details. (Modified from Smith JJ, Kampine JP: Circulatory physiology: the essentials, ed 3, Baltimore, 1990, Williams & Wilkins.)

opposite effect (i.e., sodium and water retention and an increase in plasma volume). Chemoreceptors are small, highly vascularized tissues located near the high-pressure sensors in the aortic arch and carotid sinus that are sensitive to changes in blood chemistry. They are strongly stimulated by decreased O2 tensions, low pH or high levels of CO2. Simply put, the major cardiovascular effects of chemoreceptor stimulation are vasoconstriction and increased HR.

ADH µ units/mL (log scale)

CHAPTER 10  The Cardiovascular System

RULE OF THUMB  As the arterial oxygen content or the pH drops, chemoreceptors will cause an increased in the HR and systemic vasoconstriction.

10

180 Heart rate Cardiovascular responses (% control)

Blood Volume Regulation The coordinated response of the cardiovascular system is best shown under abnormal or stressful conditions. Among the most common clinical conditions in which all essential regulatory mechanisms come into play is the large blood loss that occurs with hemorrhage. Fig. 10.14 illustrates changes in these key factors during progressive blood loss in an animal model. With 10% blood loss, the immediate decline in the CVP causes a 50% decrease in the discharge rate of the low-pressure (atrial) baroreceptors; however, there is little change in the activity of the high-pressure (arterial) receptors. The initial response, mediated through the medullary centers, is an increase in sympathetic discharge to the sinus node, which causes a progressive increase in HR. At the same time, plasma levels of antidiuretic hormone (vasopressin) begin to increase and thus maintaining normal arterial blood pressure. As the blood loss becomes more severe (20%), atrial receptor activity decreases further, which increases the intensity of sympathetic discharge from the cardiovascular centers. Plasma antidiuretic hormone and HR continue to increase, as does peripheral vasculature tone. An increase in vascular tone occurs through the constriction of the capacitance vessels in the venous system, slowing the decrease in CVP.4 The arterial pressure does not start to decrease until blood loss approaches 30%. At this point, arterial receptor activity begins to decrease, resulting in a marked increase in systemic vascular tone. Despite the magnitude of blood loss, CVP levels off. If no further hemorrhage occurs, blood pressure and tissue perfusion can be maintained at adequate levels. If blood loss continues, however, central control mechanisms begin to take over, causing massive peripheral vasoconstriction, shunting blood away from skeletal muscle to maintain blood flow to the brain and heart. Increasing levels of local metabolites such as CO2 and other acids override central control and cause further vessel dilation and increased blood flow to these vital organs; however, as these metabolites build up, tissues become hypoxic, cardiac function becomes impaired and vasodilation occurs throughout the body. In such an instance, this vasodilation signals the onset of late stage and irreversible hypovolemic

100

1

Venomotor tone

140

100

Arterial blood pressure

60

Central venous pressure

20

Receptor firing rate (% control)

These changes occur only when the cardiopulmonary system is overtaxed and so the chemoreceptors probably have little influence under normal conditions; however, their influence on respiration is clinically important and therefore discussed in greater detail in Chapter 9.

221

100 Arterial receptors 50

0

Atrial receptors –10%

–20%

–30%

Decrease in blood volume

Fig. 10.14  Plasma levels of antidiuretic hormone (ADH), cardiovascular responses and receptor firing rates in response to graded hemorrhage in the dog. See text for details. (From Richardson DR: Basic circulatory physiology, Boston, 1976, Little, Brown; venomotor tone data are those of W. Sears J, as cited in Gauer OH, Henry JP, Behn C: The regulation of extracellular fluid volume, Annu Rev Physiol 32:547, 1970. All other data are from Henry JP, et al: Can J Physiol Pharmacol 46:287, 1968.)

shock, after which death often occurs. Similar events can occur in the presence of severe dehydration and volume depletion by other means such as severe vomiting and diarrhea.

EVENTS OF THE CARDIAC CYCLE This chapter has emphasized the mechanical properties of the heart; the electrical activities of the heart are discussed in Chapter 18. Although they are discussed separately, the mechanical and electrical events are interdependent. Given the role of RTs in dealing with cardiovascular problems, in-depth knowledge of how these events relate is quite useful.3 The events of the cardiac cycle are depicted in Fig. 10.15. The top of the figure shows a time axis scaled in tenths of a second;

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Atrial systole (atria contract)

Ventricular systole (ventricles contract)

Atrial and ventricular diastole

A 0

0.1

0.2

0.3

0.4

Systole

120

Completion of ventricular filling

Systole

Pressure (mm Hg)

0.7

0.8

Diastole

Ejection Isometric contraction

Dicrotic notch

B

0.6

Diastole

Diastole Diastasis

0.5

80

Diastasis

Seconds Atria Ventricles

Rapid ventricular filling

Isometric relaxation

Aortic pressure Semilunar valves close

Semilunar valves open Ventricular pressure 40

Atrioventricular valves close

Atrial pressure

a

Atrioventricular valves open

c 0

v

D

P wave

T wave

First heart sound

Frequency (cycles/sec)

C

Millivolts

QRS complex

Second heart sound

Third heart sound

E

Volume (mL)

150

100

50

Fig. 10.15  Cardiac Cycle. (A) Timing of cardiac events. (B) Simultaneous pressures created in the aorta, left ventricle and right atrium during the cardiac cycle. (C) Electrical activity during the cardiac cycle. (D) Heart sounds corresponding to the cardiac cycle. (E) Ventricular blood volume during the cardiac cycle. (Modified from Moffett DF, Moffett SB, Schauf CL: Human physiology: foundations and frontiers, ed 2, St Louis, 1993, Mosby.)

CHAPTER 10  The Cardiovascular System

next are the timing bars for ventricular systole and diastole and pressure events in the atria, ventricles and aorta; these are followed by an ECG, heart sounds, and ventricular flow (see Chapter 18 for an explanation of the ECG waves). Going from left to right, the P wave (atrial depolarization) begins the ECG. Earlier, the ventricles have been passively filling with blood through the open AV valves. Within 0.1 seconds, the atria contract, causing a slight increase in both atrial and ventricular pressures (a waves). This atrial contraction helps preload the ventricles, increasing their volume by 25%. This help from the atria to ventricular filling is called the atrial kick. Toward the end of diastole, the electrical impulses from the atria reach the AV node and bundle branches and ventricular depolarization (QRS complex) is initiated. Within a few hundredths of a second after depolarization, the ventricles begin to contract. As soon as ventricular pressures exceed pressures in the atria, the AV valves close, with closure of the mitral valve occurring first, followed immediately by the closure of the tricuspid valve. This closure marks the end of ventricular diastole, producing the first heart sound on the phonocardiogram.3 Immediately after AV valve closure, the ventricles become closed chambers. During this short isovolemic phase of contraction, ventricular pressures increase rapidly. Upward bulging of the AV valves during this phase causes a slight upswing in atrial pressure graphs, called the c wave. Within 0.05 seconds, ventricular pressures increase to exceed the pressures in the aorta and pulmonary artery and open the semilunar valves. Toward the end of systole, as repolarization starts (indicated by the T wave), the ventricles begin to relax. Consequently, ventricular pressures decrease rapidly. When arterial pressures exceed pressures in the relaxing ventricles, the semilunar valves shut. Closure of the semilunar valves generates the second heart sound. Rather than immediately dropping off, aortic and pulmonary pressures increase again after the semilunar valves close. The dicrotic notch is caused by the elastic recoil of the arteries. This recoil provides the extra “push” that helps maintain the pressure created by the ventricles. As the ventricles continue to relax, their pressures decrease to less than the pressures in the atria and this decline in pressure reopens the AV valves. As soon as the AV valves open, the blood collected in the atria rushes to fill the ventricles, causing a rapid decrease in atrial pressures (the v wave). Subsequently, ventricular filling slows as the heart prepares for a new cycle. Knowledge of these events can help in understanding many of the diagnostic and monitoring procedures used for patients with cardiopulmonary disorders, including balloon-directed pulmonary artery catheterization and direct arterial pressure monitoring.

SUMMARY CHECKLIST • The heart is a four-chambered muscular organ approximately the size of a fist. It is positioned in the mid mediastinum of the chest, behind the sternum. • The cardiovascular system consists of the heart and a vascular network that accounts for normal distribution and regulation of blood flow throughout the body to ensure tissue perfusion.

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• Inflammation of the pericardium results in a clinical condition called pericarditis. • An abnormal amount of fluid can accumulate between the pericardial layers, resulting in a pericardial effusion. A large pericardial effusion may lessen the pumping function of the heart, resulting in cardiac tamponade. • The two lower-heart chambers, or ventricles, make up the bulk of the heart’ ’s muscle mass and do most of the pumping that circulates the blood. • Common valve problems include regurgitation and stenosis. Regurgitation is the backflow of blood through a malfunctioning valve. Stenosis is a pathologic narrowing or constriction of a valve outlet, which causes blood to back up and results in increased pressure in the proximal chamber and vessels. Both conditions affect cardiac performance. • The heart’s circulatory system is called the coronary circulation. To meet the heart’s needs, the coronary circulation provides an extensive network of branches to all myocardial tissue. • Complete obstruction of a coronary artery may cause tissue death or infarct, a condition called myocardial infarction (MI). • ACS is the name given to three types of CAD that are associated with gradual and/or sudden obstruction of the coronary arteries: (1) unstable angina or angina pectoris, (2) NSTEMI, and (3) STEMI. • Heart diseases remain responsible for approximately one third of all deaths in individuals over the age of 35.7 years. Nearly one-half of all middle-aged men and one-third of middleaged women in the USA will develop some manifestation of a CHD. • Symptoms of a MI include tightness or pain in the chest, neck, back or arms, as well as fatigue, lightheadedness, abnormal heartbeat and anxiety. Women are more likely to have atypical symptoms than men. • The thebesian veins bypass or shunt around the pulmonary circulation as part of the normal anatomy, this phenomenon is called an anatomic shunt. When combined with a similar bypass in the bronchial circulation, these normal anatomic shunts account for approximately 2% to 3% of the total CO. • Myocardial tissue possesses the following four key properties: excitability, inherent rhythmicity or automaticity, conductivity and contractility. • During a resuscitation attempt even in the presence of a “normal” cardiac rhythm in a monitor but with an absent pulse, chest compressions must continue to guarantee adequate perfusion to central organs. • Mechanical and electrical properties of cardiac tissue, combined with internal and external control mechanisms, provide the basis for coordinated cardiac function. • According to the Frank-Starling law, the more a cardiac fiber is stretched (up to a point), the greater the tension it generates when contracted. • The systemic circulation has three major components: (1) arterial system, (2) capillary system, and (3) venous system. These vessels regulate not only the amount of blood flow per minute (CO) but also the distribution of blood to organs and tissues (perfusion).

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• The venous system consists of small, expandable venules and veins and larger, more elastic veins. Besides conducting blood back to the heart, these vessels act as a reservoir for the circulatory system. • The heart is a single organ, but it functions as two separate pumps. The right side of the heart generates a systolic pressure of approximately 25 mm Hg to drive blood through the low-resistance, low-pressure pulmonary circulation. The left side of the heart generates systolic pressures of approximately 120 mm Hg to propel blood through the higher pressure, highresistance systemic circulation. • The sum of all frictional forces opposing blood flow through the systemic circulation is called systemic vascular resistance (SVR). • According to Ohm’s law, changes in resistance are the primary means by which blood flow is regulated within organs because control mechanisms in the body generally maintain arterial and venous blood pressures within a narrow range. • Resistance to blood flow in the pulmonary circulation is approximately one-tenth of the systemic circulation. • The vascular system is regulated by local and central control mechanisms. • CO is primarily determined by four factors: preload, afterload, contractility and HR and is equivalent to the product of the SV × HR. • Increased HR decreases CO by decreasing filling times (decreasing EDV) and decreasing contraction times, hence increasing ESV. • To avoid organ and tissue damage and maintain adequate perfusion pressures under changing conditions, the cardiovascular system attempts to balance relative volume and resistance. • The cardiovascular system regulates blood flow mainly by altering the capacity of the vasculature and the volume of blood it holds. • Central control of blood flow is primarily achieved by the sympathetic division of the autonomic nervous system. • Blood pressure is regulated by changing the volume of circulating blood, changing the capacity of the vascular system, or both. • The body can generally maintain adequate blood (and perfusing) pressures until blood loss reaches or exceeds approximately 30%, at which point hypovolemic shock is likely, and death may even occur. During increased demand, special compensatory mechanisms are called on to maintain stable blood flow. • SV is affected primarily by intrinsic control of three factors: (1) preload, (2) afterload, and (3) contractility. • Preload represents the combined force of all the factors that contribute to ventricular wall stretch at the end of diastole. Many factors determine preload, including venous return, total blood volume and distribution and atrial activity. • Afterload can be described as the combined force of all the factors the ventricles encounter and must overcome when stimulated to contract and achieve the end of systole. • Several factors determine afterload; most notably peripheral vascular resistance and the physical characteristics of arterial blood.

• All else being constant, the greater the afterload on the ventricles, the harder it is for the ventricles to eject their volume. • EF is the proportion of the EDV ejected on each stroke (SV/ EDV). • Low EF can be caused by many cardiac and vascular conditions such as cardiomyopathy, CAD, MI, heart valve disease and systolic heart failure. • Heart failure, also known as CHF, occurs when a person’s heart is weakened and not able to pump blood the way it should, therefore the EF falls below normal, healthy levels. • Factors that increase HR are called positive chronotropic factors. Likewise, factors that decrease HR are called negative chronotropic factors. • Failure of cardiovascular control mechanisms often requires clinical intervention to help restore normal function.

REFERENCES 1. Patton KT: Anatomy and physiology, ed 9, St Louis, 2016, Elsevier. 2. Neumar RW, Shuster M, Callaway CW, et al: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care, Circulation 132:S315–S367, 2015. 3. Marieb EN, Hoehn KN: Human anatomy and physiology, ed 11, San Francisco, 2018, Pearson Benjamin Cummings. 4. Des Jardins T: Cardiopulmonary anatomy and physiology, ed 6, New York, 2013, Delmar Cengage Learning. 5. Berne RM, Levy MN, editors: Physiology, ed 7th, St Louis, 2017, Elsevier. 6. Barret KE, Barman SM, Boitano S, et al: Ganong’s review of medical physiology, ed 25, New York, 2016, McGraw-Hill. 7. Sanchis-Gomar F, Perez-Quilis C, Leischik R, et al: Epidemiology of coronary heart disease and acute coronary syndrome, Ann Transl Med 4(13):256, 2016. 8. Mozaffarian D, Benjamin EJ, et al: Executive summary: Heart Disease and Stroke Statistics–2016 update: a report from the American Heart Association, Circulation 133:447–454, 2016. 9. Baldzizhar A, Manuylova E, Marchenko R, et al: Ventricular tachycardias: characteristics and management, Crit Care Nurs Clin North Am 28(3):317–329, 2016. 10. Heuer AJ, Scanlan CL: Clinical assessment in respiratory care, ed 8, St Louis, 2018, Elsevier. 11. Leone M, Asfar P, Radermacher P, et al: Optimizing mean arterial pressure in septic shock: a critical reappraisal of the literature, Crit Care 19(1):101, 2015. 12. Asfar P, Meziani F, Hamel JF, et al: High versus low blood-pressure target in patients with septic shock, N Engl J Med 370:1583–1593, 2014. 13. Norton JM: Toward consistent definitions for preload and afterload, Adv Physiol Educ 25:53, 2001.

BIBLIOGRAPHY Andreoli TE, Benjamin I, Griggs RC, et al: Cecil essentials of medicine, ed 9, Philadelphia, 2015, WB Saunders. Guyton AC, Hall JE: Textbook of medical physiology, ed 13, Philadelphia, 2015, WB Saunders. Stevens A, Lowe J: Human histology, ed 4, St Louis, 2015, Mosby.

11  Ventilation Eduardo Mireles-Cabodevila

CHAPTER OBJECTIVES After reading this chapter you will be able to: • Describe the physiologic functions provided by ventilation. • Describe the pressure gradients responsible for gas flow, diffusion, and lung inflation. • Identify the forces that oppose gas movement into and out of the lungs. • Describe how surface tension contributes to lung recoil. • Describe how lung, chest wall, and total compliance are related. • State the factors that affect resistance to breathing.

• Describe how various lung diseases affect the work of breathing. • State why ventilation is not evenly distributed throughout the lung. • Describe how the time constants affect alveolar filling and emptying. • Identify the factors that affect alveolar ventilation. • State how to calculate alveolar ventilation, dead space, and the VD/VT ratio.

CHAPTER OUTLINE Mechanics of Ventilation, 226 Pressure Differences During Breathing, 226 Forces Opposing Inflation of the Lung, 228 Static Versus Dynamic Mechanics, 234 Mechanics of Exhalation, 235

Work of Breathing, 236 Mechanical Work, 236 Metabolic Work, 238 Distribution of Ventilation, 238 Regional Factors Affecting Distribution, 239

Local Factors Affecting Distribution, 240 Efficiency and Effectiveness of Ventilation, 241 Efficiency, 241 Effectiveness of Ventilation, 244

hysteresis minute ventilation physiologic dead space plethysmograph pneumotachometer pressure gradient sub-atmospheric surface tension tidal volume (VT) transairway pressure gradient

transairway pressure (PTAW) transalveolar pressure (PTA) trans–chest wall pressure (PTCW) transmural pressure transpulmonary pressure difference (PTP) transpulmonary pressure gradient transrespiratory pressure (PTR) transthoracic pressure difference (PTT) ventilation

KEY TERMS airway resistance alveolar dead space compliance dynamic compression dynamic hyperinflation (air trapping) elastance elasticity equal pressure point (EPP) hyperventilation hypoventilation

The main functions of the lungs are to supply the body with oxygen and to remove carbon dioxide. To perform these functions, an adequate amount of gas must move from the trachea to the alveoli and then out of the lung. Ventilation is the process of moving gas (usually air) in and out of the lungs. Ventilation is to be distinguished from respiration,

which refers to the physiologic processes of using O2 by the tissues at the cellular level. The amount of air movement (ventilation) is regulated to meet the body’s needs under a wide range of conditions (e.g., exercise). In disease, this process can be markedly disrupted and often results in inadequate ventilation and/or increased work of 225

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breathing. Respiratory care is directed toward restoring and supporting adequate and efficient ventilation. To provide effective respiratory care, the respiratory therapist (RT) must have a solid understanding of the normal ventilation processes and of how diseases may affect it.

MECHANICS OF VENTILATION Ventilation occurs in a cycle with two phases: inspiration and expiration. During each cycle, a volume of gas moves in and out of the respiratory tract. This volume, measured during either inspiration or expiration, is called the tidal volume (VT). The VT refreshes the gas present in the lung, removing CO2 and supplying O2 to meet metabolic needs. The VT must be able to meet changing metabolic demands, such as during exercise or sleep. To achieve ventilation, the respiratory muscles (and/or a mechanical ventilator) have to generate changes in pressure (a pressure gradient, see later discussion) so that gas will flow in or out of the lungs. To better understand the forces that the muscles (or/and the machine) have to overcome to generate ventilation, we use a formula. This formula is a simplified version of the so-called “equation of motion” for the respiratory system: ∆Pressure = (Elastance × ∆Volume) + (Resistance × ∆Flow) where: ΔPressure = Force generated by the respiratory muscles or a mechanical ventilator, or both, during inspiration. This “pressure” is actually a pressure difference or gradient, that is, the difference in pressure (see next section). Volume = Change in volume (e.g., VT, amount of air inspired in a usual breath) Elastance = Distensibility of the lungs and thorax (Δpressure/ Δvolume); elastance is the reciprocal of compliance (Δvolume/ Δpressure) Resistance = Airflow and tissue resistance (Δpressure/Δflow) Flow = Volume change per unit of time In this equation, the terms (elastance × volume) and (resistance × flow) represent the loads (elastic and resistive) against which the respiratory muscles or ventilator must work to achieve gas movement. Thus, you can now see that in patients with high elastance or/and high resistance, the pressure needed to move gas and achieve ventilation will be high. In healthy lungs, this work is minimal and is performed only during the inspiratory phase. Normally, expiration is passive (i.e., no muscle force is involved) as energy stored from the work of inspiration is released (i.e., through the elastic recoil of the lung and chest wall, which will return to their resting volume). In discussing ventilation, it may be helpful to review some details about the equation of motion. First, remember that it is a mathematical model. This model simplifies the respiratory system into a single resistance and a single elastance. That is, it combines all the resistances of the many airways into a single flow-conducting tube and lumps all the elastances of the alveoli and airways into a single elastic compartment (see later discussions about elastance, compliance, and resistance). The graphic model is shown in Fig. 11.1.1 Surrounding the “lungs” is another elastic compartment representing the chest wall. This graphic

PAO Airway opening

Airways

Chest wall Ppl PA Alveoli

Pleural space PBS Body surface

Fig. 11.1  Schematic diagram of the respiratory system consisting of an airway connected to a single alveoli (representing the lungs) surrounded by the chest wall. PA, Alveolar pressure; PAO, pressure at the airway opening; PBS, pressure on the body surface; Ppl, pressure in the intrapleural space.

TABLE 11.1  Measurable Pressures Used in

Describing Respiratory System Mechanics Name

Symbol

Definition

Pressure at the airway opening

PAO

Pleural pressure

Ppl

Alveolar pressure

PA

Body surface pressure

PBS

Pressure measured at the opening of the respiratory system airway (e.g., mouth and nose, tracheostomy opening, and endotracheal tube opening) Pressure measured in the pleural space, changes that are often estimated by measuring pressure changes in the esophagus Pressure in the alveolar (gas space) region of the lungs Pressure measured at the body surface

depiction of the respiratory system allows us to define points in space where pressures may be measured (or inferred) as defined in Table 11.1.

Pressure Differences During Breathing A pressure gradient is needed to achieve gas flow from one place to another. Air rushing out of a punctured tire moves from higher pressure inside the tire to a lower pressure outside the tire (i.e., down a pressure gradient). Using the equation of motion, we can recognize the pressure gradients or differences in pressure between two points in space in each of the components of the model. The discussion that follows will focus on various compartments or individual components of the total respiratory system. The individual components of the model (airways, lungs, and chest wall) are defined as everything that exists between these points in space. Let’s define each of these pressure gradients across different compartments.

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Starting with the whole system, the respiratory system is everything that exists between the pressure measured at the airway opening (PAO) and the pressure measured at the body surface (PBS). The pressure difference is called the transrespiratory pressure (PTR): PTR = PAO − PBS The term PAO comes before the term PBS in the equation. This order is dictated by the direction of flow; at end inspiration, air pressure inside the lung exceeds the pressure outside the lung, so that gas flows out of the lung when expiration begins. During mechanical ventilation, at the end of inspiration, PAO is higher than PBS, and PTR is calculated by subtracting PBS from PAO. The same general principle applies to all the other pressure differences described subsequently. The components of transrespiratory pressure correspond to all the components of the graphic model (i.e., airways, lungs, and chest wall). We can further divide these components and their pressure gradients. Starting at the airways in this model, the pressure gradient across the airways is whatever exists between PAO and pressure measured in the alveoli of the lungs (PA). The graphic model makes the lungs look like one giant alveolus, which means that alveolar pressure represents an average pressure over all alveoli in real lungs. This pressure difference is called the transairway pressure (PTAW): PTAW = PAO − PA Thus, PTAW represents all the airways (physiological and artificial). The alveolar region is whatever exists between pressure measured in the alveolus and pressure measured in the pleural space (Ppl). This associated pressure difference is transalveolar pressure (PTA): PTA = PA − Ppl The PTA represents all the alveoli as if they were one single alveolus. We also take into account the chest wall. The pressure across the chest wall is the difference between the pressure measured in the pleural space and the pressure on the body surface. The pressure difference is called trans–chest wall pressure (PTCW): PTCW = Ppl − PBS Some of these components can be combined to encompass structures that are clinically important. One of the most useful combinations bundles together the airways (PTAW) and the alveolar region (PTA) to assess the whole pulmonary system (airways and alveoli), and this is called the transpulmonary pressure difference (PTP): PTP = PAO − Ppl What may be confusing is that there are other definitions of transpulmonary pressure in the literature. Some authors define PTP as PA − Ppl (i.e., the difference between the pressure in the alveoli and the pleura). The confusion arises from the fact that PTA = PTP = PA − Ppl, but only under static conditions (i.e., when there is no movement of air occurring). Static conditions can be imposed during mechanical ventilation by using an inspiratory

TABLE 11.2  Pressure Differences Used in

Describing Respiratory System Mechanics Definition

Name

Symbol

PAO − PBS PAO − PA PAO − Ppl PA − Ppl PA − PBS Ppl − PBS

Transrespiratory pressure difference Transairway pressure difference Transpulmonary pressure difference Transalveolar pressure difference Transthoracic pressure difference Trans–chest wall pressure difference Global muscle pressure difference

ΔPTR ΔPTAW ΔPTP ΔPTA ΔPTT ΔPTCW ΔPmus

or expiratory hold maneuver which stops air from flowing. This situation should be considered a special case of PTP; however, the general case is PTP = PAO − Ppl, which shows what pressures must be measured to derive the mechanical properties of the pulmonary system under either static or dynamic (active breathing when air is moving) conditions. If we want to evaluate the elastance and resistance of the pulmonary system, we substitute PTP for P in the equation of motion. Alternatively, if we want to evaluate the total respiratory system elastance and resistance, we substitute PTR for P. Sometimes, it may be useful to define the pressure required to expand the lung and chest wall components; to do this, we use the transthoracic pressure difference (PTT), which is defined as: PTT = PA − PBS We use the transrespiratory pressure gradient and the other gradients to understand the gas flow into and out of the alveoli during breathing. Table 11.2 summarizes these equations. For a spontaneously breathing person, PA is sub-atmospheric in the beginning of inspiration compared with PAO. Because “nature hates a vacuum,” and pressure differences want to equalize, air flows into the alveoli when pressure at the airway opening is higher than pressure in the alveoli. The opposite happens when exhalation begins; here, PA is higher than PAO, causing air to flow out of the airway opening as pressure in the alveoli is higher than pressure at the airway opening. During a normal breathing cycle, the glottis remains open. The PBS and PAO remain at zero (i.e., atmospheric) throughout the cycle; only changes in PA and Ppl are of interest. It is often helpful to use these to describe the changes in pressures during a breathing cycle. Before inspiration, pleural pressure is approximately −5 cm H2O (i.e., 5 cm H2O below atmospheric pressure), and alveolar pressure is 0 cm H2O. The transpulmonary pressure gradient is also approximately 5 cm H2O in the resting state, that is, PTP = PAO − Ppl = 0 − (−5) = 5. This positive end-expiratory PTP maintains the lung at its resting volume which is the functional residual capacity (FRC). The definition of functional residual capacity is the volume of the lung at the end of expiration with the glottis open. Airway opening and alveolar pressures are both zero at FRC, so the transairway pressure gradient also is zero. No gas moves into or out of the respiratory tract at FRC.

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450.00 400.00 350.00 300.00 250.00 200.00 150.00 100.00 50.00 0.00 50.00 100.00 150.00 200.00 250.00 5.010 6.000 7.000 8.000 9.000 10.000 Fig. 11.2  Waveforms for Normal Breathing. Red, Change in pleural pressure relative to end-expiratory value (cm H2O, scaled times 10); blue, alveolar pressure (cm H2O, scaled times 10); green, flow (L/min, scaled times 10); purple, volume (mL).

RULE OF THUMB  A way to imagine FRC is to think of a dead patient’s lung volume (or a paralyzed patient). where the glottis is open and there is no muscle activity, then the volume of air in the lungs (the FRC) is the result of a balance of forces; on one side the elastic lungs wanting to shrink and on the other, the recoil of the chest wall trying to expand.

Inspiration begins when muscular effort expands the thorax. Thoracic expansion causes a decrease in pleural pressure. This decrease in pleural pressure causes a positive change to PTP and PTA, which induces air to flow into the lungs down the resulting pressure gradient. The inspiratory flow (i.e., the rate at which air is moving) is proportional to the positive change in transairway pressure difference; the higher the change in PTA, the higher is the flow. Pleural pressure continues to decrease until the end of inspiration. Alveolar filling slows when alveolar pressure approaches equilibrium with the atmosphere, and inspiratory flow decreases to zero (Fig. 11.2). At this point, called end-inspiration, alveolar pressure has returned to zero, and the intrapleural pressure is maximally negative—and hence transpulmonary pressure gradient reaches the maximal value (for a normal breath) of approximately 10 cm H2O. At end inspiration, the muscle pressure relaxes, and the chest wall recoil and lung elastance will lead to an alveolar pressure higher than the pressure at the airway opening, driving flow out of the lung (for expiration). The equation of motion shows this, setting the driving pressure, Pmus, to zero: Pmus = 0 = (Elastance × Volume) + (Resistance × Flow) Rearranging the formula, we get: (Elastance × Volume) = −(Resistance × Flow) = Resistance × (− Flow)

This equation says two important things: (1) Flow is negative (i.e., going out of the lung), indicating expiration, and (2) the driving force (transthoracic pressure, equal to elastance × volume) for expiratory flow is the energy stored in the combined elastances of lungs and chest wall (the total elastance is the sum of the chest wall and lung elastances). These events occur during normal tidal volume excursions. Similar pressure changes accompany deeper inspiration and expiration. The pressure change is greater with deeper breathing. Pleural pressures are always negative (sub-atmospheric) during normal inspiration and exhalation. During forced inspiration with a big downward movement of the diaphragm, the pleural pressure can decrease to −50 cm H2O, whereas during a forced expiration, pleural pressure may increase above atmospheric pressure to 50 to 100 cm H2O.

Forces Opposing Inflation of the Lung The lungs have a tendency to recoil inward, whereas the chest wall tends to move outward; these opposing forces keep the lung at its resting end-expiratory volume (i.e., FRC). To generate the previously described pressure gradients, the lungs must be distended. This distention requires several opposing forces to be overcome for inspiration to occur. As indicated in the equation of motion, the forces opposing lung inflation may be grouped into two categories: elastic forces and frictional forces. Elastic forces involve the tissues of the lungs, thorax, and abdomen, along with surface tension in the alveoli. Frictional forces include resistance caused by gas flow through the airways (natural and artificial) and tissues moving past each other during breathing.

Surface Tension Forces Hysteresis is defined as the dependence of a system on its history or past state. When we apply it to the lungs, hysteresis refers to the difference between inspiratory and expiratory pressure-volume curves exhibited by the lung. That is, for the same pressure, the volume in the lungs in inspiration and expiration are different. The difference in expiratory pressure-volume curve is a result of surface tension forces in the alveoli. To understand this better it is good to review what happens to the lung in the saline versus air-filled state. In Fig. 11.3, you can see that if a lung is filled with fluid such as saline (fluid-filled), then less pressure is needed to a given volume (higher compliance) and minimal hysteresis than an air-filled lung. This phenomenon indicates that a gasfluid interface in the air-filled lung changes its inflation-deflation characteristics. The recoil of the lung, its tendency to collapse, is a combination of tissue elasticity and the surface tension forces in the alveoli. During inflation, additional pressure is needed to overcome surface tension forces. During deflation, surface tension forces are reduced, resulting in altered pressure-volume characteristics (i.e., the leftward shift seen in Fig. 11.3). In the intact lung (i.e., within the chest), the volume history also affects the degree of hysteresis that occurs. Factors such as the initial volume, the tidal excursion, and whether the lungs have been previously inflated or deflated help determine the volume history and the shape of the pressure-volume curves of the lung.

CHAPTER 11  Ventilation

229

MINI CLINI

Volume

Surfactant Replacement Therapy and Lung Mechanics Saline filled

Air filled

Pressure Fig. 11.3  Static Pressure-Volume Curves of Saline-Filled and AirFilled Excised Lungs. In the saline-filled lung, the distending pressure is the same during inflation and deflation. The air-filled lung shows hysteresis (i.e., higher pressure for a given volume on inflation compared with deflation). The hysteresis results in part from the effects of surface tension forces caused by the air-liquid interface in the alveoli. (Modified from Slonim NB, Hamilton LH: Respiratory physiology, ed 5, St Louis, 1987, Mosby.)

RULE OF THUMB  Patients with severe lung disease and requiring mechanical ventilation may be subject to a recruitment maneuver. These maneuvers (several techniques exist) consist of increasing the pressure in the airway to regain inflation of the lung. The goal is to open alveoli that are closed, minimize the surface tension, and regain ventilated lung tissue to decrease the pressures needed to provide mechanical ventilation.

This phenomenon is dependent on the surface tension of the lung. Surface tension is the tendency of a fluid surface to become as small as possible (think of a water drop, which is as small as it can be based on the attraction of its molecules). In the alveoli, the alveoli wall is covered with fluid, which is trying to reduce its size (collapse). Thanks to pulmonary surfactant it does not. The lung surface tension is dependent on the presence and function of pulmonary surfactant. A surfactant is any substance that reduces the surface tension. The mechanism of action of pulmonary surfactant molecules is based on their weak intra-molecular attractive forces. When surfactant molecules are mixed with other liquid molecules that have higher intra-molecular attraction, the surfactant molecules are pushed to the surface of the liquid, where they form the airliquid interface. Because of the weak intra-molecular attraction between these surfactant molecules at the surface, the liquid lining of the alveoli exhibits much less surface tension than it would in the absence of pulmonary surfactant. In a premature infant with inadequate surfactant, the intra-alveolar surface tension is abnormally high; this produces a collapsing force that increases lung recoil and reduces lung compliance. Greater muscular effort is required to overcome increased recoil during inspiration and the work of breathing is increased. The infant’s inspiratory muscles may eventually become fatigued, leading to ventilatory failure. Instillation of artificial surfactant into the lungs reduces surface tension to its normal level. Lung compliance is increased, elastic recoil is reduced, and the muscular work required to inflate the lung is reduced.

Problem If an infant is born prematurely, the lungs may be unable to produce adequate amounts of pulmonary surfactant. How does this condition affect lung mechanics and what effect does surfactant replacement therapy have on lung compliance and the work of breathing? Discussion The liquid molecules that line each alveolus attract one another. This attraction creates a force called surface tension, which tends to shrink the alveolus. A phospholipid called pulmonary surfactant reduces surface tension in the lung. Alveolar type II cells produce pulmonary surfactant. In contrast to typical surfaceactive agents, pulmonary surfactant changes surface tension according to its area.2 The ability of pulmonary surfactant to reduce surface tension decreases as surface area (i.e., lung volume) increases. Conversely, when surface area decreases, the ability of pulmonary surfactant to reduce surface tension increases. This property of changing surface tension to match lung volume helps stabilize the alveoli. Any disorder that alters this can cause significant changes in the work of breathing.

RULE OF THUMB Surfactant is essential for lung function. When the patient exhales, the size of the alveoli decreases, thus there is “more” surfactant in relation to the size of the alveoli, therefore less tension surface (less pressure needed to expand). As the lung expands, the alveoli is larger, so there is “less” surfactant in relation to the size of the alveoli, therefore more tension surface (this homogenizes lung inflation and deflation).

Elastic Forces Opposing Lung Inflation Elastin and collagen fibers are found in the lung parenchyma. These fibers give the lung the property of elasticity. Elasticity is the physical tendency of an object to return to an initial state after deformation. Like a balloon when stretched, an elastic body tends to return to its original shape. The tension developed when an elastic structure is stretched is proportional to the degree of deformation produced (Hooke’s law). An example is a simple spring (Fig. 11.4). When tension on a spring is increased, the spring lengthens. However, the ability of the spring to stretch is limited. When the point of maximal stretch is reached, further tension produces little or no increase in length. Additional tension may break the spring. In the respiratory system, inflation stretches tissue. The elastic properties of the lungs and chest wall oppose inflation. To increase lung volume, pressure must be applied. This property may be shown by subjecting an excised lung to changes in transpulmonary pressure and measuring the associated changes in volume (Fig. 11.5). To simulate the pressures during breathing, the lung is placed in an airtight jar. The force to inflate the lung is provided by a pump that creates a vacuum around the lung inside the jar, simulating the negative Ppl. This action mimics the pleural pressure changes associated with thoracic expansion and contraction. The changes in transpulmonary pressure allow the lungs to come to rest in between, so that all of the applied pressure opposes elastic forces and none of it opposes resistive forces (i.e., flow is zero when the measurements are made). The amount of

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SECTION II  Applied Anatomy and Physiology

B

C

Length

A

Force Fig. 11.4  Graphic representation of the force-length relationship applied to a simple spring (increase in length with increase in force). With increasing force, or weight in this example, the spring lengthens from A to B, but at the point of maximal stretch, further force produces no additional increase in length (B to C).

Volume (L) 1.0

Volume Pump

0.5 Pressure Lung 0 –10 –20 –30 Pressure around lung (cm water)

Fig. 11.5  Measurement of the Pressure-Volume Curve of an Excised Lung. The lung is placed in a sealed jar and connected to a spirometer (to measure volume). A pump generates sub-atmospheric pressure around the lung while its volume is measured. The curve plotting the relationship between pressure and volume is nonlinear and flattens at high expanding pressures (sub-atmospheric). The inflation and deflation curves are not the same. This difference is called hysteresis.

stretch (inflation) is measured as volume by a spirometer. Changes in volume resulting from changes in transpulmonary pressure are plotted on a graph. During inspiration in this model, increasingly greater negative pleural pressures are required to stretch the lung to a larger volume. As the lung is stretched to its maximum (total lung capacity [TLC]), the inflation curve becomes flat. This flattening indicates increasing opposition to expansion (i.e., for the same change in transpulmonary pressure, there is less change in volume).3 As with a spring when tension is removed, deflation occurs passively as pressure in the jar is allowed to return toward atmospheric pressure. Deflation of the lung does not follow the

inflation curve exactly. During deflation, lung volume at any given pressure is slightly greater than it is during inflation. This difference between the inflation and deflation curves is called hysteresis.3 In other words, the pressure needed to inflate the lung from its empty state is not the same (and greater, in fact) as the pressure gradient associated with deflating the lung from its full state. Hysteresis indicates that factors other than simple elastic tissue forces are present. The major factor contributing to the increased pressure needed to inflate the lung, particularly in sick lungs, is the opening of collapsed alveoli during inspiration that tend to stay open during expiration until very low lung volumes are reached.

CHAPTER 11  Ventilation

lungs become more distensible (i.e., more compliant) so that a normal transpulmonary pressure results in a larger lung volume. The term hyperinflation is used to describe an abnormally increased lung volume. A distinctly opposite pattern is seen in pulmonary fibrosis, where the lung becomes less compliant, or stiffer. Interstitial fibrosis is characterized by an increase in connective tissue in the lung and increased stiffness of the lung. The compliance curve of a patient with pulmonary fibrosis is therefore flatter than the normal curve (i.e., shifted down and to the right), indicating that more pressure is needed to produce the same degree of lung inflation. As a result, there is a smaller volume change for any given pressure change (decreased compliance). Inflation and deflation of the lung occur with changes in the dimensions of the chest wall. The relationship between the lungs and the chest wall can be illustrated by plotting their relaxation pressure curves separately and combined (see Fig. 11.7). In the intact thorax, the lungs and chest wall recoil against each other. The point at which these opposing forces balance determines the resting end-expiratory volume of the lungs, or FRC. This is also the point at which alveolar pressure equals atmospheric pressure. The normal FRC is approximately 40% of the TLC. The opposing forces between the chest wall and lungs are partially responsible for the sub-atmospheric pressure in the intrapleural space. Diseases that alter the compliance of either the chest wall or the lung often disrupt the balance point, usually with a change in lung volume. With stiffer lungs, FRC is reduced and with more compliant lungs, FRC increases.

Compliance Compliance (C, the reciprocal of elastance, E) is caused by the tissue elastic forces and surface tension that oppose lung inflation. Compliance is defined as the ratio between volume (V) and pressure (P) in an elastic system and is usually expressed in units of mL/cm H2O: C=

∆V 1 = ∆P E

RULE OF THUMB  A more intuitive way to think about the compliance of the respiratory system is to ask: How much pressure across the whole respiratory system is needed to inflate the lung maximally (to TLC)? The more compliant the lung, the less the pressure needed to inflate it and the less compliant (i.e., stiffer) the lung, the more pressure needed.

To calculate lung compliance, ΔPTP is substituted for ΔP. To calculate respiratory system compliance, use ΔPTR. To calculate chest wall compliance, use ΔPTCW. A graph of change in lung volume versus change in transpulmonary pressure (Fig. 11.6A) is called the compliance curve of the lungs. Fig. 11.6B compares a normal lung compliance curve with curves that might be observed in patients who have emphysema (obstructive lung disease) or pulmonary fibrosis (restrictive lung disease). The curve from a patient with emphysema is steeper and displaced to the left. The shape and position of this curve represent large changes in volume for small pressure changes (increased compliance). Increased compliance results primarily from loss of elasticity due to breakdown of elastic fibers in the alveolar walls, which occurs in emphysema. The

Combined Compliances The two lungs have their own (usually different) compliances. However, the muscles (or ventilator) see the net effect of all the combined compliances. Because the lungs have the same driving

em ph

ys

4 3

Em

Lung volume (L)

Lung volume (L)

a

5

al

m

r No

osis

Fibr

2 1

Transpulmonary pressure (cm H2O)

A

231

0

B

10

20

30

Transpulmonary pressure (cm H2O)

Fig. 11.6  (A) Compliance measurement (deflation curve). After swallowing an esophageal balloon, the person inhales a full breath and then exhales slowly. At specific lung volumes, he holds his breath with the glottis open, ensuring an alveolar pressure of zero. Lung volume is plotted against transpulmonary pressure (esophageal pressure is assumed to reflect pleural pressure) generating a compliance curve. (B) Compliance curves. Normal lung compliance is approximately 0.2 L/cm H2O (measured from the lower portion of the curve, near resting lung volume). Compliance is increased in emphysema because of the destruction of elastic tissue; conversely, it is decreased in pulmonary fibrosis because of increased elastic recoil. (Modified from Martin L: Pulmonary physiology in clinical practice: the essentials for patient care and evaluation, St Louis, 1987, Mosby.)

40

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SECTION II  Applied Anatomy and Physiology

Lung-Thorax Relaxation Pressure Curve 100

Expiration

TLC

Inspiration D

80 Thorax

Vital capacity (%)

60 40

B

a

C

b

20

Lungs Functional residual capacity

A 0

Lungs and thorax Residual volume

–30

–20

Minimal air –10

0

+10

+20

+30

Intrapulmonary pressure (mm Hg) Fig. 11.7  Relationship Between the Lungs and Chest Wall. Volumes of the lungs, thorax, and lungs and thorax combined are plotted as a percentage of vital capacity against intrapulmonary pressure (recoil pressure). The combined lung-thorax relaxation curve (solid line) is the sum of the individual lung and thorax curves. Equilibrium (zero pressure) occurs where the lung and thoracic recoil forces balance (a + b = 0). This point determines the functional residual capacity (lung B). Lung A represents low lung volume with greater recoil pressure exerted by the chest wall. Lung C shows a chest wall recoil of zero at approximately 70% of total lung capacity (TLC). When lung volume is greater than 70% of TLC, greater pressures are required to distend both the lungs and the thorax (lung D). (Modified from Beachey W: Respiratory care anatomy and physiology, ed 2, St Louis, 2007, Mosby.)

pressure but different flows in the right versus the left lung, they are said to be connected in parallel. Parallel compliances combine by simple addition: Parallel compliances : Ctotal = Cright + Cleft The total compliance of a parallel connection is more than any of the components. The total lung compliance is connected in series with the chest wall compliance, meaning they have different driving pressures but the same flow. Series compliances combine as follows: Series compliances : Ctotal =

Cchestwall × Clungs Cchestwall + Clungs

The total compliance of a series connection is less than any of the components. RULE OF THUMB  The lungs and chest wall each have their own compliance, or distensibility. In healthy adults, the compliance of the lungs and chest wall are each equal to approximately 0.2 L/cm H2O. However, because the lungs are contained within the thorax, the two systems act as springs pulling against the driving force. This reduces the compliance of the system to approximately half that of the individual components, or 0.1 L/cm H2O. Obesity, kyphoscoliosis, ankylosing spondylitis, and many other abnormalities can reduce chest wall compliance and lung volumes.

Inhalation occurs when the balance of forces between the lungs and chest wall shifts. Energy from the respiratory muscles (primarily the diaphragm) overcomes the tendency of the lungs to contract. At the beginning of the breath, the tendency of the chest wall to expand facilitates lung expansion. When lung volume nears 70% of the TLC, the chest wall reaches its natural resting level. To inspire to a lung volume greater than approximately 70% of TLC, the inspiratory muscles must overcome the recoil of both the lungs and the chest wall (see Fig. 11.7). For exhalation, potential energy “stored” in the stretched lung (and chest wall at high volumes) during the preceding inspiration allows the lungs to empty passively (i.e., without forcing air out). Still, to exhale below the resting level of the lung (FRC), muscular effort is required to overcome the tendency of the chest wall to expand.

Resistive Forces Opposing Lung Inflation Frictional forces also oppose ventilation. Frictional opposition forces differ from the elastic properties of the lungs and thorax. Frictional opposition occurs only when the system is in motion; there is no friction when there is no motion. Frictional opposition to ventilation has two components—tissue viscous resistance and airway resistance. Tissue viscous resistance.  Tissue viscous resistance is the impedance of motion (opposition to flow) caused by displacement

CHAPTER 11  Ventilation

of tissues during ventilation. Displaced tissues include the lungs, rib cage, diaphragm, and abdominal organs. The frictional resistance is generated by the movement of each organ surface sliding against the other (e.g., the lung lobes sliding against each other and against the chest wall). Tissue resistance accounts for only approximately 20% of the total resistance to lung inflation. However, in conditions such as obesity, pleural fibrosis, and ascites, the tissue viscous resistance will increase the total impedance to ventilation. Airway resistance.  Gas flow through the airways also causes frictional impedance, called flow resistance. Resistance to ventilation by the movement of gas through the airways is called airway resistance. Airway resistance accounts for approximately 80% of the frictional resistance to ventilation. Resistance is defined as the ratio between pressure (P) and flow (V̇ ) in a flow-conducting system and is usually expressed in units of cm H2O/L per second: R=

∆P ∆V

To calculate airway resistance, Raw, use ΔPTA instead of ΔP. To calculate respiratory system resistance, use ΔPTR. Airway resistance in healthy adults ranges from approximately 0.5 to 2.5 cm H2O/L per second. To cause gas to flow into or out of the lungs at 1 L/s, a healthy person needs to lower his or her alveolar pressure only 0.5 to 2.5 cm H2O below atmospheric pressure. Raw in spontaneously breathing patients is usually measured in a pulmonary function laboratory. Flow is measured with a pneumotachometer. Alveolar pressures are determined in a body plethysmograph, an airtight box in which the patient sits. By momentarily occluding the patient’s airway and measuring the pressure at the mouth, alveolar pressure can be estimated (i.e., mouth pressure equals alveolar pressure under conditions of no flow). By relating flow and alveolar pressure to changes in plethysmograph pressure, airway resistance can be calculated.

Combined Resistances The right and left main stem bronchi have their own (usually different) resistances. However, the muscles (or ventilator) see a combined resistance from both the right and left lungs together. Because these airways have the same driving pressure but different flows, they are said to be connected in parallel. Parallel compliances combine like compliances in series, as follows: Parallel resistances : Rtotal =

Rright × Rleft Rright + Rleft

The total resistance of a parallel connection is less than that of any of the components. The bronchial airway resistance is connected in series with upper airway (and artificial airway, if any), meaning that they have different driving pressures but the same flow. Series resistances combine like compliances in parallel: Series resistance : Rtotal = Rupper airway + Rbronchi

233

MINI CLINI Helium and Oxygen Therapy for Large Airway Obstruction Problem Patients with significant obstruction in the upper airway, trachea, or main stem bronchi expend a large amount of energy overcoming the resistance to breathing. What type of gas therapy would be most advantageous in this situation? Discussion Because most (approximately 80%) of the resistance to breathing occurs in the upper and large airways, disease processes that increase resistance in these airways cause tremendous increases in the work of breathing. Vocal cord edema, tumors in the trachea, and foreign bodies in main stem bronchi are examples of the types of clinical conditions that can markedly increase the work of breathing. Patients who must breathe against high levels of resistance are prone to respiratory muscle fatigue and failure. Gas flow in the upper and large airways is predominantly turbulent. Turbulent flow is highly influenced by gas density. Patients with large airway obstruction often can be treated with a mixture of helium and O2 (heliox or HeO2) because helium is approximately 6 times less dense than air. The lower density allows helium to flow more rapidly under conditions of turbulent flow. Thus, HeO2, usually an 80/20 or 70/30 mixture, can be administered to reduce the work of breathing until the obstructive process can be treated (see Chapter 42). A HeO2 mixture does little for patients with small airway obstruction, as occurs in emphysema or asthma, because flow in the small airways is mainly laminar and largely independent of the density of the gas breathed. However, heliox therapy can be used for patients with small airway obstruction to allow them to exercise longer and more strenuously with less dyspnea and dynamic hyperinflation.

The total resistance of a series connection is more than that any of the components. Factors affecting resistance.  The two main patterns that characterize the flow of gas through the respiratory tract are laminar flow and turbulent flow (see Chapter 6). A third pattern, tracheobronchial flow, is a combination of laminar and turbulent flow. Laminar flow requires less driving pressure than turbulent flow. Poiseuille’s equation (see Chapter 6) describes laminar flow through a smooth, unbranched tube of fixed dimensions (i.e., length and radius). This equation says that for gas flow to remain constant, the pressure is inversely proportional to the fourth power of the airway’s radius. That is, by reducing the radius of a tube by half requires a 16-fold pressure increase to maintain a constant flow (24 = 16)! Clinically, this means that to maintain ventilation in the presence of narrowing airways, large increases in driving pressure may be needed, resulting in marked increases in the work of breathing. RULE OF THUMB  A change in the radius of an airway by a factor of 2 causes a 16-fold change in resistance. If the size of a patient’s airway is reduced from 2 to 1 mm, airway resistance increases by a factor of 16. Similarly, increasing the size of an endotracheal tube from 4.5 to 9 decreases 16-fold the pressure needed to achieve the same flow.

Distribution of resistance.  Approximately 80% of the resistance to gas flow occurs in the nose, mouth, and large airways,

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SECTION II  Applied Anatomy and Physiology

4

500

Raw (cm H2O/L/sec)

Total cross section area (cm2)

400

300

200

Conducting zone

2

Resp. zone 0

100 Terminal bronchioles 0

5

10 15 Airway generation

20

23

Fig. 11.8  Cross-Sectional Area of the Airways Plotted Against Airway Generation. The first 15 or 16 airway generations represent a conducting zone in which gas moves primarily by bulk flow, and no gas exchange takes place. These airways make up the anatomic dead space (see Chapter 9). The gas-exchange surface increases markedly at the level of the terminal bronchiole.

TABLE 11.3  Distribution of Airway

Resistance Location

Nose, mouth, upper airway Trachea and bronchi Small airways ( 1

V/Q = 1 Normal

V/Q < 1

Venous admixture

V/Q = 0

Anatomical shunt

When a low PaO2 is observed, the RT must take into account the normal decrease in arterial O2 tension that occurs with aging. As shown in Fig. 12.17, for an individual breathing air at sea level, the “normal” DA–aO2 increases in a nearly linear fashion with increasing age (shaded area). This increase in DA–aO2 results in a gradual decline in PaO2 over time and is probably caused by reduced surface area in the lung for gas exchange and increases in V/Q mismatching. A PaO2 of 85 mm Hg in a 60-year-old adult would be interpreted as normal, but the same PaO2 in a 20-yearold adult would indicate hypoxemia. The expected PaO2 in older adults may be estimated by using the following formula: Expected PaO2 = 100 − (0.323 × Age in years)

Fig. 12.16  Range of V/Q ratios. (Modified from Martin L: Pulmonary physiology in current practice: the essentials for patient care and evaluation, St Louis, 1987, Mosby).

Hemoglobin deficiencies.  Normal PaO2 does not guarantee adequate arterial O2 content or delivery. For arterial O2 content to be adequate, there also must be enough normal Hb in the blood. If the blood Hb is low—even when PaO2 is normal—tissue

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SECTION II  Applied Anatomy and Physiology

105 100 95

PO2 (mm Hg)

90 85 80 75 70 65 20

40

60

80

100

Age in years PAO2

PaO2

Fig. 12.17  Relationship Between PA−aO2 and aging. As PaO2 naturally decreases with age, PA−aO2 increases at the rate of approximately 3 mm Hg each decade beyond 20 years. (Modified from Lane EE, Walker JF: Clinical arterial blood gas analysis, St Louis, 1987, Mosby.)

Reduction in Blood Flow (Shock or Ischemia) Because O2 delivery depends on both arterial O2 content and cardiac output, hypoxia can still occur when the CaO2 is normal and blood flow is reduced. There are two types of reduced blood flow: (1) circulatory failure (shock) and (2) local reductions in perfusion (ischemia). Circulatory failure (shock).  In circulatory failure, tissue O2 deprivation is widespread. Although the body tries to compensate

20

Hb 15 g/dL

16 CaO2 (mL/dL)

hypoxia can occur because of low O2 content in the arterial blood. Relative Hb deficiencies are caused by abnormal forms of Hb and were discussed earlier in this chapter. Hb deficiencies, or anemias, can be either absolute or relative. Absolute Hb deficiency occurs when the Hb concentration is lower than normal. Relative Hb deficiencies are caused by either the displacement of O2 from normal Hb or the presence of abnormal Hb variants. A low blood Hb concentration may be caused either by a loss of RBCs, as with hemorrhage, or by inadequate erythropoiesis (formation of RBCs in the bone marrow). Regardless of the cause, a low Hb content can seriously impair the O2-carrying capacity of the blood even in the presence of a normal supply (PaO2) and adequate diffusion.5 Fig. 12.18 plots the relationship between arterial O2 content and PaO2 as a function of Hb concentration. As can be seen, progressive decreases in blood Hb content causes large decreases in arterial O2 content (CaO2). A 33% decrease in Hb content (from 15 to 10 g/dL) reduces CaO2 as much as would a decrease in PaO2 from 100 to 40 mm Hg.

Hb 10 g/dL

12 8

Hb 5 g/dL

4 0

Hb 0 g/dL 0

20

40

60

80

100

120

140

PaO2 (torr) Fig. 12.18  Relationship Between CaO2 and PaO2 as a Function of Blood Hb Concentration. Progressive decreases in Hb cause large decreases in CaO2.

for the lack of O2 by directing blood flow to vital organs, this response is limited. Prolonged shock ultimately causes irreversible damage to the central nervous system and eventual cardiovascular collapse. Local reductions in perfusion (ischemia).  Even when wholebody perfusion is adequate, local reductions in blood flow can cause localized hypoxia. Ischemia can result in anaerobic metabolism, metabolic acidosis, and eventual death of the affected tissue. Myocardial infarction and stroke are examples of ischemic conditions that can cause hypoxia and tissue death.

265

CHAPTER 12  Gas Exchange and Transport

MINI CLINI

Pathologic

Effect of Anemia on Oxygen Content Normal

•

VO2

In its most common form, anemia is a clinical disorder in which the number of RBCs is decreased. Because RBCs carry Hb, anemia decreases the amount of this O2-carrying protein. Problem What effect would anemia that causes a progressive decrease in Hb from (a) 15 g/dL, to (b) 12 g/dL, to (c) 8 g/dL, to (d) 4 g/dL have on the amount of O2 carried in a patient’s blood? Assume that PO2 and saturation stay normal at 100 mm Hg and 97%. Discussion 1. Calculate dissolved O2 the same way for all four examples as follows: Dissolved O2 = 100 × 0.003 = 0.30 mL dL 2. Compute chemically combined O2 as follows: Chemically combined O2 = Hb (g/dL) × 1.34 mL/g × SaO2 a. 15 g/dL × 1.34 mL/g × 0.97 = 19.50 mL/dL b. 12  g/dL × 1.34 mL/g × 0.97 = 15.60 mL/dL c. 8 g/dL × 1.34 mL/g × 0.97 = 10.40 mL/dL d. 4  g/dL × 1.34 mL/g × 0.97 = 5.20 mL/dL 3. Compute total O2 content as follows: CaO2 = Dissolved O2 + Chemically combined O2 a. 0.30 + 19.50 = 19.80 mL/dL b. 0.30 + 15.60 = 15.90 mL/dL c. 0.30 + 10.40 = 10.70 mL/dL d. 0.30 + 5.20 = 5.50 mL/dL Loss of Hb decreases the amount of O2 carried in a patient’s blood even though PO2 and saturation remain normal. With an Hb concentration of 4 g/ dL, the amount of O2 carried in a patient’s blood is only approximately onefourth the normal concentration (5.50 vs. 19.80 mL/dL).

Dysoxia Dysoxia is a form of hypoxia in which the cellular uptake of O2 is abnormally decreased. The best example of dysoxia is cyanide poisoning. Cyanide disrupts the intracellular cytochrome oxidase system, preventing cellular use of O2. Dysoxia also may occur when tissue O2 consumption becomes dependent on O2 delivery. Fig. 12.19 plots tissue O2 consumption (VO2 ) against O2 delivery (DO2) in both normal and pathologic states. Normally, VO2 increases along with DO2, until a critical threshold (dashed line) is reached, after which the line becomes flat and VO2 does not change. In certain diseases, such as septic shock, trauma, or ARDS, VO2 will become more dependent on DO2 and will increase proportionally with DO2. If the demand for VO2 is not met with the proportional increase in DO2, anaerobic metabolism develops, which leads to the accumulation of lactic acid. RULE OF THUMB  Lactic acid level is often used for a quick assessment of circulatory function. In cases of circulatory failure, such as cardiogenic or septic shock, O2 delivery to the tissues is greatly reduced. Changes in lactic acid level over time can also be used as a measure of the effectiveness of medical interventions in patients with shock.

Calculate (1) O2 delivery, (2) O2 extraction ratio, and (3) shunt fraction. Discuss the causes of abnormal values. What would be the potential interventions to increase his O2 delivery?

DO2 Fig. 12.19  Supply Dependence of Oxygen Consumption (V̇ o2). Under normal conditions (solid line), V̇ o2 will increase until a critical threshold (dashed line) of delivered oxygen (Do2) is reached. Beyond this critical threshold, V̇ o2 remains stable despite the increase in Do2. In pathologic conditions (dotted line), such as acute respiratory distress syndrome, V̇ o2 may not plateau but will continue to rise as Do2 increases until well past the normal critical threshold. (From Heuer AJ, Scanlan, CL: Wilkins’ clinical assessment in respiratory care, ed 7, St. Louis, 2018, Elsevier.)

Impaired Carbon Dioxide Removal

Any disorder that decreases alveolar ventilation (V̇ A) relative to metabolic need impairs CO2 removal. Impaired CO2 removal by the lung causes hypercapnia and respiratory acidosis (see Chapter 14). A decrease in alveolar ventilation occurs when (1) the minute ventilation is inadequate, (2) the dead space ventilation per minute is increased, or (3) a V/Q imbalance exists.4–8

Inadequate Minute Ventilation Clinically, inadequate minute ventilation is caused by decreased tidal volume or respiratory rate. Inadequate minute ventilation occurs in restrictive conditions such as atelectasis, neuromuscular disorders, or impeded thoracic expansion (e.g., kyphoscoliosis). A decrease in respiratory rate is less common but may be present with respiratory center depression, as in drug overdose. Increased Dead Space Ventilation An increase in dead space ventilation, or VD/VT, is caused by either (1) decreased tidal volume (as with rapid, shallow breathing) or (2) increased physiologic dead space as in various lung diseases. In either case, wasted ventilation increases. Without compensation, alveolar ventilation per minute is decreased and CO2 removal is impaired. Ventilation/Perfusion Imbalances Theoretically any V/Q imbalance should cause an increase in PaCO2. However, PaCO2 does not always increase in these cases. Many patients who are hypoxemic because of a V/Q imbalance have a low or normal PaCO2. This common clinical finding suggests that V/Q imbalances have a greater effect on oxygenation than on CO2 removal. Careful inspection of the O2 and CO2 dissociation curves supports this finding. The O2 and CO2 dissociation curves are plotted on the same scale in Fig. 12.20. The upper CO2 curve is nearly linear in the physiologic range. The lower O2 curve is almost flat in the physiologic range. Point a on each curve is the

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MINI CLINI

Problem A patient is admitted to the ICU with pneumonia. Various devices are placed for monitoring. The following data are obtained: pH PCO2 (mm Hg) PaO2 (mm Hg) SaO2 FiO2 Cardiac output (L/min) Hgb (g/dL) VO2 (mL/min)

7.24 32 60 0.9 0.7 6 8 200.00

Discussion 1. Calculate the oxygen delivery: DO2 = CaO2 × C.O. = (1.39 × Hgb × SaO2 + 0.003 × PaO2 ) × C.O. = (1.39 × 8 × 0.9 + 0.003 × 60) × 60 = 10.18 (mL dL) × 60 (dL min) = 610.8 mL min

60 O2 or CO2 content (mL/100 mL blood)

Note that this is a comprehensive Mini Clini and will draw on information from the various parts of this chapter.

CO2

50

V/Q

40 30

V/Q 20

v/Q

a

O2

10

20 40 60 80 100 120 140 Partial pressure (mm Hg) Fig. 12.20  V/Q Imbalance and Dissociation Curves for CO2 and O2. V/Q represents low V/Q units, and V/Q represents high V/Q units. See text for discussion.

Normal values PaO2 100 PaCO2 40

VO2 DO2 = 200 610.8 = 33% Extraction fraction is increased to maintain O2 consumption in the setting of reduced O2 delivery. 3. Calculate the shunt fraction: Q s CcO2 − CaO2 = Q t CcO2 − C v O2

DA −aO2 = PAO2 − PaO2 = FiO2 × (PB − PH2O ) − (PACO2 ÷ RQ)

V/Q

a

Note that the C.O. of 6 L/min was changed to 60 dL/min to maintain the uniformity of values. Overall, O2 delivery is reduced mainly due to reduction in Hgb and SaO2 despite modest increase in C.O. 2. Calculate the oxygen extraction ratio:

Remember that the actual shunt fraction calculation is deferred in clinical practice because of its complexity. The following estimate (see this chapter’s section on shunt fraction) is often used: each increase of DA–aO2 by 100 mm Hg corresponds to a 5% increase in shunt fraction. Now, to calculate DA–aO2,

v/Q

v/Q

V/Q imbalance

PaO2 40 PaCO2 55 Response to hypercapnia and hypoxemia: increased VE

No response to hypercapnia and hypoxemia: unchanged VE

− PaO2 = 0.7 × (760 − 47) − (32 0.8) − 60 = 399 Shunt fraction is estimated to be increased by 20%. Assuming a “normal” shunt fraction of 5%, the total shunt fraction in this patient can be estimated at 25%. This increase is due to severe V/Q imbalance caused by pneumonia and possible ARDS. Potential interventions to increase O2 delivery would be aimed to improve the components of the following O2 delivery formula: Hgb (blood transfusion), SaO2 and/or PaO2 (increased PEEP or FiO2), and C.O. (administration of vasopressors). In clinical practice, the interrelationships between these variables are very complex and the ultimate decision is often made after consideration of multiple factors. For example, an increase in PEEP will increase SaO2 but may also decrease cardiac output by decreasing venous return to the heart. The overall impact on DO2 may be deleterious, as the increase in SaO2 may be dwarfed by the decrease in C.O.

PaO2 55 PaCO2 40

PaO2 40 PaCO2 55

Fig. 12.21  Changes in PaO2 and PaCO2 Caused by V/Q Imbalance. All values are given in millimeters of mercury (mm Hg).

normal arterial point for both content and partial pressure. To the right of the graph are two lung units, one with a low V/Q and the other with a high V/Q. The blood O2 and CO2 contents from each unit are plotted on the curves. The final CO2 content, arrived at by averaging the high and low V/Q points, is shown as point a on the CO2 curve. This point is the same as the normal arterial point for CO2. Patients with significant V/Q imbalances must compensate for high PCO2 coming from underventilated units. To compensate for these high PCO2 values, the patient’s minute ventilation must increase (see Fig. 12.21). Patients who can increase their minute

CHAPTER 12  Gas Exchange and Transport

ventilation tend to have either normal or low PaCO2, combined with hypoxemia. Conversely, patients with V/Q imbalance who cannot increase their minute ventilation are hypercapnic. Hypercapnia generally occurs only when the V/Q imbalance is severe and chronic, as in severe COPD. Such patient must sustain a much higher than normal minute ventilation just to maintain normal PaCO2. If the energy costs required to sustain a high minute ventilation are prohibitive, the patient opts for less work—and hence elevated PaCO2.

SUMMARY CHECKLIST • Movement of gases between the lungs and the tissues depends mainly on diffusion. • PACO2 varies directly with CO2 production and inversely with alveolar ventilation. • PAO2 is computed using the alveolar air equation. • With a constant FiO2, PAO2 varies inversely with PACO2. • Normal PAO2 averages 100 mm Hg, with mean PACO2 of approximately 40 mm Hg. • Normal mixed venous blood has a PO2 of approximately 40 mm Hg and PCO2 of approximately 46 mm Hg. • V/Q must be in balance for pulmonary gas exchange to be effective. Because of normal anatomic shunts and V/Q imbalances, pulmonary gas exchange is imperfect. • In disease, V/Q can range from zero (perfusion without ventilation or physiologic shunting) to infinity (pure alveolar dead space). • Blood carries a small amount of O2 in physical solution, and larger amounts are carried in chemical combination with erythrocyte Hb. • Hb saturation is the ratio of oxyhemoglobin to total Hb, expressed as a percentage. • To compute total O2 contents of the blood, add the dissolved O2 content (0.003 × PO2) to the amount of O2 carried by hemoglobin (1.34 × Hb × SaO2) • The arteriovenous O2 content difference, Ca–vO2, is the amount of O2 given up by every 100 mL of blood on each pass through the tissues. All else being equal, Ca–vO2 varies inversely with cardiac output.

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• Hb affinity for O2 increases with high PO2, high pH, low temperature, and low levels of 2,3-DPG. • Hb abnormalities can affect O2 loading and unloading and can cause hypoxia. • Most CO2 (approximately 80%) is transported in the blood as ionized bicarbonate; other forms include carbamino compounds and physical solution. • Changes in CO2 levels modify the O2 dissociation curve (Bohr effect). Changes in Hb saturation affect the CO2 dissociation curve (Haldane effect). These changes are mutually beneficial, assisting in gas exchange at the lung and the cellular level. • Hypoxia occurs if (1) the arterial blood O2 content is decreased, (2) blood flow is decreased, or (3) abnormal cellular function prevents proper uptake of O2. • Decreased PaO2 level may be a result of a low ambient PO2, hypoventilation, impaired diffusion, V/Q imbalances, and right-to-left anatomic or physiologic shunting. • A decrease in alveolar ventilation occurs when (1) the minute ventilation is inadequate, (2) dead space ventilation is increased, or (3) a V/Q imbalance exists.

REFERENCES 1. Mottram C: Ruppel’s manual of pulmonary function testing, ed 11, St Louis, 2017, Elsevier. 2. Hennessey I, Japp A: Arterial blood gases made easy, ed 2, St Louis, 2015, Churchill Livingstone. 3. Rose BD, Post TW, Stakes J: Clinical physiology of acid-base and electrolyte disorders, ed 6, New York, 2014, McGraw-Hill. 4. Malley WJ: Clinical blood gases: assessment and intervention, ed 2, St Louis, 2005, Saunders. 5. Lumb A, Pearl RG: Nunn’s applied respiratory physiology, ed 8, St Louis, 2016, Elsevier. 6. West JB: Pulmonary physiology and pathophysiology: an integrated, case-based approach, ed 2, Philadelphia, 2007, Lippincott Williams and Williams. 7. Des Jardins T: Cardiopulmonary anatomy and physiology, essentials for respiratory care, ed 6, Clifton Park, NY, 2013, Delmar Publications. 8. Beachey W: Respiratory care anatomy and physiology, ed 4, St Louis, 2017, Elsevier. 9. Heuer AJ, Scanlan CL: Wilkins’ clinical assessment in respiratory care, 8th ed, St Louis, 2018, Elsevier.

13  Solutions, Body Fluids, and Electrolytes Daniel F. Fisher

CHAPTER OBJECTIVES After reading this chapter you will be able to: • Describe the characteristics of and key terms associated with solutions, colloids, and suspensions. • Describe the five factors that influence the solubility of a substance in a solution. • Describe how osmotic pressure functions and what its action is in relation to cell membranes. • Describe how to calculate the solute content of a solution using ratio, weight/volume, and percent methods. • State the ionic characteristics of acids, bases, and salts.

• Describe how proteins can function as bases. • Describe how to calculate the pH of a solution when given the [H+] in nanomoles per liter. • Identify where fluid compartments are located in the body and their volumes. • Describe how water loss and replacement occur. • Define the roles played by osmotic and hydrostatic pressure in edema. • Identify clinical findings associated with excess or deficiency of the seven basic electrolytes.

CHAPTER OUTLINE Solutions, Colloids, and Suspensions, 269 Definition of a Solution, 269 Concentration of Solutions, 270 Starling Forces, 270 Osmotic Pressure of Solutions, 270 Quantifying Solute Content and Activity, 272

Solute Content by Weight, 273 Calculating Solute Content, 273 Quantitative Classification of Solutions, 273 Electrolytic Activity and Acid-Base Balance, 274 Characteristics of Acids, Bases, and Salts, 274

Designation of Acidity and Alkalinity, 276 Body Fluids and Electrolytes, 277 Body Water, 277 Electrolytes, 280

hypercalcemia hyperkalemia hypokalemia hyponatremia hyperphosphatemia hypertonic hypotonic ionic insensible interstitial fluid intracellular fluid isotonic molal solution molar solution nanomole normal solution nonpolar covalent

osmolality osmotic pressure (oncotic pressure) percent solution plasma colloid osmotic pressure (oncotic pressure) polar covalent ratio solution saturated solution sensible solute solution solvent Starling equilibrium suspensions transcellular fluid weight-per-volume (W/V) solution

KEY TERMS acid active transport anions base buffering cations colloids diluent dilute solution dilution equation Donnan effect electrolyte solution equivalent weight extracellular hydrophilic hydrostatic pressure hypocalcemia 268

CHAPTER 13  Solutions, Body Fluids, and Electrolytes

Body water and various chemicals are regulated to maintain normal bodily functions. Imbalances in such processes occur in many diseases, including those which affect the respiratory system. Therefore it is important for respiratory therapists (RTs) to have a basic understanding of body fluids, electrolytes, and related physiologic chemistry, as provided in this chapter.

TABLE 13.1  Types of Physiologic

Solutions Type

Characteristics

Ionic (electrovalent)

Ionic compounds dissolved from crystalline form, usually in water (hydration); form strong electrolytes with conductivity dependent on concentration of ions Molecular compounds dissolved in water or other solvents to produce ions (ionization); electrolytes may be weak or strong, depending on degree of ionization; solutions polarize and are good conductors Molecular compounds dissolved into electrically neutral solutions (do not polarize); solutions are not good conductors; nonelectrolytes

SOLUTIONS, COLLOIDS, AND SUSPENSIONS Definition of a Solution The body is based on liquid water chemistry and the interaction of various substances either dissolved or suspended within the fluid. Water itself is a polar (having two sides with one positive and one negative charges) covalent (capable of forming bonds by sharing electrons) molecule and is referred to in chemistry as a universal solvent. Water is the primary component of any liquid within the body, and it greatly influences other materials as they are introduced. These substances and particles combine with water in the following three ways: as (1) colloids, (2) suspensions, or (3) solutions. A solution is a stable mixture of two or more substances that cannot be separated using a centrifuge. One substance is evenly distributed between the molecules of the other. The substance that dissolves is called the solute. The medium in which it dissolves is called the solvent. Gases, liquids, and solids can dissolve to become solutes; for example, carbon dioxide, alcohol, and salt can be dissolved in water. The process of dissolving involves breaking the (relatively weak) bonds between the solute-solute molecules and the solvent-solvent molecules. These intermolecular forces must be broken before a new solute-solvent bond can be formed. A solute dissolves in a solvent if the solute-solvent forces of attraction are great enough to overcome the solute-solute and solvent-solvent forces of attraction. If the solute-solvent force is less than the solute-solute or solvent-solvent force, the solute does not dissolve. When all three sets of forces are approximately equal, the two substances typically are soluble in each other. In electrochemical terms, there are three basic types of physiologic solutions. Depending on the solute, solutions are ionic (electrovalent), polar covalent, or nonpolar covalent (Table 13.1). In ionic and polar covalent solutions, some of the solute ionizes into separate particles known as ions. A solution in which this dissociation occurs is called an electrolyte solution. If an electrode is placed in such a solution, positive ions migrate to the negative pole of the electrode (the cathode). These ions are called cations. Negative ions migrate to the positive pole of the electrode (the anode); they are called anions. In nonpolar covalent solutions, molecules of solute remain intact and do not carry electrical charges; these solutions are referred to as nonelectrolytes. These nonelectrolytes are not attracted to either the positive or the negative pole of an electrode (hence the designation nonpolar). All three types of solutions coexist in the body. These solutions also serve as the media in which colloids and simple suspensions are dispersed. Gases such as oxygen and CO2 are nonpolar molecules (along with nitrogen) and do not dissolve very well in water, which is a polar solvent. Colloids (sometimes called dispersions or gels) consist of large molecules that attract and hold water (hydrophilic: “water

269

Polar covalent

Nonpolar covalent

Physiologic Example Saline solution (0.9% NaCl)

Hydrochloric acid (HCl) (strong electrolyte); acetic acid (CH3COOH) (weak electrolyte)

Glucose (C6H12O6)

loving”). These molecules are uniformly distributed throughout the dispersion, and they tend not to settle. The protoplasm inside cells is a common example of a colloid. Physiologically, colloids provide very little free water to the patient’s system, and care should be taken not to create a hypotonic (having a lower concentration of electrolytes than body plasma) environment.1 Suspensions are composed of larger particles that float within a liquid. Unlike a solution, suspensions can be physically separated by centrifugation. Red blood cells in plasma are an example of a suspension. Dispersion of suspended particles depends on physical agitation. Particles settle because of gravity when the suspension is motionless. The ease with which a solute dissolves in a solvent is its solubility, which is influenced by the following five factors: 1. Nature of the solute. The ease with which substances go into a solution (dissociation) in a given solvent depends on the forces of the solute-solute molecules and varies widely. 2. Nature of the solvent. The ability of a solvent to dissolve a solute depends on the bonds of the solvent-solvent molecules and varies widely. The electrical properties of the solvent molecules determine how soluble a substance is for a particular solvent. Polar solvents, such as water, dissolve other polar covalent bonds; nonpolar solvents dissolve nonpolar solutes: “Like dissolves like.” 3. Temperature. The solubility of most solids increases with increased temperature. However, the solubility of gases varies inversely with temperature. 4. Pressure. The solubility of solids and liquids is not greatly affected by pressure. However, the solubility of gases in liquids varies directly with pressure. 5. Concentration. The concentration of a solute or available solvent affects how much of the substance goes into a solution.

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The effects of temperature and pressure on the solubility of gases are important. More gas dissolves in a liquid at lower temperatures. As the temperature of a liquid increases, gas dissolved in that liquid comes out of solution. Henry’s law describes the effect of pressure on solubility of a gas in a liquid. Henry’s law states that at a given temperature, the volume of a gas that dissolves in a liquid is proportional to the solubility coefficient of the gas and the partial pressure of gas to which the liquid is exposed. O2 and CO2 transport can change significantly with changes in body temperature or atmospheric pressure (see Chapter 6).

A solution is characterized as being supersaturated when the solvent contains more solute than a saturated solution at the same temperature and pressure. If a saturated solution is heated, the solute equilibrium is disturbed and more solute goes into the solution. This is because of the space between the solvent molecules increases. If undissolved solute is removed and the solution is gradually cooled, there is an excess of dissolved solute (see Fig. 13.1C). The excess solute of supersaturated solutions may be precipitated out (or come out of solution) if the solution is vibrated or if a “seed crystal” is introduced.

Concentration of Solutions

Starling Forces

The term concentration refers to the amount of solute dissolved into the solvent. Concentration can be described either qualitatively or quantitatively. Calling something a dilute solution, suggesting a small amount of solute relative to the solvent or a weak concentration, is an example of a qualitative description. Stating that a specific container holds 50 mL of 0.4 molar solution of sodium hydroxide (NaOH) is a quantitative description (Fig. 13.1A). Saturated solutions occur when the solvent can hold no more solute and additional solute added to a saturated solution will settle to the bottom of the container (see Fig. 13.1B). Solute particles precipitate into the solid state at the same rate at which other particles go into solution. This equilibrium characterizes a saturated solution.

The transport of water across the capillary wall to the tissue was first studied by Ernest Starling, a 19th-century British physiologist. He described that the driving force for fluid filtration across the wall of the capillary is determined by four separate pressures: hydraulic (hydrostatic) and colloid osmotic pressure both within the vessel and in the tissue space.2 This process can be described mathematically using the following equation:

MINI CLINI Solutions and Suspensions Problem Respiratory therapists (RTs) work with both solutions and suspensions every day—for example, providing aerosolized medication to a patient with asthma. Many of the medications are solutions of the drug in either water or saline. When the drug is nebulized, small droplets of it are suspended in a gas. Discussion The medication to be nebulized is a solution. That is, the medication has been dissolved into a solvent of either water or saline. When the medication is placed in the nebulizer chamber, the large volume of liquid is converted to small droplets that can be easily inhaled. The droplets of the aerosol float in the air to be breathed in by the patient. The aerosol is a suspension of the droplets of liquid within a gas. Given enough time, the droplets would eventually settle to the floor. For more information on aerosol therapy see Chapter 40.

A

B

Jv = Lp [(Pc − Pi ) − s(pc − pi )] where: Jv = Fluid filtration movement across the capillary wall per unit area. Lp = Permeability of the capillary wall. s = Oncotic reflection coefficient. Describes how a semipermeable membrane excludes or reflects a specific solute as water moves from one side of the membrane to the other. Pc, Pi, pc, pi = Global values for both the hydrostatic and colloid osmotic pressures in the capillary and interstitial compartments. Fluid transfer across the membrane is the net result of the aforementioned factors. If the overall result if positive, fluid will move from the capillary to the interstitium. If the overall result is negative, fluid will be reabsorbed from the tissue back into the capillary. A capillary has higher hydrostatic pressure closer to the arteriole and a lower hydrostatic pressure when closer to the venule. Assuming normal transcapillary driving forces (Table 13.2), the net force can be calculated for each end of the capillary.

Osmotic Pressure of Solutions Most of the solutions of physiologic importance in the body are dilute. Solutes in dilute solution resemble gases. This behavior

C

Fig. 13.1  (A) In the dilute solution, there are relatively few solute particles. (B) In the saturated solution, the solvent contains all the solute it can hold in the presence of excess solute. (C) Heating the solution dissolves more solute particles, which may remain in the solution if cooled gently, creating a state of supersaturation.

CHAPTER 13  Solutions, Body Fluids, and Electrolytes

271

TABLE 13.2  Typical Values of Transcapillary Pressures Capillary Blood Pressure (Pc)

Interstitial Fluid Pressure (Pi)

Effective Capillary Colloid Osmotic Pressure (s pc)

Effective Interstitial Fluid Colloid Osmotic Pressure (s pi)

Net Force

+35 mm Hg +15 mm Hg

−2 mm Hg −2 mm Hg

+25 mm Hg +25 mm Hg

+0.1 mm Hg +3 mm Hg

+12 mm Hg −5 mm Hg

Arteriolar End Venular End

Modified from Boron WF, Boulpaep EL: Medical physiology: a cellular and molecular approach, updated edition, Philadelphia, 2003, Elsevier-Saunders.

A

B

50%

D

C

30%

40%

40%

E

Fig. 13.2  Osmotic Pressure Is Illustrated by the Solutions in the Five Containers. Each container is divided into two compartments by a semipermeable membrane, which permits passage of solvent molecules but not solute (circles). The number of solute particles represents relative concentrations of the solutions. Solute particles are fixed in number and are confined by the membranes. Volume changes are a function of the diffusible solvent. Solvent movement is indicated by arrows through the membranes. Container (A) shows a state of equilibrium, in which solute and solvent are equally distributed on either side of the membrane. Containers (B) and (C) show diffusion of solvent through the membrane as a result of solvent on only one side of the membrane and the resulting pressure change (osmotic pressure indicated by the gauge). Containers (D) and (E) show what happens when different concentrations exist on either side of a semipermeable membrane. Solvent moves from the lower concentration toward the higher concentration to establish an equilibrium because of osmotic pressure.

results from the relatively large distances between the molecules of solute in dilute solutions. The most important physiologic characteristic of solutions is their ability to exert pressure. Osmotic pressure (oncotic pressure)3 is the force produced by solvent particles under certain conditions. A membrane that permits passage of solvent molecules but not solute is called a semipermeable membrane. If such a membrane divides a solution into two compartments, molecules of solvent can pass (diffuse) through it from one side to the other (Fig. 13.2A). The number of solvent molecules diffusing in one direction must equal the

number of solute molecules passing in the opposite direction. An equal ratio of solute to solvent particles (i.e., the concentration of the solution) is maintained on both sides of the membrane. A capillary wall is an example of a semipermeable membranes.4,5 If a solution is placed on one side of a semipermeable membrane and pure solvent is placed on the other, solvent molecules move through the membrane into the solution. The force driving solvent molecules through the membrane is called osmotic pressure. Osmotic pressure tries to redistribute solvent molecules so that the same concentration exists on both sides of the membrane. Osmotic pressure may be measured by connecting a manometer to the expanding column of the solution (see Fig. 13.2B and C). Osmotic pressure also can be visualized as an attractive force of solute particles in a concentrated solution. If 100 mL of a 50% solution is placed on one side of a membrane and 100 mL of a 30% solution is placed on the other side, solvent molecules move from the dilute to the concentrated side (see Fig. 13.2D and E). The particles in the concentrated solution attract solvent molecules from the dilute solution until equilibrium occurs. Equilibrium exists when the concentrations (i.e., ratio of solute to solvent) in the two compartments are equal (40% in Fig. 13.2). Osmolality is defined as the ratio of solute to solvent. In physiology, the solvent is water.1,4,6 Osmotic pressure depends on the number of particles in solution but not on their charge or identity. A 2% solution has twice the osmotic pressure of a 1% solution under similar conditions. For a given amount of solute, osmotic pressure is inversely proportional to the volume of solvent. Most cell walls are semipermeable membranes. Through osmotic pressure, water is distributed throughout the body within certain physiologic ranges. Tonicity is the relative concentration of solutions that determine the direction and extent of diffusion. Tonicity is a way of describing the response of cells immersed in an external solution. Tonicity is influenced by the concentration of solutes that cannot cross the membrane. Average body cellular fluid has a tonicity equal to a 0.9% solution of sodium chloride (sometimes referred to as physiologic or normal saline). Solutions with the same tonicity are called isotonic. Compared with body fluid, solutions with more tonicity (more oncotic pressure and higher concentration as a result of less water) are hypertonic, and solutions with less tonicity (less oncotic pressure and lower concentration as a result of more water) are hypotonic. For example, a hypotonic solution has a lower concentration of solutes outside the cell than inside the cell. In an attempt to balance the concentrations of solutes inside and outside the cell, water will move into the cell, causing it to enlarge. Pressure increases inside the cell to counteract osmotic

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MINI CLINI Sputum Induction and Hypertonic Saline Problem To obtain samples of respiratory secretions, aerosol therapy is sometimes used to increase the volume of secretions and promote coughing to recover sputum or cells or both from the respiratory tract. Sputum induction combines the effect of hypertonic aerosols on the lining of the respiratory tract and on the normal cough reflex. Discussion Sputum induction is usually performed by having the patient inhale a sterile hypertonic saline solution. Isotonic saline is approximately 0.9% (i.e., normal saline); concentrations greater than 0.9% are considered hypertonic. In clinical practice, concentrations of 3% to 10% have been used. When the particles of hypertonic saline are deposited in the airway, osmotic pressure is thought to play a key role. When hypertonic saline comes into contact with the respiratory mucosa, water moves from the cells lining the airway into the sol-gel matrix that lines the airways, increasing its volume. The combination of increased volume of respiratory secretions with irritation of the epithelial cells themselves promotes reflex coughing. The volume of sputum and the rate of clearance from the lungs seem to depend on the osmolarity of the inhaled aerosol. Exposure of mast cells normally present in the airways to hypertonic aerosols results in the release of mediators (e.g., histamine) and bronchospasm. These effects may be related to the stimulation of the cough reflex. For the same reason, hypertonic saline is also sometimes used for bronchial challenge testing.

pressure. This pressure is called turgor. Some cells have selective permeability, allowing passage not only of water but also of specific solutes. Through these mechanisms, nutrients and physiologic solutions are distributed throughout the body. RULE OF THUMB Solutions that have osmotic pressures equal to the average intracellular pressure in the body are called isotonic. This is roughly equivalent to a saline (NaCl) solution of 0.9%. Solutions with higher osmotic pressure are called hypertonic, whereas solutions with lower osmotic pressure are called hypotonic. Administration of isotonic solutions usually causes no net change in cellular water content. Hypertonic solutions draw water out of cells. Hypotonic solutions usually cause water to be absorbed from the solution into cells.

Quantifying Solute Content and Activity The amount of solute in a solution can be quantified in two ways: (1) by actual weight (grams or milligrams) and (2) by chemical combining power (electronegativity). The weight of a solute is easy to measure and specify. However, it does not indicate chemical combining power. The sodium ion (Na+) has a gram ionic weight of 23. The bicarbonate ion (HCO3−) has a gram ionic weight of 61. Both ions have equal but opposite electronegativities (+1 for Na+, −1 for HCO3−). The number of chemically reactive units is usually more meaningful than their weight.

Equivalent Weights In medicine, it is customary to refer to physiologic substances in terms of chemical combining power. The measure commonly used is equivalent weight. Equivalent weights are amounts of substances that have equal chemical combining power. For

example, if chemical A reacts with chemical B, by definition, 1 equivalent weight of A reacts with exactly 1 equivalent weight of B. No excess reactants of A or B remain. Two magnitudes of equivalent weights are used to calculate chemical combining power: gram equivalent weight (gEq) and milligram equivalent weight, or milliequivalent (mEq). One milliequivalent (1 mEq) is 11000 of 1 gEq. Gram equivalent weight values.  A gram equivalent weight of a substance is calculated as its gram molecular (formula) weight divided by its valence. Valence refers to the number of electrons that need to be added or removed to make the substance electrically neutral. The valence signs (+ or −) are disregarded. gEq = Gram molecular weight valence The gram equivalent weight of N+, with a valence of 1, equals its gram atomic weight of 23 g. The gram equivalent weight of calcium (Ca2+) is its atomic weight (i.e., 40) divided by 2, or 20 g. The gram equivalent weight of ferric iron (Fe3+) is its atomic weight (i.e., 55.8) divided by 3, or approximately 18.6 g. Gram equivalent weight of an acid.  The gram equivalent weight of an acid is the weight of the acid (in grams) that contains 1 mole of replaceable hydrogen (H). The gram equivalent weight of an acid may be calculated by dividing its gram formula weight by the number of H+ atoms in its formula, as shown in the following reaction: HCl + Na+ → NaCl + H+ The single H+ of hydrochloric acid (HCl) is replaced by Na+. In 1 mole of HCl, there is 1 mole of replaceable H+. By definition, the gram equivalent weight of HCl must be the same as its gram formula weight, or 36.5 g. The two H atoms of H2SO4 are both considered to be replaceable. In 1 mole of H2SO4, there are 2 moles of replaceable H+, and the gram equivalent weight of H2SO4 is half its gram formula weight, or 48 g. Acids in which H+ atoms are not completely replaceable are exceptions to the rule. In some acids, H+ replacement varies according to specific reactions. Carbonic acid (H2CO3) and phosphoric acid (H3PO4) are examples of such exceptions. Their equivalent weights are determined by the conditions of their chemical reactions. For example, H2CO3 has two H+ atoms. In physiologic reactions, only one is considered replaceable: H2CO3 + Na+ → NaHCO3 + H+ Only one H+ atom is released; the other remains bound. In 1 mole of H2CO3, there is only 1 mole of replaceable H+. The gram equivalent weight of H2CO3 is the same as its gram formula weight, or 61 g. Gram equivalent weight of a base.  The equivalent weight of a base is its weight (grams) containing 1 mole of replaceable hydroxyl (OH−) ions. Similar to acids, the gram equivalent weight of bases is calculated by dividing gram formula weight by the number of OH− groups in its formula. Conversion of gram weight to equivalent weight.  To determine the number of gram equivalent weights in a substance, the gram weight is divided by its calculated equivalent weight, as shown in the following example:

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CHAPTER 13  Solutions, Body Fluids, and Electrolytes

TABLE 13.3  Concentration of Ingredients

58.5 g NaCl gEq 58.5 g = 1 gEq 29.25 g NaCl gEq 58.5 = 0.5 gEq

in Lactated Ringer Solution

Milligram equivalent weights.  The concentrations of most chemicals in the body are quite small. The term milligram equivalent weight (milliequivalent) is preferred for expressing these minute values; 1 mEq is simply 0.001 gEq: mEq = gEq 1000 The normal concentration of potassium in plasma ranges from 0.0035 to 0.005 gEq/L. These values may be converted to milliequivalents by multiplying by a factor of 1000. The normal concentration of K+ in the plasma would be expressed as ranging from 3.5 to 5.0 mEq/L.

Solute Content by Weight The measurement of many electrolytes is based on actual weight rather than on milliequivalents. This weight is often expressed as milligrams per 100 mL of blood or body fluid. The units for this measurement are abbreviated as mg% (milligram percent) or mg/dL (milligrams per deciliter). This text uses the modern designation mg/dL. Some substances present in blood or body fluid are present in extremely small amounts and are expressed in micrograms ( 11000 of a milligram) per deciliter (µg/dL or mcg/ dL). Values stated in milligrams per deciliter may be converted into their corresponding equivalent weights and reported as milliequivalents per liter. Conversion between mEq/L and mg/ dL may be calculated as follows:

mEq L =

mg dL × 10 equivalent weight

mEq L × equivalent weight mEq L = 10

Substance

mg/dL

NaCl (sodium chloride)

600 Na 310 Cl 30 C3H5O3 30 K 20 Ca

NaC3H5O3 (sodium lactate) KCl (potassium chloride) CaCl2 (calcium chloride)

Approximate mEq/L 130 109 28 4 27

MINI CLINI Using Lactated Ringer Solution Over 5% Dextrose in Water Problem Patients may have electrolyte imbalances requiring replacement therapy. There are many common solutions that may be used (e.g., lactated Ringer [LR] solution or 5% dextrose in water [D5W]). Both solutions have clinical use but can have different results in fluid distribution. Discussion When D5W is given, the body will rapidly metabolize the dextrose sugar, changing the solution from isotonic to hypotonic. The resulting shift in colloid osmotic pressure will cause the water to leave the vascular system and hydrate the surrounding tissue. However, LR solution is isotonic and does not contain sugar, so it remains isotonic within the vascular system. This allows for the fluid to be more evenly distributed throughout the body while replenishing electrolytes and not further adding more fluid to the surrounding tissue.7,8

(1)

Calculating Solute Content

(2)

In addition to gEq, mEq, mg/dL, and µg/dL (mcg/dL), several other methods of calculating solute content exist. These common chemical standards are used to compute solute content and dilution of solutions.

To convert a serum Na+ value of 322 mg/dL to mEq/L, the equation is used as follows: mEq L = mg dL × 10 equivalent weight = 322 × 10 23 = 140 mEq L In clinical practice, electrolyte replacement is common when a laboratory test identifies a significant deficiency. The electrolyte content of intravenous solutions is usually stated in milligrams per deciliter or in milliequivalents per liter. Lactated Ringer (LR) solution is one such infusion used for electrolyte replacement (Table 13.3). RULE OF THUMB: Volume by Weight  Blood is a mixture of substances, including hemoglobin. Hemoglobin is a very large molecule useful in oxygen transport. Because of its relatively large molecular weight, the normal hemoglobin range is approximately 13.5−17.5 mg/dL for males and 12−15.5 mg/dL for females.

Quantitative Classification of Solutions The amount of solute in a solution may be quantified by the following six methods: 1. Ratio solution. The amount of solute to solvent is expressed as a proportion (e.g., 1 : 100). Ratio solutions are sometimes used in describing concentrations of drugs. 2. Weight-per-volume (W/V) solution. The W/V solution is commonly used for solids dissolved in liquids. It is defined as weight of solute per volume of solution. This method is sometimes erroneously described as a percent solution. W/V solutions are commonly expressed in grams of solute per 100 mL of solution. For example, 5 g of glucose dissolved in 100 mL of solution is properly called a 5% solution, according to the W/V scheme. A liquid dissolved in a liquid is measured as volumes of solute to volumes of solution. 3. Percent solution. A percent solution is weight of solute per weight of solution. For example, 5 g of glucose dissolved in 95 g of water is a true percent solution. The glucose is 5% of the total solution weight of 100 g.

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SECTION II  Applied Anatomy and Physiology

4. Molal solution. A molal solution contains 1 mole of solute per kilogram of solvent, or 1 mmol/g solvent. The concentration of a molal solution is independent of temperature. 5. Molar solution. A molar solution has 1 mole of solute per liter of solution, or 1 mmol/mL of solution. The solute is measured into a container, and solvent is added to produce the solution volume desired. 6. Normal solution. A normal solution has 1 gEq of solute per liter of solution, or 1 mEq/mL of solution. For all monovalent solutes, normal and molar solutions are the same. The equivalent weights of their solutes equal their gram formula weights. Equal volumes of solutions of the same normality contain chemically equivalent amounts of their solutes. If the solutes react chemically with one another, equal volumes of the solutions react completely. Neither substance remains in excess. In the analytic process of titration, normal solutions are often used as standards to determine the concentrations of other solutions.

Dilution Calculations Dilute solutions are made from a stock preparation. Preparation of medications often involves dilution. Dilution calculations are based on the weight-per-unit volume principle (the aforementioned W/V solution method). Diluting a solution increases its volume without changing the amount of solute it contains, and this reduces the concentration of the solution. The amount of solute in a solution can be expressed as volume times concentration. For example, 50 mL of a 10% solution (10 g/dL) contains 50 × 0.1, or 5 g. In the dilution of a solution, initial volume (V1) multiplied by initial concentration (C1) equals final volume multiplied by final concentration. This can be expressed as follows: V1C1 = V2C2 This equation is sometimes referred to as the dilution equation. Whenever three of the variables are known, the fourth can be calculated by isolating the missing variable as in the following examples: 1. Diluting 10 mL of a 2% (0.02) solution to a concentration of 0.5% (0.005) requires finding the new volume (V2) by rearranging the dilution equation as follows: V2 = V1C1 C2 V2 = 10 mL × 0.02 0.005 V2 = 40 mL 2. If 50 mL of water is added to 150 mL of a 3% (0.03) solution, the new concentration is calculated by rearranging the dilution equation to find C2 as follows: C2 = V1C1 V2 C2 = 150 mL × 0.02 (50 mL + 150 mL) C2 = 0.0225 or (2.25%) 3. To dilute 50 mL of a 0.33 normal (N) solution to a 0.1 N concentration, concentration is given as normality, but it can be used similar to a percentage. The new volume (V2)

can be calculated by rearranging the dilution equation as follows: V2 = V1C1 C2 V2 = 50 mL × 0.33 0.1 V2 = 165 mL In the last example, the volume needed to produce a 0.1 N solution would be 165 mL to 50 mL (the original volume), or 115 mL. In other words, 115 mL of solvent would have to be added to the original 50 mL of 0.33 N solution to produce the desired concentration. The added solvent is called the diluent because it dilutes the original concentration to a lower concentration. RULE OF THUMB: Isolating Missing Variables  When using the dilution equation, separate what is known and what you will need to determine. Look at the side of the equation which has the unknown value. To isolate it, divide both sides by the accompanying known value. This will leave the three known values on one side and the unknown fourth on the other side of the equation. Plug in the numbers, and solve.

ELECTROLYTIC ACTIVITY AND ACID-BASE BALANCE Acid-base balance depends on the concentration and activity of electrolytic solutes in the body. Clinical application of acid-base homeostasis is discussed in detail in Chapter 14.

Characteristics of Acids, Bases, and Salts Acids The term acid refers to either compounds that can donate [H+] (Brönsted-Lowry acid) or any compound that accepts an electron pair (Lewis acid). Although these two theories of acids differ in which is being transferred, both theories attempt to describe how reactive groups perform within an aqueous solution8,9: NH4Cl + NaOH → NH3 + NaCl + HOH In this reaction, Na+ and Cl− ions are not involved in the proton transfer. The equation can be rewritten ionically as follows to show the acidity of the ammonium ion: NH4 + + OH− → NH3 + HOH The ammonium ion donates an H+ ion (proton) to the reaction. The H+ combines with the hydroxide ion (OH−), and this converts the former into ammonia gas and the latter into water. Each of these dilutions uses the same proportions used in the first dilution as determined by the dilution equation. Methacholine is administered by nebulizer to the patient, starting with the lowest concentration (0.0625 mg/mL) and increasing until a change in FEV1 is observed. (See Chapter 20 for additional information on pulmonary function testing.) Acids with single ionizable hydrogen.  Simple compounds such as hydrochloric acid (HCl) ionize into one cation and one anion: HCl → H+ + Cl−

CHAPTER 13  Solutions, Body Fluids, and Electrolytes

MINI CLINI Methacholine Dilution The dilution equation (V1C1 = V2C2) is commonly used to calculate volumes or concentrations of medications when a specific dosage needs to be administered to a patient. If three of the variables are known, the fourth can be determined. Problem Methacholine is a drug used to induce airway constriction in patients suspected of having reactive airway disease. In healthy subjects, only higher doses of methacholine cause bronchospasm. In asthmatics, very low doses can precipitate a 20% decrease in the forced expiratory volume in 1 s (FEV1). The methacholine challenge test begins with a low dose and increases the concentration (either doubling or quadrupling) until the patient has a significant change in FEV1 or the highest dose has been given. Methacholine is supplied in vials that contain 100 mg of the active substance to which 6.25 mL of diluent (saline) can be added to produce a concentration of 16 mg/mL. This is the highest dosage administered to the patient. How can you make serial dilutions of the drug so that five different dosages are available and each one is 4 times more concentrated than the previous dose?

275

ions. The OH− may also be bound to an ammonium cation (NH4+). An example of this type of base is NaOH. The BrönstedLowry definition of a base is any compound that accepts a proton; bases are paired with acids that donate the proton, and these are called conjugate pairs. This definition includes substances other than hydroxides, such as ammonia, carbonates, and certain proteins. Hydroxide bases. In aqueous solution, the following are typical dissociations of hydroxide bases: Na+OH → Na+ + OH− K +OH → K + + OH− Ca2+ (OH− )2 → Ca2+ + 2(OH− ) Inactivation of an acid is part of the definition of a base. This inactivation is accomplished by OH− reacting with H+ to form water: NaOH + HCl → NaCl + HOH

Solution Starting with a 16 mg/mL stock solution of methacholine, how much diluent needs to be added to 3 mL of the stock to make a 4 mg/mL dose (one-fourth of the original concentration)? Using the dilution equation:

Nonhydroxide bases.  Ammonia and carbonates are examples of nonhydroxide bases. Proteins, with their amino groups, also can serve as nonhydroxide bases. Ammonia.  Ammonia qualifies as a base because it reacts with water to yield OH−:

C1V1 = C2 V2 (16)(3.0) = (4) V2 48 4 = V2 12 = V1

NH3 + HOH → NH4 + + OH− and neutralizes H+ directly: NH3 + H+ → NH4 +

Because there was 3 mL of the stock solution to begin with, the amount of diluent to add is the difference between 12 (V2) and 3, or 9 mL. Adding 9 mL of diluent to the original 3 mL of stock (16 mg/mL) provides 12 mL of methacholine with a concentration of 4 mg/mL, exactly one-fourth of the highest dose. Additional dilutions can be prepared using 3 mL of solution according to the following:

In both instances, NH3 accepts a proton to become NH4+. Ammonia plays an important role in renal excretion of acid (see Chapter 14). Carbonates.  The carbonate ion (CO32−), can react with water in the following way to produce OH−:

Start With



Na2CO3  2Na+ + CO32−

(1)



CO32− + HOH  HCO3− + OH−

(2)

3 mL of 4 mg/mL 3 mL of 1 mg/mL 3 mL of 0.25 mg/mL

To Make 9 mL 9 mL 9 mL

1 mg/mL 0.25 mg/mL 0.0625 mg/mL

Acids with multiple ionizable hydrogens.  The H+ ions in an acid may become available in stages. The degree of ionization increases as an electrolyte solution becomes more dilute. Concentrated sulfuric acid ionizes only one of its two H+ atoms per molecule, as follows: H2SO4 → H+ + HSO4 − With further dilution, second-stage ionization occurs: H2SO4 → H+ + H+ + SO4 −

Bases A base is a compound that yields hydroxyl ions (OH−) when placed into aqueous solution. A substance capable of inactivating acids is also considered a base. These compounds, called hydroxides, consist of a metal that is ionically bound to an OH− ion or

In this reaction, CO32− accepts a proton from water, becoming the HCO3− ion. It simultaneously produces a hydroxide ion. The CO32− ion also can react directly with H+ to inactivate it: CO32− + H+  HCO3− Protein bases.  Proteins are composed of amino acids bound together by peptide links. Physiologic reactions in the body occur in a mildly alkaline environment. This environment allows proteins to act as H+ receptors, or bases. Cellular and blood proteins acting as bases are transcribed as prot−. The imidazole group of the amino acid histidine is an example of an H+ acceptor on a protein molecule (Fig. 13.3). The ability of proteins to accept H+ ions limits H+ activity in solution, which is called buffering. The buffering effect of hemoglobin (Hb) is produced by imidazole groups in the protein. Each Hb molecule contains 38 histidine residues. Each O2-carrying component (heme group) of Hb is attached to a histidine residue. The ability of Hb to accept (i.e., buffer) H+ ions depends on its oxygenation state. Deoxygenated (reduced) Hb is a stronger base (i.e., a better

SECTION II  Applied Anatomy and Physiology

H C N N–

+

+H

HC C

C

140

N NH HC C

CH2 NH2

160

H C

120

CH2 COOH

H Basic form of histidine

NH2

C

COOH

H Acidic form of histidine

Fig. 13.3  Histidine portion of a protein molecule (at top) serving as a proton acceptor (base).

H+ acceptor) than oxygenated Hb. This difference partially accounts for the ability of reduced Hb to buffer more acid than oxygenated Hb can (see Chapter 14). Plasma proteins also act as buffers, although with less buffering power than Hb, which contains more histidine.

Designation of Acidity and Alkalinity Pure water can be used as a reference point for determining acidity or alkalinity. The concentration of both H+ and OH− in pure water is 10−7 mol/L. A solution that has a greater H+ concentration or lower OH− concentration than water acts as an acid. A solution that has a lower H+ concentration or a greater OH− concentration than water is alkaline, or basic. The H+ concentration [H+] of pure water has been adopted as the standard for comparing reactions of other solutions. Electrochemical techniques are used to measure the [H+] of unknown solutions. Acidity or alkalinity is determined by variation of the [H+] greater than or less than 1 × 10−7. For example, a solution with a [H+] of 89.2 × 10−4 has a higher [H+] than water and is acidic. A solution with a [H+] of 3.6 × 10−8 has fewer H+ ions than water and is by definition alkaline. Two related techniques are used for expressing the acidity or alkalinity of solutions using the [H+] of water (i.e., 10−7) as a neutral factor: (1) the [H+] in nanomoles per liter and (2) the logarithmic pH scale.

RULE OF THUMB  Pure water is considered to be the reference point for neutral pH. This is because of equilibrium between [H+] and the hydroxide ion [−OH−]. Because pH reflects the concentration of [H+], a lower pH on the scale means that the concentration of [H+] increases relative to [−OH−]. An increase in pH means that there is more [−OH−] than [H+]. Because pH is an inverse logarithm that means each pH change is a 10-times increase or decrease in [H+].

Nanomolar Concentrations The acidity or alkalinity of solutions may be reported using the molar concentration of H+ compared with that of water. The [H+] of water is 1 × 10−7 mol/L, or 0.0000001 (one ten-millionth

100 Nanomoles

276

80 60 40 20 0

6.8

7.0

7.2

7.4

7.6

7.8

8.0

pH Value Fig. 13.4  Relationship between pH scale and [H+] concentrations in nanomoles per liter (nmol/L). pH of 7.00 equals 100 nmol/L H+, whereas the normal human pH (arterial blood) of 7.40 is equal to approximately 40 nmol/L.

of a mole). The unit for one-billionth of a mole is a nanomole (nmol). The [H+] of water can be expressed as 100 nmol/L. A solution that has a [H+] of 100 nmol/L is neutral. A solution with an [H+] greater than 100 nmol/L is acidic; one with an [H+] less than 100 nmol/L is alkaline. This system is limited because of the wide range of possible [H+] but is applicable in clinical medicine because the physiologic range of [H+] is narrow. [H+] in healthy individuals is usually 30 to 50 nmol/L.

pH Scale The pH scale is used to describe the concentration of H+, ([H+]), (i.e., Brönsted-Lowry acid) in a solution. Rather than expressing the [H+] in nanomoles, it is more convenient to describe it in terms of the negative logarithm of the nanomolar [H+]. The equation for calculating pH is: pH = − log[H+ ] The pH of pure water is 7.0: The [H+] of water is 1 × 10−7 mol/L. The logarithm of 1 × 10−7 is −7, so the negative logarithm of 1 × 10−7 is 7. Using this scheme, in a solution with a pH of 7.00, the [H+] is the same as would be seen in pure water, so by convention this is called “neutral.” As the pH decreases below 7.00, the solution is termed acidic. When the pH increases above 7.00, the solution is considered to be basic. With a whole number change in pH (i.e., pH decreasing from 7.00 to 6.00), the [H+] is a factor of 10 less. With a pH increase from 7.00 to 8.00, the [H+] is 10 times greater (Fig. 13.4). A pH of 7.00 is equivalent to a [H+] of 100 nmol. A pH of 8.00 is equivalent to a [H+] concentration of 10 nmol. Similarly, a change in pH of 0.3 units equals a twofold change in [H+].

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CHAPTER 13  Solutions, Body Fluids, and Electrolytes

Applying these concepts in an example pertinent to clinical medicine yields the following: [H ] in blood = 4.0 × 10 mol L +

TABLE 13.4  Distribution of Body Fluids

−8

pH = − log(4.0 × 10−8 ) = − log 4.0 + − log10−8 = − log 4.0 + log108 = −0.602 + 8 = 7.40 In this example, the [H+] in arterial blood of a healthy adult is approximately 4.0 × 10−8 mol/L, or 40 nmol/L. RULE OF THUMB  Logarithms are the opposite of exponents. Consider the exponent: 23 = 2 × 2 × 2 =8

The exponent tells us how many times to multiply the base to itself. In the previous example, the exponent tells us to multiply 2 by itself 3 times which equals 8. A logarithm is the value of the exponent when the base number is known. Unless otherwise specified, the base is 10. RULE OF THUMB  The pH scale is logarithmic which means that it is the exponent of a base number, usually 10. For example, the logarithm of 100 is 2 (102 = 100). pH is a positive number representing the negative log of the hydrogen ion concentration [H+] of a solution. To visualize changes in acidity or alkalinity, the following two rules are helpful: 1. A pH change of 0.3 unit equals a twofold change in [H+]. 2. A pH change of 1 unit equals a tenfold change in [H+]. For example, if a patient’s blood pH decreased from 7.40 (normal) to 7.10, the [H+] concentration would be twice as high. If a patient’s urine pH decreased from 7.00 to 6.00, the [H+] would have increased by 10 times.

BODY FLUIDS AND ELECTROLYTES Body Water Water constitutes 45%–80% of an individual’s body mass, depending on the mass, gender, and age of the individual. Obese individuals have a lower percentage of body water (≤30% less) than normal-weight individuals. Men have a slightly higher percentage of total body water than women. The total percentage of body water in infants and children is substantially greater, with water accounting for 80% of a newborn’s total body weight (Table 13.4).

Distribution Body water is divided into the following two major compartments: (1) intracellular (“within the cells”) and (2) extracellular (“outside the cells”). Intracellular water accounts for approximately two-thirds of the total body water, and extracellular water accounts for the remaining one-third. Extracellular water is found in three subcompartments: (1) intravascular water (plasma), (2)

Body Water Total body Water  Intracellular  Extracellular Interstitial Intravascular Transcellular

Man (% Body Weight)

Woman (% Body Weight)

Infant (% Body Weight)

60 ± 15

50 ± 15

80

45 15–20 11–15 4.5 45 45 mm Hg) with an accompanying decreased arterial pH ( 40 mm Hg Expected pH = 7.40 − (Measured PaCO2 – 40 mm Hg)0.006

Increase 0.01 0.10 Decrease 0.006 0.06

Respiratory Acidosis

Neuromuscular Disease • Poliomyelitis • Myasthenia gravis • Guillain-Barré syndrome Trauma • Spinal cord • Brain • Chest wall • Severe restrictive disorders • Obesity (Pickwickian syndrome) • Kyphoscoliosis Abnormal Lungs (“Can’t Breathe”) • Chronic obstructive pulmonary disease • Acute airway obstruction (late phase)

MINI CLINI Acute (Uncompensated) Respiratory Acidosis Problem A 35-year-old woman was admitted to the emergency department with a diagnosis of heroin overdose. Her breathing was shallow and slow. Arterial blood gas analysis showed a pH of 7.30, PCO2 of 55 mm Hg, and HCO3− of 26 mEq/L. How would the RT assess this patient’s respiratory condition? Solution The RT should follow these steps: 1. Categorize the pH. The pH is below normal, indicating the presence of acidemia. 2. Determine respiratory involvement. PaCO2 is elevated above normal (hypercapnia), consistent with a low pH, indicating hypoventilation as a contributing factor to acidemia (respiratory acidosis). 3. Determine metabolic involvement. HCO3− is elevated slightly above normal. However, this is in the expected range for acute respiratory acidosis (1 mEq for each 10-mm Hg increase in PCO2). 4. Assess for compensation. As explained in step 3, HCO3− is within the expected range for acute respiratory acidosis. There is no evidence of metabolic compensation. Therefore, the condition is interpreted as an uncompensated respiratory acidosis.

pace with an acutely increasing PaCO2. Full compensation may take several days. Partly compensated respiratory acidosis is characterized by increased PaCO2, increased [HCO3−], and an acid pH—still not quite up in the normal range. Fully compensated respiratory acidosis is characterized by a pH on the acidic side of the normal (7.35), increased PaCO2, and increased [HCO3−]. Increased [HCO3−] in the presence of increased PaCO2 is a sign that the PaCO2 has been elevated for a considerable time (i.e., the kidneys have had sufficient time to compensate). The

Changes in PaCO2 on Arterial pH

underlying pathologic process that produced hypercapnia is still present; the kidneys simply mask the problem by maintaining a normal-range pH. Because hypercapnia is still present, the term acidosis is retained in classifying this condition (fully compensated respiratory acidosis). This terminology emphasizes that lung function is still abnormal, and, if it were unopposed by the renal compensatory mechanism, it would still produce an acidosis.

Correction The main goal in correcting respiratory acidosis is to treat the underlying problem—to improve alveolar ventilation. Various respiratory care modalities may be used, ranging from bronchial hygiene and lung expansion techniques to mechanical ventilation. If hypoventilation is chronic and compensation has restored pH to the normal range, action aimed at decreasing PaCO2 to the normal range is inappropriate and possibly harmful, because the high level of [HCO3−] in the blood created by the kidney’s compensation would produce an alkalemia (Table 14.6).

Respiratory Alkalosis Any physiologic process that decreases PaCO2 (7.45) produces respiratory alkalosis. A low PaCO2 (hypocapnia) forces the hydration reaction to the left, decreasing H2CO3 concentration and increasing the pH: CO2 + H2O ← H2CO3 ← HCO3− + H+

Causes Any process in which ventilatory elimination of CO2 exceeds the body’s production of CO2 causes respiratory alkalosis. The most common cause of hyperventilation in patients with pulmonary disease is decreased PaO2 (hypoxemia). Hypoxemia causes specialized neural structures to signal the brain, increasing ventilation (see Chapter 15). Anxiety, fever, stimulatory drugs, pain, and central nervous system injuries are possible causes of hyperventilation. Other possible causes include stimulation of irritant receptors in the lung parenchyma, which may occur in pneumonia or pulmonary edema. Hyperventilation and respiratory alkalosis also may be iatrogenically induced (caused by medical treatment). Iatrogenic hyperventilation is most commonly associated with overly aggressive mechanical ventilation. It may also be associated with aggressive

300

SECTION II  Applied Anatomy and Physiology

MINI CLINI

BOX 14.4  Common Causes of

Chronic (Compensated) Respiratory Acidosis

Respiratory Alkalosis

Problem A 73-year-old man is being treated on an outpatient basis for pulmonary emphysema, which was diagnosed 7 years earlier. His breathing is labored at rest, with marked use of accessory muscles. Arterial blood gas analysis showed a pH of 7.36, PCO2 of 64 mm Hg, and HCO3− of 35 mEq/L. How would the RT assess this patient’s arterial blood gas results?

Normal Lungs • Anxiety • Fever • Stimulant drugs • Central nervous system lesion • Pain • Sepsis

Solution The RT should follow these steps: 1. Categorize the pH. The pH is on the acidemic side of the normal range, but it is still normal. 2. Determine respiratory involvement. PaCO2 is higher than normal, indicating hypoventilation as a contributing factor to the low-normal pH (respiratory acidosis). 3. Determine metabolic involvement. HCO3− is substantially elevated. By itself, this would cause alkalemia, but because pH is on the acidemic side of normal, primary metabolic alkalosis is ruled out. Compensation for the respiratory acidosis has occurred. 4. Assess for compensation. HCO3− is approximately 8 to 10 mEq higher than normal. This is consistent with a compensatory response by the kidneys to offset the acidosis. In addition, the expected pH for a PaCO2 of 64 mm Hg is [7.40 − (64 mm Hg − 40 mm Hg) × 0.006], or 7.26 (see Table 14.6). Because the actual pH is 7.36, metabolic compensation (retention of HCO3−) must have occurred. Therefore, the interpretation is a fully compensated respiratory acidosis.

MINI CLINI Acute (Uncompensated) Respiratory Alkalosis Problem A distraught 77-year-old man experiencing anxiety of apparent psychosomatic origin was brought to the hospital by his wife. The patient exhibited rapid and deep breathing, had slurred speech, and complained about tingling in his extremities. Arterial blood gas analysis showed a pH of 7.57, PCO2 of 23 mm Hg, and HCO3− of 22 mEq/L. How would the RT interpret this patient’s acidbase condition? Solution The RT should follow these steps: 1. Categorize the pH. The pH is substantially higher than normal, indicating the presence of an alkalemia. 2. Determine respiratory involvement. PaCO2 is well below normal, which is consistent with the high pH, indicating hyperventilation as a contributing factor in alkalemia (respiratory alkalosis). 3. Determine metabolic involvement. HCO3− is slightly lower than normal. However, this is within the expected range for acute respiratory alkalosis (CO2 hydration reaction’s effect). 4. Assess for compensation. The decrease in HCO3− is within the expected range for acute respiratory alkalosis (1 mEq for each 5-mm Hg decline in PCO2). Therefore, the interpretation is an uncompensated respiratory alkalosis. Hypocapnia is synonymous with respiratory alkalosis.

deep breathing and lung expansion respiratory care procedures. Decreased PaCO2, increased pH, and normal-range [HCO3−] characterize acute respiratory alkalosis. A slight decrease in [HCO3−] is expected from the effect of the hydration reaction. Box 14.4 summarizes causes of respiratory alkalosis.

Abnormal Lungs • Hypoxemia-causing conditions • Acute asthma • Pneumonia • Stimulation of vagal lung receptors • Pulmonary edema • Pulmonary vascular disease Either Normal or Abnormal Lungs • Iatrogenic hyperventilation

Clinical Signs An early sign of respiratory alkalosis is paresthesia (numbness or a tingling sensation in the extremities). Severe hyperventilation is associated with hyperactive reflexes and possibly tetany (intermittent muscle spasms). The low PaCO2 may constrict the brain’s cerebral vessels enough to reduce cerebral circulation, causing light-headedness and dizziness. Compensation The kidneys compensate for respiratory alkalosis by excreting more HCO3− in the urine (HCO3− diuresis; see Fig. 14.4). This activity brings arterial pH down toward the normal range. As with respiratory acidosis, renal compensation is a slow process. Complete compensation may take days. Partly compensated respiratory alkalosis is characterized by decreased PaCO2, decreased [HCO3−], and a high pH—still not quite down to the normal range. Fully compensated respiratory alkalosis is characterized by decreased PaCO2, decreased [HCO3−], and pH on the alkalemic side of normal (pH > 7.40 but ≤ 7.45). Compensated respiratory alkalosis is sometimes called chronic respiratory alkalosis or chronic alveolar hyperventilation. The underlying hyperventilation and hypocapnia are still present. The terminology respiratory alkalosis is retained in classifying this condition, because although the pH is within the normal range, the PaCO2 is still below normal. Correction Correcting respiratory alkalosis involves removing the stimulus that caused the hyperventilation. If hypoxemia is the stimulus, oxygen therapy is needed. Alveolar Hyperventilation Superimposed on Compensated Respiratory Acidosis Consider a patient with a compensated respiratory acidosis who has an arterial pH of 7.38, PaCO2 of 58 mm Hg, and HCO3− of

CHAPTER 14  Acid–Base Balance

MINI CLINI Compensated (Chronic) Respiratory Alkalosis Problem A 27-year-old man was admitted to the hospital with a persistent case of bacterial pneumonia, which had not responded to 6 days of ambulatory care with antimicrobial drugs. He exhibited mild cyanosis and labored breathing. Arterial blood gas analysis (with the patient breathing room air) showed a pH of 7.44, PaCO2 of 26 mm Hg, HCO3− of 17 mEq/L, and PaO2 of 53 mm Hg. How would the RT interpret this patient’s acid-base condition? Solution The RT should follow these steps: 1. Categorize the pH. The pH is on the alkalemic side of the normal range, but it is still normal. 2. Determine respiratory involvement. PCO2 is well below normal, indicating hyperventilation as a contributing factor to the high-normal pH (respiratory alkalosis). 3. Determine metabolic involvement. HCO3− is substantially lower than normal, but because the pH is on the alkalemic side of normal, primary metabolic acidosis is ruled out. Compensation for the respiratory alkalosis has occurred. 4. Assess for compensation. HCO3− is approximately 7 mEq below normal. This is consistent with a compensatory response by the kidneys. In addition, the expected pH for PaCO2 of 26 mm Hg is [7.40 + (40 mm Hg − 26 mm Hg) × 0.01], or 7.54 (see Table 14.6). Because the actual pH is 7.44, metabolic compensation (excretion of HCO3−) must have occurred. Therefore, the interpretation is a fully compensated respiratory alkalosis.

33 mEq/L. If this patient becomes severely hypoxemic, the hypoxemia may stimulate increased alveolar ventilation if lung mechanics are not too severely impaired. If increased alveolar ventilation acutely lowers the PaCO2 from 58 to 50 mm Hg, the pH could possibly increase to the alkalemic side of the normal range. For example, the patient’s blood gas values might now be: pH 7.44, PaCO2 50 mm Hg, and HCO3− 33 mEq/L. The inexperienced clinician might wrongly interpret these values as compensated metabolic alkalosis. This example shows that blood gas data alone are not enough to make an accurate acid-base assessment. Knowledge of the patient’s medical history and the nature of the current problem are essential to evaluate this problem accurately. The blood gas values in this example would be properly classified as acute alveolar hyperventilation (even though the PaCO2 is >45 mm Hg) superimposed on chronic alveolar hypoventilation (i.e., compensated respiratory acidosis).

Metabolic (Nonrespiratory) Acidosis Any nonrespiratory process that decreases plasma [HCO3−] causes metabolic acidosis. A reduction in [HCO3−] decreases blood pH because it decreases the amount of base compared with the amount of acid in the blood.

Causes Metabolic acidosis can occur in one of the following two ways: (1) fixed (nonvolatile) acid build-up in the blood, or (2) an excessive loss of HCO3− from the body. An example of fixed acid build-up is a state of low blood flow in which tissue hypoxia and anaerobic metabolism produce lactic acid. The resulting H+

301

accumulates and reacts with HCO3−, which reduces blood [HCO3]. On the other hand, an example of HCO3− loss is severe diarrhea, in which large stores of HCO3− are eliminated from the body, also producing a nonrespiratory (metabolic) acidosis. Because these two kinds of metabolic acidosis are treated differently, it is important to identify the underlying cause. Analysis of the plasma electrolytes is helpful in distinguishing between these two types of metabolic acidosis. Specifically, measuring the anion gap is helpful in making this distinction.

Anion Gap The law of electroneutrality states that the total number of positive charges must equal the total number of negative charges in the body’s fluids. Cations (positively charged ions) in the plasma produce a charge exactly balanced by plasma anions (negatively charged ions). Plasma electrolytes (cations and anions) routinely measured in clinical medicine are Na+, potassium, Cl−, and HCO3−. Normal plasma concentrations of these electrolytes are such that the cations (Na+ and K+) outnumber the anions (Cl− and HCO3−), which leads to what seems to be an anion gap. Generally, K+ is ignored in calculating this apparent anion gap: Anion gap = [Na+ ] − ([Cl− ] + [HCO3 − ]) Fig. 14.8A shows that normal concentrations of these ions in the plasma are as follows: 140 mEq/L for Na+, 105 mEq/L for Cl−, and 24 mEq/L for HCO3−, yielding an “anion gap” of 11 mEq/L (140 mEq/L − [105 mEq/L + 24 mEq/L] = 11 mEq/L). The normal anion gap range is 9 to 14 mEq/L.6 An increased anion gap (>14 mEq/L) is caused by a metabolic acidosis in which abnormal fixed acids accumulate in the body. The H+ of these acids reacts with plasma HCO3−, lowering its concentration; this leads to a further increase in the anion gap (i.e., an increase in unmeasured anions; see Fig. 14.8B). (When the H+ of fixed acids is buffered by HCO3−, the anion portion of the fixed acid remains in the plasma, increasing unmeasured anion concentration.) A high anion gap indicates that fixed acid concentration in the body has increased. Metabolic acidosis caused by HCO3− loss from the body does not cause a further increase in the anion gap. HCO3− loss is accompanied by Cl− gain, which keeps the anion gap within normal limits (see Fig. 14.8C). The law of electroneutrality helps explain the reciprocal nature of [HCO3−] and [Cl−] in this instance. With a constant cation concentration, losing HCO3− means that another anion must be gained to maintain electroneutrality. In this case, the kidney increases its reabsorption of the most abundant anion in the tubular filtrate, the Cl−. The kind of metabolic acidosis in which HCO3− is lost from the body is sometimes called hyperchloremic acidosis because of the characteristic increase in plasma [Cl−]. Box 14.5 summarizes causes of anion gap and non–anion gap metabolic acidosis.

RULE OF THUMB Metabolic acidosis accompanied by a higher than normal anion gap means that the body has accumulated an unusual fixed acid. A metabolic acidosis accompanied by a normal anion gap means that the body has lost a greater than normal amount of base.

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Normal

Metabolic acidosis Anion gap (unmeasured anions) increased

Unmeasured cations (14)

Anion gap (11) HCO3– (24) Na+ (140)

A

Unmeasured Unmeasured cations anions (14) (25)

Anion gap (23)

Unmeasured anions (37)

Anion gap (11)

Na+ (140)

B

Cl– (105)

Cations Anions 154 154 mEq/L mEq/L

Na+ (140)

C

Unmeasured anions (25) HCO3– (12)

HCO3– (12)

Cl– (105)

Cations Anions 154 154 mEq/L mEq/L

Unmeasured cations (14)

Anion gap (unmeasured anions) constant

Cl– (117)

Cations Anions 154 154 mEq/L mEq/L

Fig. 14.8  The anion gap in normal (A) and metabolic acidosis (B and C). Fixed acid accumulation increases the anion gap (B), whereas HCO3− loss is accompanied by an equal Cl− gain, keeping the anion gap within the normal range. (Modified from Beachey W: Respiratory care anatomy and physiology: foundations for clinical practice, ed 2, St Louis, 2007, Mosby.)

BOX 14.5  Causes of Anion Gap and

Nonanion Gap Metabolic Acidosis High Anion Gap Metabolically Produced Acid Gain • Lactic acidosis • Ketoacidosis • Renal failure (e.g., retained sulfuric acid) Ingestion of Acids • Salicylate (aspirin) intoxication • Methanol (formic acid) • Ethylene glycol (oxalic acid)

Normal Anion Gap (Hyperchloremic Acidosis) Gastrointestinal Loss of HCO3− • Diarrhea • Pancreatic fistula Renal Tubular Loss: Failure to Reabsorb HCO3− • Renal tubular acidosis Ingestion • Ammonium chloride • Hyperalimentation intravenous nutrition From Beachey W: Respiratory care anatomy and physiology: foundations for clinical practice, ed 2, St Louis, 2007, Mosby.

Compensation Hyperventilation is the main compensatory mechanism for metabolic acidosis. The increased plasma [H+] of metabolic acidosis is buffered by plasma HCO3−, which reduces plasma [HCO3−]

and pH. The low pH activates sensitive receptors in the brain that signal the respiratory muscles to increase ventilation. This increased ventilation lowers the blood’s CO2 levels, and thus its volatile acid (H2CO3), which returns the pH toward the normal range. Uncompensated metabolic acidosis suggests that a ventilatory defect must be present, because ventilation usually responds to this stimulus immediately. Metabolic acidosis accompanied by PaCO2 of 40 mm Hg means that something prevents the lungs from responding appropriately to the brain’s stimulation. The defect may lie in nerve impulse transmission, the respiratory muscles, or the lungs themselves.

Symptoms Respiratory compensation in metabolic acidosis means there is a great increase in minute ventilation, which may cause patients to report dyspnea. Hyperpnea (increased tidal volume depth) is a common finding during physical examination of patients with metabolic acidosis. In patients with severe diabetic ketoacidosis, a very deep, fast breathing develops, called Kussmaul respiration. Neurologic symptoms of severe metabolic acidosis range from lethargy to coma. Correction The initial goal in severe acidemia is to increase the arterial pH greater than 7.20, a level below which serious cardiac arrhythmias become more likely, and treating them becomes more challenging. If respiratory compensation maintains the pH at or above this level, immediate corrective action is usually not required. Treatment of the underlying cause of acid gain or base loss is the reasonable approach.

CHAPTER 14  Acid–Base Balance

MINI CLINI

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MINI CLINI

Partially Compensated Metabolic Acidosis

Metabolic Alkalosis

Problem A 42-year-old woman in a diabetic coma was taken to the emergency department. She exhibited fast and deep respirations. Arterial blood gas analysis showed a pH of 7.22, PCO2 of 20 mm Hg, HCO3− of 8 mEq/L, and base excess (BE) of −16 mEq/L. How would the RT interpret this patient’s acid-base condition?

Problem An 83-year-old woman with heart disease had been taking a powerful diuretic to remove excess edematous fluid from her legs and help keep her free of pulmonary edema. Blood gas and serum electrolyte analyses showed a pH of 7.58, PaCO2 of 46 mm Hg, HCO3− of 44 mEq/L, BE of +19 mEq/L, serum K+ of 2.5 mEq/L, and serum Cl− of 95 mEq/L. How would the RT assess this patient’s acid-base condition?

Solution The RT should follow these steps: 1. Categorize the pH. The pH is below the normal range, indicating the presence of acidemia. 2. Determine respiratory involvement. PaCO2 is well below normal, indicating severe hyperventilation. By itself, this would cause alkalosis, but the presence of acidemia rules out primary respiratory alkalosis. The low PaCO2 is probably a compensatory response to primary metabolic acidosis, although this response is currently insufficient to restore pH to the normal range. 3. Determine metabolic involvement. HCO3− is severely reduced, consistent with the low pH. In the presence of low pH and low PaCO2, a low HCO3− signals primary metabolic acidosis. This is confirmed by the large BE. 4. Assess for compensation. The severe hyperventilation represents a compensatory response to primary metabolic acidosis, although compensation is far from complete. Nevertheless, the pH level would be even lower if the PaCO2 were normal. Hence the interpretation is a partially compensated metabolic acidosis.

MINI CLINI Fully Compensated Metabolic Acidosis Problem A 38-year-old man had severe diarrhea for weeks without receiving medical attention. Arterial blood gas analysis showed a pH of 7.36, PCO2 of 24 mm Hg, HCO3− of 13 mEq/L, and BE of −11 mEq/L. How would the RT assess this patient’s acid-base condition? Solution The RT should follow these steps: 1. Categorize the pH. The pH is on the acidemic side of the normal range, but it is still normal. 2. Determine respiratory involvement. PaCO2 is below normal, indicating hyperventilation. By itself, this would cause alkalemia; however, because the pH is on the acidemic side of normal, the presence of primary respiratory alkalosis is ruled out. The low PaCO2 is likely a compensatory response to a primary metabolic acidosis. 3. Determine metabolic involvement. HCO3− level is substantially lower than normal, consistent with a low pH. Given that the pH level is on the acidemic side of normal, the low HCO3− level signals a possible metabolic acidosis. This is confirmed by the large BE. 4. Assess for compensation. The hyperventilation previously described must represent a compensatory response to primary metabolic acidosis. The pH is in the normal range. Hence the interpretation is a fully compensated metabolic acidosis.

In cases of severe metabolic acidemia, intravenous infusion of NaHCO3 may be indicated. If respiratory compensation is under way, only small amounts of NaHCO3 are required to attain an arterial pH of 7.20. In any case, rapid correction of an arterial pH to greater than 7.20 by NaHCO3 infusion is undesirable.

Solution The RT should follow these steps: 1. Categorize the pH. The pH level is substantially above normal, indicating the presence of alkalemia. 2. Determine respiratory involvement. PaCO2 is slightly higher than normal, indicating mild hypoventilation. However, because alkalemia is present, the existence of primary respiratory acidosis is ruled out. The elevated PaCO2 may be a compensatory response to a primary metabolic alkalosis. 3. Determine metabolic involvement. HCO3− is substantially higher than normal. Given the high pH, the elevated HCO3− signals a metabolic alkalosis. This is confirmed by the large BE. In addition, the low serum K+ and Cl− values indicate hypokalemic/hypochloremic metabolic alkalosis. 4. Assess for compensation. Although PaCO2 is slightly elevated, compensation for metabolic alkalosis is minimal and the interpretation would be an uncompensated metabolic alkalosis.

Metabolic Alkalosis Metabolic alkalosis is characterized by increased plasma [HCO3−] or a loss of H+ and a high pH. One must keep in mind that increased [HCO3−] is not always diagnostic of a primary metabolic alkalosis because it may be caused by renal compensation for respiratory acidosis.

Causes Metabolic alkalosis can occur in one of the following two ways: (1) loss of fixed acids, or (2) gain of blood buffer base. Both processes increase plasma [HCO3−]. To explain why losing fixed acid increases the plasma [HCO3−], consider a situation in which vomiting removes gastric HCl from the body (Fig. 14.9). In response to HCl loss, H+ diffuses out of the gastric cell into the gastric fluid, where Cl− accompanies it; this forces the CO2 hydration reaction in the gastric cell to the right, which generates HCO3−. The HCO3− enters the blood in exchange for the Cl−. The plasma gains an HCO3− for each Cl− (or H+) that is lost (Fig. 14.9).6 The causes of metabolic alkalosis are summarized in Box 14.6. Metabolic alkalosis is common in acutely ill patients and is probably the most complicated acid-base imbalance to treat because it involves fluid and electrolyte imbalances. Metabolic alkalosis is often iatrogenic, resulting from the use of diuretics, low-salt diets, or gastric drainage. To understand how the loss of Cl−, K+, and fluid volume may cause alkalosis, one needs to understand how the kidney regulates Na+. Approximately 26,000 mEq of Na+ passes through the glomerular membrane daily, but the body’s daily Na+ intake averages only approximately 150 mEq.4 The kidney’s main job is to

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reabsorb Na+, not to excrete it. For this reason, and because Na+ has a major role in maintaining fluid balance, the kidney places a greater priority on reabsorbing Na+ than on maintaining Cl−, K+, or acid-base balance. Normally, Na+ is reabsorbed through primary active transport (Fig. 14.10), in which the sodium-potassium–adenosine

HCO3–

Blood

CO2 + H2O

H2CO3

triphosphatase (Na+, K+-ATPase) pump actively transports Na+ out of the renal tubule cell into the blood. This process causes Na+ to diffuse continually from the filtrate into the tubule cell. Cl− (the most abundant anion in the filtrate) accompanies Na+ because of electrostatic forces—that is, to maintain electroneutrality in the filtrate. If blood Cl− concentration is much below normal BOX 14.6  Causes of Metabolic Alkalosis

(Increased Plasma HCO3−)

Cl–

Loss of Hydrogen Ions Gastrointestinal • Vomiting • Nasogastric drainage

H+ + HCO3–

Gastric cell

Vomiting loss of HCl

HCl

H+

+

Renal • Diuretics (loss of Cl−, K+ fluid volume) • Hypochloremia (increased H+ secretion and HCO3− reabsorption) • Hypokalemia (increased H+ secretion and HCO3− reabsorption) • Hypovolemia (increased H+)

Cl–

Retention of Bicarbonate Ion • NaHCO3 infusion or ingestion

Gastric fluid +

− 3

Fig. 14.9  Gastric H loss generates HCO , creating metabolic alkalosis. (Modified from Beachey W: Respiratory care anatomy and physiology: foundations for clinical practice, ed 2, St Louis, 2007, Mosby.)

From Beachey W: Respiratory care anatomy and physiology: foundations for clinical practice, ed 2, St Louis, 2007, Mosby.

Peritubular capillary

Tubule cell 3Cl– 3Na+

K+

Cl– Na+ K+ ATPase pump

Na+

Tubular lumen Cl– Na+ Cl– Na+

2K+

Epithelial brush border

Fig. 14.10  N+ Reabsorption Through Primary Active Transport. The sodium-potassium-adenosine triphosphatase (Na+,K+-ATPase) pump generates tubular cell electronegativity by pumping out more Na+ than it pumps in K+. This creates both electrostatic and concentration gradients favoring Na+ diffusion from the filtrate into the tubular cell. Normally, negatively charged Cl− passively follows Na+ (cotransport). (Modified from Beachey W: Respiratory care anatomy and physiology: foundations for clinical practice, ed 2, St Louis, 2007, Mosby.)

CHAPTER 14  Acid–Base Balance

305

Peritubular capillary

Tubule cell Na+ HCO3–

CO2

Na+ HCO3– + H+ H2CO3 (Carbonic anhydrase) H2O + CO2

Tubular lumen HCO3– Na+ Na+ H+ + HCO3– H2CO3 CO2 + H2O

Fig. 14.11  Na+ Reabsorption Through Secondary Active H+ Secretion. Through the countertransport process, Na+ is reabsorbed as H+ is secreted into the filtrate. HCO3− ion is reabsorbed with Na+ instead of Cl−. This process becomes more predominant when Cl− is scarce, and it leads to alkalosis. (Modified from Beachey W: Respiratory care anatomy and physiology: foundations for clinical practice, ed 2, St Louis, 2007, Mosby.)

(hypochloremia), less Cl− is available for reabsorption with Na+, which means that the kidney relies more on other mechanisms to reabsorb Na+. These other mechanisms, called secondary active secretion, require the kidney to secrete either H+ or K+ into the filtrate in exchange for Na+. In this way, Na+ is reabsorbed, and filtrate electroneutrality is preserved. Figs. 14.11 and 14.12 illustrate the secondary active secretion process for H+ and Na+, which may lead to loss of plasma H+ (alkalosis) and K+ (hypokalemia). Preexisting hypokalemia (e.g., from inadequate K+ intake) in the presence of hypochloremia places an even greater demand on the kidney to secrete H+ to reabsorb Na+—that is, hypokalemia leads to alkalosis. Dehydration (fluid volume depletion or hypovolemia) further aggravates alkalosis and hypokalemia because hypovolemia profoundly increases the kidney’s stimulus to reabsorb Na+, which means the kidney depends even more on these secondary mechanisms for Na+ reabsorption.

Compensation The expected compensatory response to metabolic alkalosis is hypoventilation (CO2 retention). Traditionally, it was thought that the hypoxemia accompanying hypoventilation greatly limited respiratory compensation for metabolic alkalosis (i.e., hypoxemia itself stimulates ventilation and should prevent compensatory hypoventilation). However, metabolic alkalosis blunts the hypoxemic stimulus to ventilation—that is, neurologic receptors

sensitive to hypoxemia become less sensitive in the presence of alkalemia. Individuals with PaO2 levels of 50 mm Hg may still hypoventilate to PaCO2 levels of 55 to 60 mm Hg to compensate for metabolic alkalosis.6 Nevertheless, significant CO2 retention is not seen often in cases of metabolic alkalosis, probably because metabolic alkalosis commonly coexists with other conditions that may cause hyperventilation, such as anxiety, pain, infection, fever, or pulmonary edema.

Correction Correction of metabolic alkalosis is aimed at restoring normal fluid volume and electrolyte concentrations, especially K+ and Cl− levels. Inadequate fluid volume, especially if coupled with hypochloremia, causes excessive secretion and loss of H+ and K+ because of the great need to reabsorb Na+. In treating this type of alkalosis, it is important to supply adequate fluids containing Cl−. If hypokalemia is a primary factor, potassium chloride (KCl) is the preferred corrective agent. In rare cases of very severe metabolic alkalosis, acidifying agents, such as dilute HCl may be infused directly into a large central vein.7

Metabolic Acid-Base Indicators Standard Bicarbonate To eliminate the influence of the hydration reaction on plasma bicarbonate concentration, some laboratories report standard

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Peritubular capillary Tubular lumen Tubule cell HCO3–

Na+

HCO3– + H+ H2CO3

CO2

H2O + CO2

Na+

Na+

Na+

K+

K+

K+

Fig. 14.12  Na+ Reabsorption Through Secondary Active K+ Secretion. This mechanism is more likely to occur when Cl− is scarce and an alkalemia (low H+) exists. In such instances, hypokalemia develops. (Modified from Beachey W: Respiratory care anatomy and physiology: foundations for clinical practice, ed 2, St Louis, 2007, Mosby.)

bicarbonate. The standard bicarbonate is the plasma concentration of HCO3− (in mEq/L) obtained from a blood sample that has been equilibrated (at body temperature) with a PCO2 of 40 mm Hg. This HCO3− measurement presumably reflects only the metabolic component of acid-base balance, unhampered by the influence that CO2 changes have on HCO3−. However, the process of standardizing the bicarbonate under in vitro laboratory conditions creates an artificial situation not present in the patient’s body. The blood in the patient’s vascular system is separated from the extravascular fluid (fluid outside of the vessels) by a thin capillary endothelial membrane, readily permeable to HCO3−. When a patient hypoventilates and the blood PaCO2 increases, the plasma HCO3− also increases because of the hydration reaction. Consequently, plasma HCO3− diffuses out of the capillary into the extravascular fluid until HCO3− equilibrium is established between the blood and extravascular fluid. If the patient were now to hyperventilate so that the PaCO2 again was 40 mm Hg, blood HCO3− would decrease, and extravascular HCO3− would diffuse down its concentration gradient back into the blood until an HCO3− equilibrium was established again. This diffusion of HCO3− between vascular and extravascular spaces cannot occur in a laboratory blood sample when the blood PCO2 of a hypercapnic patient is artificially lowered to 40 mm Hg. Thus even the standard bicarbonate is not a

perfect measure of purely nonrespiratory factors that influence blood pH.

Base Excess Base excess (BE) is determined by equilibrating a blood sample in the laboratory to a PCO2 of 40 mm Hg (at 37°C) and recording the amount of acid or base needed to titrate 1 L of blood to a pH of 7.40. A normal BE is ±2 mEq/L. A positive BE (>+2 mEq/L) indicates a gain of base or loss of acid from nonrespiratory causes. A negative BE ( 3 weeks), unexplained fever despite a comprehensive work-up is called a fever of unknown origin (FUO) and is a common finding in patients with HIV disease.8 The magnitude of temperature elevation may indicate the type and virulence of the infection. Low-grade fever typically accompanies common upper respiratory tract infections, whereas a high fever occurs with influenza infection. Fever that occurs with a cough suggests a respiratory tract infection, particularly when purulent sputum is produced. Pneumonia is suspected when a high fever (i.e., 38.9°[C102°F]) persists for 2 or more days and is accompanied by chills. However, the absence of coughing or sputum production does not rule out lung infection. For many years, it was believed that a link existed between fever and atelectasis in postoperative surgical patients. However, we now know that atelectasis does not cause fever.9 Patients with a significant fever have an increased metabolic rate that increases both O2 consumption and carbon dioxide production and may cause tachypnea. Fever is particularly dangerous for patients with severe chronic cardiopulmonary

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disease because the increased ventilatory demand may induce acute respiratory failure.

Pedal Edema Heart failure is often characterized by swelling in the lower extremities referred to as dependent or pedal edema, the classic sign being “swollen ankles.” It is caused by the heart’s inability to pump blood effectively, with blood pooling in the gravity-dependent lower extremities as a consequence. The resulting increase in venous hydrostatic pressure pushes fluid into the interstitial space. It is also common in patients with end-stage liver disease. Pedal edema has two subtypes. Pitting edema is when finger pressure applied on a swollen extremity leaves an indentation mark on the skin. The highest point where pitting edema occurs suggests the severity of heart failure. For example, pitting edema that extends to the knees signifies greater heart failure than edema limited to the ankles. Weeping edema occurs when the applied finger pressure causes a small fluid leak. A standard scale is used to quantify the severity of pitting edema, with “1 plus” equating to trace pitting with rapid refill and “4 plus” meaning severe pitting with refill time in excess of 2 minutes. Any patient who is suspected to have right-sided or left-sided heart failure is examined for pedal edema. Patients with chronic hypoxemic lung disease are especially prone to right-sided heart failure (cor pulmonale) that also causes pedal edema. Chronic hypoxemia causes severe pulmonary vasoconstriction and pulmonary hypertension. Sustained elevated workloads on the thin-walled right ventricle eventually lead to failure and venous congestion.

The Medical Record and Medical History The first priority of the RT reviewing the medical record is to ensure the presence of a valid physician order for all respiratory care procedures. A valid order is one that is current, clearly written, and complete (i.e., without ambiguity as to what is being administered, the parameters or dosage, and frequency of administration). All healthcare practitioners must be familiar with the medical history of the patients they are treating regardless of the reason for contact. The medical history familiarizes clinicians with the signs and symptoms that the patient exhibited on admission and the rationale for administered therapies. Afterward, the RT should read the chief complaint and history of present illness which presents a detailed, systematic account of the patient’s major complaints written by a physician after the postadmission interview with the patient. The next step is to review the patient’s past medical history describing all past major illnesses, injuries, surgeries, hospitalizations, allergies, and health-related habits. This information is essential to building rapport with the patient as it provides context to whatever the patient shares about their experiences with illness and the healthcare system. The past history also provides context regarding medical decisions made during the current hospitalization. The past medical history also records the patient’s smoking history which is extremely important in assessing pulmonary

health. Smoking history is recorded in pack-years and is determined by multiplying the number of packs smoked per day by the number of years smoked. Typically, patients are asked how many cigarettes (on average) they smoke per day. If they state that they have smoked a pack of cigarettes a day for 20 years, then their smoking history is 20 pack-years. If patients describe their smoking in terms of the number of cigarettes, or fractions of a pack, the calculation becomes more difficult. Two examples may be helpful in this situation. There are 20 cigarettes per pack. If a patient states he or she has smoked a pack and a half of cigarettes per day for 20 years, the smoking history is calculated as follows: 30 cigarettes 20 cigarettes per pack = 1.5 packs × 20 years = 30 pack years smoking history If the patient states that he or she has smoked 15 cigarettes per day for 20 years: 15 cigarettes 20 cigarettes per pack = 0.75 packs × 20 years = 15 pack years smoking history A review of potential genetic or occupational links to disease and the patient’s current life situation are documented in the family and social/environmental history. Many patients have a genetic predisposition to pulmonary disorders such as asthma, lung cancer, and cystic fibrosis. A detailed occupational history also is important in establishing acquired pulmonary disorders from workplace exposure to inhaled organic (i.e., carbon-based) or non-organic (e.g., asbestos, silica) compounds. A strong link exists between many chronic pulmonary diseases and air pollution which predominantly affects those living in urban poverty.10 The review of systems uncovers problem areas the patient may have omitted, and is usually obtained in a head-to-toe review of all body systems. For each system, the interviewer obtains information about current symptoms. When reviewing the respiratory system, the interviewer asks about the presence or history of cough, hemoptysis, sputum production, chest pain, shortness of breath, and fever (Box 16.4).

MINI CLINI Problem During the interview a patient just diagnosed with chronic obstructive pulmonary disease (COPD) relates a complicated smoking history to the RT. For the first 10 years he smoked roughly 2 packs/day but slowly weaned himself down to 1 12 packs/day for 6 years, 1 pack/day for 2 years and then 12 pack per day for 1 year before quitting entirely. About how many pack years did this patient smoke? Solution 2 packs/day for 10 years is 20 pack-years; 1 12 packs/day × 6 years is 9 packyears, 1 pack/day for 2 years is 2 pack-years, and 12 pack/day for 1 year is 1 pack-years. The estimated smoking history then is 20 + 9 + 2 + 0.5 or 2 approximately 32 pack-years.

CHAPTER 16  Bedside Assessment of the Patient

BOX 16.4  Outline of a Complete Health

BOX 16.5  Typical Format for Recording

Demographic data (obtained from admission interview): Name, address, age, birth date, place of birth, race, nationality, marital status, religion, occupation, and source of referral Date and source of history and estimate of the reliability of the historian Brief description of the patient’s condition at the time the history or patient profile was taken Chief complaint and reason for seeking treatment History of present illness: Chronologic description of each symptom • Onset: Time, type, source, setting • Frequency and duration of symptoms • Location and radiation of pain • Severity (quantity) • Quality (character) • Aggravating and alleviating factors • Associated manifestations Past medical history • Childhood diseases and development • Hospitalizations, surgeries, injuries, accidents, and major illnesses • Allergies • Medications Family history • Familial disease history • Marital history • Family relationships Social and environmental history • Education • Military experience • Occupational history • Religious and social activities • Alcohol and cigarette consumption • Living arrangements • Hobbies and recreation • Satisfaction with and stresses of life situation, finances, and relationships • Recent travel or other event that might affect health Review of systems: Respiratory system • Cough • Hemoptysis • Sputum (amount and consistency) • Chest pain • Shortness of breath • Hoarseness or changes in voice • Dizziness or fainting • Fever or chills • Peripheral edema Patient’s printed name and signature

Initial Impression • Age, height, weight, sensorium, and general appearance

History

Finally, the medical record should indicate whether any limitations are in place on the extent of care provided in the event of cardiac or respiratory arrest. This information is known as an advance directive, whereby the patient (or a legally authorized representative) has formalized his or her wishes for resuscitative efforts. Typically this is referred to as the DNR status (“do not resuscitate”) or may be expressed as DNI (“do not intubate”). A less ambiguous acronym, AND (“allow for natural death”), emphasizes that care is focused on patient comfort. This information may be found either in the admission note or within the body of the physician progress notes. In addition to this

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the Physical Examination

Vital Signs • Pulse rate, respiratory rate, temperature, and blood pressure Head, Ears, Eyes, Nose, and Throat • Inspection findings Neck • Inspection and palpation findings Thorax • Lungs: Inspection, palpation, percussion, and auscultation findings • Heart: Inspection, palpation, and auscultation findings Abdomen • Inspection, palpation, percussion, and auscultation findings Extremities • Inspection and palpation findings

descriptive note, there must be an order written by the physician clearly specifying how care should be limited in the event of a medical emergency.

PHYSICAL EXAMINATION A careful physical examination of the patient is essential for evaluating problem(s) and determining the effects of therapy. The physical examination consists of four general steps: (1) inspection (visually examining), (2) palpation (touching), (3) percussion (tapping), and (4) auscultation (listening with a stethoscope).

General Appearance The RT’s initial impressions when encountering a patient may indicate the severity of the current problem and alter the subsequent assessment course. If the patient’s general appearance suggests an acute problem, the examination may be abbreviated and focused upon that singular issue until that condition is stabilized. When the patient appears stable, a more complete assessment can be conducted (Box 16.5). Four important indicators are used when assessing the patient’s overall appearance include: (1) their level of consciousness (see later discussion), (2) facial expression, (3) level of anxiety or distress, and (4) positioning. When observing the patient the RT should look for specific characteristics. Does the patient appear well nourished or emaciated? Weakness and emaciation (cachexia) are signs of general ill health and malnutrition that increase susceptibility to infection. Is the patient sweating? Diaphoresis (sweating) can indicate fever, pain, severe stress, increased metabolism, or acute anxiety. Facial expressions communicate a patient’s internal state, particularly in regard to stress response. In fact, specific patient facial expression patterns are found to precede clinical deterioration.11

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By observing facial expressions during encounters with patients the RT might be able to intuit the presence of pain or anxiety, as well as patient alertness and mood. Body positioning also may be useful in assessing the severity of some pulmonary problems. For example, patients with severe pulmonary hyperinflation tend to sit upright while bracing their elbows on a table. Known as the tripod sign, this position gives a mechanical advantage to the accessory breathing muscles of the upper chest and neck.

Level of Consciousness In medicine the term sensorium is used when evaluating a patient’s cognitive functioning and level of consciousness. The sensorium is evaluated by asking patients whether they are aware of their current circumstances—namely whether they are oriented to time, place, person (i.e., self), and situation. A normal sensorium is present when the patient can correctly tell the interviewer their name, the current date, their location, and their situation (e.g., “I’m in the hospital because I fell and broke my hip”). This is typically documented as “oriented × 4.” The simple rating scale shown in Box 16.6 allows clinicians to describe the patient’s level of consciousness objectively. Depressed consciousness may occur when cerebral blood flow is impaired (e.g., hypotension, neurovascular lesion) or when the brain is perfused with poorly oxygenated blood. Early signs of acutely decreased cerebral oxygenation include restlessness, confusion, or disorientation and may progress to loss of consciousness as hypoxemia worsens. In contrast, patients with severe chronic lung disease have adapted to sustained hypoxemia and often have normal mental status. Other sources of abnormal sensorium include chronic degenerative brain disorders, side effects of certain medications, and drug overdoses (particularly sedatives and narcotics). The Glasgow Coma Scale score is used to assess the level of consciousness and neurologic function and is described in more detail later in this textbook.

Vital Signs Vital signs include body temperature, pulse rate, respiratory rate, blood pressure, and pulse oximetry and constitute the cornerstone of patient monitoring. They are easy to obtain and provide useful information. Often, abnormal vital signs are the first clue of adverse reactions to treatment. In addition, improvement in a patient’s vital signs is strong evidence that a treatment is effective. For example, decreased respiratory and heart rates in response to supplemental O2 suggest the therapy is beneficial.

Body Temperature The average adult body temperature is about 37°C (98.6°F), and fluctuates approximately 0.5°C (1°F). Normally it is lowest in the early morning and highest in the late afternoon. Body temperature represents the balancing of heat production with heat loss and is regulated by the hypothalamus. Body temperature is controlled largely through skin perfusion whereby heat dissipates with peripheral vasodilation and sweating (diaphoresis) and is conserved by vasoconstriction. Minor dissipation occurs during breathing whereby some of the heat used to warm inspired air is subsequently lost during exhalation.

BOX 16.6  Levels of Consciousness Confused The patient • Exhibits slight decrease of consciousness • Has slow mental responses • Has decreased or dulled perception • Has incoherent thoughts Delirious The patient • Is easily agitated • Is irritable • Exhibits hallucinations Lethargic The patient • Is sleepy • Arouses easily • Responds appropriately when aroused Obtunded The patient • Awakens only with difficulty • Responds appropriately when aroused Stuporous The patient • Does not awaken completely • Has decreased mental and physical activity • Responds to pain and exhibits deep tendon reflexes • Responds slowly to verbal stimuli Comatose The patient • Is unconscious • Does not respond to stimuli • Does not move voluntarily • Exhibits possible signs of upper motor neuron dysfunction, such as Babinski reflex or hyperreflexia • Loses reflexes with deep or prolonged coma

Elevated body temperature (hyperthermia or hyperpyrexia) can result from disease or from normal strenuous activities. Temperature elevation caused by disease is called fever, and the patient is said to be febrile. Fever increases metabolism, causing both increased O2 consumption and CO2 production. Increased metabolism induces both increased circulation and ventilation to maintain homeostasis. This is why febrile patients often have increased heart and breathing rates. Fever increases the demand placed on the heart and lungs and often complicates clinical management. Patients with limited cardiopulmonary reserve often cannot meet the increased circulatory and ventilatory demand and are vulnerable to respiratory failure. Hypothermia is a body temperature below normal; the most common source is prolonged exposure to cold. In response the hypothalamus initiates shivering (to generate heat) and vasoconstriction (to conserve heat). Pathological sources of hypothermia include injury to the hypothalamus from trauma or stroke, decreased thyroid activity, and sepsis.

CHAPTER 16  Bedside Assessment of the Patient

Because hypothermia reduces O2 consumption and CO2 production, patients with hypothermia may exhibit slow, shallow respiratory rate and reduced pulse rate. The most common sites for measuring body temperature are the mouth, axilla, ear (tympanic membrane), and rectum. The oral site typically is used in an alert, adult patient, but cannot be used with infants, comatose, or orally intubated patients. Oral temperature measurement should be delayed for 10 to 15 minutes when patients have recently ingested hot or cold liquid or have been smoking. The axillary site (i.e., in the armpit) is acceptable for infants or small children who do not tolerate rectal thermometers, but less desirable as it may underestimate core temperature by 1° to 2°C. Accurate body temperature also can be measured using a hand-held eardrum (tympanic membrane) thermometer. However, rectal temperatures are closest to actual core body temperature.

Pulse Rate The peripheral pulse is evaluated for rate, rhythm, and strength (Box 16.7). The normal adult pulse rate is 60 to 100 beats/min, with a regular rhythm. A condition in which the pulse rate is greater than 100 beats/min is called tachycardia. Common causes of tachycardia are exercise, fear, anxiety, low blood pressure, anemia, fever, reduced arterial blood O2 levels (hypoxemia), elevated CO2 (hypercapnia), and certain medications. A condition in which the pulse rate is less than 60 beats/min is called bradycardia. Although less common, bradycardia can occur with hypothermia, traumatic brain or cervical spinal cord injury, certain cardiac arrhythmias, and certain medications. The radial artery is the most common site used to palpate the pulse. The second and third fingertip pads (but not the thumb) are used to palpate the radial pulse. Ideally, the pulse rate is counted for 1 minute, especially if the pulse is irregular. Essential pulse characteristics should be noted and documented Box 16.7. Spontaneous ventilation influences pulse strength (amplitude) during inspiration with a slight decrease in pulse pressure (the difference between the systolic and diastolic systemic blood pressure). This is caused by negative intrathoracic pressure (generated by diaphragmatic contraction) that pools blood in the pulmonary circulation while simultaneously increasing venous return and right ventricular volume. These combined effects (blood pooling in the pulmonary circulation and right ventricular engorgement) limits left ventricular filling during diastole. The end result is a brief reduction in left ventricular stroke volume and decreased systolic blood pressure. Pulse pressure normally decreases slightly with inspiration (10 mm Hg) during spontaneous inspiration that can be quantified with a blood pressure cuff (see later section). It is a common finding in acute obstructive pulmonary disease, especially in patients experiencing an asthma attack. During respiratory distress, vigorous inspiratory efforts decrease stroke volume by impeding the strength of left ventricular contraction.12 Pulsus paradoxus also may signal a mechanical restriction of the pumping action of the heart, as can occur with constrictive pericarditis or cardiac tamponade. Pulsus alternans is an alternating succession of strong and weak pulses that suggests left-sided heart failure rather than pulmonary disease. RULE OF THUMB Pulsus paradoxus is an exaggeration of the normal variation in pulse pressure caused by negative intrathoracic pressure during inspiration. During respiratory distress (e.g., COPD exacerbations) large negative intrathoracic pressure swings can greatly magnify pulse pressure swings. In contrast, alternating series of large and small pulse pressures seemingly unrelated to the breathing cycle is more indicative of left heart dysfunction.

The pulse also may be assessed by palpating the carotid, brachial, femoral, temporal, popliteal, posterior tibial, and dorsalis pedis pulses. The more centrally located pulses (e.g., the carotid and femoral) should be used when the blood pressure is abnormally low. If the carotid site is used, great care must be taken to avoid the carotid sinus area. Pressure on the carotid sinus area may cause strong parasympathetic stimulation resulting in bradycardia.

Respiratory Rate The normal resting adult respiratory rate is 12 to 18 breaths/ min. Tachypnea is defined as a respiratory rate greater than 20 breaths/min and has multiple sources: exertion, fever, hypoxemia, hypercarbia, metabolic acidosis, pulmonary edema, lung fibrosis, anxiety, and pain. Bradypnea is a respiratory rate less than 10 breaths/min and may occur with traumatic brain injury, severe myocardial infarction, hypothermia, anesthetics, opiate narcotics, and recreational drug overdoses. The respiratory rate is counted by watching the abdomen or chest wall move out and in. Sometimes the respiratory rate may need to be verified by placing a hand on the upper abdomen (i.e., detect diaphragmatic contraction). Ideally, the patient should be unaware that the respiratory rate is being counted (i.e., awareness of having one’s breathing being watched generally causes the respiratory rate to increase). One method to accomplish this is to count the respiratory rate immediately after evaluating the patient’s pulse, while keeping the fingers on the patient’s wrist. This gives the impression that the pulse rate is still being counted. Arterial Blood Pressure Arterial blood pressure is the force exerted by the heart against the systemic arteries as the blood moves through them (see Chapter 10). Arterial systolic pressure is the peak force exerted in the major arteries during contraction of the left ventricle, whereas diastolic pressure is the force in the major arteries

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remaining after relaxation of the ventricles. In an adult, normal systolic pressure is 90 to 140 mm Hg, whereas normal diastolic pressure is 60 to 90 mm Hg. Blood pressure tends to increase with age in adulthood. The blood pressure is recorded by listing systolic pressure over diastolic pressure (e.g., 120/80 mm Hg). Pulse pressure is the difference between the systolic and diastolic pressures and is normally 30 to 40 mm Hg. A pulse pressure below 30 mm Hg is difficult to detect. RULE OF THUMB  The pulse pressure is the difference between systolic and diastolic pressure and is normally 30–40 mm Hg. When the pulse pressure falls below 30 mm Hg the pulse can be difficult to palpate.

Systemic hypertension is an arterial blood pressure persistently greater than 140/90 mm Hg and is a common medical problem in adults. In approximately 90% of cases the cause is unknown (“essential” hypertension). There are three categories of hypertension.13 Stage I is defined as a systolic pressure of 140 to 159 mm Hg or a diastolic pressure of 90 to 99 mm Hg. Stage II hypertension occurs when the systolic pressure is 160 mm Hg or greater or the diastolic pressure is 100 mm Hg or greater. A third category (“prehypertension”) is used to assess the future risk of developing hypertension. It is defined as systolic pressure between 120 and 139 mm Hg or diastolic pressure between 80 and 89 mm Hg. Prehypertension is not a disease state and does not require treatment. Hypertension results from increased systemic vascular resistance (e.g., either constriction or stiffening of blood vessels) or an increased force of ventricular contraction. Sustained hypertension can cause central nervous system abnormalities, such as headaches, blurred vision, and confusion. Other potential consequences of hypertension include uremia (renal insufficiency), CHF, and cerebral hemorrhage. Acute, severe elevation of blood pressure can cause acute neurologic, cardiac, and renal failure and is called an acute hypertensive crisis. Hypotension is defined in one of three ways: (1) a systolic arterial pressure less than 90 mm Hg, (2) a mean arterial pressure less than 65 mm Hg, or (3) a decrease in systolic pressure greater than 40 mm Hg from baseline.14 The last definition acknowledges that patients with baseline hypertension may have inadequate tissue perfusion at blood pressures considered normal for most patients. The precise definition of shock is inadequate delivery of O2 and nutrients to the vital organs relative to their metabolic demand.15 Although tissue hypoperfusion often is inferred by the presence of hypotension, the two conditions are not synonymous. In shock, vital body organs are in imminent danger of receiving inadequate blood flow and tissue impaired O2 delivery (i.e., tissue hypoxia). For this reason, shock is usually treated aggressively with fluids, blood products, or vasoactive drugs, or a combination of these, depending on the cause and severity. There are two broad categories of hypotension and shock can be broadly characterized as representing either a hypodynamic or hyperdynamic cardiovascular state.15 Hypodynamic states include left ventricular failure (cardiogenic) and reduced blood volume (hypovolemia or hypovolemic) from hemorrhage or severe fluid loss. Hyperdynamic states are caused by profound

systemic vasodilation (peripheral vascular failure) associated with overwhelming infection (septic shock), systemic allergic reaction (anaphylaxis), or severe liver failure. In healthy individuals sitting or standing up causes minimal changes in blood pressure. However, similar postural changes in a hypovolemic patient often produce hypotension. This is referred to as postural hypotension and is treated with fluid administration. Postural hypotension is confirmed by measuring blood pressure with the patient supine and then measuring with the patient in the sitting (or standing) position. Postural hypotension may reduce cerebral blood flow and lead to syncope (fainting). The most common technique for measuring arterial pressure requires a blood pressure cuff (sphygmomanometer) and a stethoscope (Fig. 16.2). When the cuff is applied to the upper arm and pressurized to exceed systolic blood pressure, brachial arterial blood flow stops. The cuff pressure is then released slowly. Once the cuff pressure falls just below the systolic pressure, blood flows intermittently past the obstruction and creates turbulence and vibrations called Korotkoff sounds. These sounds are heard with a stethoscope over the brachial artery distal to the cuff. To measure the blood pressure, a deflated cuff is wrapped snugly around the patient’s upper arm, with the lower edge of the cuff 1 inch above the antecubital fossa. While palpating the brachial pulse, the clinician inflates the cuff approximately 30 mm Hg above the point at which the pulse can no longer be felt. Then, the diaphragm of the stethoscope is placed over the artery and the cuff is slowly deflated (2 to 3 mm Hg/s) while observing the manometer. The systolic pressure is recorded when the first Korotkoff sounds are heard. The point where cuff pressure equals diastolic pressure turbulence ceases. Therefore the pressure when Korotkoff sounds disappear represents the diastolic pressure. As mentioned earlier, a paradoxical pulse is when systolic blood pressure decreases more than 10 mm Hg during a resting inhalation and can only be quantified by auscultation. To measure this, inflate the blood pressure cuff until the radial or brachial pulse can no longer be palpated. Then slowly deflate the cuff until sounds are heard only on exhalation (point 1). Next, reduce the cuff pressure until sounds are heard throughout respiration (point 2). The difference between points 1 and 2 indicates the degree of paradoxical pulse. Most hospitals and clinics now use digital blood pressure measuring devices that do not require clinicians to listen for the Korotkoff sounds. These devices are very accurate and eliminate variances in recorded blood pressures based on human perception. The clinician only needs to apply the blood pressure cuff correctly and press the start button. The device inflates and deflates the cuff automatically and displays the blood pressure and pulse rate on a digital screen.

Examination of the Head and Neck Head Respiratory distress produces common facial signs such as nasal flaring, cyanosis, and pursed-lip breathing. Nasal flaring occurs when the external nares flare outward during inhalation and is associated with increased work of breathing.

CHAPTER 16  Bedside Assessment of the Patient

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Pressure mm Hg Cuff pressure Systolic pressure 110 100 90 80 70

Ar terial pressure pulses Diastolic pressure

60 50 40 30 20 10 0

Sphygmomanometer cuff Inflation bulb

Fig. 16.2  Auscultatory method for measuring arterial blood pressure, using a sphygmomanometer and a stethoscope. (Redrawn from Rushmer RR: Structure and functions of the cardiovascular system, ed 2, Philadelphia, 1976, WB Saunders.)

Cyanosis is a bluish discoloration of the skin or oral mucosa resulting from respiratory or cardiac disease (discussed later). Patients with COPD may use pursed-lip breathing during exhalation. Breathing through pursed lips during exhalation creates resistance to flow. The increased resistance creates a slight back pressure in the small airways during exhalation. This back pressure prevents premature airway collapse and allows more complete emptying of the lung.

Neck Inspection and palpation of the neck help determine the position of the trachea and the jugular venous pressure (JVP). Normally, when the patient faces forward, the trachea is located in the middle of the neck. The midline of the neck can be identified by palpating the suprasternal notch. The midline of the trachea should be directly below the center of the suprasternal notch. The trachea can shift away from the midline in certain thoracic disorders. Generally, the trachea shifts toward an area of collapsed lung and shifts away from areas with increased air or fluid (e.g., tension pneumothorax or large pleural effusion).

RULE OF THUMB Volume changes inside the hemithorax often cause the mediastinal contents to shift and are seen on a physical exam by a shift in the position of the trachea. Severe volume loss (i.e., from lobar collapse) will cause the trachea to shift toward the affected side. In contrast increased volume and positive pressure in the pleural space (i.e., from large pneumothoraces or pleural effusion) will cause the trachea to shift away from the affected side.

JVP indirectly reflects venous blood volume and pressure of the right heart. A rising JVP (and associated jugular venous distension) typically reflects the heart’s inability to adequately pump blood. JVP is estimated by determining how high the jugular vein extends above the level of the sternal angle. Individuals with obese necks may not have visible neck veins, even when the veins are distended. When lying supine healthy individuals have visible neck veins that extend up the neck. As the head of the bed is elevated (i.e., 45-degree angle) the blood column descends and their visibility diminishes to approximately the clavicular level. With elevated venous pressure, the neck veins may be distended as high as the angle of the jaw, even when the patient is sitting upright. JVP decreases during inspiration with increasing negative intrathoracic pressure causing the blood column to descend toward the thorax. During passive expiration the blood column returns to its previous position. However, during active expiration (i.e., positive intrathoracic pressure from abdominal muscular contraction) JVP and the position of the neck veins may actually rise higher than the previously observed end-expiratory baseline. Under abnormal conditions (e.g., cardiac tamponade), the JVP may increase during inhalation and is called Kussmaul sign. Jugular venous distension (JVD) is present when the jugular vein is enlarged and can be seen more than 4 cm above the sternal angle. It is common in patients with chronic hypoxemia who develop right heart failure (cor pulmonale) from hypoxemia- induced pulmonary hypertension. Other conditions associated with JVD include left heart failure, cardiac tamponade, tension pneumothoraces, and mediastinal tumors.

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A

B

Fig. 16.3  (A) Patient with normal thoracic configuration. (B) Patient with increased anteroposterior diameter. Note contrasts in the angle of slope of the ribs and development of accessory muscles.

The neck also is palpated to detect lymphadenopathy (i.e., enlarged lymph nodes) Lymphadenopathy occurs with various medical disorders, including infection, malignancy, and sarcoidosis. Tender lymph nodes in the neck suggest a nearby infection. In contrast malignancy is characterized by enlarged, non-tender lymph nodes.

TABLE 16.1  Abnormalities of Thoracic

Examination of the Thorax and Lungs

Kyphosis

Inspection Visual inspection of the chest assesses thoracic configuration, expansion, breathing pattern, and breathing effort. This should occur in a well-lit room with the patient sitting upright. When the patient is unable to sit up, the clinician should carefully roll the patient to one side to examine the posterior chest. Inspection, palpation, percussion, and auscultation require at least partial exposure of the thorax. Therefore, clinicians must be sensitive to issues of privacy and patient modesty (especially for female patients). In a semiprivate room the drapes must be drawn and whenever possible expose as little of the thorax as needed to adequately conduct the examination. Thoracic configuration.  With normal body habitus transverse diameter of the thorax exceeds the anteroposterior (AP) diameter. Normally, the AP diameter increases with age but may prematurely increase in patients with COPD. This abnormal increase in AP diameter is called barrel chest and is associated with emphysema. When the AP diameter increases, the normal 45-degree angle of articulation between the ribs and spine is increased, becoming

Configuration Name

Condition

Pectus carinatum Pectus excavatum

Abnormal protrusion of sternum Depression of part or entire sternum, which can produce a restrictive lung defect Spinal deformity in which the spine has an abnormal anteroposterior curvature Spinal deformity in which the spine has a lateral curvature Combination of kyphosis and scoliosis, which may produce a severe restrictive lung defect as a result of poor lung expansion

Scoliosis Kyphoscoliosis

more horizontal (Fig. 16.3). Other abnormalities of the thoracic configuration are listed in Table 16.1. Thoracic expansion.  The diaphragm is the primary muscle of (and power source for) breathing. Diaphragmatic contraction causes the ribs to distend both outward and upward and the anterior abdominal wall to protrude outward. Therefore, when palpating the chest wall, both the chest and abdomen should expand synchronously during inspiration. However, the relative expansion of the thorax and abdomen depend upon body position. When supine, the primary motion during normal tidal breathing is outward abdominal expansion with little noticeable chest

CHAPTER 16  Bedside Assessment of the Patient

A

331

B Fig. 16.4  Estimation of Thoracic Expansion. (A) Exhalation. (B) Maximal inhalation.

excursion. In the upright position rib cage motion becomes more pronounced.16 The normal chest wall expands symmetrically and can be evaluated anteriorly and posteriorly. Anterior expansion is evaluated by placing the hands over the anterolateral chest, with the thumbs extended along the costal margin toward the xiphoid process. To evaluate posteriorly, position the hands over the posterolateral chest with the thumbs meeting at the T-8 vertebra (Fig. 16.4). Instruct the patient to exhale slowly and completely. At maximal exhalation, gently secure the fingertips against the sides of the patient’s chest and extend the thumbs toward the midline until the tip of each thumb meets at the midline. Next instruct the patient to take a full, deep breath. Note the distance the tip of each of the thumbs moves from midline. Normally, each thumb moves an equal distance of approximately 3 to 5 cm. Diseases that restrict lung expansion also reduce chest expansion on the affected side (i.e., either unilateral or bilateral). Causes of reduced expansion include neuromuscular disorders (from muscular weakness), COPD (from lung hyperinflation), lobar consolidation (non-distensible tissue), pleural effusion, and pneumothorax (loss of pleural space integrity to transmit inspiratory muscle pressure). Breathing pattern and effort.  A healthy resting adult has a consistent breathing rate and rhythm with minimal effort and passive exhalation. There are two broad categories encompassing abnormal patterns: (1) those directly associated with cardio­ pulmonary or chest wall diseases that increase work of breathing and (2) those associated with neurologic disease (Table 16.2). The hallmark of increased breathing effort (“work of breathing”) is the recruitment of accessory breathing muscles in the neck and thorax to maintain ventilation. The most readily apparent (and palpable) is the sternocleidomastoid or “strap muscles.”

Common causes of increased work of breathing are airway obstruction (e.g., COPD, asthma), edematous (“heavy”) lungs (e.g., acute respiratory distress syndrome [ARDS], cardiogenic pulmonary edema), or a stiff chest wall (e.g., ascites, anasarca, pleural effusions). One sign of severely increased work of breathing is visible distortions in the chest wall called retractions. During labored breathing the abdominal muscles also are recruited during expiration to assist subsequent inspiratory efforts (see later: assessing the diaphragm) Retractions are an inward sinking of the chest wall during inspiration. This occurs when inspiratory muscle contractions generate large negative intrathoracic pressures. The respiratory muscles can generate negative inspiratory pressures of approximately 150 cm H2O (112 mm Hg) at maximal effort.17 There are three distinct types of retractions: (1) intercostal (seen between the ribs), (2) supraclavicular (above the clavicles), and (3) subcostal (below the rib cage). Another form of retraction is tracheal tugging, which is the downward movement of the thyroid cartilage toward the chest during inspiration in concert with sternocleidomastoid muscle recruitment. Note that retractions are difficult to see in obese patients. Two archetypal abnormal breathing patterns exist providing clues about the underlying pulmonary disease. The first is characterized by a rapid, shallow breathing pattern and the second is characterized by an abnormally prolonged exhalation with pronounced, sustained abdominal muscular contraction. An additional pattern, Kussmaul breathing, is observed during severe metabolic acidosis whereby patients breathe rapidly and deeply, similar to a normal person during strenuous exercise. Rapid, shallow breathing typically occurs in patients with increased lung inflammation or stiffness (e.g., ARDS, pulmonary fibrosis), whereas lower airway obstruction slows lung emptying

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TABLE 16.2  Abnormal Breathing Patterns Breathing Pattern

Characteristics

Causes

Agonal breathing Apnea Apneustic breathing

Intermittent prolonged gasps No breathing Deep, gasping inspiration with brief, partial expiration

Ataxic breathing

Completely irregular breathing pattern with variable periods of apnea Prolonged exhalation with recruitment of abdominal muscles Chaotic breathing pattern characterized by frequent irregularity in both rate and tidal volume that eventually deteriorates to agonal breathing and terminal apnea Irregular type of breathing; breaths increase and decrease in depth and rate with periods of apnea; variant of “periodic breathing”

Preterminal brain stem reflex Cardiac arrest, narcotic overdose, severe brain trauma Damage to upper medulla or pons caused by stroke or trauma; sometimes observed with hypoglycemic coma or profound hypoxemia Damage to medulla

Asthmatic breathing Biot respiration

Cheyne-Stokes respiration

Central neurogenic hyperventilation Kussmaul breathing Paradoxical breathing

Periodic breathing

Persistent hyperventilation Deep and fast respirations Abdominal paradox: Abdominal wall moves inward on inspiration and outward on expiration Chest paradox: Part or all of the chest wall moves in with inhalation and out with exhalation

Breathing oscillates between periods of rapid, deep breathing and slow, shallow breathing without prolonged periods of apnea

and prolongs the expiratory phase as patients attempt to minimize gas trapping inside the lungs. This causes the inspiratory-toexpiratory time ratio to decrease from a normal value of 1 : 2 to 1 : 4 or greater. In contrast, extrathoracic upper airway obstruction (e.g., epiglottitis or croup) results in a prolonged inspiratory time in an attempt to achieve an adequate tidal volume. Neurologic and some cardiac diseases also produce abnormal breathing patterns. These include Cheyne-Stokes respiration, Biot respiration, apneustic breathing, central neurogenic hypoventilation, and hyperventilation. Cheyne-Stokes respiration is when the respiratory rate and tidal volume gradually increase in intensity and then gradually decrease to complete apnea (absence of ventilation), which may last several seconds. This pattern is associated with coma from severe cerebral lesions, metabolic derangements, or low cardiac output states (e.g., CHF). However, it is not always associated with profound pathology as it sometimes occurs during sleep in the elderly.18 In comatose states, the regulatory influence of the cerebral cortex on the respiratory centers in the medulla is lost. As a result, the medulla becomes overly sensitive to CO2 resulting in the waxing and waning breathing pattern. In CHF Cheyne-Stokes respiration is caused by prolonged blood transit time between the lungs and the medulla wherein changes in respiratory center PCO2 lag behind changes in arterial PCO2. Biot respiration occurs with damage to the medulla resulting in a chaotic breathing pattern characterized by frequent irregularity in both rate and tidal volume. The pattern eventually deteriorates

Obstruction to airflow out of the lungs Damage to medulla or pons caused by stroke or trauma; severe intracranial hypertension Most often caused by severe damage to bilateral cerebral hemispheres and basal ganglia (usually infarction); also seen in patients with congestive heart failure owing to increased circulation time and in various forms of encephalopathy. Also observed in some elderly patients in the absence of neurologic or cardiac disease. Midbrain and upper pons damage associated with head trauma, severe brain hypoxia, or ischemia Metabolic acidosis Abdominal paradox: Diaphragmatic fatigue or paralysis Chest paradox: Typically observed in chest trauma with multiple rib or sternal fractures Also found in patients with high spinal cord injury with paralysis of intercostal muscles Same causes as Cheyne-Stokes respiration

to agonal breathing (i.e., intermittent prolonged gasps) and then apnea. Apneustic breathing is characterized by a prolonged inspiratory pause at full inspiration typically lasting for 2 to 3 seconds. It indicates damage to the lower pons (which regulates the transition from the inspiratory to expiratory phase) and is usually caused by basilar artery occlusion.19 Central neurogenic hyperventilation is characterized by persistent hyperventilation driven by abnormal neural stimuli. It is related to midbrain and upper pons damage associated with head trauma, severe brain hypoxia, or lack of blood flow to the brain.20 Conversely, central neurogenic hypoventilation means the respiratory centers do not respond appropriately to ventilatory stimuli, such as CO2. It also is associated with head trauma and brain hypoxia as well as narcotic suppression of the respiratory center.19

RULE OF THUMB  Patients with lung diseases that cause lung volume loss and stiffness (e.g., pulmonary fibrosis, ARDS) typically present with a rapid-shallow breathing pattern.

RULE OF THUMB  Patients with lung diseases that cause intrathoracic airways to narrow (e.g., asthma, bronchitis) tend to breathe with a prolonged expiratory phase.

CHAPTER 16  Bedside Assessment of the Patient

RULE OF THUMB  Lung diseases that cause the upper airway to narrow (e.g., croup, epiglottitis) also cause the patient to breathe with a prolonged inspiratory phase.

Assessing the diaphragm.  The diaphragm may be nonfunc­ tional or severely limited in patients with high cervical spinal cord injury, neuromuscular disease, and COPD. When the diaphragm is nonfunctional or limited, the accessory muscles of ventilation become active to maintain adequate gas exchange. Excluding strenuous exercise, heavy use of accessory muscles is reliable evidence of significant cardiopulmonary disease. In patients with emphysema, the lungs become hyperinflated, preventing the diaphragm from achieving its relaxed position whereby the muscle fibers lengthen. When the diaphragm must contract from above its relaxed position the force or pressure it can generate decreases. As hyperinflation pushes the diaphragm downward into a flat position its effectiveness in moving air is greatly limited. Contraction of a flat diaphragm tends to draw in the lateral costal margins (Hoover sign) instead of normal expansion outward. The accessory muscles therefore must assist the diaphragm. The severity of emphysema is often reflected by the magnitude of accessory muscle activity. Diaphragmatic fatigue occurs in many chronic and acute pulmonary diseases. Fatigue is the inability of a contracting muscle(s) to achieve a target pressure. In contrast, muscle weakness is the inability to achieve a target pressure in a rested muscle. For the respiratory muscles, the target pressure is that needed to maintain normal ventilation as assessed by the arterial CO2 partial pressure (PaCO2). Acute diaphragmatic fatigue often manifests with distinctive breathing patterns; the first sign is tachypnea.16 Sometimes this evolves into a breathing pattern in which the diaphragm and rib cage muscles alternately power breathing in an attempt to rest each muscle group (respiratory alternans). This pattern is noted by the upward motion of the diaphragm during inspiration on a series of breaths, followed by diaphragmatic contractions and outward abdominal movement on the following series of breaths. When the diaphragm is inactive, contraction of the rib cage muscles sucks the diaphragm upward and the abdomen moves inward. The opposite motion occurs when the diaphragm is active and the rib cage muscles are inactive: the chest moves inward as the abdomen protrudes, producing a rocking motion appearance to the chest. Abdominal paradox occurs with complete diaphragmatic fatigue, as the diaphragm is drawn upward into the thoracic cavity with each inspiratory effort of the rib cage muscles. These patterns are not always associated with impending muscle fatigue. Sometimes they reflect adaptations to high workloads when the respiratory muscle strength is normal.20 Also, during respiratory distress the expiratory muscles are recruited to increase diaphragmatic strength (i.e., maximizing muscle length).17 This situation can make it difficult to discern accurately the presence and type of abnormal breathing patterns. The RT must be careful not to offer definitive therapeutic suggestions (e.g., need for mechanical ventilation) based solely on his or her perception of an abnormal breathing pattern.

333

Palpation Palpation is the art of touching the chest wall to evaluate underlying structure and function. It is used to confirm or rule out suspected problems suggested by the history and initial examination findings. Palpation is performed to evaluate vocal fremitus, estimate thoracic expansion, and assess the skin and subcutaneous tissues of the chest. Vocal and tactile fremitus.  Vocal fremitus are vibrations created by the vocal cords during speech. These vibrations are transmitted down the tracheobronchial tree and through the lung to the chest wall. When these vibrations are felt on the chest wall, it is called tactile fremitus. Assessing vocal fremitus requires a conscious, cooperative patient. Increased intensity of fremitus occurs when the lung becomes consolidated (e.g., filled with inflammatory exudate) as in pneumonia. However, fremitus is absent when consolidated tissue is not in communication with patent airways because speech is not transmitted. In addition, fremitus is reduced in patients who are obese or overly muscular. Decreased intensity of fremitus occurs when fluid or air collects in the pleural space (e.g., pleural effusion or pneumothoraces). Speech transmission also decreases with hyperinflation (e.g., asthma, emphysema) as lung tissue density is reduced. Tactile fremitus is assessed by asking the patient to repeat the word “ninety-nine” while the RT systematically palpates the anterior, lateral, and posterior portions of the thorax. The palmar aspect of the fingers or the ulnar aspect of the hand can be used for palpation. If one hand is used, it should be moved from one side of the chest to the corresponding area on the other side. Skin and subcutaneous tissues.  Lung rupture often causes air to leak into the subcutaneous tissues of the chest and neck. Fine air bubbles collecting in subcutaneous tissues produces a crackling sound and sensation when palpated. This is referred to as subcutaneous emphysema. The tactile sensation it produces is called crepitus which is a classic sign of barotrauma. Two situations when the RT should be vigilant for the presence of subcutaneous emphysema are when high airway pressures and end-inspiratory volumes occur during mechanical ventilation and in patients with blunt or penetrating chest trauma. Percussion of the Chest Percussion is the art of tapping on a surface to evaluate the underlying structure. Percussion of the chest wall produces a sound and a palpable vibration useful in evaluating underlying lung tissue. The vibration created by percussion penetrates the lung to a depth of 5 to 7 cm below the chest wall. This assessment technique is not performed routinely on all patients but is reserved for patients with suspected pneumothorax or lung consolidation. The technique most often used in percussing the chest wall is called mediate, or indirect, percussion and can be broken down into two steps. First, place the middle finger of the non-dominant hand firmly against the patient’s chest wall, parallel to the ribs, with the palm and other fingers held off the chest. Second, the tips of middle and index fingers of the dominant hand are then used to strike the finger pressed against the chest. Alternatively, the lateral aspect of the thumb can be used. A quick, sharp blow

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SECTION III  Assessment of Respiratory Disorders

should be placed near the base of the terminal phalanx. Movement of the hand striking the chest is generated at the wrist, not at the elbow or shoulder. Percussion over lung fields.  Percussion of the lung fields is performed systematically by consecutively testing comparable areas on both sides of the chest. Percussion over the bony structures and over the breasts of female patients has no diagnostic value and should not be performed. Asking patients to raise their arms above their shoulders helps move the scapulae laterally and minimizes their interference with percussion on the posterior chest wall. The sounds generated during chest percussion are evaluated for intensity (loudness). Percussion over normal lung fields produces an easily heard, moderately low-pitched, resonate sound described as tympanic. When the percussion note is louder, deeper, and more resonant, it is said to be hypertympanic. Percussion may also produce a damped or dull noise resembling the sound of a heavily muffled drum. Unilateral problems are easier to detect than bilateral problems because the unaffected side provides a normal standard for immediate comparison. Clinical implications.  In modern practice, chest percussion enables rapid bedside assessment of chest abnormalities and may aid in deciding whether to obtain a chest radiograph. Any abnormality that either increases lung tissue density (e.g., pneumonia, tumor, or atelectasis) or increases the density of the pleural space (e.g., pleural effusion, empyema) results in decreased resonance or a dull note to percussion over the affected area. In contrast, increased resonance or a hyper-resonate note is detected when the lungs are either hyperinflated (e.g., asthma or emphysema) or when the pleural space contains large amounts of air (pneumothorax). Percussion of the chest has important limitations. Abnormalities that are small or deep below the surface are not likely to be detected during percussion of the chest. RULE OF THUMB Percussing the chest can produce two abnormal resonance sounds related to an imbalance between gas and tissue/fluid inside the chest cavity. Dull resonance is produced by the muffling effects of increased tissue density (e.g., atelectasis or consolidation) or fluid collection (e.g., pleural effusion, hemothorax), whereas hyper-resonance is produced by lung hyperinflation (e.g., COPD or asthma exacerbation) or gas trapped in the pleural space (i.e., pneumothorax).

Auscultation of the Lungs Auscultation is the process of listening for bodily sounds. The thorax is auscultated to identify normal and abnormal lung sounds and to evaluate the effects of therapy. It is a particularly useful clinical tool because it is noninvasive and can be performed quickly. Auscultation requires a stethoscope to enhance sound transmission from the patient’s lungs to the examiner’s ears. Stethoscope.  A stethoscope has the following four basic parts: (1) a bell, (2) a diaphragm, (3) tubing, and (4) earpieces (Fig. 16.5). The bell detects a broad spectrum of sounds and is useful for hearing low-pitched sounds (e.g., heart sounds). Proper technique for listening to heart sounds is to place the bell lightly against the chest. This avoids stretching the skin, which inadvertently makes auscultating heart sounds more difficult because it filters out low-frequency sounds.

Earpieces Bell

Binaurals

Diaphragm

Chestpiece

Tubing Fig. 16.5  Acoustic stethoscope.

The diaphragm is used to auscultate the lungs as it is better at capturing high-frequency sounds. The ideal tubing is thick enough to exclude external noises and approximately 25 to 35 cm (11 to 16 in) in length. Longer tubing may impair sound transmission. The stethoscope should be examined regularly for cracks in the diaphragm, wax or dirt in the earpieces, and other defects that may interfere with sound transmission. A hospital-approved disinfectant should be used to clean the stethoscope after every patient contact to minimize contamination with microorganisms.22 Patients requiring either contact or protective isolation must have a dedicated stethoscope in the room to prevent cross infection. Technique.  Ideally the patient should be relaxed, sitting upright, and instructed to breathe through the mouth a little more deeply than normal. Exhalation should be passive. Because clothing may distort lung or heart sounds the bell or diaphragm should be placed directly against the chest wall. Likewise, be careful not to allow objects to rub against the tubing as this may produce artifacts that could be mistaken for adventitious lung sounds (discussed later). Auscultating the lungs should be systematic including all lobes on the anterior, lateral, and posterior chest. Begin at the bases and compare breath sounds side to side, working upward toward the lung apexes (Fig. 16.6). Beginning at the bases is important because certain abnormal sounds only occur in the lower lobes and quickly resolve with deep breaths. Evaluate one full breath at each stethoscope position and listen to several breaths when abnormal sounds are present to clarify the characteristics. Breath sounds consist of several key features: pitch (vibration frequency), intensity (loudness), and the duration of inspiratory and expiratory phases. The acoustic characteristics of breath sounds are illustrated in breath sound diagrams (Fig. 16.7), as well as their normal features (Table 16.3). The RT must be familiar with normal breath sounds before acquiring the ability to identify changes that accompany respiratory disease. Normal lung sound terminology.  There are three normal breath sounds referred to as tracheal, bronchovesicular, and vesicular. Tracheal breath sounds have a loud, tubular quality and are heard

CHAPTER 16  Bedside Assessment of the Patient

9 5

6 3

4 1

2

10

8

7

5

6

4

3

1

2

8

7 6

5 4

1

2

3

Fig. 16.6  Sequencing for auscultation technique. (Modified from Wilkins RL, Dexter JR, editors: Respiratory diseases: a case study approach to patient care, ed 3, Philadelphia, 2007, FA Davis.)

Fig. 16.7  Diagram of Normal Breath Sound. Upstroke represents inhalation, and downstroke represents exhalation; length of upstroke represents duration; thickness of stroke represents intensity; angle between upstroke and horizontal line represents pitch.

TABLE 16.3  Characteristics of Normal

Breath Sounds Breath Sound

Pitch

Intensity Location

Vesicular Low Soft Bronchovesicular Moderate Moderate

Peripheral lung areas Around upper part of sternum, between the scapulae

Tracheal

Over the trachea

High

Loud

Diagram

when auscultating the trachea and are characterized by approximately equal durations between the inspiratory and expiratory phases. Bronchovesicular breath sounds, heard around the upper half of the sternum and between the scapulae, are slightly lower in pitch and also have equal inspiratory and expiratory components. Vesicular breath sounds are heard over normal lung parenchyma and are characterized by a soft, muffled sound quality that is lower both in pitch and intensity than bronchovesicular breath sounds. Vesicular sounds are heard primarily during inhalation, with an exhalation component approximately one-third the duration of inhalation (see Table 16.3).

335

Lung Sounds in Pulmonary Disease Respiratory diseases often alter breath sounds with descriptors such as diminished or even absent when the intensity decreases and harsh when the intensity increases. Harsh breath sounds of approximately equal duration between inspiration are described as bronchial breath sounds. Adventitious lung sounds are additional sounds or vibrations produced by air movement through diseased airways. These sounds may be loud or faint, scattered or diffuse, and inspiratory or expiratory (or both). Adventitious sounds have two classifications. Discontinuous sounds are intermittent, crackling, or bubbling sounds of short duration and are referred to as either crackles or rales (from the French word for “rattle”). Faint or low-intensity crackles are often referred to as fine crackles; more pronounced or more intense crackles are referred to as coarse crackles. In contrast continuous adventitious lung sounds are described with the term wheezes (i.e., a high or low-pitched quasi-musical sound). However, the RT may encounter the term rhonchi (derived from the Latin word for “wheezing”). Although no longer favored, it was used previously to describe low-pitched, continuous sounds associated with secretions in the larger airways (i.e., now synonymous with coarse crackles).23 It is useful to monitor the pitch and duration of wheezing. Improved expiratory flow is associated with a decrease in the pitch and length of the wheezing. Another continuous adventitious lung sound, heard primarily over the larynx and trachea during inhalation, is stridor, a loud, high-pitched sound associated with upper airway obstruction (i.e., larynx or trachea) and often heard without a stethoscope. It is more common in infants and children. Laryngomalacia is the most common cause of chronic stridor, whereas croup is the most common acute cause. Generally, inspiratory stridor is consistent with narrowing above the glottis, whereas expiratory stridor indicates narrowing of the lower trachea. In adults, stridor most often occurs from laryngeal or subglottic edema secondary to airway trauma or infection (e.g., epiglottitis). Mechanisms and significance of lung sounds.  Lung sounds are audible vibrations primarily generated by turbulent airflow in the larger airways. These sounds are altered as they travel through the lung periphery and chest wall. Normal lung tissue acts as a low-pass filter (preferentially passes low-frequency sounds). This explains the characteristic differences between tracheal breath sounds, heard directly over the trachea, and vesicular sounds, heard over the lung periphery.23 In essence vesicular lung sounds are attenuated tracheal breath sounds. However, when lung tissue density increases because of atelectasis or because it is consolidated (e.g., pneumonia), attenuation is reduced, and breath sounds over the affected area change from vesicular to something resembling that heard over the trachea. When in doubt, the RT should use tracheal sounds as a reference point for assessing lung sounds. Diminished breath sounds.  Diminished breath sounds have two sources: either diminished airflow velocity (i.e., sound intensity) in the larger airways, or when sound transmission through the lung or chest wall is blunted. Shallow and slow breathing patterns reduce sound intensity by creating less

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SECTION III  Assessment of Respiratory Disorders

turbulent flow, whereas reduced sound transmission occurs for a variety of other reasons. These include: (1) airways plugged with mucus, (2) hyperinflated lung tissue (e.g., COPD, asthma), (3) air or fluid in the pleural space (e.g., pneumothorax, hemothorax, pleural effusion), (4) anasarca (generalized body edema), and (5) obesity or when chest muscles are highly developed. Wheezes and stridor. High-velocity airflow through a narrowed airway (e.g., from bronchospasm, airway edema, foreign bodies, etc.) produces vibrations described as wheezes or stridor. Narrowing initially causes airflow velocity to increase which in turn causes lateral wall pressure to decrease, narrowing the airways to the point that airflow ceases. When airflow stops, the lateral wall pressure increases, and the airway opens back to the previous position. This cycle repeats many times per second and causes the airway walls to vibrate and make a musical sound similar to a reed instrument. RULE OF THUMB Expiratory wheezing indicates intrathoracic airway constriction typical of obstructive lung diseases (e.g., bronchitis, asthma). Wheezing may be monophonic (single note) or polyphonic (multiple notes). A monophonic wheeze indicates that a single airway is partially obstructed. Monophonic wheezing may be heard during inhalation and exhalation or during exhalation only. Polyphonic wheezing suggests that many airways are obstructed, such as with asthma, and is heard only during exhalation. Bronchitis and CHF with pulmonary edema also can cause polyphonic wheezing.

Crackles.  Crackles are primarily inspiratory sounds produced when airflow moves secretions or fluid in the airways or when collapsed airways pop open during inspiration. They are differentiated according to sound quality (e.g., course or fine) and timing (e.g., early or late). Coarse crackles, also known as rhonchi, are usually associated with airway secretions and often clear with coughing or when the airways are suctioned. Fine crackles that do not clear with coughing are either indicative of air moving through fluid-filled airways such as that which occurs with CHF, or collapsed smaller airways that re-open (“recruited”) during inspiration. When alveoli are recruited in this way, they produce a relatively fine sound quality that may appear early or late in the inspiratory phase depending on their location (depth) in the bronchial tree and the intensity of inspiratory effort (i.e., magnitude of inthoracic pressure generated) (Fig. 16.8). A summary linking adventitious breath sounds with potential mechanisms, characteristics, and associated disease states is presented in Table 16.4. RULE OF THUMB  Fine, late inspiratory crackles suggest either restrictive lung diseases such as pulmonary fibrosis or the opening of collapsed (atelectatic) alveoli.

Pleural friction rub.  Inflamed pleural surfaces create friction during breathing that produces a creaking or grating sound referred to as a pleural friction rub. It is typically heard during inspiration and usually is localized to a discreet site on the chest wall. Although it sounds similar to coarse crackles it is not affected by coughing. The intensity of pleural rubs may increase with deep breathing.

Inspiration

A

Expiration

Inspiration

B

Expiration

Inspiration

C

Expiration

Fig. 16.8  Timing of Inspiratory Crackles. (A) Early inspiratory crackles. (B) Late inspiratory crackles. (C) Pan-inspiratory crackles.

TABLE 16.4  Application of Adventitious

Lung Sounds Lung Sound

Possible Mechanism

Wheezes

Rapid airflow through obstructed airways Stridor Rapid airflow through obstructed upper airway Coarse Excess airway crackles secretions moving through airways Fine Sudden opening of crackles peripheral airways

Characteristics Causes High-pitched, usually expiratory High-pitched, monophonic

Asthma, congestive heart failure

Fine, late inspiratory

Atelectasis, fibrosis, pulmonary edema

Croup, epiglottitis, postextubation laryngeal edema Coarse, inspiratory Severe pneumonia, and expiratory bronchitis

Voice sounds.  As described above, normal, air-filled lung tissue alters sound transmission (“low pass filter”) and reduces the intensity and clarity of spoken words. In contrast, collapsed or consolidated lung tissue increases the transmission of higher- frequency vocal vibrations that enhance the clarity and resonance of spoken words. The terms used for this phenomenon are egophony or bronchophony. This is evaluated by instructing the patient to repeat the words “one,” “two,” “three,” or “ninetynine” while auscultating the chest, comparing one side with the other. When listening over consolidated lung tissue, the words will be transmitted louder and clearer. Alternatively, instruct the patient to repeatedly pronounce a long A sound. Consolidated lung will transmit the A sound as an E, which is referred to as E to A egophony.

Cardiac Examination Because of the close relationship between the heart and lungs, chronic lung diseases often cause cardiac problems. The techniques for physical examination of the chest wall overlying the heart

CHAPTER 16  Bedside Assessment of the Patient

337

1

A

P

2 3 4

T

5 M 6 7 8 9 10

Fig. 16.9  Anatomic and Auscultatory Valve Area. Location of anatomic valve sites is represented by solid bars. Arrows designate transmission of valve sounds to their respective auscultatory valve areas. A, Aortic valve; M, mitral valve; P, pulmonic valve; T, tricuspid valve.

(precordium) include inspection, palpation, and auscultation. Most clinicians examine the precordium at the same time they assess the lungs.

Inspection and Palpation Inspection and palpation of the precordium help identify normal or abnormal pulsations. Pulsations on the precordium are created by ventricular contraction. Detection of pulsations depends on the force of ventricular contraction and the thickness of the chest wall through which the vibrations travel. Normally, left ventricular contraction is the most forceful and generates a palpable pulsation called the point of maximal impulse (PMI). To identify the PMI, place the palm of the right hand over the lower left sternal border. Cardiopulmonary disease often produces changes in PMI. For example, PMI shifts laterally with left ventricular hypertrophy. In contrast, right ventricular hypertrophy produces a systolic heave (or thrust) felt near the lower left sternal border. This is a common finding in patients with chronic hypoxemia, pulmonary valvular disease, or primary pulmonary hypertension. The PMI is often difficult to palpate in severe emphysema, because hyperinflated lungs poorly transmit systolic vibrations. Both pneumothorax and lobar collapse shift the mediastinum and therefore PMI location. The PMI will shift toward lobar collapse and away from a tension pneumothorax. With severe pulmonary hyperinflation the PMI may shift centrally to the epigastric area. The second left intercostal space near the sternal border is referred to as the pulmonic area and is palpated to identify

accentuated pulmonary valve closure. Strong vibrations may be felt in this area with the presence of pulmonary hypertension or valvular abnormalities (Fig. 16.9). Valvular abnormalities may produce palpable vibrations or thrills that often are accompanied by a murmur (see later).

Auscultation of Heart Sounds Heart sounds are auscultated using either the bell or diaphragm of the stethoscope. Optimal auscultation occurs when the patient leans forward or lies on the left side, as this moves the heart closer to the chest wall. Normal heart sounds are created by closure of the heart valves (see Chapter 10). The first heart sound (S1) is produced by closure of the mitral and tricuspid (atrioventricular [AV]) valves during ventricular contraction. When systole ends and the ventricles relax, the pulmonic and aortic (semilunar) valves close, creating the second heart sound (S2). Asynchronous closure of the AV valves and semilunar valves creates a pronounced split heart sound. A third, low-pitched heart sound (S3) is heard over the apex of the heart that, in adults, may signify CHF. A fourth heart sound (S4) occurs later and may be a sign of heart disease. A patient with heart disease who has S3 and S4 is said to have a gallop rhythm. Abnormal Heart Sounds Both cardiac and extracardiac abnormalities reduce the intensity of heart sounds. Pulmonary hyperinflation, pleural effusion, pneumothorax, and obesity make it difficult to identify S1 and S2 as well as poor cardiac contractility or valvular disease. In

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SECTION III  Assessment of Respiratory Disorders

contrast, an intense S2 (loud P2) occurs in pulmonary hypertension due to forceful closure of the pulmonic valve. Cardiac murmurs are created by (1) a backflow of blood through an incompetent valve, (2) a forward flow of blood through a stenotic (“narrowed”) valve, and (3) rapid blood flow through a normal valve (i.e., strenuous exercise). Cardiac murmurs caused by incompetent or stenotic heart valves are classified as systolic or diastolic. An incompetent AV valve produces a high-pitched, “whooshing” systolic murmur during S1, whereas restricted blood flow through a stenotic semilunar valve produces a crescendo-decrescendo sound. Blood back-flowing across an incompetent semilunar valve produces an S2 diastolic murmur whereas restricted blood flow across a stenotic AV produces a turbulent diastolic murmur.

Abdominal Examination The RT’s focus in abdominal exams is detecting distension and tenderness that impairs diaphragmatic movement and contributes to or causes respiratory insufficiency. Abdominal dysfunction often inhibits deep breathing and coughing thereby promoting atelectasis and secretion retention that increases the risk of pneumonia. For example, hepatomegaly (i.e., an enlarged liver) commonly occurs in both patients with liver disease or cor pulmonale and frequently results in right lower lobe atelectasis and pleural effusion. Of particular concern is intraabdominal hypertension (i.e., intraabdominal pressure >12 mm Hg) that occurs in 20% to 30% of critically ill patients.24 Abdominal compartment syndrome occurs when intraabdominal pressures exceed 20 mm Hg, often requiring emergency decompressive surgery. This syndrome causes profound atelectasis and hypoxemia, hypotension, and renal failure. Intraabdominal hypertension is characterized by pronounced abdominal distension, and is common in patients with abdominal trauma, ruptured aortic aneurysm, bowel infarction, and end-stage liver failure. Intraabdominal pressure is measured by connecting an intraarterial pressure catheter to the culture port of a Foley urine catheter.

Examination of the Extremities Respiratory disease may cause abnormalities of the extremities, including digital clubbing, cyanosis, and pedal edema.

Clubbing Clubbing is the painless enlargement of the terminal phalanges of the fingers and toes associated with numerous cardiopulmonary and other diseases. It is a slow-emerging process whereby the angle of the fingernail to the nail base increases, and the base of the nail feels “spongy.” Although a profile view of the digits allows easier recognition (Fig. 16.10), the most important sign is the sponginess of the nail beds. Causes of clubbing include infiltrative or interstitial lung disease, bronchiectasis, various cancers (particularly lung cancer),25 congenital heart disease, severe liver failure,26 and inflammatory bowel disease. COPD alone, even when hypoxemia is present, does not lead to clubbing. Clubbing of the digits in a patient with COPD indicates that something other than obstructive lung disease is occurring.

A

B

IPD

DPD

C Fig. 16.10  (A) Normal digit configuration. (B) Mild digital clubbing with increased hyponychial angle. (C) Severe digital clubbing; the depth of the finger at the base of the nail (DPD) is greater than the depth of the interphalangeal joint (IPD) with clubbing.

Cyanosis Whenever hypoxemia is suspected the digits should be examined for cyanosis. Because the fingernails and skin are relatively translucent cyanosis is readily detectable. Cyanosis becomes visible when the amount of unsaturated hemoglobin in capillary blood exceeds 5 to 6 g/dL. This may be caused by a reduction in arterial or venous O2 content, or both. Cyanosis is classified as either peripheral or central. Peripheral cyanosis signifies poor perfusion of the extremities (particularly the digits), so that the tissues extract more O2. This reduces the venous O2 content, thereby increasing the amount of reduced hemoglobin. The term acrocyanosis is used when extensive portions of limbs are involved. The extremities are usually cool to the touch when peripheral cyanosis is present. It should be noted that a brief period of acrocyanosis is a normal finding in certain newborn babies. In contrast, central cyanosis is when the mucosa or the torso are involved and may signal severe lung disease, profound hypotension, or the presence of certain congenital heart diseases. Of note, the RT must always be mindful that cyanosis may be masked by several factors, including low room lighting, darker skin pigmentation, and severe anemia. Pedal Edema See discussions of common cardiopulmonary symptoms.

CHAPTER 16  Bedside Assessment of the Patient

MINI CLINI Evaluation of Acute-Onset Respiratory Distress Problem The RT is called to evaluate a 55-year-old woman with acute respiratory distress and worsening hypoxemia. The patient is 3 days post-admission for right-sided rib fractures. This resulted from falling down a flight of stairs during alcohol intoxication with brief loss of consciousness. Since admission her oxygenation has been adequate with pulse oximetry (SpO2) of 95% on 3 L/min of nasal O2. Over the past hour she has become febrile (maximum temperature 39.5°C), has developed tachypnea (32 breaths/min), tachycardia (heart rate 130 beats/ min), and hypotension (blood pressure 88/50 mm Hg; mean, 63 mm Hg). Her SpO2 is now 87% on 6 L/min nasal O2. This also coincides with new-onset altered mental status. Her medical history is significant for alcoholism and a 30 pack-year smoking history. What can the physical examination and history tell us about the potential source of respiratory distress? Solution The signs, symptoms, and history suggest bacterial pneumonia possibly from aspiration during her initial loss of consciousness or from a pulmonary contusion. Bacterial pneumonia has an incubation period of 1 to 3 days. The associated high fever, tachycardia, hypotension, and altered mental status also suggest that pneumonia has resulted in sepsis (systemic inflammation). Pulmonary contusion also can result in pneumonia and ARDS (see Chapter 29), with a peak occurrence at approximately 72 h.27 Rib fractures are painful and limit deep breathing and effective coughing, leading to atelectasis and retained secretions that increase the risk for pneumonia. When extensive, rib fractures also cause chest wall instability that limits effective ventilation and heightens the risk for respiratory failure. Both alcoholism and cigarette smoking further increase the susceptibility to pneumonia.28,29 Also, a history of alcohol abuse may be a contributory factor because the onset of acute alcohol withdrawal typically occurs in this time frame.30 The first priority is to increase O2 therapy to achieve adequate oxygenation (SpO2 ≥90%) while conducting an examination. Worsening oxygenation, despite doubling O2 therapy, suggests refractory hypoxemia, which is a hallmark of ARDS. This situation indicates the need for high-concentration O2 therapy, continuous pulse oximetry, and close hemodynamic monitoring. The RT should be alert for signs suggestive for heightened work of breathing (rapid-shallow breathing, accessory inspiratory muscle use, along with tracheal or intercostal retractions and expiratory muscle recruitment), chest wall instability (paradoxical chest motion), and diminished ventilation (global decrease in breath sound intensity). Breath sounds should be evaluated for evidence suggesting the presence of secretions (coarse, bubbling crackles) or pulmonary edema (fine inspiratory crackles). Another possibility is acute pulmonary embolism, which would become a more prominent consideration if the patient had also suffered pelvic or leg fractures and was immobilized or has redness and swelling of the lower extremities. Although a pneumothorax is unlikely in this situation, the chest should be inspected for signs (e.g., subcutaneous emphysema, JVD, unilateral chest excursion). Further work-up would include a chest radiograph to confirm the suspicion of pneumonia or chest contusion (and to rule out a pneumothorax), an arterial blood gas to evaluate the severity of hypoxemia and the adequacy of ventilation, and blood samples to evaluate the presence of infection (see Chapter 17). The results of these tests and the patient’s response to therapeutic interventions would determine where the patient can be safely and optimally managed.

Capillary Refill Capillary refill is an expedient method to assess peripheral perfusion by pressing firmly on the patient’s fingernail until the nail bed is blanched, and then releasing the pressure. The speed

339

at which the blood flow and color return is noted. Healthy individuals with good cardiac output and digital perfusion have capillary refill times of 3 seconds or less. Poor cardiac output and/or poor digital perfusion results in a slow capillary refill that often exceeds 5 seconds. Capillary refill time should be assessed in the context of whether or not the skin is mottled (i.e., blotched skin shade) and skin temperature.

Peripheral Skin Temperature When systemic perfusion is poor (as in heart failure or shock), there is a compensatory vasoconstriction in the extremities that diverts blood to the vital organs. This reduction in peripheral perfusion causes the extremities to become cool to the touch. The extent to which coolness extends back toward the torso indicates the degree of circulatory failure. In contrast, patients with high cardiac output and peripheral vascular failure (as occurs in septic shock) may have warm, dry skin.

SUMMARY CHECKLIST • Bedside assessment is the process of interviewing and examining a patient for signs and symptoms of disease, as well as evaluating the effects of treatment. • Signs refer to the objective manifestation of illness (e.g., increased respiratory rate) whereas symptoms refer the sensation or subjective experience of some aspect of an illness (e.g., breathlessness). • Four factors affecting communication between the RT and the patient are sensory and emotional, environmental, verbal and nonverbal communication process, and cultural-socialpersonal histories of both the RT and the patient. • Social space is socially-appropriate space (approximately 4 to 12 feet distance) from where introductions are made. Personal space is 2 to 4 feet and is the distance from which private information is exchanged. • The five common characteristics of symptoms that can be identified by asking neutral questions are: When did it start? How severe is it? Where on the body is it? What seems to make it better or worse? Has it occurred before? • Dyspnea specifically refers to the perception that breathing effort is excessive relative to the tidal volume achieved (e.g., “hard to breathe”), whereas breathlessness refers to an unpleasant urge to breathe (e.g., not being able to “catch your breath”). • The perception of breathing is complex and includes the following three major factors: neural drive emanating from the respiratory centers in the brainstem, sensory information regarding tension developed in the respiratory muscles, and the corresponding displacement of the lungs and chest wall. • The four questions used to assess dyspnea in patients during an interview are: What activities trigger dyspnea? How much activity triggers the sensation? Does the quality of dyspnea change depending upon the activity? How long ago did dyspnea first become noticeable and how rapidly did it progress over time? • An effective cough depends upon the ability to take a deep breath, the elastic recoil properties of the lungs, expiratory muscle strength, and airways resistance.

340

SECTION III  Assessment of Respiratory Disorders

• The five characteristics that RTs must monitor are whether a cough is dry or loose, productive or nonproductive, acute or chronic; occurs more frequently at particular times; and whether it is provoked by a certain body positions. • Infected or purulent sputum typically is thick, colored, sticky, and sometimes foul-smelling, whereas mucoid sputum is clear and may be thick. • Massive hemoptysis is a medical emergency defined as more than 300 mL within 24 hours and commonly occurs in patients with bronchiectasis, lung abscess, and tuberculosis. In contrast, non-massive hemoptysis produces less blood and is associated with a multitude of conditions such as airway infections, pneumonia, lung cancer, tuberculosis, blunt or penetrating chest trauma, and pulmonary embolism. • Pleuritic chest pain usually is a sharp, stabbing pain located laterally or posteriorly on the chest that worsens with deep breathing. It is a common symptom in pneumonia, empyema, pleural effusion, and pulmonary embolism. Non-pleuritic chest pain typically is a dull ache or pressure located in the center of the anterior chest and may radiate to the shoulder, neck, or back brought on by exertion or stress and is associated with coronary artery occlusion. It is not affected by breathing. • Fever is a temperature greater than 38.3°C (101°F) commonly associated with bacterial, viral, or fungal infections. But there are also numerous non-infectious causes including drug reactions, malignancies, head trauma, burns, alcoholic cirrhosis, thromboembolic disorders, and noninfectious inflammatory diseases. • Pedal edema is either pitting (e.g., leaves a dent when pushing down on the skin) or weeping (e.g., causes fluid to leak when pushing down on the skin) and is a characteristic finding in CHF and cor pulmonale as well as end-stage liver disease. • The five major categories of patient information documented in the medical record are: chief complaint and history of present illness, past medical history, family and social/ environmental history, review of systems, and advance directive (i.e., any limits of care). • Smoking history is recorded in pack-years and is determined by multiplying the number of packs smoked per day by the number of years smoked. • The physical examination consists of four general steps: visual inspection, palpation, percussion, and auscultation. • The four criteria that comprise sensorium (i.e., cognitive functioning) are the patient’s orientation to time, place, self, and their current circumstances. • The basic vital signs are temperature, pulse rate, blood pressure, respiratory rate, and oxygen saturation. • The eight anatomic locations where a pulse can be palpated are the radial, brachial, femoral, carotid, dorsalis pedis, temporal, popliteal, posterior tibial arteries. • Arterial hypertension is chronically elevated blood pressure of 140/90 mm Hg or greater that is categorized as Stage I (systolic pressure: 140 to 159 mm Hg or diastolic pressure: 90 to 99 mm Hg), stage II (systolic pressure: ≥160 mm Hg, or the diastolic pressure is ≥100 mm Hg), or prehypertension

•

•

•

•

•

• •

•

•

•

•

(systolic pressure of 120 to139 mm Hg or diastolic pressure of 80 to 89 mm Hg), which denotes increased risk of developing hypertension. Hypotension is a systolic arterial pressure less than 90 mm Hg, a mean arterial pressure less than 65 mm Hg, or a decrease in systolic pressure greater than 40 mm Hg in patients with established hypertension. Although hypotension often is associated with shock, the distinction is that shock specifically refers to tissue perfusion that fails to meet metabolic demand (i.e., it cannot reliably be determined by measuring blood pressure alone). The common signs used to infer increased work of breathing on a physical exam include nasal flaring, recruitment of the sternocleidomastoid and abdominal muscles, tracheal tugging, and chest wall retractions (i.e., intercostal, subcostal, supraclavicular). The two archetypal breathing patterns during respiratory distress are rapid shallow breathing (restrictive conditions) and a pattern characterized by a prolonged expiratory phase. Abnormal breathing patterns typically associated with neurologic disease or injury include Cheyne-Stokes respiration, Biot respiration, apneustic breathing, central neurogenic hypoventilation, and hyperventilation. Lung hyperinflation causes a flattening of the diaphragm that produces a paradoxical inward movement of the lower rib cage during inspiration (Hoover’s sign). Without clinical intervention diaphragmatic fatigue can manifest into one of two breathing patterns (respiratory alternans or abdominal paradox). The three normal breath sounds are vesicular, bronchovesicular, and tracheal and are related to specific sites of auscultation. The two main adventitious breath sounds are discontinuous sounds (rales or crackles) and continuous, quasi-musical sounds (wheezing and stridor). Rales and crackles are associated with pneumonia, bronchitis, atelectasis. Wheezing is associated with asthma and CHF whereas stridor is most frequently associated with upper airway obstruction from laryngeal edema or spasm. The PMI is a palpable pulsation over the lower left sternal border created by left ventricular contraction. In the presence of left ventricular hypertrophy the PMI shifts laterally whereas right ventricular hypertrophy produces a systolic heave that can be felt near the lower left sternal border. The PMI is often difficult to palpate in severe emphysema. The four common heart sounds are: S1 (produced by AV valve closure during ventricular contraction), S2 (closure of the semilunar valves), S3 (a low-pitched sound heard over the apex of the heart in adults that may signify CHF), and S4 that occurs later and also is associated with heart disease. Abdominal distension and tenderness impair diaphragmatic movement and inhibits deep breathing and coughing thereby promoting atelectasis and secretion retention that increases the risk of pneumonia. The four signs gleaned from examination of the extremities that suggest the presence of cardiopulmonary disease are clubbing of the digits, cyanosis, pedal edema, and skin temperature.

CHAPTER 16  Bedside Assessment of the Patient

REFERENCES 1. Von Leupoldt A, Sommer T, Kegat S, et al: Dyspnea and pain share emotion-related brain network, Neuroimage 48:200–206, 2009. 2. Schwartzstein RM, Parker MJ: Respiratory physiology: a clinical approach, Philadelphia, 2006, Lippencott Williams & Wilkins. 3. Aboussouan LS: Respiratory disorders in neurologic disease, Cleve Clin J Med 72(6):511–520, 2005. 4. Schwartzstein RM: The language of dyspnea. In Mahler DA, O’Donnell DE, editors: Dyspnea: mechanisms, measurement and management, ed 3, Boca Raton, FL, 2014, CRC Press, Taylor & Francis. 5. Boulding R, Stacy R, Niven R, et al: Dysfunctional breathing: a review of the literature and proposal for classification, Eur Respir Rev 25:287–294, 2016. 6. Terasaki G, Paauw DS: Evaluation and treatment of chronic cough, Med Clin North Am 98:391–403, 2014. 7. O’Grady NP, Barie PS, Bartlett JG, et al: Guidelines for evaluation of new fever in critically-ill adult patients: 2008 update from the American College of Critical care medicine and the Infectious Diseases Society of America, Crit Care Med 35:1330–1342, 2008. 8. Hayakawa K, Ramasamy B, Chandrasekar PH: Fever of unknown origin: an evidence-based review, Am J Med Sci 344:307–316, 2012. 9. Mavros MN, Velmahos GC, Falagas ME: Atelectasis as a cause of postoperative fever: where is the clinical evidence?, Chest 140:418–424, 2011. 10. Brugha R, Grigg J: Urban air pollution and respiratory infections, Paediatr Respir Rev 15:194–199, 2014. 11. Madrigal-Garcia MI, Rodrigues M, Shenfield A, et al: What faces reveal: a novel method to identify patients at risk of deterioration using facial expressions, Crit Care Med 46: 1057–1062, 2018. 12. Buda AJ, Pinsky MR, Ingels NB, Jr, et al: Effect of intrathoracic pressure on left ventricular performance, N Engl J Med 301: 453–459, 1979. 13. National High Blood Pressure Education Program: The 7th report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure, Besthesda, MD, 2004, National Institutes of Health National Heart, Lung and Blood Institute. 14. Antonelli M, Levy M, Andrews PJD, et al: Hemodynamic monitoring and shock and implications for management. International consensus conference, Paris, France. 27th-28th April 2006, Intensive Care Med 33:575–590, 2007. 15. Astiz ME: Pathophysiology and classification of shock states. In Fink MP, Abraham E, Vincent J-L, et al, editors: Textbook of critical care, ed 5, Philadelphia, 2005, Saunders, pp 897–904.

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16. Roussos C, Macklem PT: The respiratory muscles, N Engl J Med 307:786–797, 1982. 17. Kallet RH: Patient-ventilator interactions during acute lung injury and the role of spontaneous breathing. Part 1. Respiratory muscle function in critical illness, Respir Care 56:181–189, 2011. 18. Ropper AH, Samuels MA, Klein JP: Coma and related disorders of consciousness. In Adams and Victor’s principles of neurology, ed 10, New York, 2014, McGraw-Hill, (Chapter 17). 19. Stocchetti N, Maas AI, Chieregato A, et al: Hyperventilation in head injury: a review, Chest 127:1812, 2005. 20. Tobin MJ, Perez W, Guenther SM, et al: Does rib cage-abdominal paradox signify respiratory muscle fatigue, J Appl Physiol 63:851–860, 1987. 21. Deleted in review. 22. Longtin Y, Schneider A, Tschopp C, et al: Contamination of stethoscopes and physician’s hands after a physical examination, Mayo Clin Proc 89:291–299, 2014. 23. Sarkar M, Madabhavi I, Niranjan N, et al: Ausclatation of the respiratory system, Ann Thorac Med 10(3):158–168, 2015. 24. Rogers WK, Garcia L: Intra-abdominal hypertension, abdominal compartment syndrome and the open abdomen, Chest 153(1):238–250, 2018. 25. Rutherford JD: Digital clubbing, Circulation 127:1997–1999, 2013. 26. Varghese J, Llias-basha H, Dhanasekaran R, et al: Hepatopulmonary syndrome – past to present, Ann Hepatol 6(3):135–142, 2007. 27. Cohn SM, DuBose JJ: Pulmonary contusion: an update on recent advances in clinical management, World J Surg 34:1959–1970, 2010. 28. Kaphalia L, Calhoun WJ: Alcoholic lung injury: metabolic, biochemical and immunological aspects, Toxicol Lett 222: 171–179, 2013. 29. Huttunen R, Heikkinen T, Syrjanen J: Smoking and outcome of infection, J Intern Med 269:258–269, 2011. 30. Awassi D-K, Lebrun G, Fagnan M, et al: Alcohol, nicotine and iatrogenic withdrawals in the ICU, Crit Care Med 41:S57–S68, 2013.

BIBLIOGRAPHY Bickley LS: Bate’s guide to physical examination and history taking, ed 12, Philadelphia, 2017, Wolters Kluwer. Heuer AJ, Scanlan CL: Clinical assessment in respiratory care, ed 8, St Louis, 2018, Elsevier. Seidel HM, Ball JW, Dains JE, et al: Seidels’s guide to physical examination, ed 8, St Louis, 2015, Elsevier-Mosby.

17  Interpreting Clinical and Laboratory Data Richard H. Kallet

CHAPTER OBJECTIVES After reading this chapter you will be able to: • Describe a critical value and its importance in clinical practice. • Define leukocytosis, leukopenia, anemia, polycythemia, and thrombocytopenia. • Identify which electrolyte disturbances interfere with normal respiratory function. • Describe clinical tests used to identify cardiac stress and myocardial infarction. • Identify the three main tests used to diagnose coagulation disorders.

• Describe how the sputum Gram stain and culture are used to diagnose pulmonary infections. • Discuss the acid-fast test used to identify Mycobacterium tuberculosis. • Explain the advantages of the Xpert MTB/RIF in diagnosing Mycobacterium tuberculosis infections. • List the cut-off values of sweat chloride used to diagnose cystic fibrosis and identify borderline cystic fibrosis cases.

CHAPTER OUTLINE Interpreting Clinical Laboratory Tests, 342 Introduction to Laboratory Medicine, 343 Complete Blood Count, 343 Electrolyte Tests, 345

Enzyme Tests, 347 Coagulation Studies, 348 Microbiology Tests, 350 Sputum Gram Stain, 350 Sweat Chloride, 351

Clinical Application of Laboratory Data, 351 Coagulation Disorders, 351 Electrolyte Disorders and Conclusion, 351

hematocrit hematology hemolysis homeostasis hyperglycemia hyperkalemia hypernatremia hypoglycemia hypokalemia lactate leukocytes leukocytosis leukopenia

neutropenia neutrophilia polycythemia reference range segs sweat chloride thrombocytes thrombocytopenia total bilirubin troponin troponin I

KEY TERMS acid-fast bacterium analyte anemia anion gap bands basic chemistry panel B-type natriuretic peptide complete blood count creatine phosphokinase critical test value D-dimer erythrocytes glucose

INTERPRETING CLINICAL LABORATORY TESTS This chapter discusses common blood tests performed on patients. These tests evaluate a patient’s general health and baseline status, identify organ dysfunction, detect infection, shape the care plan, 342

and monitor its effectiveness. Hence, the respiratory therapist (RT) must be familiar with these tests and their value in helping diagnose and treat respiratory disease. Also, this chapter briefly reviews physiologic concepts related to these tests, contains referencerange values, and explains their significance in patient assessment.

CHAPTER 17  Interpreting Clinical and Laboratory Data

Introduction to Laboratory Medicine Laboratory medicine studies tissue and fluid specimens from patients and consists of five disciplines. Clinical biochemistry analyzes blood, urine, and other bodily fluids for electrolytes and proteins; hematology analyzes cellular components of blood. Clinical microbiology tests blood and other bodily fluids for infectious agents including bacteria (bacteriology), viruses (virology), fungi (mycology), and parasites (parasitology). Immunology is a discipline focusing on autoimmune and immunodeficiency diseases. Finally, anatomic pathology assists with diagnosing diseases by analyzing tissue samples.

Reference Range Laboratory tests help determine a patient’s health status and aid medical decisions. Therefore it is important to determine whether test results fall within an expected range of values considered to be “normal.” However, the term normal is not synonymous with healthy. For example, someone can have a normal red blood cell (RBC) count but the cells may not be capable of carrying or unloading oxygen, such as can occur with cyanide poisoning. In the 1970s,1 the term normal ranges was replaced with more appropriate terms such as reference ranges, biologic reference intervals, and expected value.2 This newer terminology acknowledged that what we consider normal must account for variations related to age, gender, race, and ethnicity which change over time. A reference range sets the boundaries for, and expected variability of, any analyte (the object of a test such as an electrolyte or blood cell) likely to be encountered in healthy patients. Reference ranges differ from laboratory to laboratory for various reasons. These include differences in measurement techniques, the populations of healthy individuals used to establish the reference intervals, and analytic imprecision. Most differences in reference ranges between laboratories are small.2 Reference ranges and critical values displayed in this chapter serve as representative examples; however, RTs must become familiar with the reference ranges used at their institutions. RULE OF THUMB  A normal laboratory test value is not synonymous with health. Rather, it is just one clinical finding which must be combined with many others to determine a patient’s health status.

Critical Test Value A critical test value is a result significantly outside the reference range and represents a pathophysiologic condition. A critical value may signal a potentially life-threatening condition and often warrants immediate clinical action to protect patients. Critical values are communicated by the clinical laboratory to the unit where the patient is located. The nurse or RT receiving these results must read back the critical value to the clinical laboratory or point of service to ensure accuracy. The nurse or RT then must communicate the critical value in a timely fashion to the physician, physician assistant, or nurse practitioner caring for the patient. The same read-back procedure is used. All communication of critical test values is documented in the medical record.

343

RULE OF THUMB  A critical lab value is one that may indicate a potentially life-threatening condition. These values must be communicated to the treating physician in a timely fashion.

In this chapter, critical values are listed along with pathophysiologic states in which they commonly occur. Some clinical analytes lack a critical value because none has been established. Other analytes have only a one-sided value that exists below or above a critical threshold. This occurs with substances not normally present in the blood such as intracellular enzymes and proteins released only after extensive damage following injury (see later section on enzyme tests). Normally these proteins or enzymes are virtually undetectable. When interpreting abnormal test results, clinicians must consider the context of the change. For example, a serum creatinine of 3.0 mg/dL (approximately twice the upper limit of normal) generally is not considered urgent in patients with chronic renal disease. However, in a patient with previously normal kidney function who now presents with septic shock, the same creatinine value is critical because it indicates acute kidney injury from both bloodstream infection and insufficient renal perfusion.

Complete Blood Count The complete blood count (CBC) describes the number of circulating white blood cells (WBCs), called leukocytes; RBCs, called erythrocytes; and platelets, called thrombocytes. The WBC count consists of five types of cells and is reported as a differential. RBCs are evaluated for size and hemoglobin (Hb) content. Platelets are evaluated by the number present. Table 17.1 lists the normal CBC results for adults. Leukocytosis refers to an elevated WBC count and has multiple causes including stress, infection, and trauma. The degree of leukocytosis reflects the severity of infection. A significantly elevated WBC count (>20 × 103/mcL) raises concern for serious infection and that the patient’s immune system is generating a strong response. In contrast, leukopenia (or leukocytopenia) is a WBC count below normal often occurring when the immune system is overwhelmed by infection, or with immunosuppressive conditions such as acquired immunodeficiency syndrome (AIDS) and chemotherapy given to cancer patients. RULE OF THUMB Leukocytosis often represents a vigorous immune response often to either infection or trauma.

RULE OF THUMB Leukocytopenia often signifies that either the immune system has been overwhelmed by infection or there is presence of immunosuppression.

White Blood Cell Count The WBC differential count determines the number of each type of WBC present in the blood (Table 17.2). Most circulating WBCs are either neutrophils or lymphocytes. Leukocytosis is a significant elevation in the WBC count (>15 × 103/mcL) that occurs when either neutrophils or lymphocytes are responding

344

SECTION III  Assessment of Respiratory Disorders

to an abnormality. Basophils, eosinophils, and monocytes make up a small proportion of the circulating WBCs and rarely cause a major increase in the WBC count. The WBC count differential is calculated by multiplying the percentage of each WBC subtype by the total WBC count. This prevents misinterpreting the WBC count differential when one cell type changes, causing a relative change (percentage) in the other four cell types. For example, if the neutrophil count doubles because of infection, the relative percentage of the other four cell types would decrease, although their absolute number would not change. Analyzing specific lymphocytes is crucial in identifying human immunodeficiency virus (HIV) infection that causes AIDS. HIV TABLE 17.1  Reference Range Values for

Complete Blood Count in an Adult Test

Reference Range

Red Blood Cell Count Men Women

4.4–5.9 × 106/mcL 3.8–5.2 × 106/mcL

Hemoglobin Men Women

13.3–17.7 g/dL 11.7–15.7 g/dL

Hematocrit Men Women White blood cell count

40%–52% 35%–47% 3.9–11.7 × 103/mcL

White Blood Cell Differential Segmented neutrophils Bands Eosinophils Basophils Lymphocytes Monocytes Platelet count

40%–75% 0%–6% 0%–6% 0%–1% 20%–45% 2%–10% 150–400 × 103/mcL

Values for reference ranges and critical test results are from the University of California–San Francisco Moffit-Long Hospital and San Francisco General Hospital.14 Reference ranges may differ between hospitals and laboratories so the respiratory therapist should be aware of the value in her/his own hospital.

targets and destroys CD4 T lymphocytes. Opportunistic infections such as Pneumocystis jiroveci pneumonia generally occur when lymphocytes decrease to less than 200 × 106/L, and this information is used to diagnose AIDS. Neutrophilia refers to an absolute elevation in neutrophils. Immature neutrophils are called bands because of their banded shape nucleus, and are located in the bone marrow, where they mature. Mature neutrophils are known as segs because their nucleus has a segmented shape. Severe infection causes the bone marrow to release stores of both mature and immature neutrophils, and both bands and segs into the circulating blood. When bands and segs are elevated in the CBC, the patient is likely experiencing a more severe bacterial infection. Neutropenia is a reduction in the number of circulating neutrophils observed in patients with bone marrow disease (e.g., lymphoma, leukemia), autoimmune disorders, HIV infection, and those undergoing chemotherapy for cancer. Neutropenia increases the risk for the developing opportunistic infections. RULE OF THUMB Elevation of the white blood cell count usually is caused by an increase in either neutrophils or lymphocytes in response to infection.

RULE OF THUMB  When bands and segs are elevated in the complete blood count, the patient is likely experiencing a more severe bacterial infection.

Red Blood Cell Count Erythrocytes (i.e., RBCs) supply oxygen to the tissues, so the RBC count helps determine the ability of the blood to carry O2. An abnormally low RBC count is referred to as anemia which has several potential causes: inadequate production of RBCs by the bone marrow, hemolysis (RBC destruction), or excessive blood loss (e.g., from hemorrhage). Regardless of the source, the blood’s O2-carrying capacity is reduced, placing the patient at risk for tissue hypoxia. Causes of anemia include dietary deficiencies in iron or vitamins (e.g., vitamin B12 and folate), chronic inflammatory diseases such as Crohn disease, HIV/AIDS, lymphoma, and autoimmune diseases

TABLE 17.2  Reference Range Values for White Blood Cell Count Differential and Common

Causes for Abnormalities Cell Type

a

Relative Value (%)

Absolute Value

Neutrophils

40–75

1.8–6.8 × 10 /L

Lymphocytes CD4 T lymphocytes Eosinophils Basophils Monocytes

20–45 31–60a 0–6 0–1 2–10

1.0–3.4 × 109/L 410–1590 × 106/L 0–0.4 × 106/L 0–0.1 × 106/L 0.2–0.8 × 106/L

9

Causes for Abnormalities Increased with bacterial infection and trauma; reduced with bone marrow diseases (critical value 155 mmol/L; 6.0 mmol/L; 120 mmol/L; 40 mmol/L; 13.5 mg/dL; 1.55 mmol/L; 500 mg/dL; 10 mg/dL >100 mg/dL

Test

Glucose (Glu) Creatinine (Cr) Blood urea nitrogen (BUN) Magnesium (Mg++)

Hypercalcemia: Hyperparathyroidism, lithium or thiazide diuretic therapy, metastatic cancer, multiple myeloma See above Hyperglycemia: Diabetes mellitus, severe sepsis Acute kidney injury, chronic renal failure Acute kidney injury, chronic renal failure, dehydration

>1.85 mmol/L; 4 mmol/L

Osmolarity

>320 mOsm/kg; 420 units/L >10,000 units/L >0.05 ng/mL b

>880 (moderate); >8800 (severe)

a

Critical test results vary among clinical laboratories based on instrumentation and calibration procedures. Not all tests have an associated critical result that can be reported. b No critical value established. Values for reference ranges and critical test results from the University of California–San Francisco Moffit-Long Hospital/San Francisco General Hospital.

MINI CLINIC Pulmonary Edema and BNP Problem A 60-year-old man presents to the Emergency department with altered mental status, hypotension, hypoxemia, and tachypnea. A physical exam is notable for right lower leg cellulitis. Chest radiograph shows diffuse bilateral opacities and a mildly enlarged cardiac silhouette. The physician weighs whether the initial treatment approach should be for possible cardiogenic pulmonary edema (e.g., fluid restriction and diuretics) or severe sepsis and ARDS (fluid resuscitation and vasopressors). Solution The initial BNP level is 150 pg/mL indicating sepsis and non-cardiogenic pulmonary edema rather than cardiac failure as the source of hypotension and hypoxemia.

RULE OF THUMB  In patients suffering a myocardial infarction, cardiac injury markers (CPK-2, troponin I) tend to reach peak values beginning at 12 h and up to 24 h after the onset of symptoms.

functioning) lead to excessive bleeding, whereas thrombocytosis (excessive platelets) causes excessive clotting. In addition to direct platelet measurement, the functionality of the entire process of coagulation is measured by the prothrombin time (PT) and partial thromboplastin time (PTT). These tests assess two different pathways by which fibrin clots are formed. PT is the time in seconds required by plasma to form a fibrin clot after exposure to tissue factors. It assesses the extrinsic

Reference Range

Critical Test Result

50 s

0.8–1.2 5 s a

15 mm Hg • Hemodynamic instability • Active hemoptysis • Tracheoesophageal fistula • Recent esophageal surgery • Radiographic evidence of blebs • Recent facial, oral, or skull surgery • Singultus (hiccups) • Nausea

Incentive Spirometry

Contraindicating Intermittent Positive Airway Pressure Breathing Therapy

ICP, Intracranial pressure.

Noninvasive Ventilation A

B

Pressure

Noninvasive ventilation (NIV) provides breathing support to patients with inadequate ability to ventilate. NIV has been documented to have beneficial effects for patients who may need periodic, short-term support or patients who are experiencing exacerbations of pulmonary disease. NIV offers some benefits over traditional, invasive ventilation due to lower infection risk and reduced need for sedation because of the absence of an artificial airway. NIV is discussed in detail elsewhere (Chapter 50). In addition, variations of NIV, including IPPB, CPAP, HFNC, and PEP therapy, can be potentially valuable lung expansion tools and are discussed in the following sections.

Intermittent Positive Airway Pressure Breathing Physiologic Basis IPPB is a specialized form of NIV used for relatively short treatment periods (approximately 15 minutes per treatment). The intent of IPPB, unlike NIV, is not to provide full ventilatory support but to provide machine-assisted deep breaths assisting the patient to deep breathe and stimulate a cough. This section discusses the use of IPPB as a modality for the treatment of atelectasis. IPPB has historically consisted of providing an aerosol under positive pressure, augmenting the patient’s own inspiratory efforts and thus resulting in a larger tidal volume (VT) than could be spontaneously generated. The effectiveness of IPPB as an enhancement for aerosol delivery has been shown to be incorrect. In fact, IPPB does not improve aerosol deposition at all.3 The American Association for Respiratory Care (AARC) clinical practice guidelines (CPG) for IPPB even recommends a 10-fold increase in medication dosage when compared with other aerosol delivery methods.14 Lung volumes are increased in IPPB because Palv > Ppl. Depending on the mechanical properties of the lung, Ppl may exceed atmospheric pressure during a portion of inspiration. As with spontaneous breathing, the recoil force of the lung, stored as potential energy during the positive pressure breath, causes a passive exhalation. As gas flows from the alveoli out to the airway opening, Palv decreases to atmospheric level, while Ppl is restored to its normal subatmospheric range (Fig. 43.5).

can be useful in the treatment of pulmonary complications or exacerbations of lung disease.12,15-17 IPPB should not be used as a single treatment modality for a patient with absorption atelectasis because of excessive airway secretions. Appropriate systemic hydration and airway clearance techniques should be used to assist in removal of excessive secretions. In concept, IPPB treatment should provide the patient with augmented tidal volumes, achieved with minimal effort. There are no data to support the use of IPPB as a method of preventing or expanding atelectasis. The techniques listed later are more effective.

Indications Although IPPB is not an effective aerosol delivery system, periodic sessions of positive pressure ventilation provided noninvasively

Hazards and Complications As with any clinical intervention, certain hazards and complications are associated with IPPB. These potential problems should

Inspiration

Expiration

Inspiration

Expiration

Fig. 43.5  Alveolar (solid lines) and pleural (dotted lines) pressure changes during spontaneous breathing (A) and intermittent positive airway pressure breathing (B). Note the difference in transalveolar pressure (PAL) gradients (double arrows).

Contraindications There are several clinical situations in which IPPB should not be used (Box 43.6). With the exception of untreated tension pneumothorax, most of these contraindications are relative. A patient with any of the conditions listed in Box 43.6 should be carefully evaluated before IPPB therapy is begun.

CHAPTER 43  Lung Expansion Therapy

BOX 43.7  Hazards and Complications

BOX 43.8  Potential Outcomes of

• Hyperventilation and respiratory alkalosis • Discomfort secondary to inadequate pain control • Pulmonary barotrauma • Exacerbation of bronchospasm • Fatigue

• Decrease or elimination of atelectasis • Improved breath sounds • Normal or improved chest x-ray • Increased SpO2 • Increased VC • Improved inspiratory muscle performance and cough

943

Intermittent Positive Airway Pressure Breathing Therapy

of Intermittent Positive Airway Pressure Breathing

SpO2, Oxygen saturation.

be addressed in the initial stages of planning for IPPB. The most common complication associated with IPPB is inducing respiratory alkalosis. This problem is easily avoided through proper coaching of the patient before and during treatment. Another potential complication of IPPB is gastric distention; this occurs when gas from the IPPB device passes directly into the esophagus. Gastric distention is uncommon in an alert patient but is a significant risk for an obtunded patient. Normally, the esophagus does not open until a pressure of approximately 20 to 25 cm H2O has been reached. Gastric distension represents the greatest risk in patients receiving IPPB at high pressures. The major hazards and complications of IPPB are listed in Box 43.7.

Administration Effective IPPB requires careful preliminary planning, individualized patient assessment and implementation, and thoughtful follow-up. Preliminary planning.  During preliminary planning, the need for IPPB is determined and desired therapeutic outcomes are established. Box 43.8 lists potential accepted and desired outcomes of IPPB therapy. Not all the outcomes listed in Box 43.8 apply to every patient. RULE OF THUMB IPPB was once a mainstay therapy for respiratory care. Its nearest cousin, noninvasive ventilation, uses a mask. IPPB was generally given via a mouthpiece and nose clips.

MINI CLINI Problem While covering a surgical step-down floor, you are called to provide IPPB with a bland aerosol to help a patient with postoperative atelectasis. Discussion Because you are on the floor, you go to the patient’s room, introduce yourself, and assess their pulmonary status. After you have completed your evaluation, you speak with the physician who ordered IPPB to find out what his therapeutic goals would be and you relay your evaluation of the patient. The physician states that the patient has severe atelectasis and he is concerned about developing pneumonia and wanted to try IPPB to help with lung recruitment and secretion clearance. You make the suggestion to try CPAP and give a flutter valve to the patient to use when not wearing the CPAP mask. The distending pressure from the CPAP will help to re-recruit the lung, while using PEP may aid secretion clearance by keeping the airways from collapsing on exhalation.

BOX 43.9  Monitoring Intermittent Positive

Airway Pressure Breathing Therapy Machine Performance • Sensitivity • Peak pressure • Flow setting • FiO2

Patient Responsea • Breathing rate and expired volume • Peak flow or FEV1/FVC% • Pulse rate and rhythm (from electrocardiogram if available) • Sputum quantity, color, consistency, and odor • Mental function • Skin color • Breath sounds • Blood pressure • SpO2 (if hypoxemia is suspected) • ICP (in patients for whom ICP is important) • Chest x-ray (when appropriate) • Subjective response to therapy a

Items should be chosen as appropriate for the specific patient. FEV1, Forced expiratory volume in 1 s; FVC, forced vital capacity; ICP, intracranial pressure; SpO2, oxygen saturation.

Evaluating alternatives.  Before starting IPPB, the RT and prescribing physician must determine therapeutic objectives for the treatment and whether simpler and less costly methods might be as effective in achieving the desired outcomes.

Discontinuation and Follow-Up Depending on the goals of therapy and condition of the patient, IPPB treatments typically last 10 to 15 minutes. Follow-up activities include posttreatment assessment of the patient, recordkeeping, and equipment maintenance. Posttreatment assessment.  At the end of a treatment session, the patient assessment is repeated. As with the baseline assessment, this follow-up evaluation has two components. A follow-up evaluation should focus on determining any pertinent changes in vital signs, sensorium, and breath sounds, with emphasis on identifying possible untoward effects. Treatment frequency should be determined by assessing patient response to therapy (Box 43.9). For acute care patients, orders should be reevaluated based on patient response to therapy at least every 72 hours or with any change of patient status.

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SECTION V  Basic Therapeutics

BOX 43.10  Clinical Situations A

Pressure

+

Contraindicating Continuous Positive Airway Pressure Therapy

B

• Tension pneumothorax/untreated pneumothorax • ICP >15 mm Hg • Hemodynamic instability • Active hemoptysis • Tracheoesophageal fistula • Radiographic evidence of blebs • Recent facial, oral, or skull surgery • Nausea • Hypoventilation

0

–

ICP, Intracranial pressure.

Inspiration

Expiration

Inspiration

Expiration

Fig. 43.6  Alveolar (solid lines) and pleural (dotted lines) pressures during spontaneous breathing (A) and continuous positive airway pressure (B). Note the difference in transalveolar pressure (PAL) gradients (double arrows).

Continuous Positive Airway Pressure Physiologic Basis Atelectasis causes a pulmonary shunt and contributes to impaired gas exchange. For areas with a low ventilation and perfusion (V̇ /Q) and an elevated FiO2, the patient is at risk for developing gas absorption atelectasis, further complicating the situation.25 CPAP provides a distending pressure to reinflate the collapsed airways thus improving V̇ /Q. As can be seen in Fig. 43.6, CPAP elevates and maintains high alveolar and airway pressures throughout the full breathing cycle; this increases PAL gradient throughout both inspiration and expiration. Typically, a patient on CPAP breathes through a pressurized circuit against a threshold resistor, with pressures maintained between 5 cm H2O and 20 cm H2O. To maintain system pressure throughout the breathing cycle, CPAP requires a source of pressurized gas. Indications Although evidence supports the use of CPAP therapy in the treating postoperative atelectasis, as with all mechanical techniques, the duration of beneficial effects appears limited. The corresponding increase in FRC may be lost within 10 minutes after the end of the treatment. For this reason, it has been suggested that CPAP should be used on a continuous basis until the patient recovers. CPAP by mask also has been used to treat cardiogenic pulmonary edema. In such patients, CPAP reduces venous return and cardiac filling pressures, which is helpful in reducing pulmonary vascular congestion. Lung compliance is improved, and the work of breathing is decreased. The improvement in lung compliance and the removal of the edema from the alveoli will result in improved ventilation (decreased dead space VD/VT) and thus a decrease in hypercapnia.

RULE OF THUMB Many different types of interfaces can be used for CPAP therapy. They range from nasal prongs (common in neonates, Chapter 54), nasal masks, oronasal masks, and helmets. The ideal interface is that which is comfortable for the patient, does not produce excessive pressure on the face, and minimizes dead space (VD).

Contraindications Intermittent use of CPAP for correcting atelectasis is contraindicated when certain clinical situations exist. A patient who is hemodynamically unstable is unlikely to tolerate CPAP for even a short period. For those patients who are suspected to have hypoventilation, NIV is usually a better option than CPAP. CPAP is also inappropriate when the patient has nausea, facial trauma, untreated pneumothorax, or elevated intracranial pressure (ICP). Hazards and Complications Most hazards and complications associated with CPAP are caused by either the increased pressure or the apparatus (Box 43.10). The increased work of breathing caused by the apparatus can lead to hypoventilation and hypercapnia. An improperly fitted mask can also have detrimental effects on the success of CPAP. Too large a mask will increase the VD.26 A mask that is too small would require being tightly strapped onto the patient’s face. This would increase their chances of developing a pressure-related wound. In addition, because CPAP does not augment spontaneous ventilation, patients with an accompanying ventilatory insufficiency may hypoventilate when CPAP is applied. Barotrauma is a potential hazard of CPAP and is more likely to occur in a patient with emphysema and blebs. Gastric distension may occur, especially if CPAP pressures greater than 25 cm H2O are needed. This condition may lead to vomiting and aspiration in a patient with an inadequate gag reflex. A special case is the obese patient who may actually require high levels of CPAP to counteract the weight of their abdomen on the diaphragm. Monitoring and Troubleshooting CPAP poses a risk of hypoventilation. Experience with long-term CPAP shows that patients must be able to maintain adequate elimination of carbon dioxide on their own if the therapy is to

CHAPTER 43  Lung Expansion Therapy

be successful. For these reasons, patients receiving CPAP must be closely and continuously monitored for untoward effects. In addition, it is vital that the CPAP device be equipped with a means to monitor the pressure delivered to the airways and alarms to indicate the loss of pressure owing to system disconnect or mechanical failure. There should also be a device allowing for excessive pressure to be released (pop-off). These are essential components of any CPAP device (Box 43.11). The development of new CPAP units and improvement on the interface itself have addressed some of the comfort issues

BOX 43.11  Hazards and Complications

of Continuous Positive Airway Pressure Therapy

• Barotrauma, pneumothorax • Nosocomial infection • Hypercarbia • Hemoptysis • Pressure ulcers from mask • Gastric distension • Impaction of secretions (associated with inadequately humidified gas mixture) • Impedance of venous return • Hypoventilation • Increased VD • Vomiting and aspiration VD, Dead space.

945

and correction of leakage associated with CPAP. The RT must also ensure that the flow is adequate to meet the patient’s needs with the use of CPAP systems. Flow adjustments are made by carefully observing the airway pressure. Flow generally can be considered adequate when the system pressure decreases no more than 1 to 2 cm H2O during inspiration.

Administration Early administration of CPAP has been found to be beneficial for both reversing atelectasis and improving V̇ /Q. Equipment.  CPAP is most commonly delivered using either specialized CPAP machines (Fig. 43.7) or ventilators. These devices allow for a more consistent level of positive pressure and provide the benefit of some level of patient monitoring. In the case where ICU-level ventilators are used, this includes monitoring of respiratory rate, airway pressures, and alarms. In the event of a disconnect or if the patient becomes apneic, the ventilator alarms can provide a measure of safety not realized with a high-flow system and resistor valve. Procedures.  Whether used on an intermittent or continuous basis, CPAP is a complex and potentially hazardous approach to patient management. As with all therapies, the appropriate CPAP level for a patient must be determined on an individual basis. Initial application and monitoring require a broader range of knowledge and skill than is required for simpler modes of lung expansion therapy (Box 43.12). Preliminary planning.  As with all respiratory care, effective CPAP therapy requires careful planning, individualized patient

Fig. 43.7  Various continuous positive airway pressure systems. See text for description.

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SECTION V  Basic Therapeutics

BOX 43.12  Potential Outcomes of Continuous Positive Airway Pressure Therapy • Improved VC • Increased FEV1 or peak flow • Enhanced cough and secretion clearance • Improved chest x-ray • Improved breath sounds • Improved oxygenation • Improved patient comfort

A

D

C

FEV1, Forced expiratory volume in 1 s.

BOX 43.13  Monitoring Continuous

Positive Airway Pressure Therapy Device Performance • Mask fit • Set pressure • Flow rate • FiO2

Patient Responsea • Breathing rate and expired volume • Pulse rate and rhythm (from electrocardiogram if available) • Mental function • Skin color • Breath sounds • Blood pressure • SpO2 (if hypoxemia is suspected) • Ventilation • ICP (in patients for whom ICP is important) • Chest x-ray (when appropriate) • Subjective response to therapy a

Items should be chosen as appropriate for the specific patient. ICP, Intracranial pressure; SpO2, oxygen saturation.

assessment and implementation, and thoughtful follow-up (Box 43.13). Evaluating alternatives.  The use of CPAP, NIV, or HFNC has shown promise in decreasing the development of postoperative respiratory complications.27

Discontinuing and Follow-Up Depending on the indications for CPAP (e.g., chronic heart failure [CHF]), once the underlying cause that indicated the need for CPAP has been addressed, it is possible to start to discontinue therapy. In the case of CHF, once the patient has been diuresed, they will most likely not need the positive pressure. Care for other patients may result in periods of time off therapy followed by periods back on until the patient shows signs of continued improvement. Posttreatment assessment.  Auscultation of breath sounds and monitoring oxygen saturation (SpO2) in addition to patient assessment will help to guide the clinician. High-flow nasal cannula.  Providing supplemental oxygen via a nasal cannula has been a common practice in respiratory

B

Fig. 43.8  Schematic of a high-flow nasal cannula system (A) air-oxygen blender, (B) humidifier, (C) circuit, (D) high-flow cannula.

BOX 43.14  Clinical Situations

Contraindicating High-Flow Nasal Cannula Therapy • Hypercarbic respiratory failure • Inability to protect the airway • Unable to tolerate high flow

care. The typical flow limit for these devices is approximately 6 L/min, which is a result of the upper airway to warm and humidify the inspired gas. Common patient complaints when standard nasal cannulas are used at high flows are headache, drying of nasal mucosa, and nosebleeds (Fig. 43.8).26,28,29 The small inner diameter of the standard nasal cannula also does not allow for higher flows. HFNC is specially designed with larger prongs allowing higher oxygen flow rates. In addition to the larger-bore cannula, the gas is also heated and humidified before being delivered to the patient providing a higher level of comfort. These two factors allow for the flow rate to be significantly higher, ranging from 40 to 50 L/min (Boxes 43.14 and 43.15).28-30

Physiologic Basis HFNC at elevated inspiratory flows provides a more stable FiO2. Another benefit from the enhanced flow is washing out the CO2

CHAPTER 43  Lung Expansion Therapy

BOX 43.15  Hazards and Complications of

BOX 43.17  Monitoring Continuous

• Nosocomial infection • Hypercarbia • Headache • Drying of mouth/upper airway • Impaction of secretions (associated with inadequately humidified gas mixture)

Device Performance • Mask fit • Flow rate • FiO2

High-Flow Nasal Cannula Therapy

Positive Airway Pressure Therapy

Patient Responsea • Breathing rate • Pulse rate and rhythm (from electrocardiogram if available) • Mental function • Skin color • Breath sounds • Blood pressure • SpO2 (if hypoxemia is suspected) • Ventilation • ICP (in patients for whom ICP is important) • Chest x-ray (when appropriate) • Subjective response to therapy

BOX 43.16  Potential Outcomes of High-

Flow Nasal Cannula Therapy • Improved chest x-ray • Improved breath sounds • Improved oxygenation • Improved patient comfort

from the anatomic dead space. This helps with ventilation because the CO2 contained in the nasal pharynx has been eliminated and is not the first gas that enters the lowers respiratory tract with each breath. Essentially, gas flow in the upper airway is unidirectional, in through the nose and out through the mouth. This reduces anatomic dead space by approximately one-third, reducing PCO2 by 3 to 5 mm Hg and decreasing the work of breathing.30 In addition to the washout, a small level of positive pressure is delivered as a result of resistance generated as with the patient breathing out against the high inspiratory flow. Most estimate that approximately 1 cm H2O positive end-expiratory pressure (PEEP) is established for every 10 L/min flow through the HFNC. This low positive pressure will first help to recruit collapsed alveoli by increasing the PAL and maintaining their inflation once reopened.28,29 V̇ /Q will improve as a result of the improved ventilation to previously perfused areas of the lung (Box 43.16).

Other Therapies There are other therapies available to the RT with the aim of secretion clearance and possible treatment of postoperative pulmonary complications: intrapulmonary percussive ventilation (IPV) and high-frequency chest wall compression (HFCWC). There is a lack of supporting evidence for the effectiveness of either of these therapies, although each is similar to techniques previously discussed within this chapter. IPV is similar to IPPB with a high respiratory rate, and HFCWC is similar to chest physical therapy (CPT) using a pneumatic vest that the patient wears. These modalities are mentioned for completeness, although the evidence supporting them is low-level or anectdotal.3,19

Positive Airway Pressure First introduced in Denmark during the 1970s as an airway clearance device, and similar to CPAP, PEP adjuncts use positive pressure to increase the PAL gradient and enhance lung expansion.31 In contrast to CPAP or HFNC, PAP therapy requires no complex machinery. Some methods do not even need a source of pressurized gas.

947

a

Items should be chosen as appropriate for the specific patient. ICP, Intracranial pressure; SpO2, oxygen saturation.

Physiologic Basis There are three current approaches to PAP therapy: PEP, flutter, and CPAP. All three techniques are effective in treating atelectasis in most postsurgical patients.32,33 Using either PEP or flutter as part of airway clearance is described in detail in Chapter 44. This chapter focuses on the uses of PAP for treating atelectasis. PEP threshold, resistor, and flutter valves create expiratory positive pressure only without need for continuous flow or complex machinery,28 whereas CPAP maintains a positive airway pressure throughout both inspiration and expiration. Fig. 43.6 compares the alveolar and Ppl changes occurring during a normal spontaneous breath (see Fig. 43.6A) and CPAP (see Fig. 43.6B). The following factors involving PAP, flutter, and CPAP therapy contribute to the beneficial effects: (1) recruitment of collapsed alveoli through an increase in FRC, (2) decreased work of breathing due to increased compliance or elimination of intrinsic positive end-expiratory pressure (PEEPi), (3) improved distribution of ventilation through collateral channels (e.g., pores of Kohn), and (4) increase in the efficiency of secretion removal (Box 43.17). Indications The evidence for PEP therapy suggests that patients with expiratory airflow limitation will best respond to this therapy.31,34 PEP mimics the maneuver of pursed-lip breathing by presenting expiratory resistance either through a flow or threshold resistor, and an elongated expiratory phase. Those patients who are good candidates for PEP therapy are those who can follow instructions and repeat the demonstration back to the RT. Similar to IS, there is no set duration for therapy nor a set number of repetitions during each session. Currently this therapy is given for patients who may either have atelectasis or have breathlessness.

948

SECTION V  Basic Therapeutics

Contraindications Similar to the contraindications for the other lung expansion therapies, an untreated pneumothorax should be considered before starting therapy. A good baseline assessment of the patient is helpful to identify any predisposing issues. Hazards and Complications Regardless if it is flow limited, a threshold device, or oscillating PEP, care should be taken that the patient does not hyperventilate during therapy. Signs can include dizziness, tingling in the extremities, and light-headedness. In those cases, have the patient stop therapy until they feel better and then suggest a slower regimen of breaths. Equipment PEP valve and mouthpiece. The device is designed to fit into a pocket and taken apart for cleaning. Procedures.  Show the device to the patient and have them take a tidal, or slightly larger than tidal, breath. Have the patient exhale through the PEP device and set the resistor to the desired strength. Repeat the instructions if they are breathing out too quickly or slowly.31,35 Monitoring and Troubleshooting Check the valve for obstructions if the patient cannot breathe out from the device. Some PEP devices include a 30-day diary that can be used to track progress.

MINI CLINI—PROBLEM WITH POSITIVE EXPIRATORY PRESSURE Problem During a follow-up visit with a patient that you instructed in the use of PEP therapy, it is observed that the patient is struggling on exhalation through the device and does not want to use it. Discussion Looking at the device, you see that the resistance is set to maximum. The patient had visitors who were looking at the device and may have moved the setting. You take the time to provide some education and reassurance to the patient and show how to set the resistance and enter it into the diary. With the correct settings, the patient is more willing to continue therapy.

INITIATION OF THERAPY The best approach for achieving a given clinical goal is always the safest, simplest, and most effective method for an individual patient. Selecting an approach for lung expansion therapy requires in-depth knowledge of both the methods available and the specific condition and needs of the patient being considered for therapy.

Preliminary Planning Patient education and motivation are key to the success for this therapy. The PEP devices are made to be portable and allow the

patient to carry them while outside of the hospital or home. Many devices are now dishwasher safe for easier cleaning.

Evaluating Alternatives If the patient cannot tolerate PEP, then alternative therapies could be either CPAP or HFNC. Both will aid in lung recruitment using a similar mechanism, with less patient coordination.

Discontinuing and Follow-Up PEP therapy has been shown to have a positive effect on patient self-reported breathlessness for those patients who have noncystic fibrosis bronchiectasis or severe chronic obstructive pulmonary disease (COPD).35 PEP can be continued at home as part of a daily regimen for pulmonary hygiene and dyspnea.

Posttreatment Assessment Auscultation of breath sounds and reviewing the patient diary for shortness of breath can help to guide the RT in determining if the therapy should be discontinued.

SELECTING AN APPROACH Selecting an approach for lung expansion therapy requires in-depth knowledge of both the methods available and the specific condition and needs of the patient being considered for therapy. Fig. 43.9 presents a sample protocol for selecting an approach to lung expansion therapy. As indicated in the algorithm, the patient first must meet the criteria for therapy by having one or more of the indications previously specified. For patients meeting the inclusion criteria, the RT first determines the degree of alertness. Because an obtunded patient cannot be expected to cooperate with IS or PEP or expiratory positive airway pressure (EPAP) therapy, HFNC or CPAP is initiated with appropriate monitoring. For a patient having no difficulty with secretions, if the VC exceeds 15 mL/kg of lean body weight or the IC is greater than 33% of predicted, IS is given. If either the VC or the IC is less than these threshold levels, IPPB is initiated, with the pressure gradually manipulated from the initial setting to deliver at least 15 mL/kg. If excessive sputum production is a compounding factor, a trial of PEP therapy is substituted for IS. Based on patient response, bronchodilator therapy and bronchial hygiene measures may be added to this regimen. If monitoring fails to reveal improvement and atelectasis persists, a trial of CPAP should be considered. Because evidence of the effectiveness of CPAP is still contradictory, its use should be limited to treating atelectasis after alternative approaches have been tried without success. Whether or not to keep critically ill patients on complete bed rest is being critically examined in the literature.22-27,36,37 The complications of prolonged bed rest include cardiovascular, pulmonary, gastrointestinal, and skin integrity issues. Pulmonary complications of immobility include those that have been the focus of this chapter: development of atelectasis, pneumonia, and PE.23-27,36 Rates of early mobilization for ICU patients have been increasing in both Europe and the United States, along

CHAPTER 43  Lung Expansion Therapy

949

At risk for atelectasis

No

No

Increased CO2

Awake Yes

Neuromuscular disease

No Early mobilization Yes

Yes Cough assist/MIE

Signs of improvement?

Hypoxia/ desaturation

Yes High flow nasal cannula (HFNC)

No PEP/flutter No

Signs of improvement?

No Noninvasivce ventilation (NIV)

Yes

Yes

Signs of improvement?

No

Consider escalating level of care

Yes Continue to monitor Fig. 43.9  Protocol for selecting an approach for lung expansion therapy. See text for details. PEP, Positive expiratory pressure. MIE, Mechanical insufflation exhalation.

with the an emphasis on decreasing morbidity in the ICU. Mobilization does not only include walking, but also sitting, standing, and getting out of bed into a chair. As the patient changes body position, his or her breathing changes, as does the gas distribution within the lung. Improvements in ventilation result in less alveolar collapse.

SUMMARY CHECKLIST • Atelectasis is caused by persistent ventilation with small tidal volumes or by resorption of gas distal to obstructed airways. • Patients who have undergone upper abdominal or thoracic surgery are at greatest risk for atelectasis. • A history of lung disease or significant cigarette smoking increases the risk for atelectasis. • Patients with atelectasis usually have rapid, shallow breathing; fine, late-inspiratory crackles; and abnormalities on chest radiograph.

• Lung expansion therapy corrects atelectasis by increasing the PAL gradient; this can be accomplished by deep spontaneous breaths or by the application of positive pressure. • The most common problem associated with lung expansion therapy is the onset of respiratory alkalosis, which occurs when the patient breathes too quickly. • RTs are responsible for implementing, monitoring, and documenting results of lung expansion therapy.

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31.

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33.

34.

35.

36.

37.

complications in upper abdominal surgery, Cochrane Database Syst Rev (2):CD006058, 2014. Hassanzadeh H, Jain A, Tan EW, et al: Postoperative incentive spirometry use, Orthopedics 35:e927–e931, 2012. Restrepo RD, Wettstein R, Wittnebel L, et al: Incentive spirometry: 2011, Respir Care 56:1600–1604, 2011. Eltorai AEM, Szabo AL, Antoci V, et al: Clinical effectiveness of incentive spirometry for the prevention of postoperative pulmonary complications, Respir Care 63:347–352, 2018. Freitas ERFS, Soares BGO, Cardoso JR, et al: Incentive spirometry for preventing pulmonary complications after coronary artery bypass graft, Cochrane Database Syst Rev (9):CD004466, 2012. Karcz M, Papadakos PJ: Respiratory complications in the postanesthesia care unit: a review of pathophysiological mechanisms, Can J Respir Ther CJRT Rev Can Ther Respir RCTR 49:21, 2013. Nishimura M: High-flow nasal cannula oxygen therapy in adults [Internet], J Intensive Care 3:15, 2015. Availablefrom: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4393594/. Ireland CJ, Chapman TM, Mathew SF, et al: Continuous positive airway pressure (CPAP) during the postoperative period for prevention of postoperative morbidity and mortality following major abdominal surgery, Cochrane Database Syst Rev (8): CD008930, 2014. Branson RD: The scientific basis for postoperative respiratory care, Respir Care 58:1974–1984, 2013. Roca O, Riera J, Torres F, et al: High-flow oxygen therapy in acute respiratory failure, Respir Care 55:408–413, 2010. Hernández G, Vaquero C, González P, et al: Effect of postextubation high-flow nasal cannula vs conventional oxygen therapy on reintubation in low-risk patients: a randomized clinical trial, JAMA 315:1354, 2016. FagevikOlsén M, Lannefors L, Westerdahl E: Positive expiratory pressure—Common clinical applications and physiological effects, Respir Med 109:297–307, 2015. Sehlin M, Ohberg F, Johansson G, et al: Physiological responses to positive expiratory pressure breathing: a comparison of the PEP bottle and the PEP mask, Respir Care 52:1000–1005, 2007. Squadrone V, Coha M, Cerutti E, et al: Continuous positive airway pressure for treatment of postoperative hypoxemia: a randomized controlled trial, JAMA 293:589–595, 2005. Osadnik CR, McDonald CF, Miller BR, et al: The effect of positive expiratory pressure (PEP) therapy on symptoms, quality of life and incidence of re-exacerbation in patients with acute exacerbations of chronic obstructive pulmonary disease: a multicentre, randomised controlled trial, Thorax 69:137–143, 2014. Lee AL, Williamson HC, Lorensini S, et al: The effects of oscillating positive expiratory pressure therapy in adults with stable non-cystic fibrosis bronchiectasis: a systematic review, Chron Respir Dis 12:36–46, 2015. Sorenson HM, Shelledy DC: AARC: AARC clinical practice guideline. Intermittent positive pressure breathing–2003 revision & update, Respir Care 48:540–546, 2003. Guérin C, Vincent B, Petitjean T, et al: The short-term effects of intermittent positive pressure breathing treatments on ventilation in patients with neuromuscular disease, Respir Care 55:866–872, 2010.

CHAPTER 43  Lung Expansion Therapy 38. Narita M, Tanizawa K, Chin K, et al: Noninvasive ventilation improves the outcome of pulmonary complications after liver resection, Intern Med Tokyo Jpn 49:1501–1507, 2010. 39. Pessoa KC, Araújo GF, Pinheiro AN, et al: Noninvasive ventilation in the immediate postoperative of gastrojejunal

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derivation with Roux-en-Y gastric bypass, Rev Bras Fisioter Sao Carlos Sao Paulo Braz 14:290–295, 2010. 40. Andrews J, Sathe NA, Krishnaswami S, et al: Nonpharmacologic airway clearance techniques in hospitalized patients: a systematic review, Respir Care 58:2160–2186, 2013.

44  Airway Clearance Therapy David L. Vines and Donna D. Gardner

CHAPTER OBJECTIVES After reading this chapter you will be able to: • Compare the normal airway clearance mechanisms to the factors that impair their function. • Identify pulmonary diseases associated with abnormal secretion clearance. • State the clinical indications for airway clearance therapy. • Describe the proper technique that would result in potential benefits of each of the following: • Chest physical therapy • Directed coughing and related expulsion techniques

• Vibratory positive expiratory pressure therapy • Mechanical insufflation-exsufflation (MIE) • High-frequency oscillation devices • Vibratory positive expiratory pressure • High-frequency airway pressure devices • High-frequency oscillation compression devices • Mobilization and exercise • Evaluate a patient’s response to airway clearance therapy to determine changes in the treatment plan.

CHAPTER OUTLINE Physiology of Airway Clearance Therapies, 953 Normal Clearance, 953 Abnormal Clearance, 953 Diseases Associated With Abnormal Clearance, 954 General Goals and Indications, 954 Airway Clearance Therapy for Acute Conditions, 954 Airway Clearance Therapy for Chronic Conditions, 955 Airway Clearance Therapy to Prevent Retention of Secretions, 955

Determining the Need for Airway Clearance Therapy, 955 Airway Clearance Methods, 955 Chest Physical Therapy Also Known as Postural Drainage and Percussion, 956 Coughing and Related Expulsion Techniques, 959 Active Cycle of Breathing Technique, 962 Autogenic Drainage, 962 Mechanical Insufflation-Exsufflation, 963

Positive Airway Pressure Adjuncts, 964 High-Frequency Positive Airway Pressure Devices, 966 High-Frequency Chest Wall Compression, 967 Exercise, Mobilization, and Physical Activity, 968 Selecting Airway Clearance Techniques, 968 Selection Factors, 968 Protocol-Based Airway Clearance, 969

Hertz (Hz) High-frequency chest wall compression (HFCWC) huff coughing inspissation intrapulmonary percussive ventilation (IPV)

mechanical insufflation-exsufflation (MIE) mucous plugging oscillation positive expiratory pressure (PEP) splinting

KEY TERMS active cycle of breathing technique (ACBT) autogenic drainage (AD) bronchiectasis chest physical therapy (CPT) ciliary dyskinetic syndromes forced expiratory technique (FET)

Airway clearance therapy (ACT) uses noninvasive techniques designed to assist in mobilizing and removing secretions to improve gas exchange.1 Historically, the term chest physical therapy (CPT) described the primary techniques used to assist with clearing secretions from the airways. Today, there are 952

numerous options related to airway clearance including CPT, breathing retraining techniques, positive expiratory therapy (PEP), vibratory PEP, high-frequency oscillation devices, highfrequency chest wall compression (HFCWC) devices, mechanical insufflation-exsufflation (MIE), and various exercise protocols.1–3

CHAPTER 44  Airway Clearance Therapy

This chapter focuses on ACTs or techniques used to mobilize secretions and noninvasively assist in their removal. The primary invasive method for removing airway secretions is suctioning and is discussed in Chapter 37. Successful outcomes in airway clearance techniques require knowledge of normal and abnormal physiology, understanding of how clearance devices work, careful patient evaluation, rigorous application of evidence-based methods, and ongoing assessment targeted at achieving therapeutic goals.1–4

PHYSIOLOGY OF AIRWAY CLEARANCE THERAPIES To apply ACTs properly, one must understand how normal airway clearance mechanisms work and what can impair their function.

Normal Clearance Normal airway clearance requires patent airways, a functional mucociliary escalator, adequate hydration, and effective cough.5 Mucociliary clearance normally occurs from the larynx down to the respiratory bronchioles. Mucus is produced by secretory (Clara, goblet, and serous) cells and submucosal glands.5 Ciliated epithelial cells move this mucus via a coordinated wave of ciliary motion toward the trachea and larynx, where secretions can be swallowed or expectorated. Healthy individuals produce 10 to 100 mL of secretions in the airway on a daily basis that are cleared by this mucociliary escalator.3,5 The cough is one of the most important protective reflexes. Coughing clears the larger airways of excessive mucus and foreign matter, assists normal mucociliary clearance, and helps ensure airway patency. As shown in Fig. 44.1, there are four distinct phases to a normal cough: irritation, inspiration, compression, and expulsion. In the initial irritation phase, an abnormal stimulus provokes sensory fibers in the airways to send impulses to the medullary cough center in the brain. This stimulus normally is inflammatory, mechanical, chemical, or thermal. Infection is a good example of an inflammatory process that can stimulate a cough. Foreign bodies can provoke a cough through mechanical

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stimulation. Inhaling irritating gases (e.g., cigarette smoke) can result in coughing through chemical stimulation. Finally, cold air may cause thermal stimulation of sensory nerves, producing a cough. When these impulses are received, the cough center generates a reflex stimulation of the respiratory muscles to initiate a deep inspiration (the second phase). In normal adults, this inspiration averages 1 to 2 L. During the third or compression phase, reflex nerve impulses cause glottic closure and a forceful contraction of the expiratory muscles. This compression phase is normally about 0.2 seconds and results in a rapid increase in pleural and alveolar pressures, often greater than 100 mm Hg. At this point, the glottis opens, initiating the expulsion phase. With the glottis open, a large pressure gradient between the lungs and the atmospheric pressure exists. Together with the continued contraction of the expiratory muscles, this pressure gradient causes a violent, expulsive high velocity of airflow from the lungs. This high-velocity gas flow, combined with dynamic airway compression, creates huge shear forces that displace mucus from the airway walls into the air stream. Mucus and foreign material are expelled from the lower airways to the upper airway, where they can be expectorated or swallowed.

Abnormal Clearance Any abnormality that alters airway patency, mucociliary function, strength of the inspiratory or expiratory muscles, thickness of secretions, or effectiveness of the cough reflex can impair airway clearance leading to retention of secretions.3,5 In addition, some therapeutic interventions, especially interventions used in critical care, such as an endotracheal tube, can result in abnormal clearance. Retention of secretions can result in full or partial airway obstruction. Full obstruction, or mucous plugging, can result in atelectasis which causes hypoxemia due to shunting. A partial obstruction restricts airflow, increasing work of breathing and possibly leading to air trapping, lung overdistension, and ventilation/ perfusion (V̇ /Q̇ ) imbalances. In the presence of pathogenic organisms, retention of secretions can also lead to infections.

Irritation Inspiration Compression Expulsion Fig. 44.1  The cough reflex. (Modified from Cherniack RM, Cherniack L. Respiration in Health and Disease, ed 3, Philadelphia, 1983, WB Saunders.)

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SECTION V  Basic Therapeutics

TABLE 44.1  Mechanisms Impairing

Cough Reflex Phase

Examples of Impairments

Irritation

Anesthesia Central nervous system depression Narcotic analgesics Pain Neuromuscular dysfunction Pulmonary restriction Abdominal restriction Laryngeal nerve damage Artificial airway Abdominal muscle weakness Abdominal surgery Airway compression Airway obstruction Abdominal muscle weakness Inadequate lung recoil (e.g., emphysema)

Inspiration

Compression

Expulsion

BOX 44.1  Causes of Impaired Mucociliary

Clearance in Intubated Patients • Endotracheal or tracheostomy tube • Tracheobronchial suction • Inadequate humidification • High FiO2 values • Drugs • General anesthetics • Opiates • Narcotics • Underlying pulmonary disease

Infectious processes provoke an inflammatory response and the release of chemical mediators. These chemical mediators, including leukotrienes, proteases, and elastases, can damage the airway epithelium and increase mucus production, resulting in a vicious cycle of worsening airway clearance.5 In patients with retained secretions, interference with one of the four phases of cough can result in ineffective airway clearance. This occurs in patients following thoracic or upper abdominal surgery, in the intensive care unit, or with neuromuscular diseases (NMDs) such as amyotrophic lateral sclerosis (ALS), myasthenia gravis (MG), or cervical or thoracic spinal cord injuries. Table 44.1 provides examples of factors that can impair the normal cough reflex. As indicated in Box 44.1, additional factors can impair airway clearance in critically ill patients with artificial airways, the most important of which is the airway itself.6 The presence of an artificial airway in the trachea increases mucus secretion, and the cuff of the tube mechanically blocks the mucociliary escalator. In addition, movement of the tube tip and cuff can cause erosion of the tracheal mucosa, leading to further impairment of the mucociliary escalator. The endotracheal tube also impairs the compression phase of the cough reflex by preventing closure of the glottis (see Table 44.1). Although suctioning is used to

aid secretion clearance, it too can cause damage to the airway mucosa and impair mucociliary transport. Inadequate humidification can cause thickening or inspissation of secretions, mucous plugging, and airway obstruction.7 High fractional inspired oxygen (FiO2) concentrations can impair ciliary function, resulting in retained secretions. Retained secretions can lead to acute tracheobronchitis. Several common drugs, including some general anesthetics and narcotic analgesics, may also depress mucociliary transport.5

RULE OF THUMB  Several factors impair the mucociliary escalator resulting in increased mucus production: the presence of an artificial airway, suctioning beyond the end of an artificial airway, inadequate humidification, high concentrations of oxygen, and drugs (anesthetics and narcotic—analgesics).

Diseases Associated With Abnormal Clearance Several diseases are associated with abnormal airway clearance, including diseases affecting airway patency, composition and production of mucus, ciliary structure and function, and normal cough reflex.5 Internal obstruction or external compression of the airway lumen can impair airway clearance. Examples include foreign bodies, tumors, and congenital or acquired thoracic anomalies such as kyphoscoliosis. Internal obstruction also can occur with mucus hypersecretion, inflammatory changes, or bronchospasm that narrows the lumen. Examples include asthma, chronic bronchitis, and/or acute infections. Diseases that alter normal mucociliary clearance also can cause retention of secretions. In cystic fibrosis (CF), the solute concentration of the mucus is altered because of abnormal sodium and chloride transport.5 This alteration increases the viscosity of mucus and impairs its movement up the respiratory tract. Although less common, there are several conditions in which the respiratory tract cilia do not function properly.5 The ciliary dyskinetic syndromes contribute to ineffective airway clearance. Bronchiectasis permanently damages and dilates airways that are prone to obstruction due to retained secretions.5,8 Bronchiectasis is a common finding in CF and ciliary dyskinetic syndromes.8–10 Mucociliary function may be normal, but lack of an effective cough alters airway clearance leading to retained secretions, mucous plugs, obstructions, and atelectasis. The most common conditions affecting the cough reflex are musculoskeletal and NMD, including muscular dystrophy, ALS, spinal muscular atrophy, MG, poliomyelitis, and cerebral palsy (see Chapter 33).11

GENERAL GOALS AND INDICATIONS The primary goal of ACT is to assist the patient to mobilize and remove retained secretions. Removal of these retained secretions may improve gas exchange, promote alveolar expansion, and reduce the work of breathing. Box 44.2 lists general indications for ACT.1,3

Airway Clearance Therapy for Acute Conditions Patients with acute conditions in whom ACT may be indicated include: (1) acutely or chronically ill patients with copious

CHAPTER 44  Airway Clearance Therapy

BOX 44.2  Indications for Airway

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MINI CLINI

Clearance Therapy

Assessing a Patient’s Cough Clearance

Acute Conditions • Copious secretions • Inability to mobilize secretions • Ineffective cough

Problem The respiratory therapist (RT) is called by a nurse to determine a care plan to assist a patient who is having difficulty clearing secretions. The patient is an alert, obese, 45-year-old man who underwent general anesthesia and surgery for a cholestectomy 3 h earlier. Physical signs indicate retention of secretions, but there is no history of lung disease. Auscultation reveals coarse expiratory crackles. The patient is breathing spontaneously; however, his breathing is shallow and he has a very weak cough. Visual clues indicate the patient has severe pain in the epigastric area. The patient was given an injection of morphine to assist with the pain 1 h earlier.

Chronic Conditions • Cystic fibrosis • Bronchiectasis • Ciliary dyskinetic syndromes • Chronic obstructive pulmonary disease patients with retained secretions.

secretions; (2) patients with retained secretions or ineffective cough (coarse crackles, worsening oxygenation and/or ventilation, volume loss on chest radiograph); (3) possibly patients with acute lobar atelectasis; or (4) patients with V̇ /Q̇ abnormalities.1 In treating chronic respiratory conditions, inhaled bronchodilator therapy before ACT may improve the overall effectiveness of the treatment both by opening the airways and by increasing the mucociliary activity.12 For acute pulmonary infections and those with CF, inhaled antibiotics taken after ACT can lead to improved deposition of the antibiotic.4 Acute conditions for which ACT is probably not indicated include: (1) routine care of chronic obstructive pulmonary disorder (COPD), (2) pneumonia without clinically significant sputum production, (3) routine postoperative care, and (4) uncomplicated asthma.1,3 RULE OF THUMB  Bronchodilator therapy is not indicated in the acute care setting for airway clearance therapy unless the patient is wheezing due to a bronchospasm or has a chronic pulmonary condition with retained secretions.

Airway Clearance Therapy for Chronic Conditions ACT has proved effective in secretion clearance and improving pulmonary function in chronic conditions associated with copious sputum production, including CF, bronchiectasis, and ciliary dyskinetic syndromes, and COPD patients with retained secretions.1,3,4 Generally, sputum production must exceed 20 to 30 mL/day for ACT to improve secretion removal significantly.3 RULE OF THUMB Patients with copious secretions (20–30 mL/day) or inability to mobilize and expectorate secretions may benefit from airway clearance therapy.

Airway Clearance Therapy to Prevent Retention of Secretions ACT has been used as preventive therapy in various disorders and current evidence is not supportive of this approach.1,2 The best-documented preventive uses of ACT include: (1) body positioning and patient mobilization to prevent retained secretions in acutely ill patients, and (2) ACT combined with physical activity to maintain lung function in patients with CF.1,2,4

Discussion There is no surprise that this patient is having difficulty clearing secretions considering the recent anesthesia and receiving a narcotic analgesic, which may impair his cough. In addition, obesity (abdominal restriction), weakness, and pain are impairing the inspiration, compression, and expulsion phases of his cough effort. The patient should immediately be started on ACT and hyperinflation or lung expansion therapies. Judicious use of pain medication, coinciding with therapies, should continue. Cough instruction including incisional splinting should be part of the plan. Early mobilization should be encouraged. Although the most common postoperative complication is atelectasis, pneumonia may also occur. The head of the patient’s bed should be elevated at least to 30–45 degrees to minimize the risk of aspiration.

DETERMINING THE NEED FOR AIRWAY CLEARANCE THERAPY Effective ACT requires proper initial and ongoing patient assessment (Chapter 16). Formulation of the respiratory care plan depends on review of the patient’s medical history and interview for current symptoms, physical assessment, assessment of cough and sputum, laboratory testing (including pulmonary function tests), and radiologic evaluation. Box 44.3 lists the key factors that must be considered when assessing a patient’s need for ACT.1,3,4 Physical findings, such as a loose, ineffective cough; labored breathing pattern; decreased or bronchial breath sounds; coarse inspiratory and expiratory crackles; tachypnea; tachycardia; or fever may indicate a potential problem with retained secretions.

AIRWAY CLEARANCE METHODS Five general approaches to ACT, which can be used alone or in combination, include: (1) CPT; (2) coughing and related expulsion techniques (including mechanical insufflation-exsufflation [MIE]); (3) positive airway pressure (PAP) adjuncts (positive expiratory pressure [PEP], vibratory PEP, high-frequency PAP devices); (4) high-frequency oscillation devices; and (5) mobilization and physical activity. Table 44.2 provides a brief description and limitations associated with these ACTs. Appropriate use of these techniques requires an understanding of their underlying principles, relative usefulness, and methods of application.

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SECTION V  Basic Therapeutics

BOX 44.3  Initial Assessment of Need for

Airway Clearance Therapy

Medical Record History of pulmonary problems causing increased secretions Admission for upper abdominal or thoracic surgery; consider: Age (elderly) History of chronic obstructive pulmonary disease Obesity Nature of procedure Type of anesthesia Duration of procedure Presence of artificial tracheal airway Chest radiograph indicating atelectasis or infiltrates Results of pulmonary function testing Arterial blood gas values or O2 saturation Patient Posture, muscle tone Effectiveness of cough Sputum production Breathing pattern General physical fitness Breath sounds Vital signs, heart rate and rhythm

Chest Physical Therapy Also Known as Postural Drainage and Percussion CPT has long been considered a standard of care in patients with CF. Evidence suggests that these therapies benefit mucus transport and assist in the expectoration of secretions.1,3,4 This therapy includes postural drainage (PD) and percussion or vibration. CPT involves the use of positioning, gravity, and mechanical energy to help mobilize secretions. PD places the body in various positions that are intended to drain secretions from each of the patient’s lung segments into the central airways, where they can be removed by cough or suctioning.4 This drainage is accomplished by simply placing the segmental bronchus to be drained in a more vertical position, permitting gravity to assist in the process. Positions generally are held for 3 to 15 minutes (longer in special situations such as CF) and modified as the patient’s condition and tolerance warrant. Specifically, with CF patients and all pediatric patients in general, head-down positioning should be avoided to prevent marked increases in intracranial pressure (ICP), especially during coughing.2–4,13 Cough methods are used with CPT and are discussed separately. The indications for CPT (and other ACTs) in a patient are the presence of copious secretions, the inability to mobilize and expectorate the secretions, and pulmonary disorders associated with retained secretions (CF, bronchiectasis, and ciliary dyskinetic syndromes).1,3,4 This therapy does require a trained caregiver’s assistance in order for it to be performed correctly. CPT may be most effective in conditions characterized by excessive sputum production (greater than 25 to 30 mL/day) that is not cleared by deep breathing and coughing. For maximum effect with PD, headdown positions should exceed 25 degrees below horizontal.2–4,13

In patients with CF and pediatric patients in general head-down positioning should be avoided as discussed above.2–4,13 If the patient cannot be placed in appropriate positions for the areas affected, another ACT should be considered. In spontaneously breathing patients, treatment frequency should be determined by assessing the patient’s response to therapy. Critically ill patients, especially patients being mechanically ventilated, should be moved and rotated every 2 hours.14 RULE OF THUMB To achieve the maximum secretion drainage with postural drainage and percussion the head-down positions should exceed 25 degrees below horizontal. In patients with CF and pediatric patients in general head down positioning should be avoided because of increased ICP, especially of concern during coughing. If the patient cannot be placed in appropriate drainage positions for the areas affected, another ACT should be considered.

Technique Based on a preliminary assessment of the patient and review of the physician’s order, the RT should identify the appropriate lobes and segments for drainage. The RT may need to choose a different ACT method in patients with unstable cardiovascular status, hypertension, cerebrovascular disorders, or dyspnea. To avoid gastroesophageal reflux and the possibility of aspiration, treatment times should be scheduled before or at least 2 hours after meals or tube feedings to decrease the chance of vomiting or aspiration. If the patient assessment indicates that pain may hinder treatment implementation, the RT should consider coordinating the treatment regimen with prescribed pain medication. Contraindications for CPT are listed in Box 44.4. Before positioning, the procedure (including adjunctive techniques) should be explained to the patient. The RT should inspect for incisions, monitoring leads, intravenous tubing, and oxygen (O2) therapy equipment connected to the patient and, if necessary, make adjustments to ensure continued function during the procedure or choose a different ACT method. Before starting, during, and after the procedure, the RT should measure the patient’s vital signs, auscultate the chest, and measure SpO2 to assess the presence of hypoxemia. These simple assessments serve as baseline measurements for monitoring the patient’s response during the ACT and can assist in determining outcomes. The following items also should be monitored before, during, and after CPT: subjective responses (pain, discomfort, dyspnea, response to therapy), arrhythmias, breathing pattern, sputum production (quantity, color, consistency, odor), skin color, and ICP if monitored. Fig. 44.2 depicts the primary positions used to drain the various lung lobes and segments. Generally, to obtain the proper head-down position, the RT must lower the head of the bed by at least 16 to 18 inches to achieve the desired 25-degree angle. In the ambulatory care setting, a tilt table can be used in lieu of a hospital bed. A tilt table allows precise positioning at headdown angles up to 45 degrees. When angles this large are used, shoulder supports must be provided to prevent the patient from sliding off the tilt table. After the patient is positioned, the RT confirms the patient’s comfort and ensures proper support of all joints and bony areas with pillows or towels. The indicated position is maintained for

CHAPTER 44  Airway Clearance Therapy

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TABLE 44.2  Airway Clearance Therapies, Techniques, and Devices ACT

Techniques and Devices

Limitations Associated With ACT

Chest physiotherapy (CPT) includes percussion and postural drainage

Manual percussion of the chest using cupped hands or mechanical device creates vibrations to loosen secretions and positioning uses gravity to draining secretions from the lung segments to the larger airways To mobilize secretions the breathing cycles includes alternating between relaxed breathing, deep breathing, and forced expiratory technique

• Patients who are short of breath may not tolerate being placed in Trendelenburg position. • The treatment is dependent of the patient being positioned appropriately. • Caregivers are required to perform the therapy • Patients who are unable to perform this therapy include those unable to take a deep breath or experiencing an exacerbation • This concept is difficult to perform in children less than 4 years old. • Repeated coaching may be needed in children up to the age of 10 • The patient’s coordinated breathing is necessary making it difficult to perform when they are short of breath or unable to take a deep breath. • To perform correctly the patient needs to be an older than 10 years of age

Active cycle of breathing

Autogenic drainage

Mechanical insufflatorexsufflator (MIE)

Positive expiratory pressure (PEP) or oscillatory or vibratory PEP (OPEP)

High-frequency positive airway pressure devices

High-frequency chest wall compression

Mobilization and physical activity

To loosen and move secretions into the larger airways and then expelled them, a patient can use a series of breathing patterns beginning with breaths at a low volume, then breaths at a normal tidal volume and ending with a high volume and high peak flow breath like a huff cough To expel secretions the device simulates an effective cough by using positive airway pressure on inspiration to increase tidal volume and then switching to a negative pressure to increase peak expiratory cough flows. The device may be used with a mask, mouthpiece or attached to an artificial airway. The device has an oscillatory mechanism to assist with mobilize the secretions To mobilize secretions using PEP devices, an expiratory pressure of 10–20 cm H2O is created by the patient actively exhaling against a fixed or variable orifice flow resistor. The OPEP creates flow oscillations by adding flow interruptions during the patient’s active exhalation To loosen and move secretions into the larger airways the patient breathes in and actively exhales against short, rapid positive airway pressure pulses

To mobilize the secretions in the larger airways the patient wears a vest that creates chest wall compression resulting in small pulses of volume at high frequencies Patients who participate in physical activity that results in increased tidal volume, heart rate, and cardiac output, and improved physical condition

• In patients with bulbar ALS, the negative pressure expiratory phase may be limited by upper airway closure. • Patients with obstructive airway disorders may experience airway collapse with the negative pressure phase • Contraindicated in the presence or suspicion of untreated pneumothorax, unstable hemodynamic status, increased intracranial pressure, current maxillofacial surgery or trauma, active hemoptysis, or tympanic membrane rupture. • Caregiver is needed for this therapy • Patients must be able to take a deep breath and exhale with enough force to generate the PEP and oscillations. • Contraindicated in the presence or suspicion of untreated pneumothorax, unstable hemodynamic status, increased intracranial pressure, current maxillofacial surgery or trauma, active hemoptysis, or tympanic membrane rupture • Younger patients will require a caregiver. • If the patient does not actively exhale, exhalation will depend on the patients’ chest wall elastic recoil. • Contraindicated in the presence or suspicion of untreated pneumothorax, unstable hemodynamic status, increased intracranial pressure, current maxillofacial surgery or trauma, active hemoptysis, or tympanic membrane rupture • Patients need to be at least 2 years of age begin using the device. • Avoid using the device in the presence of indwelling catheters or chest tubes • Patients may participate in physical exercise as long as their medical condition allows, or medical monitoring is available. • Caution is needed for patients at risk of developing bronchospasm in the presence of reactive airways

ACT, Airway clearance therapy; ALS, amyotrophic lateral sclerosis.

a minimum of 3 minutes if tolerated and longer if good sputum production results. Between positions, pauses for relaxation and breathing control are useful and can help prevent hypoxemia. Because postural drainage therapy can increase O2 consumption, critically ill patients should be given supplemental O2 during the procedure if SpO2 decreases. During the procedure, the patient is continually observed for any side effects or complications. Moderate changes in vital signs are expected during treatment. Table 44.3 lists complications

and the recommended interventions. Significant problems may require immediate intervention. Also, the RT should ensure that the patient uses appropriate coughing technique during and after positioning. When using the head-down position for non-CF and nonpediatric patients, the patient should avoid strenuous coughing because this markedly increases ICP.1,2 Rather, the patient should use the forced expiration technique (described later in this chapter). Generally, total treatment time should not exceed 15 minutes for a routine

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SECTION V  Basic Therapeutics

BOX 44.4  Contraindications to the Use of

Chest Physical Therapy

The decision to use postural drainage requires assessment of potential benefits versus potential risks. Therapy should be provided for no longer than necessary to obtain the desired therapeutic results. Listed contraindications are relative unless marked as absolute (A). Positioning: All positions are contraindicated for: • Head and neck injury until stabilized (A) • Active hemorrhage with hemodynamic instability (A) • Intracranial pressure (ICP) greater than 20 mm Hg • Recent spinal surgery or acute spinal injury • Active hemoptysis • Empyema • Bronchopleural fistula • Pulmonary edema associated with congestive heart failure • Aged, confused, or anxious patients who do not tolerate position changes • Pulmonary embolism • Rib fracture, with or without flail chest • Surgical wound or healing tissue • Large pleural effusions Trendelenburg position contraindicated for: • Recent gross hemoptysis related to recent lung carcinoma treated surgically or with radiation therapy • ICP greater than 20 mm Hg • Uncontrolled hypertension • Distended abdomen • Patients in whom increased ICP is to be avoided (e.g., neurosurgery, aneurysms, eye surgery) • Uncontrolled airway at risk for aspiration (tube feeding or recent meal) • Esophageal surgery • External manipulation of the thorax contraindications (in addition to contraindications previously listed): • Subcutaneous emphysema • Recent epidural spinal infusion or spinal anesthesia • Recently placed transvenous pacemaker or subcutaneous pacemaker • Lung contusion • Osteomyelitis of the ribs • Coagulopathy • Recent skin grafts, or flaps, on the thorax • Burns, open wounds, and skin infections of the thorax • Suspected pulmonary tuberculosis • Bronchospasm • Osteoporosis • Complaint of chest wall pain Excerpts from the American Association for Respiratory Care: Clinical practice guideline: postural drainage therapy. Respir Care 36:1418, 1991.

treatment and 30 minutes for extended treatment. Both the patient and the RT should understand that PD does not always result in the immediate production of secretions. More often, secretions are simply mobilized toward the trachea for easier removal by coughing. If the procedure causes vigorous coughing, have the patient sit up until the cough subsides. After the procedure, the patient is repositioned to the pretreatment position, and the RT ensures the patient’s stability and comfort. Immediate posttreatment assessment includes repeat vital signs, confirmation of satisfactory SpO2, chest auscultation, and questioning the patient regarding his or her subjective

MINI CLINI Chest Physical Therapy (Postural Drainage, Percussion, and Vibration) Problem A physician’s progress note indicates a potential bacterial pneumonia localized to a patient’s right middle lobe. The patient has coarse breath sounds on the right midlung and a nonproductive cough. The physician orders CPT four times daily “until radiograph clears.” What positions should the RT select for postural drainage, and where should the RT provide percussion? Discussion The correct position for draining the right middle lobe would be head down (foot of bed raised about 12 inches), with the patient rotated about 45 degrees left from supine (modified left side-lying position). Percussion should be performed on the right anterior chest wall, between the fourth and sixth ribs (see Chapter 16 for external anatomic landmarks).

response to the procedure. Because PD is coupled with other ACTs, the outcomes assessment and documentation are discussed later in the chapter. RULE OF THUMB  Generally, whenever you observe any patient adverse effects or complications during postural drainage, follow the “triple S rule”: stop the therapy, return the patient to the original resting position, and stay with the patient until he or she is stabilized.

Percussion and Vibration Percussion and vibration involve application of mechanical energy to the chest wall using either hands or various electrical or pneumatic devices. Both methods are designed to augment secretion clearance. In theory, percussion should help loosen secretions from the tracheobronchial tree, making them easier to remove by coughing or suctioning. The effectiveness of percussion as an adjunct to PD remains unclear. This controversy is due to variability in practice and the difficulty related to performing trials of percussion because percussion is only a part of the overall treatment regimen.15 Manual percussion.  The RT performs manual percussion with his or her hands in a cupped position, with fingers and thumb closed and positioned parallel to the ribs (Fig. 44.3). This technique compresses air between the hand and chest wall. This technique should be applied against a thin layer of cloth, such as a hospital gown or bed sheet to help improve patient comfort. This technique involves the therapist’s cupped hands rhythmically striking the chest wall, using both hands alternately in sequence with the elbows partially flexed and wrists loose (see Fig. 44.3). Slower, more relaxing rates are better tolerated by the patient and the therapist. This technique requires practice to determine the appropriate force and maintain a rhythmic pattern during this therapy (Fig. 44.4). Ideally, the RT should percuss back and forth in a circular pattern over the localized area for 3 to 5 minutes. Care should be taken to avoid tender areas or sites of trauma, surgery, or chest tubes, and one should never percuss directly over bony prominences, such as the clavicles, vertebrae or sternum.

CHAPTER 44  Airway Clearance Therapy

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Posterior Anterior

Anterior

Left Right

Right

Left

Anterior upper segment (upper lobes)

Posterior apical segment

Anterior segments Anterior

Posterior

Posterior

Left

Left

Right

Left

Right

Right

Right

Left

Raise 12 inches

Right posterior segment

Left posterior segment

Left

Left

Raise 12 inches

Left lingular

Right

Right

Raise 18 inches

Anterior segments (lower lobes)

Left

Raise 18 inches

Right lateral segment

Posterior

Anterior

Right

Anterior

Posterior

Anterior

Right

Right middle lobe

Anterior

Left

Left

Right Right

Left

Raise 18 inches

Raise 18 inches

Left lateral segment Posterior segments Superior segments Fig. 44.2  Patient positions for postural drainage. (Modified from Potter PA, Perry AG: Fundamentals of Nursing: Concepts, Process and Practice, ed 4, St Louis, 1997, Mosby.)

Hand positioned 3 inches from chest (2) Strike chest in waving movement (1)

Fig. 44.3  Movement of cupped hand at wrist, to percuss chest.

Mechanical percussion and vibration.  Mechanical vibration is used as an alternative to manual percussion in acutely ill patients with chest wall discomfort or injury. Various electrical and pneumatic devices have been developed to generate and apply the energy waves used during percussion and vibration. Typically, these devices have both a frequency and a percussion force control (Fig. 44.5). Most units provide frequencies between 20 and 50

cycles per second (20 to 50 Hertz [Hz]). Other sonic or acoustic devices may provide up to 120 Hz. Noise, excess force, and mechanical failure are all potential problems. Electrical devices also pose a potential electrical shock hazard. These devices have the advantage of reducing fatigue on the caregiver, decreasing treatment time, and delivering consistent rates, rhythms, and impact forces. These devices may improve hospitalized patients’ compliance, especially when chest wall discomfort or injury is present. However, there is no firm evidence that such devices are more effective than manual techniques. For this reason, as with other ACT techniques, the selection of manual or mechanical methods should be based on individual patient factors such as age, condition, and tolerance.2,4

Coughing and Related Expulsion Techniques Most ACTs only help move secretions into the central airways. Clearance of these secretions requires either coughing or suctioning. In this respect, an effective cough (or alternative expulsion measure) is an essential component of all ACT. These expulsion methods are also useful in obtaining sputum specimens for diagnostic analysis.

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SECTION V  Basic Therapeutics

TABLE 44.3  Complications of Postural

Drainage Therapy and Recommended Interventions Complication Hypoxemia

Increased intracranial pressure Acute hypotension during procedure Pulmonary hemorrhage

Pain or injury to muscles, ribs, or spine Vomiting and aspiration

Bronchospasm

Arrhythmias

Action to Be Taken/Possible Intervention Administer higher FiO2 during procedure if potential for or observed hypoxemia exists. If patient becomes hypoxemic during treatment, administer 100% O2, stop therapy immediately, return patient to original position, and consult physician Stop therapy, return patient to original resting position, and consult physician Stop therapy, return patient to original resting position, and consult physician Stop therapy, return patient to original resting position, and call physician immediately. Administer O2 and maintain an airway until physician responds Stop therapy that appears directly associated with pain or problem, exercise care in moving patient, and consult physician Stop therapy, clear airway and suction as needed, administer O2, maintain airway, return patient to previous resting position, and contact physician immediately Stop therapy, return patient to previous resting position, and administer or increase O2 delivery while contacting physician. Administer physician-ordered bronchodilators Stop therapy, return patient to previous resting position, and administer or increase O2 delivery while contacting physician

Fig. 44.4  Hand placement for chest physical therapy. (From Harkreader H, Hogan M, Thobaben M: Fundamentals of Nursing, Caring and Clinical Judgment, ed 3, St Louis, 2007, Saunders.)

RULE OF THUMB  Clinicians should coach the patient to create an effective cough with most airway clearance techniques to fully clear secretions.

Fig. 44.5  Example of an electrically powered mechanical percussor. (Courtesy General Physiotherapy, Inc. St Louis, MO.)

Directed Cough Directed cough is a deliberate maneuver that is taught, supervised, and monitored. It aims to assist in creating a productive cough in patients unable to clear secretions with an effective spontaneous cough. In patients with copious secretions, directed coughing is an effective clearance method clearing secretions from the central—but not peripheral—airways. In addition to aiding in the removal of retained secretions from central airways, it should be a routine part of all ACT and may be helpful in obtaining sputum specimens for diagnostic analysis. Box 44.5 lists the relative contraindications and potential complications associated with directed cough. These patients should be monitored for pain, discomfort, dyspnea, pulse rate, cardiac rhythm (if an electrocardiogram is available), breath sounds, pulse oximetry if desaturation is suspected, breathing pattern, skin color, sputum production, and ICP if elevated. To determine the effectiveness of directed cough techniques, therapists should evaluate the patient for any of the following outcome changes: increased sputum production, decreased pulse and respiratory rate, clearing of the breath sounds, improved O2 saturation, and possibly clearing of infiltrates on the chest x-ray. Standard technique.  After the clinical need for directed coughing has been established, the RT should assess the patient for any factors that could limit the success of directed cough and relative contraindications. An effective directed cough is impossible with unresponsive, paralyzed, or uncooperative patients. In addition, some patients with severe COPD or severe restrictive disorders (including neurologic, muscular, or skeletal abnormalities) may be unable to generate an effective spontaneous cough. Pain, systemic dehydration, tenaciously thick secretions, artificial airways, or use of central nervous system depressants can also impact efforts to implement an effective directed cough. If any of these limitations exist, the RT should recommend an alternative to directed cough such as an assisted cough, which is discussed later in this chapter. Patient education is a critical part of developing an effective directed cough. The three most important aspects in teaching a patient to have an effective cough are: (1) instruction on proper positioning, (2) instruction on breathing control, and (3) exercises to strengthen the expiratory muscles.16 These activities are modified according to the patient’s underlying clinical problem. RULE OF THUMB  Adequate expiratory muscle strength as well as proper instruction regarding patient positioning and breathing control are essential components to an effective directed cough.

CHAPTER 44  Airway Clearance Therapy

BOX 44.5  Directed Cough Contraindications Directed cough is rarely contraindicated. The contraindications listed must be weighed against potential benefit in deciding to eliminate cough from the care of the patient. Listed contraindications are relative: • Inability to control possible transmission of infection from patients suspected or known to have pathogens transmittable by droplet nuclei (e.g., Mycobacterium tuberculosis) • Presence of elevated intracranial pressure or known intracranial aneurysm • Presence of reduced coronary artery perfusion, such as in acute myocardial infarction • Acute unstable head, neck, or spine injury • Manually assisted directed cough with pressure to the epigastrium may be contraindicated in the presence of increased potential for regurgitation or aspiration, acute abdominal pathology, abdominal aortic aneurysm, hiatal hernia, pregnancy, bleeding diathesis, or untreated pneumothorax • Manually assisted directed cough with pressure to the thoracic cage may be contraindicated in the presence of osteoporosis or flail chest Hazards and Complications • Reduced coronary artery perfusion • Reduced cerebral perfusion • Incontinence • Fatigue • Rib or costochondral fracture • Headache • Visual disturbances, including retinal hemorrhage • Bronchospasm • Muscular damage or discomfort • Incisional pain, evisceration • Anorexia, vomiting • Gastroesophageal reflux • Spontaneous pneumothorax • Pneumomediastinum • Subcutaneous emphysema • Cough paroxysms • Chest pain • Central line displacement Excerpts from the American Association for Respiratory Care: Clinical practice guideline: directed cough. Respir Care 38:495, 1993.

First, patients are taught to assume a sitting position with one shoulder rotated inward and the head and spine slightly flexed to aid exhalation and allow easy thoracic compression. It is difficult to generate an effective cough in the supine position. The patient’s feet should be supported to provide abdominal and thoracic support for the patient. If the patient is unable to sit up, the RT should raise the head of the bed and ensure that the patient’s knees are slightly flexed with the feet braced on the mattress. Breathing control measures help ensure that the inspiration, compression, and expulsion phases of the cough are maximally effective and coordinated. For effective inspiration, the patient should be taught to inspire slowly and deeply through the nose, using the diaphragm. In patients with copious amounts of sputum, such breaths alone may stimulate coughing by loosening secretions in the larger airways. After confirming that the patient can take a good, deep inspiration, the RT has the patient bear down against the glottis, in

961

much the same manner as would occur with straining when lifting weights or during a bowel movement. For patients with pain or patients subject to bronchial collapse, it is probably best that they be shown how to “stage” their expiratory effort into two or three short bursts. For these patients, this method is generally less fatiguing and more effective in producing sputum than a single violent expulsion. Effective breathing control and effective coughing are best taught by demonstration. The RT demonstrates the various phases of the cough sequence while emphasizing the correct technique. The RT explains how to avoid common errors, such as simple throat clearing and weak cough efforts. Proper positioning and breathing control alone may not result in an effective cough and clear secretions. This limitation is usually due to weak breathing muscles. Muscle weakness is common in patients with NMD, COPD, or those needing longterm ventilatory support. The breathing muscles may atrophy due to disease progression, lack of appropriate nutrition, or lack of use during mechanical ventilation. In these cases, either suctioning or using the mechanical insufflation-exsufflation (MIE) device may be effective in helping clear these secretions. Modifications to directed cough technique.  Modifying the normal directed cough to the needs of the individual patient may lead to a productive cough effort. Good clinical examples of the need to modify directed cough are seen in surgical patients, patients with COPD, and patients with neuromuscular disorders. In surgical patients, preoperative training in deep breathing and directed cough can help prepare the patient for the postoperative regimen. This preparation can minimize the anxiety related to pain that commonly impairs an effective cough in these patients. In addition, coordinating the coughing sessions with prescribed pain medication and splinting the operative site can enhance the effectiveness of these sessions. The RT can use his or her hands with a pillow or blanket to support the area of incision during the expiratory phase of the cough. Eventually, the patient can learn to use a pillow or blanket roll to splint the incision site. The forced expiratory technique (FET) (discussed subsequently) may also be valuable in these patients. In some patients with COPD, the high pleural pressures during a forced cough may compress the smaller airways and limit the effectiveness of the cough. FET maybe beneficial in these patients because the technique reduces transpulmonary pressures and decreases airway compression or closure.15 In this situation, the patient is placed in the sitting position previously described. The patient is instructed to take in a moderately deep breath slowly through the nose. To help enhance expulsion, the patient should exhale with moderate force through pursed lips, while bending forward. This forward flexion of the thorax enhances expiratory flow by upward displacement of the abdominal contents. After three or four repetitions of this maneuver, the patient is encouraged to bend forward and initiate short staccato-like bursts of air. This technique relieves the strain of a prolonged hard cough, and the staccato rhythm at a relatively low velocity minimizes airway collapse. These staccato-like bursts of air against an open glottis are referred to as huffing. With this technique the patient is instructed to make the sound “huff, huff, huff ” rapidly with the mouth and glottis open. Huff coughing is also referred to as FET.15

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SECTION V  Basic Therapeutics

RULE OF THUMB  Huff coughing or FET should be used to prevent small airway compression due to high pleural pressures during a forced cough in patients with COPD, CF, or bronchiectasis.

Forced Expiratory Technique As stated above, FET consists of one or two forced expirations of middle to low lung volume without closure of the glottis, followed by a period of diaphragmatic breathing and relaxation.16 The goal of this method is to help clear secretions with less change in pleural pressure and less likelihood of bronchiolar collapse. To help keep the glottis open during FET, the patient is taught to phonate or “huff ” during expiration. The period of diaphragmatic breathing and relaxation following the forced expiration is essential in restoring lung volume and minimizing fatigue. Comparative clinical studies on the effectiveness of FET have shown favorable results. The technique is particularly useful in patients prone to airway collapse during normal coughing, such as patients with COPD, CF, or bronchiectasis.17,18 Manual Assisted Cough Patients with neuromuscular conditions present a special challenge in cough management. These patients typically are unable to generate the forceful expulsion needed to move secretions toward the trachea.11 If this problem results in retained secretions, there are only three options: (1) placement of an artificial airway and removal of secretions by suctioning (see Chapter 37), (2) manually assisted cough, and/or (3) MIE. Manually assisted cough (quad—cough) is an external application of pressure to the thoracic cage or epigastric region, coordinated with a forced exhalation. In this technique, the patient takes as deep an inspiration as possible, assisted as needed by the application of positive pressure using a self-inflating manual resuscitation bag or ventilator. At the end of the patient’s inspiration, the RT exerts pressure under the diaphragm (lateral costal margins or epigastrium) abruptly. This pressure increases the force of compression throughout expiration; this mimics the normal cough mechanism by generating an increase in the velocity of the expired air and may be helpful in moving secretions toward the trachea, where they can be removed by suctioning. Assisted cough with pressure to the lateral costal margins is contraindicated in patients with osteoporosis or flail chest. Assisted cough using epigastric pressure is contraindicated in unconscious patients with unprotected airways, in pregnant women, and in patients with acute abdominal pathology, an abdominal aortic aneurysm, or a hiatal hernia.

Active Cycle of Breathing Technique To emphasize that FET should include breathing exercises, the originators of this technique modified the procedure and renamed it the active cycle of breathing technique (ACBT). ACBT consists of repeated cycles of breathing control, thoracic expansion, and FET (Box 44.6). Breathing control involves gentle diaphragmatic breathing at normal tidal volumes for 5 to 10 seconds with relaxation of the upper chest and shoulders. This phase is intended to help prevent bronchospasm. The thoracic expansion exercises involve deep inhalation, approaching vital capacity, with relaxed

BOX 44.6  Active Cycle of Breathing

Technique Sequence

1. Relaxation and breathing control 2. Three or four thoracic expansion exercises 3. Relaxation and breathing control 4. Repeat three to four thoracic expansion exercises 5. Repeat relaxation and breathing control 6. Perform one or two forced expiratory techniques (huffs) 7. Repeat relaxation and breathing control

MINI CLINI Modifications to Directed Cough Problem A patient who has been diagnosed with ALS who has been attending your multidisciplinary clinic for the last few years returns for a follow-up visit. The patient states that she has noticed that her cough is not as powerful as it has been and that she is “winded” when walking distances. The RT assesses the patient and finds: pulse rate of 80, respiratory rate of 24, and breath sounds of scattered wet crackles in both lungs. The patient performs spirometry and maximum inspiratory pressure (MIP) and maximum expiratory pressure (MEP) maneuvers. Her forced vital capacity (FVC) is 70% of predicted; MIP is negative 50 cm H2O and MEP is 55 cm H2O sitting; and MIP is negative 40 cm H2O and MEP is 40 cm H2O supine. The therapist reviews the values from the previous visit 3 months earlier and finds FVC was 75% of predicted and MIP was a negative 65 cm H2O and the MEP was 70 cm H2O both sitting and supine. Discussion Based on this assessment, the patient’s lung volumes and muscle strength have declined. She also has retained secretions and would benefit from ACT and possibly MIE to assist with secretion removal. The patient began HFCWC to mobilize these secretions and MIE to assist in expectorating the secretions. This therapy should take place at least twice a day.

exhalation, which may be accompanied by percussion, vibration, or compression. The thoracic expansion phase is designed to help loosen secretions, improve the distribution of ventilation, and provide the volume needed for FET. The subsequent FET moves secretions into the central airways. Postoperative patients may require splinting at the thoracic or abdominal incision site. Although ACBT can be performed in the sitting position, it is most beneficial when combined with PD. When ACBT is compared with similar methods of secretion clearance, studies indicate that ACBT can provide comparable results in terms of both sputum production and distribution of ventilation.2,19 ACBT is not useful with young children (10–12 mL/kg predicted body weight [PBW]) to generate adequate pressure, oscillations, and prolonged exhalations during PEP therapy.

Common strategies for PEP therapy vary, with frequency determined by assessment of patient response. Studies provide conflicting results related to the amount of time and intervals of therapy sessions during acute exacerbations associated with CF and COPD. Two to four times daily are common frequencies used for PEP therapy. Aerosol drug therapy may be added to a PEP session using either an in-line handheld nebulizer or a metered dose inhaler attached to the one-way valve inlet of the

A

B

C

D

E Fig. 44.8  Positive expiratory devices. (A) Flutter. (B) TheraPEP. (C) Acapella (Choice is used for a range of flows. Green is used for flows higher than 15 L/min. Blue is used for flows less than 15 L/min.). (D) Aerobika. (E) RC-Cornet.

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SECTION V  Basic Therapeutics

BOX 44.8  Clinical Procedure for Positive

Airway Pressure Therapy

1. Assess need for positive airway pressure (PAP) therapy and design a treatment program to accomplish treatment objectives. a. Bring equipment to bedside and provide initial therapy to patient, adjusting pressure settings to meet patient need. b. After initial patient treatment or training, communicate treatment plan to physician and nurse, and provide instruction to nursing staff if required. 2. Explain purpose of PAP therapy to patient; teach patient “huff” (directed cough procedure). 3. Instruct patient to: a. Sit comfortably. b. If using a mask, apply it tightly but comfortably over the nose and mouth. If mouthpiece is used, place lips firmly around it and breathe through mouth. c. Take in a breath that is larger than normal, but do not completely fill lungs. d. Exhale actively, but not forcefully, creating a PAP of 10–20 cm H2O during exhalation (determined with manometer during initial therapy sessions). Length of inhalation should be approximately one-third of the total breathing cycle (inspiratory-to-expiratory ratio of 1 : 3 to 1 : 4). e. Perform 10–20 breaths. f. Remove the mask or mouthpiece and perform two or three “huff” coughs; rest as needed. g. Repeat above cycle four to eight times, not to exceed 20 min. 4. Evaluate patient for the ability to self-administer. 5. When appropriate, teach patient to self-administer. Observations on several occasions of proper technique, uncoached, should precede allowing the patient to self-administer without supervision. 6. When patients are also receiving bronchodilator aerosol, administer in conjunction with PAP therapy by placing a nebulizer in line with the PAP device. 7. When PAP device is visibly soiled, rinse it with sterile water and shake or air dry; leave within reach at patient’s bedside in a clear plastic bag. 8. Send the PAP device (if single-patient use) home with the patient or discard it on discharge. If device is nondisposable, send in-house for high-level disinfection. 9. Document in the patient’s medical record procedures performed (including device, settings used, pressure developed, number of breaths per treatment, and frequency), patient response to therapy, patient teaching provided, and patient ability to self-administer.

system. The combination of aerosol drug therapy with PEP seems to improve the efficacy of bronchodilator administration because of better distribution to the peripheral airways.24 Some PEP devices can be modified to incorporate a mask for patients with ALS, toddlers, or stroke patients who are unable to use a mouthpiece. High-frequency vibrations or oscillations refer to the rapid vibratory movement of small volumes of air back and forth in the respiratory tract. At frequencies of 12 to 25 Hz, these oscillations are thought to physically loosen secretions and move them toward the larger airways, which enhances airway clearance. There are two general approaches: airway application of oscillation methods such as OPEP discussed above or high-frequency airway pressure devices (HFPAP) such as intrapulmonary percussive ventilation, or external (chest wall) application referred to as high-frequency chest wall compression (HFCWC) devices.

A

B Fig. 44.9  (A) Intrapulmonary percussive ventilator, IPV. (Courtesy Percussionaire, SandPoint, Idaho.) B. MetaNeb. (Courtesy of HILL ROM.)

It is thought that the mucus moves because of the vibrations of the airways created when the oscillation frequency resembles the resonance frequency of the pulmonary system.21,25

High-Frequency Positive Airway Pressure Devices HFPAP devices include the intrapulmonary percussion ventilator (IPV) and the Metaneb (Fig. 44.9). The IPV (Percussionaire

CHAPTER 44  Airway Clearance Therapy

Corporation, Sandpoint, IN [some refer to this device as the Percussionator]) device (see Fig. 44.9A) was developed by Dr. Forest M. Bird in the late 1980s and it uses a pneumatic device to deliver a rapid series of pressurized gas minibursts at rates of 200 to 300 cycles per minute (1.7 to 5 Hz) to the airway.26 During the percussive cycle, the patient can inhale and exhale through the device as this oscillating airway pressure is applied. This device also delivers aerosolized medication through its own nebulizer and relies on chest wall recoil or active patient exhalation. Previous research suggests that interpulmonary percussive ventilation is equivalent to other airway clearance strategies in enhancing sputum expectoration in patients with obstructive pulmonary diseases and pediatric patients with NMD.4,27 The therapy is well tolerated by stable patients and may provide a more effective alternative for airway clearance in patients unable to take a deep inspiration. In a group of severe COPD patients receiving two treatments per day for 4 weeks, both IPV and HFCWC improved activities of daily living and pulmonary functions compared to the control group. IPV also significantly improved health status assessment and inflammatory cells in sputum compared to HFCWC.28 Further studies are needed to determine the impact on healthcare utilization and hospital readmission. Another HFPAP is the Metaneb device (Hill-Rom, Inc. Batesville, IN; Fig. 44.9B), which uses similar characteristics that provides a pneumatic form of chest physiotherapy. The Metaneb is able to deliver high-frequency rates, with oscillatory percussive breaths during inspiration and expiration, and resistance levels on exhalation. The Metaneb can deliver aerosol therapy during the lung expansion and secretion clearance cycles. The therapy lasts about 10 minutes alternating between the lung expansion and secretion clearance cycles depending on patient comfort. The percussion rate varies between 170 and 230 breaths/min. Both Metaneb and IPV have venturi devices housed inside the device. The venturi devices create high-frequency percussions during inspiration and expiration, which result in a pressure gradient.25 The pressure gradient creates an accelerated expiratory airflow and secretions move up into the larger airways for the patient to expel or are suctioned from an artificial airway.25 In addition, hyperinflation occurs at the same time assisting the patient with a deeper breath, which improves cough effectiveness. These devices are used in the hospital setting. Clinical trials using both devices demonstrate they are effective at enhancing secretion removal.1,2,22,25,27

967

MINI CLINI Using High-Frequency Positive Airway Pressure Devices Problem A 60-year-old postoperative patient with a 20 pack-year smoking history admits to the surgical intensive care unit following a laparoscopic procedure. The patient is currently receiving 4 L/min nasal cannula with a pulse O2 saturation of 92%. Their breath sounds are bilateral course rales that do not clear when the patient coughs. Their inspiratory vital capacity is only 550 mL which is 7.9 mL/kg of their predicted body weight. The critical care physician asks that you recommend an effective ACT. Discussion Based on this assessment, the patient’s lung volumes are too low to effectively perform vibratory PEP therapy. IPV would assist in moving the secretions into the larger airway and increasing the patient’s lung volume. This therapy should be every 4 h with the patient sitting up in the bed or chair. Fill the nebulizer with 15 mL of normal saline. Rotate the frequency knob to the easy position by turning this knob counterclockwise until it stops. Set the operating pressure at 20 psi to start. Have the patient breathe on the device through the mouthpiece. Push the button on the manual remote switch located on the nebulizer. Encourage the patient to slowly inhale and exhale through the device as it percusses. They also may need to splint their cheeks to avoid air and pressure loss. If the chest wall of the patient is not wiggling or visibly moving the operating pressure should be slowly increased to approximately 30 psi. Every few minutes the frequency can be increased or changed from easy to hard as tolerated by the patient. Provide breaks in this therapy to instruct the patient on a directed cough. Therapy should last approximately 15 min. The patient should be observed for signs of syncope or light headedness, changes in heart rate or breath sounds, and oxygen saturation.

High-Frequency Chest Wall Compression HFCWC devices are passive oscillatory devices. These devices use a two-part system: (1) a variable air-pulse generator, and (2) a nonstretch inflatable vest that wraps around the patient’s entire torso. Examples of these devices are; Electromed—SmartVest; Hill Rom—The Vest; RespirTech—inCourage, and the AfflowVest (Fig. 44.10). Either one or two large-bore tubing(s) connect the vest to the air-pulse generator. Table 44.4 lists the devices, airpulse waveforms, and hose configurations. The generator inflates and deflates the vest, creating pressure pulses against the thorax resulting in chest wall oscillations and moving secretions forward. The AfflowVest is battery operated, digitally programed and uses a

Fig. 44.10  The Vest Airway Clearance System for high-frequency chest wall oscillation. (Copyright 2011 Hill-Rom Services, Inc., Batesville, IN. Reprinted with permission. All rights reserved.)

technology that mimics hand CPT to mobilize secretions. HFCWC devices are used in hospital or home settings. The therapy is typically performed for a 30-minute session two to six times per day at oscillatory frequencies between 5 and 25 Hz. These therapy sessions depend on patient need and response. Clinical

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SECTION V  Basic Therapeutics

TABLE 44.4  High-Frequency Chest Wall

BOX 44.9  Key Factors in Selecting an

Company

Device

Air Pulse

Hose Configuration

Hill Rom Electromed RespirTech AfflowVest

Vest SmartVest InCourage AfflowVest

Sine waveform Sine waveform Triangle waveform Direct Dynamic Oscillation

Double hose Single hose Double hose None—battery operated

• Patient’s motivation • Patient’s goals • Patient’s ability to comprehend—literacy and cognition levels • Patient’s physical limitations • Physician/caregiver goals • Effectiveness of technique • Ease of learning and teaching • Skill of therapists • Patient fatigue associated, or work required to use device • Need for assistance to use the equipment • Limitations of technique based on disease type and severity • Costs (direct and indirect) • Desirability of combining methods

Oscillator Device Comparison

trials with HFCWC have reported better or equivalent secretions clearance compared to other ACTs in CF patients.17,18,22,29 Studies in other populations have shown some improvement, as measured by patient perception, increased compliance, or outcome.1,11,15 The Biphasic Cuirass Ventilation (BCV) device is an alternative to the vest devices. It may be used to provide noninvasive ventilation and/or cough assist. It uses a chest cuirass or shell that encompasses the anterior chest wall. The shell is connected to the generator that controls both phases of the respiratory cycle. The chest wall will expand when the negative pressure is applied. This device is capable of a frequency range between 1 and 999 oscillations per minute, I:E ratios of 1 : 6 and 6 : 1, and inspiratory and expiratory pressures of −70 to 70 cm H2O. The recommended application is two sets of cycles that include a few minutes at a frequency between 600 and 700 at an I:E of 1 : 1, followed by a higher frequency at an inverse I:E ratio.25

Exercise, Mobilization, and Physical Activity Immobility is a major factor contributing to complications in chronic disease and hospitalized patients. Early mobilization is recommended to reduce complications in hospitalized patients and is recommended as adjunctive therapy along with another ACT in CF to aid airway clearance and overall health benefits.1,30 Physical activity may also improve lung function, exercise tolerance, quality of life, and adherence to therapy. For more on the use of exercise in ambulatory patients with severe lung disease see Chapter 56.

SELECTING AIRWAY CLEARANCE TECHNIQUES Selection Factors Box 44.9 specifies many factors that should be considered when selecting an airway clearance strategy. The correct application and patient motivation to perform the ACT are critical components regardless of the setting. No ACT is successful if it is abandoned by the patient. Likewise, no routine strategy is likely to be followed without results. In this regard, increased sputum production, less shortness of breath, and perhaps improved physical activity are a few outcomes that can be used to motivate patients and gain their ongoing cooperation. Age, disease process, available resources, and patient preference often affect the choice of ACT. Patient and caregiver goals for treatment should be discussed jointly, with the intent of choosing the method that best fits the patient’s goals and lifestyle. The RT’s skill and patience in teaching the ACT is also a factor in determining the success of the therapy. The patient’s learning needs and barriers to learning

Airway Clearance Strategy

MINI CLINI Recommending Airway Clearance Strategies Problem The RT is asked to evaluate and recommend an appropriate ACT regimen for a 7-year-old active girl with CF who is being cared for in her home by elderly grandparents. Discussion Generally, appropriate secretion clearance strategies for this patient include exercise, vibratory PEP, CPT, ACBT, high-frequency chest wall oscillation (HFCWO), and IPV. CPT would be difficult to implement in this patient’s home setting (elderly caregivers), so emphasis should be placed on either vibratory PEP with ACBT or HFCWO and FET. An exercise plan should also be incorporated into the overall strategy. Dietary and medication considerations are also important.

also should be considered. Because patients reject methods that are fatiguing, this should be considered in method selection. In addition, the patient’s disease either may suggest the best approach or may impose certain limitations that preclude using a particular method. Cost is a critical factor in selecting all treatment strategies. There are multiple inexpensive options that are effective. Patient or caregiver education also plays an important role in the effectiveness of the therapy (see Chapter 55).

Outcome Assessment Specific outcome criteria indicating a positive response to ACT are listed in Box 44.10. Generally, achievement of one or more of these outcomes indicates that the therapy is meeting its objectives and should be continued. Not all criteria are required to justify continuing ACT. Because secretion clearance is affected by patient hydration, the RT may need to wait for at least 24 hours after optimal systemic hydration has been achieved to see any evidence of increased sputum production. In the interim, bland aerosol therapy may be useful for sputum induction and mobilizing secretions. Breath sounds may seem to “worsen” after therapy by changing from diminished breath sounds before therapy to coarse crackles. This change is due to the loosening of secretions and their movement into the larger airways, an intended purpose of the therapy. These coarse crackles should clear after coughing

CHAPTER 44  Airway Clearance Therapy

BOX 44.10  Assessment Outcomes After

Airway Clearance Therapy

The following items represent individual criteria that indicate a positive response to therapy (and support continuation of therapy). Not all criteria are required to justify continuation of therapy (e.g., a ventilated patient may not have sputum production >30 mL/day but has improvement in breath sounds, chest radiograph, or increased compliance or decreased resistance). • Change in sputum production • Change in breath sounds of lung fields being drained • Patient subjective response to therapy • Change in vital signs • Change in chest radiograph • Change in arterial blood gas values or O2 saturation • Change in ventilator variables Excerpts from the American Association for Respiratory Care: Clinical practice guideline: postural drainage therapy. Respir Care 36:1418, 1991.

or suctioning. In addition, the patient’s chest x-ray may significantly improve after receiving a few ACTs. In terms of the patient’s subjective response to therapy, the patient should be encouraged to report any pain, discomfort, shortness of breath, dizziness, or nausea during or after therapy. Any of these adverse effects may be grounds for either modifying or stopping treatment. Patient reports of easier clearance or increased volume of secretions after therapy support continuing therapy. Based on assessment results, ACT orders should be reevaluated for need at least every 2 to 3 days for hospitalized patients. Patients receiving home care should be reevaluated at least every 3 months or whenever their status changes.

Documentation and Follow-Up The chart entry for ACT should include the device, the therapy provided, the positions used, the time of treatment, patient tolerance, pre– and post–vital signs and breath sounds, subjective and objective indicators of treatment effectiveness (including amount, color, and consistency of sputum produced), and any adverse effects observed.

Protocol-Based Airway Clearance Numerous RT-driven protocols have been published for ACT. All of these protocols involve rigorous assessment of the patient both to establish preliminary need and to determine continuation of or modification in therapy. Fig. 44.11 is an algorithm used in one such protocol. Changes in therapy occur throughout and are based on the patient’s response and the RT’s evaluation.

SUMMARY CHECKLIST • Normal airway clearance requires a patent airway, a functional mucociliary escalator, and an effective cough. • Patients with copious secretions (20 to 30 mL/day) or inability to mobilize and expectorate secretions may benefit from ACT. • The primary goal of ACT is to help mobilize and remove retained secretions, improve gas exchange, and reduce the work of breathing.

969

• Retained secretions can increase the work of breathing, cause air trapping, worsen V̇ /Q̇ imbalance, promote atelectasis and shunting, and increase the incidence of infection. • Disorders associated with abnormal secretion clearance include foreign bodies, tumors, congenital or acquired thoracic anomalies, asthma, chronic bronchitis, CF, bronchiectasis, and acute infections. • Musculoskeletal and neurologic disorders can impair coughing and lead to mucous plugging, airway obstruction, and atelectasis. • Both mechanical and treatment factors impair mucociliary clearance in intubated patients. • Clinical signs consistent with retained secretions include ineffective cough, absent or increased sputum production, a labored breathing pattern, abnormal or adventitious lung sounds (e.g., coarse crackles, decreased breath sounds), tachypnea, tachycardia, and fever. • Turning promotes lung expansion, improves oxygenation, and prevents retention of secretions. • Postural drainage involves placing the segmental bronchus to be drained in a vertical position relative to gravity and holding the position for 3 to 15 minutes. • Cough methods must be modified in surgical patients, patients with COPD, and patients with neuromuscular disorders. • FET, or huff cough, consists of one or two forced expirations of middle to low lung volume without closure of the glottis, followed by a period of diaphragmatic breathing and relaxation. • ACBT consists of repeated cycles of breathing control, thoracic expansion, and FET. • During AD, the patient uses diaphragmatic breathing to mobilize secretions by varying lung volumes and expiratory airflow in three distinct phases. • MIE involves delivery of a positive pressure breath followed by the quick application of negative pressure; positive expiratory flows exceed flows developed by manually assisted coughing. • PEP or vibratory therapy is a self-administered clearance technique involving active expiration against a variable-flow resistance, followed by FET; patients frequently prefer PEP over other methods. • At high frequencies (12 to 25 Hz), airway oscillations enhance cough clearance of secretions. • Airway oscillations can be created externally (HFCWC) or at the airway opening (flutter valve, Accapella, Aerobika, IPV, Metaneb). • Adding physical activity to mobilization and coughing enhances mucus clearance, improves overall aeration and V̇ /Q̇ matching, and improves pulmonary function. • If performed correctly, no ACT has been proven better than another. • Numerous factors must be considered in trying to select the best airway clearance strategy for a given patient. • Outcomes of therapy should include subjective and objective measures. • ACT protocols are beneficial to patient and practitioner.

970

SECTION V  Basic Therapeutics BRONCHOPULMONARY HYGIENE (bph) Productive cough Copious secretions? (30 cc per day) No

Yes

Strong cough? No

Strong cough? Yes

Percussion, vibration,a suction PRNb

No

Deep breathe and cough

Yes

Postural drainage, percussion, vibration,a suction PRNb

Bph may be discontinued when secretions are no longer present (for 2 consecutive scheduled treatments) or when secretions and/or rhonchi can be cleared with cough. a b

A

Do rhonchi persist after patient coughs? No

Yes

Deep breathe and cough

Percussion, vibration,a deep breathe, and cough

Or oscillatory device Do not perform nasotracheal suctioning on a patient with a platelet count of 50,000 or neutropenia. Non-productive cough Rhonchi? No

Yes

History of mucusproducing disease?

No

Yes

Is patient able to deep breathe and cough spontaneously? Yes No additional therapy needed

B

Effective cough and rhonchi clear with cough?

No Percussion, vibration, and suctionb ×24 hours: then reassess

Percussion, vibration,a suction PRNb

Strong cough? No

Yes

No

Deep breathe and cough

Yes a

Percussion, vibration, deep breathe, and cough suction PRNb

Deep breathe and cough

Bph may be discontinued when secretions are no longer present (for 2 consecutive scheduled treatments) or when secretions and/or rhonchi can be cleared with cough. a

Or oscillatory device Do not perform nasotracheal suctioning on a patient with a platelet count of 50,000 or neutropenia.

b

Fig. 44.11  Example of algorithm underlying an airway clearance protocol. (A) An algorithm used in patients with productive cough. (B) An algorithm used in patients with a nonproductive cough. (Bronchial Hygiene Algorithm from the Cleveland Clinic Respiratory Therapy Consult Service Handbook. Courtesy of the Cleveland Clinic.)

CHAPTER 44  Airway Clearance Therapy

REFERENCES 1. Strickland SL, Rubin BK, Drescher GS, et al: AARC clinical practice guideline: effectiveness of nonpharmacologic airway clearance therapies in hospitalized patients, Respir Care 58(12): 2187, 2013. 2. Andrews J, Sathe NA, Krishnaswami S, et al: Nonpharmacologic airway clearance techniques in hospitalized patients: a systematic review, Respir Care 58(12):2160, 2013. 3. Volsko TA: Airway clearance therapy: finding the evidence, Respir Care 58(10):1669, 2013. 4. Flume PA, Robinson KA, O’Sullivan BP, et al: Cystic fibrosis pulmonary guidelines: airway clearance therapies, Respir Care 54(4):522, 2009. 5. Fahy JV, Dickey BF: Airway mucus function and dysfunction, N Engl J Med 363(23):2233–2247, 2010. 6. Mietto C, Pinciroli R, Piriyapatsom A, et al: Tracheal tube obstruction in mechanically ventilated patients assessed by high-resolution computed tomography, Anesthesiology 121(6): 1226–1235, 2014. 7. Restrepo RD, Walsh BK: Humidification during invasive and noninvasive mechanical ventilation: 2012, Respir Care 57(5): 782–788, 2012. 8. Moulton BC, Barker AF: Pathogenesis of bronchiectasis, Clin Chest Med 33(2):211–217, 2012. 9. Knowles MR, Daniels LA, Davis SD, et al: Primary ciliary dyskinesia: recent advances in diagnostics, genetics and characterization of clinical disease, Am J Respir Crit Care Med 188:913–921, 2013. 10. Harris A: Diagnosis and management of children with primary ciliary dyskinesia, Nurs Child Young People 29(7):38, 2017. 11. Chatwin M, Toussaint M, Goncalves MR, et al: Airway clearance techniques in neuromuscular disorders: a state of the art review, Respir Med 136:98–110, 2018. 12. Williams DM, Rubin BK: Clinical pharmacology of bronchodilator medications, Respir Care 63(6):641–654, 2018. 13. Strickland SL, Rubin BK, Haas CF, et al: AARC clinical practice guideline: effectiveness of pharmacologic airway clearance therapies in hospitalized patients, Respir Care 60(7):1071, 2015. 14. Winkelman C, Chiang L: Manual turns in patients receiving mechanical ventilation, Crit Care Nurse 30(4):36–44, 2010. 15. Snijders D, Fernandez Dominguez B, Calgaro S, et al: Mucociliary clearance techniques for treating non-cystic fibrosis bronchiectasis: is there evidence?, Int J Immunopathol Pharmacol 28(2):150–159, 2015. 16. Fink JB: Forced expiratory technique, directed cough, and autogenic drainage, Respir Care 52(9):1210, 2007.

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17. Lee A, Button BM, Tannenbaum E: Airway-clearance techniques in children and adolescents with chronic suppurative lung disease and bronchiectasis, Front Pediatr 5(2):2017. 18. Ides K, Vissers D, De Backer L, et al: Airway clearance in COPD: need for a breath of fresh air? A systematic review, COPD 8(3): 196–205, 2011. 19. Robinson KA, McKoy N, Saldanha I, et al: Active cycle of breathing technique for cystic fibrosis, Cochrane Database Syst Rev (11):CD007862, 2010. 20. Sahni AS, Wolfe L: Respiratory care in neuromuscular diseases, Respir Care 63(5):601–608, 2018. 21. Volsko TA, DiFiore J, Chatburn RL: Performance comparison of two oscillating positive expiratory pressure devices: acapella versus flutter, Respir Care 48(2):124, 2003. 22. Morrison L, Agnew J: Oscillating devices for airway clearance in people with cystic fibrosis, Cochrane Database Syst Rev (7): CD006842, 2014. 23. Van Fleet H, Dunn DK, McNinch NL, et al: Evaluation of functional characteristics of 4 oscillatory positive pressure devices in a simulated cystic fibrosis model, Respir Care 62(4):451–458, 2017. 24. Alcoforado L, Brandao S, Rattes C, et al: Evaluation of lung function and deposition of aerosolized bronchodilators carried by heliox associated with positive expiratory pressure in stable asthmatics: a randomized clinical trial, Respir Med 107(8): 1178–1185, 2013. 25. Chatburn RL: High-frequency assisted airway clearance, Respir Care 52(9):1224, 2007. 26. Salim A, Martin M: High-frequency percussive ventilation, Crit Care Med 33(3 Suppl):S245, 2005. 27. Reychler G, Debier E, Contal O, et al: Intrapulmonary percussive ventilation as an airway clearance technique in subjects with chronic obstructive airway diseases, Respir Care 63(5):2018. 28. Nicolini A, Grecchi B, Ferrari-Bravo M, et al: Safety and effectiveness of the high-frequency chest wall oscillation vs intrapulmonary percussive ventilation in patients with severe COPD, Int J Chron Obstruct Pulmon Dis 13:617–625, 2018. 29. Mall MA: Unplugging mucus in cystic fibrosis and chronic obstructive pulmonary disease, Ann Am Thorac Soc 13(Suppl 2): S177, 2016. 30. Cassidy MR, Rosenkranz P, McCabe K, et al: I COUGH: reducing postoperative pulmonary complications with a multidisciplinary patient care program, JAMA Surg 148(8): 740–745, 2013.

SECTION VI  Acute and Critical Care

45  Respiratory Failure and the Need for Ventilatory Support Loutfi S. Aboussouan

CHAPTER OBJECTIVES After reading this chapter you will be able to: • Define acute respiratory failure. • Differentiate between hypoxemic respiratory failure (type I) and hypercapnic respiratory failure (type II). • Discuss the causes of acute respiratory failure. • Discuss the differences between chronic respiratory failure and acute-on-chronic respiratory failure.

• Identify the complications of respiratory failure. • Discuss the indications for ventilatory support. • Discuss general management principles of hypoxemic and hypercapnic respiratory failure. • Discuss indications for noninvasive ventilation.

CHAPTER OUTLINE Hypoxemic Respiratory Failure (Type I), 973 Ventilation/Perfusion Mismatch, 973 Shunt, 974 Alveolar Hypoventilation, 975 Diffusion Impairment, 975 Perfusion/Diffusion Impairment, 975 Decreased Inspired Oxygen, 975 Venous Admixture, 975 Differentiating the Causes of Acute Hypoxemic Respiratory Failure, 976 Hypercapnic Respiratory Failure (Type II), 976 Unexpected Exposure to Breathing Carbon Dioxide, 977

Increased Carbon Dioxide Production, 977 Impairment in Respiratory Control, 977 Impairment in Exhaling Carbon Dioxide, 978 Chronic Respiratory Failure (Type I and Type II), 978 Acute-on-Chronic Respiratory Failure, 978 Complications of Acute Respiratory Failure, 979 Clinical Presentation, 979 Indications for Ventilatory Support, 980

Assessment of Respiratory Fatigue, Weakness, Failure, and Work of Breathing, 981 Respiratory Muscle Weakness, 981 Respiratory Muscle Fatigue, 981 Respiratory Failure, 981 Work of Breathing, 982 Choosing a Ventilatory Support Strategy for Different Causes of Respiratory Failure, 982 Noninvasive Ventilation, 982 Noninvasive Ventilation in Acute Conditions, 982 Noninvasive Ventilation in Chronic Conditions, 983 Invasive Ventilatory Support, 983

maximum inspiratory pressure (MIP) maximum voluntary ventilation (MVV) muscle fatigue noninvasive ventilation (NIV) orthodeoxia platypnea

positive end-expiratory pressure (PEEP) respiratory alternans sniff nasal inspiratory pressure pressure-time index work of breathing

KEY TERMS auto-PEEP barotrauma dynamic hyperinflation hypercapnic respiratory failure (type II) hypoxemic respiratory failure (type I) maximum expiratory pressure (MEP) 972

CHAPTER 45  Respiratory Failure and the Need for Ventilatory Support

The primary causes of hypoxemia are the following: • Ventilation/perfusion (V̇ /Q̇ ) mismatch • Shunt • Alveolar hypoventilation • Diffusion impairment • Perfusion/diffusion impairment • Decreased inspired O2 • Venous admixture or anatomic shunt These entities are briefly discussed here and are discussed in more detail in Chapters 11 and 12.

Ventilation/Perfusion Mismatch There are regions in healthy lungs where ventilation and perfusion are not evenly matched, so it seems logical that this is the most common cause of hypoxemia. West described a high V̇ /Q̇ ratio at the apex of the lungs and a low ratio at the bases.4 This concept can be oversimplified as there being more air than blood at the apices and more blood than air at the bases. Pathologic V̇ /Q̇ mismatch occurs when disease disrupts this balance, and hypoxemia results (Fig. 45.1A). Most commonly, areas of low V̇ /Q̇ ratio are seen in which ventilation is decreased despite adequate blood flow. Obstructive lung diseases are frequent causes. The bronchospasm, mucous plugging, inflammation, and premature airway closure that signal asthmatic or

· · V/Q normal

· · V/Q low

PAO2 = 100

PAO2 = 50

PO2 = 40 O2 Content = 15

PO2 = 40 O2 Content = 15

50 17

PaO2 = 64 CaO2 = 18.5

A

PIO2 = 285 · · V/Q normal

· · V/Q low

PAO2 = 225

PAO2 = 85

PO2 = 40 O2 Content = 15

PO2 = 40 O2 Content = 15 5 22 20.5

HYPOXEMIC RESPIRATORY FAILURE (TYPE I)

PIO2 = 150

0 10 20

Respiratory failure is a clinical problem that all respiratory care practitioners must be skilled at identifying, assessing, and treating. The hospital mortality of patients requiring intensive care unit (ICU) admission with respiratory failure significantly decreased from 43.5% in 1993 to 32.2% in 2009.1 The need for oxygen (O2) delivery, mechanical ventilation, and other modalities in the management of such patients makes the respiratory therapist’s (RT) role indispensable. Respiratory failure is the “inability to maintain either the normal delivery of O2 to the tissues or the normal removal of carbon dioxide (CO2) from the tissues”2 and often results from an imbalance between respiratory workload and ventilatory strength or endurance. Criteria based on arterial blood gases (ABGs) were established by Campbell who categorized respiratory failure into hypoxemia without hypercapnia, and hypoxemia with hypercapnia.3 Generally, failure is defined as arterial partial pressure of oxygen (PaO2) less than 60 mm Hg (also referred to as hypoxemic or type I respiratory failure), alveolar partial pressure of carbon dioxide (PaCO2) 50 mm Hg or greater (hypercapnic or type II respiratory failure), or both, while breathing room air at sea level. Respiratory failure can be an acute or a chronic process. Hypercapnic respiratory failure is also known as ventilatory failure or “bellows” failure. Patients with baseline acid–base derangement (e.g., chronic obstructive pulmonary disease [COPD], neuromuscular disease, thoracic or parenchymal restrictive lung disease) may be chronically hypercapnic and in chronic ventilatory failure. Although ABG analysis is helpful in distinguishing hypoxemic (type I) and hypercapnic (type II) respiratory failure, many patients in acute respiratory failure develop both hypoxemia and hypercapnia.

973

B

85 .5 19

PaO2 = 100 CaO2 = 20

Fig. 45.1  Hypoxemia caused by V̇ /Q̇ mismatch showing the effect of supplemental O2. V̇ /Q̇ is normal on the left side of each idealized lung unit and low on the right. Only O2 exchange is shown, and P(A − a) O2 is assumed to be zero. (A) With room air, not enough O2 reaches the poorly ventilated alveolus to saturate its capillary blood fully. (B) With 40% O2, PaO2 in this alveolus is increased enough to make capillary PO2 nearly normal. PaO2 in the mixed blood from the two capillaries is determined by the average of the O2 contents of the two streams of blood, not by the PaO2 values. (Modified from Pierson DJ, Kacmarek RM: Foundations of respiratory care, New York, 1992, Churchill Livingstone.)

emphysematous exacerbations worsen ventilation and create V̇ /Q̇ mismatch. Infection, heart failure, and inhalation injury may lead to partially collapsed or fluid-filled alveoli, also resulting in decreased ventilation and reduced blood O2 levels.

Clinical Presentation Because patients present with hypoxemia, the initial goal is always to treat the low PaO2 or SpO2 (arterial O2 saturation by pulse oximeter). V̇ /Q̇ mismatch responds to supplemental O2 (see Fig. 45.1B). Hypoxemia commonly causes dyspnea, tachycardia (rapid heart rate), and tachypnea (rapid breathing rate), but these are very nonspecific findings. However, patient observation is extremely valuable. The use of accessory muscles of respiration (scalene, pectoralis major, and sternomastoid) is an important

974

SECTION VI  Acute and Critical Care

Shunt is an extreme version of V̇ /Q̇ mismatch in which there is no ventilation to match perfusion (V̇ /Q̇ = 0). Two types of shunt can occur: anatomic and physiologic. About 2% to 3% of the blood supply is shunted via the bronchial and thebesian veins that feed the lungs and heart; this is normal anatomic shunt. Pathologic anatomic shunt occurs as a result of right-to-left blood flow through cardiac openings (e.g., atrial or ventricular septal defects) or in pulmonary arteriovenous malformations. Physiologic shunt accompanies V̇ /Q̇ mismatch and leads to hypoxemia when alveoli collapse or are filled with fluid or exudate. Common etiologies of physiologic shunting include atelectasis, pulmonary edema, and pneumonia. Shunt does not respond to supplemental O2 when the gas-exchange unit (the alveolus) is not open (Fig. 45.2A) or when the blood does not come into contact with ventilated areas of the lung (anatomic shunt).

Clinical Presentation The clinical presentation and patient observations in shunting are very similar in many ways to the presentation of V̇ /Q̇ mismatch. Bilateral or unilateral crackles are common owing to the alveolar filling process. Unilateral absence of breath sounds may

No ventilation

PAO2 = 100 PO2 = 40 O2 Content = 15

PO2 = 40 O2 Content = 15

A

40 15

PaO2 = 54 CaO2 = 17.5 PIO2 = 285 No ventilation

PAO2 = 225 PO2 = 40 O2 Content = 15

PO2 = 40 O2 Content = 15 5 22 20.5

Shunt

PIO2 = 150

0 10 20

sign that normal diaphragmatic inspiration is inadequate. In an elderly, cachectic, or barrel-chested individual who is leaning forward on his or her arms, COPD is the likely diagnosis. Nasal flaring may be present. Lower extremity edema suggests cardiac failure as the cause of hypoxemia. Cyanosis may be peripheral and primarily due to decreased blood flow. Central cyanosis, seen most easily as a bluish tint around the lips, occurs when greater than 5 g/dL of unsaturated hemoglobin is present. This finding is more common in patients with polycythemia (an increase in red blood cells) but may be subject to wide observer variability. More severe hypoxemia can lead to significant central nervous system (CNS) dysfunction, ranging from irritability to confusion to coma. Auscultation and percussion are very useful when added to patient observation. Bilateral wheezing, especially in a young patient in respiratory distress, often identifies the bronchospasm of asthma. Upper airway disease or fluid-filled airways may also result in wheezing. Breath sounds that are diminished bilaterally with increased resonance on percussion are common in emphysema. Unilateral abnormalities are significant. Wheezing in one lung may suggest an endobronchial lesion, whereas the absence of breath sounds and decreased resonance on one side of the chest may reflect collapse, infection, edema, or effusion as potential causes of V̇ /Q̇ mismatch. Discordant exam findings with increased resonance on percussion and decreased breath sounds on the same side may suggest a pneumothorax. Unilateral crackles and decreased resonance on percussion generally indicate an alveolar filling process (mass, infection, fluid). Radiographically, V̇ /Q̇ mismatch can manifest as a “black” radiograph, with large or hyperinflated lungs as in the case of obstructive disease. A “white” chest radiograph is evident when alveoli are partially occluded. The “blackness” or “whiteness” of the lung fields on the plain chest radiograph has important diagnostic value in assessing a patient with acute respiratory failure.

B

40 15

PaO2 = 57 CaO2 = 17.75

Fig. 45.2  Alveolar-capillary diagram of intrapulmonary (capillary) shunting showing why supplemental O2 fails to correct hypoxemia. Only O2 exchange is shown, and P(A − a)O2 is assumed to be zero. (A) With room air, although blood leaving the normal alveolar-capillary unit is normally saturated, blood passing the capillary on the right “sees” no O2 because its alveolus is unventilated, and it leaves the unit unsaturated. When the two streams of blood mix, the resulting PaO2 is determined by the average of the O2 contents, not by the PO2 values. (B) Addition of 40% O2 fails to correct the hypoxemia because O2 content is not significantly increased in the normal unit, and capillary blood in the unventilated unit still “sees” no O2. Even 100% O2 could not completely reverse the oxygenation defect in this example; this is very different from the effect with low V̇ /Q̇ as illustrated in Fig. 45.1. (Modified from Pierson DJ, Kacmarek RM: Foundations of respiratory care, New York, 1992, Churchill Livingstone.)

indicate significant collapse, mass, or effusion; these conditions require treatment before oxygenation can improve. The parenchyma on chest radiograph may be “white” with physiologic causes of shunting as may occur in the acute respiratory distress syndrome (ARDS). Anatomic shunts may be harder to diagnose as the chest x-ray may appear normal, but can be diagnosed by using 100% O2 breathing techniques, contrast-enhanced echocardiography, macroaggregated albumin scanning, or pulmonary angiography.5 Shunt is differentiated from V̇ /Q̇ mismatch by the lack of increase in PO2 as fractional inspired oxygen (FiO2) is increased (see Fig. 45.2B).

CHAPTER 45  Respiratory Failure and the Need for Ventilatory Support

Alveolar Hypoventilation Alveolar hypoventilation is discussed subsequently in the section on hypercapnic respiratory failure (type II).

Diffusion Impairment Diffusion refers to movement of gas across the alveolar-capillary membrane along a pressure gradient. Although diffusion impairment is rarely a cause of significant hypoxemia at rest, its effects become more pronounced with exercise, which limits the time for gas exchange. Diffusion impairment in interstitial lung disease (e.g., pulmonary fibrosis, asbestosis, sarcoidosis), in which the thickening and scarring of the interstitium prevent normal gas exchange, may contribute 19% of the alveolar-arterial O2 gradient at rest, and up to 40% during exercise).6 Emphysema, with its alveolar destruction, also has decreased transfer of O2 and CO2 between the alveolus and the capillary. The reduced ventilation in both diseases implies that V̇ /Q̇ mismatch also plays a role in the resulting hypoxemia. Pulmonary vascular abnormalities also can lead to diffusion impairment. Anemia, pulmonary hypertension, and pulmonary embolus all may reduce capillary blood flow, resulting in diminished gas transfer.

Clinical Presentation Signs and symptoms are related to the specific disease. Interstitial lung disease is a possible cause of a dyspneic patient with a dry cough and fine, basilar crackles on auscultation, and clubbing of the nail beds. Rheumatologic manifestations may be present if the underlying cause is a connective tissue disorder. Joint abnormalities, Raynaud disease, and telangiectasia (a vascular lesion formed by dilation of a group of small blood vessels) may be observed. The pallor of anemia can be a clue to poor gas exchange, although chronic hypoxemia may lead to polycythemia and possibly cyanosis. Pulmonary hypertension may cause signs of right-sided heart failure, such as edema, jugular venous distension, and a louder pulmonary component of the second heart sound. Diffusion impairment can also manifest with multiple, varied radiographic forms. The hyperinflated, dark chest x-ray of emphysema was mentioned earlier. Interstitial disease may manifest with reduced lung volumes with interstitial markings. An enlarged right ventricle and pulmonary arteries may be evident in secondary pulmonary hypertension.

Perfusion/Diffusion Impairment Perfusion/diffusion impairment is a cause of hypoxemia in individuals with liver disease complicated by the hepatopulmonary syndrome.7 In this condition, right-to-left intracardiac shunt combines with dilated pulmonary capillaries, resulting in impaired gas exchange because the normal alveolar partial pressures of O2 may be insufficient to drive the O2 molecules to the center of the dilated pulmonary vasculature. Cirrhosis is the most common liver disease associated with the hepatopulmonary syndrome, and portal hypertension is usually present. Although shunt is a component of the syndrome, significant supplemental O2 can overcome the hypoxemia, so this is commonly called a perfusion/diffusion defect.

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Clinical Presentation Obvious signs of liver disease (e.g., ascites, jaundice, and spider nevi) may or may not be present. Digital clubbing can occur in hepatopulmonary syndrome. Platypnea, which is the sensation of dyspnea when moving to the upright position from the supine position, may be a patient complaint. Orthodeoxia, an actual decrease in the measured O2 level when standing, may parallel this subjective sensation.

Decreased Inspired Oxygen Also clinically uncommon, hypoxemia may develop when the inspired O2 is less than usual. The most common situation in which this occurs is at high altitude, where hypoxemia occurs not because of a decrease in the fraction of O2 in the ambient air (which remains 21%) but from barometric pressure decreases, which results in a decrease in the partial pressure of inspired O2. Even with pressurized airplanes, air travelers with chronic hypoxemia may still need supplemental O2 because the altitude equivalent inside a commercial airliner may be up to 8000 feet.8 Similarly, mountain climbers sometimes require O2 masks. Cases of patient-O2 disconnects and delivery of an incorrect gas source are also included in this category. Inspired O2 less than 21% can also be used diagnostically and therapeutically. The Hypoxia Altitude Simulation Test replicates inspired partial pressure of O2 (PiO2) during air travel by asking the potential traveler to inhale a hypoxic mixture. Inhaling at FiO2 of 15% replicates the PiO2 found at an altitude of 8000 feet (108 mm Hg), and so is useful to assess whether the patient may require supplemental O2 during commercial air travel. For a lower altitude of 5400 feet, an equivalent FiO2 of 17% can be calculated.8 Infants with certain cyanotic congenital heart defects (e.g., hypoplastic left ventricle) may benefit from FiO2 below room air level. In the preoperative state, low FiO2 helps prevent pulmonary dilation and the excessive pulmonary blood flow, which could flood the lungs.

Clinical Presentation The signs and symptoms of hypoxemia may be present, with the cause related to the patient environment such as the altitude.

Venous Admixture A decrease in mixed venous O2 increases the gradient by which O2 needs to be stepped up as it passes through the lungs and can contribute to the development of hypoxemia. Congestive heart failure with low cardiac output is the most common cause of low mixed venous O2, owing to increased peripheral extraction of O2. Other factors may contribute to hypoxemia, such as V̇ /Q̇ mismatch and shunting.9 Other causes include low hemoglobin concentration and increased O2 consumption. A low mixed venous O2 may have a significant effect on the final arterial O2 tension when lung disease is present.

Clinical Presentation Signs and symptoms of congestive heart failure (e.g., rales on chest auscultation, pedal edema, etc.) or underlying lung disease, or both, may be present.

976

SECTION VI  Acute and Critical Care

Differentiating the Causes of Acute Hypoxemic Respiratory Failure It is important to recognize the physiologic basis of each of the three main causes of hypoxemic respiratory failure (hypoventilation, V̇ /Q̇ mismatch, and shunt). Hypoventilation differs from the other two causes in manifesting with a normal alveolar-toarterial PO2 difference [P(A − a)O2] indicating normal lung parenchyma (Table 45.1). A clinical determination of this difference is made by subtracting PaO2 from PAO2 (partial pressure of alveolar O2) derived from the alveolar air equation:

HYPERCAPNIC RESPIRATORY FAILURE (TYPE II) Hypercapnic respiratory failure (type II), also known as pump, bellows, or ventilatory failure, is characterized by an elevated PaCO2, creating an uncompensated respiratory acidosis (whether acute or acute-on-chronic). PaCO2 and alveolar ventilation (V̇ A) are inversely related, meaning that alveolar and arterial PCO2 levels are doubled when alveolar ventilation is halved. This is illustrated by the metabolic hyperbola relationship:

PAO2 = FiO2 (PB − PH2O ) − PaCO2 R

RULE OF THUMB  The mean alveolar-to-arterial difference [P(A − a)O2] in PO2 increases slightly with age and can be estimated with the following equation: Mean age −specific P(A − a)O2 = (age 4) + 4 Example: A 76-year-old person living at sea level: P(A − a)O2 = (76 4) + 4 = 19 + 4 = 23 mm Hg

A V̇ /Q̇ mismatch and shunt both result in elevated P(A − a) O2 levels, indicating that the resultant hypoxemia is due to an abnormality of lung tissue, requiring treatment to address that abnormality. When the RT encounters an increased P(A − a)O2, a V̇ /Q̇ mismatch and anatomic shunt can be differentiated by means of O2 administration (see Figs. 45.1 and 45.2). A significant response to applying even small amounts of O2 identifies V̇ /Q̇ mismatch as the cause of hypoxemia because altered P(A − a) O2 has not been totally obliterated. True hypoxemia shows little or no improvement in oxygenation even with 100% FiO2 (see Table 45.1). As a result, treatment of intrapulmonary shunt must be directed toward opening collapsed alveoli or clearing fluid or exudative material before O2 can be beneficial at below toxic levels. Testing to rule out anatomic shunt should be done in the right clinical setting (e.g., clear or black parenchyma on the chest radiograph). TABLE 45.1  Differentiating the Cause

of Hypoxemia Cause

P(A − a)O2

Response to Increased FiO2

Hypoventilation Shunt V̇ /Q̇ mismatch

Normal Increased Increased

Marked Minimal Marked

FiO2, Fractional inspired oxygen.

A

D

T

where V̇ A is alveolar ventilation (L/min), MV is minute ventilation (L/min), VD/VT is dead space–to–tidal volume ratio, and V̇ CO2 is CO2 production (mL/min). This equation demonstrates a rectangular hyperbola relation between the PaCO2 and ventilation (Fig. 45.3). Patients with chronic hypercapnia and low ventilation are on a steeper section of the metabolic hyperbola such that a minor drop in ventilation results in a significant increase in PaCO2, making them more susceptible to developing a sudden further increase in PaCO2 when even minor respiratory exacerbations occur. Also, with chronically elevated arterial PaCO2, the ventilatory response to a further increase in PaCO2 is more blunted.10 This leads to an acute ventilatory failure superimposed on chronic ventilatory failure. Similarly, this relationship shows that PaCO2 may increase as dead space (VD/VT) rises or as CO2 production (V̇ CO2) increases. Additionally, a change in the V̇ /Q̇ distribution of the lung toward lower ratios not only causes hypoxemia, as shown in Figs. 45.1 and 45.2, but also, to a lesser extent, can cause an elevation of PaCO2 by reducing the CO2 discharge from the pulmonary circulation to the alveoli. However, increased dead space, increased V̇ CO2, and shifts in the V̇ /Q̇ distribution toward lower ratios all are usually matched by a corrective increase in ventilation because respiratory control mechanisms tend to maintain the PaCO2 constant. The following sections describe mechanisms of hypercarbia caused by an imbalance between

160 140 120

pCO2 (mm Hg)

where PB is barometric pressure, PH2O is water vapor tension, and R is the respiratory exchange ratio (0.8). The P(A − a)O2 ranges from 10 mm Hg in young patients to approximately 25 mm Hg in elderly patients while breathing room air (see the accompanying Rule of Thumb). In patients with hypoxemia caused by hypoventilation, treatment can be focused on improving ventilation because the hypoxemia is purely a result of alveolar displacement of O2 by elevated CO2.

  PaCO2 = (0.863 VCO 2 ) VA V = MV (1− V V )

100 80 60 40 20 0

0

2

4

6 8 10 12 Minute ventilation L/min

14

16

18

Fig. 45.3  The metabolic hyperbola. Due to the hyperbolic relationship between the pCO2 and ventilation, a minor drop of ventilation occurring at an already low minute ventilation results in a significantly greater increase in the pCO2 relative to an equivalent drop occurring at a higher minute ventilation.

CHAPTER 45  Respiratory Failure and the Need for Ventilatory Support

assessment by a normal P(A − a)O2, as discussed previously. The presence of an increased P(A − a)O2 indicates that accompanying hypoxemia is present, most likely as a result of V̇ /Q̇ mismatch or shunt. The disorders that cause hypercapnic respiratory failure (ventilatory failure) are discussed next.

MINI CLINI Differentiating Causes of Hypoxemia Problem Two patients present with the following ABG values at sea level: Patient A pH PaCO2 PaO2 HCO3− SaO2 FiO2

Patient B 7.45 33 mm Hg 40 mm Hg 22 mEq/L 70% 0.21

pH PaCO2 PaO2 HCO3− SaO2 FiO2

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7.21 72 mm Hg 53 mm Hg 28 mEq/L 81% 0.21

1. Define the respiratory condition indicated by each ABG analysis. 2. What is the P(A − a)O2 for each blood gas? 3. Identify the type of respiratory failure in each case. 4. In which case would administration of 100% FiO2 help improve oxygenation? Discussion: 1. Patient A exhibits uncompensated respiratory alkalosis with hypoxemia. Patient B exhibits partially compensated respiratory acidosis with hypoxemia. 2. Patient A: PAO2 = 0.21 (760 − 47) − 33/0.8 = 108 mm Hg PaO2 = 40 mm Hg P(A − a)O2 = 108 − 40 = 68 mm Hg on room air Patient B: PAO2 = 0.21 (760 − 47) − 72/0.8 = 60 mm Hg PaO2 = 53 mm Hg P(A − a)O2 = 60 − 53 = 7 mm Hg on room air The normal values for P(A − a)O2 range from 10 mm Hg in young people to approximately 25 mm Hg in elderly people while breathing room air. 3. Patient A has hypoxemic respiratory failure (type I) as characterized by below-normal PaO2 (40 mm Hg). PaCO2 is also below normal (33 mm Hg), indicating hyperventilation is occurring in an effort to improve the oxygenation. Patient B has hypercapnic respiratory failure (type II) as characterized by an above-normal PaCO2 (72 mm Hg), indicating that hypoventilation (ventilatory failure) is occurring. There is also an elevation of HCO3− (28 mEq/L), indicating that the acute ventilatory failure is superimposed on chronic ventilatory failure. This patient is also hypoxemic (53 mm Hg). 4. Patient A has hypoxemic respiratory failure with P(A − a)O2 of 68 mm Hg, which is well above normal, indicating an oxygenation defect. The administration of 100% O2 in this case would help to determine the cause of the defect. Specifically, a marked rise in PO2 in response to 100% FiO2 would point to V̇ /Q̇ mismatch as the cause, whereas shunt would be implicated if PaO2 did not respond to the increase in delivered O2. In the latter condition, some form of positive end-expiratory pressure (PEEP) would be necessary to improve gas exchange by improving functional residual capacity. Patient B has hypercapnic respiratory failure (ventilatory failure) with hypoxemia, but with P(A − a)O2 of 7 mm Hg, which is within the normal range. A pure ventilatory defect is the cause of hypoxemia, and administration of 100% FiO2 would not raise the PO2 value. Depending on the full patient scenario, this patient may require noninvasive mechanical ventilation or intubation and invasive mechanical ventilation to restore normal acid–base status.

CO2 exposure (external or internal) and CO2 clearance (central and respiratory effector mechanisms). Hypoxemia may often accompany pump failure simply because of the displacement of alveolar PO2 (PAO2) by the increased PaCO2 from alveolar hypoventilation. This situation is identified on a room air ABG

Unexpected Exposure to Breathing Carbon Dioxide Although most cases of increased PaCO2 are due to hypoventilation, an unexpected exposure to breathing CO2 can occur in certain situations.

Clinical Presentation These unexpected exposures follow unusual clinical situations including defective CO2 scrubbers in anesthesia machines or life-support systems in scuba units, airtight chambers, spacecrafts, or submersible crafts. Occupational exposures also occur in spelunkers in caves (from groundwater seepage), individuals who work with dry ice (dry ice is a solid form of CO2), miners, and firefighters.

Increased Carbon Dioxide Production Fever, agitation, exertion, shivering, hypermetabolism, and excess caloric intake all can result in an increase in V̇ CO2, with resulting hypercapnia in patients with additional impairment in respiratory control and CO2 exhalation mechanisms.

Clinical Presentation The most common clinical scenario involving increases in CO2 production probably involves mechanically ventilated patients with already compromised lung function, in whom attempts to liberate from artificial ventilation are complicated by type II respiratory failure. Recognition and correction of fever, agitation, hypermetabolic states, and excess caloric intake, particularly due to carbohydrate-rich enteral solutions, may contribute to a favorable outcome.

Impairment in Respiratory Control Both central (medullary) and peripheral (aortic and carotid bodies) chemoreceptors responding to CO2 tension and O2 tension stimulate the drive to breathe.10 This ventilatory drive can be decreased by various factors, such as drugs (overdose or sedation), bilateral carotid endarterectomy with incidental resection of the carotid bodies, brainstem lesions, diseases of the CNS (multiple sclerosis, Parkinson disease, or elevated intracranial pressure [ICP]), hypothyroidism, morbid obesity (e.g., obesityhypoventilation), and sleep apnea.11 Patients at risk of having a decreased ventilatory drive usually can be identified by their clinical situation (e.g., CNS insult, overdose of sedative medications), and the clinician should be attentive to reversible causes.

Clinical Presentation The key feature of decreased ventilatory drive is bradypnea (slow breathing) and perhaps ultimately apnea. A normal respiratory rate is usually no less than 12 breaths/min in adults. Drug overdose or a brain disorder can manifest with an altered level of consciousness, ranging from being merely lethargic to being obtunded and comatose, with decreased respirations. Evidence

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of drug use by history or toxicity screen confirms the diagnosis of drug overdose. Evidence of head trauma and brain computed tomography (CT) scan abnormalities are important in the diagnosis of a brain disorder. Although hypothyroidism classically manifests with fatigue, weight gain, hyporeflexia, and constipation, it can also progress to significant hypoventilation and myxedema coma. Patients with obesity-hypoventilation may have a rapid, shallow breathing pattern, which results from decreased compliance and microatelectasis. Although these patients may also have nighttime sleep apnea, daytime PaCO2 is also elevated because of a decrease in the drive to breathe and metabolic factors.12 See Fig. 45.3 for the relationship between PCO2 and minute volume.

Impairment in Exhaling Carbon Dioxide Neurologic Diseases The lungs inhale and exhale under the guidance of the CNS. In some patients, the CNS signal does not reach its goal, resulting in neuromuscular dysfunction. Examples include spinal trauma, motor neuron disease in which lesions of the anterior horn cells may gradually lead to progressive ventilatory failure (e.g., amyotrophic lateral sclerosis or poliomyelitis), motor nerve disorders (including Guillain-Barré syndrome and Charcot-Marie-Tooth disease), disorders of the neuromuscular junction (e.g., myasthenia gravis and botulism), and muscular diseases (including muscular dystrophy, myositis, critical care myopathy, and metabolic disorders).13 Clinical presentation. Although hypercapnia may be a common end point, these diseases have varied clinical presentations. Patient observation is a key skill. Drooling, slurred speech (dysarthria), and weak cough are common bulbar signs in amyotrophic lateral sclerosis and myasthenia gravis. In progressive neuromuscular disease, as muscle wasting and weakness become more severe, diaphragmatic insufficiency develops, and supine paradoxical breathing and orthopnea are common.14 GuillainBarré syndrome commonly causes lower extremity weakness progressing to respiratory failure in 20% to 30% of patients.15 Weak cough and gag may be seen, which can threaten airway patency and lead to microatelectasis, hypoxemia, and uncompensated respiratory acidosis. Myasthenia gravis does not always cause respiratory failure.16 These diseases are quite different in clinical course, but there is much overlap in their presentations, and they commonly result in respiratory muscle fatigue and failure and elevated PaCO2. Increased Work of Breathing Despite normal respiratory drive, nerve transmission, and neuromuscular response, hypercapnic respiratory failure can still occur if the imposed workload cannot be overcome.2 Most commonly, this situation occurs when increased dead space accompanies COPD, or when elevated airway resistance accompanies asthma. Both of these obstructive airway diseases may increase respiratory work requirements excessively due to the presence of intrinsic positive end-expiratory pressure (auto-PEEP). Increased workload can also result from thoracic abnormalities such as pneumothorax, rib fractures with a flail chest, pleural effusions, and other conditions creating a restrictive burden on

the lungs. Finally, requirements for increased minute ventilation can arise when increased CO2 production accompanies hypermetabolic states, such as in extensive burns. Clinical presentation.  The RT must be alert to the possibility of respiratory failure when a heavy load is imposed on the respiratory system. Patients with asthma or COPD should present with hyperventilation during an exacerbation, but if breathing becomes more rapid but shallow, it may indicate impending failure. This increased VD/VT ratio leads to hypercapnia because the significant airway obstruction does not resolve with treatment. Diminished breath sounds in a young patient with asthma likewise can be a concerning sign. Irritability, confusion, and ultimately coma are possible signs in worsening hypercapnia, as they are in hypoxemic respiratory failure. More subtle findings include muscle tremor owing to catecholamine release and papilledema resulting from cerebral vasodilation in states of elevated arterial PCO2.17 In summary, hypercapnic (type II) respiratory failure, also known as ventilatory failure, develops when ventilation is impaired due to intrinsically or extrinsically increased CO2 exposure; impairment in respiratory control; or impairment in exhalation mechanisms, including neurologic disease or pulmonary and chest wall disorders associated with increased work of breathing (Table 45.2).

CHRONIC RESPIRATORY FAILURE (TYPE I AND TYPE II) For some patients with pulmonary disease and respiratory failure, the condition has developed over weeks to months to years and has become a chronic state, allowing compensatory adaptive mechanisms to develop. Most commonly, chronic hypercapnic respiratory failure accompanying COPD or obesity-hypoventilation syndrome prompts a renal response, and the kidneys retain bicarbonate to elevate the abnormally low blood pH. However, this compensatory metabolic alkalosis would not be expected to restore the pH all the way to normal. Chronic hypercapnic respiratory failure is also known as chronic ventilatory failure. RULE OF THUMB  Chronic and acute hypercapnic respiratory failure can be differentiated by the severity of change in pH.18 • Acute hypercapnic failure (acute ventilatory failure): pH decreases 0.08 for every 10 mm Hg increase in PaCO2 • Chronic hypercapnic failure (chronic ventilatory failure): pH decreases 0.03 for every 10 mm Hg increase in PaCO2.

Similarly, polycythemia may result from prolonged hypoxemic respiratory failure (e.g., sleep apnea) when O2 delivery to the tissues is compromised, and erythropoietin levels increase to elicit erythrocytosis. Hemoglobin also releases O2 more easily as the O2 dissociation curve shifts to the right in the face of acidosis. Finally, O2 delivery to the brain is enhanced when hypercapnia results in increased cerebral blood flow.19

Acute-on-Chronic Respiratory Failure Chronic respiratory failure can be complicated by acute setbacks that create acute-on-chronic respiratory failure. Patients with

CHAPTER 45  Respiratory Failure and the Need for Ventilatory Support

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TABLE 45.2  Causes of Respiratory Failure TYPE II (HYPERCAPNIC) Type I (Hypoxemic) ARDS Pulmonary embolism Pulmonary edema Septic shock Pulmonary infection  Viral  Bacterial  Fungal Inhalation  Smoke  Chemical  Water Pleural effusion Interstitial lung disease Obstructive lung disease Aspiration Primary pulmonary hypertension

Increased Exposure

Impaired Respiratory Control

Neurologic Disease

Increased Work of Breathing

Extrinsic Defective CO2 scrubbers (anesthesia or life-support systems) Occupational exposure (miners, spelunkers, dry-ice workers, firemen) Intrinsic

Drug overdose Bilateral endarterectomy with carotid body resection Central sleep apnea

Spinal cord trauma Motor neuron

Obstructive lung disease COPD

Poliomyelitis

Asthma

Hypocapnia

Amyotrophic lateral sclerosis

Fever Shivering Hypermetabolism Agitation Excess caloric intake

Cheyne-Stokes Acromegaly Hypothyroid Brainstem lesions Cerebrovascular accident Encephalitis Multiple sclerosis Parkinson disease Metabolic alkalosis Primary alveolar hypoventilation (Ondine’s curse) Congenital central hypoventilation Carotid body resection Obesity-hypoventilation

Motor nerve Phrenic nerve Guillain-Barré Charcot-Marie-Tooth Neuromuscular junction Myasthenia gravis Botulism Muscular Muscular dystrophy Myositis Myopathy Acid maltase

Upper airway obstruction Obesity-hypoventilation Pneumothorax Severe burns Chest wall disorders Kyphoscoliosis Ankylosing spondylitis

Metabolic

ARDS, Acute respiratory distress syndrome; CO2, carbon dioxide; COPD, chronic obstructive pulmonary disorder.

chronic hypercapnic respiratory failure are at significant risk for this condition, as indicated by the fact that COPD is now the third leading cause of death in the United States.20 Acute-onchronic respiratory failure can also be the presenting manifestation of neuromuscular disease that is complicated by pulmonary infection.21 Most common precipitating factors include bacterial or viral infections, congestive heart failure, pulmonary embolus, pneumothorax, chest wall dysfunction, and noncompliance with treatment. In these patients, the presence of respiratory failure cannot be judged by the normal ABG criteria but by a significant change from the baseline PaCO2 to a level having the potential to cause morbidity and mortality. Treatment goals include normalizing pH (avoiding mechanical ventilation if possible), elevating SaO2 to 90% (if hypoxemia is also present), improving airflow, treating infection, monitoring and maintaining fluid status, and preventing or treating complications as necessary. Deaths are less due to respiratory failure, and are more associated with older age, the underlying illness, associated complications, and whether intubation was required.22 Episodes of acute respiratory failure in these patients seem to have a significant long-term hazard, with mortality rates reaching 59% within the year after a critical illness requiring mechanical ventilation and tracheostomy.23 Patients with chronic hypoxemic respiratory failure (type I) are at similar risk for acute deterioration of hypoxemia. Infection and heart failure can result in worsening of the marginal oxygenation status of patients with interstitial pulmonary fibrosis or primary pulmonary hypertension.

Complications of Acute Respiratory Failure Although respiratory failure is life-threatening by itself, complications frequently arise that can add significantly to morbidity and mortality. Especially in patients with ARDS, more deaths are due to complications (e.g., sepsis, multiorgan failure) than to the primary disease.24 Modern ICUs with sophisticated mechanical ventilation can prolong but may not preserve life. Pulmonary complications such as emboli, barotrauma, and infection may be due to treatment strategies such as catheters, mechanical ventilation, and endotracheal tubes. A wide array of nonpulmonary complications may develop, including bacteremia, malnutrition, psychosis due to prolonged ICU stays, cardiac disorders (e.g., arrhythmias, hypotension), gastrointestinal ailments (e.g., hemorrhage, dysmotility), and renal disturbances (e.g., acute renal failure, positive fluid balance).

Clinical Presentation Clinically, a patient with respiratory muscle fatigue shows an initially increased respiratory rate followed by bradypnea (slowed respiratory rate) and apnea as fatigue ensues. Respiratory alternans, which is a phasic alternation between rib cage and abdominal breathing, may also occur. Opinions vary on the sensitivity and specificity of abdominal motion paradox in patients with respiratory muscle weakness, but at least some investigators suggest that respiratory muscle paradox is an early sign (see Chapter 16). When ventilatory failure is full-blown, ABG results show hypercapnia with acidosis. As mentioned earlier, the

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MINI CLINI

TABLE 45.3  Physiologic Indicators for

Acute or Chronic Hypercapnic Respiratory Failure Problem: A 55-year-old man presents to the emergency department complaining of increased shortness of breath and yellow-green sputum production for 1 week. He is alert and oriented. He has a 60 pack-year smoking history. Vital signs are blood pressure 165/90 mm Hg, pulse 120 beats/min, respirations 25 breaths/ min, and temperature 100.5°F oral. ABG values on room air are as follows: pH PaCO2 PaO2 HCO3− SaO2

7.28 70 mm Hg 35 mm Hg 36 mm Hg 66%

1. Define the respiratory condition indicated by the ABG results. 2. What is the P(A − a)O2? 3. What type of respiratory failure is present? 4. What kind of therapy is indicated? Discussion: 1. The ABG values indicate a partially compensated respiratory acidosis with hypoxemia. 2. PAO2 = 0.21 (760 − 47) − 70/0.8 = 62 mm Hg PaO2 = 35 mm Hg P(A − a)O2 = 62 − 35 = 27 mm Hg on room air 3. This is hypercapnic respiratory failure (type II), also known as ventilatory failure. However, in acute failure, the pH decreases 0.08 for every 10 mm Hg increase in PaCO2. In this patient, PaCO2 has increased 30 mm Hg (70 − 40), and the pH has decreased 0.12. The pH would be expected to decrease 0.24 (3 × 0.08) if this were acute ventilatory failure. This is a case of acuteon-chronic failure. The HCO3− of 36 mEq/L (normal 22 to 26 mEq/L) also indicates that renal compensation has occurred, which takes days to achieve. The P(A − a)O2 is 27 mm Hg, which is above normal, indicating that hypoxemia cannot be explained fully by hypoventilation. 4. Because the patient is alert, conservative therapy to improve lung function is indicated. O2 administration to achieve SaO2 of at least 90% is required. If PaO2 does not respond to O2 administration, shunt is present, and positive airway pressure may be necessary. Antibiotics are indicated for the probable infection (fever, discolored sputum), and bronchopulmonary hygiene (bronchodilators, steroids, cough assist) is indicated to improve ventilation.

presence of hypercapnia with acidosis can also indicate that the respiratory center is not responding properly.10 Tachypnea is the cardinal sign of increased work of breathing. Tachypnea occurs when the respiratory center increases breathing frequency in an attempt to lessen respiratory excursion and reduce the amount of work performed by the respiratory muscles.25 Overall workload is reflected in the minute volume needed to maintain normocapnia.

Indications for Ventilatory Support For each type of oxygenation and ventilatory failure, the goal of mechanical ventilation is either to support the patient until the underlying problem resolves or to maintain support of the patient with chronic ventilatory problems. These goals may be achieved by improving alveolar ventilation and arterial oxygenation, increasing lung volume, or reducing work of breathing.26

Ventilatory Support, Classified by Mechanism Underlying Respiratory Failure Mechanism

Normal Values

Support Indicated

Inadequate Alveolar Ventilation PaCO2 (mm Hg) pH

35–45 7.35–7.45

>55 30 kg/m2) when no other cause of hypoventilation is present. Factors associated with daytime hypercapnia include an increased body mass index, sleep apnea, a lower mean overnight O2 saturation, and severity of restrictive pulmonary function.50 In a randomized study comparing CPAP to NIV in the management of the obesity-hypoventilation syndrome, both interventions reduced the PaCO2 and improved quality without a significant difference between the two interventions.51 Stable Chronic Obstructive Pulmonary Disease NIV in the home setting for patients with severe COPD can prolong survival, improve quality of life, reduce hospitalization, and improve lung function, provided the patients and device setting are well chosen. For example, hypercapnic patients are most likely to benefit from NIV, and general recommendations for NIV use include those with a daytime PaCO2 ≥ 50 mm Hg or greater than 53 mm Hg more than 2 weeks after a hospital stay for an acute exacerbation.52 The settings that have been found to be helpful include higher pressures and higher pressure support with inspiratory positive airway pressure (IPAP) of 22 to 24 cm H2O while keeping the expiratory positive airway pressure (EPAP) low at 4 to 5 cm H2O, and with a backup rate of 14 to 18 breaths per minutes.52 Neuromuscular Diseases and Thoracic Cage Abnormalities Even in progressive neuromuscular disorders, NIV can prolong survival, improve quality of life, and reduce hospitalization rates.53 Other NIV techniques using rocking beds, pneumobelts, and negative pressure ventilation are much less frequently used and are becoming less easily available.

Invasive Ventilatory Support Patients with profound hypoxemia from a process that is expected to resolve slowly, such as acute lung injury, usually require intubation and mechanical ventilation. Other indications for intubation include conditions where NIV may be poorly tolerated or

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MINI CLINI Indications for Continuous Positive Airway Pressure Versus Continuous Mechanical Ventilation With Positive End-Expiratory Pressure Problem: A patient in the ICU is severely tachypneic and hypoxemic. The respiratory rate is 30 breaths/min. On approximately 50% O2 by mask at sea level, PaO2 is 50 mm Hg, PaCO2 is 30 mm Hg, pH is 7.51, and HCO3− is 23 mEq/L. The patient is in distress but alert and able to cooperate and follow instructions. 1. What is this patient’s P(A − a)O2? 2. What type of respiratory failure is this? 3. What is the appropriate initial therapy? Discussion: This patient does not have hypercapnic respiratory failure, as is confirmed by the low PaCO2 (30 mm Hg). The patient does have a serious oxygenation defect, as confirmed by the increased P(A − a)O2. PAO2 = 0.50 (713) − 30 0.8 = 318 mm Hg P(A − a)O2 = 318 − 50 = 268 mmHg The elevated P(A − a)O2 is explained by the presence of severe intrapulmonary shunt. Shunts this severe can occur only when significant airway closure and atelectasis are present. The mode of therapy should be aimed at reinflating collapsed alveoli and keeping the alveoli open throughout the breathing cycle. In this patient, alveolar ventilation is not impaired (PaCO2 = 30 mm Hg). CPAP alone may be effective in reducing shunt. (CPAP does not provide ventilation.) CPAP may be applied noninvasively via face mask, as would be indicated in this alert, cooperative patient. If hypercapnia and acidemia develop, mechanical ventilation with PEEP would be indicated.

even possibly harmful, such as the presence of upper airway obstruction, inability to clear secretions or protect the airway, or inability to achieve a proper mask fit. Both hypoxemic and hypercapnic types of respiratory failure can be managed effectively by invasive mechanical ventilation.

Acute Respiratory Distress Syndrome Profound hypoxemic respiratory failure is often due to severe pneumonia and ARDS. Patients with these conditions have very noncompliant lungs. Volume-cycled ventilation in patients with ARDS frequently leads to high peak airway and plateau pressures. Ventilating these patients with small tidal volumes (about 4 to 8 mL/kg) and aiming for a plateau pressure below 30 cm H2O reduces complications associated with mechanical ventilation and improves survival.54 Increased Intracranial Pressure Hyperventilation applied acutely and for short periods may be used to reduce ICP. The goal is to lower PaCO2 to between 25 mm Hg and 30 mm Hg, which causes alkalosis. Alkalosis helps reduce cerebral blood flow until ICP can be controlled by other measures. Ongoing ventilatory support should maintain PCO2 in the range of 30 to 40 mm Hg. By maintaining PCO2 in this range, sudden increases in ICP can be quickly controlled by short-term hyperventilation. Although reducing blood flow can reduce brain swelling and ICP, cerebral ischemia can also result. Another concern in ventilating patients with elevated ICP is

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MINI CLINI Acute Hypercapnic Respiratory Failure Problem: A patient with COPD presents to the emergency department in moderate respiratory distress. He is alert and cooperative. The respiratory rate is 26 breaths/min. Lung examination shows poor air entry with expiratory wheezing. Room air ABGs show pH 7.24, PaCO2 60 mm Hg, and PaO2 60 mm Hg. 1. What type of respiratory failure is this? 2. How should the patient be managed? Discussion: ABGs show an acute respiratory acidosis with normal PAO2 − PaO2 gradient. PAO2 = 0.21∗ (713) − 60 0.8 = 74 P(A − a)O2 = 74 − 60 = 14 mm Hg This patient has hypercapnic respiratory failure related to obstructive lung disease, also known as ventilatory failure. In addition to bronchodilators and corticosteroids, the RT should aim to improve ventilation to reverse the respiratory acidosis. In this patient, who is alert and cooperative, NIV using a face mask may be tried. Initial mask ventilation can start in the pressure support ventilation mode with a level of support of 10 cm H2O and 5 cm H2O PEEP. Tidal volume should be maintained at approximately 6 to 8 mL/kg. If this patient deteriorates despite therapy, he will need to be intubated and mechanically ventilated.

using PEEP to manage hypoxemia. There is a concern that increased intrathoracic pressure due to PEEP would cause decreased cerebral venous return leading to increased ICP. Also, there is concern that PEEP can decrease cerebral perfusion by limiting cardiac output. The use of PEEP in patients with elevated ICP may require invasive monitoring of ICP because the combination of decreased cerebral perfusion and elevated ICP can (but not always) narrow cerebral perfusion pressure.55 Elevation of the head of the bed can offset the increased ICP associated with the application of PEEP.

Obstructive Lung Disease Patients with obstructive lung disease have markedly increased airway resistance that leads to a decrease in the rate of expiratory flow with resulting hyperinflation. These patients frequently have problems with elevated airway pressure or dynamic hyperinflation (auto-PEEP), which can cause barotrauma and ineffective triggering of the ventilator.56 The goal in managing patients with obstructive lung disease and respiratory failure is to oxygenate and ventilate the patient successfully, while avoiding dyssynchrony and dynamic hyperinflation. In these patients, lower tidal volumes (6 to 8 mL/kg), moderate respiratory rates, and high sustained (square wave) inspiratory flow rates (70 to 100 L/min) are recommended to avoid dynamic hyperinflation.57 These maneuvers reduce inspiratory time and prolong expiratory time, which allows a patient with obstructive lung disease to have a longer time to exhale. Another consideration in patients with obstructive lung disease is the inspiratory threshold load imposed by auto-PEEP, resulting in increased patient inspiratory work.33 In this case, applied (or

extrinsic) PEEP can compensate for this threshold load and reduce the work of breathing for patient-triggered breaths in any assisted ventilatory mode.33

Ventilatory Support in Chronic Hypercapnic Respiratory Failure The goal of therapy in hypercapnic respiratory failure (acute ventilatory failure) is to guarantee a set minute ventilation. In treating patients with chronic ventilatory failure, the goal is to normalize the pH but not the PaCO2. Correction of PaCO2 in a patient with chronic hypoventilation from diverse causes can lead to a posthypercapnic metabolic alkalosis, which can produce hypokalemia, seizures, and arrhythmias.

SUMMARY CHECKLIST • Acute respiratory failure is identified by PaO2 less than 60 mm Hg or PaCO2 greater than 50 mm Hg, or both, in otherwise healthy individuals at sea level. • Hypoxemic respiratory failure is most commonly due to V̇ /Q̇ mismatch, shunt, or hypoventilation. • Hypercapnic respiratory failure, also known as ventilatory failure, results from decreased ventilatory drive, neurologic disease, or increased work of breathing. • Chronic respiratory failure may manifest with hypercapnia and evidence of a compensatory metabolic alkalosis (chronic ventilatory failure) or with polycythemia reflecting chronic hypoxemia. • The clinical condition of the patient is the most important factor in determining the need for ventilatory support. • Excessive work of breathing is the most common cause of respiratory muscle fatigue. • Acute exacerbations of COPD and cardiogenic edema represent two acute conditions in which NIV has benefit. • Increased FiO2 and PEEP are the main treatments for severe hypoxemia. • The goal of treating hypercapnic respiratory failure (acute ventilatory failure) is to normalize the pH.

REFERENCES 1. Mehta AB, Syeda SN, Wiener RS, et al: Epidemiological trends in invasive mechanical ventilation in the United States: a population-based study, J Crit Care 30:1217–1221, 2015. 2. Greene KE, Peters JI: Pathophysiology of acute respiratory failure, Clin Chest Med 15:1–12, 1994. 3. Campbell EJ: Respiratory failure, Br Med J 1:1451–1460, 1965. 4. West JB, Luks A: West’s respiratory physiology: the essentials. 2016. 5. Ming DK, Patel MS, Hopkinson NS, et al: The ‘anatomic shunt test’ in clinical practice; contemporary description of test and in-service evaluation, Thorax 69:773–775, 2014. 6. Holland AE: Exercise limitation in interstitial lung disease— mechanisms, significance and therapeutic options, Chron Respir Dis 7:101–111, 2010. 7. Rodriguez-Roisin R, Krowka MJ: Hepatopulmonary syndrome– a liver-induced lung vascular disorder, N Engl J Med 358:2378– 2387, 2008.

CHAPTER 45  Respiratory Failure and the Need for Ventilatory Support 8. Aboussouan LS, Stoller JK: Traveling with supplemental oxygen for patients with chronic lung disease. In Maurer JR, editor: Non-neoplastic advanced lung disease, New York, 2003, Marcel Dekker, pp 711–730. 9. Sarkar M, Niranjan N, Banyal PK: Mechanisms of hypoxemia, Lung India 34:47–60, 2017. 10. Caruana-Montaldo B, Gleeson K, Zwillich CW: The control of breathing in clinical practice, Chest 117:205–225, 2000. 11. Nogues MA, Benarroch E: Abnormalities of respiratory control and the respiratory motor unit, Neurologist 14:273–288, 2008. 12. Berger KI, Norman RG, Ayappa I, et al: Potential mechanism for transition between acute hypercapnia during sleep to chronic hypercapnia during wakefulness in obstructive sleep apnea, Adv Exp Med Biol 605:431–436, 2008. 13. Benditt JO, Boitano LJ: Pulmonary issues in patients with chronic neuromuscular disease, Am J Respir Crit Care Med 187:1046–1055, 2013. 14. Brown RH, Al-Chalabi A: Amyotrophic lateral sclerosis, N Engl J Med 377:162–172, 2017. 15. Willison HJ, Jacobs BC, van Doorn PA: Guillain-Barre syndrome, Lancet 388:717–727, 2016. 16. Gilhus NE: Myasthenia gravis, N Engl J Med 375:2570–2581, 2016. 17. Jozefowicz RF: Neurologic manifestations of pulmonary disease, Neurol Clin 7:605–616, 1989. 18. Sood P, Paul G, Puri S: Interpretation of arterial blood gas, Indian J Crit Care Med 14:57–64, 2010. 19. Corfield DR, McKay LC: Regional cerebrovascular responses to hypercapnia and hypoxia, Adv Exp Med Biol 903:157–167, 2016. 20. Murphy SL, Xu J, Kochanek KD, et al: Deaths: final data for 2015, Natl Vital Stat Rep 66:1–75, 2017. 21. Chen R, Grand’Maison F, Strong MJ, et al: Motor neuron disease presenting as acute respiratory failure: a clinical and pathological study, J Neurol Neurosurg Psychiatry 60:455–458, 1996. 22. Moskowitz A, Andersen LW, Karlsson M, et al: Predicting in-hospital mortality for initial survivors of acute respiratory compromise (ARC) events: development and validation of the ARC Score, Resuscitation 115:5–10, 2017. 23. Damuth E, Mitchell JA, Bartock JL, et al: Long-term survival of critically ill patients treated with prolonged mechanical ventilation: a systematic review and meta-analysis, Lancet Respir Med 3:544–553, 2015. 24. Stapleton RD, Wang BM, Hudson LD, et al: Causes and timing of death in patients with ARDS, Chest 128:525–532, 2005. 25. Banner MJ: Respiratory muscle loading and the work of breathing, J Cardiothorac Vasc Anesth 9:192–204, 1995. 26. Slutsky AS: Consensus conference on mechanical ventilation— January 28-30, 1993 at Northbrook, Illinois, USA. Part I. European Society of Intensive Care Medicine, the ACCP and the SCCM, Intensive Care Med 20:64–79, 1994. 27. Stoller JK: Physiologic rationale for resting the ventilatory muscles, Respir Care 36:290–296, 1991. 28. American Thoracic Society/European Respiratory Society: ATS/ ERS Statement on respiratory muscle testing, Am J Respir Crit Care Med 166:518–624, 2002. 29. NHLBI Workshop summary: Respiratory muscle fatigue. Report of the Respiratory Muscle Fatigue Workshop Group, Am Rev Respir Dis 142:474–480, 1990. 30. Macklem PT, Roussos CS: Respiratory muscle fatigue: a cause of respiratory failure?, Clin Sci Mol Med 53:419–422, 1977.

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31. Laghi F, Cattapan SE, Jubran A, et al: Is weaning failure caused by low-frequency fatigue of the diaphragm?, Am J Respir Crit Care Med 167:120–127, 2003. 32. Cabello B, Mancebo J: Work of breathing. In Pinsky MR, Brochard L, Hedenstierna G, et al, editors: Applied physiology in intensive care medicine 1: physiological notes—technical notes—seminal studies in intensive care, Berlin, Heidelberg, 2012, Springer, pp 11–14. 33. MacIntyre NR, Cheng KC, McConnell R: Applied PEEP during pressure support reduces the inspiratory threshold load of intrinsic PEEP, Chest 111:188–193, 1997. 34. Kirton OC, DeHaven CB, Morgan JP, et al: Elevated imposed work of breathing masquerading as ventilator weaning intolerance, Chest 108:1021–1025, 1995. 35. Mehta S, Hill NS: Noninvasive ventilation, Am J Respir Crit Care Med 163:540–577, 2001. 36. MacIntyre NR, Leatherman NE: Ventilatory muscle loads and the frequency-tidal volume pattern during inspiratory pressure-assisted (pressure-supported) ventilation, Am Rev Respir Dis 141:327–331, 1990. 37. Kato T, Suda S, Kasai T: Positive airway pressure therapy for heart failure, World J Cardiol 6:1175–1191, 2014. 38. Mahmoud KM, Ammar AS: A comparison between two different alveolar recruitment maneuvers in patients with acute respiratory distress syndrome, Int J Crit Illn Inj Sci 1:114–120, 2011. 39. Sullivan CE, Issa FG, Berthon-Jones M, et al: Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares, Lancet 1:862–865, 1981. 40. Verbraecken J, Willemen M, De Cock W, et al: Continuous positive airway pressure and lung inflation in sleep apnea patients, Respiration 68:357–364, 2001. 41. Rochwerg B, Brochard L, Elliott MW, et al: Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure, Eur Respir J 50:2017. 42. Hannan LM, Dominelli GS, Chen Y-W, et al: Systematic review of non-invasive positive pressure ventilation for chronic respiratory failure, Respir Med 108:229–243, 2014. 43. Osadnik CR, Tee VS, Carson-Chahhoud KV, et al: Non-invasive ventilation for the management of acute hypercapnic respiratory failure due to exacerbation of chronic obstructive pulmonary disease, Cochrane Database Syst Rev (7):CD004104, 2017. 44. Gray A, Goodacre S, Newby DE, et al: Noninvasive ventilation in acute cardiogenic pulmonary edema, N Engl J Med 359:142–151, 2008. 45. Ho KM, Wong K: A comparison of continuous and bi-level positive airway pressure non-invasive ventilation in patients with acute cardiogenic pulmonary oedema: a meta-analysis, Crit Care 10:R49, 2006. 46. Stefan MS, Nathanson BH, Lagu T, et al: Outcomes of noninvasive and invasive ventilation in patients hospitalized with asthma exacerbation, Ann Am Thorac Soc 13:1096–1104, 2016. 47. Bellani G, Laffey JG, Pham T, et al: Noninvasive ventilation of patients with acute respiratory distress syndrome. Insights from the LUNG SAFE study, Am J Respir Crit Care Med 195:67–77, 2017. 48. Frat J-P, Thille AW, Mercat A, et al: High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure, N Engl J Med 372:2185–2196, 2015. 49. Patel BK, Wolfe KS, Pohlman AS, et al: Effect of noninvasive ventilation delivered by helmet vs. face mask on the rate of

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endotracheal intubation in patients with acute respiratory distress syndrome: a randomized clinical trial, JAMA 315:2435– 2441, 2016. 50. Kaw R, Hernandez AV, Walker E, et al: Determinants of hypercapnia in obese patients with obstructive sleep apnea: a systematic review and metaanalysis of cohort studies, Chest 136:787–796, 2009. 51. Howard ME, Piper AJ, Stevens B, et al: A randomised controlled trial of CPAP versus non-invasive ventilation for initial treatment of obesity hypoventilation syndrome, Thorax 72: 437–444, 2017. 52. Storre JH, Callegari J, Magnet FS, et al: Home noninvasive ventilatory support for patients with chronic obstructive pulmonary disease: patient selection and perspectives, Int J Chron Obstruct Pulmon Dis 13:753–760, 2018.

53. Annane D, Orlikowski D, Chevret S: Nocturnal mechanical ventilation for chronic hypoventilation in patients with neuromuscular and chest wall disorders, Cochrane Database Syst Rev (12):CD001941, 2014. 54. Howell MD, Davis AM: Management of ARDS in adults, JAMA 319:711–712, 2018. 55. Videtta W, Villarejo F, Cohen M, et al: Effects of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure, Acta Neurochir Suppl 81:93–97, 2002. 56. Murias G, Lucangelo U, Blanch L: Patient-ventilator asynchrony, Curr Opin Crit Care 22:53–59, 2016. 57. Shapiro JM: Management of respiratory failure in status asthmaticus, Am J Respir Med 1:409–416, 2002.

46  Mechanical Ventilators Robert L. Chatburn and Teresa A. Volsko CHAPTER OBJECTIVES After reading this chapter you will be able to • Define a mechanical ventilator • Describe the key design features of ventilator displays • Discuss the importance of properly setting alarm thresholds • Explain how the compliance of the patient circuit affects volume delivery

• Describe the 10 maxims used to develop a standardized ventilator taxonomy • Demonstrate how to classify any mode of ventilation • List the three main goals of mechanical ventilator support • Discuss the differences between conventional and high-frequency ventilators

CHAPTER OUTLINE How Ventilators Work, 987 The Operator Interface, 989 The Patient Interface, 991 Identifying Modes of Mechanical Ventilation, 993 The 10 Maxims for Understanding Modes, 993

A Taxonomy for Mechanical Ventilation, 1004 How to Classify Modes, 1005 Comparing Modes of Mechanical Ventilation, 1008 Types of Ventilators, 1008

Conventional Versus High-Frequency Ventilators, 1008 Classification of Ventilators by Use, 1010

KEY TERMS adaptive targeting scheme assisted breath bio-variable targeting scheme continuous mandatory ventilation (CMV) continuous spontaneous ventilation (CSV) control circuit cycling driving pressure dual targeting scheme

elastance intelligent targeting scheme intermittent mandatory ventilation (IMV) loaded breathing machine cycled machine triggered mandatory mode pressure-control ventilation resistance

To safely and effectively initiate and manage a mechanical ventilator, the respiratory therapist (RT) must have a basic understanding of (1) ventilator design principles related to patientventilator interaction; (2) appropriate clinical application of ventilatory modes (i.e., the proper matching of ventilator capability with physiologic need); and (3) the physiologic effects of mechanical ventilation, including gas exchange and pulmonary mechanics. This chapter focuses on the first of these. It explains classification terminology and outlines a framework for understanding current and future ventilatory support devices.1

servo targeting scheme optimal targeting scheme patient cycled patient triggered spontaneous breath targeting scheme tidal pressure time constant time-control trigger volume-control ventilation

HOW VENTILATORS WORK Some basic knowledge of mechanics is helpful to understand how ventilators work. A ventilator is simply a machine that is designed to perform some portion of the work of breathing. These machines deliver a variety of medical gas mixtures, such as nitric oxide, helium, and oxygen. Sophisticated software and advanced monitoring systems make it possible to deliver a variety of breathing patterns to meet patient needs for safety, comfort, and, eventually, liberation (i.e., extubation). 987

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Ventilators are used along the whole continuum of care, from intensive care units (ICUs) to patient transport to long-term and home care. They all require energy in the form of either electricity or compressed gas to function. The energy is transmitted or transformed (by the ventilator’s drive mechanism) in a predetermined manner (by the control circuit) to augment or replace the patient’s muscles in performing the work of breathing (the desired output).

RULE OF THUMB  For patient transport, you must use either a pneumatically powered ventilator or one that can run solely on batteries. Always take along a manually powered bag-valve-mask resuscitator, and for long transports be sure to have backup power available (extra cylinders or batteries).

A basic schematic of an ICU ventilator is shown in Fig. 46.1. A simplified description of ventilator operation is as follows: High-pressure gas (air and oxygen, usually from a centrally located compressor and liquid oxygen source and piped into ICU rooms) enters the ventilator at 50 psi (in the United States). Inside the ventilator, the gas pressures of air and oxygen sources are usually

reduced. The flow of gas to a reservoir is then controlled by two valves. The relative flows of air and oxygen to the reservoir controls the FiO2. Output flow from the reservoir to the patient is managed by a high-flow proportional valve (i.e., flow is proportional to the voltage applied to the valve). The flow to the patient is coordinated with the exhalation valve that intermittently occludes the exhalation path. Thus, when the output flow valve is open and the exhalation valve is closed, gas flows into the lungs. When the output flow valve is closed and the exhalation valve is open, gas flows from the lungs, through the exhalation system, and to the atmosphere. Software controls the intricate interaction between the output valve and the exhalation valve to produce a variety of breathing patterns. These patterns can be dictated by the ventilator or entirely controlled by the patient’s brain or ventilatory demand.

RULE OF THUMB Ventilators used near magnetic resonance imaging (MRI) equipment must be MRI compatible. Even when an MRI-compatible ventilator is used during imaging, it is important to maintain the ventilator within the designated safe distance from the MRI device.

Fig. 46.1  Simplified Schematic of a Modern Intensive Care Ventilator. High-pressure gas enters the ventilator through the gas inlet connections for oxygen and air (1,2). Mixing takes place in a reservoir (5) and is controlled by two valves (3,4). Inspiratory flow from the reservoir is controlled by a separate proportional valve (6). On the inspiratory circuit there is a safety valve (7) and two nonreturn valves (8,9). In normal operation the safety valve is closed so that inspiratory flow is supplied to the patient’s lungs. When the safety valve is open, spontaneous inspiration of atmospheric air is possible through the emergency breathing valve (8). The emergency expiratory valve (9) provides a second channel for expiration when the expiratory valve (17) is blocked. Also on the inspiratory circuit are an inspiratory pressure (P) sensor (11) and a pressure sensor calibration valve (10). The exhalation circuit consists of the expiratory valve (17), expiratory pressure sensor (13) with its calibration valve (12), and an expiratory flow (F) sensor (18). The expiratory valve is a proportional valve and is used to adjust the pressure in the patient circuit. Conversion of mass flow to volume (barometric temperature and pressure saturated, BTPS) requires knowledge of ambient pressure, measured by another pressure sensor (not shown). Pressure in the patient circuit is measured with two independent pressure sensors (11,13). Oxygen flow to the nebulizer port (19) is controlled by a pressure regulator (14) and a solenoid valve (15). (Reproduced, with permission Mandu Press Ltd.)

CHAPTER 46  Mechanical Ventilators

The Operator Interface The ventilator’s operator interface (i.e., control panel) has evolved a lot over the last 45 years. Originally the displays on ventilators were very simple: operator inputs, or settings, were accomplished with hard-wired knobs, buttons, and dials. The ventilator outputs, such as alarm conditions and ventilating pressure, were displayed with bulbs, light-emitting diodes (LEDs), and meters. Some simple transport ventilators still use analog displays. The development of inexpensive microprocessors has led manufacturers to use digital displays almost exclusively on all types of ventilators. Today most ICU ventilators have computer touch screens for visual displays of ventilator data. They are usually designed as “virtual” instruments, meaning that knobs, buttons, dials, and meters are simulated on the screen, and may rely on only a single mechanical dial and perhaps a few buttons to set multiple parameters (Fig. 46.2).

Ventilator Displays Ventilator displays serve three main functions: (1) to display the inputs—that is, the current state of the settings and allow changes to be made; (2) to show the outputs—meaning the measured values that characterize normal patient–ventilator interactions; and (3) to show alarm conditions. Additional functions include trends of past settings or measured values, performance of special monitoring or automated procedures such as the determination of optimal positive end-expiratory pressure (PEEP), and miscellaneous ventilator configuration settings and patient data. Alphanumeric values.  Measured or calculated data in the form of alphanumeric values are presented in numbers or text. Typically FiO2, pressures (mean, baseline, peak, and plateau), volumes (inhaled/exhaled tidal volume, minute ventilation), peak

989

inspiratory and expiratory flow, and frequency are represented as numeric values. A variety of calculated parameters including I:E ratio, percent leak, resistance, and compliance may also be displayed. Trends.  Trends provide clinicians with measured or calculated data related to ventilatory support over time. Gradual or sudden changes in the patient’s ventilatory status can be identified by evaluating trends. Alarm logs can also be accessed and provide an additional layer of detail important for adjusting alarm limits to minimize nuisance alarms and enhance safety. Alarm logs can be invaluable in the event of a suspected ventilator failure and may be used as evidence in a legal investigation if significant patient harm has occurred. Waveforms and loops.  Graphic displays of pressure, volume, and flow convey a wealth of information. Not only is it possible to determine the mode of ventilation by examining these graphics, but the causes of patient–ventilator asynchrony can also be determined, including flow asynchrony, delayed or premature cycling, and missed triggers. Graphic representations of respiratory mechanics are helpful for identifying the ventilator parameters to be adjusted to improve the ventilator–patient interaction.2 When pressure, volume, or flow is graphed on the vertical axis with time on the horizontal axis, a waveform or “scalar” display (Fig. 46.3) is the result. Loop displays plot one variable against another as x-y graphs (Fig. 46.4). Pressure-volume (PV) loops can be used to set optimal PEEP and tidal volume levels (Fig. 46.5). PV loops are manually created by using a “super syringe” to inject discrete volumes of gas and then measuring static pressures (static pressure–volume curve). Alternatively, one can use the ventilator at very low constant inspiratory flows ( 0 Prs = 0

Fig. 47.3  Changes in Pressure, Volume, and Flow During a Single Mechanical Negative Pressure Breath. The box surrounding the lungs represents the enclosure formed by the negative pressure ventilator. FRC, Functional residual capacity. (Modified from Martin L: Pulmonary physiology in clinical practice: the essentials for patient care and evaluation, St. Louis, 1987, Mosby.)

(O2) cannot be provided to the patient through the negativepressure ventilator. Depending on patient need, low-flow or high-flow O2 delivery devices must be used to provide O2 therapy. Immediate access to patients requiring routine or emergent medical care may be difficult in systems that enclose the entire thorax and lower body, such as the iron lung and Porta-Lung (Respironics Inc., Murrysville, PA) (see Chapter 50). These systems may impede venous return by creating a negative pressure in the abdomen and lower half of the body, which may lead to hypotension, a phenomenon known as “tank shock.” The risk of glottis closure and the development of obstructive sleep apnea have been reported in association with NPV of patients with chronic obstructive pulmonary disease (COPD) and neuromuscular dysfunction. RULE OF THUMB A negative end-expiratory transpulmonary pressure results in collapse of alveoli, atelectasis. During mechanical ventilation PEEP is applied to maintain a positive end-expiratory transpulmonary pressure.

Airway, Alveolar, and Intrathoracic Pressure, Volume, and Flow During Positive Pressure Mechanical Ventilation Pressure mechanical ventilation (positive pressure ventilation [PPV]) causes air to flow into the lungs because of an increase in airway pressure, not a decrease in pleural pressure as occurs during spontaneous breathing and NPV (Fig. 47.4). However, similar to spontaneous breathing and NPV, PPV causes an increase in PTP, which allows gas to flow into the lungs. Gas flows into the lungs because Pawo is positive, and Palv is initially zero or less positive. Palv rapidly increases during the inspiratory phase of PPV. The increased Palv expands the airways and alveoli. Because Palv is greater than pleural pressure (Ppl) during PPV, positive pressure is transmitted from the alveoli to the pleural space, causing pleural pressure to increase during inspiration. Depending on the compliance and resistance of the lungs, pleural pressure may markedly exceed atmospheric pressure during a portion of inspiration. These changes in pleural pressure during PPV

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SECTION VI  Acute and Critical Care Inspiration

Expiration

Volume

Airflow

Alveolar pressure

Intrapleural pressure

0

2

4

Time(s)

Fig. 47.4  Changes in Pressure, Volume, and Flow During a Single Decelerating Flow, Positive Pressure Breath. Arrows into and out of the trachea represent airflow. (Modified from Martin L: Pulmonary physiology in clinical practice: the essentials for patient care and evaluation, St. Louis, 1987, Mosby.)

can lead to significant physiologic changes (see later sections). Pressure gradients during PPV are similar to pressure gradients during spontaneous breathing and NPV except that they are created by a positive Pawo instead of a negative pressure in the pleural space (see Table 47.1). All pressure gradients change in the same direction as during NPV and spontaneous breathing except the PTR, which changes in the opposite direction and becomes more positive instead of negative. Similar to spontaneous breathing, the recoil force of the lungs and chest wall, stored as potential energy during the positive pressure breath, causes passive exhalation. As gas flows from the alveoli to the airway opening, Palv decreases to atmospheric level, while pleural pressure is restored to its normal subatmospheric level (see Fig. 47.4). Volume and flow during PPV are also described by the equation of motion. The magnitude of Pvent depends not only on the patient’s lung mechanics but also on the Pmusc of the patient. If the patient makes no effort, Pvent is responsible for all volume and flow. During volume-controlled ventilation, as muscle effort increases, Pvent decreases and VT remains constant. During pressure-controlled ventilation, as Pmusc increases, VT increases and Pvent remains unchanged.

RULE OF THUMB  Ideally, the transpulmonary pressure should be as low as possible during mechanical ventilation. A transpulmonary pressure less than approximately 28 cm H2O minimizes the development of ventilator-induced lung injury. If the plateau pressure is kept less than 28 cm H2O, the transalveolar pressure can never exceed this level during controlled ventilation.

EFFECTS OF MECHANICAL VENTILATION ON VENTILATION Minute Ventilation The primary indication for mechanical ventilation is hypercapnic respiratory failure, also known as ventilatory failure. For patients with acute ventilatory failure, the goal of mechanical ventilation is improving alveolar ventilation to compensate for the patient’s inability to maintain a normal PaCO2. PaCO2 is inversely related to alveolar ventilation, which is related to minute ventilation. Minute ventilation (V̇ E) is the product of VT and ventilatory rate (f): V = VT × f Use of a mechanical ventilator usually implies a change in VT, ventilatory rate, or both from preintubation values. A normal

CHAPTER 47  Physiology of Ventilatory Support

spontaneous VT is approximately 5 to 7 mL/kg. The currently accepted VT for all patients acutely requiring mechanical ventilation is 4 to 8 mL/kg predicted body weight (PBW). These volumes are always based on PBW regardless of the size of the patient. The mechanical ventilator rate depends on the patient’s status. For postoperative ventilation, a rate of 12 to 20 breaths/min may be adequate. Conditions that necessitate a higher initial rate include acute respiratory distress syndrome (ARDS), pulmonary fibrosis, acutely increased intracranial pressure (ICP) (with caution; see later), and metabolic acidosis. Conditions that may necessitate a lower rate include acute asthma exacerbation, to allow an increased expiratory time to minimize air trapping. When an appropriate VT is established, the set rate is adjusted to achieve desired PaCO2. Mechanical ventilation increases minute ventilation by increasing VT, ventilator rate, or both.

MINI CLINI Alveolar, Transpulmonary, and Transalveolar Pressures Problem Mr. Jones is 58 years old, 5 feet 8 inches tall, and weighs 410 lb and is being ventilated because of ARDS. His current ventilator settings are pressure control mode, peak pressure 37 cm H2O, PEEP 20 cm H2O, FiO2 0.50, respiratory rate 26 breaths/min, and VT 400 mL. At the end of expiration gas flow returns to zero approximately 100 ms before the end of the breath. What are the endinspiratory and end-expiratory alveolar, transpulmonary, and transalveolar pressures for Mr. Jones? Solution Because there is a short end-inspiratory pause, it is reasonable to assume that the peak airway pressure in pressure control is equal to the average peak Palv. The term average is used here because alveolar units have different time constants and as a result different peak pressures, but when there is an endinspiratory equilibration of pressure, the resulting value is the average pressure across all lung units. To be more confident of this value, an additional endinspiratory pause can be added for a single breath to determine better the end-inspiratory pause pressure or plateau pressure. End-expiratory transpulmonary is determined by an end-expiratory pause. As with the end-inspiratory pause, this ensures that the pressure reading reflects the average pressure across all alveoli at end-exhalation.

To determine the end-inspiratory and end-expiratory PTP (Pawo − Ppl) and PL (Palv − Ppl), an estimate of pleural pressure must be made. The ideal method is to measure the esophageal pressure. Although not exactly equal to the pleural pressure, it accurately reflects changes in pleural pressure. Some authors have also recommended evaluation of bladder pressure, which changes in the same manner as esophageal pressure. The reading from the esophageal catheter at the time an end-expiratory pause was applied was 23 cm H2O. The end-expiratory PTP and PL are the same: 25 to 23 cm H2O or 2 cm H2O. The reading at endinspiration is 28 cm H2O. The end-inspiratory PTP and PL are the same: 37 to 28 cm H2O or 9 cm H2O. This is because Mr. Jones was ventilated in pressure control, and there was a short end-inspiratory pause, so both peak and plateau pressures were

1019

equal. However, if he was ventilated in volume ventilation and the peak airway pressure might be 45 cm H2O, while the plateau pressure (Pplat) remained 37 cm H2O when an end-inspiratory pause was added, the transalveolar pressure and PTP would still be the same: 37 – 28 cm H2O or 9 cm H2O. Mr. Jones is receiving lung protective ventilation because his transalveolar pressure is only 9 cm H2O at end-inspiration. The high airway pressures are needed because of his large body mass, which minimizes the transmission of pressure across the lung, reducing lung stretch.

Increased Alveolar Ventilation

Alveolar ventilation (V̇ A) is inversely related to PaCO2 as defined by the following relationship:  V A = (VCO 2 × 0.863) PaCO2 where V̇ CO2 is carbon dioxide (CO2) production.2 As alveolar ventilation decreases, PaCO2 increases. As CO2 production increases, alveolar ventilation must increase to maintain the same PaCO2. Mechanical ventilation may be needed in either case. It is more useful to look at this equation solved for PaCO2 because changes in PaCO2 usually correlate with the need for mechanical ventilation:   PaCO2 = (VCO 2 × 0.863) VA If V̇ A decreases or V̇ CO2 increases, PaCO2 increases, and hypercapnic respiratory failure follows; mechanical ventilation may be indicated in this setting. Because mechanical ventilation increases ventilation, PaCO2 can be decreased to the desired level depending on the total ventilatory rate.

Ventilation/Perfusion Ratio Spontaneous ventilation results in gas distribution mainly to the dependent and peripheral zones of the lungs. Controlled PPV tends to reverse this normal pattern of gas distribution, and most of the delivered volume is directed to nondependent lung zones (Fig. 47.5). This phenomenon is caused partly by the inactivity of the diaphragm and chest wall during controlled PPV. Although these structures actively facilitate gas movement during spontaneous breathing, inactivity of these structures during controlled PPV impedes ventilation to dependent lung zones. An increase in ventilation to the nondependent zones of the lung, where there is less perfusion, increases the ventilation/ perfusion (V̇ /Q̇ ) ratio, effectively increasing physiologic dead space. The increase in P(A − a)O2 often observed with PPV is caused by areas of low V̇ /Q̇ ratio. PPV decreases the V̇ /Q̇ ratio in the bases and dependent lung zones mainly as a result of ventilation being primarily distributed to nondependent lung zones. The V̇ /Q̇ ratio may also increase in nondependent lung zones because of the effect of PPV on perfusion. PPV can compress the pulmonary capillaries. This compression increases pulmonary vascular resistance and decreases perfusion. Minimal blood flow perfuses the areas with the greatest VT and contributes to a further increase in dead space. Conversely, blood intended for these areas is diverted to regions with lower vascular resistance—generally more dependent lung regions. Pulmonary blood flow during PPV tends to perfuse

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SECTION VI  Acute and Critical Care Anterior

A

embolism, an excessive level of positive end-expiratory pressure (PEEP), or advanced dead space–producing disease such as emphysema or pulmonary embolism. When inappropriate PEEP is used and blood flow is diverted from ventilated alveoli to hypoventilated alveoli; the result is an increased V̇ /Q̇ ratio. In emphysema, formation of bullae is coincident with the destruction of pulmonary capillaries; the result is large areas of poorly perfused but ventilated alveoli. Pulmonary emboli may completely occlude pulmonary vessels; the result is lack of perfusion to alveoli distal to the blockage.

Acid–Base Balance Anterior

Respiratory acidosis, occurs when minute ventilation and alveolar ventilation per minute (V̇ A) are inadequate to meet the needs of the body. Volume delivery also decreases if high airway pressures develop secondary to volume loss as a result of ventilator circuit tubing compliance (compressible volume loss). Ventilator circuits may have compliance of 1 to 3 mL/cm H2O, which effectively reduces VT: Volume lost = Tubing compliance × (Peak pressure − PEEP)

B

Ventilation Perfusion Fig. 47.5  Effect of Spontaneous Ventilation and Positive Pressure Ventilation (PPV) on Gas Distribution in a Supine Subject. (A) During spontaneous ventilation, diaphragmatic action distributes most ventilation to the dependent zones of the lungs, where perfusion is greatest. The result is a nearly normal V̇ /Q̇ ratio. (B) Partly because of diaphragmatic inactivity, PPV reverses this normal pattern of gas distribution, and most delivered volume is directed to the upper lung zones. An increase in ventilation to the upper lung zones, where there is less perfusion, increases the V̇ /Q̇ ratio, effectively increasing physiologic dead space. At the same time, higher alveolar pressure in the better ventilated upper lung zones diverts blood flow away from these areas to the areas receiving the least ventilation. The result is areas of low V̇ /Q̇ ratio and impaired oxygenation. (Modified from Kirby RR: Clinical application of ventilatory support, New York, 1990, Churchill Livingstone.)

the least well-ventilated lung regions. This perfusion decreases the V̇ /Q̇ ratio in those areas and increases the P(A − a)O2.

Alveolar and Arterial Carbon Dioxide Normal alveolar carbon dioxide tension (PACO2) is 40 mm Hg, whereas mixed venous blood typically has a PvCO2 of 45 mm Hg. Under normal circumstances, CO2 moves out of the blood at the pulmonary capillary interface; the result is a PaCO2 of 40 mm Hg. In the event of a decrease in alveolar ventilation or an increase in CO2 production, PaCO2 increases. Mechanical ventilation can increase minute volume and alveolar ventilation and reduce PACO2 and PaCO2. With an increase in VD/VT, PaCO2 increases if there is no change in minute volume; this may occur when alveolar blood flow is decreased by acute pulmonary

Tubing compliance was a concern with older ventilators; however, most intensive care unit (ICU) ventilators in use at the present time allow the user to compensate for compressible volume loss as a result of tubing compliance. When activated, the volume set is the volume delivered to the patient. This issue is discussed in more detail later in the chapter. An increase in VD/VT ratio can cause a reduction in alveolar ventilation, even though minute ventilation may be normal or increased. These problems emphasize the importance of proper selection of VT and mandatory rate. When respiratory acidosis exists, the patient may become restless and anxious, resulting in patient–ventilator asynchrony (see Chapter 48). A communicative patient may complain of dyspnea. If these symptoms are observed, especially when PaCO2 is increased, minute ventilation generally should be increased. Respiratory alkalosis occurs if the minute ventilation is too high. A patient who is dyspneic, anxious, or in pain may develop this condition; the usual manifestations are an increased ventilatory rate or patient–ventilator asynchrony or both. The ventilator can cause respiratory alkalosis secondary to an inappropriately high VT or rate. Regardless, the result is excessive minute and alveolar ventilation. This condition requires that the RT adjust the ventilator appropriately and address the patient’s pain or anxiety to avoid the systemic effects of a prolonged alkalosis. With metabolic acidosis, the patient tries to compensate by increasing minute ventilation to blow off CO2 in an effort to increase the pH. The resulting increase in work of breathing (WOB) may lead to ventilatory muscle fatigue and continued respiratory failure. The best therapy for metabolic acidosis is to manage the underlying cause while supporting the patient’s ventilation as needed. Many patients cannot be liberated from mechanical ventilation until the underlying acidosis is controlled. With metabolic alkalosis, in an effort to compensate for the increased pH, the patient tries to decrease minute ventilation. If weaning is attempted when the patient has a metabolic alkalosis, the patient may continue to hypoventilate and weaning

CHAPTER 47  Physiology of Ventilatory Support

may fail. As with metabolic acidosis, the underlying cause should be determined and managed. Common causes of metabolic alkalosis include hypochloremia or hypokalemia secondary to gastrointestinal loss, diuretics, or steroid administration. See Chapter 14 for details on acid–base balance.

1021

EFFECTS OF MECHANICAL VENTILATION ON OXYGENATION

causes of hypoxemia, an increase in FiO2 is needed to increase arterial O2 content. O2 content (see Chapter 12) is directly related to arterial oxygenation and hemoglobin concentration. Under circumstances of normal diffusion, FiO2, and hemoglobin concentration, the arterial content is normal at approximately 19.8 mL O2/100 mL blood. As defined by this equation, CaO2 decreases if hemoglobin concentration, arterial saturation, or PaO2 decreases.

Inspired Oxygen

Decreased Shunt

Mechanical ventilators usually deliver an increased fractional inspired oxygen (FiO2) ranging from room air (0.21) to 100% O2 (1.0). As a result, the alveolar partial pressure of oxygen (PAO2) and arterial partial pressure of oxygen (PaO2) may be restored to normal with appropriate management. The effectiveness of increased FiO2 in the management of hypoxemia depends on the cause of hypoxemia. Hypoxemia caused by a decrease in the V̇ /Q̇ ratio or hypoventilation is more responsive to increased FiO2 than hypoxemia caused by a diffusion defect or shunt. Hypoxemia caused by hypoventilation responds well to an increase in FiO2, but alveolar ventilation can be restored only by improved ventilation. Hypoxemia caused by diffusion defect and shunt generally respond better to an increase in PEEP than to an increase in FiO2. If the patient is receiving mechanical ventilation and has adequate alveolar ventilation, failure of the PaO2 to respond to increased FiO2 likely means that hypoxemia is due to a diffusion defect or shunt. It should be remembered that FiO2 in an acutely ill patients should not be applied excessively.3 Sufficient current data indicate that hyperoxia increases mortality of critically ill patients. As a result, the FiO2 should be adjusted to ensure that the PaO2 is 55 to 80 mm Hg and/or the SpO2 is 88% to 95%.

Mechanical ventilation alone does not decrease shunt. Otherwise, it would be much easier to restore PaO2 in patients with ARDS. Administration of PEEP with mechanical ventilation or to a spontaneously breathing patient in the form of continuous positive airway pressure (CPAP) helps to maintain open alveoli and stabilize small, collapsed, or fluid-filled alveoli. The results are an increase in alveolar surface area for diffusion and improvement in V̇ /Q̇ matching and arterial oxygenation. PEEP or CPAP should be used judiciously (see later in this chapter and Chapter 49). High pressure can overdistend alveoli and redistribute pulmonary blood flow to capillaries surrounding poorly ventilated alveoli, resulting in increased shunt.

Alveolar Oxygen and Alveolar Air Equation Increasing FiO2 increases PAO2, according to the alveolar air equation (see Chapter 11).2 When FiO2 is increased, PAO2 increases as well, if there is no change in PaCO2 or the respiratory exchange ratio. PaCO2 may change with a change in alveolar ventilation or metabolic rate. O2 consumption and CO2 production increase with an increase in metabolic rate, such as with fever or overfeeding. If metabolic rate and alveolar ventilation are constant, an increase in FiO2 results in a proportional increase in PAO2. RULE OF THUMB It should be remembered that FiO2 in an acutely ill patients should not be applied excessively. Sufficient current data indicate that hyperoxia increases mortality of critically ill patients. As a result, the FiO2 should be adjusted to ensure that the PaO2 is 55–80 mm Hg and/or the SpO2 is 88%–95%.

Arterial Oxygenation and Oxygen Content Mechanical ventilation at FiO2 of 0.21 may restore arterial oxygenation if the only cause of hypoxemia was hypoventilation. Hypoventilation may be the sole cause with central nervous system depression, apnea, and neuromuscular disease. With other

Increased Tissue Oxygen Delivery When a mechanical ventilator is used to improve arterial oxygenation by increasing FiO2 or PEEP, CaO2 increases. However, the increase in CaO2 represents only part of tissue O2 delivery because O2 delivery is defined by CaO2 and cardiac output, as follows2: DO2 (tissue oxygen delivery in ml min )= CaO2 (ml O2 100 ml blood) × Cardiac output (L min) ×10 where 10 is a constant for converting deciliters to milliliters. Normal tissue O2 delivery is approximately 990 mL/min because the normal CaO2 is approximately 20 vol%, and the normal cardiac output is approximately 5 L/min. When PaO2, CaO2, and cardiac output are adequate, so is tissue O2 delivery. When PEEP is needed to improve PaO2, it must be used cautiously because PEEP increases intrathoracic pressure. When intrathoracic pressure is increased, pleural pressure around the heart also increases, and the increase can affect the mechanical activity of the heart and impede venous return and decrease cardiac output. As discussed in Chapter 49, careful titration of PEEP must include monitoring the cardiovascular status of the patient. Optimal PEEP provides adequate arterial oxygenation and tissue O2 delivery.

EFFECTS OF POSITIVE PRESSURE MECHANICAL VENTILATION ON LUNG MECHANICS Time Constants The time necessary for passive inflation and deflation of the lung or each alveolus is determined by the product of compliance and resistance. This product is the time constant of the lung or alveolar unit. The compliance of a “normal” lung is approximately 0.1 L/cm H2O, and resistance of a normal lung

1022

SECTION VI  Acute and Critical Care

MINI CLINI Oxygen Delivery Problem Oxygen delivery (DO2) depends on PaO2, hemoglobin concentration, and cardiac output. The formula for DO2 is: DO2 = CaO2 × Cardiac output (L min) × 10 where CaO2 is the arterial oxygen content, and 10 is the conversion factor between deciliters and milliliters. Normal DO2 is 990 mL/min. DO2 is normal when the hemoglobin concentration is 15 g/dL, cardiac output is 5.0 L/min, and PaO2 is 100 mm Hg: DO2 = [15 g Hb × 1.34 mlO2 g Hb × 0.97 (SaO2 ) + 0.003 × 100 mmHg] × (5.0 L min) × 10 = 19.8 (CaO2 ) × 5 (L min) × 10 = 990 ml min When the practitioner calculates DO2 and determines it to be low, the component of the formula that is low denotes the problem and the therapeutic target. If CaO2 is low because of a low hemoglobin concentration, increasing the hemoglobin concentration with blood transfusion is indicated. If CaO2 is low because of low PaO2 or SaO2, increasing PaO2 and SaO2 with O2 or PEEP is indicated. If cardiac output is low, the cause (decreased preload, increased afterload, decreased contractility, or bradycardia) is determined, and appropriate therapy is initiated. Frequently, a decrease in CaO2 results in an increase in the cardiac output to compensate for decreased DO2. Example: Given PaO2 of 65 mm Hg, hemoglobin concentration of 10 g/dL, SaO2 of 91%, and cardiac output of 4.8 L/min, what increase in cardiac output is necessary to maintain DO2 of 900 mL/min? DO2 at given values is [(1.34 × 10 × 0.97) + (0.003 × 65)] × 4.8 × 10 = 633 ml min An increase in cardiac output to 6.8 L/min results in DO2 that is close to normal: [(1.34 × 10 × 0.97) + (0.003 × 65)] × 6.8 × 10 = 897 mL/min. However, an increase in cardiac output to 6.8 L/min increases myocardial work. Because the cause of decreased DO2 in this patient is hypoxemia and anemia, the goal of therapy should be to increase PaO2. This strategy allows cardiac output and work to return to normal while adequate DO2 is maintained. Increasing the hemoglobin concentration is normally not performed by transfusion unless the hemoglobin concentration is less than 8–10 g/dL because of the adverse effects associated with transfusions.

is approximately 2.5 cm H2O/L/s. The time constant for a normal lung is 0.25 second (1.0 L/cm H2O × 0.25 cm H2O/L/s). For patients with normal lungs, 95% of the alveoli are inflated within three time constants (i.e., within 0.75 second). In four time constants (1.0 second), 98% of alveoli are inflated, and in five time constants (1.25 second), 99.3% of alveoli are inflated. The same numbers apply for exhalation. The two major factors that affect alveolar time constants are changes in compliance and changes in resistance. If compliance or resistance decreases, the time constant for a given lung unit decreases, and the lung fills and empties faster. If compliance or resistance increases, the time constant increases, and it takes more time to fill and empty the lung. There are clinical implications for patients with disorders consistent with abnormal time constants. A longer inspiratory time may be needed for patients with asthma because Raw is increased. Attempting to ventilate these patients with a normal

inspiratory time may result in inadequate volume to affected lung units because the airways are obstructed, and volume is likely to travel to airways with the lowest resistance. Inspiratory time in severe asthma needs to be set between approximately 1.0 to 1.5 seconds to ensure adequate gas delivery. The primary limiting factor is that the airways are also obstructed during exhalation. The expiratory time must also be longer to allow as complete an exhalation as possible. Asthma is very different from COPD, in which the inspiratory time constant is normal, but the expiratory time constant is long. In general, asthma requires very slow respiratory rates with longer than normal inspiratory and expiratory times to account for the altered time constants during both inspiration and expiration. Patients with COPD generally tolerate a more rapid rate because only the expiratory time constant is lengthened. In both of these situations, air trapping is very common because of the long expiratory time constants. In patients with COPD, inspiratory times are generally short (approximately 0.7 to 0.9 second). In patients with ARDS or acute lung injury (ALI), time constants are very short, and as a result inspiratory times can also be very short. Most patients with ARDS require an inspiratory time of only 0.5 to 0.8 second. Expiratory time constants are also short— hence the ability to ventilate these patients rapidly with small VT. Respiratory rates greater than 30 breaths/min are frequently well tolerated by patients with ARDS. The major concern with patients with ARDS and their short time constants is that any disruption of the airway rapidly results in a loss of lung volume. Atelectasis occurs with disconnections from the ventilator in 1 seconds. As a result, all patients with ARDS should be suctioned only with inline suction catheters, and any circuit disconnection should be avoided. Ventilator management in the care of patients with COPD, asthma, and ARDS is described in detail in Chapter 49.

Increased Pressure Peak inspiratory pressure (PIP) is the highest pressure produced during the inspiratory phase. It is the sum of the pressures necessary to overcome Raw and lung and chest wall compliance. PIP is also known as peak pressure or peak airway pressure. Pplat is the pressure observed during a period of inflation hold or end-inspiratory pause. To obtain a Pplat, the RT initiates an inspiratory pause time of 0.5 to 2.0 seconds. During inspiration, the peak pressure is reached and then immediately followed by the inspiratory pause. During the pause, pressure decreases to a pressure plateau. When a valid Pplat is obtained, the inspiratory pause time is returned to zero. Pplat represents the average peak Palv. In volume-controlled ventilation, Pplat is always lower than peak pressure because the peak pressure is the sum of the Palv and the pressure needed to overcome Raw. When flow is delivered by a square waveform, the difference between Pplat and peak pressure is the pressure necessary to overcome Raw. If the VT is divided by the difference between the Pplat and total PEEP (applied plus auto-PEEP), the quotient is the quasistatic lungthorax compliance4: The reason for this is that the baseline pressure prior to the start of inspiration is the total PEEP, not the applied PEEP.4 Cstatic = VT (Pplat − PEEP)

CHAPTER 47  Physiology of Ventilatory Support

This value is referred to as the lung-thorax compliance because the compliance of the lungs and the compliance of the rib cage are being calculated as a unit. The lung compliance cannot be determined without the use of an esophageal balloon.4 Ideally, the volume lost owing to tubing compliance should be subtracted from the VT if the ventilator does not compensate for it, making the equation4: Cstatic = Adjusted VT Pplat − total PEEP) It may be more useful to follow trends in lung compliance, rather than making judgments on only one calculation. A downward trend in compliance means that the lungs or chest wall is stiffer, as in ARDS. Raw during volume ventilation is estimated by the difference between PIP and Pplat divided by the inspiratory flow (V̇ I) in L/s, provided that the flow is constant (square waveform)4: Raw = (PIP − Pplat ) VI During mechanical ventilation, the Pplat should be less than 28 cm H2O.5,6 At levels greater than 28 cm H2O, alveolar damage from overdistention is likely. This form of ventilator-induced lung injury (VILI) is referred to as volutrauma (see later). This trauma can result in air leakage from alveoli, the release of inflammatory mediators, and multisystem organ failure (MSOF). When the Pplat approaches 28 cm H2O during either volume or pressure ventilation, the pressure limit or the VT should be decreased. This approach to ventilation is referred to as lung protective ventilation.4–6 In addition the driving pressure, Pplat minus PEEP should be less than 15 cm H2O.7 Driving pressure greater than 15 cm H2O increases mortality and driving pressures less than 15 cm H2O decreases mortality. Many consider the driving pressure the most important variable in relation to ventilator induced lung injury.7 RULE OF THUMB  When measuring lung mechanics, Raw and compliance always use the same ventilator settings to make comparisons from one point in time to another much easier. In adults, typical settings are volume ventilation, VT 500 mL, square wave flow, and peak flow set at 60 L/min.

Mean Airway Pressure Mean airway pressure is the average pressure across the total cycle time (TCT). The mean airway pressure (PAW ) can be calculated manually if the flow is constant, as follows4: PAW =

1 2

(PIP − PEEP) × (Inspiratory time TCT) + PEEP

Mean airway pressure is computed by the ventilator as the integral of the pressure signal over the TCT (as a rolling average), so the RT can record the ventilator computed value rather than manually calculating it. Because expiratory (baseline) pressure is lower than inspiratory pressure, the mean pressure is between peak and end-expiratory pressure. The variables affecting mean pleural and mean airway pressure are summarized in Box 47.1. For a given minute volume, partial ventilatory support modes such as synchronized intermittent mandatory ventilation (SIMV) result in lower mean airway and pleural pressures than continuous

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BOX 47.1  Factors That Increase Mean

Airway Pressure

• Absence of spontaneous ventilation • Increasing positive pressure • Increasing duration of inspiration • Decreasing duration of expiration • Nature of inspiratory waveform • Increasing level of positive end-expiratory pressure • Decreasing compliance, increasing airways resistance

P

A

B

C

Fig. 47.6  Pressure patterns resulting from a descending ramp flow waveform (A), a sine wave flow waveform (B), and a constant flow waveform (C). Because waveform A has the highest pressure for the longest inspiratory time, it also has the greatest mean airway pressure.

mandatory ventilation (CMV) modes. For a specific mandatory breath, as peak pressure increases, so does mean pressure. Likewise, long inspiratory times increase mean pressure. Prolonging expiratory time has the opposite effect on mean airway pressure. In general, the harmful cardiovascular effects of PPV are more likely to occur when PAW or inspiratory-to-expiratory (I:E) ratio increases (e.g., >1 : 1). The pressure waveform of a mandatory breath affects mean pressure. In Fig. 47.6, for a given inspiratory time, the constant pressure pattern (curve A) results in the greatest area under the airway pressure curve and the highest mean airway pressure. A constant pressure pattern is normally produced by a pressure targeted breath that provides decreasing (descending ramp) flow. The effect of PEEP on mean airway pressure is simple: Every 1 cm H2O of applied PEEP increases the mean airway pressure 1 cm H2O.

Effect of Peak Airway Pressure on Lung Recruitment As peak airway pressure increases, previously collapsed, small, or partially fluid-filled alveoli are recruited (i.e., reopened).8 This reopening of alveoli increases alveolar surface area and restores functional residual capacity (FRC). At the alveolar level, the surface area available for diffusion is increased. As a result, PaO2 increases, consistent with Fick’s law. The use of extrinsic PEEP maintains the airways and recruited open alveoli. Extrinsic PEEP is controlled directly by the PEEP control on the ventilator, and the RT always knows how much extrinsic PEEP is present. Several factors, including inverse ratio ventilation (IRV), may add intrinsic

SECTION VI  Acute and Critical Care

Intrinsic PEEP (auto-PEEP) = Total PEEP − Extrinsic PEEP

Increased Lung Volume: Tidal Volume The volume delivered during pressure-controlled modes varies with changes in set pressure, patient effort, and lung mechanics. For all pressure-targeted modes, the volume delivered at a given pressure decreases as compliance decreases. An increase in resistance, active exhalation, or muscle tensing by the patient during inspiration also decreases delivered volume in pressure ventilation. If pressure serves as the limit variable instead of the cycle variable, changes in Raw during pressure-limited ventilation may or may not affect delivered volume. In this case, the key factor is the time available for pressure equilibration. Volume can remain constant even if Raw increases, as long as there is sufficient time for alveolar and airway pressures to equilibrate. However, if insufficient time is available for pressure equilibration, delivered volume decreases as Raw increases. The length of time needed for pressure equilibration is usually at least three times greater than the time constant for the respiratory system. In pressure modes, ventilatordelivered flow varies with patient effort and lung mechanics; this tends to avoid patient–ventilator asynchrony.9

Increased Functional Residual Capacity FRC is not known to change significantly with the application of PPV alone because passive exhalation allows the end-expiratory pressure to return to atmospheric pressure with each breath. If an increase in FRC is to be achieved, PEEP or CPAP must be applied. PEEP or CPAP does not recruit collapsed lung units but prevents lung units that have been opened from collapsing at end-expiration. Peak airway pressure recruits lung volume. The magnitude of the increase in FRC sustained by PEEP or CPAP is proportional to the lung-thorax compliance. With acute restriction, as PEEP is increased, lung compliance improves. Initially, the FRC gain as PEEP is added is small. There is no practical way of measuring FRC in all patients, so other methods of determining an increase in FRC are used, such as improving PaO2 at a constant FiO2, increasing PaO2/FiO2 ratio, decreasing shunt fraction, or decreasing FiO2 while maintaining PaO2. The management of PEEP is described in more detail in Chapter 49.

Pressure-Volume Curve and Lung Recruitment in Acute Respiratory Distress Syndrome Fig. 47.7 depicts the pressure-volume (P-V) relationship of the lung-thorax in an idealized patient with ARDS.8 On the inflation P-V curve, there are two points of inflection: the lower inflection point referred to as Pflex or lower corner pressure, and an upper inflection point, also referred to as upper corner pressure. These

1000 900 800 700 600 500 400 300 200 100 0

Pmc

lim b io n

Pcu lim b

la t In

fla

tio

n

D ef

PEEP or auto-PEEP by starting the next breath before the previous exhalation has ended. The amount of intrinsic PEEP added by IRV can be estimated by an end-expiratory pause, which stops the next breath from being delivered. During this endexpiratory pause, alveolar and mouth pressures equilibrate, and the total PEEP is now presented by the ventilator. The amount of auto-PEEP present is the difference between the total PEEP and the extrinsic PEEP:

Volume (mL)

1024

Pflex 0

10

20 30 Pressure (em H2O)

40

50

Fig. 47.7  Pressure-Volume (P-V) Curve of the Lung-Thorax Indicating the Inflation and Deflation Limbs. Arrows indicate direction of flow. PCL, Lower corner pressure or Pflex or lower inflection point; PCU, upper corner pressure or upper inflection point; PMC, point of maximum compliance change. (Modified from Godon S, Fujino Y, Hromi JM, et al: Optimal mean airway pressure during high frequency oscillation, Anesthesiology 94:862–868, 2001.)

two points represent defined changes in compliance. The lower inflection point represents an abrupt increase in lung-thorax compliance as collapsed or atelectatic lung begins to be recruited.10 The upper deflection point represents the point where the rate of lung recruitment decreases and over inflation begins.10 It is most important to realize from this graph that the lung is recruited by pressure and that the higher the peak airway pressure, the greater the potential for lung to be recruited. The maximum pressure needed to recruit a given patient’s lung is unknown; however, pressures up to 50 cm H2O most likely are safe with most patients when applied for short (1 to 3 minutes) periods.11–13 If these pressures were applied for longer periods, lung injury would most likely result. The deflation limb of the P-V curve is similar in shape to the inflation limb but is separated from the inflation limb. This hysteresis (separation) is a result of surfactant and surface tension interactions. Basically, less pressure is required to keep the lung open on the deflation limb of the P-V curve than on the inflation limb; this is obvious on examination of the volume maintained in the lung at Pflex, or 20 cm H2O. On the inflation limb, lung volume increases approximately 200 mL at 20 cm H2O, but on the deflation limb, lung volume increases approximately 550 mL. The goal of an open lung approach to ventilation that has been proposed by many authors is to open the lung and then to ventilate the patient on the deflation limb of the P-V curve at the least PEEP maintaining the lung open.11–13 Fig. 47.7 is an idealized P-V curve; actual patient P-V curves in ARDS are not as well defined. In approximately 20% of patients with ARDS, Pflex cannot be identified on the inflation P-V curve. As a result, despite two positive randomized controlled trials using Pflex to set PEEP,14,15 the use of P-V curves clinically has not become common practice; a second reason for this is the difficulty of measuring the P-V curve. However, many newer ICU ventilators are including algorithms that allow P-V curves to be performed by the ventilator with the ventilator identifying Pflex.

CHAPTER 47  Physiology of Ventilatory Support

The approach to setting PEEP that ensures ventilation on the deflation limb of the P-V curve and the minimal PEEP to sustain the benefit of lung recruitment is a decremental PEEP trial immediately after a lung recruitment maneuver (RM).13,14,16 Many different approaches to performing lung RMs have been published, but the approach that is considered the safest and most efficacious is the use of pressure-controlled continuous mandatory ventilation (PC-CMV).13,14,16 To perform a lung RM with PC-CMV, high enough PEEP must be set to avoid derecruitment after each inspiration. Essentially, a minimum of 20 cm H2O PEEP is required during the RM. Peak pressure is usually stopped at 40 cm H2O, but if the patient tolerates the pressure hemodynamically, it may be increased to 50 cm H2O (PEEP 35 cm H2O), ensuring a driving pressure of no more than 15 cm H2O (Box 47.2). Inspiratory time is increased to approximately 2.0 to 3.0 seconds, and respiratory rate is decreased to approximately 10 to 15 breaths/min. The maneuver is applied for 1 to 3 minutes. During the RM, the patient must be sedated to apnea to avoid fighting the ventilator. Before any RM, the patient must be hemodynamically stable. RMs should not be performed in patients with existing barotrauma or with a high likelihood of developing barotrauma (blebs or bullae) or in patients who are hemodynamically unstable. In addition, RMs are most effective and result in the least adverse reaction if performed early during ARDS. During and after the RM, the patient must be carefully monitored for hemodynamic and oxygenation instability and the development of barotrauma. After an RM, the best way to identify the minimum effective PEEP level that maintains the lung open is to perform a decremental PEEP trial.13,14,16 This trial is performed by changing the mode from PC-CMV to volume-controlled continuous mandatory ventilation (VC-CMV), VT 4 to 6 mL/kg, inspiratory time 1.0 second or less, PEEP 20 to 25 cm H2O, and rate set at the maximum that does not cause auto-PEEP.17 After stabilization (3 to 5 minutes), dynamic compliance is measured.17 PEEP is then decreased 2 cm H2O, the patient allowed to stabilize (30 to 45 seconds), and measurement of dynamic compliance is repeated;

BOX 47.2  Effects of Positive Pressure

Ventilation on System Other Than the Lungs Increased intracranial pressure Decreased cerebral perfusion pressure Decreased renal blood flow Decreased urinary output Decreased sodium and potassium excretion Increased plasma renin activity Increased plasma aldosterone level Increased vasopressin level Decreased atrial natriuretic hormone level Decreased liver and splanchnic perfusion Increased serum bilirubin level Decreased gastrointestinal function Gastric mucosal ischemia Development of stress ulcers Gastric distention

1025

this is continued until the PEEP level at which the compliance decreases is identified. In general, compliance at 20 to 25 cm H2O PEEP is low and increases as PEEP is decreased; compliance then decreases as PEEP is decreased further. Open lung PEEP is the PEEP associated with the highest compliance. Set PEEP is open lung PEEP plus 2 cm H2O. After open lung PEEP is identified, the lung is again recruited because during the decremental PEEP trial derecruitment occurred. After recruitment, PEEP is set at the identified level, ventilation is adjusted using a lung protective VT (4 to 8 mL/kg), and rate is adjusted to normalize PCO2. After all is set, FiO2 is decreased to the level that maintains PaO2 in the range of 55 to 70 mm Hg. Repeat RMs may be needed if the patient did not respond to the initial RM or if the patient is disconnected from the ventilator and derecruitment occurs. A successful RM is one that allows the FiO2 to be reduced to less than 0.5. The use of RM has been documented in many case series; however, no data have been published indicating that outcome is improved as a result of RMs and decremental PEEP settings. Research is ongoing. RULE OF THUMB A lung RM is most likely to be successful if it is performed early in the course of ARDS. Ideally a lung RM should be performed once the patient is fully stabilized after intubation and initiation of mechanical ventilation. The longer the patient is mechanically ventilated, the less likely it is that the RM would be successful.

Increased Dead Space The dead space fraction is increased with the institution of mechanical ventilation owing to inspiratory mechanical bronchodilation and the preferential ventilation of more nondependent alveoli, the reduction of blood flow away from ventilated alveoli, and the continued perfusion of basilar or dependent alveoli (see Fig. 47.5). This increase is concurrent with a decrease in V̇ /Q̇ ratio.

Decreased Work of Breathing Although improper ventilator management can increase WOB (poor patient–ventilator interaction, see Chapter 48 for details), one of the primary objectives of mechanical ventilation is to decrease WOB. PPV can significantly reduce WOB in patients with actual or impending respiratory muscle fatigue. RTs frequently see patients relax as the ventilator assumes a major portion of their WOB. To lessen WOB, ventilation must be sufficient to meet the patient’s needs. Otherwise, a spontaneously breathing patient tends to resist the ventilator, and an asynchronous breathing pattern develops. Inappropriately applied PPV can result in alveolar hypoventilation and consequently a considerable increase in the patient’s WOB. Mode, trigger setting, and inspiratory flow have an effect on WOB. WOB consists of two components: (1) ventilator work (WOBvent) occurring as the ventilator forces gas into the lungs and (2) patient work (WOBpt) as the inspiratory muscles draw gas into the lungs. The magnitude of WOBpt depends on compliance, resistance, and ventilatory drive and on ventilator variables,

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SECTION VI  Acute and Critical Care

such as trigger sensitivity, peak flow, cycling coordination, and VT.18,19 Regardless whether flow or pressure triggering is selected, either should always be set as sensitive as possible without causing autotriggering. The less sensitive the setting, the greater the patient effort. In older generation ventilators, flow triggering was shown to require less effort than pressure triggering.20 However, with the newest generation of ICU ventilators, both are equally effective.21 As described in Chapter 46, a mode of ventilation is a ventilatory pattern that can be described by identifying the control variable, breath sequence, and targeting scheme. The breath sequence may be thought of as being on a continuum from assuming very little to assuming all WOB. As the breath sequence is changed from continuous spontaneous ventilation (CSV) to CMV, the ventilator assumes more WOB. An example of this transition would be from CPAP to pressure support to CMV. In CPAP, a continuous spontaneous mode of ventilation, the patient assumes all WOB. The ventilator merely provides constant positive pressure throughout the patient’s breathing cycle. The ventilator assumes more WOB during CMV. Pressure support is also an example of CSV. During pressure support ventilation (PSV), the patient determines breath timing (length of inspiration and expiration) and frequency. Depending on the set inspiratory pressure, the clinician may program the ventilator to provide a minimal to a maximal amount of WOB. In instances where the patient has no spontaneous efforts, all breaths during CMV are time triggered and all work performed is WOBvent. Although it may be advantageous for the ventilator to assume all WOB for a while, extended periods of passive ventilation may cause diaphragmatic atrophy, which may unnecessarily prolong the need for mechanical ventilation and delay weaning. At initiation of patient-triggered pressure or volume modes, WOBpt resumes. During assisted ventilation, pressure-targeted modes are generally more capable of meeting patient ventilatory demands and minimizing WOBpt.22 As pressure level is increased, ventilatory muscles are unloaded, VT increases for a given amount of patient effort, and WOBpt decreases. Most clinicians increase pressure level until the breathing pattern approaches normal—that is, until the spontaneous ventilatory rate is 15 to 25 breaths/min and the spontaneous VT is normal (5 to 8 mL/kg). Measuring WOB is technically difficult. It is often accomplished by esophageal balloon monitoring, in which a balloon is placed in the distal third of the esophagus, and a pneumotachometer is attached to the airway (see Chapter 52). WOB is the integral of the esophageal pressure and VT. Normal WOB is 0.6 to 0.9 J/L.23

MINIMIZING ADVERSE PULMONARY EFFECTS OF POSITIVE PRESSURE MECHANICAL VENTILATION Decreasing Pressure The main objective of mechanical ventilation is to provide a minute ventilation appropriate to achieve adequate alveolar ventilation and supplemental O2 and PEEP to provide adequate arterial oxygenation.

MINI CLINI Overcoming an Increase in the Work of Breathing Problem A patient’s WOB is minimal during mechanical ventilation with an appropriate VT and rate. As the ventilator support is gradually discontinued and the patient is expected to take over more of WOB, Raw associated with breathing through an endotracheal tube may become clinically important. The RT must be able to recognize this problem readily and know how to correct it. A patient has received mechanical ventilation in volume-controlled continuous mandatory ventilation mode for the past week. The patient’s condition is now clinically stable, and ventilation is provided by PSV. As the PSV pressure level is reduced to 8 cm H2O, the patient begins using accessory muscles to breathe, the spontaneous respiratory rate increases to 30 breaths/min, and the patient reports shortness of breath. Blood gas values are acceptable, and no abnormal lung sounds are present. What is the problem, and what should the RT do? Solution The patient may be experiencing excessive WOB because of Raw associated with the endotracheal tube; a small sized tube or partial obstruction of the tube with secretions may be the problem. Other possibilities that should be considered include deterioration in the patient’s cardiopulmonary status, but the normal blood gas values and lung sounds suggest the problem is not the lungs. Passing a suction catheter through the tube may help to identify the problem. If the catheter does not pass easily, the tube may be partially obstructed. Two options exist: change the tube or extubate the patient. Because the tube would need to be removed regardless of the choice, a trial extubation should be considered. Because this patient is at risk immediately after extubation, noninvasive ventilation should be started. If the patient cannot tolerate extubation, an appropriate-sized endotracheal tube can be reinserted.

Peak pressure is the result of the pressure required to overcome system resistance and compliance. Although there is no absolute maximum pressure, most practitioners try to avoid peak pressures greater than 40 cm H2O. As the peak pressure approaches 40 cm H2O, it is important to consider the causes. Factors that increase Raw include airway edema, bronchospasm, and secretions and ETT obstruction. The RT can manage or avoid these problems by ensuring adequate humidity, bronchial hygiene (suctioning, airway care), and administration of bronchodilators and antiinflammatory drugs. Factors that increase the pressure needed to inflate the lung and overcome compliance include alveolar and interstitial edema, atelectasis, fibrosis, and chest wall restriction. Pplat reflects mean maximum Palv. Pplat of 28 cm H2O or greater has an increased likelihood of causing lung injury.4–6 If Pplat approaches 28 cm H2O during volume ventilation, the VT should be decreased so that the Pplat is less than 28 cm H2O, or with pressure ventilation, target pressure should be set less than 28 cm H2O.5,24 The patient population where this guideline is most likely violated is the markedly obese patient who may require more than 20 cm H2O PEEP. (See Chapter 30.) Driving pressure is the difference between Pplat and total PEEP and should not exceed 15 cm H2O.7 As described earlier, the lower the driving pressure the lower the risk of mortality. Even in the markedly obese patient, if the VT and PEEP are set properly the driving pressure can be kept below 15 cm H2O, even when the Pplat exceeds 28 cm H2O.

CHAPTER 47  Physiology of Ventilatory Support

Mean airway pressure is decreased by decreasing inspiratory time, VT, respiratory rate, PEEP, or PIP. Increased mean airway pressure reduces venous return and may reduce cardiac output. RULE OF THUMB  Driving pressure (plateau pressure minus PEEP) should be less than 15 cm H2O. Driving pressure greater than 15 cm H2O increase mortality and driving pressures less than 15 cm H2O decrease mortality. Many consider the driving pressure the most important variable in relation to ventilator induced lung injury.

Positive End-Expiratory Pressure or Continuous Positive Airway Pressure PEEP is the application of positive pressure at end-exhalation. PEEP is used primarily to improve oxygenation in patients with refractory hypoxemia. As a rule, refractory hypoxemia exists when PaO2 cannot be maintained at greater than 50 to 60 mm Hg with FiO2 0.50 or greater. PEEP improves oxygenation in these patients by maintaining alveoli open, restoring FRC, and decreasing physiologic shunting. The improved alveolar volume provided by PEEP allows a lower FiO2. Other values such as lung compliance, shunt fraction, and PaO2/FiO2 ratio also may improve when PEEP is appropriately applied. PEEP may be indicated in the care of patients with COPD who have dynamic hyperinflation (auto-PEEP).25,26 (See discussion later in this chapter.) Beneficial and harmful effects are associated with the use of PEEP (Table 47.2). Detrimental effects of inappropriately high levels of PEEP include decreased cardiac output, increased pulmonary vascular resistance, and increased dead space. When one or more of these problems occur, PEEP is decreased to the previous level or to a value between the current level and the previous level. If cardiac output decreases and an increase in PEEP is necessary to maintain oxygenation, intravenous fluid, inotropic cardiac drugs, or both are administered to restore cardiac output. PEEP is contraindicated in the presence of a tension pneumothorax. PEEP should be applied cautiously in patients with severe unilateral lung disease because PEEP would overinflate the lung with higher compliance. The result is lung overdistention and compression of adjacent pulmonary capillaries. Independent lung ventilation can be used to apply separate inspiratory and baseline pressures to the right and the left lung when severe

TABLE 47.2  Physiologic Effects of Positive

End-Expiratory Pressure Beneficial Effects of Appropriate PEEP

Detrimental Effects of Inappropriate PEEP

Restored functional residual capacity, avoids derecruitment Decreased shunt fraction

Increased pulmonary vascular resistance Potential decrease in venous return and cardiac output Decreased renal and portal blood flow Increased intracranial pressure Increased dead space

Increased lung compliance Decreased work of breathing Increased PaO2 for a given FiO2

PEEP, Positive end-expiratory pressure.

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unilateral lung disease is present.27 PEEP is not contraindicated in the care of patients with increased ICP, caution must be used to prevent the application of PEEP from increasing ICP further. In general, if the head of the bed can be elevated to a height equal to the amount of PEEP applied, the hydrostatic pressure increase caused by the PEEP can by offset by the elevation of the head of the bed. RULE OF THUMB Refractory hypoxemia exists when PaO2 cannot be maintained at greater than 50–60 mm Hg with FiO2 0.50 or greater. This situation is an indication for PPV with PEEP or CPAP because an increased endexpiratory pressure with either of these modalities improves oxygenation by stabilizing lung open decreasing physiologic shunting.

Effects of Ventilatory Pattern The most commonly used inspiratory flow patterns are constant or square and descending ramp during volume-controlled ventilation and exponential decay during pressure-controlled ventilation. In mechanical and computer models, a descending ramp (volumecontrolled ventilation and pressure control ventilation) flow pattern improves gas distribution to lung units with long-time constants. The literature often refers to the descending ramp as a decelerating flow pattern. Similar findings in humans have been reported. Compared with a square flow waveform, a descending ramp has been shown to reduce peak pressure, inspiratory work, VD/VT, and P(A − a)O2 without affecting hemodynamic values.28 In addition, compared with volume-controlled ventilation with a square flow waveform, pressure-controlled ventilation with an exponential decay flow waveform may result in a higher PaO2, lower PaCO2, and lower PIPs. However, mean airway pressure is higher with pressure-controlled ventilation compared with volume-controlled ventilation because pressure rapidly increases to the set inspiratory pressure and remains constant throughout inspiration. During pressure-controlled ventilation, flow is responsive to patient demand. The ventilator delivers flow to the patient in proportion to patient demand. Flow is also greater at the onset of inspiration, resulting in VT delivery at a time when the lungs are most compliant, the beginning of the breath. As a breath ends, flow is least, and the volume delivered is small. The result is a lower peak airway pressure for any given VT. In most spontaneously breathing persons, lower inspiratory flows improve gas distribution. However, during PPV, low inspiratory flow may lead to lengthy inspiratory times and air trapping if expiratory time is too short. High ventilator inspiratory flow allows more time for exhalation and reduces the incidence of air trapping. Avoidance of air trapping improves gas exchange and reduces WOB in patients with high ventilatory demands.19,29 An inflation hold also affects gas exchange. By momentarily maintaining lung volume under conditions of no flow, an inflation hold allows additional time for gas redistribution between lung units with different time constants. In both animal and human studies, increasing the length of an inflation hold decreases the VD/VT, PaCO2, and inert gas washout time. Adding an inflation hold effectively increases total inspiratory time, shortening the time available for exhalation and predisposes patients with airway obstruction to auto-PEEP. In practice, an inflation hold

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should be used only to obtain Pplat values. Because the technique prevents the onset of exhalation, asynchrony occurs if the patient is actively breathing.

Trigger Site and Work of Breathing Studies have examined the effects of sensing a patient’s inspiratory effort at the tip of the endotracheal tube rather than in the ventilator circuit, as is done with all ventilators. Triggering and managing gas delivery by measurement of pressure at the tip of the endotracheal tube decreases patient effort and improves synchrony; however, no practical system has been designed.30 In addition, the efficiency of ventilator flow and pressure triggering seems to improve with each new generation of mechanical ventilator.

PHYSIOLOGIC EFFECTS OF VENTILATORY MODES Volume-Controlled Ventilation Versus Pressure-Controlled Ventilation Fig. 46.5 illustrates the important variables for volume ventilation modes. The figure shows that the primary variable to be

controlled is the patient’s minute ventilation. A particular ventilator may allow the operator to set minute ventilation directly. More frequently, minute ventilation is adjusted by means of a set VT and frequency. VT is a function of the set inspiratory flow and the set inspiratory time. Inspiratory time may be affected by the set frequency and, if the I:E ratio is set. The mathematical relationships among all these variables are shown in Table 47.3. With pressure-controlled ventilation, the goal is also to maintain adequate minute ventilation. However (as the equation of motion shows), when pressure is controlled, VT and minute ventilation are determined not only by the ventilator’s pressure settings but also by the elastance and resistance of the patient’s respiratory system. Minute ventilation and hence gas exchange are less stable in pressure-controlled modes than in volumecontrolled modes. Fig. 46.6 shows the important variables for pressure-controlled ventilation. VT is not operator set. It is the result of the patient inspiratory effort, the set inspiratory pressure, the patient’s lung mechanics, and the inspiratory time. On most ventilators, the speed with which inspiratory pressure is achieved (i.e., the pressure rise time) is adjustable. That adjustment affects the shape of the pressure waveform and the mean airway pressure.

TABLE 47.3  Equations Relating the Important Parameters for Volume-Controlled and

Pressure-Controlled Ventilation Mode

Parameter

Symbol

Volume-controlled

Tidal volume (L)

VT

Mean inspiratory flow (L/min)

V1

Tidal volume (L)

VT

Instantaneous inspiratory flow (L/min)

v̇ 1

Pressure gradient (cm H2O) Exhaled minute ventilation (L/min) Total cycle time or ventilatory period (s)

ΔP V̇ E TCT

I:E ratio

I:E

Time constant (s)

τ

Resistance (cm H2O/L/s)

R

Compliance (L/cm H2O)

C

Elastance

E

Mean airway pressure (cm H2O)

Paw

Pressure (cm H2O) Volume (L) Flow (cm H2O/L/s) Time (s) Inspiratory time (s) Expiratory time (s) Frequency (breaths/min) Base of natural logarithm (≈2.72)

P V V̇ τ TI TE f e

Pressure-controlled

Both modes

Primary variables

Equation VT = V̇ E ÷ f VT = V̇ I ÷ TI VI = 60 × VT ÷ TI v × TCT v1 = E T1 VT = ΔP × C × (1 − e−t/τ) ∆P v 1 =   e− t τ  R  ΔP = PIP − PEEP V̇ E = VT × f TCT = TI + TE = 60 ÷ f T I : E = TI : TE = 1 TE τ=R×C ∆P R=  ∆V ∆V ∆P 1 E= C t = TCT 1  Paw =   ∫ Paw dt  TCT  t =0 C=

CHAPTER 47  Physiology of Ventilatory Support

Continuous Mandatory Ventilation CMV (also referred to as assist/control) is a mode of ventilation in which total ventilatory support is provided by the mechanical ventilator. All breaths are mandatory and delivered by the ventilator at a preset volume or pressure, breath rate, and inspiratory time. If the patient has spontaneous respiratory efforts, the ventilator delivers a patient-triggered breath. If patient efforts are absent, the ventilator delivers time-triggered breaths. The clinician needs to set an appropriate trigger level and flow rate for the patient in this mode of ventilation. There is a potential for the ventilator to autotrigger when the trigger level is set too sensitive. As a result, hyperventilation, air trapping, and patient anxiety often ensue. However, if the trigger level is not sensitive enough, the ventilator does not respond to the patient’s inspiratory efforts, which results in increased WOB. Occasionally, all attempts to optimize patient comfort, reduce WOB, and achieve the goals of this mode of ventilation are futile. In cases in which this mode is poorly tolerated and spontaneous triggering is counterproductive to the goals set for a particular patient, sedation or paralysis or both may be required. These agents may be used to minimize patient effort and normalize WOB.

Volume-Controlled Continuous Mandatory Ventilation VC-CMV is indicated when a precise minute ventilation or blood gas parameter, such as PaCO2, is therapeutically essential to the care of patients.29 Theoretically, volume control (with a constant inspiratory flow) (Fig. 47.8) results in a more even distribution of ventilation (compared with pressure control) among lung units with different time constants where the units have equal resistances but unequal compliances (e.g., ARDS).30

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During VC-CMV, volume is guaranteed, but airway pressure varies depending on changes in the patient’s lung mechanics. A reduction in lung compliance or an increase in resistance causes higher peak airway pressures. Care should also be taken when setting the inspiratory flow. Avoid setting a flow that fails to match patient needs or exceeds patient demand. An insufficient flow rate would result in an imposed increase in the patient’s WOB and a concomitant increase in O2 consumption. The inspiratory phase may be prematurely shortened if the set inspiratory flow exceeds patient demands. Meticulous patient monitoring and use of VC-CMV allow the clinician to achieve precise and predictable physiologic results. VC-CMV results in gas exchange and hemodynamic stability at the same level as PC-CMV, and either can be used effectively during controlled ventilation; the patients are passively ventilated. However, when the patient is actively triggering the ventilator, better patient ventilator synchrony and less WOB are achieved during PC-CMV than VC-CMV.

Pressure-Controlled Continuous Mandatory Ventilation Similar to VC-CMV, PC-CMV can be used as a basic mode of ventilatory support. The primary difference between volumecontrolled and pressure-controlled ventilation is the control variable with which the clinician is most concerned.31,32 Theoretically, pressure control (with a constant inspiratory pressure) (Fig. 47.9) results in a more even distribution of ventilation (compared with volume control) among lung units with different time constants when units have equal compliances but unequal resistances.30 The instability of VT caused by airway leaks can be minimized by using pressure-controlled rather than volumecontrolled ventilation. Increased VT stability may lead to better gas exchange and lower risk of pulmonary volutrauma.33

Fig. 47.8  Volume-Controlled Continuous Mandatory Ventilation. Top, VT; middle, flow; bottom, airway pressure waveform. VT, Tidal volume.

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Fig. 47.9  Pressure-Controlled Continuous Mandatory Ventilation. Top, VT; middle, flow; bottom, airway pressure waveform. VT, Tidal volume.

Use of a rectangular pressure waveform opens alveoli earlier in the inspiratory phase during PC-CMV and results in a higher mean airway pressure than VC-CMV with a rectangular flow waveform, allowing more time for oxygenation to occur.34 However, in PC-CMV, inspiratory flow is not a parameter set by the clinician. It is variable and dependent on patient effort and lung mechanics, improving patient comfort and patientventilator synchrony. However, as lung mechanics or patient effort or both change, volume delivery (VT and minute ventilation) changes. Because VT is not directly controlled, the driving pressure (Pplat − PEEP) is the primary parameter used to alter the breath size and CO2 tensions. Typically, PIP is adjusted to provide the patient with a VT within the desired range.35 As with VC-CMV, the mandatory breath rate set by the clinician depends on the presence of ventilatory muscle activity and the severity of lung disease. When higher mandatory breath rates are needed (>30 breaths/min), it is essential for the clinician to provide a sufficient expiratory time and prevent air trapping. As long as lung mechanics and patient effort remain constant, the volume and peak flow delivered to the patient remain unchanged.36 When patient effort decreases, or compliance decreases, or resistance increases, less volume is delivered for the preset pressure for each breath. Conversely, improvements in patient effort and mechanics can dramatically increase the volume delivery to the patient in this mode. Close VT monitoring is required to avoid ventilator-induced hyperventilation or hypoventilation and ventilator-induced lung injury. The patient’s cardiac index and O2 consumption should be closely monitored as well. Higher mean airway pressures may impair cardiac output. In addition, PC-CMV with IRV can lead

to the development of auto-PEEP, which can impair venous return, compromise O2 delivery to the tissues, and result in marked air trapping.37

Pressure-Controlled Inverse Ratio Ventilation PC-CMV may be used to accomplish pressure-controlled inverse ratio ventilation (PC-IRV), by increasing the inspiratory time directly or by increasing the I:E ratio to the desired value. PC-IRV is defined as pressure-controlled ventilation with an I:E ratio greater than 1 : 1 (Fig. 47.10). Although some studies have shown improvement in oxygenation with PC-IRV versus CMV with PEEP, others have shown concurrent decreases in cardiac output.31,38 In general, if applied PEEP in normal ratio ventilation is equal to total PEEP (applied and intrinsic PEEP) in PC-IRV, the oxygenation benefits are equivalent without the marked depression in cardiac output.

Intermittent Mandatory Ventilation As a partial support mode, IMV allows or requires the patient to sustain significant WOB. The level of mechanical support needed depends on the specific physiologic process causing the need for mechanical ventilation, presence or degree of ventilatory muscle weakness, and presence and severity of lung disease. In this mode, mandatory breaths are delivered at a set rate. Between the mandatory breaths, the patient can breathe spontaneously at his or her own VT and rate (Fig. 47.11). Breaths can occur separately (e.g., IMV); breaths can be superimposed on each other (e.g., spontaneous breaths superimposed on mandatory breaths, as in bilevel positive airway pressure [bilevel PAP] or airway pressure release ventilation [APRV]); or mandatory breaths can be superimposed on spontaneous breaths, as in

CHAPTER 47  Physiology of Ventilatory Support

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Fig. 47.10  Pressure-Controlled Inverse Ratio Ventilation. The flow waveform for any breath does not return to baseline before the next breath, resulting in auto–positive end-expiratory pressure and an increase in mean airway pressure. Top, VT; middle, flow; bottom, airway pressure waveform. VT, Tidal volume.

MINI CLINI Using Pressure-Controlled Ventilation Problem The RT is caring for a 20-year-old patient with ARDS. The patient has no respiratory effort. Current ventilator settings are as follows: Mode: VC-CMV VT: 400 mL Frequency: 25 breaths/min PEEP: 14 cm H2O FiO2: 1 PIPs monitored on the ventilator: 35–40 cm H2O Mean airway pressure: 20–22 cm H2O Plateau pressure: 27 cm H2O An arterial blood gas is obtained, which reveals pH 7.28, PCO2 41 mm Hg, and PO2 50 mm Hg. The physician would like to employ pressure-controlled ventilation. What are the appropriate initial settings in PC-CMV mode to maintain the current minute ventilation? Solution Initial ventilator setting would be as follows: Ventilator frequency, PEEP, and FiO2: the same Frequency: 25 breaths/min PEEP: 14 cm H2O FiO2: 1

high-frequency ventilation administered during spontaneous breathing. Spontaneous breaths may be assisted (e.g., PSV) (Fig. 47.12) or unassisted. When the mandatory breath is patient-triggered, modern day ventilators deliver the mandatory breath in synchrony with the patient’s inspiratory effort. If no spontaneous efforts occur, the ventilator delivers a time-triggered breath. Because spontaneous

To keep the minute ventilation constant, the RT needs to set the PIP high enough to deliver the same VT as in volume control (400 mL). 1. Calculate the patient’s respiratory system compliance: Compliance = VT Pplat − total PEEP = 400 mL 27 cm H2O − 14 cm H2O = 31mL cm H2O 2. Calculate the pressure limit in PC-CMV mode to achieve the target VT. Because the pressure limit is measured relative to PEEP on this ventilator, the equation is: Ventilating pressure = VT Compliance = 400 mL 31mL cm H2O = 13 cm H2O PIP in PC = ventilating pressure + PEEP PC set 13 cm H2O + peep 14 cm H2O or 27 cm H2O A shortcut is to realize that the required pressure limit is the Pplat on VC-CMV. The PIP (relative to atmospheric pressure) is 27 cm H2O.

breaths decrease pleural pressure, ventilatory support with IMV usually results in a lower mean intrathoracic pressure than CMV, which can result in a higher cardiac output.39 When used to wean a patient from mechanical ventilation, the intent of IMV is to provide respiratory muscle rest during the mandatory breaths and exercise during spontaneous breaths. However, studies have shown that IMV increases the WOB,

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MINI CLINI Determining Appropriate Ventilator Rate Problem A 36-year-old woman with traumatic brain injury was intubated in the emergency department with a 7-mm endotracheal tube and transferred to the RT in the neurointensive care unit. She is paralyzed and sedated. Her current ventilator settings are as follows: Mode: VC-CMV VT: 405 mL Frequency: 15 breaths/min FiO2: 0.5 The pulse oximeter displays 97%, and end-tidal CO2 monitor is reading 49. The patient’s weight is estimated at 45 kg. End-tidal CO2 is stable and 4 mm Hg higher than PaCO2. The clinical goal is to minimize ICP. Because intracranial blood flow is inversely proportional to PaCO2, ventilation should be increased to maintain PaCO2 at approximately 35–40 mm Hg. The RT needs to make appropriate ventilator changes to achieve the target PaCO2. Discussion The current VT is already large at 8 mL/kg. The increase in ventilation must be achieved by increasing frequency. Because the patient is paralyzed, the ventilation level is controlled by the set frequency, and PaCO2 is predictable. The new frequency required is calculated using the following equation: Required frequency = Current frequency × Current PaCO2 Desired PaCO2 Re quired frequency = 15 breaths min × 49 mm Hg 35 mm Hg = 21breaths min

asynchrony and weaning prolongs the duration of mechanical ventilation compared with PSV and spontaneous breathing trials.40,41 In general at this stage in the development of ventilatory support we would recommend against the routine use of SIMV.

Volume-Controlled Intermittent Mandatory Ventilation Volume-controlled intermittent mandatory ventilation (VC-IMV) has been advocated for patients with relatively normal lung function recovering from sedation or rapidly reversing respiratory failure.42,43 However, the use of IMV has greatly decreased over the years in favor of VC-CMV, PC-CMV, and PSV, and there are no specific situations in adults where IMV would be the optimal mode. Pressure-Controlled Intermittent Mandatory Ventilation PC-IMV has been traditionally associated with mechanical ventilation of infants not only because of their oxygenation problems but also because traditionally it had been difficult to control VT at such small values.44,45 Liberation from this mode involves the gradual reduction of the PIP and the mandatory breath rate. As lung compliance improves, adjustments in PIP are necessary to prevent overdistention of the lung. Adjustments in PIP and set mandatory breath rate are critical to prevent hyperventilation. Airway Pressure Release Ventilation A mode related to both PC-IRV and PC-IMV is APRV, in which the patient breathes spontaneously throughout periods of high and low applied CPAP (Fig. 47.13).46 APRV intermittently

Fig. 47.11  Volume-Controlled Synchronized Intermittent Mandatory Ventilation + Continuous Positive Airway Pressure. Top, VT; middle, flow; bottom, airway pressure waveform. VT, Tidal volume.

CHAPTER 47  Physiology of Ventilatory Support

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Fig. 47.12  Volume-Controlled Synchronized Intermittent Mandatory Ventilation + Pressure Support Ventilation (PSV). The addition of PSV to the spontaneous breaths increases spontaneous tidal volume. Top, VT; middle, flow; bottom, airway pressure waveform. VT, Tidal volume.

Fig. 47.13  Airway Pressure Release Ventilation (APRV). In APRV, the patient is able to breathe spontaneously throughout the total cycle time. Top, VT; middle, flow; bottom, airway pressure waveform. VT, Tidal volume.

decreases or “releases” the airway pressure from an upper pressure (Phigh) or CPAP level to a lower pressure (Plow) or CPAP level. The pressure release usually lasts approximately 0.2 to 1.5 seconds depending on whether or not air trapping is desired. In Fig. 47.13, inspiratory time is longer than expiratory time, and spontaneous breaths are superimposed on this mandatory

pattern of pressurization and release. Spontaneous breaths may be supplemented by PSV. This is a feature of APRV available on some ventilators, where APRV is referred to as bilevel ventilation. In APRV, the I:E ratio is usually greater than 1 : 1, which is similar to PC-IRV, but APRV allows spontaneous breathing throughout inspiratory and expiration.47

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SECTION VI  Acute and Critical Care

APRV also provides ventilation and oxygenation without adversely affecting hemodynamic values because of the periodic reductions in intrathoracic pressure during the spontaneous breaths. In addition, peak airway pressure during APRV may be less than with VC-IRV for comparable oxygenation and ventilation.48 APRV compared with conventional volume-controlled or pressure-controlled SIMV showed that with APRV there was a decrease in peak airway pressures, improved hemodynamics, and a decreased need for vasopressor and inotropic support.49 However, the cost of these potential benefits is patient effort; WOB is markedly increased and PTP is excessive, potentially inducing lung injury during APRV.47 There are no data to indicate a better outcome with APRV than with other approaches to ventilatory support when a similar approach to managing oxygenation is used. Specific indications for APRV are unclear. Recent data imply that APRV results in greater mortality in pediatric patients than conventional ventilatory modes of ventilation,

Continuous Spontaneous Ventilation Spontaneous breath modes include modes in which all breaths are initiated and ended by the patient. The level of support these modes of ventilation provide determines the amount of WOB the patient ultimately assumes. CPAP, PSV,50 automatic tube compensation (ATC), proportional assist ventilation (PAV), and neurally adjusted ventilatory assist (NAVA) are continuous spontaneous breath modes.51

Continuous Positive Airway Pressure CPAP is spontaneous breathing at an elevated baseline pressure (Fig. 47.14). Breaths are patient-triggered and cycled.52,53 VT depends on patient effort and lung mechanics. CPAP increases Palv and maintains alveoli open. In contrast to NPV and PPV,

airway pressure with CPAP is theoretically constant (baseline pressure ±2 cm H2O) throughout the respiratory cycle. Because airway pressure does not change, CPAP does not provide ventilation. For gas to move into the lungs during CPAP, the patient must create a spontaneous PTA gradient. Although NPV and PPV produce the pressure gradients needed for gas flow into the lungs, CPAP maintains alveoli at greater inflation volume, restoring FRC. An important physiologic feature of CPAP is that as alveoli are maintained open, FiO2 needed to maintain adequate PaO2 may decrease. Oxygenation becomes more efficient at any given FiO2, as measured by PaO2/FiO2 ratio and shunt fraction. The potential side effects associated with PPV also exist for CPAP but usually to a lesser degree.

Pressure Support Ventilation PSV is a form of PC-CSV that assists the patient’s inspiratory efforts (Fig. 47.15). At very low levels of support, this mode unloads WOB the ventilator circuitry imposes on the respiratory muscles.54 If the level of support is maximized, the ventilator may assume all WOB.55 The result of high levels of support is a reduction in the respiratory rate, reduction in respiratory muscle activity, reduction in O2 consumption, and improvement or stabilization of spontaneous VT.56,57 However, the positive attributes of this mode of ventilation can be negated if ventilator parameters are not properly set. The ventilator must be able to detect spontaneous patient effort. It is critical for the clinician to adjust the trigger sensitivity correctly. Of equal importance is the clinician-set rise time, the time required for the ventilator to reach the inspiratory pressure limit, and termination criteria, the minimal flow resulting in cycling to exhalation (see Chapter 48). Ventilator graphics are often helpful when adjusting these parameters and optimizing patient–ventilator synchrony.

Fig. 47.14  Continuous Positive Airway Pressure. Top, VT scalar; middle, flow scalar; bottom, airway pressure scalar. VT, Tidal volume.

CHAPTER 47  Physiology of Ventilatory Support

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Fig. 47.15  Pressure Support Ventilation. Top, VT; middle, flow; bottom, airway pressure waveform. VT, Tidal volume.

Regardless of the level of support provided, the patient has primary control over the breath rate and inspiratory time and flow rate delivered during this mode of assisted ventilation. The VT resulting from a PSV breath depends on the preset pressure level, patient effort, and mechanical forces opposing ventilation (lung–chest wall compliance and Raw). Of all of the classic modes of ventilation, PSV exerts the least control over the patient’s ventilatory pattern and as a result should improve patientventilator synchrony. Since the first description of PSV in 1982, it has been used either to overcome the imposed resistance associated with the artificial airway or to provide ventilatory support with minimal control.58 PSV is useful in any patient with an intact ventilatory drive and a stable ventilatory demand. Bilevel PAP (BiPAP; Respironics, Inc., Murrysville, PA) is simply PSV with PEEP applied noninvasively.59 With bilevel PAP, inspiratory positive airway pressure (or PSV) and PEEP are set. The duration of inspiratory positive airway pressure and expiratory positive airway pressure can be independently adjusted to set the I:E ratio. Although it was originally developed to enhance the capabilities of home CPAP systems used for management of obstructive sleep apnea, bilevel PAP has been successfully used in the home and the hospital for noninvasive ventilatory support of patients with acute and chronic respiratory failure.60 (See Chapter 50 for details.) Example.  An example of the use of PC-CSV is noninvasive PSV and PEEP in the management of a patient with COPD in an acute exacerbation. As described in detail in Chapter 50, noninvasive ventilation has been shown in this setting to decrease the frequency of intubation, length of mechanical ventilation, development of ventilator-associated pneumonia, and patient mortality.

Proportional Assist Ventilation PAV is based on both the mechanics of the total respiratory system and the resistive properties of the artificial airway; that is, the ventilator delivers a pressure assist in proportion to the patient’s desired VT (volume assist) and to the patient’s instantaneous inspired flow (flow assist). The response of these two aspects of ventilatory assistance is automatically adjusted to meet changes in the patient’s ongoing ventilatory demand. This algorithm is based on the law of motion as it applies to the respiratory system: Pmusc + Pappl = (Volume × E) + (Flow × R) where Pmusc is pressure generated by the respiratory muscles, Pappl is pressure applied by the ventilator, and E and R are elastic and resistance properties of the respiratory system. Assuming that E and R are linear during inspiration, the instantaneous flow and volume to be delivered are proportional to the resistive and elastic WOB. The ventilator continuously measures the instantaneous flow and volume and periodically measures the E and R. Using this information, the ventilator software adjusts gas delivery by estimating Pmusc and assisting Pmusc in a proportional manner, the percentage of support set by the clinician. The patient is the determinant of the ventilatory pattern. Patients are given the freedom to select a ventilatory pattern that is rapid and shallow or slow and deep. If the patient desires a small VT, a low level of pressure is applied, and if a large VT is desired, a high pressure is applied. The ventilator does not force any control variable except the unloading of E and R in a proportional manner. See Chapter 46 for details on operation of PAV. Numerous studies have evaluated the effect of PAV during noninvasive PPV.61–65 Most of these comparisons were between

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PAV and PSV,61,65 and in almost all of these comparisons the patients evaluated had chronic respiratory failure and were in an acute exacerbation. Patients managed with PAV had a lower refusal rate, had a more rapid reduction in respiratory rate, and developed fewer complications.63,64 In these studies, gas exchange and respiratory pattern did not differ between PSV and PAV, but the patients ventilated with PAV were more comfortable. PAV has also been shown to be essentially equivalent to PSV in stable patients with chronic ventilatory failure62 and in patients with acute cardiogenic pulmonary edema.65 PAV has been most widely studied during invasive mechanical ventilation.66–68 As with the evaluation of PAV in other settings, most of the comparisons focused on the physiologic response observed when PSV is changed to PAV. In general, during invasive ventilation, the change from PSV to PAV results in lower VT, more rapid respiratory rate, lower peak airway pressure, and lower mean airway pressure without significant changes in gas exchange or hemodynamics.69–71 In a randomized comparison of PAV versus PSV each for a 48-hour period in a series of critically ill patients,68 the percentage of patients’ failing the transition to PAV or PSV differed, 11% failing PAV versus 22% failing PSV. In addition, the proportion of patients developing asynchrony was greater with PSV versus PAV. The current data on PAV indicate it can sustain the same patients as PSV— patients who can breathe spontaneously and manage their ventilator drive normally.

Neurally Adjusted Ventilatory Assist From a conceptual perspective, NAVA is essentially the same as PAV except that PAV responds to changes in airway pressure and flow, whereas NAVA responds to changes in diaphragmatic electromyograph (EMG) activity. However, for NAVA to function properly, a specially designed nasogastric catheter with a 10-cm length of EMG electrodes must be in place. Both PAV and NAVA respond to patient effort providing ventilatory support in a proportional manner. The clinician does not set pressure, volume, flow, or time in either mode. The only parameter set is the proportion of effort unloaded by the ventilator; in NAVA, this is set as the number of cm H2O pressure applied per microvolt of inspiratory diaphragmatic EMG activity. NAVA responds similarly to PAV; when compared with pressure support, NAVA results in low airway pressures, smaller tidal volumes, more rapid rates, and increased patient–ventilator synchrony.72,73 PEEP titration also affects baseline diaphragmatic EMG activity. As PEEP is increased, EMG activity decreases. Minimal EMG activity seems to correspond to optimal PEEP level.74 NAVA application in neonates results in similar outcomes as observed in adults.75,76 After the change to NAVA, VT tends to decrease, respiratory rate to increase, and peak diaphragmatic EMG activity to decrease. In addition, despite the open ventilating system (uncuffed artificial airway), triggering and cycling are still primarily neurally activated.75,76 The most important advantage of PAV and NAVA over traditional modes of ventilation is improved synchrony. The specific indications for PAV and NAVA are not fully established; however, both can be reasonably used in any patient with an intact

ventilatory drive. The primary indication would be a patient with a significant level of asynchrony.

Automatic Tube Compensation ATC is similar to the flow assist aspect of PAV but considers only the resistance of the endotracheal tube.77 ATC is an adjunct that automatically adjusts the airway pressure to compensate for endotracheal tube resistance to gas flow by maintaining tracheal pressure constant at the baseline level.77 The goal is to eliminate WOB imposed by the endotracheal tube. In ATC, the RT inputs into the ventilator the type and size of artificial airway (endotracheal tube or tracheostomy tube) and the percentage compensation desired (10%–100%). The ventilator continuously measures flow and calculates the amount of pressure needed to overcome the resistance of the airway (pressure = resistance × flow). As a result, the greater the inspiratory demand, the greater the pressure applied. Pressure varies throughout the breath. ATC may be applied during inspiration (positive airway pressure) or during both inspiration and expiration (negative airway pressure). However, expiratory ATC may result in early airway closure and increased air trapping. ATC has been referred to as electronic extubation, meaning that if the airway pressure is low during inspiration (5 to 7 cm H2O), it is simply overcoming the resistance of the endotracheal tube with a normal inspiratory effort.78 Consequently, many clinicians consider this an indication that spontaneous ventilation can be maintained without ventilatory support and the patient should be considered for extubation. Although in theory the use of ATC to wean patients appears ideal, no data to date have indicated that ATC weans patients faster than spontaneous breathing trials. Adaptive Modes and Dual Control The first adaptive control/dual control mode was described by Amato and colleagues.79 Their major finding was that the ventilatory workload imposed on the inspiratory muscles during volume-assured PSV was significantly reduced using dual control. In this mode, pressure support is combined with volume control. However, this benefit was due to the fact that inspiration started out in pressure support and stayed there unless the VT target was not met. The improvement was mostly a result of the improved synchrony between the patient and the machine. These investigators did not show a specific benefit of the actual dual nature of the mode (i.e., switching from pressure support to volume control), and no evidence has been published in the literature since then supporting this mode. Anecdotal reports indicate that it is difficult to adjust pressure, volume, and flow settings to make the mode work properly, in particular, if the mechanical properties of the patient’s respiratory system are changing rapidly. Pressure-regulated volume control (PRVC), or PC-CMV, and volume support (VS), or PC-CSV, are examples of adaptive control/ dual control modes. PRVC is based on pressure-controlled ventilation, and VS is based on PSV. In both modes, the ventilator attempts to maintain a target VT by adjusting the pressure level based on the previous breath. When a clinician places a patient in PRVC, a target VT, minimal breath rate, and maximum (i.e., alarm) pressure limit are clinician set, whereas for a patient placed

CHAPTER 47  Physiology of Ventilatory Support

in VS, a target VT and maximum (i.e., alarm) pressure limit are clinician set. In both modes, once the patient is connected to the ventilator, the patient–ventilator interaction that occurs in the first few breaths is critical. Initially, the ventilator calculates total system compliance. On the succeeding three or four breaths, the ventilator monitors the peak airway pressures and expiratory VT. The ventilator determines the pressure level necessary to deliver the clinician-set “target” VT, for the given total system compliance. The patient–ventilator interaction is monitored on a breathby-breath basis. If the patient’s lung compliance improves (or patient effort increases), the ventilator delivers subsequent breaths at a lower pressure level to maintain the target VT. This adjustment by the ventilator reduces the risk of alveolar overdistention and volutrauma. Conversely, the ventilator responds to worsening pulmonary compliance (or decreasing patient effort) by increasing the pressure limit until the VT is achieved. The ventilator makes pressure level changes in small increments, 1 to 3 cm H2O per breath, and does not exceed the maximum pressure limit set by the clinician. These automatic ventilator responses to changes in a patient’s lung mechanics minimize the risk of ventilator-induced hyperventilation or hypoventilation. The desired outcome is a stable or consistent minute ventilation and enhanced patient comfort. However, the major problem with these modes is that the ventilator cannot distinguish between the patient improving and heightened levels of ventilator demand. If patient demand results in a larger VT, the ventilator ventilates less.80 In most ventilators, pressure can be decreased all the way to the PEEP level. This situation can lead to ventilatory failure.80 Both RPVC and VS should be used very cautiously in all patients with a normal or increased ventilatory demand. Randomized comparison between these modes and other, more traditional, modes failed to show any outcome benefit.81,82 Example.  PRVC or VS has been used in infants with respiratory distress syndrome.83 Rapidly changing pulmonary mechanics from surfactant administration are associated with complications such as pulmonary air leaks, intraventricular hemorrhage, and bronchopulmonary dysplasia. These adaptive modes respond to changes in a patient’s lung mechanics and may reduce the incidence of these common complications. Adaptive support ventilation (ASV), or PC-IMV, is an example of optimal control in adaptive ventilation. ASV is a pressuretargeted mode that optimizes the relationship between VT and respiratory frequency based on lung mechanics as predicted by Otis.84 ASV uses a pressure ventilation format establishing a ventilatory pattern that minimizes WOB and auto-PEEP, while limiting peak airway pressure. In this regard, ASV is similar to PC-CMV and PRVC in its gas delivery format. It differs from PC-CMV and PRVC by its additional algorithmic control of the ventilatory pattern.85 ASV automatically determines the VT and respiratory rate that best maintains the peak pressure below the target level.86 The clinician inputs the patient’s ideal body weight, high pressure limit, PEEP, FiO2, inspiratory rise time, flow cycle percentage, and percentage of predicted minute volume desired. The ventilator periodically measures dynamic compliance and the respiratory time constant and determines the desired

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mandatory rate. Ideal body weight is used by the ventilator to calculate the minute volume, which is divided by the rate for determination of VT.87 The newest adaption to ASV is referred to as Intellivent. With this adaption the ventilator operates the same as with ASV but in addition has the ARDSnet PEEP/FIO2 tables programed into the ventilator algorithm. Thus, as the patient’s SpO2 changes, PEEP and FIO2 are adjusted as dictated by the ARDSnet protocols. When ASV is compared with VC-IMV, ASV decreases inspiratory load and improves patient–ventilator synchrony.88 Others have shown that ASV resulted in a shorter duration of intubation than VC-IMV in postoperative cardiac patients with no complications.89 More recently, Belliato and colleagues90 comparing PC-IMV (optimal) to ASV showed that the ventilator was able to differentiate between patient types and select appropriate settings.91 Using a lung model, Sulemanji and coworkers92 determined that ASV could provide better lung protection than a fixed VT of 6 mL/kg ideal body weight. ASV control has been adapted to respond to end-tidal CO2 levels.92 This new adaptation allows specific algorithms to be selected based on patient diagnosis: ARDS, COPD, brain injury, or healthy lung. This mode is the most sophisticated of the closed loop control modes available on ICU ventilators at the present time. However, additional study is needed to determine fully the type of patient in whom ASV is most useful. Current data would indicate ASV works very well in patients under controlled approaches to ventilatory support, but additional data in spontaneously ventilated patients are needed before it can be recommended in these patients. RULE OF THUMB Most patients requiring ventilatory support can be effectively ventilated with volume assist/control, pressure assist/control, and PSV modes.

Patient Positioning to Optimize Oxygenation and Ventilation Patients receiving mechanical ventilation are turned frequently, usually at least every 2 hours, unless turning is contraindicated. Kinetic beds continually rotate patients and are designed to help prevent atelectasis, hypoxemia, secretion retention, and pressure ulcers. When patients are kept immobile, pooling of secretions in dependent lung zones can promote nosocomial pneumonia, and shrinking of dependent alveoli leads to decreases in ventilation and hypoxemia. However, the use of rotating kinetic beds is controversial in the prevention of nosocomial pneumonia.93 No data are available to indicate that these very expensive beds improve patient outcome. Patients with unilateral lung disease benefit from being placed in positions that promote matching of ventilation and perfusion. In unilateral lung disease, only one lung is affected by atelectasis, consolidation, or pneumonia. If the affected lung is placed in the dependent position, blood flow follows. The resultant poor V̇ /Q̇ ratio in the affected lung contributes to venous admixture and hypoxemia. However, if the patient is rotated so that the good lung is in the dependent position, these relationships are reversed. With the good lung down, blood flows to well-ventilated

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alveoli, and V̇ /Q̇ matching and arterial blood gas values improve. An added benefit of this maneuver is that the affected lung is placed in a postural drainage position, which promotes gravity drainage of retained secretions so that they can be removed.

RULE OF THUMB  Patients who have unilateral or dependent consolidation or atelectasis and severe hypoxemia may benefit from positioning with the affected lung or segments in the nondependent position to promote improvement in V̇ /Q̇ relationships. Prone positioning is indicated only if the PaO2/FiO2 is less than 100 mm Hg. When positioning the patient, great care should be taken to avoid the hazards associated with prone positioning.

Prone Positioning A similar phenomenon has been described in ARDS. In a supine patient with ARDS, alveoli in the bases and posterior segments become atelectatic. Shunt increases, and the patient requires a high FiO2 and PEEP for adequate oxygenation. If the patient is rotated into the prone position, several mechanisms have been proposed to improve oxygenation.94 Blood flow is redistributed to areas that are better ventilated. This redistribution improves V̇ /Q̇ relationships. Prone positioning removes the weight of the heart from its position over the lungs while the patient is supine. Pleural pressure in the now nondependent collapsed lung becomes more negative, improving alveolar recruitment. In addition, the stomach no longer lies over the dependent basilar posterior segments of the lower lobes. A number of studies have demonstrated some benefit of prone positioning.95–98 However, several persons are needed to “flip” the patient while ensuring monitoring lines and catheters are not disrupted and the patient is not inadvertently extubated. Wound dehiscence, facial or upper chest wall necrosis despite extensive padding, cardiac arrest immediately after movement to the prone position, dependent edema of the face, and corneal abrasion have been reported.96 A recent meta-analysis of existing randomized controlled trials indicated no outcome benefit from prone positioning in patients with ARDS.97 However, this metaanalysis also found that patients with PaO2/FiO2 less than 100 mm Hg were the group most likely to benefit from prone positioning. A subsequent randomized controlled trial showed the same results.98 Considering the complications associated with prone positioning, only patients with very severe hypoxemia (PaO2/ FiO2 95% have greater mortality than those maintained at an FiO2 that maintains PaO2 of 55 to 80 mm Hg or SpO2 of 88% to 95%.35,36 Patients who have undergone previous blood gas measurement or oximetry who are doing well clinically, and patients with disease states or conditions that normally respond to low to moderate concentrations of O2, may begin ventilation with a lower O2 concentration (50%). These typically are patients with normal ventilation/perfusion (V̇ /Q̇ ) or a V̇ /Q̇ imbalance without shunt (V̇ /Q̇ 0). Patients who often do well with lowto-moderate concentrations of O2 include patients with acute exacerbation of COPD, emphysema, chronic bronchitis, drug overdose without aspiration, or neuromuscular disease and postoperative patients with normal lungs. For example, a patient with an acute exacerbation of COPD who needs mechanical ventilatory support may have had PaO2 of 50 mm Hg with a nasal cannula at 4 L/min before intubation and mechanical ventilation. This patient would probably do well with FiO2 of approximately 0.50 when adequate ventilation is restored. The patient can begin with 50% O2 and be immediately assessed for assurance of adequate SpO2. FiO2 can be adjusted according to the patient’s response. Many ICU patients are now managed with an FiO2 of 21% because that is all that is needed to maintain appropriate oxygenation.

Positive End-Expiratory Pressure and Continuous Positive Airway Pressure PEEP and CPAP are effective techniques for improving and maintaining lung volume and improving oxygenation for patients with acute restrictive disease such as pneumonia, pulmonary edema, and ARDS.1,9 PEEP and CPAP should be cautiously applied in the treatment of patients with an already elevated functional residual capacity (FRC), such as patients with COPD or acute asthma, except at levels that are applied to offset auto-PEEP and air trapping.9 Generally, the indication for PEEP or CPAP is inadequate arterial O2 with moderate-to-high concentrations of O2 caused by unstable lung units that are collapsed. PaO2 less than 50 to 60 mm Hg with FiO2 greater than 0.40 is a good general starting place for considering use of PEEP or CPAP. In terms of ventilator initiation, initial PEEP or CPAP levels are usually 5 to 8 cm H2O, even in the absence of unstable lung units or auto-PEEP. Most experts advocate for the use of 5 cm H2O PEEP for all patients who have an artificial airway in place. Intubation results in small reductions in FRC,1,9 which can be balanced with the application of PEEP or CPAP. PEEP has been advocated in the presence of auto-PEEP, in particular in the care of patients with obstructive lung disease.37 Applied PEEP in the presence of auto-PEEP is indicated only if the patient has difficulty triggering the ventilator. During controlled ventilation, increasing PEEP in the presence of auto-PEEP is usually not indicated (see Chapter 48 for auto-PEEP details). An absolute contraindication to PEEP is an uncontrolled tension

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pneumothorax; however, PEEP should be cautiously applied in any patient with severe intrinsic lung disease, hypotension, and elevated intracranial pressure.

Open Lung Strategy, Recruitment Maneuvers, and Positive End-Expiratory Pressure In the care of patients with ARDS, it is usually necessary to initiate PEEP at 10 to 15 cm H2O;24,25,38,39 however, many clinicians use the ARDS Clinical Network PEEP/FiO2 tables to set PEEP initially during the establishment of ventilatory support (see Box 49.7). When patients are stabilized, the use of an open lung ventilation strategy in early-stage ARDS has been recommended.1,5 Such a strategy incorporates VT of 4 to 8 mL/kg IBW with either pressure-targeted or volume-targeted ventilation and a PEEP level set after a lung recruitment maneuver using a decremental PEEP trial.1,5,40,41 The lung recruitment maneuver is intended to open collapsed lung units, and the setting of PEEP using a decremental PEEP trial is intended to apply PEEP based on the patient’s lung mechanics to keep the recruited lung units open. Although all patients with ARDS require PEEP, not all patients with ARDS respond to low-level PEEP, and patients with pulmonary (vs. nonpulmonary) causes of ARDS, such as pneumonia, may be less likely to respond to low to moderate levels of PEEP.12 Nonpulmonary causes of ARDS (e.g., extrathoracic trauma, intraabdominal sepsis) seem to respond well to PEEP.12 In practice, some authors have suggested that higher levels of PEEP (>15 cm H2O) be reserved for patients with a high percentage of recruitable lung.4 High levels of PEEP have been shown to improve outcomes in ARDS in patients with the most severe forms of ARDS (PaO2/FiO2 < 150 mm Hg).42,43 (See later section on the performance of recruitment maneuvers and the setting of PEEP by decremental trial.)

Pressure Rise Time or Slope Most newer, critical care ventilators include an inspiratory pressure rise time or pressure slope. This control functions only with pressure-limited breaths (PSV, PCV, PRVC, volume support, APRV, pressure SIMV). The purpose of this control is to adjust the rate at which flow increases from baseline to peak (see Chapter 48 for details).44-46

Limits and Alarms Ventilator alarms and limits warn of ventilator malfunction and changes in patient status. Ventilator malfunction alarms include power or gas supply loss and electronic or pneumatic malfunction. These alarms are usually preset by the manufacturer. Patient status alarms are usually set by the RT. These include maximum inspiratory pressure, low-pressure and low-PEEP alarms, high-volume, low-volume and rate alarms, O2 and humidification alarms, and apnea alarms. After initiation of ventilation, alarms and limits are readjusted as needed. Alarms are usually set so that they warn the clinician of important changes or problems. Without proper setting, these alarms can become a nuisance by falsely signaling problems that are not real.9 In volume ventilation, a pressure limit should be set. Generally, before the patient is connected to the ventilator, the limit should be set at 40 cm H2O to avoid over pressuring the system

TABLE 49.6  Alarm and Backup Ventilation

Setting of Initial Ventilatory Setup (Adults) Low pressure Low PEEP/CPAP High pressure limit Low exhaled VT Low exhaled minute ventilation High minute ventilation O2 percentage (FiO2) Temperature Apnea delay Apnea values

5–10 cm H2O below PIP 3–5 cm H2O below PEEP Max 50 cm H2O, adjusted to 10–15 cm H2O above PIP 100 mL or 50% below set VT 2–5 L/min or 50% below minimum SIMV or assist/control backup minute ventilation 50% above baseline minute ventilation 5% above and below set O2 percentage 2°C above and below set temperature, do not exceed 37°C 20 s VT and rate set to achieve full ventilatory support (VT 8–10 mL/kg; rate 10–12 breaths/min) with 100% O2

CPAP, Continuous positive airway pressure; FiO2, fractional inspired oxygen; PEEP, positive end-expiratory pressure; PIP, peak inspiratory pressure.

when the patient is connected. After the patient is connected to the ventilator, the peak and plateau pressures should be assessed. If Pplat is greater than 28 cm H2O, consideration should be given to decreasing the set VT. If Pplat is less than 28 cm H2O, the highpressure limit can be adjusted to 10 to 15 cm H2O above PIP. One can decrease peak pressure by decreasing the peak flow rate, increasing the inspiratory time, changing the inspiratory flow waveform from a square to a down ramp, or decreasing the delivered VT. For spontaneously breathing patients, inspiratory flow and time must meet or exceed the patient’s inspiratory demand to ensure one does not increase the patient’s WOB further (see Chapter 48 for details). Preset or adjustable alarms common to most ventilators include pressure (high-low), volume (highlow VT, minute ventilation), apnea, O2 percentage, and temperature. Suggested initial settings for these alarms and backup ventilator settings are presented in Table 49.6.

Humidification Humidification is required during both invasive and noninvasive mechanical ventilation. A heated humidifier or a HME should provide a minimum of 30 mg/l of water with a temperature of 30°C or greater.47 Use of HMEs should be avoided in the care of patients with thick and or retained secretion and patients with low body temperature (10 L/min), or air leaks in which exhaled VT is less than 70% of delivered VT.47 Heated humidifiers may be used to deliver saturated gas at 100% relative humidity at body temperature (see Chapter 39). Current clinical practice guidelines suggest an inspired gas temperature of 35 ± 2°C.48 The optimal humidity approach uses a heated humidifier to deliver gas in the range of 35 to 37°C at the airway and at a temperature consistent with patient comfort during noninvasive ventilation; however, in patients without primary pulmonary dysfunction and short-term ventilation, HMEs are very useful. Generally, these are postoperative patients after elective surgery, patients in the emergency department, and patients recovering from an overdose.

CHAPTER 49  Initiating and Adjusting Invasive Ventilatory Support

Periodic Sighs Constant, monotonous tidal ventilation at a small volume (140 beats/min or 28 cm H2O).

Open Lung Approach The use of a high PEEP, low VT lung-protective strategy using VT of 4 to 8 mL/kg and PEEP set after a lung recruitment maneuver and decremental PEEP, as discussed previously, may improve mortality in patients with persistent ARDS.24,25 Because VT is reduced, respiratory rate should be increased incrementally up to 35 to 40 breaths/min. The limitation on rate is the development of auto-PEEP; if auto-PEEP does not develop, the rate can be increased. The primary concern in patients with severe ARDS is acidosis; however, most patients without severe sepsis, cardiovascular dysfunction, or renal failure can tolerate severe acidosis. The ARDS Clinical Network defined the limit for acidosis as pH less than 7.15.2 PaCO2, although important, should be allowed to increase before accepting VT that results in Pplat greater than 28 mm Hg. The need to allow PaCO2 to increase to avoid inducing lung injury is referred to as permissive hypercapnia; however, the goal is not to allow the PaCO2 to increase but to avoid Pplat

Mode Increase

Ventilation (↓ PaCO2)

Decrease Ventilation (↑ PaCO2)

Volume-Controlled Ventilation VC-CMV control ↑ VT; ↑ f; remove VDmach VC-CMV assist ↑ VT; ↑ f (to greater than control assist rate); remove VDmach SIMV ↑ VT; ↑ f; add/increase PSV; remove VDmach

↓ VT; ↓ f ↓ VT; ↓ f (may require sedation, control mode) ↓ VT; ↓ f; reduce PSV (may require sedation)

Pressure-Controlled Ventilation PCVa ↑ ΔP; ↑ f (maintaining same Ti); remove VDmatch PSV ↑ ΔP; remove VDmatch Bilevel PAP ↑ IPAP (↑ ΔP); remove VDmatch APRV ↑ ΔP ↑ release frequency

↓ ΔP; ↓ f (maintaining same Ti) ↓ ΔP ↓ IPAP (↓ ΔP) ↓ ΔP ↓ release frequency

Note: In assist (patient-triggered) mode, the patient may simply alter the trigger rate after a ventilator change, and it becomes difficult to predict the results of a ventilator change on PaCO2 in the assist mode. a In PCV, if %Ti is preset, an increase in respiratory rate results in a decrease in inspiratory time and may reduce VT. If %Ti is set at 50% in PCV mode, an increase in rate from 15 to 20 breaths/min causes inspiratory time to decrease from 2 s (50% of 4 s) to 1.5 s (50% of 3 s). If the pressure limit is not changed, VT is likely to decrease. APRV, Airway pressure release ventilation; IPAP, inspiratory positive airway pressure; PCV, pressure-controlled ventilation; PSV, pressure support ventilation; SIMV, synchronized intermittent mandatory ventilation; VC-CMV, volume controlled-continuous mechanical ventilation.

that may induce lung injury. With this approach in severe ARDS, VT is frequently 4 to 5 mL/kg IBW, and PaCO2 is greater than 60 mm Hg. Table 49.10 compares the effect of acute changes in PaCO2 on pH. When applying this approach, PEEP is set after it is determined by a lung recruitment maneuver and a decremental PEEP trial, Table 49.11. VT or pressure level is adjusted, ensuring that Pplat or pressure control setting is less than 28 cm H2O. Because VT is small, inspiratory times can be short (frequently 0.6 to 0.8 second). The respiratory rate is set to achieve CO2 elimination, with its limit being the development of auto-PEEP. Initially, FiO2 is set to 1.0 but then titrated downward until PaO2 is greater than 55 mm Hg. Generally, PEEP is sustained at the set level until FiO2 is less than 0.5, and when PEEP is decreased it should be decreased in increments of 2 cm H2O no more frequently than approximately every 6 to 8 hours. If PaO2 decreases when PEEP is decreased, the correct decision is to reestablish PEEP level, not increase FiO2, because if this occurs, the lung is derecruited and lung volume needs to be reestablished. When to repeat a recruitment maneuver is a difficult question to answer, and data are insufficient at this time to provide an answer; however, if the PaO2 does not decrease after the initial lung recruitment maneuver, there is no reason to perform an additional recruitment maneuver. Suctioning may cause derecruitment and hypoxemia, and ventilator disconnection always results in derecruitment. If either of these situations occurs, the

CHAPTER 49  Initiating and Adjusting Invasive Ventilatory Support

MINI CLINI

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TABLE 49.10  Effect of Acute Changes in

Adjusting Ventilation in PA/C Mode

PaCO2 on pH

Problem A 70 kg (IBW) patient with ARDS is receiving PCV in the control mode with the following ventilator settings: Pressure: 15 cm H2O Rate: 25 breaths/min Inspiratory time: 0.8 FiO2: 0.60 PEEP: 12 cm H2O VT (exhaled): 425 mL Arterial blood gas values with these ventilator settings are as follows: PaO2: 60 mm Hg SaO2: 90% pH: 7.30 PaCO2: 50 mm Hg HCO3: 23 mEq/L Base excess: −2 mEq/L The physician requests that the respiratory rate be increased to 18 breaths/ min to decrease the patient’s PaCO2 to 40 mm Hg and normalize the pH. What should the RT do?

PaCO2

pH

80 70 60 50 40 35 30 25 20

7.16 7.22 7.28 7.34 7.40 7.45 7.50 7.55 7.60

Solution This patient has a PaO2/FiO2 ratio of 100 (60/0.60), which is consistent with the diagnosis of ARDS. Special considerations for the ventilatory management of ARDS include maintaining Pplat less than 28 cm H2O. VT is started at 8 mL/ kg IBW and gradually reduced to 6 mL/kg IBW to achieve this goal and minimize ventilator-induced lung injury. Respiratory rate may be increased to maintain PaCO2 and pH closer to normal, as long as volume and Pplat are acceptable. PaCO2 may be allowed to increase if necessary to maintain Pplat less than 28 cm H2O as long as pH is acceptable for the patient (usually >7.25). Oxygenation problems are managed initially with PEEP to achieve PaO2 of 60 mm Hg or more with an acceptable FiO2. If PEEP fails to improve PaO2, lung recruitment maneuvers and prone positioning may be used. For this patient, the VT is acceptable at approximately 6 mL/kg (70 kg × 6 mL/kg = 420 mL), and Pplat is 27 cm H2O. PaCO2 (50 mm Hg) and pH (7.30) are acceptable, and PEEP of 12 cm H2O may be appropriate for a patient with ARDS. To decrease PaCO2, the rate could be increased as follows: Initial Desired f(1) × PaCO2(1) = f(2) × PaCO2 25 × 50 = f(2) × 40 f(2) Desired = (25 × 50 40) = 31.25 If VT is maintained at 425 mL, a rate of 30–32 breaths/min should bring PaCO2 and pH into normal range; however, if respiratory rate is increased, air trapping and auto-PEEP may develop. If auto-PEEP develops, VT is likely to decrease. In pressure ventilation, an auto-PEEP increase is equal to an equivalent decrease in pressure control level, decreasing VT. The rate should be increased cautiously, constantly evaluating the impact of the rate increase on VT. More importantly, there is no reason to try to normalize PaCO2 in this patient. PaCO2 of 50 mm Hg with pH of 7.30 is acceptable.

lung needs to be recruited again, but PEEP is reestablished at the previous PEEP level because the hypoxemia was not a result of deterioration in lung function. A recruitment maneuver and decremental PEEP trial should be repeated only if the patient’s lung function deteriorates.

From Malley WJ: Clinical blood gases: assessment and intervention, ed 2, Philadelphia, 2005, Saunders.

In all patients with severe ARDS, mechanical dead space should be eliminated, in-line suction catheters should be in place, and airway suctioning should be performed only to the level of the main stem bronchus. In addition, ideally the ventilator circuit should not be disconnected.

Other Lung Protective Strategies Alternative techniques for facilitating CO2 removal during lung protective ventilation in patients with ARDS include extracorporeal CO2 removal (ECMO, see Chapter 51), reduction of CO2 production by control of fever, avoidance of overfeeding, and neuromuscular paralysis. Patients with severe ARDS (PaO2 < 150 mm Hg) should receive neuromuscular paralysis for the first 12 to 48 hours to allow for stabilization and titration of therapy. This has been shown to improve mortality in these patients.48 Other authors have advocated the use of HFOV;76–78 however, recent data in adults indicate that the use of HFOV in ARDS patients results in poorer outcome than the continued use of conventional ventilation.21,22 As a result, HFOV cannot be recommended in the management of ARDS.

SUMMARY CHECKLIST • Pplat should ideally be maintained at less than 28 cm H2O in all patients to prevent ventilator-induced lung injury. • Driving pressure should be maintained at less than 15 cm H2O in all patients to prevent ventilator-induced lung injury and improve mortality. • PEEP is used primarily to maintain lung volume, resulting in improved oxygenation and lower FiO2 in patients with severe oxygenation problems and refractory hypoxemia. • Initially, all acutely ill patients should be ventilated with VT of 4 to 8 mL/kg IBW with a respiratory rate to maintain adequate CO2 removal. • Patients with ARDS may begin mechanical ventilation with VT of 8 mL/kg but may need volume adjusted to less than 6 mL/kg IBW to maintain Pplat less than 28 cm H2O. • Lung protective strategies in the management of ARDS include use of lower VT (6 mL/kg), maintaining Pplat less than 28 cm H2O, permissive hypercapnia, and PEEP set above the lower inflection point on the static pressure-volume curve.

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TABLE 49.11  Example of a Decremental Positive End-Expiratory Pressure Study Following a

Lung Recruitment Maneuvera Value

PEEP = 20

PEEP = 18

PEEP = 16

PEEP = 14

PEEP = 12

Time (s) VT (L) f (breaths/min) FiO2 (%) I:E ratio Ppeak (cm H2O) Pplat (cm H2O) Cs (mL/cm H2O) SaO2 (%) Blood pressure (mm Hg)

0 4–6 mL/kg PBW 24 100 1 : 2 36 28 24 96 131/78

30 4–6 mL/kg PBW 24 100 1 : 2 34 26 27 97 133/82

75 4–6 mL/kg PBW 24 100 1 : 2 32 24 32 98 130/79

120 4–6 mL/kg PBW 24 100 1 : 2 30 22 34 100 125/74

175 4–6 mL/kg PBW 24 100 1 : 2 34 26 28 98 110/69

a

The best compliance PEEP is 14 cm H2O. Because the process of doing a decremental PEEP trial results in derecruitment, the lung must be recruited again and then PEEP is set at the best compliance PEEP plus 2 cm H2O. FiO2, fractional inspired oxygen; I:E, inspiratory-to-expiratory; PEEP, Positive end-expiratory pressure.

• FiO2 should be adjusted in all patients who are mechanically ventilated to maintain PaO2 55 to 80 mm Hg and SpO2 88% to 95%. • An open lung approach to mechanical ventilation includes the application of lung recruitment maneuvers, decremental PEEP trial, choosing VT that maintains Pplat less than 28 cm H2O, and accepting permissive hypercapnia. • Inspiratory flow for most adult patients should initially be set at approximately 60 L/min or greater to achieve an inspiratory time of approximately 0.6 to 1 second. • Patient ventilator synchrony is a major problem in patients during patient-triggered ventilation. • In all modes of pressure ventilation, the pressure level should be set to ensure that VT of 4 to 8 mL/kg IBW is delivered. • When in doubt, initial FiO2 should be set at 1.0. • Auto-PEEP is a problem in patients with obstructive lung disease (COPD, asthma). • In spontaneously breathing patients with COPD and autoPEEP, applied PEEP should be added to ensure that all patient efforts result in triggering of the ventilator. • An appropriate goal of PEEP would be to achieve PaO2 55 to 80 mm Hg with FiO2 less than 0.50. • Alternative lung protective strategies in patients with ARDS include prone positioning and ECMO. • Careful attention to acid–base homeostasis and the effect of PaCO2 on pH is an essential part of ventilator management.

REFERENCES 1. Hess DR, Kacmarek RM: Essentials of mechanical ventilation, ed 4, New York, 2019, McGraw-Hill. 2. The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome, N Engl J Med 342:1301–1308, 2000. 3. Sutherasan Y, D’Antini D, Pelosi P: Advances in ventilator-associated lung injury: prevention is the target, Expert Rev Respir Med 8:233–248, 2014. 4. Chiumello D, Carlesso E, Cadringher P, et al: Lung stress and strain during mechanical ventilation for acute respiratory

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distress syndrome, Am J Respir Crit Care Med 178:346–355, 2008. Amato MPB, Meade MO, Slutsky AS, et al: Driving pressure and survival in the acute respiratory distress syndrome, N Engl J Med 372:747–755, 2015. Kacmarek RM: The cost in some is an increase in the work of breathing: is it too high? (editorial), Respir Care 50:1624–1626, 2005. Slutsky AS, Ranieri VM: Ventilator-induced lung injury, N Engl J Med 369:2126–2136, 2013. Esteban A, Ferguson ND, Meade MO, et al., VENTILA Group: evolution of mechanical ventilation in response to clinical research, Am J Respir Crit Care Med 177:170–177, 2008. Tobin MJ: Principles and practice of mechanical ventilation, ed 2, New York, 2006, McGraw-Hill. Marini JJ, Rodriguez RM, Lamb V: The inspiratory workload of patient-initiated mechanical ventilation, Am Rev Respir Dis 134:902, 1986. Marini JJ, Capps JS, Culver BH: The inspiratory work of breathing during assisted mechanical ventilation, Chest 87:612, 1985. Tobin MJ: Advances in mechanical ventilation, N Engl J Med 344:1986, 2001. Esteban A, Anzueto A, Alia I, et al: How is mechanical ventilation employed in the intensive care unit? An international utilization review, Am J Respir Crit Care Med 161:1450, 2000. Brochard L, Rauss A, Benito S, et al: Comparison of three methods of gradual withdrawal from ventilatory support during weaning from mechanical ventilation, Am J Respir Crit Care Med 150:896–903, 1994. Estaban A, Frutos F, Tobin MJ, et al: A comparison of four methods of weaning patients from mechanical ventilation, N Engl J Med 332:345–350, 1995. Williams P, Muelver M, Kratohvil J, et al: Pressure support and pressure assist/control: are there differences? An evaluation of the newest ICU ventilators, Respir Care 45:1169–1181, 2000. Uchiyama A, Yoshida T, Yamanaka H, et al: Estimation of tracheal pressure and imposed expiratory work of breathing by the endotracheal tube, heat and moisture exchanger, and ventilator during mechanical ventilation, Respir Care 58:1157– 1169, 2013. Derdak S, Mehta S, Stewart TE, et al: High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a

CHAPTER 49  Initiating and Adjusting Invasive Ventilatory Support

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randomized, controlled trial, Am J Respir Crit Care Med 166: 801–808, 2002. Bollen CW, Well G, Sherry T, et al: High frequency oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a randomized controlled trial [ISRCTN2422669], Crit Care 9:R430–R439, 2005. Eastman A, Holland D, Higgins J, et al: High frequency percussive ventilation improves oxygenation in trauma patients with respiratory distress syndrome: a retrospective review, Am J Surg 192:191, 2006. Ferguson ND, Cook DJ, Guyatt GH, et al: High-frequency oscillation in early acute respiratory distress syndrome, N Engl J Med 368:795–805, 2013. Young D, Lamb SE, Shah S, et al: High-frequency oscillation for acute respiratory distress syndrome, N Engl J Med 368:806–813, 2013. Jesus J, Kacmarek RM, Hedensternia G: From ventilator-induced lung injury to physician-induced lung injury: why the reluctance to use small tidal volumes?, Acta Anaesthesiol Scand 48:267–271, 2004. Amato MBP, Barbas CSV, Medeiros DM, et al: Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome, N Engl J Med 338:347–354, 1998. Villar J, Kacmarek RM, Perez-Mendez L, et al: ARIES Network: a high positive end-expiratory pressure, low tidal volume ventilatory strategy improves outcome in persistent acute respiratory distress syndrome: a randomized, controlled trial, Crit Care Med 34:1311–1318, 2006. Gajic O, Dara SI, Mendez JL, et al: Ventilator associated lung injury in patients without acute lung injury at the onset of mechanical ventilation, Crit Care Med 32:1817–1824, 2004. Hill LL, Pearl RG: Flow triggering, pressure triggering and auto triggering during mechanical ventilation, Crit Care Med 28:579, 2000. Sassoon CSH: Mechanical ventilator design and function: the trigger variable, Respir Care 37:1056, 1992. Branson RD: Flow-triggering systems, Respir Care 39:138, 1994. Oto J, Chenelle CT, Marchese AD, et al: A comparison of leak compensation in acute care ventilators during noninvasive and invasive ventilation: a lung model study, Respir Care 58:2027– 2037, 2013. Oto J, Chenelle CT, Marchese AD, et al: A comparison of leak compensation during pediatric noninvasive ventilation: a lung model study, Respir Care 59:241–251, 2014. Rau JL, Shelledy DC: The effect of varying inspiratory flow waveforms on peak and mean airway pressures with a timecycled volume ventilator: a bench study, Respir Care 36:347, 1991. Lindahl S: Influence of an end inspiratory pause on pulmonary ventilation, gas distribution, and lung perfusion during artificial ventilation, Crit Care Med 7:540, 1979. Langevin PB, Hellein V, Harms SM, et al: Synchronization of radiograph film exposure with the inspiratory pause: effect on the appearance of bedside chest radiographs in mechanically ventilated patients, Am J Respir Crit Care Med 160:2067, 1999. Girardis M, Busani S, Damiani E, et al: Effect of conservative vs conventional oxygen therapy on mortality among patients in an intensive care unit: the Oxygen-ICU randomized clinical trial, JAMA 316:1583, 2016. Chu DK, Kim LHY, Young PJ, et al: Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen

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therapy (IOTA): a systemic review and meta-analysis, Lancet 391:1693–1701, 2018. Sethi J, Siegel MD: Mechanical ventilation in chronic obstructive lung disease, Clin Chest Med 21:799, 2000. Mercat A, Richard JC, Vielle B, et al: Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome, JAMA 299:646–655, 2008. Talmor D, Sarge T, Malhotra A, et al: Mechanical ventilation guided by esophageal pressure in acute lung injury, N Engl J Med 359:2095–2104, 2008. Kacmarek RM, Villar J: Lung recruitment maneuvers during acute respiratory distress syndrome: is it useful?, Minerva Anestesiol 77:85–89, 2011. Gattinoni L, Caironi P, Cressoni M, et al: Lung recruitment in patients with acute respiratory distress syndrome, N Engl J Med 354:1175, 2006. Phoenix SI, Paravastu S, Columb M, et al: Does a higher positive end expiratory pressure decrease mortality in acute respiratory distress syndrome?, Anesthesiology 110:1098–1105, 2009. Briel M, Meade M, Mercat A, et al: Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis, JAMA 303:865–873, 2010. Bonmarchand G, Chevron V, Menard JF, et al: Effects of pressure ramp slope values on the work of breathing during pressure support ventilation in restrictive patients, Crit Care Med 27:715, 1999. Branson RD, Campbell RS, Davis K, et al: Altering flow rate during maximum pressure support ventilation (PSVmax): effect on cardiorespiratory function, Respir Care 35:1056–1069, 1990. Branson RD, Campbell RS: Pressure support ventilation, patient-ventilatory synchrony and ventilator algorithms, Respir Care 43:1045–1053, 1998. American Association for Respiratory Care: AARC clinical practice guideline: humidification during mechanical ventilation, Respir Care 37:887, 1992. Papazian L, Forel JM, Gacouin A, et al: Neuromuscular blockers in early acute respiratory distress syndrome, N Engl J Med 363: 1107–1116, 2010. Bendixen HH, Egbert LD, Hedley-Whyte J, et al: Respiratory care, St Louis, 1965, Mosby. MacIntyre N: Of Goldilocks and ventilatory muscle loading, Crit Care Med 28:588, 2000. Hickling KD: Best compliance during a decremental, but not incremental, positive end-expiratory pressure trial is related to open-lung positive end-expiratory pressure: a mathematical model of acute respiratory distress syndrome lung, Am J Respir Crit Care Med 163:69–78, 2001. O’Keefe GE, Gentilello LM, Erford S, et al: Imprecision in lower “inflection point” estimation from static pressure-volume curves in patients at risk for acute respiratory distress syndrome, J Trauma 44:1064, 1998. Girgis K, Hamed H, Khater Y, et al: A decremental PEEP trial identifies the PEEP level that maintains oxygenation after lung recruitment, Respir Care 51:1132, 2006. Suarez-Sipmann F, Bohm SH, Tusman G, et al: Use of dynamic compliance for open lung positive end-expiratory pressure titration in an experimental study, Crit Care Med 35:214–221, 2007. Borges JB, Okamoto V, Gustavo M, et al: Reversibility of lung collapse and hypoxemia in early acute respiratory distress syndrome, Am J Respir Crit Care Med 174:268–278, 2006.

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56. Lin SC, Alander A, Simonson DA, et al: Transient hemodynamic effects of recruitment maneuvers in three experimental models of acute lung injury, Crit Care Med 32:2371–2384, 2004. 57. Toth I, Leiner T, Mikor A, et al: Hemodynamic and respiratory changes during lung recruitment and descending optimal positive end-expiratory pressure titration in patients with acute respiratory distress syndrome, Crit Care Med 35:787–793, 2007. 58. Medoff BD, Harris SR, Kesselman H, et al: Use of recruitment maneuvers and high positive end expiratory pressure in a patient with acute respiratory distress syndrome, Crit Care Med 28:1210, 2000. 59. Tugrul A, Akinci O, Ozcan PE, et al: Effects of sustained inflation and postinflation positive end-expiratory pressure in acute respiratory distress syndrome: focusing on pulmonary and extrapulmonary forms, Crit Care Med 31:738–744, 2003. 60. Pirrone M, Fisher D, Chipman D, et al: Recruitment maneuvers and positive end-expiratory pressure titration in morbidly obese ICU patients, Crit Care Med 44:300, 2016. 61. Fumagalli J, Berra L, Zhang C, et al: Transpulmonary pressure describes lung morphology during decremental positive end-expiratory pressure trials in obesity, Crit Care Med 45:1374, 2017. 62. Mauri T, Mercat A, Grasselli G: What’s new in electrical impedance tomography, Intensive Care Med 2018, doi:10.1007/ s00134-018-5398-z. [Epub ahead of print]. 63. Jacopo F, Santiago RRS, Droghi MT: Positive end expiratory pressure titration in obese patients with acute respiratory distress syndrome, Anesthesiology. In Press. 64. Saptharishi LG, Jayashree M, Singhi SC, et al: Airway pressure release ventilation in pediatric acute respiratory distress syndrome: a randomized controlled trial, Am J Respir Crit Care Med 198:1199, 2018. 65. Drakulovic MB, Torres A, Bauer TT, et al: Supine body position was a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomized trial, Lancet 354:1851, 1999. 66. Chatte G, Sab JM, Dubois JM, et al: Prone position in mechanically ventilated patients with severe acute respiratory failure, Am J Respir Crit Care Med 155:473–478, 1997. 67. Gattinoni L, Tognoni G, Pesnti A, et al: Effect of prone positioning on the survival of patients with acute respiratory failure, N Engl J Med 345:568–573, 2001.

68. Mancebo J, Fernandez R, Blanch L, et al: A multicenter trial of prolonged prone ventilation in severe acute respiratory distress syndrome, Am J Respir Crit Care Med 173:1233–1239, 2006. 69. Taccone P, Pesenti A, Latini R, et al: Prone positioning in patients with moderate and severe acute respiratory distress syndrome: a randomized controlled trial, JAMA 302:1977–1984, 2009. 70. Sud S, Friedrich JO, Taccone P, et al: Prone ventilation reduces mortality in patients with acute respiratory failure and severe hypoxemia: systematic review and meta-analysis, Intensive Care Med 36:585–599, 2010. 71. Curley MA: Prone positioning in patients with acute respiratory distress syndrome: a systematic review, Am J Crit Care 8:397, 1999. 72. Hirvela E: Advances in the management of acute respiratory distress syndrome: protective ventilation, Arch Surg 135:126, 2000. 73. Guérin C, Reignier J, Richard JC, et al: Prone positioning in severe acute respiratory distress syndrome, N Engl J Med 368:2159–2168, 2013. 74. Izurieta R, Rabatin J: Sedation during mechanical ventilation: a systematic review, Crit Care Med 30:2644–2648, 2002. 75. Girard TD, Kress JP, Fuchs BD, et al: Efficacy and safety of a paired sedation and ventilation weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomized controlled trial, Lancet 371:126–134, 2008. 76. Derdak S, Mehta S, Stewart TE, et al: High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial, Am J Respir Crit Care Med 166: 801–808, 2002. 77. Bollen CW, Well G, Sherry T, et al: High frequency oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a randomized controlled trial [ISRCTN2422669], Crit Care 9:R430–R439, 2005. 78. Mentzelopoulos SD, Malachias S, Tzoufi M, et al: High frequency oscillation and tracheal gas insufflation for severe acute respiratory distress syndrome, Intensive Care Med 33:S142, 2007.

50  Noninvasive Ventilation Purris F. Williams

CHAPTER OBJECTIVES After reading this chapter you will be able to: • List the goals and benefits of noninvasive ventilation (NIV). • Discuss indications for NIV and the relative strength of the supporting evidence for each indication. • List the selection and exclusion criteria for successful NIV. • List the factors that predict successful NIV. • Describe how to recognize NIV failure and discuss when and why this is important. • Identify the types of patient interfaces available for NIV and describe how to choose an appropriate interface for a patient.

• List common interface-related adverse effects and discuss how to avoid them. • Discuss the types of mechanical ventilators and ventilation modes used to provide NIV. • Discuss the causes and resolution of patient–ventilator asynchrony in NIV. • Describe the role of the respiratory therapist during the initial application of NIV. • Describe the ongoing ventilator management of NIV in the acute care setting. • List potential complications associated with NIV and possible solutions.

CHAPTER OUTLINE History and Development of Noninvasive Ventilation, 1106 Indications for Noninvasive Ventilation, 1107 Goals and Benefits of Using Noninvasive Ventilation, 1107 Acute Care Indications, 1108 Long-Term Care Indications, 1110 Selecting Appropriate Patients for Noninvasive Ventilation, 1111 Acute Care Setting, 1111 Long-Term Care Setting, 1112

Equipment Used for Noninvasive Ventilation, 1113 Patient Interfaces, 1113 Types of Mechanical Ventilators and Modes of Ventilation, 1116 Heated Humidifiers, 1119 Management of Noninvasive Ventilation, 1120 Initial Application of Noninvasive Ventilation, 1120 Clinical Assessment Criteria to Identify Success or Failure of Noninvasive Ventilation, 1121

Adjusting Noninvasive Ventilator Settings, 1121 Aerosolized Medication Delivery, 1122 Safe Delivery of Noninvasive Ventilation, 1123 Weaning from Noninvasive Ventilation, 1123 Complications of Noninvasive Ventilation, 1123 Time and Costs Associated With Noninvasive Ventilation, 1124

inspiratory positive airway pressure (IPAP) iron lung negative pressure ventilator nocturnal hypoventilation noninvasive positive pressure ventilation (NPPV)

noninvasive ventilation (NIV) obesity hypoventilation syndrome palliative care pneumobelt rocking bed Trendelenburg position

KEY TERMS chest cuirass continuous positive airway pressure (CPAP) erythema expiratory positive airway pressure (EPAP) hypercapnic respiratory failure hypoxemic respiratory failure

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Noninvasive ventilation (NIV) is a means of delivering ventilatory support without using an invasive artificial airway, such as an endotracheal or tracheostomy tube. NIV can be provided by applying either negative or positive pressure to the airways. Almost any type of mechanical ventilator can be used to deliver NIV, and many noninvasive patient interfaces are available. However, at the present time, NIV is almost always delivered using a positive pressure ventilator designed specifically for noninvasive use or an ICU ventilator with a noninvasive mode in conjunction with an oronasal or nasal mask. NIV is generally understood to include both noninvasive positive pressure ventilation (NPPV) and the noninvasive application of continuous positive airway pressure (CPAP). Interest in NIV has increased in recent years with the publication of findings from clinical trials using NIV in the management of respiratory failure. At the same time, technologically advanced noninvasive ventilators have been introduced. Most intensive care unit (ICU) ventilators now include a specific noninvasive mode of ventilation. Improvements in the design of noninvasive interfaces have increased patient tolerance of NIV. The net effect of these developments is that NIV has become a familiar intervention in both acute and long-term care settings.1 This chapter reviews the evidence supporting the use of NIV to manage various disease processes and makes recommendations on the types of patients and specific techniques for its successful application.

Fig. 50.1  Pneumobelt, an intermittent abdominal pressure device. (From Albert RK, Spiro SG, Jett JR: Clinical respiratory medicine, ed 2, Philadelphia, 2004, Mosby.)

HISTORY AND DEVELOPMENT OF NONINVASIVE VENTILATION Many of the early devices used for NIV were developed in the 20th century during the polio epidemic. These devices are most effective when used for patients with neuromuscular disease in the absence of primary pulmonary disease. First described in the 1930s, the pneumobelt consists of a rubber bladder that is strapped around the abdomen and periodically inflated by a positive pressure ventilator (Fig. 50.1).2 This simple, innovative device is most effective when the patient is in a sitting position. Inflation of the rubber bladder compresses the abdomen. The resulting increase in abdominal pressure pushes the diaphragm upward, actively assisting exhalation. When the rubber bladder deflates, abdominal pressure drops and the diaphragm moves down with the force of gravity, facilitating inspiration.3 The rocking bed (Fig. 50.2) is a motorized bed that frequently rocks from the Trendelenburg position to reverse Trendelenburg position. This repetitive motion facilitates inspiration and exhalation by using gravity to move the abdominal contents and the diaphragm upward and downward.4 Rocking beds were used in the 1950s as an alternative to negative pressure ventilators for patients following recovery from polio.2 The device can provide adequate minute ventilation but it is not tolerated by some patients. Negative pressure ventilators were widely used during the polio epidemic and a few are still used in the home setting.2 A negative pressure ventilator generates negative pressure within a chamber that surrounds the thorax. The chest wall expands, negative pressure is created in the alveoli and inspiration occurs when air flows into the lungs. When the negative pressure is

Fig. 50.2  Rocking bed.

released, elastic recoil causes the lungs and chest wall to return to their normal size, resulting in passive exhalation. The first electrically powered negative pressure ventilator, known as the iron lung (Fig. 50.3), surrounded the entire body from the neck down. Other designs were introduced, such as the chest cuirass, which enclosed only the chest.2 A disadvantage of negative pressure ventilators is that their design limits access to the patient unless ventilation is interrupted. Effective negative pressure ventilation can be challenging to achieve if the device has air leaks or does not fit properly. In addition, collapse of the upper airway can occur during inspiration when excessive negative pressure is applied.3 The first reported use of NPPV was in 1780, when Chaussier used a bag and face mask during resuscitation.1 However, widespread clinical use of NPPV did not begin until much later, with the introduction of intermittent positive pressure breathing (IPPB) in 1947.1,2 IPPB was used extensively to deliver aerosolized medications until the mid-1980s2 when new evidence showed

CHAPTER 50  Noninvasive Ventilation

1107

C A

B

D Fig. 50.3  Various devices used for negative pressure ventilation. (A) Emerson iron lung. (B) Chest cuirass. (C) Poncho wrap. (D) Porta-Lung. (A–C, From Albert RK, Spiro SG, Jett JR: Clinical respiratory medicine, ed 2, Philadelphia, 2004, Mosby; D, Courtesy Phillips Respironics, Murrysville, PA.)

no benefit compared to small volume nebulizers.5 Around this time, nasal mask CPAP was suggested as a therapy for obstructive sleep apnea.6 In 1989, NPPV was used successfully to support patients with acute respiratory failure (ARF).7 Since then, many studies have examined the use of NIV. The next section provides evidence-based recommendations for the application of NIV in the management of respiratory failure for selected clinical conditions.

INDICATIONS FOR NONINVASIVE VENTILATION Goals and Benefits of Using Noninvasive Ventilation Impaired gas exchange is the hallmark of ARF. Endotracheal intubation and mechanical ventilation are often necessary to

improve gas exchange in patients with severe ARF. The primary goal of NIV is to improve gas exchange without endotracheal intubation and its associated complications. The potential benefits of using NIV in the acute care setting include improved survival, less time on mechanical ventilation, shorter hospitalization, and lower rates of ventilator-associated pneumonia. In the long-term care setting, major goals are improving the patient’s quality of life and relieving symptoms of hypoventilation. The goals of NIV in acute and long-term care settings are listed in Box 50.1. The primary indication for NIV is hypercapnic respiratory failure due to chronic obstructive pulmonary disease (COPD) exacerbation. Hypercapnic ARF is characterized by inadequate alveolar ventilation, elevated arterial PCO2, and respiratory acidosis. Although patients with hypercapnic ARF are the most likely to benefit from the use of NIV, it is also indicated for selected patients with hypoxemic respiratory failure or with

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BOX 50.1  Goals of Noninvasive

Ventilation

Acute Care Setting • Improve gas exchange • Avoid intubation • Decrease mortality • Decrease length of time on ventilator • Decrease length of hospitalization • Decrease incidence of ventilator-associated pneumonia • Relieve symptoms of respiratory distress • Improve patient–ventilator synchrony • Maximize patient comfort Long-Term Care Setting • Relieve or improve symptoms • Enhance quality of life • Avoid hospitalization • Increase survival • Improve mobility Modified from Mehta S, Hill NS: Noninvasive ventilation, Am J Respir Crit Care Med 163:540, 2001.

respiratory failure resulting from numerous other conditions (Box 50.2).8–12

Acute Care Indications Hypercapnic Respiratory Failure Chronic obstructive pulmonary disease.  NIV is the standard of care for treatment of hypercapnic respiratory failure secondary to COPD exacerbation and should be available as first-line therapy in all institutions treating patients with COPD. Current data show that patients with COPD and ARF require intubation less often when they receive NIV. Other benefits of NIV use in this group of patients include lower risk of mortality, fewer complications, and reduced length of hospital stay.13,14 Early intervention with NIV should be considered before severe respiratory acidosis develops. However, NIV can be used successfully and safely in much sicker patients. Successful application of NIV has occurred in patients with hypercapnic coma and in awake, noncomatose patients. RULE OF THUMB The use of NIV in managing COPD exacerbation is strongly supported by evidence from numerous randomized, controlled trials.

BOX 50.2  Acute and Chronic Disease

Processes for Which Noninvasive Ventilation May Be Indicated Acute Conditions • Hypercapnic respiratory failure • Chronic obstructive pulmonary disease (COPD) exacerbation • Asthma • Facilitation of extubation, especially in COPD • Hypoxemic respiratory failure but cautiously • Acute cardiogenic pulmonary edema • Respiratory failure in immunocompromised patients • End-of-life care, do-not-intubate (DNI) and comfort-measures-only (CMO) orders • Postoperative respiratory failure • Prevention of reintubation in high-risk patients • Postextubation respiratory failure Chronic Conditions • Nocturnal hypoventilation • Restrictive thoracic disease • Amyotrophic lateral sclerosis (ALS) • COPD • Obesity-hypoventilation syndrome (OHS)

in this setting. If patients with severe asthma receive a trial of NIV, they must be monitored closely. Unless significant improvement in the symptoms of respiratory failure is evident within 1 to 2 hours, intubation should proceed without delay.

Facilitation of Weaning in Chronic Obstructive Pulmonary Disease There is reasonable evidence that patients with COPD who were intubated for ARF and have failed at least one spontaneous breathing trial (SBT) should be considered for a trial of extubation directly to NIV.20,21 However, early extubation to NIV does not influence weaning time for similar difficult-to-wean patients if ARF is caused by a condition other than COPD. Success is more likely for COPD patients with no exclusion criteria, for example, excessive amount of secretions and for those who have used NIV previously (and many patients with COPD are familiar with NIV from prior exacerbations). Interestingly, the failure of NIV to prevent intubation does not preclude the successful use of NIV to facilitate extubation at a later time.

RULE OF THUMB  All patients with an acute COPD exacerbation should be evaluated for NIV as an alternative to intubation and invasive mechanical ventilation. NIV is the standard of care in these patients.

RULE OF THUMB  A trial of extubation directly to NIV should be considered for patients with COPD and hypercapnic ARF who are likely to receive a tracheostomy for failure to wean.

RULE OF THUMB  Severe hypercapnia and decreased level of consciousness should not be considered absolute contraindications to a cautious trial of NIV in selected patients. The RT should be present until the patient is alert, oriented and able to protect his or her airway.

Hypoxemic Respiratory Failure Many conditions can cause hypoxemic respiratory failure, defined as impaired oxygenation (PaO2/FiO2 ratio 9 mL/kg PBW) during pressure support ventilation (PSV). The impact of NIV success or failure on survival remains unclear. NIV failure results in worse outcomes than NIV success but better than outcomes when patients are initially intubated. Most importantly, profound hypoxemia (PaO2/FiO2 ratio 40 kg/m2).67 The prevalence of obesity has increased significantly in the 21st century. Obesity hypoventilation syndrome is a common, underdiagnosed condition in hospitalized extremely obese patients. Obesity-hypoventilation syndrome (OHS) is characterized by chronic daytime hypercapnia, sleep-disordered breathing and obesity (body mass index >30 kg/m2) when no other known cause for hypoventilation is present. Excess weight on the chest wall and abdomen impose a load on the inspiratory muscles, especially in sitting or supine positions. Extreme obesity decreases the compliance of the chest wall and the respiratory system and increases resistance in the airways. These changes in pulmonary mechanics can cause small airways to close completely before exhalation is complete. The result of this air trapping is the development of intrinsic PEEP, further increasing work of breathing for these patients. Patients with OHS have a defective respiratory drive with a blunted response to increased PaCO2.68 NIV improves daytime hypercapnia and relieves symptoms associated with nocturnal hypoventilation within 1 to 4 months. Respiratory drive improves but may not return to normal. CPAP and NPPV have been shown to be equally effective in decreasing daytime PaCO2 in patients with OHS, and both are generally well tolerated. CPAP is usually the first-line treatment for OHS. If hypercapnia persists with CPAP, a switch to NPPV is recommended. Typically, an IPAP setting of at least 6 cm H2O above expiratory positive airway pressure (EPAP) is necessary to increase alveolar ventilation.69

SELECTING APPROPRIATE PATIENTS FOR NONINVASIVE VENTILATION Acute Care Setting The success or failure of NIV depends to a large degree on the clinician’s clinical judgment in choosing appropriate patients. Candidates for NIV in the acute care setting should show signs and symptoms of respiratory distress and have moderately abnormal gas exchange. NIV selection criteria for ARF are detailed in Box 50.3.2 Candidates for NIV must have an intact respiratory drive and stable vital signs. Patients with facial anatomy or injury that prevents use of a noninvasive interface should be excluded. The

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BOX 50.3  Noninvasive Ventilation

BOX 50.4  Noninvasive Ventilation

Signs of Impaired Gas Exchange (at Least One of the Following) • PaCO2 >45 mm Hg and pH 50 Cannulas: sites have been Tolerated HOB up, Hgb ≥8–9 stable—no migration or dangling, OOB ACT at goal bleeding to chair a. Obtain MD order for ambulation after assessment by RN, PT, RT b. Ensure ECMO cannulas, airway and all other lines are secured c. Equipment checklist: 1. Full O2 tank 2. Clamps 3. Portable SpO2 monitor 4. Wheelchair/recliner 5. ECMO emergency equipment 6. Assess battery life for all equipment d. Contingency plan: 1. Identify red plug outlets 2. Identify location of backup circuit e. Team discussion prior to take off to include destination & roles 1. RN: IVs, tubing, chest tubes 2. RT: ECMO pump/cannula (circuit), monitor flow/speed, airway 3. PT: manages patient mobility 4. A minimum of three staff must be present during ambulation 5. *Each discipline to monitor hemodynamic parameters and alert team members if significant changes noted f. Ensure hallways are clear of obstruction g. Limit ambulation to within the ICU III. Ambulate IV. Documentation Per Each Discipline’s Standards ECMO, Extracorporeal membrane oxygenation; HOB, head of bed; ICU, intensive care unit; MD, physician; OOB, out of bed; PT, prothrombin time; RN, nurse; RT, respiratory therapist.

CHAPTER 51  Extracorporeal Life Support

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MINI CLINI Problem A patient in the Cardiac Care Unit coded suddenly and was placed on VA ECMO. The patient is now somewhat stabilized on ECMO but needs to travel to the Cardiac Cath Lab as soon as possible to investigate and hopefully treat the cause of the arrest. He is on a pump flow of 5l pm and sweep flow of 4l pm. He is on multiple blood pressure medications. Who should travel with this patient besides the ECMO Specialist? What other considerations should be brought to the team’s attention? Discussion Every effort should be made to support this patient in the event an arrest reoccurs. The ECMO Specialist will be focused on the equipment that moves along with the patient. There should be a doctor from the Surgical Team available in case any cannulas are dislodged. A nurse or anesthesiologist should also be available to handle the medication pumps and help monitor the vital signs. Team members should all agree that the patient is able to travel. A dry run to the destination should be made to clear any obstacles. Back-up equipment should be brought to the Cath Lab in case of any circuit failures.

BOX 51.9  Common Complications Mechanical Complications • Pump failure • Tubing rupture • Cannula problems • Oxygenator failure Physiologic Complications • Seizures • Hemolysis • Renal failure • Bleeding; intracranial, surgical site • Neurologic complications • Arrhythmias • Pneumothorax

equipment should be identified and checked for function prior to beginning ambulation. There should be specific reasons to abort the exercise such as tachycardia, desaturation, patient fatigue or concerns for equipment or patient safety.

RISKS AND COMPLICATIONS ECMO poses significant risks. The complications can be classified as mechanical as a result of equipment failure or patient from clinical issues. Box 51.9 outlines ECMO complications.1 ECMO specialists are clinicians specifically trained in all aspects of ECMO. It is essential that the ECMO specialist have a thorough understanding of ECMO physiology and ECMO patient management. These individuals must have critical thinking skills and be technically adept at assessing all components of the ECMO circuit. Monitoring and frequent inspection of the circuit and evaluating circuit functions are among the primary roles of the ECMO specialist. The risk of the many complications inherent in providing ECMO support diminishes with diligence by the specialist.

Fig. 51.15  Oxygenator with significant clot accumulation.

The most common mechanical complication during ECMO is clot formation.1 Clots can occur anywhere in the circuit but more frequently occur in the oxygenator, at connectors, in the circuit bladder or any place with relatively low flow. Clots can result in increased resistance and may impede flow, limiting support of the patient. Clot formation within the fibers of the oxygenator will reduce gas exchange and, if significant, may require the oxygenator to be replaced (Fig. 51.15). Inadvertent decannulation and pump failure are other significant complications that can cause circuit interruption and require immediate attention. These conditions might result in the need for an entire circuit to be replaced. Replacement of oxygenators or circuits requires the patient to be briefly removed from support. Practitioners trained in this procedure need to maintain competency to efficiently change out the oxygenator or circuit in the least amount of time to minimize patient decompensation from interruption of support. Proper coordination with the team caring for the patient is essential during this loss of support. Air in the circuit is a major risk during ECMO. Despite the ECMO system being a closed system, air emboli can occur when air is entrained into the system. This can occur inadvertently through cavitation—air being pulled out of a solution due to increased negative pressure—if venous return is inadequate. It can occur from drainage ports of a cannula migrating out of a vessel or from access lines, such as through the CVVH port, infusion lines or other monitoring lines. The presence of air in the circuit, if not redirected or withdrawn, may enter the patient’s circulation. In VA ECMO this is particularly life threatening because air will not be filtered through the pulmonary circulation as it is in VV ECMO. As with most mechanical complications, prevention is vital. Bleeding is a common risk of ECMO due to anticoagulation and the multiple surgical sites where bleeding can easily occur. Bleeding in the chest can lead to the complication of cardiac tamponade, an emergency needing immediate intervention,

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without which the patient will not likely survive. Cannula placement in the awake and active patient on ECMO can also contribute to the occurrence of tamponade. Loss of pump flow, hemodynamic changes with a narrowing of pulse pressure, arrhythmias, and decreases in hemoglobin and hematocrit levels are symptomatic of tamponade. Bleeding from any source resulting in low pump flow causes risks not only to the patient but to the circuit as well. Lower flows result in higher potential for clot formation in a circuit. The drop in hemoglobin is also a major concern because the oxygen-carrying capacity is greatly reduced. Bleeding can occur from any surgical site, including cannula sites, chest tubes or IVs. Bleeding becomes a risk with any venopuncture, NG or OG tube placement, rectal tube placement, suctioning or anything that might cause mild trauma to the tissues. Internally, intracranial hemorrhage, GI and pulmonary bleeding are also bleeding risks associated with ECMO. RULE OF THUMB  A set up primed circuit and/or backup ECMO equipment should be kept easily accessible to the patient on an ECMO run in case any circuit complications that require a component or full circuit change.

BLOOD PRODUCTS DURING EXTRACORPOREAL MEMBRANE OXYGENATION The most common blood product used during an ECMO run is packed red blood cells (PRBCs). PRBCs are transfused to maintain adequate levels of hemoglobin to ensure adequate oxygen carrying capacity. Typically, hemoglobin is maintained at approximately 8 to 10 g/dL. Platelets, FFP, and cryoprecipitate are often used to target specific clotting factors. Protocols identify when transfusion of each individual product is indicated. Albumin may also be used intermittently throughout the run for volume expansion.

WEANING AND DECANNULATION Daily assessments for the possibility of weaning should be made first by considering why the patient was initially placed on ECMO and whether or not the problem has been resolved. Other questions to consider are if additional issues have been identified that either indicate the necessity to continue support or identify the need to discontinue support. Throughout the run, the team must consider if the risks of ECMO outweigh the benefits. The process of weaning off ECMO is different in VA support than in VV support. During VA weaning, the function of the heart must be assessed as increased blood flow is redirected to the native circulation. This evaluation is often accomplished via cardiac ultrasound while pump flow is decreased. At the same time, hemodynamic stability, right ventricule, left ventricule (RV, LV) function, and the degree of pulmonary hypertension should be evaluated. Ventilator support may need to be adjusted as pump flows are decreased, particularly ventilator FiO2 to supplement the decrease in pump flow. At this time, the risk of clots developing in the circuit at the low flow states is present. Therefore the duration of the wean should be limited to no more than an hour, with close attention to anticoagulation.

MINI CLINI Problem A patient is cannulated for VV ECMO due to acute lung injury secondary to H1N1 flu. The patient initially required a pump flow of 4 L/min and sweep of 10 L/min to achieve the desired gas exchange. After 5 days on resting ventilator settings, an improvement in both CXR and lung compliance is noted. Additionally, PaO2 with the ventilator FiO2 at 1.0 is markedly improved: on day 1 it had been 50 mm Hg and after 5 days is now 220 mm Hg. What changes should be made to assess the patient’s readiness to wean off of VV support? Discussion Gradually decreasing the sweep flow will allow assessment of the patient’s native lung’s ability to effectively ventilate. Simultaneously, ventilator adjustments should be made to support the transition when ECMO is discontinued. The patient is ready to be decannulated when gas exchange can be maintained without sweep flow and ventilator settings that will not induce any further lung injury (i.e., plateau pressures less than 28 and FiO2 less than 0.6).

For the patient who requires VA ECMO for both cardiac and pulmonary support, there is the option to convert to VV ECMO if the heart function recovers before adequate lung function is achieved. The patient can be supported on VV ECMO until there is further evidence of lung improvement. Patients on VV ECMO must demonstrate improvement in their pulmonary status before weaning can be considered. This includes an increase in lung compliance, improved aeration on CXR, and the ability for effective gas exchange on conventional ventilator settings that are not likely to produce lung injury. A test to evaluate the native lung’s ability to oxygenate can be achieved while maintaining the same ECMO support and obtaining an arterial blood gas with the ventilator FiO2 at 1.0. A daily assessment using this “100% gas” can demonstrate the improvement in oxygenation. Early stages of support will not reveal much change, but as the lungs improve then significant increases in the PaO2 will be obvious. The process of weaning off VV ECMO involves maintaining pump flow and weaning sweep flow to assess the native lung’s ability to remove CO2. Adjustments in ventilator support to accommodate the decrease in sweep flow should be made at this time. Once there is an improvement in ventilation evidenced by reasonable levels of PCO2 on moderate ventilator settings with an improvement in the 100% oxygen gas, the sweep flow can be removed. The pump flow continues while a period of assessment off ECMO occurs to determine if the patient is ready for decannulation, with the decannulation approach determined by the cannulation sites. Percutaneously inserted cannulas may be simply withdrawn at the bedside if vascular repair is not anticipated. If surgical repair or reconstruction of the vessel is required or if the patient is centrally cannulated, decannulation will typically take place in the operating room. Post-decannulation anticoagulation is most often discontinued or adjusted to desired levels. RULE OF THUMB  Weaning from VA support is accomplished by turning down the pump flow and assessing hemodynamics. Weaning from VV support is accomplished by turning down the sweep flow and assessing gas exchange.

CHAPTER 51  Extracorporeal Life Support

SUMMARY CHECKLIST • ECMO is an option for newborn, pediatric, and adult patients with severe cardiac or respiratory failure who meet the criteria outlined in Boxes 51.2 and 51.3 and who otherwise have no absolute contraindications. • The primary goals of ECMO are to deliver adequate amounts of oxygen, remove carbon dioxide, and, in cases of VA ECMO, provide hemodynamic support. ECMO physiology mimics native cardiopulmonary physiology in that it allows oxygen to diffuse into the blood and carbon dioxide to be removed. This is accomplished through a circuit that contains a pump and an artificial oxygenator. • The patient is cannulated with either a double-lumen cannula or multiple single-lumen cannulas. • During VV support, cannulas are usually placed in the right internal jugular vein, right atrium, and left or right femoral veins. In VA support, the venous cannulas are placed in the same locations as with VV support, with the arterial cannula inserted into the aorta or either femoral artery. • Blood is either drained or siphoned into the pump, which propels it forward into an oxygenator. The oxygenator provides gas exchange before returning the blood to the patient containing hemoglobin that is fully saturated and has the desired carbon dioxide level. • A blood warmer/cooler keeps the blood at the desired temperature and additional monitors provide clinicians with valuable information regarding circuit pressures, flows, and additional lab values. Several of the monitors can be set to sound audible alarms when the values of certain parameters are outside of the acceptable range. • Additional safety components can be added to the ECMO system for additional blood parameter monitoring such as venous and arterial saturations, hemoglobin and hematocrit. • The circuit and cannulas are made of materials foreign to blood. These surfaces will cause the normal activation of blood clotting reactions. Anticoagulation is necessary to decrease the risk of clots in the circuit, cannulas, and, most importantly, in the patient. • Bedside coagulation testing is typically performed at regular intervals to keep a close watch on the level of anticoagulation, along with frequent inspection for clot development in any of the circuit components. • A major advantage of ECMO is that ventilator support can be decreased once ECMO is initiated, thus reducing the potential of ventilator-induced lung injury. At times the ventilator can even be discontinued, reducing the potential of ventilator-associated pneumonia and allowing the patient to more actively participate in activities of daily living. This is of particular importance in the pre-transplant patient. • As technology advances and proper candidate selection is achieved, ECMO is certain to be more frequently utilized in ICU management of the critically ill patient. • Ambulating and/or intrahospital transports on ECMO are more common occurrences made possible by portable equipment, proper planning and team effort.

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REFERENCES 1. ECLS Registry Report International Summary, Extracorporeal Life Support Organization; Ann Arbor, MI. Available at: www.elso.org/Registry/Statistics.aspx. (Accessed August 2018). 2. ELSO Guidelines for all Extracorporeal Life Support Cases: Neonatal Respiratory Failure v 1.4, Ann Arbor, MI. Available at: www.elsonet.org/Resource/guidelines.aspx. December 2017. 3. ELSO Guidelines for Adult Respiratory Failure v1.4, Ann Arbor, MI. Available at: www.elso.org/Resource/guidelines.aspx. December 2017. 4. ECMO: Extracorporeal cardiopulmonary support in critical care, ed 5, Ann Arbor, MI, 2017, Extracorporeal Life Support Organization. 5. Hintz SR, Suttner DM, Sheehan AM, et al: Decreased use of neonatal extracorporeal membrane oxygenation (ECMO): how new treatment modalities have affected ECMO utilization, Pediatrics 106:1339, 2000. 6. Abrams D, Brody D: Emerging indications for ECMO in adults with respiratory failure, Ann Am Thorac Soc 10:371, 2013. 7. Martinez G, Vuylsteke A: Extracorporeal membrane oxygenation in adults, Cont Edu Anaesth Crit Care Pain 12:57, 2012. 8. Turner DA, Cheifetz IM: Extracorporeal membrane oxygenation for adult respiratory failure, Respir Care 58:1038, 2013. 9. Esper SA, Levy J, Waters J, et al: ECMO in the adult: a review of anticoagulation monitoring and transfusion, Anesth Analg 118: 731, 2014. 10. ELSO Anticoagulation Guidelines 2014. Extracorporeal Life Support Organization. Available at: elso.net/resources/guidelines. Oct. 1, 2014. 11. Liveris A, Bello RA, Friedmann P, et al: Antifactor Xa assay is a superior correlate of heparin dose than activated partial thromboplastin time or activated clotting time in pediatric extracorporeal membrane oxygen, Pediatr Crit Care Med 15:e72, 2014. 12. Betit P: Are contraindications to extracorporeal membrane oxygenation slowly vanishing?, Respir Care 56:1054–1055, 2011. 13. Randucci M, Ballotta A, Kandil H, et al: Bivalirudin-based versus conventional heparin anticoagulation for postcardiotomy extracorporeal membrane oxygenation, Crit Care 15:R275, 2011. 14. Olsson KM, Simon A, Strueber M, et al: Extracorporeal membrane oxygenation in nonintubated patients as bridge to lung transplantation, Am J Transplant 10:2173, 2013. 15. Hayanga AJ, Aboagye J, Esper S, et al: Extracorporeal membrane oxygenation as a bridge to lung transplantation in the United States: an evolving strategy in the management of rapidly advancing pulmonary disease, J Thorac Cardiovasc Surg 149:291, 2015. 16. Garcia JP, Kon ZN, Evans C, et al: Ambulatory veno-venous extracorporeal membrane oxygenation: innovation and pitfalls, J Thorac Cardiovasc Surg 142:755, 2011. 17. Hill N: Extracorporeal CO2 removal with the Hemolung RAS for mechanical ventilation avoidance during acute exacerbation of COPD (VENT-AVOID). Unpublished manuscript. 2018. Clinical Trial: NCT03255057. 18. McAuley D: Protective ventilation with veno-venous lung assist in respiratory failure (REST). Unpublished manuscript. 2018. Clinical Trial: NCT02654327.

52  Monitoring the Patient in the Intensive Care Unit Thomas Piraino CHAPTER OBJECTIVES After reading this chapter you will be able to: • Discuss the principles of monitoring the respiratory system, cardiovascular system, neurologic status, renal function, liver function, and nutritional status of patients in intensive care. • Explain why the caregiver is the most important monitor in the intensive care unit (ICU). • Describe various measures of patient oxygenation in the ICU. • Explain why the partial pressure of carbon dioxide (PaCO2) is the best index of ventilation for critically ill patients. • Describe the approach used to evaluate changes in respiratory rate, tidal volume, minute ventilation, PaCO2, and end-tidal pressure of carbon dioxide values for monitoring purposes. • Identify monitoring techniques used in the ICU to evaluate lung and chest wall mechanics, auto–positive end-expiratory pressure, work of breathing, and respiratory drive. • Describe the importance of measuring transpulmonary pressure in select patients.

• Discuss the importance of monitoring peak, plateau, and driving pressures in patients receiving mechanical ventilatory support. • Identify monitoring techniques that have become available more recently, such as lung stress and strain, functional residual capacity, stress index, electrical impedance tomography, and lung ultrasound. • Describe the approach used to interpret the results of ventilator graphics monitoring. • Describe the cardiovascular monitoring techniques used in the care of critically ill patients and how to interpret the results of hemodynamic monitoring. • Discuss the evaluation of renal function, liver function, and nutritional status in the ICU. • List and discuss the use of composite and global scores to measure patient status in the intensive care unit, such as the acute physiology, age, chronic health evaluation system for scoring the severity of illness. • Discuss the importance of monitoring neurologic status in the ICU and the variables that should be monitored. • Discuss monitoring and troubleshooting of the patient-ventilator system in the ICU.

CHAPTER OUTLINE Principles of Monitoring, 1147 History, 1148 Pathophysiology and Monitoring, 1148 Monitoring Oxygenation, 1148 Arterial Pulse Oximetry, 1148 Oxygen Consumption, 1149 Alveolar-Arterial Oxygen Tension Difference, 1149 PaO2/FiO2 Ratio, 1149 Murray Lung Injury Score, 1149 Other Oxygenation Measurements, 1149 Monitoring Ventilation, 1149 Capnography, 1150 Dead Space, 1150 Monitoring of Inspired and Exhaled Gas Volumes, 1151 Inspired Versus Expired Tidal Volume During Mechanical Ventilation, 1151 1146

Peak and Plateau Pressures, 1151 Mean Airway Pressure, 1151 Driving Pressure, 1151 Resistance, 1151 Monitoring Lung and Chest Wall Mechanics, 1152 Respiratory System Compliance, 1153 Chest Wall Compliance, 1153 Transpulmonary Pressure, 1154 Lung Stress and Strain, 1154 Monitoring the Patient-Ventilator System, 1155 Graphics Monitoring, 1157 Monitoring During Lung-Protective Ventilation, 1157 Stress Index, 1161 Auto–Positive End-Expiratory Pressure (Intrinsic Positive End-Expiratory Pressure), 1162

Methods for Determining Auto– Positive End-Expiratory Pressure, 1162 End-Expiratory Hold by the Ventilator, 1162 Esophageal Pressure Measurements, 1162 Using Positive End-Expiratory Pressure With Auto–Positive End-Expiratory Pressure, 1162 Monitoring Breathing Effort and Patterns, 1163 Work of Breathing, 1163 Pressure-Time Product, 1163 Oxygen Cost of Breathing, 1163 Assessing Ventilatory Drive, 1164 Airway Occlusion Pressure, 1164 Diaphragm Ultrasound, 1165

CHAPTER 52  Monitoring the Patient in the Intensive Care Unit

Rapid Shallow Breathing Index, 1165 Respiratory Inductive Plethysmography, 1165 Monitoring Strength and Muscle Endurance, 1165 Endurance: Maximal Voluntary Ventilation, 1166 Lung Imaging at the Bedside, 1166 Lung Ultrasound, 1166 Electrical Impedance Tomography, 1167 Cardiac and Cardiovascular Monitoring, 1167 Electrocardiography, 1169 Monitoring of Arterial Blood Pressure, 1169

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Monitoring of Central Venous Pressure–Right Atrial Pressure, 1170 Monitoring of Pulmonary Artery Pressure, 1170 Preload, 1172 Contractility, 1172 Afterload, 1172 Cardiac Output, 1172 Cardiac Muscle Injury, 1172 Monitoring Renal Function, 1172 Monitoring Liver Function, 1173 Nutritional Monitoring, 1174 Assessment of Nutritional Status, 1174 Global Monitoring Indices, 1174 Acute Physiology and Chronic Health Evaluation (APACHE), 1175

Neurologic Monitoring, 1175 Neurologic Status and Examination, 1175 Pupillary Response, 1176 Eye Movements, 1176 Corneal Responses, 1177 Gag Reflex, 1177 Respiratory Rate and Pattern, 1177 Motor Evaluation, 1178 Sensory Evaluation, 1178 Glasgow Coma Scale, 1178 Intracranial Pressure Monitoring, 1178 Troubleshooting, 1178

driving pressure electrical impedance tomography esophageal balloon factitious events Fick’s principle frequency/tidal volume ratio Glasgow Coma Scale lung stress and strain lung ultrasonography maximal inspiratory pressure maximum voluntary ventilation mean airway pressure

Murray lung injury score oxygen consumption (V̇ O2) preload pressure-time product respiratory inductive plethysmography stress index Swan-Ganz catheter transpulmonary pressure venous admixture vital capacity

KEY TERMS afterload alveolar and arterial oxygen tension difference APACHE scoring system artifacts bladder pressure capnography capnometry cardiac output contractility dead space/tidal volume ratio diaphragm ultrasound

When patients are admitted to the intensive care unit (ICU), it is generally for the purpose of providing diagnostic and therapeutic interventions that require continuous or periodic monitoring of physiologic parameters. ICU patients often require multiple medications, fluids, and nutrition, as well as noninvasive or invasive ventilatory support for respiratory failure. The monitoring of these patients is essential to assess the effectiveness of treatment in the ICU and to minimize, limit, or prevent adverse events. Although diagnostic procedures such as radiographic imaging can be used to monitor the progression of disease over time, this chapter focuses on the periodic and/or continuous monitoring of the respiratory system, cardiovascular system, renal function, liver function, nutritional status, and neurologic function of patients in the ICU.

PRINCIPLES OF MONITORING The best monitoring options provide detailed, easily interpreted data, obtained noninvasively or minimally invasively with the

fewest hazards and side effects. A monitoring tool that is highly invasive and carries a certain level of risk with use must provide a high level of valuable and required information to make the benefit of using it outweigh the risk. New advancements in technology aim to make monitoring less invasive and at the same time provide the most clinically relevant data. The data provided should be accurate (reflect the true value) and precise (not vary widely when repeated). When monitoring involves images, graphs, or waveforms, the data must be easily distinguishable from artifacts, factitious events, or normal variation and still require an understanding of the overall status of the patient to understand their significance. The best monitor in the ICU is the caregiver who understands how to use and interpret the various monitoring tools and techniques available to him or her. However, observing a monitor while ignoring the patient does not take into consideration the patient’s global status. We must combine the “seen” with the “unseen” to truly understand the patient (Box 52.1).

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BOX 52.1  Monitors and Monitoring Data

BOX 52.2  Values Affecting Pulse Oximetry

• Monitored values can exhibit physiologic and instrument variability. • Monitoring devices can be noninvasive or invasive. • Alarm systems should be set to alert caregivers properly yet avoid false alarms. • Monitors can run continuously and measure what caregivers cannot see. • The best monitors are caregivers who can assess and make decisions based on understanding the patient’s global status.

• Motion artifact • Environmental light (e.g., sunlight, fluorescence) • Anemia • Deeply pigmented skin • Carboxyhemoglobin, methemoglobin • Nail polish • Blood-borne dyes

RULE OF THUMB  The caregiver must understand and interpret the information provided through monitoring. The key to the proper interpretation of information is understanding how it applies to the global status of the individual patient.

HISTORY Obtaining a history from a critically ill patient—in particular a patient with altered state of consciousness—can be difficult. However, attempting to obtain a history by speaking with the patient or family members can provide extremely useful information in the ICU. Information regarding the patient’s past medical history, psychologic status, habits of smoking and alcohol use, and physical abilities is important, especially considering some of the challenges that may arise in the course of care in ICU. In particular, it is important to know how a patient’s baseline state may affect the normal ranges of monitored values or the ability to be weaned quickly from mechanical ventilation.

PATHOPHYSIOLOGY AND MONITORING The problem often faced at the bedside when one is presented with monitoring data is that clinicians may begin treating the numbers rather than the underlying pathophysiology. For example, when a patient is mechanically ventilated and the peripheral capillary oxygen saturation (SpO2) level drops, the first step is to quickly determine whether the SpO2 reading seems correct by confirming a good waveform or correlation with clinical findings such as the patient’s appearance and objective measures such as the heart rate. If a drop in SpO2 seems real, the respiratory therapist (RT) may recommend increasing the fraction of inspired oxygen (FiO2) or adjusting the positive end-expiratory pressure (PEEP) in cases of refractory hypoxemia when there has been no response to moderate or high FiO2. Treating the patient rather than the number requires the clinician to consider first if the readings seem accurate and then to address the underlying cause (Box 52.2).

of the gas exchange (discussed in Chapter 19). Although ABGs can be drawn at the bedside, they usually require processing outside of the patient’s room, either at a point-of-care machine or by the hospital laboratory. The most common bedside monitoring surrogates for O2 uptake and CO2 clearance are the SpO2 and respiratory rate (minute ventilation when the patient is mechanically ventilated). Both monitoring options have benefits, but each also has considerable limitations.

MONITORING OXYGENATION Tissue oxygenation depends on FiO2, inspired partial pressure of oxygen (PiO2), alveolar oxygen tension (PAO2), arterial oxygenation (PaO2, SaO2, oxygen content of arterial blood CaO2), oxygen delivery, tissue perfusion, and O2 uptake.

ARTERIAL PULSE OXIMETRY ABG analysis has been the accepted method of detecting hypoxemia in critically ill patients, but obtaining arterial blood can be painful and cause complications; moreover, ABG analysis does not provide immediate or continuous data. For these reasons, SpO2 has become the standard for a continuous, noninvasive assessment of SaO2. However, it too has significant limitations (see Box 52.2).1,2 SpO2 does not measure PaCO2, and patients breathing an elevated FiO2 can retain CO2 (increased PaCO2), although SpO2 values are acceptable. Ventilatory failure may go unnoticed unless ABGs are measured (see Chapter 19).

RULE OF THUMB  There are two very important problems with relying on SpO2 to monitor adequate respiratory function: (1) SpO2 values reflect oxygenation, not ventilation; and (2) SpO2 measurement is susceptible to numerous factors that can produce false values.

MINI CLINI Trusting the Pulse Oximeter

RULE OF THUMB  Treating the patient rather than the number requires the clinician to consider first whether the readings seem accurate and then to address the underlying cause.

The function of the lungs is the uptake of oxygen and the removal of carbon dioxide (see Chapter 12). The arterial blood gas (ABG) gives valuable information regarding the effectiveness

Problem A newborn of 32 weeks’ gestation is intubated and receiving continuous positive airway pressure (CPAP) therapy. The patient appears to be in mild to moderate respiratory distress, yet her SpO2 is 98%. Hurricane spray (20% benzocaine) had been used to reduce the irritation of the endotracheal tube. Analysis of ABG values reveals a PaO2 of 325 mm Hg, and the co-oximeter shows a methemoglobin value of 38%.

CHAPTER 52  Monitoring the Patient in the Intensive Care Unit

MINI CLINI—cont’d

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BOX 52.3  Murray Lung Injury Score

Trusting the Pulse Oximeter

Component

Solution The most common problems with the fidelity of pulse oximeter readings are motion artifacts, interference by external light sources, or malposition of the sensor. Each of these problems can be assessed easily and quickly. In this case, the clinical symptoms did not correlate with an acceptable SpO2 value. Because adequate O2 delivery is the ultimate goal, CO2 and O2-carrying ability must be considered as causes of the respiratory distress. The high methemoglobin value, most likely caused by the hurricane spray, necessitates immediate therapy with methylene blue dye. Although the pulse oximeter can be an excellent, safe means of monitoring blood oxygenation, there must be a wary vigilance regarding the values it provides.

Chest X-Ray No alveolar consolidation 0 Alveolar consolidation confined to one quadrant 1 Alveolar consolidation confined to two quadrants 2 Alveolar consolidation confined to three quadrants 3 Alveolar consolidation in all four quadrants 4 Hypoxemia Score 0 PaO2/FiO2 >300 1 PaO2/FiO2 225–299 2 PaO2/FiO2 175–224 3 PaO2/FiO2 100–174 4 PaO2/FiO2 15 cm H2O Respiratory System Compliance Score (When Available) 0 Compliance ≥80 mL/cm H2O Compliance 60–79 mL/cm H2O 1 Compliance 40–59 mL/cm H2O 2 Compliance 20–39 mL/cm H2O 3 4 Compliance ≤19 mL/cm H2O

OXYGEN CONSUMPTION Oxygen consumption (V̇ O2) is the volume of O2 consumed by the body in milliliters (mL) per minute. Normal resting V̇ O2 is approximately 250 mL/min, and V̇ O2 increases with activity, stress, and temperature. Oxygen consumption and measurement are discussed in Chapter 12.

Alveolar-Arterial Oxygen Tension Difference The alveolar-arterial oxygen tension difference (P[A–a]O2) is a useful measurement of the efficiency of gas exchange. A healthy person breathing room air has a P(A−a)O2 of approximately 5 to 15 mm Hg. This value increases with age to approximately 10 to 20 mm Hg in elderly adults. P(A−a)O2 also increases normally with an increase in FiO2. An abnormal increase in P(A−a) O2 is associated with gas-exchange problems. This measurement is discussed in greater detail in Chapter 12.

PaO2/FiO2 Ratio The PaO2/FiO2 ratio is easy to calculate and a reliable index of gas exchange; it is one of the commonly used oxygenation measurements in research studies involving patients in acute respiratory failure. The PaO2/FiO2 ratio provides an index for the effect of O2 on PaO2 when a range of FiO2 settings may be prescribed. The index allows comparisons of severity between patients or when FiO2 changes in the same patient. Every bedside clinician should be aware of the PaO2/FiO2 in their patients when ABG values are available. More information may be found in Chapter 12.

Murray Lung Injury Score To monitor the severity of acute respiratory distress syndrome (ARDS), Murray and colleagues3 developed a lung injury score. This score quantifies the injury level using the following four factors: chest radiographic findings, PaO2/FiO2 ratio, PEEP setting, and compliance. The Murray lung injury score is an example of a composite score that allows quantification of lung status according to different aspects of the injury—gas exchange, radiographic findings, and mechanics. This score is used as an index of the effectiveness of therapy or for interstudy comparisons. The method for calculating the Murray lung injury score is shown in Box 52.3. Other measures of lung injury are listed in Box 52.4.

Value

The final value is obtained by dividing the aggregate sum by the number of components used. Score   No lung injury: 0   Mild to moderate lung injury: 0.1–2.5   Severe lung injury (ARDS): >2.5

BOX 52.4  Measures of Decreased Blood

Oxygenation or Lung Injury • • • • • •

↓ SpO2 ↓ PaO2 ↑ P(A−a)O2 (PAO2−PaO2) ↓ P/F ratio (PaO2/FiO2) ↑ Shunt/venous admixture ↑ Murray lung injury score

Other Oxygenation Measurements Other important measures of oxygenation (not as routinely measured), including oxygen consumption, the alveolar-arterial oxygen tension difference (A–aO2), the oxygenation index (OI), and the quantification of shunt. These are covered in detail in Chapter 12.

MONITORING VENTILATION As in the case of oxygenation, the adequacy and efficiency of ventilation is routinely evaluated in the ICU (Box 52.5). Monitoring of patients receiving mechanical ventilatory support in the ICU includes measurement of the patient’s tidal volume (VT), respiratory rate (f), and minute ventilation (V̇ E). It is

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SECTION VI  Acute and Critical Care

BOX 52.5  Monitoring the Adequacy

BOX 52.6  Causes of Increased and

• Respiratory volume and rate (VT, f, V̇ E) • PaCO2 • VD/VT • Capnometry (not for routine use but in special situations, such as ensuring tracheal intubation and cardiac blood flow in resuscitation efforts)

Increased PETCO2 • Decreased effective ventilation (↓ VT, ↓ V̇ E, ↓ V̇ A, ↑ PaCO2) • Increased CO2 production (V̇ CO2) (agitation, stress, shivering, fighting the ventilator, pain, anxiety, recovery from sedation or paralysis)

of Ventilation

Begin inhalation

PCO2

III

II

Decreased End-Tidal Carbon Dioxide Values

Decreased PETCO2 • Increased effective ventilation (↑ VT, ↑ V̇ E, ↑ V̇ A, ↓ PaCO2) • Marked decrease in effective ventilation (↓↓V̇ T approaching dead space volume; rapid shallow breathing) • Decreased CO2 production (V̇ CO2) (sedation, sleep, cooling) • Decrease in lung perfusion (pulmonary embolus, decreased CO) Absent PETCO2 • Apnea • Cardiac arrest • Ventilator disconnect or malfunction • Airway obstruction

I Begin exhalation

Time

Fig. 52.1  Time-Based Capnograph. Phase I, anatomic dead space; Phase II, transition from anatomic dead space to alveolar plateau; Phase III, the alveolar plateau.

important to understand that the effectiveness of minute ventilation depends on alveolar ventilation (V̇ A). Significant changes in arterial pH can still occur despite the maintenance of minute ventilation when patients have a significant change in dead space and intrapulmonary shunt.

CAPNOGRAPHY As discussed in Chapter 19, capnometry is the measurement of CO2 at the airway opening during the ventilatory cycle. Capnography refers to plotting CO2 concentration against time or against exhaled volume. The normal CO2 waveform is displayed in Fig. 52.1. Patients for whom capnometry may be a useful monitoring tool include those with normal lungs but an unstable ventilatory drive who are breathing spontaneously or receiving low-level ventilatory support. In these patients, capnometry readings should initially be validated by comparison with PaCO2. Changes in end-tidal PCO2 (PETCO2) can be used to alert the clinician to potential changes in patient ventilation. Thereafter, periodic reevaluation should be performed as the patient’s clinical state changes. Capnometry has been extremely useful in emergency situations, such as to verify endotracheal intubation and assess blood flow during or after cardiac arrest. Small in-line CO2 monitors that employ colorimetry are now routinely used to verify endotracheal intubation.4 Although PETCO2 and PaCO2 values tend to correlate at a single point in time, correlation between changes in PETCO2 and in PaCO2 is weaker.5 Decreases in ventilation are reflected by

increases in PETCO2 and PaCO2. However, with very small VT, PaCO2 increases, whereas PETCO2 may decrease. Although the appropriate role of capnometry in critical care may be unclear, integration of capnometry into modern ventilators is reasonable because the primary role of the ventilator is CO2 elimination. As a guide for clinicians, the American Association for Respiratory Care (AARC) has created a clinical practice guideline for using capnometry in ventilated patients.6 Box 52.6 lists common causes of changes in monitored PETCO2 values. Volumetric CO2 monitoring holds promise in continuously monitoring ventilation efficiency. VCO2 can be continuously monitored in a patient being liberated from mechanical ventilation as an indicator of adequate or improving ventilatory efficiency.7 The volumetric capnogram has been examined as a potential tool for detecting a pulmonary embolism,8 tracking the efficiency of mechanical ventilation,8 and calculating dead space.9 The relationship between VCO2 and dead space also makes it a valuable tool in the optimization of PEEP.

Dead Space As discussed in Chapter 11, the dead space/tidal volume (VD/ VT) ratio is a measure of the efficiency of gas exchange. This ratio is an estimate of the proportion of ventilation participating in the diffusion of CO2. VD/VT can be calculated from the Enghoff modification of the Bohr equation, as follows: VD VT = (PaCO2 − PECO2 ) PaCO2 where PECO2 is the CO2 concentration in mixed expired gas. Frequently, the VD/VT ratio is increased in patients with congestive heart failure, pulmonary embolism, ARDS, or pulmonary hypertension and in those undergoing mechanical ventilation. The VD/VT ratio has been used to evaluate patients being considered for liberation from mechanical ventilation. A VD/VT ratio greater than 0.60 generally requires continuation of ventilatory support. Increased VD/VT in the early phase of ARDS has been associated with an increased risk of death.3,10

CHAPTER 52  Monitoring the Patient in the Intensive Care Unit

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MONITORING OF INSPIRED AND EXHALED GAS VOLUMES

of developing ventilator-induced lung injury. However, the limit for Pplat depends on the resulting lung stress and strain.

Although the best index of effective ventilation is the measurement of PaCO2, measurement of inspired and expired gas volumes is an important aspect of monitoring patients receiving mechanical ventilatory support. For patients receiving controlled mechanical ventilation, minute ventilation (V̇ E), respiratory rate (f), and VT are assessed by

MEAN AIRWAY PRESSURE

VE = (VT )(f) and VT average = VE f With an adequate VT, increases in V̇ E tend to increase alveolar ventilation and decrease PaCO2, whereas decreases in V̇ E tend to have the opposite effect. However, in the presence of rapid shallow breathing with normal or elevated V̇ E, a decrease in effective ventilation can result in an increase in PaCO2. This effect is caused by ineffective shallow tidal breaths that are at or below the volume of the dead space. Spontaneous respiratory rate often is a sensitive indicator of the need for mechanical ventilation. Rates greater than 25 breaths/min in adults may indicate distress, and a rate greater than 30 breaths/min with a spontaneous VT of less than 300 mL often indicates the need for mechanical ventilatory support in adults because a large proportion of ventilatory effort is being expended to move dead-space gases.

Inspired Versus Expired Tidal Volume During Mechanical Ventilation Normal inspired VT and expired VT should be nearly the same. However, in the presence of an air leak, inspired VT may be larger than expired VT, and measurement of delivered VT versus exhaled VT may be useful in detecting and quantifying the size of a leak—a situation that may require immediate attention. When a significant mismatch between inspired and expired VT is noticed, consider not only the possibility of a cuff leak with the endotracheal or tracheostomy tube but also check the circuit connections. Alternatively, be sure to monitor the ventilator waveform graphics and assess the patient’s respiratory rate, looking for the presence of an insufficient expiratory time leading to auto-PEEP.

PEAK AND PLATEAU PRESSURES The maximum value of pressure at the airway opening during a ventilatory cycle is routinely monitored in the ICU as peak airway pressure. Peak airway pressure greater than 50 to 60 cm H2O is generally discouraged because high values of peak pressure carry an increased risk of lung injury and hypotension.11 During volume-targeted modes of ventilation, an increase in peak pressure results from increased resistive pressure or increased elastic pressure from decreased lung or chest wall compliance. During pressure-targeted modes of ventilation, increased resistive pressure or increased elastic pressure results in a decrease in delivered tidal volume rather than the increase in peak or plateau pressure (Pplat). Measurement of Pplat helps to differentiate between the resistive and elastic components. The Pplat level should be monitored for all ventilated patients. Pplat ideally should not exceed 28 cm H2O, because elevated Pplat increases the likelihood

Mean airway pressure (MAP) represents the average airway pressure over the total ventilatory cycle. Correct measurement of this value requires continuous sampling of airway pressure at the airway opening; this is an automated feature of modern ventilators. MAP is related to mean lung volume, which correlates with oxygenation if perfusion is adequate. When MAP is increased, arterial O2 levels often improve, but venous return and subsequently arterial pressure can be adversely affected. In an effort to increase oxygenation while monitoring arterial pressure, the clinician can manage MAP by several means, including VT, frequency, inspiratory-to-expiratory (I:E) ratio, and PEEP. The management of MAP relates to a concern for improving oxygenation balanced against its detrimental influence on venous return. Normally, expiratory resistance is greater than (twice) inspiratory resistance, and mean alveolar pressure normally is greater than MAP. For patients with chronic obstructive pulmonary disease (COPD) and elevated expiratory resistance, high mean alveolar volume can be significant during mechanical ventilation. There is an understandable caution when MAP is being increased, usually by increasing PEEP, yet two ventilator modes apply dramatic increases in MAP—high-frequency oscillation and airway pressure release ventilation. The marked improvements in oxygenation seen with these modes can be attributed to high MAP. In the case of high-frequency oscillation, the lungs are never allowed to derecruit between breaths. Airway pressure release ventilation is more complicated because the lung deflates to varying unknown alveolar volumes on exhalation. In using either mode, end-expiratory alveolar lung volume status cannot easily be determined, but oxygenation is often improved.

DRIVING PRESSURE Driving pressure is a measure of the pressure difference between Pplat and total PEEP (PEEP plus auto-PEEP). The swing in pressure from end-expiration to end-inspiration may be an independent stress factor on the lungs. Consider driving pressure as the amount of energy applied to the lung: the higher the energy applied to the lung, the greater the potential for lung injury. In general, the driving pressure should be kept below 15 cm H2O.12 RULE OF THUMB  Driving pressure is a simple bedside value obtained by determining the pressure difference between plateau pressure and total PEEP. Clinicians should attempt to keep this value below 15 cm H2O. The use of lower tidal volume and proper levels of PEEP can help to achieve this ventilation goal.

RESISTANCE Depending on the driving pressure measured, various resistances can be calculated, including airway, pulmonary, chest wall, and

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total respiratory system resistance. An airway resistance (Raw) can be determined dynamically from simultaneous measurements of airflow and the pressure difference between the airway opening (Pao) and the alveoli (Palv) by Raw = (Pao − Palv)/flow. Because resistance changes throughout inspiration and expiration and expiratory resistance generally is greater than inspiratory resistance, instantaneous measures of resistance are not commonly performed clinically. Inspiratory resistance can be calculated simply during constant-flow volume ventilation by using a short (0.5-second) pause at the end of volume delivery. This allows for the separation of peak and plateau pressures in real time. It allows monitoring of airway status over time or after the effects of bronchodilator therapy and is determined by dividing the pressure change by the flow rate, as follows: Raw = ∆P ∆F = (Ppeak − Pplat ) flow where Ppeak is peak airway pressure and Pplat is plateau pressure. Automated methods of measuring expiratory resistance have been integrated into some ventilators. In ventilated patients, a significant component of the total flow resistance is from endotracheal tubes.13 In healthy persons, flow is relatively laminar during tidal ventilation and becomes turbulent only with increasing ventilatory demands. The flow resistance offered by the endotracheal tube increases markedly with increasing flow and varies with the size of the tube. Normal airway resistance is approximately 1 to 2 cm H2O/L/s; however, intubated patients receiving mechanical ventilatory support typically have an airway resistance of 5 to 10 cm H2O/L/s or more. Automated tube compensation modes have been added to mechanical ventilators to deliver flow that accounts for the added resistance of the endotracheal tube. Common causes of changes in airway resistance in mechanically ventilated patients are listed in Box 52.7.

MINI CLINI Airway Resistance Problem A patient receiving volume-assist controlled ventilation with a constant flow of 60 L/min has high peak airway pressures of 35 cm H2O. You perform an inspiratory hold on the ventilator and determine that the plateau pressure is 22 cm H2O. Upon auscultation you hear bilateral wheezes on exhalation. What does this finding indicate? Solution The patient has high airway resistance (13 cm H2O), which could be caused by bronchospasm. The response to any intervention, such as administering bronchodilators, can be monitored in real time by using a pause time on the ventilator of 0.2 to 0.3 seconds. This will allow a plateau pressure to be displayed in real time and breath by breath on the ventilator. The change in the difference between peak and plateau pressure will indicate a decrease in airway resistance.

MONITORING LUNG AND CHEST WALL MECHANICS Ventilation of the lungs involves overcoming the flow-resistive, inertial, and elastic properties of the respiratory system. In a

BOX 52.7  Common Causes of Changes in

Compliance and Resistance in Mechanically Ventilated Patients

Decreased Compliance • ↓ Lung compliance (atelectasis, pneumonia, pulmonary edema, ARDS, pneumothorax, fibrosis, bronchial intubation) • ↓ Thoracic compliance (ascites, chest wall deformity) Increased Compliance • ↑ Lung compliance (improvement in any of the foregoing conditions, pulmonary emphysema) • ↑ Thoracic compliance (improvement in any of the foregoing conditions; flail chest; position change—sitting patient up) Increased Resistance • Small endotracheal tube, secretions plugging endotracheal tube, biting on endotracheal tube • ↑ Bronchospasm, mucosal edema • ↑ Secretions • ↑ Airway obstruction • High gas flow rate (or ↑ gas flow) Decreased Resistance • ↓ Improvement in any of the foregoing conditions • ↓ Bronchodilator administration • ↓ Suctioning and airway care • ↓ Use of lower inspiratory gas flow rate

ventilated patient, change in airway pressure during ventilation is used to determine the compliance of the total respiratory system. Pressure changes measured by an esophageal balloon reflect compliance of the chest wall. The difference between the compliance of the respiratory system and chest wall is the lung compliance (lung compliance can also be measured in the passively ventilated patient using the change in transpulmonary pressure). One method to assess the compliance of the respiratory system and its relation to lung volume is through the use of a pressurevolume (P-V) curve. There is normally a difference in the P-V relationship during inflation and deflation. However, a large difference between inflation and deflation, called hysteresis, typically implies that lung units have been recruited after a threshold level of pressure was applied. To measure a static P-V curve of a ventilated patient from resting at functional residual capacity (FRC) to total lung capacity, until more recently a calibrated syringe (referred to as a supersyringe) ranging from 1.5 to 3 L was used to inject 50 to 100 mL increments into the lungs while airway pressure was recorded. A P-V curve can be measured more easily by the continuous delivery of a low flow of gas into the lung (65% 15—left ventricular failure, fluid overload) 20 mm Hg (same as ↑ PAP) 18 mm Hg (left ventricular failure, fluid overload) >20 mm Hg (interstitial edema) >25 mm Hg (alveolar filling) >30 mm Hg (frank pulmonary edema) 8 L/min (elevated) (see cardiac index) 4 L/min/m2 (elevated owing to stress, septic shock, fever, hypervolemia, or drugs [dobutamine, dopamine, epinephrine, isoproterenol, and digitalis]) 1400 dynes-s/cm5 (increased owing to vasoconstrictors [dopamine, norepinephrine, and epinephrine], hypovolemia, late septic shock) 250 dynes-s/cm5 (hypoxemia, ↓ pH, PaCO2, vasopressors, emboli, emphysema, interstitial fibrosis, pneumothorax) 10 s), visual stimulation Briefly awakens with eye contact to voice (10 mm Hg) suggest a position near the critical inflection point of the cranial P-V curve. Elevations in ICP to 15 to 20 mm Hg compress the capillary bed and compromise microcirculation. At ICP levels of 30 to 35 mm Hg, venous drainage is impeded, and edema develops in uninjured tissue. Even when autoregulatory mechanisms are intact, cerebral perfusion cannot be maintained if ICP increases to within 40 to 50 mm Hg of the mean arterial pressure. When ICP approximates mean arterial pressure, perfusion stops and the brain dies. Two categories of ICP monitoring techniques are currently available. Fluid-filled systems have external transducers, such as an intraventricular catheter and subarachnoid bolts. Solid-state systems have miniature pressure transducers that can be inserted in the lateral ventricle, brain parenchyma, or subarachnoid or epidural space.

TROUBLESHOOTING Identification and correction of patient- and ventilator-related problems during mechanical ventilatory support are primary responsibilities of the RT. Under ideal circumstances, potential problems are identified before they occur or before they can cause harm to the patient. Potential problems with the patient include anxiety, agitation, altered mental status, fighting the ventilator, hypoxemia, hypoventilation, and the development of metabolic acidosis. The patient may experience acute changes in respiratory rate, heart rate, blood pressure, and CO2. Other common patient-related problems include excessive secretions, bronchospasm, and other causes of decreased compliance or increased resistance. Recognition of signs of pneumothorax, pneumomediastinum or subcutaneous emphysema, airway malfunction or leaks, and chest tube leaks should receive prompt attention. Problems associated with the ventilator include leaks or malfunctions in the system, inappropriate ventilator settings (including trigger sensitivity and inspiratory flow rate), development of auto-PEEP, and improper humidification. Box 52.14 lists causes of sudden respiratory distress in patients receiving mechanical ventilatory support. Box 52.15 lists steps for managing sudden respiratory distress. Table 52.11 summarizes troubleshooting of the patient–ventilator system. Pharmacologic paralysis should be considered only when no other alternatives are effective. The one exception to this guideline is the patient presenting with severe ARDS (PaO2/FiO2 100 mm Hg). In order to gain control of the patient’s physiologic status, it is now recommended to paralyze these patients for up to 48 hours. The use of neuromuscular blocking agents can mask other patient problems, and ventilator malfunction or disconnection

CHAPTER 52  Monitoring the Patient in the Intensive Care Unit

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BOX 52.14  Causes of Sudden Respiratory Distress in a Patient Receiving Ventilatory Support Patient-Related Causes • Artificial airway problems • Movement of endotracheal tube • Cuff herniation • Cuff leak • Kinking of endotracheal tube • Foreign body • Transesophageal fistula • Innominate artery rupture • Malpositioned nasogastric tube • Secretions • Bronchospasm • Pneumothorax • Pulmonary edema • Pulmonary embolism • Acute hypoxemia

• Blood in endotracheal tube • Dynamic hyperinflation • Abnormal respiratory drive • Alteration in body posture • Drug-induced problems • Abdominal distention • Agitation Ventilator-Related Causes • Ventilator malfunction • Circuit malfunction • Leaks or disconnects • Condensate • In-line nebulizers • Inadequate ventilatory support • Patient–ventilator asynchrony

From Tobin MJ, Alex CJ, Fahey PJ: Fighting the ventilator. In: Tobin MJ, editor: Principles and practice of mechanical ventilation, New York, 2006, McGraw-Hill.

BOX 52.15  Steps for Managing Sudden Distress in a Patient Receiving Ventilatory Support 1. Remove the patient from the ventilator. 2. Initiate manual ventilation with 100% O2. 3. Patient improvement indicates that the ventilator is the cause of distress. 4. Lack of improvement indicates the problem is within the patient.

5. If death appears imminent, consider and manage the most likely causes; check for airway obstruction (by passing a suction catheter), a dislodged endotracheal tube, or a pneumothorax. 6. If death is not imminent, wait until the patient’s condition is stable before attempting a more detailed assessment including a chest radiograph.

Modified from Tobin MJ, Alex CJ, Fahey PJ: Fighting the ventilator. In: Tobin MJ, editor: Principles and practice of mechanical ventilation, New York, 2006, McGraw-Hill.

TABLE 52.11  Troubleshooting the Patient–Ventilator System Clue to Problem

Possible Cause

Corrective Action

Decreased minute ventilation or VT

Leak around endotracheal or chest tube Decreased patient-triggered respiratory rate

Check all connections for leaks. Evaluate patient. Check sensitivity. Measure auto-PEEP. Increase set rate. Change mode. Evaluate patient. Clear airway of secretions. Check patient–ventilator system. Check with external respirometer. Check respiratory rate. Check sensitivity. Change mode. Check patient–ventilator system. Evaluate patient. Consider ABG and SpO2 values. Decrease pressure. Decrease inspiratory time. Check with external respirometer. Check patient–ventilator system. Evaluate patient. Evaluate patient. Consider ABG and SpO2 values.

Increased minute ventilation or VT

Decreased lung compliance Airway secretions Altered settings Malfunctioning volume monitor Increased patient-triggered respiratory rate

Altered settings Hypoxia Increased lung compliance

Change in respiratory rate

Malfunctioning volume monitor Altered setting Increased metabolic demand Hypoxemia

Continued

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TABLE 52.11  Troubleshooting the Patient–Ventilator System—cont’d Clue to Problem

Possible Cause

Corrective Action

Sudden increase in peak airway pressure

Coughing Airway secretions or plugs Ventilator tubing kinked or filled with water Changes in patient position Endotracheal tube in right mainstem bronchus Patient–ventilator asynchrony

Alleviate uncontrolled coughing. Clear airway secretions. Check for kinks and water. Consider repositioning patient. Verify position. Correct asynchrony. Check for adequate peak flow. Verify with waveforms. Identify cause and treat. Insert chest tube. Evaluate for problems, such as atelectasis, increasing lung water, bronchospasm. Check patient–ventilator systems for leaks. Verify with waveforms. Check for active inspirations. Evaluate patient. Calibrate analyzer. Change O2 sensor. Correct failure. Correct failure. Check ventilator reservoir. Check flow setting and correct. Check settings and correct. Check setting and correct. Clear airway of secretions. Measure minute ventilation. Wait. Correct temperature control setting. Turn off heater during treatment. Replace heater. Adjust PEEP level. Adjust PEEP level. Check settings and correct. Evaluate patient and correct if possible. Determine whether current settings are the intended ones.

Gradual increase in peak airway pressure Sudden decrease in peak airway pressure

FiO2 drift

I:E ratio too high or too low

Inspired gas temperature too high

Changes in PEEP

Changes in static pressure Changes in ventilator setting

Bronchospasm Pneumothorax Diffuse, reactive, or obstructive process Volume loss from leaks in the system

O2 analyzer error Blender piping failure O2 source failure O2 reservoir leak Altered inspiratory flow Alteration in other settings that control I:E ratio Alteration in sensitivity setting Airway secretions (pressure ventilator) Subtle leaks Addition of cool water to humidifier Altered settings Adding cool gas by small-volume nebulizer treatment Thermostat failure Change in VT Change in compliance Altered settings Changes in lung compliance Changes in these settings resulting from deliberate or accidental adjustment of dials or knobs

PEEP, Positive end-expiratory pressure. Modified from Martz K, Joiner JW, Shepherd RM: Management of the patient-ventilator system: a team approach, ed 2, St. Louis, 1994, Mosby.

BOX 52.16  Pharmacologic Agents Used to Produce Sedation or Paralysis I. Benzodiazepine tranquilizing agents A. Diazepam (Valium) B. Lorazepam (Ativan) C. Midazolam (Versed) II. Sedative hypnotics and miscellaneous agents A. Sodium thiopental (Pentothal) B. Etomidate (Amidate) C. Haloperidol (Haldol) D. Propofol (Diprivan) E. Dexmedetomidine (Precedex) III. Narcotic analgesics A. Morphine B. Fentanyl (Sublimaze) IV. Neuromuscular blocking agents A. Nondepolarizing (competitive) agents 1. Steroidal agents I. Pancuronium (Pavulon)

II. Pipecuronium (Arduan) III. Rocuronium (Zemuron) IV. Vecuronium (Norcuron) 2. Benzylisoquinolinium esters I. Atracurium (Tracrium) II. Cisatracurium (Nimbex) III. Doxacurium (Nuromax) IV. Metocurine (Metubine) V. Mivacurium (Mivacron) VI. Tubocurarine (Tubarine) B. Depolarizing agents 1. Succinylcholine (Anectine, Quelicin) 2. Decamethonium (Syncurine)

CHAPTER 52  Monitoring the Patient in the Intensive Care Unit

in the care of a paralyzed patient can be catastrophic. In addition, some patients receiving neuromuscular blocking agents in the ICU may experience prolonged neuropathy. Pharmacologic agents used to produce sedation or paralysis in the ICU are listed in Box 52.16.

SUMMARY CHECKLIST • Caregivers must be experienced at filtering the noise from the changes in monitored variables that require attention. Caregivers must recognize false alarms. They must also discriminate real pathophysiologic changes from normal physiologic variations and variations inherent in the data. • Because only caregivers can make choices about altering care, caregivers continue to be the most important monitors. • Monitoring of the respiratory system includes assessment of ventilation, gas exchange, and respiratory system mechanics and function. • Ventilation is monitored by measurement of VT, respiratory rate, and minute ventilation and by assessment of dead space and alveolar ventilation. • Gas exchange is routinely monitored with ABG analysis and pulse oximetry. Derived values such as VD/VT, P(A−a)O2 difference, PaO2/FiO2 ratio, shunt, and lung injury score can clarify the nature and severity of gas-exchange abnormality. Arterial PaCO2 is the best index of alveolar ventilation. • Respiratory system mechanics are routinely monitored by tracking peak pressure, Pplat, driving pressure, auto-PEEP, compliance, and resistance. • When any patient is being mechanically ventilated, ideally, the tidal volume should be 4 to 8 mL/kg of predicted body weight, and the plateau pressure should be less than 28 cm H2O. • Monitoring of transpulmonary pressure is becoming increasingly important in managing patients with decreased chest wall compliance and those with severe ARDS requiring high PEEP levels. • Factors such as WOB, f/VT, VC, MIP, and MVV can be extremely helpful in assessing the need to increase ventilatory support or in assessing the potential for weaning. • Advanced monitoring techniques include EIT, diaphragm and lung ultrasound, lung stress and strain, stress index, and esophageal pressure monitoring. • The most important responsibility of the RT in the ICU is monitoring of the patient–ventilator system. • Monitoring of the patient–ventilator system includes overall assurance of the integrity and safety of the system. Monitoring requires complete knowledge of the ventilator settings; all aspects of ventilator function; the circuitry; airway status; gas exchange; ventilator graphics; lung mechanics; alarms; and the overall care, safety, and comfort of the patient. • Acute changes in cardiac performance, cardiovascular status, or impulse conduction (ECG) can be life threatening; some form of monitoring of the heart, vascular system, and ECG is necessary in the care of nearly all patients in the ICU. • Hemodynamic monitoring requires the use of invasive pulmonary arterial, central venous, and arterial catheters. Values

•

•

•

•

1181

obtained with these monitoring lines must be carefully interpreted by experienced caregivers. All ICU patients should receive ECG monitoring. Monitoring of changes in neurologic status is extremely important and is more often overlooked than the monitoring of other organ systems. The neurologic examination includes assessment of mental status, pupillary response, eye movements, corneal response, gag reflex, and respiratory rate and pattern and a general motor and sensory evaluation. ICP monitoring may be needed to detect or manage elevated ICP. Global index monitoring is calculation of an illness level score that is an estimate of the risk of mortality from numerous monitoring values. Illness scores are not used in the care plan for an individual patient, but scoring systems are widely used in clinical studies. The APACHE II system is among the most popular of these estimates. Troubleshooting the patient–ventilator system is aimed at identifying and correcting problems before they harm the patient.

REFERENCES 1. Mendelson Y: Pulse oximetry: theory and applications for noninvasive monitoring, Clin Chem 38:1601–1607, 1992. 2. Cairo JN, Pilbeam SP: Mosby’s respiratory care equipment, ed 7, St Louis, 2004, Mosby. 3. Murray JF, Matthay MA, Luce JM, et al: An expanded definition of the adult respiratory distress syndrome, Am Rev Respir Dis 138:720–723, 1988. 4. Rabitsch W, Nikolic A, Schellongowski P, et al: Evaluation of an end-tidal portable ETCO2 colorimetric breath indicator (COLIBRI), Am J Emerg Med 22:4–9, 2004. 5. Hinkelbein J, Floss F, Denz C, et al: Accuracy and precision of three different methods to determine Pco2 (Paco2 vs. Petco2 vs. Ptcco2) during interhospital ground transport of critically ill and ventilated adults, J Trauma Acute Care Surg 65:10–18, 2008. 6. AARC Clinical Practice Guideline: Capnography/capnometry during mechanical ventilation: revised 2003, Respir Care 48:534–539, 2003. 7. Suarez-Sipmann F, Bohm SH, Tusman G: Volumetric capnography: the time has come, Curr Opin Crit Care 20:333–339, 2014. 8. Yem JS, Turner MJ, Baker AB: Sources of error in partialrebreathing pulmonary blood flow measurements in lungs with emphysema and pulmonary embolism, Br J Anaesth 9:732– 741, 2006. 9. Siobal MS, Ong H, Valdes J, et al: Calculation of physiologic dead space: comparison of ventilator volumetric capnography to measurements by metabolic analyzer and volumetric CO2 monitor, Respir Care 58:114–1151, 2013. 10. Nuckton TJ, Alonso JA, Kallet RH, et al: Pulmonary dead-space fraction as a risk factor for death in the acute respiratory distress syndrome, N Engl J Med 346:1281–1286, 2002. 11. Stewart TE, Meade MO, Cook DJ, et al: Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. Pressure- and Volume-Limited Ventilation Strategy Group, N Engl J Med 338:35–361, 1998.

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12. Amato MBP, Meade MO, Slutsky AS, et al: Driving pressure and survival in the acute respiratory distress syndrome, N Engl J Med 372:74–755, 2015. 13. Schumann S, Haberthuer C, Guttmann J: Compensating for endotracheal tube resistance, Anesth Analg 110:631–639, 2010. 14. Hubmayr RD: Perspective on lung injury and recruitment: a skeptical look at the opening and collapse story, Am J Respir Crit Care Med 165:164–1653, 2002. 15. Villar J, Pérez-Méndez L, Basaldúa S, et al: A risk tertiles model for predicting mortality in patients with acute respiratory distress syndrome: age, pressure, and P(aO(2))/F(IO(2)) at ARDS onset can predict mortality, Respir Care 56:420–428, 2011. 16. Gattinoni L, Carlesso E, Brazzi L, et al: Positive end-expiratory pressure, Curr Opin Crit Care 16:39–44, 2010. 17. Loring SH, O’Donnell CR, Behazin N, et al: Esophageal pressures in acute lung injury: do they represent artifact or useful information about transpulmonary pressure, chest wall mechanics, and lung stress?, J Appl Physiol 108:515–522, 2010. 18. Talmor DS, Fessler HE: Are esophageal pressure measurements important in clinical decision-making in mechanically ventilated patients, Respir Care 55:162–164, 2010. 19. Gattinoni L, Chiumello D, Carlesso E, et al: Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distresssyndrome patients, Crit Care 8:350–355, 2004. 20. Yoshida T, Amato MBP, Grieco DL, et al: Esophageal manometry and regionaltranspulmonary pressure in lung injury, Am J Respir Crit Care Med 197:1018–1026, 2018. 21. Chiumello D, Carlesso E, Cadringher P, et al: Lung stress and strain during mechanical ventilation for acute respiratory distress syndrome, Am J Respir Crit Care Med 178:346–355, 2008. 22. Graf J, Santos A, Dries D, et al: Agreement between functional residual capacity estimated via automated gas dilution versus via computed tomography in a pleural effusion model, Respir Care 55:1464–1468, 2010. 23. Yilmaz M, Gajic O: Optimal ventilator settings in acute lung injury and acute respiratory distress syndrome, Eur J Anaesthesiol 25:89–96, 2008. 24. Briel M, Meade M, Mercat A, et al: Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome, J Am Med Assoc 30:865–873, 2010. 25. Grasso S, Terragni P, Mascia L, et al: Airway pressure-time curve profile (stress index) detects tidal recruitment/hyperinflation in experimental acute lung injury, Crit Care Med 32:1018–1027, 2004. 26. Sun X-M, Chen G-Q, Chen K, et al: Stress index can be accurately and reliably assessed by visually inspecting ventilator waveforms, Respir Care 63:1094–1101, 2018. 27. Formenti P, Graf J, Santos A, et al: Non-pulmonary factors strongly influence the stress index, Intensive Care Med 37:59– 600, 2011. 28. Mughal MM, Culver DA, Minai OA, et al: Auto-positive end- expiratory pressure: mechanisms and treatment, Cleve Clin J Med 72:801–809, 2005. 29. Blanch L, Bernabé F, Lucangelo U: Measurement of air trapping, intrinsic positive end-expiratory pressure, and dynamic hyperinflation in mechanically ventilated patients, Respir Care 50:110–123-124, 2005. 30. Junhasavasdikul D, Telias I, Grieco DL, et al: Expiratory flow limitation during mechanical ventilation, Chest 2018, doi:10.1016/j.chest.2018.01.046.

31. Kapasi M, Fujino Y, Kirmse M, et al: Effort and work of breathing in neonates during assisted patient-triggered ventilation, Pediatr Crit Care Med 2:9–16, 2001. 32. Purro A, Appendini L, De Gaetano A, et al: Physiologic determinants of ventilator dependence in long-term mechanically ventilated patients, Am J Respir Crit Care Med 161:111–1123, 2000. 33. Telias I, Damiani F, Brochard L: The airway occlusion pressure (P0.1) to monitor respiratory drive during mechanical ventilation: increasing awareness of a not-so-new problem, Intensive Care Med 2018, doi:10.1007/s00134-018-5045-8. THIS IS ONLINE AHEAD OF PRINT. 34. Mancebo J, Albaladejo P, Touchard D, et al: Airway occlusion pressure to titrate positive end-expiratory pressure in patients with dynamic hyperinflation, Anesthesiology 93:81–90, 2000. 35. Goligher EC, Fan E, Herridge MS, et al: Evolution of diaphragm thickness during mechanical ventilation. Impact of inspiratory effort, Am J Respir Crit Care Med 19:108–1088, 2015. 36. Goligher EC, Dres M, Fan E, et al: Mechanical ventilation– induced diaphragm atrophy strongly impacts clinical outcomes, Am J Respir Crit Care Med 197:204–213, 2018. 37. Yang KL, Tobin MJ: A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation, N Engl J Med 324:1445–1450, 1991. 38. Marini JJ, Smith TC, Lamb V: Estimation of inspiratory muscle strength in mechanically ventilated patients: the measurement of maximal inspiratory pressure, J Crit Care 1:3238, 1986. 39. Adams A: Pulmonary function in the mechanically ventilated patient, Respir Care Clin N Am 3:30–331, 1997. 40. Costa EL, V, Borges JB, Melo A, et al: Bedside estimation of recruitable alveolar collapse and hyperdistension by electrical impedance tomography, Intensive Care Med 35:1132–1137, 2009. 41. Bouhemad B, Mongodi S, Via G, et al: Ultrasound for ‘lung monitoring’ of ventilated patients, Anesthesiology 122:437–447, 2015. 42. Yoshida T, Torsani V, Gomes S, et al: Spontaneous effort causes occult pendelluft during mechanical ventilation, Am J Respir Crit Care Med 188:1420–1427, 2013. 43. Yoshida T, Uchiyama A, Fujino Y: The role of spontaneous effort during mechanical ventilation: normal lung versus injured lung, J Intensive Care Med 3:18–25, 2015. 44. Frerichs I, Amato MBP, van Kaam AH, et al: Chest electrical impedance tomography examination, data analysis, erminology, clinical use and recommendations: consensus statement of the TRanslational EIT developmeNt stuDy group, Thorax 72:8–93, 2017. 45. Wiener RS, Welch HG: Trends in the use of the pulmonary artery catheter in the United States, 1993-2004, JAMA 298: 423–429, 2007. 46. Mehta Y, Arora D: Newer methods of cardiac output monitoring, World J Cardiol 6:10229, 2014. 47. Liquori ME, Christenson RH, Collinson PO, et al: Cardiac biomarkers in heart failure, Clin Biochem 47:327–337, 2014. 48. TenHoor T, Mannino DM, Moss M: Risk factors for ARDS in the United States: analysis of the 1993 National Mortality Follow Back Study, Chest 119:1179–1184, 2001. 49. Nussbaum MS, Fischer JE: Pathogenesis of hepatic steatosis during total parenteral nutrition, Surg Annu 23:1–11, 1991. 50. Wong DT, Knaus WA: Predicting outcome in critical care: the current status of the APACHE prognostic scoring system, Can J Anaesth 3:374–383, 1991.

CHAPTER 52  Monitoring the Patient in the Intensive Care Unit 51. Wheeler MM: APACHE: an evaluation, Crit Care Nurs Q 32:4– 48, 2009. 52. Riker RR, Picard JT, Fraser GL: Prospective evaluation of the Sedation-Agitation Scale in adult ICU patients, Chest 112:32S33S, 1997. 53. Sessler CN, Gosnell MS, Grap MJ, et al: The Richmond Agitation–Sedation Scale: validity and reliability in adult intensive care unit patients, Am J Respir Crit Care Med 166:1338–1344, 2002. 54. Hayhurst CJ, Pandharipande PP, Hughes CG: Intensive care unit delirium: a review of diagnosis, prevention, and treatment, Anesthesiology 125:1229–1241, 2016.

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55. Bergeron N, Dubois M-J, Dumont M, et al: Intensive Care Delirium Screening Checklist: evaluation of a new screening tool, Intensive Care Med 27:859–864, 2001. 56. Ely EW, Inouye SK, Bernard GR, et al: Delirium in mechanically ventilated patients: validity and reliability of the confusion assessment method for the intensive care unit (CAM-ICU), JAMA 286:2703–2710, 2001. 57. Larson MD, Singh V: Portable infrared pupillometry in critical care, Crit Care 20:161, 2016.

53  Discontinuing Ventilatory Support Robert M. Kacmarek CHAPTER OBJECTIVES After reading this chapter you will be able to: • Discuss the relationship between ventilatory demand and ventilatory capacity as well as their relationship with ventilator discontinuance. • List the factors associated with ventilator dependence. • Explain how to evaluate a patient before attempting ventilator discontinuation or weaning. • List acceptable values for specific weaning indices used to predict a patient’s readiness for discontinuation of ventilatory support. • Describe factors that should be optimized before an attempt is made at ventilator discontinuation or weaning. • Describe techniques used in ventilator weaning, including daily spontaneous breathing trials, synchronized

• •

• • • • •

intermittent mandatory ventilation, pressure support ventilation, and other newer methods. Contrast the advantages and disadvantages associated with various weaning methods and techniques. Discuss the use of esophageal pressure, diaphragm electrical activity (EAdi), and ultrasound to assess weaning capabilities and predict weaning success. Discuss weaning of the morbidly obese patient. Discuss the new weaning guidelines provided by the ATS/ ACCP. Describe how to assess a patient for extubation. List the primary reasons why patients fail a ventilator discontinuance trial. Explain why some patients cannot be successfully weaned from ventilatory support.

CHAPTER OUTLINE Reasons for Ventilator Dependence, 1186 Ventilatory Workload and Demand, 1186 Ventilatory Capacity, 1186 Global Criteria for Discontinuing Ventilatory Support, 1187 Patient Evaluation, 1187 The Most Important Criterion, 1188 Weaning Indices, 1188 Ventilation, 1189 Oxygenation, 1190 Acid–Base Balance, 1190 Metabolic Factors, 1190 Renal Function and Electrolytes, 1191 Cardiovascular Function, 1191 Psychologic Factors and Central Nervous System Assessment, 1191 Integrated Indices, 1191 Evaluation of the Airway, 1192 Preparing the Patient, 1192 Optimizing the Patient’s Medical Condition, 1192 Patients’ Psychologic and Communication Needs, 1193 1184

Caregiver Preparation, 1193 Methods, 1194 Rapid Ventilator Discontinuation, 1194 Patients Who Need Progressive Weaning of Ventilatory Support, 1194 Spontaneous Breathing Trials, 1195 Continuous Positive Airway Pressure, 1197 Synchronized Intermittent Mandatory Ventilation, 1197 Pressure Support Ventilation, 1197 Synchronized Intermittent Mandatory Ventilation With Pressure Support Ventilation, 1198 Spontaneous Awaking Trials, 1198 Newer Techniques for Facilitating Ventilator Discontinuance, 1199 Mandatory Minute Volume Ventilation, 1199 Adaptive Support Ventilation/ Intellivent, 1199 Computer-Based Weaning, 1200 Automatic Tube Compensation, 1200 Volume Support, 1200

Newer Techniques for Evaluation of Diaphragm Function and Prediction of Successful Discontinuation, 1201 Noninvasive Ventilation/Continuous Positive Airway Pressure, 1201 High-Flow Nasal Cannula, 1201 Role of Mobility, 1201 Respiratory Therapist–Driven Protocols, 1202 Recent ATS/ACCP Ventilation Liberation Guidelines, 1202 Selecting an Approach, 1202 The Morbidly Obese Patient, 1203 Monitoring the Patient During Weaning, 1203 Ventilatory Status, 1203 Oxygenation, 1204 Cardiovascular Status, 1204 Extubation, 1204 Artificial Airways and Weaning, 1204 Ventilator Discontinuance Failure, 1205 Prolonged Mechanical Ventilation, 1206 Chronically Ventilator-Dependent Patients, 1206 Terminal Weaning, 1206

CHAPTER 53  Discontinuing Ventilatory Support

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KEY TERMS adaptive support ventilation (ASV) airway occlusion pressure automatic tube compensation (ATC) continuous positive airway pressure (CPAP) diaphragm electrical activity (EAdi) esophageal pressure

Intellivent mandatory minute volume ventilation (MMV) pressure support ventilation (PSV) progressive mobility prolonged mechanical ventilation (PMV)

The purpose of mechanical ventilation is to support the patient until the disease state or condition that caused the need for ventilatory support is alleviated or resolved. Ventilatory support can sustain life, but it cannot cure disease. Further, many complications and hazards are associated with mechanical ventilation. Consequently, ventilatory support should be withdrawn as soon as the patient is able to adequately resume spontaneous breathing.1 All patients who are mechanically ventilated should be evaluated daily, beginning with the day of intubation, for their ability to be liberated from ventilatory support.2,3 Frequently this evaluation is very quick, but it should be performed at least daily regardless of the patient’s status. After the problem or condition that caused the need for mechanical ventilation is resolved, most patients can be quickly and easily liberated from ventilatory support. For example, for most patients who need mechanical ventilation as a result of a drug overdose or severe asthma, for those who are recovering from postoperative anesthesia, and for those who have received ventilation for 72 hours or less, one may simply discontinue ventilation when the precipitating condition has resolved.1,4 However, some patients require mechanical ventilation for longer periods. The term ventilator dependent is usually reserved for patients who need ventilatory support for lengthy periods (i.e., 2 weeks or more) or who have not responded to attempts at ventilator discontinuation. For these patients, a more prolonged ventilator discontinuation process is required.1 Ventilator discontinuation should be carefully timed. Premature removal from the ventilator may severely stress the cardiopulmonary system and delay the patient’s recovery.4 Premature discontinuation also exposes the patient to the hazards of reintubation. However, delays in discontinuing ventilation expose the patient to an increased risk of complications, including nosocomial pneumonia, lung injury, myocardial infarction, and death.4 There are three basic historical methods for discontinuing ventilatory support, which can be used alone or in combination with one another1: 1. Spontaneous breathing trials (SBTs) alternating with mechanical ventilation 2. Synchronized intermittent mandatory ventilation (SIMV) 3. Pressure support ventilation (PSV) Other techniques that may facilitate ventilator discontinuation include the use of volume-support ventilation (VSV); adaptive support ventilation (ASV)/Intellivent; automatic tube compensation (ATC); proportional assist ventilation (PAV), which is

rapid, shallow breathing index (f/VT) spontaneous awaking trial (SAT) spontaneous breathing trial (SBT) synchronized intermittent mandatory ventilation (SIMV) ultrasound, diaphragm

also known as proportional pressure support (PPS); neurally adjusted ventilatory assist (NAVA); and continuous positive airway pressure (CPAP). However, little data exist that support the use of any of these techniques except for CPAP, which seems potentially beneficial during the ventilator discontinuation process, especially in morbidly obese patients.5 RULE OF THUMB  All patients who are mechanically ventilated should be evaluated at least daily, beginning with the day of intubation, for their ability to be liberated from ventilatory support.

Techniques for predicting when patients are ready for ventilator discontinuation and weaning have been studied extensively.4 Many weaning indices designed to predict successful ventilatory discontinuation have been proposed. Despite this, there are no universally applicable indices for predicting success. Of all the methods studied, SBTs and PSV have been shown to be the most effective methods for ventilator discontinuation and weaning. Evidence-based reviews recommend the use of at least daily SBTs.1 Protocols for ventilator discontinuation administered by an interdisciplinary team of respiratory therapists, nurses, and physicians can be highly effective, and have been recommended.1,4,6–10 Regardless of the method used, success is unlikely unless the precipitating problems that caused the ventilator dependency have been resolved.1,4,10 After these problems are resolved, an organized plan or protocol should be followed, and variations from the plan should be based on each patient’s response.1,4,6 Some patients cannot be successfully removed from mechanical ventilatory support. This group of ventilator-dependent patients poses clinical, economic, and ethical concerns.11,12 The term weaning has been used as a general term to refer to the process of discontinuing ventilatory support, regardless of the time frame or method involved. The term has also been used to refer to reductions in fractional inspired oxygen concentration (FiO2), positive end-expiratory pressure (PEEP), and CPAP. Alternatively, the term ventilator discontinuation or liberation has been used to refer to the process of disconnecting a patient from mechanical ventilatory support. For the purposes of this chapter, the term weaning is defined as a gradual reduction in the level of ventilatory support, whereas liberating from or discontinuing ventilatory support refers to the overall process of removing the patient from the ventilator, regardless of the method used. In general, patients who are being considered for removal from ventilatory support fall into one of five categories:

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1. Those for whom removal is quick and routine, normally the majority of ventilated patients. 2. Those who need a more systematic approach to discontinuing ventilatory support, which is normally about 15% to 20% of ventilated patients. 3. Those who require days to weeks to wean from ventilatory support, which is usually less than 5% of ventilated patients. 4. Those ventilator-dependent or “unweanable” patients, who compose less than 1% of patients who require ventilatory support. 5. Those who have no chance for survival in whom the ventilator is discontinued while comfort measures are provided, normally referred to as terminal weaning or terminal extubation.13 RULE OF THUMB  After the problem or condition that caused the need for mechanical ventilation is resolved, most patients can be quickly and easily liberated from ventilatory support.

REASONS FOR VENTILATOR DEPENDENCE Patients may require mechanical ventilation because of apnea, acute or impending ventilatory failure, or severe oxygenation problems that necessitate high levels of PEEP or CPAP. Regardless of the reason for initiating mechanical ventilation, patients remain dependent on the ventilator because of respiratory, cardiovascular, neurologic, or psychologic factors.1

Ventilatory Workload and Demand Patients who need mechanical ventilation often have a ventilatory workload and demand that exceeds their ventilatory capacity. This is the most common cause of ventilator dependence.1,4 The term ventilatory workload refers to the amount of work that the respiratory muscles are asked to perform to provide an appropriate level of ventilation. A patient’s total ventilatory workload is primarily determined by the following: (1) the level of ventilation needed, (2) the compliance of the lungs and thorax, (3) the resistance to gas flow through the airways, and (4) any imposed work of breathing (WOBI) due to ventilatory system mechanical factors.1,4 The level of ventilation required is determined by the following: (1) the metabolic rate, (2) the central nervous system (CNS) ventilatory drive, and (3) the ventilatory dead space. Common causes of an increased demand for ventilation include increased carbon dioxide production (i.e., fever, shivering, agitation, trauma, or sepsis) and increased dead space (i.e., pulmonary emboli or chronic obstructive pulmonary disease [COPD]). Other common causes of increased ventilatory demand include metabolic acidosis, severe hypoxemia, pain, and anxiety. Compliance is determined by the elastic nature of the lung– thorax system. Resistance is largely related to the nature of the conducting airways. Common causes of decreased lung compliance include atelectasis, obesity, pneumonia, pulmonary edema, pulmonary fibrosis, acute lung injury, and acute respiratory distress syndrome. Thoracic compliance may be reduced because of ascites, or abdominal distention. Airway resistance increases with bronchospasm, excessive secretions, and mucosal edema.

BOX 53.1  Factors That May Increase

Ventilatory Workload

Increased Ventilatory Demand: Increased Level of Ventilation Required • Increased central nervous system drive: hypoxia, acidosis, pain, fear, anxiety, and stimulation of J receptors (e.g., pulmonary edema) • Increased metabolic rate: increased carbon dioxide production, fever, shivering, agitation, trauma, infection, and sepsis • Increased dead space: chronic obstructive pulmonary disease and pulmonary embolus Decreased Compliance • Decreased lung compliance: atelectasis, obesity, pneumonia, fibrosis, pulmonary edema, and acute respiratory distress syndrome • Decreased thoracic compliance: ascites, abdominal distention, and pregnancy Increased Resistance • Increased airway resistance: bronchospasm, mucosal edema, and secretions • Artificial airways: endotracheal tubes, tracheostomy tubes, and partial obstruction of the artificial airway or the patient airway • Other mechanical factors: ventilator circuits, demand flow systems, and inappropriate ventilator flow or sensitivity settings

BOX 53.2  Factors That May Reduce

Ventilatory Drive

• Decreased PaCO2 (respiratory alkalosis) • Metabolic alkalosis • Pain (visceral) • Electrolyte imbalance • Pharmacologic depressants (narcotics, sedatives) • Fatigue • Decreased metabolic rate • Increased PaCO2 associated with chronic carbon dioxide retention • Neurologic or neuromuscular disease

Mechanical factors that can increase the work of breathing (WOB) include artificial airways (i.e., endotracheal and tracheotomy tubes), partial obstruction of the airway, ventilator circuits, demand flow systems, auto-PEEP, and inappropriate ventilator flow and sensitivity settings. Factors that may increase ventilatory workload are summarized in Box 53.1.

Ventilatory Capacity Ventilatory capacity is determined by ventilatory drive, ventilatory muscle strength, and ventilatory muscle endurance. Most patients who are being withdrawn from ventilatory support have a normal or an increased drive to breathe. Patients with neuromuscular disorders and those who are receiving sedatives, narcotics, or neuromuscular blocking agents may have a reduced or absent drive to breathe or impaired neuromuscular transmission. Patients with metabolic alkalosis, hypothyroidism, and sleep deprivation also may have a reduced ventilatory drive. Box 53.2 summarizes the factors that may reduce ventilatory drive. Muscle strength is influenced by age, sex, muscle bulk, and overall health. Malnutrition, starvation, and electrolyte imbalances (especially involving calcium, magnesium, potassium, and

CHAPTER 53  Discontinuing Ventilatory Support Partial support

Total support

Mechanical ventilation needed (intolerable loads)

Demands • Pressure loads CLT RAW • Ventilation loads • • • V• A ( VCO2, VO2) VD • Imposed loads

Increasing reserve Spontaneous ventilation possible (tolerable loads)

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BOX 53.3  Factors That Contribute to

Ventilator Dependence Normal reserve

Capabilities • Neural drive • Muscle function strength endurance

Fig. 53.1  Ventilatory failure and the need for ventilatory support depend on the balance between ventilatory muscle demands (i.e., loads) and ventilatory muscle capabilities. CLT, Lung–thorax compliance; RAW, airway resistance, V̇ , minute alveolar ventilation; V̇ , minute dead space ventilation. (Modified from MacIntyre NR: Respiratory factors in weaning from mechanical ventilatory support. Respir Care 40:244–259, 1995.)

phosphate) can lead to ventilatory muscle weakness. Critical illness myopathy, critical illness polyneuropathy, and the prolonged use of neuromuscular blocking agents are major causes of the development of ventilatory muscle weakness in the intensive care unit (ICU).14 Controlled ventilation for prolonged periods can result in ventilatory muscle discoordination and atrophy. Ventilatory muscle endurance is a function of energy supply versus demand. Energy supply is related to nutrition, perfusion, and cell energy use, whereas demand is related to the amount of work performed and is a function of minute ventilation, compliance, and resistance. Fig. 53.1 summarizes the relationship between ventilatory demands and capabilities. RULE OF THUMB  If patient workload exceeds capacity, the patient will not be successfully weaned from ventilatory support.

Global Criteria for Discontinuing Ventilatory Support Success with liberation from ventilatory support is related to the patient’s condition in four main areas1–4: 1. Ventilatory workload versus ventilatory capacity 2. Oxygenation status 3. Cardiovascular function 4. Psychologic factors Simply put, when ventilatory workload or demand exceeds ventilatory capacity, successful ventilator discontinuation is unlikely. Excessive ventilatory workload may lead to ventilatory muscle fatigue. When the ventilatory muscles fatigue, they must be rested for at least 24 hours to recover.15 Ventilatory workload

Respiratory Factors • Ventilatory workload exceeds ventilatory capacity • Decreased compliance: lung or chest wall • Increased resistance: artificial airways, bronchospasm, mucosal edema, secretions, and mechanical demand flow systems • Increased dead space: pulmonary embolus and chronic obstructive pulmonary disease • Ventilatory muscle weakness or fatigue • Oxygenation problems • ↓ V̇ /Q̇ • Increased shunt • ↓ DO2 • ↓ Oxygen extraction ratio Nonrespiratory Factors • Cardiovascular factors • Myocardial ischemia • Heart failure • Hemodynamic instability, hypotension, and arrhythmias • Neurologic factors • Decreased or increased central drive to breathe • Decreased peripheral nerve transmission • Psychologic factors • Fear and anxiety • Stress • Confusion or altered mental status • Depression • Poor nutrition • Multiple-system organ failure • Equipment shortcomings

increases with decreased compliance, increased airway resistance, or an increased requirement for ventilation. Ventilatory capacity can be reduced by ventilatory muscle fatigue and by a loss of muscle strength and endurance. Other factors that may contribute to ventilator dependence include inadequate arterial oxygenation, poor tissue oxygen delivery, myocardial ischemia, arrhythmias, low cardiac output, and cardiovascular instability. Neurologic problems that may contribute to ventilator dependence include decreased central drive to breathe and impaired peripheral nerve transmission. Psychologic issues that may contribute to ventilatory dependence include the fear of removal of the life-support system, anxiety, stress, depression, and sleep deprivation. Box 53.3 summarizes the major factors that contribute to ventilator dependence.

PATIENT EVALUATION Careful patient assessment is required to determine which patients are ready to be quickly removed from ventilatory support, which patients may need a prolonged ventilator discontinuation phase, and which patients are not yet ready for the discontinuation of ventilatory support. An important factor to consider as part of this assessment is the length of time that the patient has been receiving mechanical ventilation. In general, those who receive support for 72 hours

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BOX 53.4  Factors Associated With

Readiness for the Discontinuation of Ventilatory Support

• Reversal or partial reversal of reason for instituting mechanical ventilation • Good baseline functional status • Ventilatory capacity that is capable of meeting ventilatory workload • Good oxygenation status • Good cardiovascular performance • Good functional status of other organs and systems • Short duration of the critical illness • Short duration of mechanical ventilation • No psychologic factors affecting current status Modified from Pierson DJ: Nonrespiratory aspects of weaning from mechanical ventilation. Respir Care 40:263–270, 1995.

or less often can be removed quickly from the ventilator.16,17 Those who need a longer period of support may need a more prolonged approach. Current guidelines recommend that patients who need mechanical ventilation for more than 48 to 72 hours be carefully assessed to determine the possible causes of ventilator dependence.1,4 These include the respiratory, cardiovascular, neurologic, and psychologic causes of ventilator dependence that are listed in Box 53.3. This recommendation is especially important for the care of patients who have had unsuccessful attempts at the discontinuation of ventilation.1,4 Factors associated with readiness for the discontinuation of ventilatory support are summarized in Box 53.4.

The Most Important Criterion The single most important criterion to consider when evaluating a patient for ventilator liberation or weaning is whether there has been significant alleviation or reversal of the disease state or condition that necessitated use of the ventilator in the first place.1,4,10 The clinician should determine whether the patient’s condition is improving, whether the initial reason for providing ventilatory support is improved or resolved, and whether the patient’s clinical condition is stable. The following specific questions for patient evaluation have been suggested1: 1. Is there evidence of improvement or reversal of the disease state or condition that caused the need for mechanical ventilation? 2. Is the patient’s oxygenation status adequate? Specific criteria may include the following: PaO2 of 60 mm Hg or more, FiO2 of less than 0.40 to 0.50, PEEP of less than 5 to 10 cm H2O; PaO2/FiO2 of 150 to 200 or greater; and pH of 7.25 or greater. 3. Is the patient medically and hemodynamically stable? Specific criteria may include the absence of acute myocardial ischemia or marked hypotension. Patients should have adequate blood pressure without vasopressor therapy or with only low-dose intermittently delivered vasopressor therapy (i.e., less than 5 mcg/kg/min of dopamine or dobutamine). 4. Can the patient breathe spontaneously? The patient must be able to breathe spontaneously at sufficient tidal volumes and have a sufficient drive to breathe if ventilator liberation is being considered. If the patient’s condition is improving, if the alleviation or reversal of the precipitating disease state or condition has occurred,

if the patient is capable of spontaneous breathing, and if the oxygenation status and hemodynamic values are stable, then ventilator liberation should be attempted.1 RULE OF THUMB  In general, those who receive support for 72 hours or less often can be removed quickly from the ventilator.

Weaning Indices Mechanical ventilation is hazardous, and unnecessary delays in ventilator discontinuation increase the associated complication rate. Unfortunately, premature ventilator discontinuation may also cause serious problems, including difficulty with reestablishing the artificial airway and serious compromise of the patient’s clinical status. General clinical judgment alone has been found to be a poor guide to determining whether a patient is ready for ventilator discontinuation, and as a result, more specific indicators have emerged. Specific indicators or weaning indices that clearly show whether a patient is ready to have the ventilator removed and help avoid inappropriate ventilator discontinuation have been sought. Unfortunately, none of the current weaning indices predict readiness for ventilator discontinuance with a high level of accuracy.1,4 Traditional discontinuation indices include the PaO2/FiO2 ratio, the alveolar-to-arterial partial pressure of oxygen difference [P(A − a)O2], the maximum inspiratory pressure (MIP), the vital capacity (VC), the spontaneous minute ventilation (VEsp), and the maximum voluntary ventilation (MVV).3,18 Newer indices include the rapid, shallow breathing index (f/VT), airway occlusion pressure (P0.1), and measures of WOB.1,4 Although all of these values can be useful, there are enormous discrepancies in the literature regarding their accuracy with regard to the prediction of “weanability.”1,4 With respect to the more traditional discontinuation indices, VC and MIP can be highly variable, whereas minute ventilation, respiratory rate (f), and f/VT tend to be more reliable.1,4 However, these measures may not correlate well with discontinuation success among all patients and especially among those receiving long-term ventilatory support, the elderly, and those with major pulmonary abnormalities.1,4,19 A comprehensive review of related research identified a possible role for 66 specific measurements as predictors of weaning success.4 Of these, eight values were found to be the most useful for the prediction of successful ventilator discontinuation.1,4 Useful predictive measures included spontaneous respiratory rate, spontaneous tidal volume, f/VT, minute ventilation, MIP, P0.1, P0.1/MIP, and a combined index called the CROP (Compliance Rate Oxygenation and Plmax) score that included compliance, respiratory rate, oxygenation, and MIP.1,4 Unfortunately, these measures all have limitations and can falsely suggest that a patient is ready for weaning. It is doubtful that a single index will be found that can be used for consistent discrimination between discontinuation success and failure. Moreover, none of these traditional indicators alone has proved useful for the prediction of improvements in patient outcome or in the selection of a particular discontinuation method.5,19

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Notwithstanding these limitations, the measurement of discontinuation indices in the difficult-to-wean patient may provide guidance regarding the reasons that patients fail discontinuation trials. Many find it useful to trend these indicators daily for those patients who require lengthy weaning times.11,16 Specific values for respiratory indices that are used to predict the successful discontinuation of ventilatory support are found in Table 53.1. RULE OF THUMB  None of the indices predicting success or failure of weaning predict with sufficient accuracy the results of a weaning trial. The trial itself is the BEST determinant of ability to be liberated from the mechanical ventilator.

Ventilation Increased thoracic cage movement during spontaneous breathing and asynchronous chest wall–to–diaphragm movement are related to an increased workload that may lead to ventilatory muscle fatigue and failure. Tachypnea (i.e., more than 30 to 35 breaths/min in adults) is a sensitive marker of respiratory distress, but it can prolong intubation if it is used as the only criterion. One explanation for this is that when sedation is lessened to facilitate weaning, the more awake patient may become anxious about having an endotracheal tube in place and being on a ventilator, which may itself cause their tachypnea. On the other end of the spectrum, irregular spontaneous breathing or periods of apnea indicate that the patient is at risk for weaning failure. Asynchronous and rapid shallow breathing patterns— although not definitive—suggest respiratory decompensation.19 However, decreased ventilatory variability over time (rate, VT, minute ventilation) has been clearly shown to identify patients who will fail an SBT.20,21 The evaluation of patients for the presence of palpable scalene muscle use during inspiration, an irregular ventilatory pattern, palpable abdominal muscle tensing during expiration, and the inability to alter the ventilatory pattern on command can be helpful for the assessment of the potential for prolonged spontaneous ventilation. Patients with none of these signs have a very high probability of successful ventilator discontinuance. Patients with one or two of these signs usually need continued support. The presence of three or more of these signs can mean that the patient’s condition is unstable and that the patient has a poor prognosis for ventilator removal.22 P0.1 is the inspiratory pressure that is measured 100 ms after airway occlusion.1,4 The P0.1 is effort-independent, and it correlates well with central respiratory drive. Patients who have a P0.1 more negative than −5 cm H2O have an increased WOB; the more negative the P0.1 the less likely it is that the patient will be able to be liberated from ventilatory support.1,4 Daily monitoring of P0.1 can provide very useful information on patients’ ventilatory drive and WOB (see Chapter 48 for more details).1,4 The f/VT is the ratio of spontaneous breathing frequency (breaths/min) to tidal volume (liters), and it has been found to be a good predictor of discontinuation success for many patients who need mechanical ventilation.1,4,19 The f/VT has less predictive ability for patients who need ventilatory support for longer than 8 days, and it may be less useful for predicting discontinuation

TABLE 53.1  Indices That Are Used to

Predict the Success of Weaning and Ventilator Discontinuation Measurement

Criterion

Oxygenation FiO2 PEEP (cm H2O) PaO2 (mm Hg) SaO2 (%) SvO2 (%) PaO2/PAO2 ratio PaO2/FiO2 ratio P(A-a)O2 (mm Hg) Q̇ s/Q̇ T (% shunt) No lactic acidosis, adequate Q̇ T, blood pressure

≤0.40–0.50 ≤5–8 ≥60 ≥90 ≥60 ≥0.35 >150–200 25