Lung Biology in Health & Disease Volume 213 Practical Pulmonary and Critical Care Medicine: Respiratory Failure

Practical Pulmonary and Critical Care Medicine LUNG BIOLOGY IN HEALTH AND DISEASE Executive Editor Claude Lenfant For...

Author: Zab Mohsenifar | Guy W. Soo Hoo

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Practical Pulmonary and Critical Care Medicine

LUNG BIOLOGY IN HEALTH AND DISEASE Executive Editor Claude Lenfant Former Director, National Heart, Lung, and Blood Institute National Institutes of Health Bethesda, Maryland

1. Immunologic and Infectious Reactions in the Lung, edited by C. H. Kirkpatrick and H. Y. Reynolds 2. The Biochemical Basis of Pulmonary Function, edited by R. G. Crystal 3. Bioengineering Aspects of the Lung, edited by J. B. West 4. Metabolic Functions of the Lung, edited by Y. S. Bakhle and J. R. Vane 5. Respiratory Defense Mechanisms (in two parts), edited by J. D. Brain, D. F. Proctor, and L. M. Reid 6. Development of the Lung, edited by W. A. Hodson 7. Lung Water and Solute Exchange, edited by N. C. Staub 8. Extrapulmonary Manifestations of Respiratory Disease, edited by E. D. Robin 9. Chronic Obstructive Pulmonary Disease, edited by T. L. Petty 10. Pathogenesis and Therapy of Lung Cancer, edited by C. C. Harris 11. Genetic Determinants of Pulmonary Disease, edited by S. D. Litwin 12. The Lung in the Transition Between Health and Disease, edited by P. T. Macklem and S. Permutt 13. Evolution of Respiratory Processes: A Comparative Approach, edited by S. C. Wood and C. Lenfant 14. Pulmonary Vascular Diseases, edited by K. M. Moser 15. Physiology and Pharmacology of the Airways, edited by J. A. Nadel 16. Diagnostic Techniques in Pulmonary Disease (in two parts), edited by M. A. Sackner 17. Regulation of Breathing (in two parts), edited by T. F. Hornbein 18. Occupational Lung Diseases: Research Approaches and Methods, edited by H. Weill and M. Turner-Warwick 19. Immunopharmacology of the Lung, edited by H. H. Newball 20. Sarcoidosis and Other Granulomatous Diseases of the Lung, edited by B. L. Fanburg

21. Sleep and Breathing, edited by N. A. Saunders and C. E. Sullivan 22. Pneumocystis carinii Pneumonia: Pathogenesis, Diagnosis, and Treatment, edited by L. S. Young 23. Pulmonary Nuclear Medicine: Techniques in Diagnosis of Lung Disease, edited by H. L. Atkins 24. Acute Respiratory Failure, edited by W. M. Zapol and K. J. Falke 25. Gas Mixing and Distribution in the Lung, edited by L. A. Engel and M. Paiva 26. High-Frequency Ventilation in Intensive Care and During Surgery, edited by G. Carlon and W. S. Howland 27. Pulmonary Development: Transition from Intrauterine to Extrauterine Life, edited by G. H. Nelson 28. Chronic Obstructive Pulmonary Disease: Second Edition, edited by T. L. Petty 29. The Thorax (in two parts), edited by C. Roussos and P. T. Macklem 30. The Pleura in Health and Disease, edited by J. Chrétien, J. Bignon, and A. Hirsch 31. Drug Therapy for Asthma: Research and Clinical Practice, edited by J. W. Jenne and S. Murphy 32. Pulmonary Endothelium in Health and Disease, edited by U. S. Ryan 33. The Airways: Neural Control in Health and Disease, edited by M. A. Kaliner and P. J. Barnes 34. Pathophysiology and Treatment of Inhalation Injuries, edited by J. Loke 35. Respiratory Function of the Upper Airway, edited by O. P. Mathew and G. Sant’Ambrogio 36. Chronic Obstructive Pulmonary Disease: A Behavioral Perspective, edited by A. J. McSweeny and I. Grant 37. Biology of Lung Cancer: Diagnosis and Treatment, edited by S. T. Rosen, J. L. Mulshine, F. Cuttitta, and P. G. Abrams 38. Pulmonary Vascular Physiology and Pathophysiology, edited by E. K. Weir and J. T. Reeves 39. Comparative Pulmonary Physiology: Current Concepts, edited by S. C. Wood 40. Respiratory Physiology: An Analytical Approach, edited by H. K. Chang and M. Paiva 41. Lung Cell Biology, edited by D. Massaro 42. Heart–Lung Interactions in Health and Disease, edited by S. M. Scharf and S. S. Cassidy 43. Clinical Epidemiology of Chronic Obstructive Pulmonary Disease, edited by M. J. Hensley and N. A. Saunders 44. Surgical Pathology of Lung Neoplasms, edited by A. M. Marchevsky

45. The Lung in Rheumatic Diseases, edited by G. W. Cannon and G. A. Zimmerman 46. Diagnostic Imaging of the Lung, edited by C. E. Putman 47. Models of Lung Disease: Microscopy and Structural Methods, edited by J. Gil 48. Electron Microscopy of the Lung, edited by D. E. Schraufnagel 49. Asthma: Its Pathology and Treatment, edited by M. A. Kaliner, P. J. Barnes, and C. G. A. Persson 50. Acute Respiratory Failure: Second Edition, edited by W. M. Zapol and F. Lemaire 51. Lung Disease in the Tropics, edited by O. P. Sharma 52. Exercise: Pulmonary Physiology and Pathophysiology, edited by B. J. Whipp and K. Wasserman 53. Developmental Neurobiology of Breathing, edited by G. G. Haddad and J. P. Farber 54. Mediators of Pulmonary Inflammation, edited by M. A. Bray and W. H. Anderson 55. The Airway Epithelium, edited by S. G. Farmer and D. Hay 56. Physiological Adaptations in Vertebrates: Respiration, Circulation, and Metabolism, edited by S. C. Wood, R. E. Weber, A. R. Hargens, and R. W. Millard 57. The Bronchial Circulation, edited by J. Butler 58. Lung Cancer Differentiation: Implications for Diagnosis and Treatment, edited by S. D. Bernal and P. J. Hesketh 59. Pulmonary Complications of Systemic Disease, edited by J. F. Murray 60. Lung Vascular Injury: Molecular and Cellular Response, edited by A. Johnson and T. J. Ferro 61. Cytokines of the Lung, edited by J. Kelley 62. The Mast Cell in Health and Disease, edited by M. A. Kaliner and D. D. Metcalfe 63. Pulmonary Disease in the Elderly Patient, edited by D. A. Mahler 64. Cystic Fibrosis, edited by P. B. Davis 65. Signal Transduction in Lung Cells, edited by J. S. Brody, D. M. Center, and V. A. Tkachuk 66. Tuberculosis: A Comprehensive International Approach, edited by L. B. Reichman and E. S. Hershfield 67. Pharmacology of the Respiratory Tract: Experimental and Clinical Research, edited by K. F. Chung and P. J. Barnes 68. Prevention of Respiratory Diseases, edited by A. Hirsch, M. Goldberg, J.-P. Martin, and R. Masse 69. Pneumocystis carinii Pneumonia: Second Edition, edited by P. D. Walzer

70. Fluid and Solute Transport in the Airspaces of the Lungs, edited by R. M. Effros and H. K. Chang 71. Sleep and Breathing: Second Edition, edited by N. A. Saunders and C. E. Sullivan 72. Airway Secretion: Physiological Bases for the Control of Mucous Hypersecretion, edited by T. Takishima and S. Shimura 73. Sarcoidosis and Other Granulomatous Disorders, edited by D. G. James 74. Epidemiology of Lung Cancer, edited by J. M. Samet 75. Pulmonary Embolism, edited by M. Morpurgo 76. Sports and Exercise Medicine, edited by S. C. Wood and R. C. Roach 77. Endotoxin and the Lungs, edited by K. L. Brigham 78. The Mesothelial Cell and Mesothelioma, edited by M.-C. Jaurand and J. Bignon 79. Regulation of Breathing: Second Edition, edited by J. A. Dempsey and A. I. Pack 80. Pulmonary Fibrosis, edited by S. Hin. Phan and R. S. Thrall 81. Long-Term Oxygen Therapy: Scientific Basis and Clinical Application, edited by W. J. O’Donohue, Jr. 82. Ventral Brainstem Mechanisms and Control of Respiration and Blood Pressure, edited by C. O. Trouth, R. M. Millis, H. F. Kiwull-Schöne, and M. E. Schläfke 83. A History of Breathing Physiology, edited by D. F. Proctor 84. Surfactant Therapy for Lung Disease, edited by B. Robertson and H. W. Taeusch 85. The Thorax: Second Edition, Revised and Expanded (in three parts), edited by C. Roussos 86. Severe Asthma: Pathogenesis and Clinical Management, edited by S. J. Szefler and D. Y. M. Leung 87. Mycobacterium avium–Complex Infection: Progress in Research and Treatment, edited by J. A. Korvick and C. A. Benson 88. Alpha 1–Antitrypsin Deficiency: Biology • Pathogenesis • Clinical Manifestations • Therapy, edited by R. G. Crystal 89. Adhesion Molecules and the Lung, edited by P. A. Ward and J. C. Fantone 90. Respiratory Sensation, edited by L. Adams and A. Guz 91. Pulmonary Rehabilitation, edited by A. P. Fishman 92. Acute Respiratory Failure in Chronic Obstructive Pulmonary Disease, edited by J.-P. Derenne, W. A. Whitelaw, and T. Similowski 93. Environmental Impact on the Airways: From Injury to Repair, edited by J. Chrétien and D. Dusser 94. Inhalation Aerosols: Physical and Biological Basis for Therapy, edited by A. J. Hickey

95. Tissue Oxygen Deprivation: From Molecular to Integrated Function, edited by G. G. Haddad and G. Lister 96. The Genetics of Asthma, edited by S. B. Liggett and D. A. Meyers 97. Inhaled Glucocorticoids in Asthma: Mechanisms and Clinical Actions, edited by R. P. Schleimer, W. W. Busse, and P. M. O’Byrne 98. Nitric Oxide and the Lung, edited by W. M. Zapol and K. D. Bloch 99. Primary Pulmonary Hypertension, edited by L. J. Rubin and S. Rich 100. Lung Growth and Development, edited by J. A. McDonald 101. Parasitic Lung Diseases, edited by A. A. F. Mahmoud 102. Lung Macrophages and Dendritic Cells in Health and Disease, edited by M. F. Lipscomb and S. W. Russell 103. Pulmonary and Cardiac Imaging, edited by C. Chiles and C. E. Putman 104. Gene Therapy for Diseases of the Lung, edited by K. L. Brigham 105. Oxygen, Gene Expression, and Cellular Function, edited by L. Biadasz Clerch and D. J. Massaro 106. Beta2-Agonists in Asthma Treatment, edited by R. Pauwels and P. M. O’Byrne 107. Inhalation Delivery of Therapeutic Peptides and Proteins, edited by A. L. Adjei and P. K. Gupta 108. Asthma in the Elderly, edited by R. A. Barbee and J. W. Bloom 109. Treatment of the Hospitalized Cystic Fibrosis Patient, edited by D. M. Orenstein and R. C. Stern 110. Asthma and Immunological Diseases in Pregnancy and Early Infancy, edited by M. Schatz, R. S. Zeiger, and H. N. Claman 111. Dyspnea, edited by D. A. Mahler 112. Proinflammatory and Antiinflammatory Peptides, edited by S. I. Said 113. Self-Management of Asthma, edited by H. Kotses and A. Harver 114. Eicosanoids, Aspirin, and Asthma, edited by A. Szczeklik, R. J. Gryglewski, and J. R. Vane 115. Fatal Asthma, edited by A. L. Sheffer 116. Pulmonary Edema, edited by M. A. Matthay and D. H. Ingbar 117. Inflammatory Mechanisms in Asthma, edited by S. T. Holgate and W. W. Busse 118. Physiological Basis of Ventilatory Support, edited by J. J. Marini and A. S. Slutsky 119. Human Immunodeficiency Virus and the Lung, edited by M. J. Rosen and J. M. Beck

120. Five-Lipoxygenase Products in Asthma, edited by J. M. Drazen, S.-E. Dahlén, and T. H. Lee 121. Complexity in Structure and Function of the Lung, edited by M. P. Hlastala and H. T. Robertson 122. Biology of Lung Cancer, edited by M. A. Kane and P. A. Bunn, Jr. 123. Rhinitis: Mechanisms and Management, edited by R. M. Naclerio, S. R. Durham, and N. Mygind 124. Lung Tumors: Fundamental Biology and Clinical Management, edited by C. Brambilla and E. Brambilla 125. Interleukin-5: From Molecule to Drug Target for Asthma, edited by C. J. Sanderson 126. Pediatric Asthma, edited by S. Murphy and H. W. Kelly 127. Viral Infections of the Respiratory Tract, edited by R. Dolin and P. F. Wright 128. Air Pollutants and the Respiratory Tract, edited by D. L. Swift and W. M. Foster 129. Gastroesophageal Reflux Disease and Airway Disease, edited by M. R. Stein 130. Exercise-Induced Asthma, edited by E. R. McFadden, Jr. 131. LAM and Other Diseases Characterized by Smooth Muscle Proliferation, edited by J. Moss 132. The Lung at Depth, edited by C. E. G. Lundgren and J. N. Miller 133. Regulation of Sleep and Circadian Rhythms, edited by F. W. Turek and P. C. Zee 134. Anticholinergic Agents in the Upper and Lower Airways, edited by S. L. Spector 135. Control of Breathing in Health and Disease, edited by M. D. Altose and Y. Kawakami 136. Immunotherapy in Asthma, edited by J. Bousquet and H. Yssel 137. Chronic Lung Disease in Early Infancy, edited by R. D. Bland and J. J. Coalson 138. Asthma’s Impact on Society: The Social and Economic Burden, edited by K. B. Weiss, A. S. Buist, and S. D. Sullivan 139. New and Exploratory Therapeutic Agents for Asthma, edited by M. Yeadon and Z. Diamant 140. Multimodality Treatment of Lung Cancer, edited by A. T. Skarin 141. Cytokines in Pulmonary Disease: Infection and Inflammation, edited by S. Nelson and T. R. Martin 142. Diagnostic Pulmonary Pathology, edited by P. T. Cagle 143. Particle–Lung Interactions, edited by P. Gehr and J. Heyder 144. Tuberculosis: A Comprehensive International Approach, Second Edition, Revised and Expanded, edited by L. B. Reichman and E. S. Hershfield

145. Combination Therapy for Asthma and Chronic Obstructive Pulmonary Disease, edited by R. J. Martin and M. Kraft 146. Sleep Apnea: Implications in Cardiovascular and Cerebrovascular Disease, edited by T. D. Bradley and J. S. Floras 147. Sleep and Breathing in Children: A Developmental Approach, edited by G. M. Loughlin, J. L. Carroll, and C. L. Marcus 148. Pulmonary and Peripheral Gas Exchange in Health and Disease, edited by J. Roca, R. Rodriguez-Roisen, and P. D. Wagner 149. Lung Surfactants: Basic Science and Clinical Applications, R. H. Notter 150. Nosocomial Pneumonia, edited by W. R. Jarvis 151. Fetal Origins of Cardiovascular and Lung Disease, edited by David J. P. Barker 152. Long-Term Mechanical Ventilation, edited by N. S. Hill 153. Environmental Asthma, edited by R. K. Bush 154. Asthma and Respiratory Infections, edited by D. P. Skoner 155. Airway Remodeling, edited by P. H. Howarth, J. W. Wilson, J. Bousquet, S. Rak, and R. A. Pauwels 156. Genetic Models in Cardiorespiratory Biology, edited by G. G. Haddad and T. Xu 157. Respiratory-Circulatory Interactions in Health and Disease, edited by S. M. Scharf, M. R. Pinsky, and S. Magder 158. Ventilator Management Strategies for Critical Care, edited by N. S. Hill and M. M. Levy 159. Severe Asthma: Pathogenesis and Clinical Management, Second Edition, Revised and Expanded, edited by S. J. Szefler and D. Y. M. Leung 160. Gravity and the Lung: Lessons from Microgravity, edited by G. K. Prisk, M. Paiva, and J. B. West 161. High Altitude: An Exploration of Human Adaptation, edited by T. F. Hornbein and R. B. Schoene 162. Drug Delivery to the Lung, edited by H. Bisgaard, C. O’Callaghan, and G. C. Smaldone 163. Inhaled Steroids in Asthma: Optimizing Effects in the Airways, edited by R. P. Schleimer, P. M. O’Byrne, S. J. Szefler, and R. Brattsand 164. IgE and Anti-IgE Therapy in Asthma and Allergic Disease, edited by R. B. Fick, Jr., and P. M. Jardieu 165. Clinical Management of Chronic Obstructive Pulmonary Disease, edited by T. Similowski, W. A. Whitelaw, and J.-P. Derenne 166. Sleep Apnea: Pathogenesis, Diagnosis, and Treatment, edited by A. I. Pack 167. Biotherapeutic Approaches to Asthma, edited by J. Agosti and A. L. Sheffer

168. Proteoglycans in Lung Disease, edited by H. G. Garg, P. J. Roughley, and C. A. Hales 169. Gene Therapy in Lung Disease, edited by S. M. Albelda 170. Disease Markers in Exhaled Breath, edited by N. Marczin, S. A. Kharitonov, M. H. Yacoub, and P. J. Barnes 171. Sleep-Related Breathing Disorders: Experimental Models and Therapeutic Potential, edited by D. W. Carley and M. Radulovacki 172. Chemokines in the Lung, edited by R. M. Strieter, S. L. Kunkel, and T. J. Standiford 173. Respiratory Control and Disorders in the Newborn, edited by O. P. Mathew 174. The Immunological Basis of Asthma, edited by B. N. Lambrecht, H. C. Hoogsteden, and Z. Diamant 175. Oxygen Sensing: Responses and Adaptation to Hypoxia, edited by S. Lahiri, G. L. Semenza, and N. R. Prabhakar 176. Non-Neoplastic Advanced Lung Disease, edited by J. R. Maurer 177. Therapeutic Targets in Airway Inflammation, edited by N. T. Eissa and D. P. Huston 178. Respiratory Infections in Allergy and Asthma, edited by S. L. Johnston and N. G. Papadopoulos 179. Acute Respiratory Distress Syndrome, edited by M. A. Matthay 180. Venous Thromboembolism, edited by J. E. Dalen 181. Upper and Lower Respiratory Disease, edited by J. Corren, A. Togias, and J. Bousquet 182. Pharmacotherapy in Chronic Obstructive Pulmonary Disease, edited by B. R. Celli 183. Acute Exacerbations of Chronic Obstructive Pulmonary Disease, edited by N. M. Siafakas, N. R. Anthonisen, and D. Georgopoulos 184. Lung Volume Reduction Surgery for Emphysema, edited by H. E. Fessler, J. J. Reilly, Jr., and D. J. Sugarbaker 185. Idiopathic Pulmonary Fibrosis, edited by J. P. Lynch III 186. Pleural Disease, edited by D. Bouros 187. Oxygen/Nitrogen Radicals: Lung Injury and Disease, edited by V. Vallyathan, V. Castranova, and X. Shi 188. Therapy for Mucus-Clearance Disorders, edited by B. K. Rubin and C. P. van der Schans 189. Interventional Pulmonary Medicine, edited by J. F. Beamis, Jr., P. N. Mathur, and A. C. Mehta 190. Lung Development and Regeneration, edited by D. J. Massaro, G. Massaro, and P. Chambon 191. Long-Term Intervention in Chronic Obstructive Pulmonary Disease, edited by R. Pauwels, D. S. Postma, and S. T. Weiss

192. Sleep Deprivation: Basic Science, Physiology, and Behavior, edited by Clete A. Kushida 193. Sleep Deprivation: Clinical Issues, Pharmacology, and Sleep Loss Effects, edited by Clete A. Kushida 194. Pneumocystis Pneumonia: Third Edition, Revised and Expanded, edited by P. D. Walzer and M. Cushion 195. Asthma Prevention, edited by William W. Busse and Robert F. Lemanske, Jr. 196. Lung Injury: Mechanisms, Pathophysiology, and Therapy, edited by Robert H. Notter, Jacob Finkelstein, and Bruce Holm 197. Ion Channels in the Pulmonary Vasculature, edited by Jason X.-J. Yuan 198. Chronic Obstuctive Pulmonary Disease: Cellular and Molecular Mechanisms, edited by Peter J. Barnes 199. Pediatric Nasal and Sinus Disorders, edited by Tania Sih and Peter A. R. Clement 200. Functional Lung Imaging, edited by David Lipson and Edwin van Beek 201. Lung Surfactant Function and Disorder, edited by Kaushik Nag 202. Pharmacology and Pathophysiology of the Control of Breathing, edited by Denham S. Ward, Albert Dahan and Luc J. Teppema 203. Molecular Imaging of the Lungs, edited by Daniel Schuster and Timothy Blackwell 204. Air Pollutants and the Respiratory Tract: Second Edition, edited by W. Michael Foster and Daniel L. Costa 205. Acute and Chronic Cough, edited by Anthony E. Redington and Alyn H. Morice 206. Severe Pneumonia, edited by Michael S. Niederman 207. Monitoring Asthma, edited by Peter G. Gibson 208. Dyspnea: Mechanisms, Measurement, and Management, Second Edition, edited by Donald A. Mahler and Denis E. O'Donnell 209. Childhood Asthma, edited by Stanley J. Szefler and Søren Pedersen 210. Sarcoidosis, edited by Robert Baughman 211. Tropical Lung Disease, Second Edition, edited by Om Sharma 212. Pharmacotherapy of Asthma, edited by James T. Li 213. Practical Pulmonary and Critical Care Medicine: Respiratory Failure, edited by Zab Mosenifar and Guy W. Soo Hoo 214. Practical Pulmonary and Critical Care Medicine: Disease Management, edited by Zab Mosenifar and Guy W. Soo Hoo The opinions expressed in these volumes do not necessarily represent the views of the National Institutes of Health.

Practical Pulmonary and Critical Care Medicine Respiratory Failure

Edited by

Zab Mosenifar Cedars–Sinai Medical Center Los Angeles, California, U.S.A.

Guy W. Soo Hoo VA Greater Los Angeles Healthcare System Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

New York London

Published in 2006 by Taylor & Francis Group 270 Madison Avenue New York, NY 10016 © 2006 by Taylor & Francis Group, LLC No claim to original U.S. Government works Printed in the United States of America on acid-free paper 10 9 8 7 6 5 4 3 2 1 International Standard Book Number-10: 0-8493-6663-1 (Hardcover) International Standard Book Number-13: 978-0-8493-6663-5 (Hardcover) Library of Congress Card Number 2005044634 This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. No part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC) 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe.

Library of Congress Cataloging-in-Publication Data Practical pulmonary and critical care medicine / edited by Zab Mosenifar, Guy W. Soo Hoo p. ; cm. -- (Lung biology in health and disease ; v. 213-214) Includes bibliographical references and index. Contents: v. 1. Respiratory failure-- v. 2. Disease management. ISBN-13: 978-0-8493-6663-5 (v. 1 : alk. paper) ISBN-10: 0-8493-6663-1 (v. 1 : alk. paper) ISBN-13: 978-0-8247-2597-6 (v. 2 : alk. paper) ISBN-10: 0-8247-2597-2 (v. 2 : alk. paper) 1. Lungs--Diseases. 2. Respiratory intensive care. I. Mosenifar, Zab, 1951- II. Soo Hoo, Guy W. III. Series. [DNLM: 1. Lung Diseases--therapy. 2. Acute Disease--therapy. 3. Critical Care--methods. WF 600 P8947 2006] RC941.P73 2006 616.2'4--dc22

2005044634

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Introduction

Surely, all of us would certainly concur with the ﬁrst sentence of the Preface prepared by Drs. Mosenifar and Soo Hoo: “Over the past decade, the pace of progress in medicine has been astounding. New developments in diagnosis, management, and therapeutics occur at a breathtaking rate.” On the other hand, one could argue with the time frame, that is, why only the past decade? This is a signiﬁcant point, especially when it comes to pulmonary and critical care. Pulmonary medicine started to blossom many, many decades ago but especially during the last 30 years or so. Critical care started its course, to what it is today, with the development of the oxygen electrode (and later oximetry) and with the recognition of the value of blood pH measurements in the late 1950s. At the same time, the use of ventilators and respiratory assist devices became more common. However, in reality it matters little when progress began. Today, what counts is that new developments are being introduced at such a fast pace that progress may exceed the ability to fully transfer and utilize all this knowledge in the practice of medicine. Sure enough, tertiary hospitals have the facilities and work force to adjust to and quickly adapt the changes as they occur. On the other hand, hospitals which are community based and distant from academic centers may ﬁnd iii

iv

Introduction

it more difﬁcult to take full advantage of the newer approaches for the management of pulmonary patients and/or critical care situations. What could be considered a dual standard between tertiary and community hospitals is well recognized today, and has raised concerns of policy makers, politicians, and medical leaders. The question is frequently raised about how fast, and how well, research advances are translated into the practice of medicine, including pulmonary and critical care medicine. This monograph, Practical Pulmonary and Critical Care Medicine: Respiratory Failure and its companion volume titled Practical Pulmonary and Critical Care Medicine: Disease Management represent important steps to minimize translation difﬁculties. Indeed, they both present a very practical approach to pulmonary and critical care medicine. The ﬁrst volume addresses, and very carefully describes, the “tools” to provide the most optimal care and management of respiratory failure. The second volume examines a number of situations—both pulmonary and non-pulmonary—that require the use of these tools. Together, these volumes will not only enrich the knowledge of the readers, but also will provide a wealth of practical information that has the potential to positively impact on the care of their patients. The editors, Dr. Zab Mosenifar and Dr. Guy W. Soo Hoo, have assembled contributors with outstanding expertise and a wealth of practical experience, coming from institutions/environments with large patient populations, and a wide variety of cases and medical situations. They share their very practical and real experiences throughout the volumes. As the Executive Editor of the series of monographs Lung Biology in Health and Diseases, I am proud to present these two volumes and to express my most sincere thanks to the editors and the authors. Claude Lenfant, MD Gaithersburg, Maryland, U.S.A.

Preface

Over the past decade, the pace of progress in medicine has been astounding. New developments in diagnosis, management, and therapeutics occur at a breathtaking rate. A new disease emerges and, aided by the ease of transcontinental travel, threatens to become the next pandemic. And just as quickly, the causative agent is identiﬁed with diagnostics and therapeutics soon to follow. Old diseases have their mysteries unraveled, and targeted therapeutics provide hope where there was once despair. Some conditions come under control in less than a generation’s span, while others plod along inexorably to the end, with little available to alter their course. Just as the conditions of disease have changed, so have the conduits for information. The speed and availability of electronic databases now allow access to vast warehouses of information at the click of a mouse or ﬂick of a stylus. Where once the resident or houseofﬁcer carried a worn copy of a spiral bound manual, handheld computers are now the essential accessories. The grand old textbooks have followed suit, available in versions abbreviated to ﬁt ﬁle-size limits or available in their own electronic internet-based versions. This electronic world not only allows but mandates frequent content changes. Information can be updated daily and even more frequently if necessary. The online resource is now predominant in an arena that was once the domain of the print journal. v

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Preface

Whereas attendance at national or international meetings once offered the latest developments, this information can now be accessed from a remote site and disseminated at near-instantaneous speed, certainly before one can return home. Why then, in this information rich era, would there be a need for this book? First of all, even though there is instant access and availability to volumes of information, there remains a dearth of practical information. No one functions in the vacuum of cyberspace or isolation of an information warehouse. Everyone faces the limitations of available technology, restricted formularies, time pressures, and treatment preferences. In addition to the wealth of knowledge, one requires the wisdom of experience and expediency of practical management. The best technology or therapeutic is only as effective as the treatment that can be instituted by the lone practitioner. Treatment available only to the few or the very specialized usually has no role in general management. Filling this void is the guiding premise of this book. Even if mutations threaten to render current antimicrobials ineffective or new disease entities emerge, there remains a need for comprehensive and effective supportive care. This care is best provided not by the disease specialist, but by physicians who carry a broader perspective while also maintaining focus on the most pressing problems. In the new lexicon of medicine, this is the hospitalist or intensivist. Because many of the most immediate life-threatening conditions involve the respiratory tract, management often falls under the domain of pulmonary and critical care, either as the pulmonologist and/or intensivist. The need for coordinated comprehensive care is further highlighted by increasingly vulnerable patients as a result of increased longevity, treatment modalities that strip a patient’s immune system, and emerging disease entities. The modern pulmonary and critical care physician not only has to deal with the many complexities of illness, but also must choose the best available approach to facilitate recovery. This has required the intensivist to assume many roles in patient management, but none more important than as the functional equivalent of a chief executive with oversight over total management. This has required familiarity with areas where they are not generally considered expert, and reliance on a multi-disciplinary approach to care. These sections in the text are authored by experts in the area who provide a broad overview, but highlight those issues most important in managing critically ill patients. This brings the intensivist’s view to the specialist’s world. As every bibliophile knows, the advantage of a textbook often lies in the additional or complementary information that is often encountered through perusal of its pages. Electronic sources are often unforgiving in their searches, limiting access to pre-determined and pre-deﬁned categories. With a book, one can often identify the needed content within its covers even if one is not quite certain of the initial focus of inquiry. The topic may not be in the ﬁrst section, but is invariably covered in a subsequent area. Practical Pulmonary and Critical Care is divided into two volumes based partly on space limitations and partly by design. This ﬁrst volume focuses

Preface

vii

on immediate management and diagnosis. For the practicing physician, this is often referred to in billing as the ﬁrst hour or more of critical care management. This often involves the patient with respiratory failure, one of the most common entry conditions into a hospital or critical care unit. These patients often present in extreme distress and the underlying diagnosis may not be immediately apparent or may require further investigation. Other patients are intubated as part of support measures while therapy is directed at other organs. This volume includes chapters and strategies on immediate management of these patients. This includes an extensive treatise on oxygen strategies, helium – oxygen, and non-invasive ventilation. If the patient fails these conservative measures, the focus shifts to intubation and ventilator management. The alphabet soup of ventilator modes and waveform interpretation is clariﬁed with a section that allows comparisons between multiple vendors. These patients demand close monitoring, and a chapter is dedicated to the nuances of monitoring their response to therapy as well as mechanical ventilation. Other sections deal with the delicate task of discontinuing mechanical ventilation and patients who require long-term ventilatory support. These patients often have multi-organ system dysfunction. In addition to ventilatory support, they often require other invasive procedures, either therapeutically or to provide or guide therapeutics. A comprehensive section is dedicated to the most commonly performed procedures, with an abundance of detailed ﬁgures and tables. This includes coverage of procedures once reserved for surgical colleagues, such as tube thoracostomy or tracheostomy. Equally important are imaging studies that help diagnose and monitor a patient’s response to therapy. The section on radiology covers the gamut with respect to patient management, including the use of the radiograph for conﬁrmation of location of invasive devices, diagnosis, and illustrative cases. The radiographs are all derived from recent cases and reproduce well, providing important detail useful in management. Each topic is covered with a focus on details that facilitate its implementation and potential pitfalls, as well as a practical perspective on its role in overall management. It is this perspective that not only deﬁnes this book, but hopefully lends an enduring quality to its content. There have been very few scientiﬁc developments that have completely altered the management of patients. Changes are often incremental and incorporated over several years of practical experience, although medications may be the one exception. The experience of time allows techniques to undergo further reﬁnement. Practical aspects of management are highlighted with detailed descriptions of procedures, protocols, or guidelines. There is often much to gain from historical perspective, and this information is judiciously included as well as that which is evidence based. Therefore, even though technology, medications, and formularies have changed over the past decade, patients with acute respiratory failure still have the same basic requirements in their management. Ventilators must provide the best support while inﬂicting the least amount of ventilator-associated injury. And once the road to recovery is

viii

Preface

reached, assisted ventilation should be removed as soon as possible. These basic tenets will not change in the foreseeable future, only the details in implementation. Although a paper-based textbook may not have the allure of electronic media, it can provide a roadmap and framework for efﬁcient and pragmatic care. Once in place, additional information can only enhance the work and ﬁnal product. We share a common goal to enhance the recovery of patients from a critical illness. We hope this textbook can contribute to that end result. Zab Mosenifar Guy W. Soo Hoo

Contributors

Janet Au Division of Pulmonary and Critical Care, Olive View – UCLA Medical Center and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Bruce M. Barack Department of Imaging, VA Greater Los Angeles Healthcare System and Department of Radiological Science, Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Sharad Dass Division of Pulmonary and Critical Care Medicine, Cedars –Sinai Medical Center and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Scott K. Epstein Department of Medicine, Caritas– St. Elizabeth’s Medical Center and Tufts University School of Medicine, Boston, Massachusetts, U.S.A. Dani Hackner Transitional Critical Care Service, Cedars –Sinai Medical Center and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Dean R. Hess Department of Respiratory Care, Massachusetts General Hospital and Department of Anesthesia, Harvard Medical School, Boston, Massachusetts, U.S.A. ix

x

Contributors

C. Matilda Jude Department of Imaging, VA Greater Los Angeles Healthcare System and Department of Radiological Science, Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Nader Kamangar Division of Pulmonary and Critical Care, Olive View –UCLA Medical Center and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Hsin-Yi Lee Department of Imaging, VA Greater Los Angeles Healthcare System and Department of Radiological Science, Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Michael I. Lewis Division of Pulmonary and Critical Care Medicine, Cedars –Sinai Medical Center and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Zab Mosenifar Division of Pulmonary and Critical Care Medicine, Cedars –Sinai Medical Center, Los Angeles, California, U.S.A. Michael L. Nevins Division of Pulmonary and Critical Care and Department of Medicine, Group Health Permanente, University of Washington School of Medicine, Seattle, Washington, U.S.A. Brian Richards Division of Pulmonary and Critical Care Medicine, Cedars –Sinai Medical Center, Los Angeles, California, U.S.A. Antoinette R. Roth Department of Radiological Science, Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Ammar Sakkour UCLA – Santa Monica Specialties, Geffen School of Medicine at UCLA, Santa Monica, California, U.S.A. Silverio Santiago Pulmonary and Critical Care Section, West Los Angeles Healthcare Center, VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Nikhil Shah Pulmonary and Critical Care Section, West Los Angeles Healthcare Center, VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Guy W. Soo Hoo Pulmonary and Critical Care Section, West Los Angeles Healthcare Center, VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Irawan Susanto UCLA– Santa Monica Specialties, Geffen School of Medicine at UCLA, Santa Monica, California, U.S.A.

Contributors

xi

Sanjay Vadgama Pulmonary and Critical Care Section, West Los Angeles Healthcare Center, VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. Steve Y. Wong Mission Hospital, Mission Viejo, Long Beach VA, Long Beach, California, U.S.A.

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Contents

Introduction Claude Lenfant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iii Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix

1. Oxygen Therapy and Airway Management . . . . . . . . . . . . . . . 1 Steve Y. Wong and Dean R. Hess I. Introduction . . . . 1 II. Oxygen Therapy . . . . 1 III. Airway Management . . . . 13 IV. Conclusions . . . . 25 References . . . . 25 2. Non-Invasive Ventilation in Critical Care Guy W. Soo Hoo I. Introduction . . . . 33 II. Rationale for Use . . . . 34 III. Clinical Conditions . . . . 35 IV. Other Conditions . . . . 45

. . . . . . . . . . . . . . . 33

xiii

xiv

Contents

V. Clinical Aspects of NIMV . . . . 50 VI. Monitoring the Response to Treatment . . . . 61 VII. Conclusion . . . . 67 References . . . . 68 3. Modes of Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . . . 77 Brian Richards and Zab Mosenifar I. Introduction . . . . 77 II. The Breath . . . . 78 III. Breath Phases . . . . 78 IV. Breath Types . . . . 87 V. Breath Patterns or Modes . . . . 94 VI. Fine Tuning the Ventilator Breath . . . . 99 References . . . . 101 4. Monitoring During Mechanical Ventilation . . . . . . . . . . . . . 105 Dean R. Hess I. Introduction . . . . 105 II. Arterial Blood Gases . . . . 105 III. Arterialized Capillary Blood Gases . . . . 108 IV. Point-of-Care Testing . . . . 108 V. Blood Gas Monitors . . . . 109 VI. Mixed Venous Blood Gases . . . . 110 VII. Pulse Oximetry . . . . 112 VIII. Gastric Tonometry and Sublingual PCO2 . . . . 116 IX. Capnography . . . . 117 X. Lung Mechanics and Graphics . . . . 127 XI. Monitoring in Perspective . . . . 135 References . . . . 136 5. Weaning from Mechanical Ventilation . . . . . . . . . . . . . . . . . 153 Dani Hackner, Sharad Dass, and Michael I. Lewis I. Introduction . . . . 153 II. Pathophysiologic Factors Determining Weaning Success or Failure: An Introductory Overview . . . . 154 III. Predicting Weaning Success . . . . 160 IV. Protocols and Pathways . . . . 164 V. Weaning from Prolonged Ventilation . . . . 167 VI. Sedation . . . . 168 VII. Goals of Therapy: Conversations About Ventilation . . . . 174 References . . . . 178

Contents

xv

6. Prolonged Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . 187 Scott K. Epstein and Michael L. Nevins I. Introduction . . . . 187 II. How Is Prolonged Mechanical Ventilation Deﬁned and How Often Does It Occur? . . . . 188 III. Who Requires Prolonged Mechanical Ventilation? . . . . 189 IV. Site of Care for Patients with Prolonged Mechanical Ventilation . . . . 190 V. What Are the Outcomes for Patients Requiring Prolonged Mechanical Ventilation? . . . . 191 VI. Why Do Patients Become Ventilator-Dependent? . . . . 192 VII. What Assessment Tools Are Available to Predict Weaning Outcome for Patients with Prolonged Mechanical Ventilation? . . . . 202 VIII. What Is the Best Approach to Weaning Patients with Prolonged Mechanical Ventilation? . . . . 204 IX. Conclusion . . . . 207 References . . . . 207 7. Procedures in the Intensive Care Unit . . . . . . . . . . . . . . . . . 219 Sanjay Vadgama, Janet Au, and Nader Kamangar I. Introduction . . . . 219 II. Arterial Catheters . . . . 219 III. Central Venous Catheters . . . . 225 IV. Pulmonary Artery Catheters . . . . 236 V. Chest Tube Thoracostomy . . . . 261 References . . . . 273 8. Bronchoscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285 Nikhil Shah, Irawan Susanto, and Silverio Santiago I. Introduction . . . . 285 II. Speciﬁcations, Indications, and Contraindications . . . . 286 III. Patient Preparation, Sedation, and Anesthesia . . . . 288 IV. Insertion Techniques . . . . 289 V. Diagnostic Techniques . . . . 289 VI. Post-Procedure Care . . . . 291 VII. Complications . . . . 291 VIII. Speciﬁc Diagnostic Indications . . . . 292 IX. Speciﬁc Diagnostic and Therapeutic Indications . . . . 297 X. Therapeutic Bronchoscopy: Indications and Options . . . . 298 XI. Potential Therapeutic Indications . . . . 305 References . . . . 306

xvi

Contents

9. Percutaneous Tracheostomy . . . . . . . . . . . . . . . . . . . . . . . . . 313 Ammar Sakkour and Irawan Susanto I. Introduction . . . . 313 II. Indications, Beneﬁts, and Timing of Tracheostomy . . . . 315 III. Contraindications . . . . 316 IV. The Technique of Bedside PDT: How We Do It . . . . 317 V. Complications . . . . 321 VI. OST vs. PDT . . . . 324 VII. Care of Patients with Tracheostomy . . . . 324 VIII. Future . . . . 325 References . . . . 325 10. Radiology in the Intensive Care Unit . . . . . . . . . . . . . . . . . . 331 Bruce M. Barack, C. Matilda Jude, Hsin-Yi Lee, and Antoinette R. Roth I. Introduction . . . . 331 II. The Portable Chest Radiograph . . . . 331 III. Devices Used in the ICU . . . . 338 IV. Common Thoracic Abnormalities Encountered in the ICU . . . . 364 V. Computerized Tomography . . . . 385 VI. Image-Guided Interventional Procedures in the ICU . . . . 387 References . . . . 392 Index

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407

1 Oxygen Therapy and Airway Management

STEVE Y. WONG

DEAN R. HESS

Mission Hospital, Mission Viejo Long Beach VA, Long Beach, California, U.S.A.

Department of Respiratory Care Massachusetts General Hospital and Department of Anesthesia Harvard Medical School Boston, Massachusetts, U.S.A.

I.

Introduction

Oxygen administration and airway management are two of the fundamental aspects of management in a patient with acute respiratory failure. Proper application of technical aspects of oxygen therapy and airway management can be life saving. Despite the importance of these therapies and their frequent use in the acute care setting, their nuances are often under-appreciated. II.

Oxygen Therapy

Oxygen (O2) is an elemental gas that is necessary for life in aerobic organisms. In the absence of O2 (hypoxia), cellular respiration ceases and irreversible cellular injury and death occur within minutes. At normal atmospheric pressure and temperature, O2 exists as an odorless, tasteless, and colorless gas. It represents one-ﬁfth of the earth’s atmosphere by volume (20.96%). A. Medical Oxygen

Medical grade O2 is manufactured by fractional distillation of liqueﬁed air (1,2). It is stored as a liquid to reduce the size of the storage container (1 L of liquid O2 produces 860 L of gaseous O2). The liquid O2, stored outside the hospital in a cryogenic container, is converted to gaseous O2 and delivered to the patient 1

2

Wong and Hess

care areas via a bulk gas delivery system. By convention, O2 is supplied at a pressure of 50 lbs/in2. Oxygen can also be delivered from a medical gas cylinder at a pressure of 2000 lbs/in2 when full. Cylinders are frequently used to supply O2 during transport of patients to remote locations of the hospital, such as diagnostic areas. Cylinders are identiﬁed by letter codes to indicate size and gas capacity. The cylinders most frequently used in the hospital are small E-cylinders. They are typically green in color, and a label afﬁxed to the side of the cylinder indicates the cylinder contents. When cylinders are used, it is important to calculate the duration of ﬂow to avoid inadvertent loss of O2 supply (Table 1). B. Indications for Oxygen Therapy

The most important indication for O2 therapy is to treat hypoxemia. The alveolar gas equation illustrates how increasing the inspired O2 fraction (FIO2) increases the alveolar PO2 (PAO2) and subsequently the arterial PO2 (PaO2): PA O2 ¼ FI O2 EBP 1:25 Pa CO2 where EBP is the barometric pressure corrected for water vapor pressure. The effect of increasing FIO2 on the PaO2 is a function of the physiologic cause of hypoxemia. In cases of shunt (V/Q ¼ 0), supplemental O2 therapy has little effect on PaO2. If the cause of hypoxemia is low V/Q or diffusion defect, supplemental O2 therapy will effectively increase the PaO2. Table 1 Duration of Flow (in Hours) from an E-Cylinder as a Function of O2 Flow and the Pressure of Gas Remaining in the Cylinder Cylinder pressure (lbs/in2) 1 500 600 700 800 900 1000 1100 1200 1300 1400 1500 1600 1700 1800 1900 2000

2.3 2.8 3.3 3.7 4.2 4.7 5.1 5.6 6.1 6.5 7.0 7.5 7.9 8.4 8.9 9.3

Flow (L/min) 2

3

4

5

6

7

8

9

10

11

12

13

14

15

1.2 1.4 1.6 1.9 2.1 2.3 2.6 2.8 3.0 3.3 3.5 3.7 4.0 4.2 4.4 4.7

0.8 0.9 1.1 1.2 1.4 1.6 1.7 1.9 2.0 2.2 2.3 2.5 2.6 2.8 3.0 3.1

0.6 0.7 0.8 0.9 1.1 1.2 1.3 1.4 1.5 1.6 1.8 1.9 2.0 2.1 2.2 2.3

0.5 0.6 0.7 0.7 0.8 0.9 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9

0.4 0.5 0.5 0.6 0.7 0.8 0.9 0.9 1.0 1.1 1.2 1.2 1.3 1.4 1.5 1.6

0.3 0.4 0.5 0.5 0.6 0.7 0.7 0.8 0.9 0.9 1.0 1.1 1.1 1.2 1.3 1.3

0.3 0.4 0.4 0.5 0.5 0.6 0.6 0.7 0.8 0.8 0.9 0.9 1.0 1.1 1.1 1.2

0.3 0.3 0.4 0.4 0.5 0.5 0.6 0.6 0.7 0.7 0.8 0.8 0.9 0.9 1.0 1.0

0.3 0.3 0.4 0.4 0.5 0.5 0.6 0.6 0.7 0.7 0.7 0.8 0.8 0.9 0.9

0.3 0.3 0.3 0.4 0.4 0.5 0.5 0.6 0.6 0.6 0.7 0.7 0.8 0.8 0.8

0.3 0.3 0.4 0.4 0.4 0.5 0.5 0.5 0.6 0.6 0.7 0.7 0.7 0.8

0.3 0.3 0.3 0.4 0.4 0.4 0.5 0.5 0.5 0.6 0.6 0.6 0.7 0.7

0.3 0.3 0.3 0.4 0.4 0.4 0.5 0.5 0.5 0.6 0.6 0.6 0.7

0.3 0.3 0.3 0.4 0.4 0.4 0.5 0.5 0.5 0.6 0.6 0.6

Oxygen Therapy and Airway Management

3

An unusual, but occasionally effective, use of O2 therapy is the re-absorption of air leaks, such as a small pneumothorax, subcutaneous emphysema, or pneumocephalous (3,4). If the patient is breathing room air, the composition of the leaked gas is presumably 21% O2 and 78% nitrogen. Breathing 100% O2 clears nitrogen from the blood, creates a diffusion gradient for nitrogen to diffuse from the extra-vascular space, and thus effectively reduces the volume of the leaked gas. In a theoretical assessment of normobaric O2 therapy to treat pneumocephalus, Dexter and Reasoner (3) reported that modestly increasing the FIO2 from 0.21 to 0.4 decreased the total air absorption time by 67%, whereas increasing the FIO2 from 0.8 to 1.0 decreased the total air absorption time by only an additional 3%. Another important use of O2 is treatment of carbon monoxide poisoning. The half-life of carboxyhemoglobin is about ﬁve hours breathing 21% O2 at ambient pressure, a little more than one hour breathing 100% O2 at ambient pressure, and ,30 min breathing 100% O2 at 3 atm of pressure. Weaver et al. (5) conducted a double-blind, randomized trial to evaluate the effect of hyperbaric-oxygen treatment on cognitive sequelae that commonly occur following carbon monoxide poisoning. Patients with symptomatic acute carbon monoxide poisoning were assigned to three hyperbaric oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Cognitive sequelae at six weeks were less frequent in the hyperbaric-oxygen group (25%) than in the normobaric-oxygen group (46%). Anaerobic infections and necrotizing fasciitis (6) may also be responsive to O2 therapy. However, the treatment is usually with hyperbaric oxygen, rather than normobaric oxygen, and this application of hyperbaric O2 therapy is controversial. C. Monitoring Oxygen Therapy

Oxygen should not be administered without an objective assessment of its effect. Because the most frequent indication for O2 therapy is to treat hypoxemia, the clinical effect of O2 administration is usually monitored with pulse oximetry or arterial blood gas analysis. Most commonly, pulse oximetry is used and a target O2 saturation (SpO2) of .92% is acceptable. If the O2 therapy is assessed by arterial blood gas analysis, a PaO2 . 60 mm Hg is usually acceptable. SpO2 or PaO2 should always be assessed relative to the amount of inspired O2. In the case of low-ﬂow O2 delivery systems (e.g., nasal cannula), the arterial O2 level is assessed relative to the administered O2 ﬂow. In the case of highﬂow O2 delivery systems and during mechanical ventilation, the arterial O2 level is assessed relative to the FIO2. Oxygen analyzers use one of several methods to measure O2 concentration(2). Polarographic and galvanic cell analyzers use an electrochemical principle to measure changes in PO2, which is then converted to a display of %O2. Paramagnetic analyzers use the Pauling principle, which is based on the fact that

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Wong and Hess

O2 is a paramagnetic gas. A wheatstone bridge O2 analyzer uses the principle of thermoconductivity. In the zirconium analyzer, an electric potential is developed across heated zirconium oxide that is proportional to the PO2. Zirconium analyzers are very precise and used in applications such as indirect calorimetry.

D. Physiologic Complications of Oxygen Therapy

Worsening hypercapnia with O2 administration in patients with chronic obstructive pulmonary disease (COPD) has been of concern for many years. This has resulted in conservative use of O2 in these patients and has likely produced unnecessary hypoxemia in some patients. In patients with stable COPD, continuous O2 administration has been shown to be life-prolonging (7). Oxygen should never be withheld from a hypoxemic patient in acute respiratory failure. Moreover, the risk may be relatively low (8), and the mechanism for hypercarbia when O2 is administered to the patient with COPD is controversial. When hypercarbia occurs with O2 administration, this may be due to the Haldane effect (9), an increase in alveolar dead space due to the effects of O2 on pulmonary blood _ mismatch, or suppression of the respiratory drive. Aubier et al. _ Q ﬂow and V= (10) reported that an increased PaCO2 following O2 administration in patients with COPD occurred with no change in minute ventilation. Crossley et al. (11) reported that an increased FIO2 in mechanically ventilated patients with COPD (PaO2 increase to about 200 mm Hg) did not change PaCO2, respiratory drive, or dead space. Gomersall et al. (12) reported no signiﬁcant difference in requirement for mechanical ventilation or mortality for patients with COPD in acute respiratory failure in whom O2 was administered with a goal PaO2 . 50 or .70 mm Hg. However, Robinson et al. (13) reported a reduction in minute ventilation and an increase in alveolar dead space in patients with COPD who had worsening hypercapnia with O2 administration. These results, as well as those by Dick et al. (14) and Dunn et al. (15), suggest that a decrease in ventilatory drive may contribute to the hypercapnia that occurs with O2 administration in some patients with COPD. Concern for hypercapnia is also reported in patients with asthma exacerbation. Chien et al. (16) reported an increase in PaCO2 in patients with acute asthma who received an FIO2 of 1.0, but the increase in PaCO2 was modest (maximum of 10 mm Hg) and the clinical signiﬁcance of this is unclear. Absorption atelectasis has been demonstrated in patients breathing 100% O2 (17). Absorption of gas behind occluded airways is more likely to produce atelectasis if the alveolar gas composition is 100% O2 rather than room air. If the alveolar gas is room air, uptake of O2 results in an alveolar volume change of 20%, delaying the onset of atelectasis. Although this effect has been demonstrated primarily during anesthesia, it is likely that it might also occur during acute respiratory failure. In mechanically ventilated patients, this complication may be avoided by the use of positive end-expiratory pressure (PEEP).

Oxygen Therapy and Airway Management

5

Experimental evidence implicates the formation of reactive O2 species (superoxide anion, hydroxyl radical, and hydrogen peroxide) in the pathogenesis of pulmonary O2. The clinical importance of this, however, has been debated for many years (18,19). It is common teaching that maintaining the FIO2 , 0.6 avoids O2 toxicity, although there are few data to support this. Early human reports of “respirator lung” showed septal edema, endothelial cell damage, hyaline membrane deposition, and interstitial ﬁbrosis. However, these ﬁndings may have been the result of high ventilating pressure rather than hyperoxia per se. Normal human volunteers exposed to hyperoxia develop chest discomfort, dyspnea, cough, headache, and paresthesia within 12 hours of exposure and these effects persist for several days. However, similar effects have not been shown to occur in patients with acute respiratory failure. Patients treated with bleomycin have an increased risk for oxygen-induced lung toxicity (20). An FIO2 of 0.35 to 0.4 is sufﬁcient to cause toxicity in this setting. Bleomycin may impair the lungs’ antioxidant defenses, increasing the burden of reactive O2 species produced in the lung by a high FIO2. Bleomycin O2 toxicity may be steroid responsive. Retinopathy of prematurity (21) and bronchopulmonary dysplasia (22) are complications that are associated with O2 therapy in infants. Similar disorders are not known to occur in patients older than neonates. E.

Technical Hazards of Oxygen Therapy

An important physical characteristic of O2 is its ability to support combustion. Accordingly, the potential ﬁre hazard of O2 should be appreciated when supplemental O2 is administered. Improper handling and storage of high-pressure gas cylinders can result in rapid escape of gas, turning the cylinder into a dangerous projectile. Because O2 is stored dry, it must be humidiﬁed when delivered at high concentrations. This is of particular concern when the upper airway is bypassed with an endotracheal tube (ETT) or tracheostomy tube. When lowﬂow O2 is administered, the need for humidiﬁcation is less, and humidiﬁers for this application have not been shown to be useful (23 –25). F. Oxygen Administration Devices

Oxygen therapy systems are generally categorized as either low- or high-ﬂow devices (1,2). Low-ﬂow devices deliver O2 at ﬂow rates insufﬁcient to meet the inspiratory ﬂow demand of the patient. The additional required ﬂow is inhaled from the room air. The FIO2 from low-ﬂow devices may vary from breath-to-breath, depending on the breathing pattern. High-ﬂow devices provide ﬂow sufﬁcient to meet the patient’s inspiratory ﬂow demand and thus maintain a precise FIO2 that is unaffected by changes in breathing pattern. Relevant characteristics of O2 delivery devices are shown in Table 2. The nasal O2 cannula (Fig. 1) is the most widely used O2 delivery device. It consists of two short, soft, pliable plastic prongs, each about one-half inch in

6

Wong and Hess

Table 2 Oxygen Delivery Devices for Adult Applications

Device

Usual ﬂow range

Approximate oxygen concentration

Nasal cannula

1 –6 L/min

24– 40%

Simple mask

5 –10 L/min

30– 60%

Comments FIO2 is reduced with nasal obstruction; can be less effective with mouth breathing; FIO2 varies with breathing pattern Flows ,5 L/min result in rebreathing; FIO2 varies with breathing pattern If SpO2 remains low despite use of a non-rebreathing mask, consider using a high-ﬂow O2 delivery device

Theoretically, a Flow must non-rebreathing be high enough mask will deliver to prevent close to 100% O2; full collapse of reservoir bag in reality, however, during inhalation; it delivers ﬂows 12 L/min concentrations of are often required 60– 80% because the mask does not ﬁt tightly over the face When mask is AirO2 concentration is Use at least the removed, administer stamped on the ﬂow stamped entrainment O2 by nasal cannula colored adapter on colored mask to provide target SpO2 adapter Gas should be .30 L/min 24– 100%, set by High-ﬂow humidiﬁed with air and O2 ﬂow oxygen meters on high-ﬂow system system blender Nonrebreathing mask

length. The cannula is easily applied and well tolerated by most patients when used with ﬂows of 6 L/min. It is held in place by an elastic band around the head or, more commonly, by looping the delivery tubing over the ears and holding it in place with an adjustable slide under the chin. Oxygen delivery by nasal cannula produces an FIO2 of approximately 0.24 at 1 L/min to about 0.40 at 6 L/min. The FIO2 from a nasal cannula is highly variable even if the O2 ﬂow remains constant (Table 3). A number of studies using various methodologies conﬁrm that the FIO2 resulting from use of a nasal cannula is highly variable and dependent upon the O2 ﬂow, inspiratory ﬂow, and minute ventilation (26–36). The amount of delivered O2 is reduced if O2 is breathed from only one of the prongs, as may occur if the prongs are displaced or there is unilateral nasal obstruction (37). There are

Oxygen Therapy and Airway Management

7

nasal cannula

simple mask

Figure 1

Nasal cannula and simple mask.

conﬂicting data regarding the effect of mouth breathing when a nasal cannula is used (38,39). Although mouth breathing may decrease the FIO2, O2 therapy by nasal cannula can be effective even with mouth breathing. The majority of O2 is wasted when it is delivered by nasal cannula. Most of the O2 ﬂow during the expiratory phase is wasted. It is only during the initial period of inspiration that the supplemental ﬂow of O2 is needed. It is this ﬁrst part of inspiration that is delivered to the alveoli and participates in gas exchange. The remainder of the inspired gas ﬁlls the anatomic dead space and is exhaled without contributing in gas exchange. Oxygen-conserving devices conserve O2 by using a reservoir, which provides O2 ﬂow only during the inspiratory phase,

Table 3 Estimation of FIO2 from a Nasal Cannula Cannula ﬂow Tidal volume Anatomic reservoir Inspiratory time Volume of O2 inspired 33 mL 50 mL 88 mL

2 L/min (33 mL/sec) 500 mL 50 mL (nasal passages and nasopharynx) 1 sec O2 ﬂow Anatomic reservoir Amount of O2 in the inspired air; 417 mL 0.21

Volume O2 inspired 171 mL FIO2 ¼ 171 mL (O2)/500 mL (tidal volume) ¼ 0.34. Similar calculations can be used to calculate the effects of changes in O2 ﬂow or inspiratory time.

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Wong and Hess

Table 4 Oxygen Delivery Systems Designed to Conserve O2 by Eliminating Waste During the Expiratory Phase Reservoir O2 cannula (moustache and pendant types): A small reservoir ﬁlls with O2 (20 mL for the moustache style and 40 mL for the pendant) during exhalation. At the beginning of inhalation, a bolus of O2 is drawn from the reservoir. This may allow a reduction in O2 ﬂow by 50– 75%. Reservoir cannulae are not well accepted by patients due to their appearance. Transtracheal O2 catheter: This is a small-diameter catheter surgically inserted into the trachea. It is connected to a small ﬂange and held in place by an adjustable chain. As O2 is continuously delivered directly into the trachea, a reduction in the O2 ﬂow by about 50% is possible. Complications of the catheter placement include infection, bleeding, and subcutaneous emphysema. The catheter must be cleaned regularly to prevent mucus accumulation. Catheter obstruction is prevented by instilling saline and inserting a cleaning wire into the lumen of the catheter. Demand oxygen conservers: These devices only deliver O2 during the inspiratory phase. When the patient begins an inspiration, this creates a negative pressure in the supply tubing and causes a demand valve to open and supply a dose of O2.

either by providing an O2 bolus at the beginning of inspiration or by administering O2 directly into the trachea (Table 4) (40,41). These devices are not commonly used in the acute care settings, but patients receiving chronic O2 therapy may use one of these systems. Considerable variability in the performance of these devices has been reported (42). The simple O2 mask (Fig. 1) is used when a higher FIO2 is needed than can be attained with a nasal cannula or when a cannula is not appropriate (e.g., with nasal obstruction). The simple mask increases the FIO2 over that achieved by a nasal cannula because it adds a volume of 100 to 200 mL over the face, which serves as an O2 reservoir. Additional air is inhaled through small holes in the mask. To avoid rebreathing, a minimum ﬂow of 5 L/min must be used with O2 delivery by face mask (43). The simple mask is a low-ﬂow O2 delivery device capable of providing an FIO2 of 0.3 to 0.6 at ﬂows of 5 to 10 L/min (44). The FIO2 is dependent on the size of the mask and the patient’s breathing pattern. Simple masks are subjectively less appealing than nasal cannulae and may cause claustrophobia, mufﬂing of speech, and difﬁculty eating and drinking. The non-rebreathing mask (Fig. 2) increases the FIO2 by adding a reservoir bag. It has a one-way valve between the bag and the mask and another oneway valve over one or both mask ports. All of the exhaled tidal volume is directed through the mask ports because of the valve between the mask and the bag. The bag ﬁlls with 100% O2 during exhalation. During inhalation, the mask valves close and the bag valve on the reservoir opens. The O2 ﬂow must be high enough to prevent the bag from emptying during inhalation. Theoretically, the

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9

valves reservoir reservoir bag bag

Figure 2 Non-rebreathing mask.

non-rebreathing mask will deliver 100% O2. However, these masks do not provide an airtight ﬁt on the face, and the valves do not provide a perfect seal (45). At ﬂows of 10 to 15 L/min, an FIO2 of 0.6 to 0.8 may be achieved. Moreover, the non-rebreathing masks have a valve over only one of the exhalation ports. This allows inhalation of room air if the O2 supply ﬂow becomes inadequate.

O2

lower FIO2

O2

O2

higher FIO2

O2

Figure 3

The air-entrainment mask and its principle of operation.

10

Wong and Hess G. High-Flow Devices

An air-entrainment mask (Fig. 3) consists of a mask, a jet nozzle, and air-entrainment ports (46 –49). Oxygen is delivered through the jet nozzle, which increases its velocity. The high-velocity O2 entrains ambient air into the mask due to the viscous shearing forces between the gas traveling through the nozzle and the stagnant ambient air. The FIO2 depends on the nozzle size and the size of the entrainment ports. Commercially available systems use interchangeable jets or adjustable entrainment ports. Obstruction of the entrainment port or downstream obstruction decreases entrainment and increases FIO2. To deliver a ﬁxed FIO2, the ﬂow to the mask must exceed the peak inspiratory ﬂow of the patient. This may be difﬁcult to achieve with a higher FIO2 settings (Table 5). A high-ﬂow O2 delivery system can be used to deliver a precise FIO2 and any concentration between 0.21 and 1.0. Such a system provides sufﬁcient ﬂow to meet the inspiratory demands of the patient (50). Because the total ﬂow is set higher than the inspiratory ﬂow of the patient (typically 30– 60 L/min), the gas should be humidiﬁed. An air and an O2 ﬂow meter can be used to deliver a precise FIO2 (Fig. 4) and a variety of patient interfaces can be used (Fig. 5). The FIO2 can be calculated from the ﬂow rates of air and O2 (Table 6). A blender uses pressurized sources of air and O2 to deliver a precise FIO2. Blenders are compact and convenient but more expensive than using two ﬂow meters.

H. Heliox

Heliox is a gas mixture of helium and oxygen that is clinically useful in some circumstances due to its low density. Because helium does not support life, it must always be delivered in a gas mixture containing at least 20% oxygen. There is an increasing interest in its therapeutic use in patients with obstructive lung Table 5 FIO2, Minimum Flow Requirements, Outputs, and Entrainment Ratios for an Air-Entrainment Mask FIO2 setting 0.24 0.28 0.31 0.35 0.40 0.50 0.60 0.70

Minimum O2 ﬂow (L/min)

Entrainment ratio (O2:Air)

Total ﬂow (L/min)

4 4 6 8 8 12 12 12

1:25 1:10 1:7 1:5 1:3 1:1.7 1:1 1:0.6

104 44 48 48 32 32 24 19

Source: From Branson RD. The nuts and bolts of increasing arterial oxygenation: devices and techniques. Respir Care 1993; 38:672– 686.

Oxygen Therapy and Airway Management

Figure 4

11

High-ﬂow O2 delivery system.

aerosol mask

tracheostomy mask

T-piece

Figure 5 Patient interfaces used with high-ﬂow O2 delivery systems.

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Table 6 Air:O2 Ratios and Determination of Air and O2 Flows Air:O2 ¼ (1.0 2 FIO2)/(FIO2 2 0.21) If an FIO2 of 0.4 is desired: Air:O2 ¼ (1.0 2 0.4):(0.4 2 0.21) ¼ 0.6:0.2 ¼ 3:1 If a total ﬂow of 60 L/min is required, an air ﬂow of 45 L/min and an O2 ﬂow of 15 L/min will produce a FIO2 of 0.4. If an FIO2 of 0.6 is desired: Air:O2 ¼ (1.0 2 0.6):(0.6 2 0.21) ¼ 0.4:0.4 ¼ 1:1 If a total ﬂow of 60 L/min is required, an air ﬂow of 30 L/min and an O2 ﬂow of 30 L/min will produce a FIO2 of 0.6.

diseases, and this has been the source of several reviews (51,52) and meta-analyses (53,54). Although the role of heliox has been reported beneﬁcial in case series and anecdotal reports, current evidence is insufﬁcient to allow a recommendation for the use of heliox as a standard therapy for any speciﬁc patient population. One use of heliox is to reduce resistance with upper airway obstruction (55,56). An example is post-extubation stridor, where use of heliox has been reported to be beneﬁcial (57). There is also interest in the use of heliox for acute asthma (58,59). In spontaneously breathing patients with asthma, heliox decreases PaCO2, increases peak ﬂow, and decreases pulsus paradoxus. There may be beneﬁt related to the combination of heliox with aerosol bronchodilator delivery in patients with acute asthma or COPD (60 – 63). When heliox (rather than air or oxygen) is used to power the nebulizer, the ﬂow should be increased by about 50% to assure adequate output from the nebulizer (64). As demonstrated in several meta-analyses, however, the beneﬁt of heliox in the management of patients with acute asthma has yet to be conclusively demonstrated (53,54). The role of heliox in the treatment of COPD is unclear (65 – 67). COPD is a disease of small airways—a region of the lungs in which ﬂow is density independent. Heliox has been reported to decrease work of breathing in some, but not all, patients with COPD when evaluated just prior to extubation (68). Beneﬁt has been reported for the use of heliox with non-invasive ventilation in patients with COPD (69 –72), and methods to administer heliox with a BiPAP ventilator have been described (73). Care must be taken to administer heliox in a safe and effective manner. To avoid administration of a hypoxic gas mixture, it is recommended that 20% oxygen/80% helium is mixed with oxygen to provide the desired helium concentration and FIO2. If an FIO2 greater than 0.40 is required, the limited concentration of helium is unlikely to produce clinical beneﬁt. For spontaneously breathing patients, heliox is administered by face mask with a reservoir bag (Fig. 6). A Y-piece attached to the mask allows concurrent delivery of aerosolized medications. Sufﬁcient ﬂow is required to minimize contamination of

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Figure 6 Delivery system for heliox administration for spontaneously breathing patients.

the heliox with ambient air. This is often at least 12 to 15 L/min and requires 3 to 6 H-size cylinders per day. When using an oxygen-calibrated ﬂow meter for heliox therapy, it must be remembered that the ﬂow of heliox (80% helium and 20% oxygen) will be 1.8 times greater than the indicated ﬂow. Heliox administration during mechanical ventilation can be problematic (74 – 78). Ventilators are designed to deliver a mixture of air and oxygen. The density, viscosity, and thermal conductivity of helium affect the delivered tidal volume and the measurement of exhaled tidal volume. With some ventilators (e.g., Puritan – Bennett), no reliable tidal volume is delivered with heliox, whereas there may be a much higher delivered tidal volume than desired for other ventilators. One commercially available ventilator has been approved for use with heliox (VIASYS AVEA, Palm Springs, California, U.S.A.).

III.

Airway Management

When oxygen delivery remains compromised without mechanical assistance, endotracheal intubation should be considered. The goal of this section is to describe the practical aspects of endotracheal intubation. Fundamental key points useful in enhancing a successful endotracheal intubation will be discussed.

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Wong and Hess A. Indications

Endotracheal intubation is indicated to protect the airway and reduce the risks of pulmonary aspiration. It also offers a pathway for patients who require prolonged positive pressure ventilation and frequent suctioning. In addition, the ETT can be used to administer emergency medications when intravenous access is not available. Most frequently, endotracheal intubation enables the patient to undergo surgical procedures and allow delivery of inhalational anesthetics. Outside the operation room, endotracheal intubation typically involves patients who are in respiratory failure, shock, or cardiopulmonary arrest (79). Despite the increasing use of non-invasive ventilation, most patients receive mechanical ventilation invasively via an ETT.

B. Nasotracheal vs. Orotracheal Intubation

The ETT can be placed either nasally or orally. Nasotracheal intubation is typically indicated for patients undergoing oral surgeries or when intubation through the mouth is unsuccessful. It is contraindicated in patients with basilar skull fracture, mid-facial trauma, coagulopathy, nasal polyps, and epistaxis. For long-term mechanical ventilation, orotracheal intubation is preferred because a nasotracheal tube may increase the work of breathing as well as the risk of sinusitis. Because the orotracheal route usually permits placement of a larger ETT, clearance of secretions may also be easier.

C. Airway Assessment

A thorough airway evaluation should be performed prior to intubation to assess the degree of difﬁculty in airway management. Careful review of the medical history and a detailed examination of the anatomic characteristics allow identiﬁcation of potential difﬁcult mask ventilation or tracheal intubation. Anatomic features such as a short muscular neck, receding mandible, prominent upper incisors, small mouth with a high arched palate, and limited movement of the mandible suggest increased likelihood of potential airway problems (80).

D. Predicting Difﬁcult Mask Ventilation

Langeron and colleagues (81) identiﬁed ﬁve independent predictors for difﬁcult mask ventilation: age .55 years, body mass index .26 kg/m2, lack of teeth, presence of a beard, and history of snoring. When two or more of the risk factors are present, the likelihood of difﬁculty with mask ventilation is high. Furthermore, difﬁcult intubation is encountered more frequently when difﬁcult ventilation is present.

Oxygen Therapy and Airway Management

Figure 7 E.

15

An example of the Mallampati class I airway.

Predicting Difﬁcult Tracheal Intubation

The Mallampati classiﬁcation (82) is widely used in predicting the ease of laryngoscopy. It compares tongue versus pharyngeal size. The observation is divided into four categories. The evaluation is performed while the patient is sitting with mouth open and tongue protruding. Visualization of the oropharyngeal structures is then noted (Fig. 7). . Class I: the soft palate, uvula, and faucial pillars are all visible. . Class II: the tonsillar pillars and the base of uvula are obscured by the base of the tongue. . Class III: only the soft palate is visible. . Class IV: soft palate is not visible. When the pharyngeal class is Mallampati III or IV, a more difﬁcult intubation is expected. Unfortunately, it is not easy to use the Mallampati classiﬁcation for urgent or emergent intubation. Simple measurement of the thyromental distance, which is the length between the prominence of the thyroid cartilage and the bony point of the chin, can be used to aid in predicting difﬁcult intubation. When the thyromental distance is ,7 cm and the Mallampati class is III or IV, difﬁcult intubation can be anticipated (83). The performance of the Mallampati test and the measurement of the thyromental distance should identify most cases of difﬁcult intubation and allow appropriate preparations.

16

Wong and Hess F.

Laryngeal Visualization by Direct Laryngoscopy

Laryngoscopic view of the glottic opening is also used to predict the ease of tracheal intubation (84). The extent of laryngeal exposure is categorized into grades I to IV. When the glottic opening is fully visualized (grade I view), endotracheal intubation is relatively easy. If only the posterior portion of the glottic opening is seen (grade II view), intubation is technically more difﬁcult. When the laryngoscopic view is grade III (only the tip of epiglottis is visible) or grade IV (only the soft palate is seen), success of tracheal intubation by direct laryngoscopy is expected to be low. G. Maneuvers to Improve Laryngoscopic Visualization

Better laryngeal visualization of the glottic opening facilitates endotracheal intubation. Several simple techniques have been advocated to improve laryngoscopic visualization of the glottis. The “BACK” maneuver (simple back-pressure on the thyroid or cricoid cartilage) displaces the larynx posteriorly and reduces the failure rate to visualize any part of the glottis from about 9.2% to 1.6% (85). The “BURP” maneuver (backward, upward, and rightward pressure of the larynx) has also been reported to improve laryngeal visualization (86). In a comparative study (87), both the BURP maneuver and the BACK maneuver were found to be effective. However, the BURP maneuver was shown to be superior. Neither maneuver was associated with signiﬁcant complications. The jaw thrust maneuver is a technique commonly used to relieve laryngeal obstruction caused by the base of the tongue. By grasping the angles of the jaw with one hand on each side, the mandible can be displaced forward to keep the pharyngeal airway patent (88). The mandibular advancement can also improve

Figure 8

Equipment for endotracheal intubation.

Medications Commonly Used to Facilitate Endotracheal Intubation Induction agent

Medication Concentration Dosage Absolute contraindications

Propofol 10 mg/mL 1 – 2 mg/kg Hypersensitivity to propofol, soybean oil, egg, and glycerol

Etomidate 2 mg/mL 0.2– 0.6 mg/kg Known sensitivity to etomidate

Side effects/ clinical considerations

Hypotension, apnea, pain at injection site

Myoclonus, adrenal suppression

Depolarizing muscle relaxant Succinylcholine 20 mg/mL 1 – 2 mg/kg Malignant hyperthermia susceptibility, myopathies, burns, increased intracranial pressure Bradycardia, hyperkalemia, increased intracranial pressure

Non-depolarizing muscle relaxant Rocuronium 10 mg/mL 0.6 – 1.2 mg/kg Known hypersensitivity to rocuronium

Vecuronium 1 mg/mL 0.08– 0.1 mg/kg Known hypersensitivity to vecuronium

Increased sensitivity in patients with myasthenia gravis, Eaton– Lambert syndrome

Increased sensitivity in patients with myasthenia gravis, Eaton– Lambert syndrome

Oxygen Therapy and Airway Management

Table 7

Source: From Donnelly AJ, Cunningham FE, Baughman VL. Anesthesiology and Critical Care Drug Handbook. Ohio: Lexi-Comp Inc., 2000.

17

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laryngeal inlet view during nasal ﬁberoptic laryngoscopy (89). Tamura and colleagues (90) have also demonstrated that such a maneuver can improve laryngeal view during laryngoscopy performed by inexperienced physicians. When the mandibular advancement is combined with the BURP maneuver, further improvement of laryngeal visualization can be obtained.

H. Preparation for Orotracheal Intubation

Before attempting endotracheal intubation, preparation is needed to ensure that the equipment (Fig. 8) is working and medications (Table 7) are available. 1.

2.

3.

4.

Laryngoscope: a laryngoscope consists of a handle and a blade. The number on the blade reﬂects its length; therefore, an adult with a long neck may require a larger blade. The blade can be curved (MacIntosh), straight (Jackson –Wisconsin), or straight with a curved tip (Miller). A curved (MacIntosh) #3 blade is most commonly used for intubation in adults; however, the choice of the blade is entirely dependent on individual preference. A MacIntosh blade may provide more room to pass the ETT, while the straight blade gives better exposure of the glottic opening. Regardless, blades of different size and shape should be readily available. When checking the laryngoscope, it is important to ensure that there are batteries in the handle and the light in the blade illuminates well. ETT: a proper-sized ETT should be determined prior to intubation, usually an internal diameter of 7.5 mm for adult males and 7.0 mm for adult females. If bronchoscopy is anticipated, endotracheal tubes with 8.0 mm or larger internal diameters are preferred, as the smaller ETTs may hinder or prevent the passage of the adult bronchoscope. When examining the ETT, the cuff should be gently inﬂated with a syringe and checked for leaks. A stylet can be inserted in the ETT to provide rigidity, which can allow the practitioner to direct the ETT with more control. Oral airway: 8.0 and 9.0 mm oral airways are commonly used in adults to maintain a patent conduit above the laryngeal inlet, just cephalad to the epiglottis. Choosing the proper size oral airway is important as airway obstruction can occur if the inserted oral airway is too big or too small. When an ideal size oral airway is placed on the side of the patient’s face, the proximal end of the oral airway should be at the lip and the distal tip of the oral airway at the angle of the jaw. Medications: induction agents are commonly used to sedate or ensure unconsciousness in patients prior to direct laryngoscopy. Muscle relaxants, either depolarizing or non-depolarizing, are often utilized to facilitate orotracheal intubation. Vasoconstrictors, such as phenylephrine, and antihypertensive drugs, such as labetalol, should be readily available to maintain hemodynamic stability.

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Figure 9 Technique for endotracheal intubation. (A) Snifﬁng position. (B) Visualization of the glottic opening. (C) Advancement of the endotracheal tube between the vocal cords under direct visualization. Source: Adapted from Dr. R. Steadman, UCLA.

5. Suction: Yankauer handle, connected to suction, should be available. It is needed to clear oropharyngeal secretions to improve visualization during direct laryngoscopy. 6. Manual ventilation (Ambu) bag: a manual ventilation bag permits temporary assisted ventilation and should be connected to 100% oxygen. 7. CO2 detector: a method of detecting CO2 is helpful in conﬁrming ETT placement, especially when auscultation is equivocal. I.

Technique for Orotracheal Intubation

The basic intubation procedure (91) for an adult is outlined below in a stepby-step manner (Fig. 9A –C):

20

Wong and Hess 1.

2.

3.

4.

5.

6.

7.

8.

9.

With the manual ventilation bag connected to 100% oxygen, place the mask over the patient’s nose and mouth. Assist ventilation as needed to maintain adequate oxygen saturation. Make sure the patient is completely supine and adjust the bed to a comfortable height, usually at the level of the practitioner’s xiphoid cartilage. Place the patient in a “snifﬁng position” by putting pads under the patient’s head and gently extending the neck. The head elevation aligns the oral and pharyngeal axes, whereas the neck extension aligns the oral axis to create a nearly straight view of the glottic opening. This position maximizes exposure of the glottis and greatly enhances the chance of a successful intubation. However, in a patient with suspected or conﬁrmed neck injury, the neck should be kept in a neutral position. Administer induction agent of choice and insert the oral airway. It is crucial that the ability to ventilate the patient is conﬁrmed before any muscle relaxant is given. In a patient at risk of pulmonary aspiration, pressure should be applied at the cricoid cartilage to occlude the esophageal lumen, prevent insufﬂation of the stomach, and minimize regurgitation of the gastric contents (92). This is known as the Sellick’s maneuver. Cricoid pressure should be discontinued only after the endotracheal placement is conﬁrmed and the ETT cuff is inﬂated. When adequate anesthetic depth is achieved, remove the oral airway. Hold the laryngoscope with the left hand and insert the blade from the right side of the patient’s mouth. Sweep the tongue to the left and advance the blade until the epiglottis is visualized. If a MacIntosh blade is used, the tip of the blade should be placed in the vallecula, which is the space between the base of the tongue and the epiglottis. If a straight blade is used, the tip of the blade should be passed beneath the laryngeal surface of the epiglottis. With the blade properly positioned, lift the laryngoscope handle in a forward and upward motion to visualize the glottic opening. To prevent dental injury, the practitioner should maintain the wrist in a neutral position and avoid levering the laryngoscope backward. Clear any secretions with the tip of the Yankauer suction catheter. Once the glottic opening is well exposed, insert the ETT, usually with a stylet, from the right side of the blade. Advance the ETT between the vocal cords under direct vision. After the endotrachael tube is advanced to a depth of about 23 cm in men and 21 cm in women, inﬂate the cuff to obtain a seal in the presence of 20 to 30 cm H2O positive airway pressure. With the right hand holding the ETT, remove the stylet with the left hand. Connect the ETT to the oxygen source and conﬁrm the ETT placement before securing it with adhesive tape.

Oxygen Therapy and Airway Management J.

21

Conﬁrmation of Proper ETT Placement

Conﬁrming proper ETT position is a crucial step in airway management. Unrecognized misplacement of the ETT (either into the esophagus or a mainstem bronchus) can lead to serious complications and even death. Evidence suggestive of proper endotracheal intubation includes equal and bilateral breath sounds, absence of epigastric airﬂow, condensation in the ETT, and chest movement with assisted ventilation. Most practitioners consider the detection of exhaled CO2 as the gold standard for conﬁrming intra-tracheal intubation. This method is based on the principle that CO2 is eliminated through the lungs and no CO2 is present in the stomach. While a CO2 analyzer is part of the anesthesia equipment in the operating room, a disposable colorimetric end-tidal CO2 detector (93) is often used in the intensive care unit and the emergency room. This commercially available device contains a pH-sensitive paper that changes color when CO2 is detected, such as the single-use Easy Capw II CO2 detector (Fig. 10), which turns from purple to yellow when CO2 is sensed. However, in the presence of low cardiac output state or in the absence of pulmonary blood ﬂow, CO2 may not be detected despite a properly positioned ETT (94). In a multicenter study of a portable colorimetric end-tidal CO2 detection device, Ornato et al. (95) reported that endotracheal placement of the ETT was conﬁrmed in a cardiac arrest patient if more than 0.5% end-tidal CO2 was detected. In contrast, if it detected less than 0.5% end-tidal CO2 during CPR, esophageal intubation remained a possibility.

Figure 10

Single-use CO2 detector.

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Wong and Hess

Cuff palpation at the suprasternal notch is a reliable method used to reduce the risk of endobronchial intubation or impingement on the carina (96). After conﬁrming intra-tracheal intubation, repetitive gentle pressure is applied with the ﬁngers to the suprasternal notch while the ETT is advanced and withdrawn. At the same time, the pilot balloon, held in the other hand, is palpated for expansion. If the balloon distends with the pressure at the suprasternal notch, the ETT is secured. It is important to keep in mind that this technique is used not to verify endotracheal location but to prevent endobronchial intubation. Other useful adjuncts to establish proper ETT position include chest X-ray examination, ﬁberoptic visualization of the carina through the ETT, and use of the esophageal detector device. The esophageal detector device uses a syringe or squeeze bulb to aspirate air from the ETT. Easy aspiration of air suggests tracheal placement, whereas difﬁcult aspiration of air suggests esophageal placement.

K. Difﬁcult Airway

When endotracheal intubation is unsuccessful with direct laryngoscopy, it is crucial to call for help from an experienced intubator. Even though the American Society of Anesthesiologists (97) provides practice guidelines for management of the difﬁcult airway (Fig. 11), difﬁcult intubation should be handled by clinicians who are most experienced in airway management. A practitioner not accustomed to difﬁcult airway management may have trouble remembering or following the complicated difﬁcult airway algorithm. As insertion of the laryngeal mask airway (LMA) (Fig. 12) is easy to learn, it has been utilized in the difﬁcult airway algorithm as a temporary approach to ventilation (98). Despite its usefulness, the LMA has two major limitations. First, it does not protect against aspiration. Second, it may fail to provide adequate ventilation in patients with high airway resistance or low pulmonary compliance. Therefore, it is contraindicated in individuals with gastroesophageal reﬂux, full stomach, pregnancy, obesity, or bronchospasm. Other techniques of intubation or ventilation, such as ﬁberoptic intubation (99), esophageal tracheal Combitube (97,100), intubating LMA (101), and transtracheal jet ventilation (102), all require extensive practice to achieve proﬁciency and should not be attempted by anyone unfamiliar with them. Commercially available kits for cricothyrotomy and retrograde tracheal intubation can also be utilized in the management of the difﬁcult airway. Both involve entering the cricothyroid membrane to establish a conduit for ventilation. In a life-threatening situation, emergency cricothyrotomy should be performed to provide an airway quickly until tracheostomy can be established. When extubation is planned in a patient with a known difﬁcult airway, a wellformulated plan must be established for possible re-intubation. A tube exchanger can be placed to serve as a guide over which the new ETT can be threaded.

Oxygen Therapy and Airway Management

Figure 11

23

Difﬁcult airway algorithm. Source: American Society of Anesthesiologists.

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Wong and Hess

Figure 12

The laryngeal mask airway.

Although this approach does not guarantee a successful re-intubation, the tube exchanger can be used to insufﬂate oxygen until a deﬁnitive airway is secured. L.

Care of the ETT

Once the endotracheal position is established, the ETT should be secured so that the distal end of the ETT is approximately 5 cm above the carina, with the head in a neutral position (103). Taping the ETT at the 23 cm mark in men and the 21 cm mark in women seems to reduce the risk of endobronchial intubation (104). Once the proper position is determined, the centimeter mark on the tube at the level of the patient’s lip should be recorded and checked on a regular basis. In addition, cuff pressure should be monitored closely, as excessive pressure can lead to tracheal mucosa injury and subsequently tracheal stenosis (105,106). Routine morning radiographic examination should be used to verify ETT position (107). Furthermore, meticulous efforts and attention should focus on preventing unplanned self-extubation, especially in patients who have a lengthy stay in the intensive care unit (108). M. Complications of Orotracheal Intubation

Complications of tracheal intubation are rare, especially in the controlled environment of the operating room (109). In contrast, emergency intubation in critically ill adults carries a much higher rate of complication (110). During direct laryngoscopy, transient hypertension and tachycardia are frequently observed. Aspiration of regurgitated gastric contents can occur when the patient’s protective reﬂexes are blunted or abolished. If difﬁcult intubation is encountered,

Oxygen Therapy and Airway Management

25

dental injury can result with repeated attempts and increased physical force. Malpositioning of the ETT is a serious complication and has been reported to occur more frequently in women after emergency intubation (111). Patients who are hemodynamically unstable and receiving vasopressor therapy prior to intubation have the highest mortality rate associated with intubation (110).

IV.

Conclusions

Oxygen administration is a basic part in the management of patients with respiratory failure. Attention must be directed to select the appropriate oxygen delivery device to meet the needs of the patient and thus avoid sequelae related to hypoxia. Airway management plays an important role in ensuring adequate oxygenation and ventilation for patients. The clinician should be familiar with airway evaluation and orotracheal intubation using direct laryngoscopy. With meticulous preparation and practice, proﬁciency in basic airway management can be achieved. If difﬁcult intubation is encountered, assistance from an experienced clinician in airway management may prove to be life saving.

References 1. 2. 3. 4.

5. 6. 7.

8.

9.

10.

Hess DR, MacIntyre NR, Mishoe SC, Galvin WF, Adams AB, Saposnick AB. Respiratory care: principles and practice. Philadelphia: WB Saunders, 2001. Branson RD, Hess DR, Chatburn RL. Respiratory care equipment. Philadelphia: J.B. Lippincott Company, 1999. Dexter F, Reasoner DK. Theoretical assessment of normobaric oxygen therapy to treat pneumocephalus. Anesthesiology 1996; 84:442– 447. Annane D, Troche G, Delisle F, et al. Effects of mechanical ventilation with normobaric oxygen therapy on the rate of air removal from cerebral arteries. Crit Care Med 1994; 22:851 – 857. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002; 347:1057 – 1067. Green RJ, Dafoe DC, Rafﬁn TA. Necrotizing fasciitis. Chest 1996; 110:219 – 229. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trial. Nocturnal Oxygen Therapy Trial Group. Ann Intern Med 1980; 93:391 –398. Moloney ED, Kiely JL, McNicholas WT. Controlled oxygen therapy and carbon dioxide retention during exacerbations of chronic obstructive pulmonary disease. Lancet 2001; 357:526– 528. Hanson CW, Marshall BE, Frasch HF, Marshall C. Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease. Crit Care Med 1996; 24:23 – 28. Aubier M, Murciano D, Milic-Emili J, et al. Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis 1980; 122:747 – 754.

26 11.

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2 Non-Invasive Ventilation in Critical Care

GUY W. SOO HOO Pulmonary and Critical Care Section West Los Angeles Healthcare Center, VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

I.

Introduction

Non-invasive ventilation mechanical (NIMV), broadly deﬁned as ventilatory support without an endotracheal tube, has gained an increasing acceptance in the management of patients with acute respiratory failure. Its role has evolved over the past decade to the point that it may be part of ﬁrst-line management in those who do not require immediate intubation and has been endorsed in numerous reviews and consensus recommendations (1– 3). Most of the experience with NIMV has been with non-invasive positive pressure ventilation (NPPV), either pressure or volume cycled, but ventilatory support can also be provided with continuous positive airway pressure (CPAP) or negative pressure ventilation (NPV). Respiratory failure is generally characterized by its effects on gas exchange and reﬂects conditions in which the demands on the ventilatory system exceed its ability to maintain adequate gas exchange. This is broadly separated into type I or hypoxemic respiratory failure and type II or hypercapnic respiratory failure, and patients may present with a combination of the two. Assisted ventilatory support delivered through an endotracheal tube or tracheostomy tube connected to a volume or pressure ventilator has been the standard of therapy since its introduction during the height of the polio epidemics of the 1950s (4). Although most patients are successfully treated with intubation and mechanical ventilation, the risks and associated adverse effects are legion and have always tempered 33

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their beneﬁcial effects (5,6). It is these complications (airway trauma, barotrauma, nosocomial sinusitis, pneumonia, tracheal stenosis, etc.) that spurred investigation into alternative methods of support. This was facilitated by the success of nasal CPAP in patients with obstructive sleep apnea. Success in patients with neuromuscular disease using a mask or mouthpiece led to its application in other conditions (7). In addition, there was increasing recognition that many of the patients with severe underlying lung disease and respiratory failure may not recover from the episode or be destined for ventilator dependence (8). This provided additional impetus for NIMV as an effective alternative that also spared patients the long-term morbidities associated with intubation. The following sections focus on diseases most amenable to NIMV, highlighting crucial clinical investigations to provide a better understanding of the role of NIMV in the management of the critically ill patient. Later sections will review practical issues in the application of NIMV.

II.

Rationale for Use

A. Demonstration of Efﬁcacy

Ventilatory support can be effectively delivered through a nasal or face mask with improvement in both physiologic and clinical variables. Short-term application of nasal NPPV in normal and stable patients with obstructive or restrictive lung disease provided ventilatory support and unloaded the ventilatory muscles, with reduction in transdiaphragmatic pressure, diaphragmatic electromyogram (EMG), and other indices of muscle work (9,10). In patients with exacerbations of underlying chronic obstructive pulmonary disease (COPD), face mask NPPV with pressure support ventilation (PSV) decreased transdiaphragmatic pressure and diaphragmatic EMG. This produced increases in tidal volume and a reduction in respiratory rate associated with correction of hypoxemia, hypercapnia, and respiratory acidosis (11). This also decreased the intubation rate, duration of ventilation, and intensive care unit (ICU) stay compared with historical controls, but had no impact on mortality. Others have reported comparable results and noted improvement in pH and PaCO2 after as little as one hour of treatment (12). These reports spurred a variety of investigations, utilizing nasal and oronasal face masks for pressure and volume ventilation with nearly uniform success in correcting a patient’s respiratory acidosis and avoiding intubation. In an early summary of these reports, the success rate for NIMV was 67% with an aggregate initial pH of 7.30 in treated patients (13). These trials primarily involved COPD patients, and most experience has continued to be in those with COPD. A few general principles that emerged from this initial experience are summarized in Table 1. Patients who require immediate intubation, are deeply comatose, or are close to cardiopulmonary arrest are not candidates for NIMV. Deﬁnitive therapy should not be delayed by a trial of NIMV. Another crucial and often unappreciated element is that the most favorable results with NIMV

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Table 1 Non-Invasive Ventilation: General Guidelines for Patient Selection Absolute contraindications Coma Respiratory arrest Cardiac arrest Any condition requiring immediate intubation Clinical conditions Rapidly reversible clinical conditions COPD exacerbations Cardiogenic pulmonary edema After discontinuation of mechanical ventilation Early extubation ? Post-extubation ? Pneumonia COPD and pneumonia Use non-invasive ventilation concomitantly with other therapy Abbreviation: COPD, chronic obstructive pulmonary disease.

have been in patients with rapidly reversible conditions. The greatest experience has accrued in these conditions. This virtually eliminates candidates with conditions that may require an extended period (weeks) of ventilatory support or an illness that may require weeks for resolution. Of course, patients with mild disease may be candidates for NIMV, but must be evaluated on a case by case basis. Patients also need to be treated concomitantly with therapy directed at their underlying disease. NIMV provides an important adjunct to therapy, best suited for those who require a brief period of support to prevent frank respiratory failure while allowing the other components of therapy to take effect. These clinical conditions will be examined in detail in the following sections. III.

Clinical Conditions

A. Chronic Obstructive Pulmonary Disease

Most experience with NIMV has been in patients with acute exacerbations of COPD. These patients often develop dynamic hyperinﬂation, ineffective ventilation, incipient ventilatory muscle fatigue, and hypercapnia in association with their illness. NIMV has been demonstrated to be particularly effective in these patients, providing ventilatory support and unloading the ventilatory muscles to facilitate recovery. The often rapid reversibility in these exacerbations seems particularly suited for NIMV. There are over a dozen prospective randomized trials comparing NPPV to standard therapy in the treatment of these patients. This section will focus on NPPV, though there are reports of efﬁcacy, but no randomized trials, with NPV (14).

36

Soo Hoo Randomized Trials

The ﬁrst prospective randomized trial, reported by Bott et al. (15), involved 60 COPD patients and compared NPPV via nasal mask volume-cycled ventilation plus conventional treatment with conventional treatment administered in a specialized ward setting. They demonstrated greater improvement in respiratory acidosis (pH and PaCO2) in treated patients compared with conventional therapy, along with lower dyspnea scores. Mortality was lower but did not reach statistical signiﬁcance. Those who died were more acidemic (pH 7.31 vs. 7.35) and hypercapnic (PaCO2 ¼ 71 vs. 64 mmHg) on admission than survivors. Another single-center study reported by Kramer et al. (16), compared nasal mask bi-level positive airway pressures (BiPAP) plus standard therapy to standard therapy alone in 31 patients (23 COPD). The intubation rate was markedly reduced in the BiPAP group, 31% versus 73%, and 9% versus 67% for COPD patients, but with no difference in mortality. They noted marked improvement in PaCO2, with a decline in heart rate, respiratory rate, and dyspnea score after just one hour of BiPAP. In a multi-center, multi-national study reported by Brochard et al. (17), 85 patients with COPD exacerbations were randomized to either NPPV with face mask pressure support of 20 cmH2O plus conventional therapy or to conventional therapy alone. Endotracheal intubation was signiﬁcantly lower in the non-invasive group (26% vs. 74%). The response rates were not different between the participating institutions, and this treatment modality was demonstrated effective in more than one institution. The non-invasive group had fewer complications, speciﬁcally fewer episodes of nosocomial pneumonia and sepsis, lower mortality rate, and shorter length of stay. It should be pointed out, though, that the one-hour decline in PaCO2 noted by others was not evident in this study. The largest multi-center, prospective, randomized trial, reported by Plant et al., compared BiPAP using either face or nasal masks and randomized 236 patients (7,18). This occurred in a non-specialist ward setting in contrast to the previously reported ward and ICU settings. They focused on those with mild to moderate acidosis with a pH 7.25 as an exclusion criterion. Patients were treated according to an established protocol, primarily initiated by nursing staff. The primary outcome measure was the “need for intubation,” but once this criterion was met, intubation was at the discretion of the attending physician and management could continue with NPPV or even standard medical care. The non-invasive group had a statistically signiﬁcantly lower number of patients who met the “need for intubation,” 15% compared with 27%, as well as a lower mortality rate, 10% versus 20%. However, there was much less difference in the actual intubation rate (NPPV, 6% vs. 10%). In a sub-group analysis, the difference was most evident in those with a pH . 7.30. There was no beneﬁt of NPPV in patients with an initial pH , 7.30. The methodology of these and other trials have varied widely, ranging from single-center to multi-center trials, different mask interfaces (nasal, face, or

Non-Invasive Ventilation in Critical Care

37

both), different modes of assisted ventilation (volume vs. pressure), with different inclusion and exclusion criteria, outcome measures, intubation criteria, and even cross-over therapy, making consistent comparisons difﬁcult. These studies often represent narrowly selected groups of patients. In the trial reported by Brochard et al., only 31% of those evaluated were enrolled in their study. Intubation is probably the most important outcome measure, but conclusions are tempered when one outcome is “meeting criteria for intubation” and the other is intubation. Some trials enrolled relatively small numbers of patients, and although with signiﬁcant differences, they are limited by potential problems with statistical power. Meta-analyses may help to provide better insight into the effects of therapy by pooling patients and ameliorating differences in study design. Meta-Analyses

Three meta-analyses have been reported, largely focusing on the use of NPPV in COPD patients, although other causes of respiratory failure are included (19 – 22). They have all reached the same general conclusion that NPPV reduces the intubation rate, mortality, and length of stay in COPD patients. Peter et al. analyzed 15 studies, eight involving patients with COPD exacerbations. Focusing on the reports of COPD patients, they noted a signiﬁcant reduction in mortality of 13% (95%CI: 6 –21%), need for intubation of 18% (95%CI: 3 – 33%), and decrease in hospital length of stay of 5.7 days (95%CI: 1.2– 10.1 days). Keenan et al. restricted their analysis to COPD patients and found a risk reduction of 10% (95%CI: 5 –15%) in mortality, a risk reduction of 28% (95%CI: 15 –40%) for endotracheal intubation, and a decrease in the length of hospital stay by 4.6 days (95%CI: 2.3– 6.8 days). They also performed sub-group analysis and found NPPV had the most impact in those with moderately severe exacerbations deﬁned by a pH , 7.30. It should be noted that patients in two studies reporting no beneﬁt with NPPV had very mild disease with an average pH of 7.33 + 0.01 and 7.40 + 0.04, respectively. This may have skewed their analysis against those with less severe disease, as they did not identify any differences in outcome in those with less severe exacerbations. This conclusion runs contrary to the experience reported by Plant et al., who found that the greatest beneﬁt appeared to be in those with less severe disease deﬁned by a pH . 7.30. In summary, the majority of reported data supports the use of NIMV in COPD. It is particularly effective in patients with hypercapnic respiratory failure. The optimal thresholds of treatment remain to be deﬁned. There are reports matching our own experience that COPD patients with an initial pH range 7.10 can be successfully managed with NIMV, with the best results probably in patients with an initial pH . 7.25 (moderate severity). It does not add to the management of patients with mild exacerbations (deﬁned by a pH . 7.35). When successful, it decreases the intubation rate, length of stay, and mortality of these patients. In addition to reversing respiratory failure, mortality seems to be decreased because of fewer episodes of nosocomial pneumonia. There

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exists great heterogeneity in the study design of these trials, and generalization is tempered by differences in many areas, including threshold for intubation. B. Cardiogenic Pulmonary Edema

Respiratory failure due to cardiogenic pulmonary edema is a rapidly reversible condition, much like decompensated COPD, that is amenable to treatment with NIMV. The adverse effects of cardiogenic pulmonary edema are related to the development of pulmonary vascular congestion and interstitial and alveolar edema. This leads to hypoxemia with metabolic acidosis and hypercapnia preceding frank respiratory failure. The beneﬁcial effects of positive pressure ventilation include increases in functional residual capacity, breathing on a more compliant portion of the lung’s pressure –volume curve, recruitment of alveolar lung units, improving ventilation/perfusion relationships, and gas exchange (23). The sum of these effects is improved oxygenation and ventilation, unloading of the respiratory muscles, and lower work of breathing. Positive intrathoracic pressure also improves left ventricular function (24). Positive intrathoracic pressure decreases transmural systolic left ventricular pressure, which reduces the afterload to the left heart, improving left ventricular emptying and cardiac output. Reductions in venous return also decrease left ventricular preload. This has a salutary effect in patients with pulmonary edema who are volume overloaded. It is important to note that the beneﬁcial effects of positive airway pressure are present as long as preload is elevated. If preload decreases, the detrimental effects of positive pressure on venous return may outweigh the beneﬁcial effects on left ventricular function, resulting in decreased cardiac output and arterial pressure. The beneﬁts of positive pressure ventilation in cardiogenic pulmonary edema have been noted in endotracheally intubated and ventilated subjects. Improvement might be expected with CPAP, which represents augmented airway pressure in its most basic form. This represents the most rudimentary form of NIMV but requires an intact ventilatory drive, as it will not support apneic patients. Investigations using nasal CPAP in the 5 to 15 cm H2O range in heart failure patients have demonstrated reduction in the work of breathing, with over 30% reduction in esophageal pressures, and improvement in cardiovascular function, with greater than 15% improvement in stroke volume and cardiac index (25 –27). Randomized Trials: CPAP

There has been a long-standing recognition of the beneﬁt of CPAP in cardiogenic pulmonary edema (28), but randomized trials were not performed for almost 50 years following the initial reports. Three noteworthy trials compared face mask CPAP either ﬁxed at 10 cm H2O or titrated from 2.5 to 12.5 cm H2O along with conventional therapy (oxygen, nitrates, diuretics, etc.) to conventional therapy alone (29 – 31). Rasanen et al. utilized face mask CPAP at 10 cm H2O in a

Non-Invasive Ventilation in Critical Care

39

total of 40 patients and noted improvement in respiratory rate, heart rate, blood pressure, PaCO2, and oxygenation after as little as 10 minutes of support. The intubation rate in CPAP patients was 30%, compared with 60% in control patients. Bersten et al. compared face mask CPAP at 10 cm H2O in a total of 39 patients with severe pulmonary edema. Their series is noteworthy for the severity of illness of their patients, with mean APACHE II scores of 20 and arterial blood gases in the CPAP-treated patients of a pH of 7.18 + 0.08, PaCO2 of 58 + 8 mmHg, and PaO2/FIO2 of 138 + 32. Control patients had a similar severity of disease. None of the CPAP patients required intubation, compared with 35% of the controls. Lin et al. reported the largest series with CPAP, involving a total of 100 patients, all with invasive hemodynamic monitoring, treated with face mask CPAP and titrated over a three-hour period from 2.5 to 12.5 cm H2O. Their results mirrored that of the two prior studies but also demonstrated a reduction in shunt fraction and improvement in cardiac indices with CPAP. The intubation rate in CPAP patients was 16%, compared with 36% in controls. The improvement in outcome measures did not achieve statistical signiﬁcance in these studies, but there were strong trends towards a reduction in intubation rate and mortality. In a meta-analysis of the three studies, pooled results demonstrated a risk reduction in intubation of 26% (95%CI: 13 –38%), with a trend towards decreased mortality of 6.6% (95%CI: 23– 16%) (32). The duration of hospitalization was not different, although there was a decrease in the ICU stay of patients in the study by Bersten et al. by about a day. In another randomized study in patients with pulmonary edema complicating acute myocardial infarction, Takeda et al. provided 4 to 10 cm H2O nasal CPAP to 11 patients and demonstrated a reduction in intubation rate (18% vs. 73%), mortality (6% vs. 64%), and cardiac hemodynamics (pulmonary artery wedge pressure, cardiac index, stroke volume index) with CPAP. Randomized Trials: NPPV

Given this experience with CPAP, it follows that NPPV would be equally or even more efﬁcacious in cardiogenic pulmonary edema. This might be expected because NPPV breaths are augmented and assisted, unlike CPAP breaths. Work of breathing would be expected to be less with NPPV than CPAP. While several investigators have included patients with cardiogenic pulmonary edema, four have focused on the addition of NPPV to conventional therapy in cardiogenic pulmonary edema (33 –35). All used a combination of pressure cycled ventilation with positive end-expiratory pressure (PEEP), either PSV with PEEP or BiPAP with bedside or portable ventilators. Three were conducted at a single institution, with the largest a multi-center study. Demonstration of beneﬁt with NPPV was not as evident as in the other studies that used CPAP. Masip et al. (33) randomized a total of 40 patients and noted a lower intubation rate (5% vs. 33%) with more rapid improvement in tachypnea,

40

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oxygenation, and hypercapnia with pressure support NPPV than conventionally treated patients (oxygen, diuretics, etc.). Improvement occurred in as little as 15 minutes. Hypercapnia in the control group was associated with intubation (44%) as opposed to none of the hypercapnic patients treated with NPPV. The mean amount of pressure support was 15.2 + 2.4 cm H2O in addition to 5 cm H2O of PEEP. No differences were noted in the length of stay and mortality. This contrasts with the ﬁndings by Sharon et al. (34), who randomized 40 patients to either BiPAP and intravenous nitroglycerin or high-dose intravenous nitroglycerin. The mean level of ventilatory support was an inspiratory positive airway pressure (IPAP) ¼ 9.3 + 2.3 cm H2O and expiratory positive airway pressure (EPAP) ¼ 4.2 + 3.1 cm H2O. This is relatively low compared with other investigators, and they never improved their study patients’ mean oxygenation. The investigators found that 80% of the BiPAP group required intubation compared with 20% of controls, with a BiPAP group myocardial infarction rate of 55% compared with 10% in controls. The amount of ventilatory support was probably suboptimal in this study, and the high intubation rate and infarction rate is quite unusual. In another study initiated in the Emergency Department, Leavitt randomized 38 patients with congestive heart failure to either BiPAP or high-ﬂow oxygen, in addition to conventional therapy. There was a trend toward a lower intubation and myocardial infarction rate in the BiPAP group, but no outcome measures were statistically signiﬁcant (36). Nava et al. (35) conducted a multi-center study, randomizing a total of 130 patients to either conventional therapy with face mask PSV and PEEP or conventional therapy. They used a portable ventilator and provided an average inspiratory pressure support of 14.5 + 2.1 cm H2O and PEEP of 6.1 + 3.2 cm H2O. While NPPV provided more rapid improvement in tachypnea, dyspnea, and oxygenation, no differences were noted in the intubation rate or mortality. Sub-group analysis indicated a reduction in the intubation rate (6% vs. 29%) in hypercapnic patients (PaCO2 . 45 mmHg). Randomized Trials: CPAP vs. NPPV

Both of these modes of NIMV have undergone direct comparison in patients with cardiogenic pulmonary edema. In a small efﬁcacy study, the two modes were compared in a cross-over study in six patients that included esophageal pressure monitoring and pressure monitoring with a pulmonary artery catheter (37). Evaluation was made in 20-minute blocks, and patients treated with NPPV delivered at an inspiratory pressure support of 10 cm H2O and PEEP of 5 cm H2O had greater reduction in indices of ventilatory muscle work than CPAP of 10 cm H2O, but no difference was noted in cardiac indices between the two modes. Mehta et al. (38) randomized a total of 27 patients to either nasal CPAP at 10 cmH2O or BiPAP with settings of IPAP/EPAP ¼ 15/5 cm H2O, both in addition to standard therapy. The ventilatory support was delivered using the same device. Within 30 minutes, patients randomized to BiPAP had

Non-Invasive Ventilation in Critical Care

41

improvement of more indices (tachypnea, hypercapnia, dyspnea, pH, and mean arterial pressure) than the CPAP group (tachypnea), but the differences between the two groups were not signiﬁcant. However, over the course of the hospitalization, there was a higher incidence of myocardial infarction (71%) in the BiPAP group compared with the CPAP group (31%) and a group of matched historical controls (38%). The latter ﬁnding resulted in termination of the investigation. On review of patient characteristics, a greater number of patients in the BiPAP group had chest pain on study entry (71% vs. 31%), suggesting an unequal distribution of patients with active ischemia. In addition, there may have been issues with the bedside ventilator with respect to its mechanisms for limiting the inspiratory time and triggering expiratory cycling. Air leaks, if present, may not trigger expiratory cycling and would result in continued inspiratory pressures. This failure to cycle off could subject patients to prolonged increased intrathoracic pressures and potentially worsen intravascular hemodynamics and coronary blood ﬂow. This group has reported preliminary results of a comparable study using a later generation bedside ventilator with a more sophisticated expiratory triggering system that eliminates the risk of a prolonged inspiratory phase (39). They randomized 27 patients to NPPV or CPAP and, similar to their initial report, noted greater improvement in oxygenation and dyspnea with NPPV, with few patients requiring ICU admission, but without any differences in intubation rate, mortality, or incidence of myocardial infarction. In summary, the evidence to support the use of NPPV in cardiogenic pulmonary edema is not as compelling as that with CPAP. While symptoms and oxygenation are more rapidly corrected with NPPV and possibly to a greater extent than CPAP, this has not translated into improvement in the important clinical outcomes of intubation and mortality. There are several issues that have contributed to this, including small sample size, unequal randomization, and technical issues (operator and mechanical). At this time, it does not appear that there is much advantage in using NPPV over CPAP in patients with cardiogenic edema, except possibly more rapid symptom relief. There may be a role for NPPV in those with hypercapnia who do not improve with CPAP of 10 cm H2O given the beneﬁt noted in sub-group analysis.

C. NIMV in the Post-Extubation Period

Many of the initial series of patients treated with NIMV included patients in the post-operative or post-extubation period (40,41). NIMV was used either to facilitate discontinuation of mechanical ventilation or as a means to prevent reintubation in those developing post-extubation respiratory distress. This is a particularly vulnerable period, and post-extubation respiratory insufﬁciency and failure may occur in 20% or more of the patients (42). A number of mechanisms may contribute singly or in unison to difﬁculty with discontinuation of

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mechanical ventilation. The removal of positive airway pressure after mechanical ventilation may produce an increase in left ventricular preload and afterload, which may worsen cardiac failure and lead to respiratory failure as previously described. Respiratory muscle weakness or fatigue and increased work of breathing are common. Other mechanisms leading to failure included increased CO2 production, upper airway obstruction, and inadequate ventilatory drive. These are manifested as either hypercapnic or hypoxemic respiratory failure. The possibility of post-extubation upper airway obstruction is particularly intriguing. Upper airway edema and trauma are acknowledged complications of prolonged endotracheal intubation, although the incidence and timeframe for resolution are not well characterized. In patients intubated an average of seven days, Nathan and colleagues (43,44) noted increased work of breathing following extubation. A sawtooth pattern on ﬂow volume loops suggestive of upper airway abnormalities was also noted. This was attributed to redundant upper airway tissue and may represent upper airway or laryngeal edema in these patients. It follows that NIMV would be effective in correcting these abnormalities as well as the aforementioned disturbances. NPPV is effective in reducing the work of breathing in the post-extubation period. Vitacca et al. (45) evaluated 12 patients with respiratory failure, comparing the same level of ventilatory support (PSV ¼ 18.2 + 2.4 cm H2O plus PEEP ¼ 3.6 + 1.3 cm H2O) delivered through an endotracheal tube prior to extubation and immediately postextubation using a face mask. There was equivalent reduction in the indices of respiratory work with both endotracheally administered ventilatory support as well as NPPV when compared with T-tube trials or spontaneous breathing. During NPPV treatment, subjects had less dyspnea and were more comfortable with this modality. Randomized Trials

Investigations have evaluated NPPV in two basic strategies in the post-extubation period. One can be designated an early extubation approach in which patients who do not meet standard criteria for extubation are extubated early in their course and managed with NPPV. Nava et al. (46) ﬁrst reported on this early extubation approach in 50 COPD patients with hypercapnic respiratory failure after 48 hours of intubation. Those unable to tolerate a T-tube weaning trial were randomized to either continued ventilator support or extubation with face mask PSV. The NPPV patients received an average pressure support of 17.6 + 2.1 cm H2O, comparable to those continuing with mechanical ventilation. Those treated with NPPV had greater success at discontinuation of mechanical ventilation (88% vs. 68%) as shorter duration of mechanical ventilation, few ICU days, and reduced mortality. These patients had no episodes of nosocomial pneumonia compared with seven in the invasive ventilation group. In a similar trial, Girault et al. (47) randomized 33 mostly COPD patients to this early extubation approach if they had met established weaning criteria but

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43

had failed a two-hour T-tube trial. Those randomized to NPPV had been intubated an average of 4.6 + 1.9 days. By study design, the duration of invasive ventilation was shorter for the NPPV group, but the NPPV patients actually required a longer period of ventilatory assistance related to weaning (11.5 + 5.2 days vs. 3.5 + 1.4 days) than invasively ventilated patients albeit for a shorter time period each day. No differences were noted in the numbers of patients eventually able to discontinue mechanical ventilation, duration of ICU and hospital stay, complications, and mortality. Ferrer et al. (48) also used this strategy but chose patients who had failed T-tube trials for three consecutive days prior to randomization to either BiPAP or continued mechanical ventilation. In their 43 mostly COPD patients, those randomized to NPPV had greater success with eventual discontinuation of mechanical ventilation, fewer episodes of nosocomial pneumonia, fewer ICU days, and improved mortality. As expected from their study design, the NPPV patients also had a shorter duration of invasive ventilation. They noted that hypercapnia (PaCO2 . 45 mmHg) during their T-tube trials was an indicator of prolonged ICU stay and decreased survival. On the other hand, using a similar approach, Hill et al. (49) reported a trial involving 21 patients, which constituted less than 10% of their ICU patients with respiratory failure. While the NPPV-treated patients had fewer days of endotracheal intubation, the re-intubation rate was also higher in this group. All of the patients in these trials were intubated on average a week or less prior to extubation and treatment with NPPV. In conclusion, while this approach is promising, the experience is somewhat mixed. Nosocomial pneumonia may be averted by this approach, but patients may still require continued ICU care because of a tenuous respiratory status. The ideal candidate for this approach remains to be deﬁned but might be an otherwise improving COPD patient who just requires a small amount of assistance to regain the balance between ventilatory load and strength. This early extubation approach seems to be effective up to a week following intubation. The other approach in this arena involves the use of NPPV to treat postextubation respiratory distress and thereby avoid re-intubation and its adverse effects. The available data casts some doubt on the efﬁcacy of NPPV under these circumstances. Jiang et al. (50) randomized 93 patients after extubation to either face mask BiPAP or oxygen therapy. It should be noted that extubation in 37 of these patients was unplanned (self-extubation). There was a 22% re-intubation rate but no signiﬁcant difference between the two treatment groups, although the re-intubation rate was higher in those receiving BiPAP. Keenan et al. (51) randomized 81 patients who developed post-extubation respiratory distress within 48 hours of extubation to either NPPV or standard therapy. Patients developed respiratory distress on average about 10 + 10 hours following extubation. No differences were noted in the re-intubation rate, duration of mechanical ventilation, episodes of pneumonia, duration of ICU or hospital stay, or mortality. The study patients represented only about 10% of screened patients who met inclusion criteria. In addition, they identiﬁed 24 patients who met inclusion

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criteria but were treated with NPPV outside the study during the study period. Their re-intubation rate was lower (44%) as opposed to 70% in the study patients. It was unclear if selection bias may have skewed the outcome of this trial. Subsequently, a multi-center trial involving 221 patients, also did not identify any difference in the re-intubation rate (48%) with NPPV and noted increased mortality in those assigned to NPPV (25% vs 14%) (52). These ﬁndings temper the use of NPPV in this group of patients, but sub-group analysis suggests possible beneﬁt in those with COPD. In summary, the support for NPPV after discontinuation of mechanical ventilation is inconclusive. It appears to work best in an early extubation strategy in which patients who do not meet conventional weaning criteria are extubated and treated with NPPV within a week of intubation. Patients with COPD may be the sub-group most likely to beneﬁt from this approach. The evidence to support the use of NPPV in patients who meet weaning criteria and then develop respiratory distress after extubation is disappointing. D. Pneumonia

Although this has been the primary focus of only one randomized trial, patients with community-acquired pneumonia constitute a large proportion of study patients in several other investigations. As in other conditions, patients with pneumonia may beneﬁt from the improvement in oxygenation and relief of dyspnea with NIMV, but there may be concerns with hemodynamic instability, secretion clearance, and refractory respiratory failure. While the gas exchange defects of pneumonia can be corrected, there may not be the rapid recovery that is characteristic of the other conditions for which NIMV has demonstrated efﬁcacy. Confalonieri et al. (53) randomized ﬁfty-six consecutive patients with severe community-acquired pneumonia to either NPPV with PSV (14.8 + 4.7 cmH2O) and PEEP (4.9 + 1.7 cmH2O) plus standard therapy or standard therapy alone. There was a reduction in the intubation rate and duration of ICU stay, but the improvement was noted only in those patients with concomitant COPD. There was no improvement in any outcome measures in patients without obstructive lung disease. It was unclear if the beneﬁt of NPPV may actually have been due to the effect of NPPV on COPD, as opposed to pneumonia. The COPD patients had a respiratory acidosis and actually had a higher PaO2/FIO2 than their non-COPD counterparts. As noted earlier, CPAP has potential to be of beneﬁt in patients with hypoxemic respiratory failure, most notably cardiogenic pulmonary edema. Evaluation of its efﬁcacy in a larger group of heterogeneous patients with acute hypoxemic respiratory failure has not conﬁrmed this beneﬁt. Delclaux et al. (54) randomized 123 patients to face mask CPAP (up to 10 cm H2O) in addition to standard therapy. Sixty-seven of these patients had pneumonia, and as a group, there was improvement in PaO2/FIO2 and symptoms at one hour, but ultimately no differences in these outcome measures, intubation rate, duration of ICU stay, or mortality.

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There were four cardiac arrests in the CPAP group, possibly related to delays in intubation. There was no separate analysis presented about pneumonia patients. CPAP may not have been the optimal mode of NIMV. In another prospective trial of patients with acute hypoxemic respiratory failure, Ferrer et al. (55) randomized 105 patients to NPPV with either BiPAP (IPAP ¼ 16 + 3 cm H2O; EPAP ¼ 7 + 2 cm H2O) plus standard therapy or standard therapy in a heterogeneous group of patients with hypoxemic respiratory failure. Thirty-four patients had pneumonia without COPD, and they were able to demonstrate a difference in the intubation rate (26% vs. 73%) with NPPV. NPPV patients also had greater improvement in hypoxemia and tachypnea, as well as a decrease in the incidence of septic shock, presumably due to decreased nosocomial pneumonia, decreased ICU mortality, and 90-day mortality. Although data were presented for the whole cohort, the beneﬁt of NPPV seemed to be restricted to the pneumonia patients. Of note, there was no difference in the intubation rate for patients with cardiogenic edema, mirroring the experience reported by Nava et al. Other randomized investigations of NPPV that include pneumonia patients have not had more than a handful of patients with pneumonia, making it difﬁcult to reach any meaningful conclusions (56 – 58). These ﬁndings urge caution in the use of NPPV in patients with pneumonia. It is important to note that in analyses of large groups of patients treated with NPPV, pneumonia has been identiﬁed as a predictor of failure with NPPV (59,60). This concern may lessen as improvements in ventilatory devices occur and clinicians gain experience and understanding of the limitations of NPPV. As in other conditions, careful patient selection and close monitoring is warranted. The above constitutes the bulk of the favorable experience with NIMV. These conditions and the primary beneﬁts of NIMV are summarized in Table 2. NIMV has also been used in other conditions, but the evidence to recommend its routine use is limited. Those conditions that have undergone single randomized controlled trials are discussed in the following section and also noted in Table 3. Endorsement of the use of NIMV may be limited to sub-groups or limited by relatively modest experience, thereby tempering its widespread use in these conditions. IV.

Other Conditions

A. Immunocompromised Patients

Immunocompromised patients are difﬁcult to manage, especially those with hematologic malignancies or post-transplant, as they can have a very high severity of illness and have an extraordinarily poor prognosis if they develop respiratory failure requiring intubation. Bone marrow transplant patients with respiratory failure requiring intubation are a group with a particularly dismal prognosis (61). Nevertheless, there is the possibility that a select group of patients may beneﬁt from NPPV and avoid intubation.

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Table 2 Non-Invasive Ventilation in Clinical Conditions with Randomized Controlled Trials: Summary of Effects Outcome variable

Condition Chronic obstructive pulmonary disease Cardiogenic pulmonary edema CPAP PSV BiPAP CPAP vs. BiPAP After discontinuation of mechanical ventilation Early extubation Post-extubation Pneumonia

Gas exchange

Intubation rate

Length of stay

Mortality

þþ

þþ

þ

þ

þþ þþ + þ (BiPAP)

þþ + 2 2

2 2 2 2

+ 2 2 2

þ + þ

þ 2 þ

þ 2 þ

þ 2 þ

Notes: þþ, Uniform beneﬁt; þ, Beneﬁt in selected groups; +, Possible beneﬁt; 2, No difference. Abbreviations: BiPAP, Bi-level positive airway pressure; CPAP, continuous positive airway pressure; PSV, pressure support ventilation.

In a group of mostly liver and renal transplant patients, Antonelli et al. (62) randomized 51 with acute hypoxemic respiratory failure to either NPPV with pressure support and PEEP plus supportive therapy or supportive therapy alone. The major causes of respiratory failure were pneumonia, cardiogenic Table 3 Non-Invasive Ventilation: Experience in Other Conditions Demonstrated beneﬁt (Single randomized controlled trial) Asthma Immunocompromised patients Solid organ transplants (liver, renal, lung) Febrile neutropenic patients Post-operative lung resection Rib fractures (trauma with non-penetrating chest injuries/ﬂail chest) Demonstrated efﬁcacy (Case series) Acute respiratory distress syndrome Cystic ﬁbrosis Do not intubate patients Kyphoscoliosis Muscular dystrophy Obstructive sleep apnea (decompensated) Pneumocystis carinii pneumonia (mild) Post-polio syndrome

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pulmonary edema, acute respiratory distress syndrome (ARDS), and mucus plugging. They were able to demonstrate greater improvement in oxygenation, intubation rate, incidence of fatal complications, most notably in septic shock, duration of ICU stay, and mortality. However, the beneﬁt was most evident in those with cardiogenic pulmonary edema, as the beneﬁt was not substantially different from standard therapy in the other sub-groups. In another study of mostly neutropenic patients with hematologic malignancies or bone marrow transplants, Hilbert et al. randomized 52 of these patients with febrile hypoxemic respiratory failure and pulmonary inﬁltrates to NPPV with pressure support (15 + 2 cm H2O) and PEEP (6 + 1 cm H2O). About half of the patients had a microbiologic diagnosis of pneumonia. They were able to demonstrate improved oxygenation, with lower intubation rates, complications, ICU stay, and hospital mortality. The beneﬁt was most pronounced in those with an identiﬁed cause of their pneumonia. It should be noted that NPPV was only administered, on average, eight hours a day for an average of four days. This indirect measure of severity would suggest that these patients had a relatively modest case of pneumonia as highlighted in the accompanying editorial (63). In summary, NPPV may beneﬁt a very select group of immunocompromised patients. Experience from these single-center studies would suggest that those with cardiogenic pulmonary edema and an identiﬁed cause of pneumonia may be the best candidates for successful application. Caution should be used in its application in any other sub-group of immunocompromised patients because a delay in more appropriate intubation may increase their risk for adverse events and death. B. Asthma

Although the treatment of decompensated asthma closely mirrors that of COPD, there is a striking paucity of reported experience with NIMV in this condition. There are sufﬁcient differences in the pathophysiology of these two conditions that may not allow the experience in COPD patients to be translated to asthma patients. Dynamic hyperinﬂation may play more of a role in COPD patients than in asthma patients, who while subject to dynamic hyperinﬂation, are also subject to increased airway resistance and sudden asphyxia not typically seen in the COPD patients. Most of the reported experience in asthma is found in case series, but there has been a randomized evaluation in asthma patients in an emergency room setting (64). Soroksky et al. randomized 30 patients with asthma to nasal BiPAP (maximum settings of IPAP ¼ 15 cm H2O; EPAP¼ 5 cm H2O) plus standard therapy or standard therapy plus sham BiPAP with settings of 1 cm H2O. They noted a more rapid and greater improvement in lung function as well as a lower hospitalization rate. This experience is promising, but it should serve as the impetus for larger studies. As with other conditions, this is a reasonable option provided there is careful patient selection and close monitoring of response to therapy.

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Respiratory failure following lung resection for lung cancer can carry devastating consequences, with mortality approaching 80% in the most severe cases (65). The major causes of decompensation include cardiogenic and non-cardiogenic pulmonary edema, mucus plugging, and pneumonia. Endotracheal intubation and mechanical ventilation also carry a risk of exacerbating bronchial stump disruption, with attendant complications including broncho-pleural ﬁstula and infection. NIMV may ameliorate some of the risk factors as patients would not be subject to the high peak airway pressures usually associated with mechanical ventilation. In a focused evaluation of patients following lung resection, Auriant et al. (66) randomized 48 patients who developed hypoxemic respiratory failure after extubation following lung cancer resection (lobes or pneumonectomy). They had been extubated in the operating room and developed respiratory distress within two days of their ICU admission. Decompensation was attributed to either pulmonary edema, atelectasis, or pneumonia. Patients were treated with BiPAP at relatively modest levels (IPAP ¼ 9 + 2 cm H2O; EPAP ¼ 4 + 0.1 cm H2O) and with a marked reduction in the intubation rate (21% vs. 50%) as well as a reduction in overall mortality. It should be noted that this experience represents a very select group of patients, comprising less than 10% of their patients who required ICU admission and 0.06% of all patients who underwent lung resection at their institution during the study period. While this is a promising option, it requires further study and due caution must be exercised when used in these patients. D. Rib Fractures/Chest Wall Trauma

Rib fractures due to non-penetrating injuries to the chest (trauma) may predispose to adverse complications due to pulmonary contusion, ineffective cough (pain), atelectasis, and pneumonia. Although patients with multiple rib fractures and respiratory compromise have often been managed with intubation and mechanical ventilation, NIMV may be able to provide this same pneumatic splint. Bolliger et al. (67) randomized 70 patients with multiple rib fractures to face mask CPAP (5 + 1 cm H2O) and regional analgesia or intubation and mechanical ventilation. Only one of the CPAP patients subsequently required intubation. The CPAP-treated patients recovered more quickly and had their hospitalization decreased by almost a week, with fewer episodes of pneumonia and no difference in mortality. While this appears promising, it should be noted that ventilator management has changed since this report. Patients undergoing intubation in the study may not be intubated in current practice. However, this is an option that can be considered in patients with chest wall trauma in whom physicians may wish to avoid intubation. E.

Acute Respiratory Distress Syndrome

This has not been the focus of any prospective, randomized study of NIMV, although patients with severe hypoxemia due to ARDS or non-cardiogenic

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49

pulmonary edema have been included in many of the prospective studies. Case series would suggest that patients with ARDS can be successfully treated with NIMV, but the success seemed to be in those with less severe disease (68). In their evaluation of hypoxemic respiratory failure, Ferrer et al. (55) enrolled 15 patients with ARDS and found no beneﬁt in any outcome variable in this sub-group. In multi-variate analysis, ARDS was identiﬁed as a risk factor for intubation. This mirrors the ﬁnding by Antonelli et al. (60), who identiﬁed ARDS as a risk factor for NPPV failure. There is insufﬁcient data to make any recommendations on the use of this modality, but the time course of this illness and many associated complications make it unlikely that it can be efﬁciently managed with NIMV, except in very mild cases. F. Do Not Intubate Status

Patients with advanced or end-stage disease, whether respiratory or otherwise, constitute a sub-group of patients who may also beneﬁt from NIMV. These patients may have previously designated a treatment preference of “do not resuscitate” or “do not intubate” or are otherwise considered poor candidates for invasive ventilatory support. These are frequently advanced stage COPD patients. They often present with profound hypercapnic respiratory failure and would expire without further supportive care. Intubation and mechanical ventilation is tempered by the risk of ventilator dependence, which is why a trial of NIMV is a consideration. While a prospective, randomized trial is not feasible, several case series suggest successful treatment is possible in these patients. Early investigations in two series (30 and 11 patients, respectively), suggested that NIMV can successfully treat 60% and 64% of these patients, although the numbers discharged home were 53% and 45%, respectively (69,70). In another series of 37 COPD patients, the median survival after an episode of hypercapnic respiratory failure treated with NIMV was 179 days, and one year survival was 30% (71). Despite some modest beneﬁt, patients or family of patients treated with NIMV in this situation must be counseled carefully to understand that this still constitutes life support. Even if this provides an opportunity for recovery, there remains the distinct possibility that application only prolongs the inevitable. Some patients will experience dyspnea relief, but in others the mask may be uncomfortable and add to their distress. While this approach does afford some patients some extra time to resolve their affairs, this therapy also consumes valuable health-care resources (staff, monitored beds, supplies, etc.) in what may be an ultimately futile situation (72,73). Drawing from the general experience with NIMV, the “do not intubate” COPD patient may comprise the group best suited for these trials. Trials in other patients would necessarily require a case by case evaluation. G. Other Conditions

There are many other respiratory conditions for which NIMV may be beneﬁcial during episodes of respiratory failure, and they are listed in Table 3. However,

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many of these are reported in case series format and not randomized, controlled studies. These conditions include cystic ﬁbrosis, kyphoscoliosis, neuromuscular disease, decompensated obstructive sleep apnea, and mild Pneumocystis carinii pneumonia. Except for Pneumocystis carinii pneumonia, most represent acute decompensation of chronic respiratory failure. With cystic ﬁbrosis, extensive experience has accumulated and been reported by Madden et al. (74). They have treated over 100 patients, and in 90 patients awaiting or undergoing evaluation for lung transplantation, 38 (42%) have been stabilized with NIPPV, with 28 having received a lung transplant and the others still on the list. Some patients were maintained for over a year and a half with NIMV. Even in a sub-group not composed of lung transplant candidates, some were able to survive using NIMV for over a year. This experience indicates that NIPPV can help provide a bridge of support until transplantation and thereby avoid the complications associated with intubation and mechanical ventilation.

V.

Clinical Aspects of NIMV

Despite over a decade of experience with NIMV, its use remains limited and often conﬁned to medical centers with expertise or a special interest in its application. Recent surveys on its actual use are telling. In a questionnaire survey, Doherty and Greenstone (75) found that NIMV was available in 48% of the hospitals surveyed in the United Kingdom. Even then, about 70% of hospitals treated ,20 patients per year. Less than 10% treated .60 patients per year. In another month long, multi-country survey on ventilator use, over 4000 patients were ventilated for .12 hours (76). Of that group, only 202 (4.7%) were treated with NIMV, and the use was even less (1%) in a point prevalence study (77). In another European survey of mostly French institutions, some with familiarity with NIMV, only 16% of their ICU patients were treated with NIMV (78). They found a wide range in the use of NIMV in the 42 ICUs surveyed, with eight ICUs never using NIMV and one ICU using NIMV in 67% of their ICU patients requiring ventilatory support. Hypercapnia (COPD), post-operative respiratory failure, pneumonia, and cardiogenic pulmonary edema were the frequent conditions treated with NIMV. Therefore, despite the success reported, relatively few patients with respiratory failure are placed on this treatment. There are areas of its application that require close attention. Patient selection, mask leaks, patient synchrony, ventilator efﬁciency, nursing, and respiratory therapy time are all potential limiting factors in successful application of NIMV. These were potential stumbling blocks for initial investigators and are issues that continue to limit the use of NIMV. A better understanding of these factors not only helps deﬁne the optimal treatment group, but also helps predict its success.

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A. Patient Selection

Patient selection is probably the most important factor to consider prior to initiating NIMV. This is an added element that encompasses all of the clinical conditions being treated. Once it is determined that the patient has a condition readily treatable with NIMV (i.e., COPD exacerbation, cardiogenic pulmonary edema, pneumonia, etc.), then a determination needs to be made if other aspects of their presentation may preclude treatment with NIMV. This is cruial as those destined to fail or only achieve a partial response with NIMV may be better served with immediate intubation and mechanical ventilation. This spares what may be ineffective therapy, avoids further progression of respiratory failure, and limits associated complications from incompletely treated respiratory failure or intubation under duress. Factors that inﬂuence the success of NIMV can be grouped into areas that deal with severity of illness, co-morbidities, technical issues, and patient cooperation. One of the unanswered questions involving patient selection (and in turn predicting the success of NIMV) has been the limits imposed by the patient’s severity of illness. This applies to both ends of the spectrum. Patients may have a relatively mild severity of illness, destined to improve with medical therapy, and not require NIMV. NIMV would be unnecessary and excessive. There is general agreement that the most severely ill patients are better served by immediate intubation without a trial of NIMV. Deﬁning the limits of application has been elusive. The severity of acidosis correlates closely with the likelihood for intubation in those presenting with hypercapnic respiratory acidosis. Thresholds have been identiﬁed based on prospective and retrospective analyses. A pH of 7.25 has been associated with a .50% intubation rate. It is noteworthy that a pH of 7.25 has been used to limit enrollment in several NIMV studies. Plant et al. (79) analyzed their database of patients with respect to pH and PaCO2 as predictors of failure and meeting criteria for intubation. These two variables are obviously linked and co-dependent. The pH may be the more important variable. The relative risk of failure was greater with worsening pH for the same level of hypercapnia than hypercapnia for the same level of pH. The relative risk for failure with a pH 7.25 and PaCO2 ¼ 45 was 3.89 for those treated with NIMV and 9.98 for those treated with standard therapy. This compares to a relative risk of unity for standard therapy with a pH 7.35, and 0.39 with NIMV. Higher APACHE II scores indicative of an increased severity of illness have predicted NIMV failures in several series (59,80). As medical staff gain more expertise with this modality, the success rate improves as expected. Carlucci et al. (81) have analyzed their experience with COPD patients during 208 episodes of acute respiratory failure. While the failure rate was constant (17.2%) over an eight-year period, patients were being treated with a greater severity of respiratory acidosis (mean pH: 7.20 + 0.08 vs. 7.25 + 0.07) and with greater successful treatment of the more severe patients

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during the latter periods of their survey compared with the early years. The failures during the early period of their survey (1992 – 1996) were very similar in terms of severity of illness to those successfully treated during the latter years (1997 – 1998). One consistent ﬁnding in both periods was that successfully treated patients had a marked improvement with NIMV after one hour of therapy (pH improvement: 0.06 –0.09), while failures had no improvement at all. The lower limit of effectiveness remains to be deﬁned, but limiting NIMV to patients with hypercapnic respiratory acidosis to a pH . 7.10 is a reasonable common sense limitation. It should be noted that there is very little experience in these severely acidemic patients since most have been excluded from clinical trials.

B. Co-Morbidities

In addition to severity of illness, co-morbidities also limit effective NIMV. These are summarized in Table 4. These limitations generally involve issues that render optimal management difﬁcult without intubation and mechanical ventilation. These include cardiac instability involved with acute myocardial infarction, ventricular dysrhythmias, shock, GI bleeding, coma, profound lethargy, and status epilepticus. The main limiting factor revolves around the need to protect the airway from aspiration or the need to control the airway during treatment. Hemodynamically unstable patients are best managed with intubation, eliminating a potentially confounding factor in already critically ill patients. Those who require airway protection or with mechanical upper airway obstruction are

Table 4 Non-Invasive Ventilation: Other Aspects of Patient Selection Co-Morbidities that Prevent Effective Non-Invasive Ventilation Hemodynamic instability Acute complicated myocardial infarction Hemodynamically signiﬁcant cardiac dysrrhythmias Severe septic shock GI bleeding Need for airway protection Coma or any condition with an unstable respiratory drive Extensive cerebral vascular accident or hemorrhage Status epilepticus Potential for life-threatening airway compromise Head and neck tumors Any tumor with extrinsic airway compression Angioedema or anaphylaxis Abbreviation: GI, gastrointestinal.

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better served with endotracheal intubation to limit further aspiration of oropharyngeal or gastic contents to the extent possible with endotracheal intubation. Patients with upper airway obstruction because of tumors, extrinsic masses, anaphylaxis, or angioedema should be intubated to maintain the patency of the airway. Comatose, severely obtunded patients or those with unstable respiratory drive are not candidates for NIMV. Patients need to be able to cooperate with mask ﬁtting and be able to coordinate with the ventilator. They can be lethargic but arousable and need to be able to cooperate and provide feedback. Those with severe pneumonia and copious secretions are problematic because mask ventilation makes it difﬁcult to control and clear secretions; however, there has been successful management in selected patients. Craniofacial defects may limit the ability to achieve an effective mask seal. Patients with bony deformities following resection of head and neck tumors fall into this category. Edentulous patients may have problems with nasal ventilation, but this can be solved by using an oronasal mask. Beards may prevent an adequate mask seal, but they can be shaved. Nasogastric tubes were once considered essential to prevent gastric insufﬂation. However, the pressures utilized with NIMV rarely exceed the lower esophageal sphincter pressure (25 cmH2O) (82). They are no longer recommended as their presence makes it difﬁcult to achieve an adequate mask seal and predisposes to air leaks.

C. Technical Issues: Masks

In the most basic conﬁguration, NIMV substitutes the endotracheal tube with a mask. However, this transforms the ventilatory system from a closed system to one with potential for substantial leaks. The leaks usually occur along the patient –mask interface or from the mouth if nasal masks are used. Substantial mask leaks lead to patient discomfort and ineffective ventilation. In addition to improperly ﬁtted masks, the masks may become dislodged during therapy or leaks may occur around nasogastric tubes or any other device that prevents an adequate seal between the skin and the mask. Fitting and maintaining a proper mask may be as important as patient selection in successful NIMV. Failure rates of NIMV can be as high as 40%, and many are due to technical issues related to the mask leaks and mask intolerance (60). Over the past decade, there has been signiﬁcant progress in mask development. Masks are clear to allow visualization of face and facilitate diagnosis in patients with emesis or excess secretions. They are softer than the past, usually with silicone or an airﬁlled cushion in the contact points with the face. There may be other cushions at the greatest pressure points, and straps have become less cumbersome and more secure. Other design improvements prevent circuit rebreathing in the event of machine failure and allow rapid mask removal in the event of emesis. Masks can be custom ﬁtted, but may be problematic in those with acute respiratory distress, and most of them are available in a variety of sizes.

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Generally, the most effective mask is the smallest mask that provides an adequate ﬁt. Patients should be upright, with the head of the bed elevated 458 or more at the time of mask placement. Patients may hold the mask up to their face, or the mask and attached head straps are loosely placed over the patient’s head prior to strapping it in place. Allowing patients to hold the mask also allows them to become accustomed to the mask. It is important that the head straps are in place prior to mask placement as this facilitates placement. For nasal masks, the mask should allow adequate clearance for the nose, but not cover the vermillion of the upper lip. The soft palate and teeth allow proper closure of the oronasal cavity during positive pressure and help minimize leaks. Edentulous patients may have difﬁculty with maintaining proper mask position and are often better served with a face mask. A face mask should ﬁt comfortably on the mandible, just below the lower vermillion. A mask that encroaches on the chin is subject to large leaks and ineffective ventilation. The straps should be tight but allow easy passage of one to two ﬁngers between the face and straps. Very tight straps are not only uncomfortable, but they increase the likelihood of developing pressure ulcers over the nose or face. Chin straps are available if mouth leaks are unavoidable. A small amount of leak may be unavoidable despite multiple manipulations. Leaks around the nose into the eyes are the most distressing for patients. Nasal plugs or nasal pillows are not suitable for acutely ill patients. A mouthpiece is an alternative, although that would require more active cooperation by the patient than a mask that is anchored to the patient by head straps. Most masks have the option of bleeding oxygen directly into the mask via oxygen tubing, but this runs the risk of creating excess pressure in this enclosed space. If oxygen is necessary, it is better delivered via an adaptor attached to ventilator tubing. In a bench study assessing the inﬂuence of the site of oxygen delivery (mask or circuit), with various combinations as to the leak port site (mask, plateau exhalation value, or circuit) and increasing levels of IPAP and EPAP (10–25 and 5–10 cm H2O, respectively), the highest concentrations of oxygen were delivered with oxygen delivered at the mask and the leak in the circuit with the lowest levels of pressure (83). This might be an issue with some of the older, smaller bi-level ventilatory assist devices. Newer ventilators are able to blend oxygen and deliver through the ventilator tubing to allow precise control of FIO2. Nasal and oronasal (including full face) masks are the primary interfaces used in NIMV. A summary of their advantages and disadvantages is provided in Table 5. For most patients, the nasal mask is more comfortable, less obtrusive, has less dead space, and allows easier communication. The nasal mask does require a more coordination by the patient. Patients must be able to maintain a mouth seal and are subject to more mouth leaks. Some patients may be unable to prevent mouth leaks (edentulous, mouth breathing pattern, pursed lips breathing, and obtundation). The oronasal mask allows for mouth breathing, creates more difﬁculty with speech and expectoration, and may cause claustrophobia in some patients. Most experience has been with an oronasal mask that covers the nose and the mouth. Face masks that cover the whole face including the

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Table 5 Non-Invasive Ventilation: Comparison of Masks Nasal Better suited for More cooperative patients Lower severity of illness Claustrophobic patients

Physiologic beneﬁts Better tolerated, ? better compliance

Other notes Less frequently used (30%)

Face (oronasal) Less cooperative patients Higher severity of illness Mouth breathing Pursed lips breathing pattern Edentulous patient More effective ventilation, higher tidal volumes More efﬁcient CO2 removal Possibly improved outcome measures (? Lower intubation rate) Most frequently used (70%)

eyes are available as an alternative to nasal and oronasal masks, although with limited experience (84). Helmet masks have also been developed, but likewise with limited experience (85,86). It follows that nasal masks are better suited for the less dyspneic patient and the oronasal face mask better for the more dyspneic patient who is more likely to be a mouth breather and subject to mouth leaks. Because this comprises the majority of candidates for NIMV, face mask NIMV is the modality of choice at our institution. Face mask ventilation is also the predominant interface for NIMV in reported studies, used in about 70% of treated patients (87). Nasal ventilation would be reserved for those cooperative patients who are unable to tolerate the face mask. It has been observed that issues with claustrophobia or mask discomfort are often outweighed by the relief obtained with unloading of the respiratory system. As might be expected, differences in randomized comparisons of the masks in acute respiratory failure primarily reﬂect difference related to leaks and efﬁcacy. In a prospective, randomized trial, Kwok et al. (88) compared nasal and oronasal masks in 70 patients with acute respiratory failure (primarily pulmonary edema and COPD). They noted comparable effects on physiologic indices (dyspnea, comfort, oxygenation, and CO2 reduction) with both masks, but there was greater mask intolerance with the nasal mask (34% vs. 11%). They also noted more deaths (11% vs. 6%) and less success in the nasal mask group (49% vs. 66%), but these differences were not statistically different, with the same intubation rate (23%) in both groups. This mirrors other evaluations in acutely ill patients, although there have been trends toward more efﬁcient removal of CO2. In a study of stable patients, there was greater CO2 reduction and higher minute ventilation with face masks, but better tolerance with nasal masks (89,90).

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In summary, once properly ﬁtted, effective ventilation can be accomplished using either a nasal or an oronasal mask. Most patients who are candidates for NIMV are best treated ﬁrst with face mask (oronasal) ventilation because their dyspnea often mandates mouth breathing. It follows that less acutely ill patients can be successfully ventilated with a nasal mask. D. Ventilators

There has been great diversity in the types of ventilators used to provide ventilatory support in NIMV. There is experience with both volume- and pressurecycled ventilators, large bedside and portable devices, and a variety of ventilatory modes, including assist control, CPAP, pressure support, proportional assist ventilation (PAV), or some combination of all of these modalities. In the appropriate setting, all of these can provide effective ventilatory support with relief of dyspnea, correction of gas exchange abnormalities, and successful prevention of endotracheal intubation. The success rates are probably comparable, provided that patients receive an adequate level of support. In this sense, one modality cannot be endorsed above another, but in reality, pressure support with PEEP in one survey was used in almost 75% of patients treated with NIMV (78). In the survey, volume ventilation was used in only 15% of patients. Similarly, the vast majority of the experience with NIMV has been accumulated with pressure ventilation with volume ventilation used in only one major randomized trial, comprising less than 10% of patients analyzed in a recent meta-analysis. Volume ventilators may pose more problems during NIMV, primarily because of mask or mouth leaks and potentially wide ﬂuctuations in peak airway pressures. The leaks obviously impede delivery of adequate tidal volume and can trigger more alarms, which may require more attention from medical staff. This may occur even with drastic changes in alarm limits. Compensation for the leaks often requires tightening of mask straps, which can contribute to skin breakdown and pressure sores. High pressures may also lead to gastric distension. On the other hand, volume ventilators may be better suited for patients with rapidly changing respiratory system compliance or drive who would require some minimum minute ventilation. However, despite these potential limitations, no signiﬁcant differences have been demonstrated between the two modes, although there appears to be better compliance with pressure ventilation (91,92). Pressure-cycled ventilators, whether provided by larger bedside critical care ventilator or smaller, more mobile bi-level ventilatory assist devices, seem to be better adapted for NIMV. The pressure ventilators are more tolerant of system leaks, and some of the bi-level models have leak compensation features, which result in fewer alarms requiring medical staff attention. The bi-level devices are designed speciﬁcally with NIMV in mind, whereas NIMV is one of the many options available in the bedside critical care ventilator. There are signiﬁcant cost differences between the two types of ventilators, and versatility among patients may also inﬂuence the use of one over the other.

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There have been improvements in other areas. Earlier models of bi-level pressure ventilators were limited by the maximal pressures that could be delivered, possible CO2 rebreathing through single-hose tubing, and imprecise FIO2 delivery (93,94). Reﬁnements have allowed higher levels of pressure support delivery (up to 40 cm H2O of inspiratory pressure) and limited potential for CO2 rebreathing (use of PEEP and modiﬁcations of the expiratory valve), and newer models are equipped with blenders that allow precise FIO2. The devices have become more responsive to patient efforts with adjustable triggering sensitivities, involving both the inspiratory and expiratory cycles. Flow triggered breaths provide for better patient–ventilator synchroncy and lower work of breathing (95). The termination of the inspiratory cycle or initiation of expiratory cycling may potentially adversely affect patients. Common criteria include termination at a threshold representing a 25–40% decrease from peak inspiratory ﬂow rates or at a set time. There is the potential for continued cycling due to mask leaks, and in a mathematical and lung model, these lead to marked variations in the duration of the inspiratory cycle as well as the development of intrinsic PEEP (96). This may have adverse consequence on patient–ventilator synchrony and possibly even some hemodynamic consequences. Modiﬁcations in newer generation devices have eliminated this potential problem. Perhaps the key to these ventilators is that their breaths are patient initiated. This certainly facilitates patient–ventilator synchrony and may improve patient comfort. There has been further blurring of the differences between these critical care ventilators and bi-level devices. There are models that now incorporate both invasive and non-invasive modes in their conﬁguration. Table 6 provides

Table 6 Non-Invasive Ventilation: Comparison of Ventilators Full function critical care ventilators

Bedside bi-level assist devices

Multiple ventilatory options Assist control/volume Pressure support Pressure control Synchronized intermittent mandatory ventilation Positive end-expiratory pressure Inverse ratio ventilation Higher inspiratory ﬂow rates

Ventilatory options (maximum pressures) Inspiratory positive airway pressure (40 cm H2O) Expiratory positive airway pressure (20 cm H2O) Continuous positive airway pressure (20 cm H2O)

Multiple alarms Not very leak tolerant

Limited number of alarms Leak tolerant and leak compensation

Adjuncts Humidiﬁcation, nebulization, oxygen, in line Patient waveforms available

Adjuncts Some models with features incorporated Other models require addition or adaptation for use

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a comparison of the key differences between the major types of ventilators used in NIMV. As the distinction between ventilators has blurred, it becomes more important to recognize that different masks are used based on the ventilator used. This would probably never be an issue except for those unfamiliar with NIMV. The bi-level devices use a single-hose to deliver ventilatory support with exhalation of gases usually through a hole in the mask or circuit. This exhalation port should never be blocked. Likewise, there is also a ﬂapper valve that allows delivery of pressure and entrainment of air. If it is not functional, the mask should be replaced. A separate mask without any openings in the mask or circuit is used for those critical care ventilators that can also deliver NIMV. The critical care ventilators use a closed two-hose system (inspiratory and expiratory) and therefore are not designed to be used with a conﬁguration with a ﬁxed leak. This type of mix-up may result in ineffective ventilation, and there is always the potential for untoward consequences. Figures 1 and 2 demonstrate the differences in the masks used with different ventilators and also illustrate the similarities between the two conﬁgurations. PAV may provide even better patient – ventilator synchrony and patient comfort. It uses an inline pneumotachometer to provide ventilatory assistance proportional to the patient’s efforts. It incorporates ﬂow and volume assistance with each breath, and expiratory cycling occurs with cessation of inspiratory effort. It is more responsive to changes in patient effort than the previously

Figure 1 Patient supported with face mask non-invasive ventilation using a bedside bi-level ventilator with a single-hose tubing attached to the mask. The connection has an exhalation port and a ﬂapper valve attached at the interface between the mask and tubing.

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Figure 2 Patient supported with face mask non-invasive ventilation using a critical care ventilator that can be used in patients who are also endotracheally intubated. The mask is the same as the mask used for the patient in Figure 1, but the head straps and ventilator tubing attachments are different. The attachment to the mask is of a single-piece construction, different conﬁguration, without any exhalation ports and is meant to be used with double-hose tubing.

discussed models. This conﬁguration should drastically reduce or even eliminate problems with patient – ventilator synchrony. Clinical experience indicates efﬁcacy equal to pressure support NIMV, but better overall tolerance and comfort (97,98). The ventilator is not yet commercially available in the United States. E.

Ventilators: Other Issues

Initial settings are goal directed to achieve adequate tidal volumes. A goal tidal volume of 5 to 7 mL/kg is appropriate with additional support added as necessary to reduce the respiratory rate to 25/min. Appropriate initial settings in most patients would be an IPAP or pressure support equal to 10 cmH2O and EPAP or PEEP equal to 5 cm H2O. These pressures are tolerated by most, although some will require lower pressures. However, it is not recommended that initial inspiratory pressures be lower than 8 cm H2O or expiratory pressures much lower than 4 cm H2O. Settings with lower pressures are usually inadequate for ventilatory support, subjecting the patient to more dyspnea and distress, and lead to premature termination of therapy. Maximal inspiratory pressures should be limited to about 20 to 25 cm H2O. Patients do not tolerate these higher pressures, and in this range, there is a risk for overcoming the lower esophageal sphincter pressure with subsequent gastric distension. Changes in settings

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should target the primary respiratory defect. Hypoxemic patients are best treated with an increase in the PEEP (CPAP) or EPAP with a proportionate increase in the IPAP effectively maintaining the same tidal volume. Hypercapnic patients beneﬁt most from an increase in tidal volume resulting from increases in pressure support or IPAP without much change in the EPAP. If using BiPAP, the difference between IPAP and EPAP represents the level of pressure support supplied to the patient. A back-up respiratory rate can be set to achieve a minimum minute ventilation. NIMV is best delivered in three to four hours blocks with 30 to 60 minutes breaks. Early in the course of treatment, some patients develop intolerable dyspnea off NIMV and receive near continuous support. The breaks in therapy are encouraged to minimize ischemia and necrosis that can develop at the skin – mask interface. This also allows a chance for the patient to clear secretions, eat, and drink. These breaks can serve as short “weaning” trials, and the duration of the break can be extended at any time based on the comfort of the patient. In this sense, ventilatory support and “weaning” occur at the same time, and ventilatory support is continued only as long as absolutely necessary. In some patients, NIMV is required for most of the ﬁrst day (20þ hours), but some may sufﬁce with only eight hours of support. Patients are often very cognizant of the beneﬁt with NIMV, and it is not infrequently that they not only dictate the duration of ventilatory support, but can also “self-wean” themselves from NIMV. Humidiﬁcation may be an issue if NIMV is administered using one of the earlier models of the portable bi-level devices. The drying effects of unhumidiﬁed air may dry and thicken airway secretions as well as mucosal surfaces. Drawing from the experience with CPAP masks in patients with obstructive sleep apnea, humidiﬁcation prevents this complication and improves compliance (99). It is a reasonable addition to patients during NIMV, especially those who require more than eight hours of daily support. This is not a signiﬁcant issue with the latest models of NIMV ventilators because most have inline humidiﬁcation systems. Treatment of COPD and asthma patients includes bronchodilators. There may be an advantage of delivering these nebulized bronchodilators inline during NIMV ventilation. There is potential for more drug to be delivered, and in one small clinical study, this seemed to translate to more rapid improvement. Potentially more drug may be able to be delivered with an inline nebulizer. However, it should be noted that improvement may not be due to improved drug delivery and distribution, but rather the beneﬁts of respiratory support with NIMV (100,101). While this requires further investigation, there are no known major adverse effects with this approach. Along the same line, a helium – oxygen mixture used in conjunction with NIMV may also enhance the beneﬁt of NIMV in selected patients. The lower density gas is known to be effective by reducing the resistive load of breathing in obstructed patients, thereby decreasing dyspnea and lowering the work of breathing while improving gas exchange. In a randomized, cross-over study of primarily COPD patients, the

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helium – oxygen mixture during pressure support NIMV reduced indices of work of breathing by one-third or more with greater improvement in hypercapnia than with NIMV (102). These are both important adjuncts in the use of NIMV in respiratory failure and have the potential of possibly averting intubation in some patients. More extensive studies are required to gain a better appreciation of the role of these adjuncts in management.

VI.

Monitoring the Response to Treatment

A. Predictors of Success and Failure

Once NIMV has been initiated, there needs to be close attention to the patient’s response to therapy. This is crucial so as to avoid any unnecessary delay in intubation and associated untoward complications. The main goal of NIMV has been to avoid intubation, and this has been a long-standing outcome measure by which to gauge the success of NIMV. Other factors may also help in this assessment. This is a crucial area and the subject of a recent review of data from multiple studies (103). Patient cooperation is crucial for the successful NIMV. This in turn serves as an indirect reﬂection of a patient’s severity of illness and level of consciousness. Some of this has been addressed in the section “Patient Selection.” Patients need to be able to coordinate their respiratory efforts with the ventilator, ensuring patient –ventilator synchrony to allow effective ventilatory support. Patients with severe tachypnea (RR . 35) may be so dyspneic that they are unable to coordinate with the ventilator. At these extremes, the mask can be claustrophobic, heightening their sense of dyspnea. Airway pressures are low, making it easy for some patients to successfully “ﬁght” the ventilator, leading to ineffective ventilation and failure. This may be more of an issue with volume ventilators, especially if with signiﬁcant mask leaks. Some patients are so obtunded that effective ventilation is impossible. Measures of level of consciousness or neurologic scores have been demonstrated to correlate with successful NIMV (21 –22, 59,104). The response of physiologic variables, speciﬁcally pH, PaCO2, respiratory rate, and heart rate, provide additional support for the effectiveness of NIMV and its eventual success. This response is an indirect reﬂection of aforementioned variables, including patient selection, patient cooperation, and patient – ventilator synchrony. The response of these variables to a short period of NIMV (30 minutes to a few hours) has been cited as an important factor in predicting the successful application of NIMV. This can be considered a trial of therapy, and improvement represents success on several fronts. Improvement in hypercapnia, respiratory acidosis, and oxygenation reﬂects adequate ventilation and therefore patient synchronization. This has been a near uniform ﬁnding, although there are successfully treated patients who do not demonstrate this pattern of response. The magnitude of the decline in PaCO2 is a variable based on the initial severity of hypercapnia. Pooled studies suggest an average decline of 8 mm Hg after one

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to three hours of ventilatory support (1). Patients who eventually fail and require intubation either have an increase, no change, or a minimal decline in PaCO2. This can cause somewhat of a conundrum in management. Unless patients require immediate intubation, a case can be made for some groups of patients (COPD) with respiratory failure to undergo a trial of NIMV. However, it may not be clear whether failure to improve represents a failure of NIMV or a patient who is slow to improve. There must be a time frame that constitutes an effective trial of NIMV. In some patients, it will be clear that NIMV is ineffective within a few minutes to an hour of initiation. In others, there may still be uncertainty after three to six hours or longer. One would like to avoid extended trials in patients destined to fail because problems may be encountered at the time of intubation, with associated morbidity and mortality. In the two largest studies, (17, 18) failure of NIMV occurred in the vast majority within 12 and 24 hours of initiation, in 82% and 61% of patients, respectively. Moretti et al. (105) identiﬁed predictors of late failure (deﬁned as .48 hours after initiation of NIMV). In their multi-center study of 186 patients, 31 were designated as late failures after an initial response to NIMV. These patients experienced a relapse on average 8.2 + 2.8 days after initial therapy. Lower initial functional status scores, hospital complications (pneumonia, shock, and coma), and lower initial pH (7.22 + 0.08) were predictive factors. These late failures also had an increased mortality rate (68% vs. 15%). In summary, a three- to four-hour trial is a reasonable time period to assess the response to NIMV. There should be some improvement in physiologic parameters within this time frame, although resolution may require a much longer period. If patients fail to demonstrate any improvement within this time frame, intubation may be likely within the initial 12 to 24 hours of presentation. The greatest success with NIMV has been in COPD and cardiogenic pulmonary edema. While patients with other conditions can also be treated with NIMV, they may not respond as favorably, and there may be a lower threshold for intubation in these conditions. Higher failure rates or slower responses to therapy (compared with COPD or cardiogenic pulmonary edema) have been noted in patients with ARDS, pneumonia, and underlying restrictive lung disease (60,106,107). This information provides additional perspective on the use of NIMV in these conditions and may inﬂuence not only the decision to use NIMV, but also the duration of NIMV prior to proceeding to endotracheal intubation. Table 7 provides a summary of the most useful measures of the success or failure of NIMV. Of course, each patient must be evaluated individually, but these parameters should provide a framework for guidance. The next great hurdle involves the decision to terminate NIMV in favor of intubation. Reported criteria for intubation have included a pH , 7.20, pH 7.20 to 7.25 on two occasions one hour apart, hypercapnic coma (Glasgow coma scale ,8 and PaCO2 . 60 mm Hg, PaO2 , 45 mm Hg), or cardiopulmonary arrest (18). Others have used a combination of major or minor clinical criteria (17). Major criteria have included respiratory arrest, loss of consciousness with respiratory

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Table 7 Non-Invasive Ventilation: Predictors of Success or Failure Severity of illness Acidosis (pH , 7.25) Hypercapnia (PaCo2 . 80 and pH ,7.30) APACHE II (.20) Level of consciousness Neurologic score (.4, stuporous, arousal only after vigorous stimulation; inconsistently follows commands) Encephalopathy score (.3, major confusion, daytime sleepiness, or agitation) Glasgow coma score (,8) Disease conditions Acute respiratory distress syndrome Pneumonia Restrictive lung disease Predictors of success Response to brief trial of NIMV (1 –3 hr) Decrease in PaCO2 . 8 mm Hg Improvement in pH . 0.06 Correction of respiratory acidosis Time frame for failure requiring intubation Failure of improvement with NIMV Within 12– 24 hr Late failures (.48 hr after initiation of non-invasive ventilation) Admission predictors of failure Lower functional status (Activity score ,2, dyspnea with light activity) Initial acidosis (pH 7.22) Hospital complications (pneumonia, shock, coma) Abbreviation: NIMV, non-invasive ventilation.

pauses, gasping for air, psychomotor agitation making nursing impossible requiring sedation, heart rate ,50 with loss of alertness, and hemodynamically instability with systolic blood pressure ,70 mm Hg. Minor criteria require two of the following: respiratory rate .35, pH , 7.30 and decreased from onset, PaO2 , 45 mm Hg despite oxygen, and increase in encephalopathy or decreased level of consciousness. These recommendations are outlined in Table 8, and additional guidelines used in our institution are included for comparison. However, despite established criteria, there still exist different thresholds for intubation by the individual physician. Arterial blood gases are a major predictor of respiratory failure, yet there is quite a difference between a pH of 7.30 and 7.20. Many patients with severe respiratory distress are able to maintain “acceptable” gas exchange and oxygenation, yet undergo intubation because of other factors or because of the potential for developing frank respiratory failure. Investigations in NIMV are not amenable to treatment blinding for obvious reasons. Therefore, there exists an extraordinary study bias with

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Table 8 Non-Invasive Ventilation: Intubation Criteria Brochard et al. (17) Major (any one of the following) Respiratory arrest Loss of consciousness with respiratory pauses Gasping for air Psychomotor agitation requiring sedation Heart rate , 50 with loss of alertness Hemodynamic instability with systolic blood pressure , 70 mm Hg Minor (two of the following) Respiratory rate . 35 pH , 7.30 and decreased from onset PaO2 , 45 mm Hg despite oxygen Increase in encephalopathy or decreased level of consciousness Plant et al. (18) pH , 7.20 pH 7.20 – 7.25 on two occasions one hour apart Hypercapnic coma (Glasgow coma scale , 8 and PaCO2 . 60 mm Hg) PaO2 , 45 mm Hg Cardiopulmonary arrest Intubation guidelines (two or more in the context of respiratory distress) RR . 35/min or ,6/min Tidal volume , 5 mL/kg Blood pressure changes: systolic ,90 mm Hg Oxygen desaturation ,90% despite adequate supplemental oxygen Hypercapnia (PaCO2 . 10 mm increase) or acidosis (pH decline .0.08) from baseline Obtundation Diaphoresis Abdominal paradox

respect to the outcome measure of intubation. There is often a natural tendency to intubate early if there is a decision to intubate, but to defer intubation as long as possible in those patients who wish to avoid intubation. This can lead to signiﬁcant discrepancies in treatment. It should be noted that in the multi-center trial that used major and minor criteria for intubation, major criteria for intubation were met in 73% of the non-invasive group, but only 32% of the control group. The guidelines are not meant to be absolute criteria, but to supplement other clinical data and to provide some guidance, especially in cases where laboratory data or measures of gas exchange may not be immediately available. B. Complications

There are markedly different proﬁles reported for complications associated with intubation and mechanical ventilation and NIMV (82). The vast majority of these

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complications can be attributed to direct injury from the patient interface, and in the case of NIMV, represent pressure injury and skin necrosis from the mask. This is by far the most frequent complication, occurring in about 10% of reports. Some of these lesions can be quite extensive, with erosions of the nasal bridge to the nasal cartilage or even bone. Gauze or other types of protective skin dressing have been used to minimize this complication. Softer masks, reducing strap pressure, and padding in key pressure points are other adjustments that may lessen the incidence of this complication. This underscores the need to provide breaks off NIMV for patients. Other reported complications are relatively minor and include problems with nasal congestion, sinusitis, gastric distension, and eye irritation. Major complications such as barotrauma, nosocomial pneumonia, and sepsis are distinctly uncommon. There have been case reports of unusual complications such as esophageal perforation, re-opening of an esophageal – pleural ﬁstula, and orbital herniation (108 –110). C. Reduction in Nosocomial Pneumonia

The reduction in nosocomial pneumonia is particularly noteworthy. This is related to the advantage NIMV has over endotracheal intubation in preserving speech function and upper airway defenses and permitting oral intake. This prevents aspiration or microaspiration and allows more effective clearance of secretions. Patients do not require sedation. This has the net effect of reducing the risk of acquiring nosocomial pneumonia. In their randomized trial, Brochard et al. noted a reduced incidence of nosocomial pneumonia and sepsis. His group has extended this observation to retrospectively analyze, in a matched case-control study, 50 patients treated with NIMV and 50 endotracheally intubated patients (111). They found a marked reduction in the nosocomial infections (18% vs. 60%), especially nosocomial pneumonia (4% vs. 11%), in those treated with NIMV. The reduction in the other sites of nosocomial infection were attributed to shorter ICU stays for the NIMV patients. There was also less antibiotic use, fewer days of ventilatory support (6 + 6 days vs. 10 + 12 days), and lower mortality. They concluded that this beneﬁt was due in part to elimination of the adverse effects of endotracheal intubation and mechanical ventilation and reduction in nosocomial infections. NIMV would also eliminate any post-extubation risks for nosocomial pneumonia (upper airway edema, stridor, and aspiration). They extended this observation to 479 patients with acute respiratory failure (COPD or cardiogenic pulmonary edema), of which 313 (65%) were treated with NIMV (112). In their retrospective analysis of this cohort, they noted that NIMV was associated with a reduction in the incidence of nosocomial infections, especially nosocomial pneumonia, reduction in ICU stay by two days, and a threefold reduction in mortality. D. Personnel and Systems Issues

The early experience with NIMV was tempered by an inordinate amount of time (over 90%) spent by nursing staff in the care of some patients during

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NIMV (113). This was attributed to alarms, mask adjustments, constant monitoring, and equipment issues (nasal masks and portable volume ventilators). This was likely a reﬂection of the initial learning curve that all personnel must encounter with this modality. This is clearly a technique that only improves with repeated administration and experience. Patients treated with NIMV also comprise a somewhat tenuous group of patients. Intubation and mechanical ventilation may be perceived as easier, requiring less time and attention, increasing resistance to its use. However, several controlled trials have subsequently demonstrated that the time commitment is very comparable to that required for those treated with conventional therapy undergoing intubation and mechanical ventilation. Kramer et al. (16) were the ﬁrst to address this issue and found an average greater initial time commitment by respiratory therapists of 56 minutes during the ﬁrst eight hours of therapy, which declined the next eight hours, so that they actually spent less time in NIMV patients compared with control patients. This experience mirrors that of Nava et al. (114), who found that the respiratory therapist spent on average an extra 74 minutes during the initial eight hours of NIMV, decreasing to equivalent time commitments at the end of 48 hours. In an analysis of workload by Plant et al. (18), they found that nursing workload increased by an average of only 26 minutes during the ﬁrst eight hours of NIMV, but by 48 hours the difference was only 21 minutes and not signiﬁcant. This represents a special situation as nursing staff provided the primary respiratory care for the patients in the study. Other investigators have also reported greater efﬁciencies over time, evidenced by improving success rates with NIMV (81). The other systems issue with NIMV involves the optimal location for its applications. There is a wide range of experience that probably reﬂects differences in health-care systems and practices, as well as local familiarity with the technique. Although this has been demonstrated to a feasible technique in an unmonitored ward setting, with or without specialty expertise, the vast majority of patients are treated in a monitored setting. This includes the Emergency Department, where treatment can be initiated, and it can be continued in a specialized respiratory unit (with continuous monitoring), step-down unit, or ICU. The need for monitoring stems from the potential need for intubation and mechanical ventilation in those that fail therapy. This has obvious implications with respect to health care costs. While early studies indicate that the resources and costs required for NIMV were comparable to that for endotracheal intubation and mechanical ventilation, other analysis suggest cost savings with this technique (16,114). One evaluation reﬂected the experience of utilizing NIMV in a ward setting, but another analyzed its use in critical care units (19,115). These analyses are probably not applicable to the United States, where the use of NIMV requires a monitored setting. The other unrecognized element of this analysis is that the health-care reimbursement system has not yet recognized NIMV as a viable treatment. It is difﬁcult to code under current guidelines, resulting in suboptimal reimbursement when compared with intubation and mechanical ventilation. In some

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centers, the code for CPAP (used to treat obstructive sleep apnea) is used to code for NIMV. It may be similar in concept but vastly different in personnel and resource utilization. This serves as a negative incentive for its use and may explain why this technique seems more prevalent in Europe and Canada than in the United States.

VII.

Conclusion

Although the efﬁcacy of NIMV has been clearly demonstrated and is endorsed by many, its utilization remains limited. The enthusiasm for treatment is tempered by some research and practical limitations. Despite well-designed and wellconducted prospective randomized studies, the actual numbers of patients undergoing study are relatively small. The studies cannot be blinded for obvious reasons, and the comparison intubation rates in those managed with standard therapy is inﬂuenced by a treatment bias inherent in this type of study. There is likely a lower threshold for the intubation of standard therapy patients than NIMV patients despite the presence of intubation guidelines. Issues with increased nursing staff and respiratory therapy time have been cited as possible limiting factors. It is acknowledged that there exists a learning curve with this technique, and it may be steeper in some institutions or situations. This treatment does require patience and commitment by all involved. In some circumstances, it is often easier for the patient to be endotracheally intubated. On the other hand, once staff has gained sufﬁcient experience with NIMV, it is an invaluable treatment option. It is ideally suited for patients with COPD with hypercapnic respiratory failure because this is often a rapidly reversible condition. Patients with cardiogenic pulmonary edema are probably the other major group that can be managed with NIMV. It allows dyspnea relief and ventilatory support, preventing further deterioration while allowing other treatments to take effect. It is intermittently applied, and treatment is discontinued once the mask is removed. Therefore, short breaks off NIMV serve a dual purpose. Patients are provided relief from skin and facial ischemia and necrosis, and the breaks serve as “weaning trials.” Patients who do not tolerate these breaks can be placed immediately back on support. This reduces much of the time and uncertainty involved with discontinuing mechanical ventilation in those who are endotracheally intubated. Patients are spared the potential complications and adverse effects associated with re-intubation. Preservation of upper airway function reduces the nosocomial/ventilator-associated pneumonia rate. All of these factors serve to reduce the duration of ventilatory support, ICU stay, and possibly duration of hospitalization. Reduction in mortality has not been universally noted. However, the positive experiences call for continued study in the modality, reﬁning issues regarding patient selection and delivery of ventilatory support. As it becomes easier to provide NIMV, barriers to its use will disappear, and it will be the treatment of choice in select patients.

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Soo Hoo Anton A, Tarrega J, Giner J, Guell R, Sanchis J. Acute physiologic effects of nasal and full-face masks during noninvasive positive-pressure ventilation in patients with acute exacerbations of chronic obstructive pulmonary disease. Respir Care 2003; 48(10):922– 925. Vitacca M, Rubini F, Foglio K, Scalvini S, Nava S, Ambrosino N. Non-invasive modalities of positive pressure ventilation improve the outcome of acute exacerbations in COLD patients. Intensive Care Med 1993; 19(8):450 – 455. Girault C, Richard JC, Chevron V, Tamion F, Pasquis P, Leroy J, Bonmerchand G. Comparative physiologic effects of noninvasive assist-control and pressure support ventilation in acute hypercapnic respiratory failure. Chest 1997; 111(6):1639– 1648. Ferguson GT, Gilmartin M. CO2 rebreathing during BiPAP ventilatory assistance. Am J Respir Crit Care Med 1995; 151(4):1126– 1135. Lofaso F, Brochard L, Touchard D, Hang T, Harf A, Isabey D. Evaluation of carbon dioxide rebreathing during pressure support ventilation with airway management system (BiPAP) devices. Chest 1995; 108(3):772– 778. Nava S, Ambrosino N, Bruschi C, Confalonieri M, Rampulla C. Physiological effects of ﬂow and pressure triggering during non-invasive mechanical ventilation in patients with chronic obstructive pulmonary disease. Thorax 1997; 52(3):249–254. Hotchkiss JR, Adams AB, Dries DJ, Marini JJ, Crooke PS. Dynamic behavior during noninvasive ventilation: chaotic support? Am J Respir Crit Care Med 2001; 163(2):374– 378. Gay PC, Hess DR, Hill NS. Noninvasive proportional assist ventilation for acute respiratory insufﬁciency. Comparison with pressure support ventilation. Am J Respir Crit Care Med 2001; 164(9):1606– 1611. Wysocki M, Richard JC, Meshaka P. Noninvasive proportional assist ventilation compared with noninvasive pressure support ventilation in hypercapnic acute respiratory failure. Crit Care Med 2002; 30(2):323 – 329. Massie CA, Hart RW, Peralez K, Richards GN. Effects of humidiﬁcation on nasal symptoms and compliance in sleep apnea patients using continuous positive airway pressure. Chest 1999; 116(2):403 –408. Pollack CV Jr, Fleisch KB, Dowsey K. Treatment of acute bronchospasm with betaadrenergic agonist aerosols delivered by a nasal bilevel positive airway pressure circuit. Ann Emerg Med 1995; 26(5):552 – 557. Chatmongkolchart S, Schettino GP, Dillman C, Kacmarek RM, Hess DR. In vitro evaluation of aerosol bronchodilator delivery during noninvasive positive pressure ventilation: effect of ventilator settings and nebulizer position. Crit Care Med 2002; 30(11):2515– 2519. Jaber S, Fodil R, Carlucci A, Boussarsand M, Pigeot J, Lemaire F, Hharf A, Lofuso F, Isabey D, Brochard L. Non invasive ventilation with helium – oxygen in acute exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000; 161(4 Pt 1): 1191– 1200. Nava S, Ceriana P. Causes of failure of noninvasive mechanical ventilation. Respir Care 2004; 49(3):295– 303. Anton A, Guell R, Gomez J, Serrano J, Castellano A, Carrasco JL, Sanchis J. Predicting the result of noninvasive ventilation in severe acute exacerbations of patients with chronic airﬂow limitation. Chest 2000; 117(3):828– 833.

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Moretti M, Cilione C, Tampieri A, Fracchia C, Marchioni A, Nava S. Incidence and causes of non-invasive mechanical ventilation failure after initial success. Thorax 2000; 55(10):819– 825. Robino C, Faisy C, Diehl JL, Rezgui N, Labrousse J, Guerot E. Effectiveness of non-invasive positive pressure ventilation differs between decompensated chronic restrictive and obstructive pulmonary disease patients. Intensive Care Med 2003; 29(4):603– 610. Domenighetti G, Gayer R, Gentilini R. Noninvasive pressure support ventilation in non-COPD patients with acute cardiogenic pulmonary edema and severe community-acquired pneumonia: acute effects and outcome. Intensive Care Med 2002; 28(9):1226– 1232. Van de LA, Brocas E, Boiteau R, Perrin-Gachadoat D, Tenaillon A. Esophageal perforation associated with noninvasive ventilation: a case report. Chest 2002; 122(5):1857– 1858. Hurst JR, Polkey MI, Goldstraw P, Yung B. Oesophagopleural ﬁstula as a novel cause of failed non-invasive ventilation. Thorax 2003; 58(7):642 – 643. Lazowick D, Meyer TJ, Pressman M, Peterson D. Orbital herniation associated with noninvasive positive pressure ventilation. Chest 1998; 113(3):841– 843. Girou E, Schortgen F, Delclaux C, Brun-Buisson C, Blot F, Lefort Y, Lemaire F, Brochard L. Association of noninvasive ventilation with nosocomial infections and survival in critically ill patients. J Am Med Assoc 2000; 284(18):2361– 2367. Girou E, Brun-Buisson C, Taille S, Lemaire F, Brochard L. Secular trends in nosocomial infections and mortality associated with noninvasive ventilation in patients with exacerbation of COPD and pulmonary edema. J Am Med Assoc 2003; 290(22):2985– 2991. Chevrolet JC, Jolliet P, Abajo B, Toussi A, Louis M. Nasal positive pressure ventilation in patients with acute respiratory failure. Difﬁcult and time-consuming procedure for nurses. Chest 1991; 100(3):775– 782. Nava S, Evangelisti I, Rampulla C, Compagnoni ML, Fracchia C, Rubini F. Human and ﬁnancial costs of noninvasive mechanical ventilation in patients affected by COPD and acute respiratory failure. Chest 1997; 111(6):1631– 1638. Plant PK, Owen JL, Parrott S, Elliott MW. Cost effectiveness of ward based noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease: economic analysis of randomised controlled trial. Br Med J 2003; 326(7396):956.

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3 Modes of Mechanical Ventilation

BRIAN RICHARDS and ZAB MOSENIFAR Division of Pulmonary and Critical Care Medicine, Cedars–Sinai Medical Center, Los Angeles, California, U.S.A.

I.

Introduction

In recent years, advances in ventilator technology have given rise to many new and often confusing terms and acronyms used to describe modes of ventilator function and patient interface. In an effort to bring order to this new terminology, a system for understanding modes of mechanical ventilation has been developed (1) and recently included in textbooks of respiratory care (2). This new classiﬁcation scheme enables logical description of new ventilator modes that function in the same way but are given different “brand” names. It also allows for grouping of ventilators in terms of the number of breathing pattern options each ventilator offers. Despite the simplicity and logic of this new system for describing ventilator modes, the terms and abbreviations used in the system are not necessarily those used by physicians who order mechanical ventilation or by respiratory care practitioners who implement these orders. Instead, when new ventilator modes are applied, they are usually ordered by the terminology the manufacturers coin (and often trademark), which is reinforced by their own clinical consultants when taught to end-users. In short, the end-users of newer ventilator systems use a mix of community-accepted terms and ventilator-speciﬁc labels to describe, order, and implement ventilator mode and breath control settings. To expect otherwise would presume years of re-educating physicians, nurses, and respiratory care practitioners in the meaning and application of the new ventilator taxonomy and in the utility of the new ventilator modes it describes. 77

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Accordingly, the reader is referred to the new system for classifying ventilator modes, but herein familiar terms will be used to describe popular ventilator modes whenever possible and, when not, the manufacturer-labeled modes will be described in simple terms. II.

The Breath

In the context of mechanical ventilation, the breath is the building block of breath patterns called ventilator modes. A breath is deﬁned as one inspiratory ﬂow event paired with one expiratory ﬂow event. The areas circumscribed by each of these ﬂow events (i.e., the integral of ﬂow) are deﬁned as the inspiratory tidal volume (Vt insp) and the expiratory tidal volume (Vt exp). A zero-ﬂow inspiratory tidal volume hold may or may not precede the expiratory ﬂow event. A breath may or may not include a passive expiratory phase that precedes the next breath (Fig. 1). III.

Breath Phases

The ventilator breath can be divided into four phases: the trigger phase, the limit phase, the cycle phase, and the expiratory phase (2). 80 60 Zero Flow

40 . VL/min

20 0 20

Passive Exp

40 60 80

1.0 sec IT (1.5 sec)

500

1.5 sec

0.5 sec

ET (2.0 sec) V O L

400 Vt ml

0.5 sec

300 200 100 0

Vt insp

H O L D

Vt exp

Figure 1 Machine breath, “volume control” with square ﬂow wave. Computer rendering of sketch drawn using common test lung, resistor, and Nellcor Puritan Bennett 840 Ventilator graphics. Source: Courtesy of Tyco Health Care, Nellcor Puritan Bennett, 2004.

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A. The Trigger Phase

The trigger phase deﬁnes what initiates an inspiratory ﬂow event. In mechanical ventilation, inspiration may be time-triggered or patient-triggered (2). Time-Triggering

Time-Triggering is typically associated with “control mode” ventilation of the patient who is apneic due to pathology or pharmacologic control of respiration. The lapse of the ventilator’s breath cycle time [60 sec/min divided by set respiratory rate (RR)] automatically triggers inspiration. Patient-Triggering

Patient-triggering occurs when patient inspiratory effort is translated into a negative pressure signal (i.e., a “pressure-trigger”) or a negative ﬂow signal (i.e., a “ﬂow-trigger”) that activates ventilator gas delivery. 1. “Pressure-triggering” occurs when a small user-set 1 to 2 cmH2O pressure drop caused by patient inspiratory effort is communicated to an upstream demand valve, which then opens to deliver ventilator gas. Small pressure-trigger settings are “more sensitive” to patient inspiratory efforts and make it easier for the patient to trigger ventilator gas delivery. However, when positive end expiratory pressure (PEEP) is set and a ventilator system leak causes expiratory baseline pressures to fall below set PEEP, small pressure-trigger settings can result in ventilator “auto-triggering” and ventilator–patient dyssynchrony (3). Conversely, large pressure-trigger settings are “less sensitive” to patient breathing effort, increase patient trigger work, and delay ventilator demand valve activation. Large pressure-trigger settings are especially problematic where expiratory air trapping results in autoPEEP that must be exceeded by patient-generated negative pressures sufﬁcient to overcome the auto-PEEP plus the user-set trigger pressure (Fig. 2). Reducing the trigger pressure and setting a low-level PEEP that approximates the auto-PEEP can decrease patient-trigger effort and better synchronize it with machine breath delivery (4 –7). 2. “Flow-triggering” employs a low level background (or “bias”) ﬂow of gas that is measured by ﬂow sensors located at the ventilator circuit’s gas inﬂow port and the ventilator circuit’s gas outﬂow port. When the patient makes an inspiratory effort, part of this background ﬂow of gas goes to the patient, causing circuit outﬂow to fall below circuit inﬂow. This difference in ﬂow translates into a user-set ﬂow signal, usually 1 to 3 lpm, that triggers inspiratory gas delivery to meet machine breath settings or spontaneous breath demands (Fig. 3). In current generation ventilators, the user can select ﬂow-triggered or pressure-triggered mechanisms to enable patient triggering of all breath types. Some studies

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Richards and Mosenifar 40 30 20

3cm H2O Auto PEEP*

10 PcmH2O

0 -10

(-2 cm) Set Trigger Pressure

-20

(-5 cm)Actual trigger threshold; add PEEP of 3 cm to restore trigger threshold to 2cm below baseline.

80 60 40 . VL/min

Air Trapping

20 0 20 40 60 80 Time (sec)

Figure 2 Machine breath, “volume control” with auto-PEEP, resulting in increased trigger work. Next machine breath electronically delayed so that rising pressure of next breath does not mask auto-PEEP. Modeled after Nellcor Puritan Bennett 840 Ventilator graphics. Source: Courtesy of Tyco Health Care, Nellcor Puritan Bennett, 2004.

suggest that ﬂow-triggering at minimum settings requires less trigger time and trigger effort than pressure-triggering at minimum settings (8,9), but the overall effect on total inspiratory effort generated throughout the machine breath is small (7). Moreover, ﬂow-triggers which are set low to minimize trigger work are particularly sensitive to circuit leaks that cause background gas outﬂow to fall below background gas inﬂow. In such cases, ventilator ﬂow sensors cannot distinguish between patientinitiated trigger ﬂow and leak ﬂow. Thus, low-ﬂow trigger settings activated by chest tube leak (10) or artiﬁcial airway leak may result in ventilator auto-triggering and resultant ventilator–patient dyssynchrony. If such leaks cannot be ﬁxed, auto-triggering can be stopped by gradually increasing trigger ﬂow until it exceeds leak ﬂow (11). Low-ﬂow trigger settings can also be activated by ﬂuctuations in background ﬂow caused by agitation of circuit condensate or strong cardiac contractions (12). Again, resultant auto-triggering can be remedied by correcting the problem and, if necessary, setting a higher trigger ﬂow.

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Prior to Patient Inspiratory Effort 5L Inspiratory pm Flow Sensor VENTILATOR Expiratory Flow Sensor

Patient (Zero Flow) m 5 Lp

At onset of Patient Inspiratory Effort 5 Lp Inspiratory m Flow Sensor Patient VENTILATOR (2 Lpm Expiratory Trigger Flow) m Flow Sensor 3 Lp

Figure 3 Conceptual depiction of ﬂow triggering. B. Limit Phase

The limit phase deﬁnes the limit to which a user-set inspiratory control, like ﬂow or pressure, can rise without terminating inspiration (2). Volume Control Ventilation

In volume control (VC) ventilation (VCV), a maximum (or “peak”) ﬂow is reached and a ﬁxed-pattern ﬂow waveform is sustained until the user-set tidal volume is delivered. The ﬂow waveform set in VCV is usually a ﬁxed-pattern “square” ﬂow wave or a ﬁxed-pattern “descending” ﬂow wave. When compared with the square ﬂow wave at the same peak ﬂow setting, use of the ﬁxed-pattern descending ﬂow wave necessarily increases inspiratory time to preserve the area under the ﬂow curve and the constancy of the user-set Vt. In sedated patients on VCV, the use of the ﬁxed-pattern descending ﬂow wave has been reported to result in higher mean airway pressures (MAWP) and better oxygenation at lower peak inspiratory pressures (PIP) (13). However, in actively breathing patients who trigger high mechanical respiratory rates, conversion from the square ﬂow wave to the longer ﬁxed-pattern descending ﬂow wave increases risks of ﬂow starvation and air trapping (Fig. 4). A major problem in VCV is matching user-set Vt, peak ﬂow and ﬁxed-pattern ﬂow wave settings with breath-to-breath changes in the inspiratory demand of the actively breathing, tachypneic patient (13,14). Pressure Control Ventilation

In pressure control (PC) ventilation (PCV), a constant pressure is sustained until the user-set inspiratory time (I-Time) elapses. Because ﬂow rates generated during PCV can rise quickly to peak ﬂows sometimes exceeding 100 lpm, initial proximal airway pressures can spike above set control pressures (15). To

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Square Wave Decelerating Wave

60 . VL/min

0 Air Trapping from prolongation of I-Time when Decelerating Flow curve used.

60

120 120 PcmH2O

60

Scooped Pressure Curve due to inadequate flow output relative to patient demand

0 Time (sec)

Figure 4 Volume control: square ﬂow versus decelerating ﬂow. Source: Adapted from Chang DW. Clinical Application of Mechanical Ventilation. 2nd ed. Delmar Thomson Learning, 2001; 11:304 (Fig. 11.29).

minimize pressure spiking, to stabilize set control pressures, and to properly reference high-pressure alarm settings to set control pressures, some ventilator manufacturers include a “Rise Time” control. The “Rise Time” control modiﬁes the initial ﬂow output from the ventilator that determines the rate of rise to set control pressure (16). Higher initial ﬂows result in rapid rise to control pressure, while lower initial ﬂows prolong rise to control pressure. An appropriate “Rise Time” setting is one in which initial ﬂow output is high enough to meet patient demand (17), but slow enough to eliminate pressure spiking (Fig. 5). The decreasing ﬂow proﬁle that follows from peak ﬂow is characteristic of PC breaths and varies with patient demand and lung mechanics. Thus, PC breaths may better match breath-to-breath changes in patient demand than the constant Vt peak ﬂow and ﬁxed-pattern ﬂow wave settings of VCV (14,18). Further, the decreasing ﬂow proﬁle of PC breaths minimizes the resistive components of proximal airway pressure, allowing for “same tidal volume ventilation” at lower PIP’s than associated with VC “square” ﬂow wave breaths. However, during VC of the acute respiratory distress syndrome (ARDS) patient, a high alveolar plateau pressure (Pplat . 32 cmH2O), not a high PIP, is the risk factor associated with ventilator-induced lung injury (19,20). Plateau pressure, in turn, is measured under conditions of no ﬂow, where airway resistance pressure is not a factor, and equals the sum of the alveolar pressure caused by tidal volume

Modes of Mechanical Ventilation 80

Rapid Rise Time

60

83 Slower Rise Time

Pressure Spike Control Pressure

PcmH2O 40 20 0

200 150 100 . VL/min

50 0 50 100 150 200

Time (sec)

Figure 5 Effect of rise time control on pressure control breath. Computer rendering of sketch drawn using common test lung, resistor, and Nellcor Puritan Bennett 840 Ventilator graphics. Source: Courtesy of Tyco Health Care, Nellcor Puritan Bennett, 2004.

stretch þ alveolar (PEEP) (Fig. 6). Thus, Vt and PEEP combine to determine alveolar stretch and related lung damage risks. While it remains controversial as to which combination of Vt and PEEP provides the best pulmonary gas exchange with the least risk of ventilator-induced lung injury (21), the pressure generated by the sum of the set PC pressure and PEEP should be maintained at no more than 30– 35 cmH2O whenever feasible (21 – 23). C. Cycle Phase

The cycle phase determines the inspiratory variable that terminates inspiration (2). Primary Cycling Mechanisms

There are four primary cycling mechanisms (24): pressure cycling (as when an intermittent positive pressure breath terminates inspiration upon reaching a user-set pressure); volume cycling (as when a volume control breath terminates inspiration upon delivery of a user-set tidal volume); time cycling (as when a PC breath terminates inspiration upon lapse of a user-set I-Time); Flow cycling [as when a pressure support (PS) breath terminates inspiration upon reaching a factory- or user-set decreasing ﬂow threshold].

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120

. VL/min

60 40

Zero Flow VT

0

60

PcmH2O

40

PIP = 40 cm H2O

20

2 Unit Lung Model

Pplat =28cm H2O Raw = (PIP - Pplat ) / Flow PEEP = C = V / (P -PEEP) T plat 5cm H2O ST

VT + PEEP => PA ~ Pplat

Time (sec) Figure 6 Conceptual relationship between peak inspiratory pressure and plateau pressure estimate of peak alveolar pressure in a volume control machine breath. Secondary Cycling Mechanisms

Secondary cycling mechanisms are often used as alarm thresholds or safety limits to terminate inspiration when primary intended cycling mechanisms fail (2). For example, the high-pressure alarm level set during VCV may be activated and terminate inspiration when airway resistance (RAW) and/or static lung – thorax compliance (CST) worsen acutely. When high-pressure alarm cycling occurs, the undelivered portion of the set tidal volume is vented to atmosphere, often leading to air hunger, tachypnea, and ventilator – patient dyssynchrony. Similarly, delivered Vt may fall when a normally ﬂow-cycled PS breath is pressure-cycled off at a few cmH2O above set control pressure because the patient coughs, sneezes, or tenses the abdomen during a PS breath (24). Flow-cycled PS breaths will also time-cycle “off” after three to ﬁve seconds if a circuit leak prevents inspiratory ﬂow from decreasing to the terminal ﬂow-cycling threshold (24). Some ventilators offer a “terminal ﬂow” control that enables the user to ensure ﬂow-cycling during pressure support ventilation (PSV) by increasing terminal ﬂow-cycling thresholds above leak ﬂows (24) (Fig. 7). An adjustable terminal ﬂow control also enables the clinician to better synchronize ﬂowcycling of PS breaths in chronic obstructive pulmonary disease patients who, because of long pulmonary ﬁlling times, often display expiratory muscle activity before PS ﬂow can decrease to low ﬂow-cycling thresholds (7). D. Expiratory Phase

The expiratory phase deﬁnes the time it takes for expiratory ﬂow to return to baseline ﬂow (i.e., active expiration) plus the time in which the variable known as PEEP or continuous positive airway pressure (CPAP) is applied

Modes of Mechanical Ventilation

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25 18 cm H2O PS

20

PcmH2O

15 10 0 80 60

Max Flow (60 Lpm)

40

. VL/min

25% Terminal Flow (15 Lpm)

50% Terminal Flow (30 Lpm)

20 0 20 40 60 80

Time (sec)

Figure 7 Effect of terminal ﬂow control on pressure support breath. Computer rendering of sketch drawn using common test lung, resistor, and Nellcor Puritan Bennett 840 Ventilator graphics. Note: Area under ﬂow curve and therefore V1 decrease as terminal ﬂow cycling threshold is increased. Source: Courtesy of Tyco Health Care, Nellcor Puritan Bennett, 2004.

(i.e., passive expiration). PEEP is an acronym used to label above-ambient baseline pressures set in ventilator modes in which machine breaths appear. CPAP is an acronym used to label above-ambient baseline pressures set in modes in which only spontaneous breaths appear. Both PEEP and CPAP are used to keep marginally inﬂated air sacs from collapsing between mechanical or spontaneous breaths, thereby reducing pulmonary shunt and improving oxygenation. Systemic PaO2’s thus rise and enable clinicians to decrease high FIO2’s (.0.5) that are commonly believed to predispose to cellular lung damage (i.e., O2 toxicity) (25). However, improved PaO2’s and a decrease in O2 toxicity risk are not the only goals of PEEP therapy. Recent evidence suggests that PEEP and low-tidal volumes should be used in acute lung injury and ARDS as part of a lung protective strategy to maximize alveolar recruitment and minimize uneven tidal volume distribution, focal hyperinﬂation, interalveolar shear stress, and resultant lung damage (26,27). Within the past few years, three approaches to applying lung protective levels of PEEP have emerged. FIO2: PEEP Relationship

The ﬁrst approach uses the FIO2:PEEP relationships (Table 1) that were used to achieve a PaO2 of 55 to 80 mmHg (or an SpO2 88 –95%) in the ARDS Network Study (28,29).

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Table 1 PEEP Values FO2 PEEP

0.3 5

0.4 5

0.4 8

0.5 8

0.6 10

0.7 10

0.7 12

0.7 14

0.8 14

0.9 14

0.9 16

1.0 20 – 24

Source: From Ref. 29.

In ARDS patients, this PEEP strategy, when used in conjunction with a tidal volume of 6 cc/kg and Pplat 30 cmH2O, resulted in patient outcome data that demonstrated less days on the ventilator and improved survival. Pressure –Volume Curve

The second approach to setting PEEP uses the patient’s static pressure – volume (P –V) curve to identify a low inﬂection point (LIP) and a high inﬂection point (HIP) that correspond, respectively, to the most effective and safest levels of PEEP and tidal volume (30). The LIP is a slight concavity that appears on the initial portion of the inspiratory static P – V curve. The point just beyond this concave zone represents the critical opening pressure at which a majority of alveoli are recruited and, therefore, the approximate x-axis value at which PEEP should be set (31,32). The straight segment of the curve that follows the LIP is the zone of maximum compliance and may give rise to a convex zone or HIP near the end of the inspiratory P – V curve that indicates an excessive tidal volume (30). If excessive, the Vt setting of the ventilator should be decreased to the y-axis value on the static inspiratory P– V curve that just precedes the HIP zone (Fig. 8). Problems with this inﬂection point PEEP strategy include: having to sedate the patient so that long low-ﬂow (non-resistive) static P –V curves can be generated; determining when to make these P – V curve measurements with respect to rapidly changing disease status; reconciling differences in inﬂection point locations that appear on inspiratory versus expiratory portions of the static P –V curve; and setting PEEP when the LIP is absent (33). Open Lung Approach

The third approach to determining how PEEP should be set is often referred to as “the open lung” approach. Proponents of this PEEP strategy recommend using a sustained alveolar recruitment maneuver in which 30 –50 cmH2O CPAP (i.e., no machine-generated breaths) is applied over 20– 90 seconds to recruit atelectatic alveoli (34,35), then decreased to a level that preserves oxygenation without hemodynamic compromise [e.g., 15 cmH2O PEEP (35) or LIP þ 2 cmH2O (36) with low Vt mechanical ventilation]. It is noteworthy that these alveolar recruitment maneuvers used in the management of ARDS (albeit temporarily) employed CPAP levels in excess of the 30 cmH2O plateau pressure limit used in the ARDS Network Study. Additional concerns with the open lung approach

Modes of Mechanical Ventilation 50 Lpm P-V Curve 10 Lpm P-V Curve

87

Vol ml Pplat (22cmH2O)

Expiration

500

PIP=32 cmH2O

400

HIP (300ml)

300

HIP

200

Inspiration

100

LIP (2 cmH2O) -20

-10

10

20

30

40

50

Pcirc cmH2O

LIP

Figure 8 Quasi-static pressure – volume curve at 10 Lpm ﬂow using test lung and resistor. Computer rendering of sketch drawn using common test lung, resistor, and Nellcor Puritan Bennett 840 Ventilator graphics. Source: Courtesy of Tyco Health Care.

include a limited number of randomized human studies, inconsistency of method, limited efﬁcacy in consolidative ARDS, and mixed conclusions as to patient safety and outcomes (37). IV.

Breath Types

There are two types of breaths possible during mechanical ventilation, the “machine breath” and the “spontaneous breath.” A. Machine Breath

The machine breath is a breath in which inspiration is time- or patient-triggered and cycles into expiration when a user-set Vt or I-Time is delivered by the machine. Examples of machine breath are discussed subsequently. Volume Control Ventilation

In VC ventilation, the VC breath is considered a machine breath because inspiration is either time- or patient-triggered “on” and cycles “off” after the machine delivery of a user-set tidal volume at a user-set ﬂow or I-Time. Pressure, the dependent variable in VCV, rises as lung mechanics worsen or ventilator circuit resistance

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increases and falls as lung mechanics improve or ventilator circuit resistance decreases. Pressure Control Ventilation

In PCV, the PC breath is considered a machine breath because inspiration is either time- or patient-triggered “on” and cycles “off” after the machine delivery of a user-set control pressure sustained over a user-set I-Time interval. Flow, the dependent variable, decelerates as alveolar-ﬁlling pressures approach set control pressure as a function of patient demand and lung mechanics. However, in PC ventilation, the user-set I-Time, not the patient, determines when inspiration cycles to expiration. Thus, too short an I-Time setting can cut off inspiratory ﬂow before alveolar ﬁlling is complete, causing delivered tidal volume to fall. Or, too long an I-Time setting can exceed alveolar-ﬁlling time, resulting in a period of no ﬂow or a “volume hold” (Fig. 9). This “volume hold” increases mean airway pressure and may result in improved PaO2 (38). However, a decrease in cardiac output from increasing I-Time settings and mean airway pressures can result in decreased oxygen transport (38,39) that may offset increases in PaO2. A prolonged I-Time setting that persists into “neural expiration” also leads to patient agitation (7) and the need for patient sedation. 600 500 400

Vtml

V O L

300 200 100

H O L D

Vt Vt Insp. Exp.

80 60 40

. VL/min

V tc

20 0 20 40 60 80

ut

of

f

I-Time too short for complete filling TIME

Vt hold*

I-Time too long, now exceeding fill time

Figure 9 Effect of I-Times setting on Vt delivery during pressure control ventilation. Note: too long an I-Time may also result in air trapping and auto-PEEP if resultant alveolar emptying time is shorter than alveolar ﬁlling time.

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Bi-Level Ventilation

In “bi-level” ventilation (Nellcor-PB 840), like PC ventilation, the breath delivered is considered a machine breath in which inspiratory ﬂow is either time- or patient-triggered “on” and cycled “off” after the machine delivers a sustained, pressure-limited breath over a user-set I-Time interval. In the absence of spontaneous breathing, the ﬂow and pressure waveform graphics generated during a bi-level machine breath resemble those generated by a time-cycled PC breath. The bi-level machine breath differs from a PC breath in that the bi-level inspiratory pressure limit is labeled as the “High PEEP” from which the “Low PEEP” is subtracted to determine the ventilating pressure (DP). For example, if the high PEEP is set at 30 cmH2O and the low PEEP is set at 5 cmH2O, then the maximum pressure reached is 30 cmH2O with a ventilating pressure (DP) of 25 cmH2O. In PC ventilation, the user-set inspiratory pressure limit is the ventilating pressure (DP) and is added to set PEEP to determine PIP. For example, if the PC pressure limit is set at 30 cmH2O and the PEEP at 5 cmH2O, then the maximum pressure reached is 35 cmH2O with a ventilating pressure (DP) of 30 cmH2O. The bi-level machine breath is further differentiated from the PC breath in that it allows for spontaneous breathing atop the user-set inspiratory pressure – time curve; a decrease in sedation is an alleged advantage (40). PS is also available to augment spontaneous breathing on both inspiratory and expiratory phases of the bi-level breath (41) (Fig. 10). 50

PcmH2O

40

Expiratory Effort

Inspiratory Effort

30 20

P=25cmH2O

HI PEEP (30 cmH2O) PS (15 cm H2O)

Lo PEEP (5 cm H2O)

10 SET IT

SET ET

SET IT

SET ET

80 60

. VL/min

40 20 0 20 40 60 80

Figure 10 Bi-Level machine breath with spontaneous breathing atop and between machine breaths. Computer rendering of sketch drawn using common test lung, resistor, and Nellcor Puritan Bennett 840 Ventilator graphics. Source: Courtesy of Tyco Helath Care, Nellcor Puritan Bennett, 2004.

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Richards and Mosenifar Airway Pressure-Release Ventilation

In “Airway Pressure-Release Ventilation” (APRV), the breath delivered is a variation on the bi-level machine breath in which the user-set inspiratory pressure limit (High PEEP) is sustained over a user-set I-Time that exceeds expiratory time. Using more familiar terminology, APRV is “pressure controlled inverse ratio ventilation” (PCIRV), with the added feature that the patient is able to breathe spontaneously atop the user-set inspiratory pressure –time curve (42). Spontaneous breathing atop the APRV inspiratory pressure curve may enhance hemodynamic function and reduce the need for sedation when compared with PCIRV (43,44). Pressure-Regulated Volume Control Ventilation

In “Pressure-Regulated Volume Control Ventilation” (PRVC; Maquet Siemens Servo 300, Maquet GmbH & Co Kg, Rastatt, Germany), like PC ventilation, the breath delivered is considered a machine breath in which inspiration is either time- or patient-triggered “on” and cycled “off” after the machine delivers a sustained pressure-limited breath over a user-set I-Time interval. Inspiratory ﬂow is decelerating and variable as a function of lung mechanics and patient demand within the user-set I-Time window. However, unlike PC ventilation, in PRVC ventilation the control pressure limit is not user-set, but instead is autoregulated in small increments or decrements between machine breaths, and in response to changing lung mechanics, to achieve a user-set tidal volume at a minimum control pressure (45). Adaptive Support Ventilation

In “Adaptive Support Ventilation” (ASV; Hamilton Medical Galileo, Hamilton Medical AG, Rhazuns, Switzerland), the breath delivered is a variation on PRVC in which each machine breath is pressure-limited, with the pressure limit and RR automatically adjusted between breaths, in response to changing lung mechanics to achieve a user-set minute Ventilation (V˙E) (46). While the targeted V˙E can be achieved with a variety of V˙t RR combinations, ASV breaths allegedly provide the safest combinations by imposing program Vt boundaries to prevent over- or under-inﬂation and RR boundaries to prevent bradypnea or tachypnea and breath stacking (46). Volume-Assured Pressure Support Ventilation

In Volume-Assured Pressure Support Ventilation (VAPS; VIASYS Healthcare, Bird VIP GOLD), PC changes to VC within the same machine breath, rather than over a series of breaths (2). In the VAPS breath, a low constant ﬂow is user-set along with a Vt target. The inspiratory ﬂow event begins as a patienttriggered or time-triggered PC breath with the pressure limit sustained as ﬂow decelerates towards a ﬂow-cycling threshold set just above the constant ﬂow. If the set Vt is not delivered when the PC ﬂow-cycling threshold is reached, then

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the breath switches to a VC breath in which the pre-set, low level, constant ﬂow is delivered (and the PC pressure limit overridden) until the target Vt is reached or (in the event of leak) a VAPS time-limit elapses (46). If the targeted Vt is delivered before PC ﬂow decays to the constant set ﬂow of VC, then inspiratory ﬂow is ﬂow-cycled “off” like a spontaneous PS breath (Fig. 11). However, unlike a spontaneous PS breath which must be patient-triggered, subsequent VAPS breaths may be time-triggered as a function of a user-set RR. B. Spontaneous Breath

The spontaneous breath is a breath in which inspiration is always patienttriggered and cycles into expiration as a function of patient demand and lung mechanics, not machine control settings. Examples of ventilator breaths considered to be spontaneous in nature follow. Pressure Support Breath

A PS breath is considered a spontaneous breath in which inspiratory ﬂow is patient triggered “on,” decelerates at a rate determined by patient demand and lung mechanics, and cycles “off” when alveolar ﬁlling is nearly complete (i.e., when a low ﬂow-cycling threshold is reached). As with normal spontaneous PS Limit Override 25 20

PcmH2O

Pressure Support Limit

15 10 5 0

45

Vt on Target

Vt below Target

Flow-cycled

. VL/min

Constant flow

0

-45 Time (sec)

Figure 11 Effect of failure to meet Vf target in VAPS breath. Computer rendering of sketch drawn using common test lung, resistor, and Viasys Health Systems, VIP Gold Ventilator graphics. Source: Courtesy of Viasys Health Care Inc., 2004.

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breathing, during PS, inspiratory ﬂow, inspiratory time, and inspiratory tidal volume vary breath-to-breath as a function of proximal airway pressure, patient demand, airway resistance, and pulmonary compliance (47). During PSV, only the user-set control pressure and the low terminal ﬂow-cycling threshold distinguish PS inspiration from true spontaneous inspiration. The main drawback of PSV is that the set control pressure, in the absence of the clinician, does not vary in response to acute changes in lung mechanics or breath-to-breath changes in inspiratory effort that reﬂect changing pulmonary workload. Moreover, during PSV there is no ventilator back-up respiratory rate to safeguard against bradypnea or apnea (47). Setting ventilator alarms to indicate inadequacy or excess in monitored volumes and respiratory rate is crucial to safe patient management during PSV. Volume Support Breath

A volume support (VS) breath (Maquet Siemens Servo 300, Maquet GmbH & Co Kg, Rastatt, Germany) is a PS breath in which inspiratory ﬂow is patienttriggered “on,” decelerates at a rate determined by patient demand and lung mechanics, and cycles “off” when a low, ﬂow-cycling threshold is reached. Unlike a PS breath, in which the inspiratory control pressure is user-set and constant, in VS the inspiratory control pressure is auto-regulated over several breaths to achieve a user-set Vt. As lung mechanics improve during VS, PS levels needed to maintain the target Vt are down-regulated, which, according to the manufacturer, should facilitate weaning (45). When the “Automode” control option is set to “On,” if the patient does not trigger a VS breath within a user-set time frame (12 seconds for adults, 8 seconds for pediatrics, and 5 seconds for newborns), then the ventilator will switch back to the applicable, user-set machine breath mode: VC or PRVC (45). When the patient triggers two consecutive breaths in the applicable machine breath mode, the ventilator switches back to spontaneous VS breaths (45). Automode also enables the ventilator to switch from PS to PC breaths based on the same age-speciﬁc time intervals (45). Resumption of spontaneous PS breathing occurs when the patient triggers two consecutive PC breaths. Concern has been expressed about the risk of deleterious changes in mean airway pressure that may occur as breath types ﬂuctuate between time-cycled machine breaths and ﬂow-cycled spontaneous breaths during Automode application (46). Tube Compensation Breath

A “Tube Compensation” breath (TC; Nellcor-Puritan Bennett 840) is another form of auto-adjusting PS. In TC, the PS level auto-adjusts to overcome the “resistive” work of breathing imposed by the artiﬁcial airway (48). In the patient-triggered TC breath, the PS compensates for the ﬂow-dependent pressure drop across an artiﬁcial airway of a known internal diameter. As a patient’s inspiratory ﬂow increases through a tube of a known diameter, the PS level is

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up-regulated to match the increased pressure drop across the airway (PS DP ¼ RAW Flow). Conversely, as a patient’s inspiratory ﬂow decreases, the PS level is down-regulated to match the decreased pressure drop across the artiﬁcial airway. A second control option offered in TC breathing enables the user to set fractional portions of the calculated TC PS level, thus gradually increasing the patient’s resistive work of breathing (48). Patients unable to tolerate these incremental increases in resistive work due to the artiﬁcial airway may be weanable only if the airway is removed. If the airway is not removable, then the possibility of ventilator dependence becomes a consideration (49,50). Proportional Assist Ventilation Breath

A “Proportional Assist Ventilation” breath (PAV; available in Europe on the Drager Evita 4, Drager Medical Inc, Telford, PA, U.S.A.) is yet another form of auto-adjusting PS. In a PAV breath, the PS level varies with patient inspiratory effort to offset the resistive load imposed by the patient’s airways [DPRaw ¼ (PIP 2 Pplat) ¼ RAW Flow], plus the elastic load imposed by the patient’s alveoli and chest wall [DPCST ¼ (Pplat 2 PEEP) ¼ Vt 1/CST] (51). The greater the patient effort, the higher the PS level generated by the ventilator. In the decelerating ﬂow proﬁle characteristic of a PAV PS breath, the high initial ﬂow generates signiﬁcant airway resistance that can be offset by setting the ventilator control to deliver a percentage of the measured pressure drop (DPRAW) across the airway. In the lower portion of the decelerating ﬂow proﬁle, where airway resistance is minimal and increasing elastic forces reﬂect increasing volume delivery, the ventilator control can be independently set to deliver a percentage of the pressure (DCST) generated during “tidal stretch” of the alveolar compartment and chest wall (51). Setting PAV elastance and airway resistance control pressures requires a practical and reproducible bedside measurement of the spontaneously breathing patient’s respiratory system elastance and airway resistance, a measurement task as yet not standardized and complicated by circuit leak that the ventilator interprets as increased patient effort (51). C. Closed-Loop Control Systems

Both machine and spontaneous breaths may be further described in terms of “closed-loop” control systems in which ventilator output variables are automatically adjusted in response to physiologic measurements to achieve inputted, breath targets. A review of some of the more commonly used closed-loop, breath types follows. In the volume-controlled, ﬂow-limited machine breath of VCV, tidal volume output from the ventilator auto-adjusts in response to compressible volume loss to maintain a user-inputted target tidal volume. Compressible volume loss is a ventilator-calculated variable in which a pre-determined circuit stretch and gas compression factor is multiplied by proximal airway pressures that increase or decrease as lung mechanics worsen or improve. Thus, as lateral tubing stretch increases at higher circuit pressures, patient tidal volume would fall if this

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compressible volume loss were not automatically offset by an increase in ventilator output. In the pressure-controlled, time-cycled machine breath of PCV, the clinician inputs a pressure target, and ﬂow output from the ventilator auto-adjusts in response to patient demand and lung mechanics to sustain the target pressure until a user set I-Time elapses. In the PRVC machine breath, a more complex closed-loop control system combines the main advantage of PCV (a decelerating ﬂow that varies with patient demand and lung mechanics) with the main advantage of VCV (delivery of consistent tidal volumes). In PRVC, the clinician sets a minute volume and respiratory rate combination that results in input of a target tidal volume. At the onset of PRVC, the ventilator imposes a pressure-controlled test breath in which ventilator ﬂow output peaks and decelerates as a function of patient demand and lung mechanics. The output ﬂow signal over time translates into an output tidal volume that is compared with the user inputted target tidal volume. The PC level is then automatically regulated in small increments or decrements between breaths to achieve the targeted tidal volume at minimal control pressures. ASV is a variation on PRVC that also involves complex closed-loops designed to achieve a targeted VE using output variables that minimize inspiratory work while limiting RR and Vt combinations to “lung protective” levels of support. Spontaneous breath types such as PS and VS incorporate closed-loop control mechanisms similar to their machine breath counterparts, PCV and PRVC. The complexity of closed-loop control systems that typify ventilator breaths increases as multiple target inputs are achieved with multiple ventilator output variations, based on multiple physiologic measurements. The goal driving design of these increasingly complex closed-loop control systems is the development of computer-based auto-adjusting ventilator breaths that use rapid measurement and feedback of pulmonary function variables to achieve as comfortable, safe, and brief a time on mechanical ventilation as possible. Yet ironically, rapid liberation of the adult patient from mechanical ventilation currently appears to depend less on computer-driven automatic adjustment of breath types and breath patterns that minimize the human element, than it does on clinician driven weaning protocols that use best evidence, weaning readiness criteria, and a once-daily spontaneous breathing trial (59). D. Breath Types, Vendors, and Special Features

Breath types, vendors and special features are shown in Table 2. V.

Breath Patterns or Modes

Machine and spontaneous breath types, as described earlier, are sequenced into three traditional breathing patterns or “modes of mechanical ventilation”: Assist/Control (A/C), intermittent mandatory ventilation (IMV), and CPAP. (Text continues on p. 98.)

Breath Types and Special Features

Breath typea

Availabilitya

Volume control ventilation

Ubiquitous

Pressure control ventilation

Ubiquitous

Pressure control inverse ratio ventilation

Ubiquitous

Bi-level ventilation

Nellcor Puritan Bennett 840; Drager Evita Series (i.e., Evita, Evita 2 Dura, and Evita 4)

Special features Machine breath type in which set Vt and ﬂow remain constant while pressure varies in response to changing lung mechanics and patient demand. For better control over delivered Vt, many current generation ventilators auto-compensate for volume loss due to gas compression and circuit stretch during the VCV breath. Patient–ventilator dyssynchrony can occur when patient ﬂow and Vt demands exceed ventilator ﬂow and Vt control settings. Machine breath type in which control pressure remains constant while ﬂow and Vt vary as a function of patient demand and lung mechanics. Tends to better match the ventilatory pattern of patients with high, variable inspiratory demands than the VCV breath, but at the risk of excessive Vt delivery. Conversely, acute deterioration in CST and/or RAW may result in inadequate Vt delivery. Often valued for decreasing ﬂow proﬁle that minimizes the resistive component of peak airway pressure, thus enabling same tidal volume ventilation at lower PIP’s than typically associated with VC square ﬂow wave breaths. A PCV breath in which the I-time is set to exceed E-time, thus inverting the physiologic I/E ratio for purposes of increasing volume hold, mean airway pressure, and PaO2. As set I-time exceeds E-time, risks of auto-PEEP and hemodynamic compromise may offset any improvements in PaO2. Moreover, as set I-time encroaches on “neural expiration”, patient agitation and the need for sedation increase. Resembles a PCV machine breath when spontaneous breathing is absent. But, is more like a distinct ventilator mode during spontaneous breathing, as an “active exhalation valve” enables the patient to breathe in an “unrestricted” manner atop the user-set, inspiratory pressure–time curve. A decrease in sedation is a manufacturer-alleged advantage. PS is also available to augment spontaneous breathing atop and between Bilevel machine breaths.

Modes of Mechanical Ventilation

Table 2

(Continued)

95

Breath Types and Special Features (Continued)

Breath typea

96

Table 2

Availabilitya

Special features

Airway pressure release ventilation

Nellcor Puritan Bennett 840; Drager Evita Series (i.e., Evita, Evita 2 Dura, Evita 4), Hamilton Galileo Gold

Pressure regulated volume control

Maquet Siemens Servo 300; Maquet Siemens Servo i, “Adaptive Pressure Ventilation” on the Hamilton Galileo; “AutoFlow” on the Drager Evita 4; “VCVþ” on the Nellcor Puritan Bennett 840 Hamilton Galileo

Is a variation on the Bi-level breath in which I-time is set to exceed E-time, resulting in a PCIRV breath atop which the patient is able to breath spontaneously. Like PCIRV, APRV is used to improve oxygenation, but unrestricted spontaneous breathing atop the high Control Pressure – time curve is alleged to reduce the patient-ventilator dyssynchrony and the high cardio-inhibitory mean airway pressures associated with the conventional PCIRV breath. PS is also available to augment spontaneous breathing atop and between APRV machine breaths. The PRVC machine breath is a PCV breath in which the control pressure is automatically regulated between breaths in small increments or decrements and in response to changing lung mechanics to achieve a target tidal volume. Thus, the advantage of the PCV breath, a decreasing ﬂow that varies with patient demand and enables same Vt ventilation at lower peak pressures than the VCV square wave breath are combined with the volume guarantee of the VCV breath.

Volume assured pressure support

Viasys Bird 8400Sti; Viasys T-Bird AVS III; Viasys Bird VIP Gold; “Pressure Augment” on Viasys Bear 1000

A variation on the PRVC machine breath in which the control pressure is up-regulated or down-regulated between breaths and in response to changing lung mechanics to achieve a targeted VE comprised of multiples of safe RR and Vt combinations. Program breath boundaries prevent over- or under-inﬂation and tachypnea or bradypnea from occurring during VE targeted automatic control pressure adjustments. Intended for use on patients with an intact respiratory drive, the VAPS breath combines the high initial ﬂow and ﬂow decay pattern of a PS breath with, if necessary to achieve the targeted Vt, the constant ﬂow of a VCV breath. If the target Vt is not reached as the PS breath decreases to its ﬂow-cycling threshold, then the breath switches to a volume control breath in which a low constant ﬂow is delivered until the target Vt is reached or a safety time-limit elapses. While intended for patients capable of triggering the ventilator, a user-set RR technically qualiﬁes the VAPS breath as a machine breath.

Richards and Mosenifar

Adaptive support ventilation

Ubiquitous

Volume support ventilation

Maquet Siemens Servo 300; Maquet Siemens Servo i; Nellcor Puritan Bennett 840.

Tube compensation

Nellcor Puritan Bennett 840; “Automatic Tube Compensation” on Draeger Evita 4; “Tube Resistance Compensation” on Hamilton Galileo Gold

Proportional assist ventilation

Available in Europe on the Drager Evita 4 as Proportional Pressure Support (aka: PPS)

Breath type brand names and their manufacturers from Pilbeam SP, Mechanical Ventilators: General-Use Devices. Pilbeam SP, Cairo JM, eds. Mosby’s Respiratory Care Equipment, 7th ed., St. Louis: Mosby, 2004; 12:391 –661.

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a

The PSV breath is considered a spontaneous breath because it is always patient-triggered, never time-triggered. PSV control pressure is user-set and sustained while ﬂow decreases as alveolar ﬁlling pressures approach set control pressures as a function of patient demand and lung mechanics. PSV is often used during the weaning process to offset the work of spontaneous breathing through restrictive artiﬁcial airways. However, a ﬁxed level of PS, in the absence of the clinician, does not vary in response to acute changes in lung mechanics or breath to breath changes in inspiratory effort. Thus, consistent Vt delivery cannot be guaranteed. A variation on the PSV breath in which the inspiratory control pressure is not user-set, but instead is auto-regulated over several breaths and in response to changing lung mechanics and patient demand to achieve a target Vt. Manufacturer literature suggests that weaning should be expedited as the pressure support levels used to maintain the target Vt are automatically down-regulated in response to improving lung mechanics. An auto-adjusting PSV breath in which control pressures automatically increase or decrease to overcome ﬂow-dependent resistive work of breathing through an artiﬁcial airway of a known diameter. As a patient’s inspiratory ﬂow demand increases, the PS level is up-regulated to match the increased pressure drop across the artiﬁcial airway. Patient resistive work is thus minimized. However, Vt delivery is not guaranteed and may become inadequate if the patient’s inspiratory effort wanes in response to worsening lung– thorax compliance or declining nutritional status. An auto-adjusting PSV breath in which control pressure varies directly with patient inspiratory effort to offset the resistive workload imposed by gas ﬂow through the airways and elastic load generated during tidal stretch of alveoli and chest wall. A “Flow Assist” control is used to offset the pressure change that occurs over the upper portion of the PSV ﬂow curve where measured resistance is greatest and a “Volume Assist” control is used to offset the pressure change that occurs over the lower portion of the PSV curve where airway resistance is minimal and measured elastance highest. As with the Tubing Compensation breath, Vt delivery is not guaranteed and may become inadequate if patient effort wanes or excessive if a ventilator circuit leak is misinterpreted as increased patient effort.

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Richards and Mosenifar A. Assist/Control Ventilation

A/C is a ventilator mode in which the patient’s entire minute volume is comprised of machine breaths delivered in response to small patient-initiated inspiratory efforts (“Assist” mode) or at the user-set mechanical respiratory rate (“Control” mode). The A/C mode machine breath may be a volume-controlled breath, a pressure-controlled breath, or a pressure-regulated/volumetargeted breath. However, A/C mode with volume control remains the mode that physicians most commonly use in the initial ventilator management of ARDS (23,52). A/C mode has also been used to rest ventilatory muscles in patients who display signs of intolerance to daily two-hour spontaneous breathing trials and, when used in this fashion, may result in quicker weaning from mechanical ventilation than protocols that gradually reduce levels of ventilator support (7). When managing patients on the A/C mode of ventilation, the clinician should remember that the ventilator’s set RR serves as an apnea safeguard and should therefore be set at approximately three-fourths the patient’s assist RR. It is especially important to set the machine RR only a few breaths below the assist RR if severe metabolic acidemia is present. Depending on the ventilator, examples of machine breath types available in the A/C mode of mechanical ventilation include: VC, PC, PRVC, and VAPS.

B. Intermittent Mandatory Ventilation

IMV is a ventilator mode in which the patient’s minute volume is comprised of a mix of machine breaths and spontaneous breaths. Most modern ventilators offer a synchronized variant of IMV called synchronized intermittent mandatory ventilation (SIMV). In SIMV, machine breath delivery is triggered by a spontaneous inspiratory effort that occurs within a “synchronization window” immediately prior to a scheduled machine breath. SIMV machine breaths may be volume-controlled or pressure-controlled. Spontaneous breaths are interspersed between machine breaths and include spontaneous breaths augmented by constant or auto-adjusting levels of PS (or TC). SIMV is frequently used to wean patients off the ventilator by gradually decreasing the machine breath rate as the patient is able to assume progressively more of the work of breathing. However, when excessive spontaneous ventilatory loads are incurred at low SIMV frequencies, machine breath delivery does not transiently lessen the excess spontaneous load (53,54). Thus, the strategy of gradually reducing SIMV frequencies may contribute to the persistence of respiratory muscle fatigue in patients not ready to wean and unnecessarily prolong mechanical assistance in patients who are ready to wean. In recent years, two highly regarded randomized studies showed that most patients deemed medically ready for weaning tolerated a two-hour spontaneous breathing trial and were extubated (55,56). Moreover, in those failing the initial spontaneous breathing trial, SIMV produced the poorest weaning outcomes, with one study ﬁnding the

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greatest success with once daily T-piece breathing trials (55) and the other with progressive PS reductions in CPAP mode (56). C. Continuous Positive Airway Pressure

CPAP is a ventilator mode in which the patient’s entire minute volume is comprised of spontaneous breaths. For this reason, one manufacturer refers to the CPAP mode as the “SPONT” mode (Nellcor Puritan Bennett 840, Puritan Benett, Carlsbad, CA, U.S.A.). The ventilator CPAP mode can be used with ﬂow-triggering as an alternative to the traditional T-piece spontaneous breathing trial via large volume O2/aerosol generator. Advantages of the CPAP mode version of the spontaneous breathing trial include less labor, as there is no additional equipment to set-up, and the availability of the ventilator’s continuous monitoring and alarm systems to indicate patient intolerance of the spontaneous breathing trial (57). Failure to tolerate the CPAP mode spontaneous breathing trial may prompt trials with graded PS (56), low-level PS (58), or auto-adjusting variants of PS (49,50) in the CPAP mode. Examples of breath types available in the ventilator CPAP mode or labeled as spontaneous breathing modes unto themselves include: PS, VS, TC and PAV. Yet, despite the spontaneous breath type selected to manage the ventilator weaning process, liberation of the patient from the mechanical ventilator is best achieved by consistent application of an evidenced-based weaning protocol in which the ﬁrst and most important step is determination of patient readiness to wean (59). VI.

Fine Tuning the Ventilator Breath

Clinical management objectives embodied in the foregoing text include reduction in the inspiratory work of breathing and in risk factors associated with ventilatorinduced lung injury. Suggested ventilator –patient management guidelines for achieving these objectives follow. Use of a ﬂow trigger (e.g., 1– 3 lpm) instead of the traditional pressure trigger (e.g., 1 –2 cmH2O) may reduce trigger work, although the impact of trigger work on total WOBi is small unless auto-PEEP is present. If autoPEEP must be overcome by the patient’s inspiratory effort before the set trigger point can be reached, then setting a low-level PEEP (e.g., 2 –5 cmH2O) that elevates the set trigger point into the auto-PEEP zone should reduce trigger work necessary for ventilator demand valve actuation. However, in the actively breathing ventilator patient, the bulk of inspiratory work is incurred after demand valve actuation, whenever ventilator ﬂow output falls below patient inspiratory ﬂow demand. In VCV, the ﬂow demand of the actively breathing ventilator patient can usually be met with a peak ﬂow setting of 40 – 80 lpm and a ﬁxed-pattern “square” ﬂow wave. But, should the clinician opt for a ﬁxedpattern “descending” ﬂow wave at the same peak ﬂow setting (presumably to reduce high PIPs), decreasing ﬂow output from the ventilator may fall below patient demand, as indicated by concave curvature or “scooping” of the

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inspiratory pressure – time curve. In patients with high and variable ﬂow demands, even high peak ﬂow and ﬁxed-pattern “square” ﬂow wave settings may be insufﬁcient to avoid tell-tail scooping on the inspiratory pressure –time curve along with inspiratory ﬂow – time curve sequences that are missing their expiratory ﬂow curve components. When inspiratory pressure curve “scooping” and inspiratory ﬂow curve “humping” occur together on the VCV graphics display, ﬂow and tidal volume settings are too low to meet patient ﬂow and tidal volume demand. A trial of PCV wherein peak ﬂow often tops 80 lpm and a descending ﬂow pattern conforms to breath-to-breath changes in patient demand and lung mechanics may reduce inspiratory work and discomfort the high demand patient experiences in VCV. The availability of a rise time control to attenuate the initial blast of gas and resultant “pressure overshoot” sometimes seen in PCV, along with a terminal ﬂow control that synchronizes termination of inspiratory ﬂow with the onset of patient expiratory activity within the PCV I-Time window, provides further means for achieving patient comfort and inspiratory workload reduction. However, persistent variability in PCV tidal volume delivery, especially if in excess of 4 –8 mL/kg in heterogeneous lung diseases like ARDS, is associated with alveolar stretch injury and may require sedation of the high demand patient and conversion back to volume controlled breaths. The concomitant use of effective levels of PEEP between breaths in this tidal range prevents atelectasis and related sheer stress that is also considered damaging to parenchymal tissue, but controversy exists as to how much PEEP should be used to recruit and prevent derecruitment of atelectatic alveoli. In managing the ARDS ventilator patient, the best approach to this controversy seems to lie in the use of the 4 – 6 mL/kg tidal volumes and FIO2:PEEP relationships used in the NIH ARDS Network trial that resulted in reduced ventilator days and mortality. Yet in severe ARDS, use of even these low-end tidal volumes and FIO2:PEEP combinations may not yield adequate gas exchange without exceeding the “lung protective” target Pplat of 30 – 35 cmH2O. At this point, high-frequency oscillatory ventilation (HFOV) has been proposed as a ventilator strategy for managing severe ARDS that may maximize lung recruitment and oxygenation while minimizing ventilator-induced stretch injury. While relatively new to adult ventilator management, HFOV has been used for nearly two decades to manage severe respiratory failure in neonates and infants. In HFOV, MAWP is the control determinate of oxygenation and is initially set at a few centimeters above the conventional ventilator MAWP. A user-set control pressure (“pressure amplitude”) is then oscillated at a high user-set frequency (e.g., 3– 5 Hz in adults) above and below the MAWP baseline to achieve visual chest wall vibration (“wiggle from shoulder to thigh”) that determines CO2 clearance while minimizing cyclic alveolar stretch. HFOV might be thought of as a vibrating CPAP and in adults represents an evolutionary extension of conventional ventilation “lung protective” strategies that aim to minimize alveolar stretch injury while maintaining maximum alveolar recruitment and adequate gas exchange.

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Acknowledgment Computer rendering of waveform sketches by Jihane Bishara, Management Assistant, Division of Pulmonary/Critical Care Medicine, CSMC.

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Richards and Mosenifar Chiumello D, Pelosi P, Croci M, Bigatello LM, Gattinoni L. The effects of pressurization rate on breathing pattern, work of breathing gas exchange and patient comfort in pressure support ventilation. Eur Respir J 2001; 18(1):107 – 114. Bonmarchand G, Chevron V, Menard J, Girault C, Moritz-Berthelot F, Pasquis P, Leroy J. Effects of pressure ramp slope values on the work of breathing during pressure support ventilation in restrictive patients. Crit Care Med 1999; 27(4):715– 722. Kallet RH, Campbell AR, Alonso JA, Morabito DJ, Mackersie RC. The effects of pressure control versus volume control assisted ventilation on patient work of breathing in acute lung injury and acute respiratory distress syndrome. Respir Care 2000; 45(9):1085– 1096. Tobin MJ. Culmination of an era of research on the acute respiratory distress syndrome. N Eng J Med 2000; 342(18):1360– 1361. Gattinoni L, Vagginelli F, Chiumello D, Taccone P, Carlesso E. Physiologic rationale for ventilator setting in acute lung injury/acute respiratory distress syndrome patients. Crit Care Med 2003; 31(4):S300 – S304. Petrucci N, Iacovelli W. Ventilation with lower tidal volumes versus traditional tidal volumes in adults for acute lung injury and acute respiratory distress syndrome. Cochraine Database Syst Rev 2003; (3):CD003844. Tobin MJ. Medical progress: advances in mechanical ventilation. N Eng J Med 2001; 344(26):1986– 1996. Thompson BT, Hayden D, Matthay MA, Brower R, Parsons PE. Clinicians’ approaches to mechanical ventilation in acute lung injury and ARDS. Chest 2001; 120:1622 –1627. Pilbeam SP. Introduction to ventilators. In: Pilbeam SP, Cairo JM, eds. Mosby’s Respiratory Care Equipment. 7th ed. St. Louis: Mosby 2004; 11:317 –390. Carmichael LC, Dorinsky PM, Higgins SB, Bernard GR, Dupont WD, Swindell B, Wheeler AP. Diagnosis and therapy of acute respiratory distress syndrome in adults: an international survey. J Critical Care 1996; 11(1):9 – 18. Slutsky AS. Lung injury caused by mechanical ventilation. Chest 1999; 116:9S – 15S. Uhlig S. Mechanotransduction in the lung, ventilation-induced lung injury and mechanotransduction: stretching it too far? AJP Lung Cell Mol Physiol 2002; 282(5):L892– L896. 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 2000; 342(18):1301– 1308. NIH/NHLBI ARDS Clinical Network: Mechanical ventilation protocol summary, 2000: Available from http://hedwig.mgh.havard.edu/ardsnet/6 ml.html/:1– 4. Jonson B, Svantesson C. Elastic pressure volume curves: what information do they convey? Thorax 1999; 54(1):82– 87. Amato MBP, Barbas CSV, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, Kairalla RA, Deheinzelin D, Munon C, Oliveira R et al. Effect of bioprotective ventilation on mortality in the acute respiratory distress syndrome. N Engl J Med, 1998; 338(6):347– 354. Mancini M, Zavala E, Moncebo J, Fernandez C, Babera JA, Rossi A, Roca J, Rodriguez-Roisin R. Mechanisms of pulmonary gas exchange improvement

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4 Monitoring During Mechanical Ventilation

DEAN R. HESS Department of Respiratory Care Massachusetts General Hospital and Department of Anesthesia Harvard Medical School Boston, Massachusetts, U.S.A.

I.

Introduction

Monitoring is the continuous, or nearly continuous, evaluation of the physiologic function of a patient in real time to guide diagnosis and management decisions, including when to make therapeutic interventions and assessment of those interventions (1). Many physiologic parameters can be monitored during mechanical ventilation (Fig. 1). These include both invasive and non-invasive monitoring. Although its impact on patient outcomes has not been well studied, monitoring has become an integral part of the care of mechanically ventilated patients. II.

Arterial Blood Gases

Arterial blood gas (ABG) analysis is commonly regarded as the “gold standard” for evaluation of arterial oxygenation and acid-base balance, althought the indications for ABG remain unclear (2). There are numerous problems associated with the measurement and use of ABG (Table 1). ABGs are the most frequently ordered laboratory test in many critical care units. A rate of 4.8 ABG/patient/day was reported from a surgical ICU, and the presence of an arterial line was most predictive of the number of ABGs drawn per patient (3). The presence of an arterial line also affects the pattern of transfusion requirements related to phlebotomy for diagnostic tests in adults (4– 7). In one study, patients with an arterial line were phlebotomized at a rate twice that of patients who did not have a line (5). Another study reported increases in the number of blood tests (29% increase), 105

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Tissue Oxygenation

Hemodynamics heart rate & rhythm blood pressure cardiac output wedge pressure oxygen delivery

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Lung mechanics airway pressure, flow, volume esophageal pressure pressure-volume curve

Sedation and Neuromuscular Blockade

Ventilator function disconnect leak occlusion humidification FIO2

Figure 1 Many physiologic parameters can be monitored during mechanical ventilation.

blood-drawing procedures (30% increase), and the amount of blood volume loss (44% increase) from patients with arterial lines compared with those without (6). Several strategies might be used to decrease blood loss because of ABGs (and other laboratory testing) in critically ill patients (7). Routine-use arterial lines should be avoided. Blood conservation systems can be used to eliminate the discard volume from arterial line blood draws (8– 11). Multiple diagnostic tests may be performed on a single sample of blood. Clinically accurate and precise invasive and non-invasive technology can be substituted for some diagnostic tests. Blood sample volume can be reduced, such as by using pediatric phlebotomy tubes and reduced syringe volume (12). Table 1 Problems Associated with Arterial Blood Gas Analysis Pain Pre-analytical errors: air contamination, heparin dilution, storage, delay before analysis Analytic errors: accuracy differences between models of blood gas analyzers Post-analytical errors: transcription errors, delays in reporting results Infection risk to patient (particularly with arterial catheter) Infection risk to clinician (particularly with arterial puncture) Thrombosis and distal embolization (particularly with arterial catheter) Blood loss (particularly with arterial catheter) Intermittent information Cost Regulation: CLIA-88

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Beasley et al. (13) established procedural, clinical, and therapeutic indicators for ABGs in a surgical ICU. A forced interaction between respiratory therapists and nurses was established by making therapists responsible for ABGs analysis. The result of this interaction between therapists and nurses regarding ABGs has resulted in an improvement in the appropriateness of ABGs requested by the nurses. Pilon et al. (14) developed institutional guidelines for ABGs and reported a decrease in the number of blood gases by about 50% with near-doubling of the appropriateness of ABGs. It is important to develop a behavior among respiratory therapists, physicians, and nurses that carefully considers the need for blood gas analysis. There is no indication for “routine” blood gases (e.g., after each ventilator change). One frequently unappreciated feature of intermittent ABGs is spontaneous variability (i.e., changes without any intervention or interaction with the patient) (15 – 18). In one report, the coefﬁcient of variation in PaO2 between four ABGs drawn at 20-minute intervals in stable mechanically ventilated trauma patients, who were not disturbed during the study period, was 5.1 + 3.2%, median 3.6%, 95th percentile 9.8%) (15). Changes in PaO2 within the limits of spontaneous variability, and without an associated clinical change, might be the result of spontaneous variability. An important clinical issue relates to the amount of time required to establish a new steady state after changing the FIO2 provided for the patient. If too little time is allowed, the blood gas results will not reﬂect the new clinical conditions. If too much time is allowed, this could subject the patient to a long period of potentially harmful hypoxemia. The time required to reach a steady state after an FIO2 change depends upon the alveolar ventilation and the functional residual capacity. A small alveolar ventilation or a large functional residual capacity requires a longer time for equilibration. Unless the patient has obstructive lung disease (which results in a lower alveolar ventilation and a larger functional residual capacity), ﬁve minutes is usually an adequate time to reach a new steady state after a change in FIO2 (19). For patients with obstructive lung disease, 30 minutes should be allowed to reach a new steady state after a change in FIO2. The gold standard for measurement of hemoglobin oxygen saturation (O2Hb) is CO-oximetry. CO-oximetry uses multi-wavelength spectrophotometry to measure O2Hb, deoxyhemoglobin (HHb), carboxyhemoglobin (COHb), and methemoglobin (metHb). Fractional oxyhemoglobin (FO2Hb) is then calculated as: FO2 Hb ¼

O2 Hb O2 Hb þ HHb þ metHb þ COHb

Oxygen saturation can also be calculated from the measured PO2 using an empirical equation for the oxyhemoglobin dissociation curve, as is commonly done using software in blood gas analyzers. Clinically important errors can result from use of calculated oxygen saturation in applications such as the shunt equation (20–23). Several errors are related to CO-oximetry. Owing to differences in the light

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absorption spectra of fetal hemoglobin (HbF) and adult hemoglobins, the presence of HbF may result in false elevations of COHb (24). Correction factors for the presence of HbF have been published (25), but these may not be appropriate under all conditions (such as transfusion) (26). Intralipid infusions (27) and propofol infusions may result in falsely elevated metHb levels measured by CO-oximetry. III.

Arterialized Capillary Blood Gases

To obtain capillary blood gas samples, a puncture is made with a lancet or similar device into the cutaneous layer of the skin at a highly vascularized area. To accelerate blood ﬂow and reduce the difference between arterial and venous gas pressures, vasodilation is achieved by warming or use of a vasoactive cream. Common sites used for arterialized capillary blood gases are the heel (in neonates), ﬁnger, toe, or earlobe. Several studies have reported the use of arterialized capillary blood gases in adults. Pitkin et al. (28) reported good agreement between capillary PO2 and arterial PO2 (bias 21 mm Hg, limits of agreement 28 to 6 mm Hg). Dar et al. (29) reported “trivial and non-signiﬁcant” differences between arterial and capillary PO2. In contrast to these reports, Sauty et al. (30) reported a signiﬁcant underestimation (4 mm Hg) of PaO2 by earlobe capillary blood gases with wide limits of agreement (24 to 13 mm Hg). Arterialized capillary blood gases produce a mixture of blood from capillaries and venules (31). The difference between arterial and venous PO2 is usually large (about 60 mmHg), but this difference can be reduced by vasodilation. Furthermore, the difference between arterial and venous PO2 decreases with hypoxemia. Thus, the accuracy of arterialized capillary blood PO2 improves as the PaO2 decreases. None the less, arterialized capillary PO2 systematically underestimates the PaO2. Moreover, capillary blood samples are difﬁcult to obtain anaerobically. Exposure of the blood to room air raises the PO2, and this may explain the agreement between arterialized capillary PO2 and PaO2 reported in some studies. Arterialized capillary blood gases have also been advocated because they are less painful, but the pain of arterial puncture can be lessened by the use of local anesthesia (32). IV.

Point-of-Care Testing

Samples for blood gas analysis are drawn from the patient, packaged and transported to the laboratory, and analyzed, and the results are then communicated back to the patient care unit. This model may result in pre-analytical errors (e.g., failure to properly transport the sample), post-analytical errors (e.g., transcription errors in reporting the results), and delay in reporting the results. There has been increasing interest in point-of-care (POC) testing, in which blood gases are measured at or near the site of patient care (33 – 40). Several

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studies have reported acceptably accurate blood gas results using POC testing devices (41 – 45). Kendall et al. (46) performed a randomized controlled trial of POC on clinical outcome in an emergency department and reported that POC testing resulted in signiﬁcantly faster decision-making. However, POC testing did not affect the amount of time spent in the emergency department, the length of stay in the hospital, admission rates, or mortality. POC testing devices are portable (some are hand-held), and they typically require a small volume of blood for testing (a few drops). Blood is introduced into a single-use disposable cartridge that is introduced into the portable analyzer. The cartridge chosen determines the tests that will be run (e.g., blood gases, electrolytes, hematocrit, glucose, BUN, creatinine, ionized calcium, and others). The sensor calibrates automatically, after which the blood sample is drawn over the biosensors. The POC analyzer then calculates, displays, and stores the results. The POC testing device can communicate with the central laboratory or hospital information system for reporting and archiving results. The role of POC testing is evolving and is likely to expand in the future. Quality control and quality assurance must be appropriately addressed. This is typically achieved by following the manufacturer’s recommendations for use of the device. The costs of the base unit the and the test cartridges must be balanced against a quicker test turn-around time (potentially resulting in more rapid treatment and better patient outcomes), the lower overhead (compared to the central laboratory), and the smaller blood volume required for testing (resulting in lower transfusion requirements).

V.

Blood Gas Monitors

Blood gas monitors measure pH, PCO2, and PO2 without permanently removing blood from the patient (47). Blood gas monitors use ﬂuorescent optodes, which are optical biosensors. Light is used to activate electrons in a dye to a higher energy state. When the light exposure ends, the electrons return to their basal state and light is re-emitted. The lower frequency of re-emitted light is augmented as the concentration of hydrogen ions or carbon dioxide increases, and the re-emitted light is quenched as the concentration of oxygen increases. Photosensors are used to quantify the amount of quenching, and a microprocessor is used to translate the signal into a display of PO2, PCO2, and pH. Various conﬁgurations of optodes for intra-arterial blood gas monitors have been developed. Optode systems are electrically isolated from the patient, they can be miniaturized so that they ﬁt through an arterial catheter without affecting other catheter functions, they are stable over time, they respond rapidly to changes in substrate concentration, and they are not consumed in the measurement process. Several approaches can be taken to blood gas monitoring in conjunction with an arterial catheter. The ﬁrst approach uses a probe that passes through the arterial catheter and resides directly within the arterial lumen (i.e., in vivo

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blood gas monitor). With the second approach, the optode system is connected to the proximal arterial line but does not pass through the catheter. With this method, when blood gas and pH levels are desired, blood is drawn into a chamber containing the optodes (i.e., ex vivo blood gas monitor). After analysis, the blood is ﬂushed back into the artery. Thus, frequent (but not continuous) blood gas measurements are possible without blood loss. Studies evaluating these devices (48 – 64) have generally reported acceptable overall accuracy of blood gas monitors. Some of these studies, however, report occasional discrepancies between the blood gas monitor and a blood gas analyzer. The reasons for this may relate to issues such as sensor position and catheter ﬂushing. One problem with these systems is their cost. Blood gas analyzers are equally expensive, but they are not dedicated to a single patient. Although manufactures are striving to design user-friendly systems that are easy to use, the amount of technical attention that these systems are likely to require in a busy ICU remains to be determined. The life of the sensor in a busy ICU also remains to be seen. The quality control and quality assurance requirements for clinical and regulatory purposes are unclear. Whether or not the beneﬁts of continuous blood gas and pH measurements will outweigh the costs and technical support required remains to be seen. VI.

Mixed Venous Blood Gases

Blood obtained from the central venous circulation or pulmonary artery is used to assess mixed venous oxygenation. If the catheter is positioned in a distal branch of the pulmonary artery, rapid aspiration can contaminate the mixed venous blood with pulmonary capillary blood (65). Although the importance of this has been questioned (66), it is prudent to use a slow aspiration rate (,1 mL/ 30 sec) when blood is sampled from a pulmonary artery catheter. The mixed venous oxygenation has been commonly thought to represent tissue oxygenation. However, several points are important in relation to the ability of mixed venous oxygenation to reﬂect tissue oxygenation. Sv¯O2 (or Pv¯O2) depends on the oxygen content derived from many vascular beds, and it thus does not necessarily reﬂect well the Sv¯O2 of any individual vascular bed. With septic shock, peripheral arteriovenous shunts open, resulting in an Sv¯O2 higher than expected (67). Sv¯O2 will also be falsely elevated (i.e., “not” reﬂect tissue oxygenation) in patients with ventricular septal defect or cyanide poisoning. During circulatory arrest, large concentrations of CO2 may accumulate in the venous circulation. With cardiac arrest, very high Pv¯CO2 (venous respiratory acidosis) has been reported in the presence of normal or low PaCO2 (arterial respiratory alkalosis) (68,69). Sv¯O2 can be mathematically derived from the Fick equation: Sv O2 ¼ 1

_ 2 VO DO2

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where V˙O2 is oxygen consumption and DO2 is oxygen delivery. The relationship V˙O2/DO2 is the oxygen utilization coefﬁcient or the oxygen extraction ratio. Sv¯O2 is thus determined by the balance between V˙O2 and DO2. Mixed venous blood is obtained from the pulmonary artery. Oxygen saturation is slightly higher in the inferior vena cava than the superior vena cava due to the relatively low levels of oxygen extraction relative to perfusion in the renal and mesenteric vasculature (70). During periods of stress (e.g., shock, hypovolemia, exercise), however, there is a drop in the oxygen saturation of the inferior vena cava, so the saturation in the superior vena cava is greater than that of the inferior vena cava. This occurs as the result of decreased renal and splanchnic perfusion during these conditions. Use of central venous blood other than that obtained from the pulmonary artery may be an inadequate reﬂection of true mixed venous blood. Although mixed venous blood samples should ideally be obtained from the pulmonary artery, a high correlation between pulmonary shunt calculations using pulmonary artery samples and central venous samples (e.g., right atria or superior vena cava) has been reported (70). A peripheral venous blood gas reﬂects the PO2 and PCO2 of the tissue bed served by that vein. Thus peripheral venous blood gases are not useful as a proxy for either an arterial blood gas sample or a central venous blood gas sample. The ability to continuously measure mixed venous oxygen saturation via oximetric methodology became commercially available in the early 1980s. This system uses a microprocessor, an optical module with light sources and photodetectors, and a ﬂow-directed pulmonary artery catheter (71 –73). Using ﬁberoptics, wavelengths of light between 650 and 1000 nm are pulsed into the pulmonary artery. This light is reﬂected off red blood cells in the pulmonary artery and returned to the optical module via another ﬁberoptic bundle. Sv¯O2 is determined by the ratio of transmitted and reﬂected light. Before insertion, the system is calibrated with an in vitro calibration standard, and this can be updated periodically by in vivo calibration using a CO-oximetry determined Sv¯O2. Factors that affect the measurement of Sv¯O2 using this method include temperature, pH, blood ﬂow velocity, hematocrit, and occlusion of the catheter tip (e.g., clot or vessel wall). A number of studies have evaluated the accuracy of Sv¯O2 catheter systems (74 – 81). Most of them reported that the three wavelength systems correlate better with CO-oximeter Sv¯O2 than two wavelength systems and that drift is less with three wavelength systems. Studies reporting bias and precision analysis have found greater degrees of inaccuracy than those claimed by the manufacturer. However, if meticulous attention is paid to care of the catheter system (e.g., in vivo calibrations, updating the hematocrit setting), either of these systems may be acceptable to detect changes or trends. These systems do require more technical attention than other monitoring systems, such as pulse oximetry or a conventional pulmonary artery catheter. Regardless of their technical performance, the clinical usefulness of Sv¯O2 monitoring remains controversial. The results of a large multi-center study

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(.10,000 patients in .50 ICUs) showed that targeting Sv¯O2 . 70% did not affect mortality (82). More recently, Rivers et al. (83) evaluated the efﬁcacy of early goal-directed therapy before admission to the ICU. Patients who arrived at an emergency department with severe sepsis or septic shock were randomized to receive either six hours of early goal-directed therapy or standard therapy before admission to the ICU. In-hospital mortality was 30.5% in the group assigned to early goal-directed therapy, compared with 46.5% in the group assigned to standard therapy. In this study, a central venous catheter capable of measuring oxygen saturation was used, with a targeted central venous oxygen saturation 70%. VII.

Pulse Oximetry

Continuous pulse oximetry has become a standard of care for critically ill patients. With pulse oximetry, two wavelengths of light (660 and 940 nm) are passed through a pulsating vascular bed (84,85). This is accomplished using two light-emitting diodes (LEDs) and a photodetector. There is some error in the wavelength of light emitted by the LEDs (+30 nm) that can affect accuracy. Also, the photodetector is not speciﬁc (i.e., if will respond to any wavelength of light, which can result in interference). Although some of the light emitted from the LEDs is absorbed by each constituent of the tissue, the only variable absorption is due to arterial pulsations. This is translated into a plethysmographic waveform. The ratio of the amplitudes of these two plethysmographic waveforms is translated into oxygen saturation. A probe is used to pass light from the LEDs through a pulsating vascular bed. Disposable and reusable probes are available and equally accurate (86). Pulse oximeter probes can become contaminated with pathogenic bacteria and serve as a source of nosocomial infection. A protective sheath can be used to allow the same disposable probe to be used on multiple patients (87). The use of disposable pulse oximeter probes can become very expensive for the hospital, and it has been shown that disposable probes can be gas sterilized and recycled (88). A number of limitations of pulse oximetry should be recognized, appreciated, and understood by everyone who uses pulse oximetry data. Most pulse oximeter errors can be explained as too little signal (e.g., low perfusion, improper probe placement) or too much noise (e.g., motion, ambient light). .

Accuracy: Many clinical evaluations of the accuracy of pulse oximeters have been published, including a meta-analysis (89). At saturations .80%, the accuracy of pulse oximetry is +4% to +5%. Below 80%, the accuracy is worse, but the clinical importance of this is questionable. To appreciate the implications of the limits of accuracy of pulse oximetry, one must consider the oxyhemoglobin dissociation curve (Fig. 2). If the pulse oximeter displays a SpO2 of 95%, the true saturation could be as low as 90% or as high as 100%. If the true

SO2 (%)

Monitoring During Mechanical Ventilation 100 90 80 70 60 50 40 30 20 10 0

pH 7.25

pH 7.40

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PO2 (mm Hg)

Figure 2 Oxyhemoglobin dissociation curve. If a pulse oximeter indicates a SpO2 of 95%, the true HbO2 may be as low as 90% or as high as 100% due to an accuracy of pulse oximetry of +5%. As indicated in the ﬁgure, the SpO2 will change if the oxyhemoglobin dissociation curve shifts (e.g., a change in pH), even though there is no change in PaO2.

.

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saturation is 90%, the PO2 will be about 60 mmHg. If the true saturation is 100%, however, one does not know how high the PO2 might be. Also, a shift of the oxyghemoglobin dissociation curve can change the SpO2, although no change in PaO2 has occurred. Misunderstanding by those who use pulse oximetry: Although pulse oximetry is commonly used, it may be misunderstood by users. Several studies (90,91) have reported that physicians and nurses lacked adequate knowledge of pulse oximetery and made serious errors in the interpretation of SpO2. Differences between devices and probes: The pulse oximeter is unique in that it requires no user calibration. However, manufacturerderived calibration curves programmed into the software vary from manufacturer to manufacturer, and they can vary among pulse oximeters of a given manufacturer. Moreover, the output of LEDs can vary from probe to probe. The accuracy of pulse oximetry has been shown to vary among devices (91 – 97). The same pulse oximeter and probe should ideally be used for each SpO2 determination on a given patient. Penumbra effect: If the ﬁnger pulse oximeter probe does not ﬁt correctly, light can be shunted from the LEDs directly to the photodetector (98). Theoretically, this will cause a falsely low SpO2 if SaO2 . 85%, and a falsely elevated SpO2 if SaO2 , 85%. Dyshemoglobinemias: Because commercially available pulse oximeters use only two wavelengths of light, they are only able to evaluate O2Hb and HHb. Pulse oximeters assume that COHb and metHb concentrations are low. Abnormal elevations of COHb (99 – 102) and

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. .

metHb (103) both result in signiﬁcant inaccuracy in pulse oximetry. Pulse oximetry is reliable with sickle cell anemia (104). Endogenous and exogenous dyes and pigments: Vascular dyes can affect the accuracy of pulse oximetry, with methylene blue having the greatest effect (105,106). Nail polish can also affect the accuracy of pulse oximetry, and it should be removed before monitoring with pulse oximetry is begun (107). Hyperbilirubinemia does not affect the accuracy of pulse oximetry (108,109). Skin pigmentation: Several studies have found that the accuracy and performance of pulse oximeters is affected by deeply pigmented skin (110 – 112). Perfusion: Pulse oximeters require a pulsating vascular bed to function correctly. Under conditions of low ﬂow (e.g., cardiac arrest or severe peripheral vasoconstriction), pulse oximetry becomes unreliable. Under these conditions, an ear probe may be more reliable than a ﬁnger probe. Anemia: Although pulse oximeters are generally reliable over a wide range of hemoglobin levels, they become less accurate and reliable with conditions of severe anemia (Hb , 8 g/dL at low saturations, and hematocrit ,10% at all saturations) (113,114). Motion: Motion of the probe can produce considerable artifact, and produce unreliable and inaccurate pulse oximetry readings. This problem can sometimes be corrected by using an alternate probe site (such as the ear or toe rather than the ﬁnger). High-intensity ambient light: Because the photodetector of the pulse oximeter is non-speciﬁc, high-intensity ambient light can produce interference. The problem can be corrected by wrapping the probe with a light barrier. The current generation of pulse oximeters may be affected less by the presence of ambient light (115). Abnormal pulses: Venous pulses and a large dicrotic notch have been shown to affect the accuracy of pulse oximetry (116 –118). Safety: Pulse oximetry is generally considered safe. However, burns as the result of defective probes and pressure necrosis have been reported during the use of pulse oximetry (119 – 122).

Motion artifact and low perfusion are common causes of pulse oximetry errors (123,124). A technique that uses mathematical manipulation of the pulse oximeter signals to measure and subtract the noise components of motion and low perfusion is commercially available (Masimo Corporation, Mission Viejo, California, U.S.) (125). Barker (126) performed a human volunteer experiment to compare the performances of 20-pulse oximeters during combinations of motion and hypoxemia. A motorized table produced different hand motions, and each motion was studied during both room air breathing and hypoxemia. Pulse oximeters on the non-moving hand were used to provide control

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measurements for comparison. The Masimo Signal Extraction Technology (SET) pulse oximeter exhibited the best overall performance, with a performance index (percentage of time in which the SpO2 reading is within 7% of control value) of 94%. Durbin and Rostow (127) evaluated the impact on clinical care of the Masimo pulse oximetry technology. Post-cardiac surgery patients were monitored with two oximeters, one employing conventional oximetry and one using the Masimo technology, on different ﬁngers of the same hand. The amount and percentage of non-functional monitoring time was collected and found to be much greater for the conventional pulse oximetery. Time to extubation was not different between the two groups, but clinicians managing patients with the Masimo technology weaned patients faster to an FIO2 of 0.40 and obtained fewer arterial blood gas measurements. The impact of pulse oximetry on patient outcomes is unclear. A large study (.20,000 patients) of pulse oximetry use in anesthesia and postanesthesia care found no difference in outcome (128,129). Pulse oximetry is indicated in unstable patients likely to desaturate, in patients receiving a therapeutic intervention that is likely to produce hypoxemia (such as bronchoscopy), and in patients having interventions likely to produce changes in arterial oxygenation (such as changes in FIO2 or PEEP). The pulse oximeter is no better at detection of a ventilator disconnect than the alarms already available on the ventilator. None the less, pulse oximetry is routinely used in mechanically ventilated patients in the ICU. Jubran and Tobin (111) evaluated the use of pulse oximetry in titrating supplemental oxygen in 54 critically ill ventilator-dependent patients (Fig. 3). In caucasian patients, they found that a SpO2 of 92% was reliable

Figure 3 (Left): In caucasian patients (open circles), a SpO2 92% is reliable in predicting a PaO2 60 mmHg. (Right): In patients with deeply pigmented skin (ﬁlled circles), a SpO2 95% was required to reliably predict a PaO2 60 mmHg. Source: Adapted from Ref. 111.

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Figure 4 Pulse oximeter tracings from a 60-year-old woman with an exacerbation of chronic obstructive pulmonary disease who was admitted to the ICU in ventilatory failure. (A) The patient’s pulse oximetry tracing at the time of admission, revealing the respiratory variability in the pulse oximeter plethysmography tracing. Her measured pulsus paradoxus at this time was 16 mm Hg. (B) The patient’s pulse oximetry tracing after 12 hours of aggressive therapy. Her pulsus paradoxus at this time was 8 mm Hg. Note the absence of RWV in the baseline of the oximeter tracing after the clinical improvement in airﬂow and the resolution of elevated pulsus paradoxus. Abbreviation: RWV, respiratory waveform variation. Source: Adapted from Ref. 130.

in predicting a PaO2 60 mmHg. In patients with deeply pigmented skin, however, a SpO2 of 95% was required. There may be important non-oxygenation monitoring applications for pulse oximetry. For example, Hartert et al. (130) reported the effect of pulsus paradoxus, and therefore the severity of air trapping in obstructive airway disease, on the pulse oximetry plethysmographic waveform (Fig. 4). They reported that, in patients with obstructive lung disease and elevated pulsus paradoxus, there was an altered pulse oximetry baseline tracing manifested as the respiratory waveform variation. Pulsus paradoxus was signiﬁcantly correlated with the degree of respiratory waveform variation of the pulse oximetry tracing and the amount of auto-PEEP.

VIII.

Gastric Tonometry and Sublingual PCO2

Gastric tonometry has been suggested as a minimally invasive method to assess tissue oxygenation in critically ill patients (131 –146). Perfusion of the gut is affected early in the course of systemic hypoxia, which should result in a decrease in gastric intramucosal pH (pHi). Normal pHi is 7.38 + 0.03. Hypoperfusion of the gut also increases gastric intramucosal PCO2, which is referred to as regional PCO2 (PrCO2). The PrCO2 can increase with either decreased perfusion or increased PaCO2. With decreased perfusion, the gap between PrCO2 and

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PaCO2, the Pr – aCO2 increases. Levy et al. reported an increased mortality when the Pr – aCO2 gap was .20 mm Hg (145). The gastric tonometer consists of a nasogastric tube with a distal CO2permeable silastic balloon. The balloon is ﬁlled with 2.5–3 mL of physiologic saline solution. An equilibration time of one to two hours allows CO2 in the gastric lumen to equilibrate with the saline inside the balloon. After discarding 1–1.5 mL of aspirate from the gastric tube (dead volume), the remaining 1–1.5 mL is analyzed for PCO2 using a blood gas analyzer. A simultaneous arterial blood sample is analyzed to determine HCO2 3 . Gastric pHi is calculated from the Henderson–Hasselbalch equation, using the PCO2 of the saline from the gastric balloon and the HCO2 3 of arterial blood. Several studies have reported substantial preanalytical errors related to air contamination of the saline sample (147–149). This has led to the development of gas tonometry techniques (146,150–153). Another advantage of these newer techniques is that they are automated and can be used for nearly continuous monitoring. Even with improvements in the technical aspects of gastric tonometry, its use remains controversial (154,155). Sublingual PCO2 (PSLCO2) correlates well with gastric intramucosal PCO2 and is relatively easy to perform (156 – 158). PSLCO2 is measured by using a CapnoProbe subingual PCO2 measurement system (Nellcor, Pleasanton, CA, U.S.A.). The CapnoProbe consists of a disposable PCO2 sensor and a batterypowered handheld instrument. The sensor is a CO2-sensing optode. The optode has a CO2-permeable capsule ﬁlled with a ﬂuorescent indicator at the distal end of an optical ﬁber. The ﬂuorescent indicator is excited by light conducted through the optical ﬁber, with the ﬂuorescent emission of the indicator being monitored by the optical ﬁber. As CO2 enters the capsule, carbonic acid is formed, resulting in a lower pH. The pH change causes a shift in the ﬂuorescence of the indicator, which is detected through the ﬁber optics. The change in ﬂuorescence is then converted to a PCO2 via the Henderson– Hasselbalch equation.

IX.

Capnography

Capnometry is the measurement of CO2 at the airway opening during the ventilatory cycle (159). Capnography is the graphic waveform display of CO2 as a function of volume or time. The waveform displayed by a capnograph is called a capnogram. Most bedside capnometers measure CO2 by infrared absorption, which uses the absorption peak for CO2 at 4.26 mm. The CO2 in the sample cell decreases the radiation transmitted to the detector. The increased radiation transmitted from the reference cell (relative to that from the sample cell) is detected and used to determine the CO2 concentration. The mass spectrometer can also be used to measure CO2, in which the sample is aspirated into a vacuum chamber where the gas is ionized by an electron beam. The charged fragments are accelerated into a dispersion chamber where they are separated

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according to mass and charge. When light strikes gas molecules, energy is absorbed and reemitted at the same wavelength and direction, and a small fraction of the absorbed energy is reemitted at new wavelengths in a phenomenon known as Raman scattering. Raman scattering results in a red-shifted spectrum, and the wavelength shift and amount of scattering can be used to measure the PCO2. A portable non-electronic single-patient-use device is commonly used to produce a color change (colorimetric end-tidal CO2 detection) in the presence of exhaled CO2 (i.e., tracheal intubation). The color changes from purple with a low CO2 concentration to yellow with a CO2 concentration of 2.0% to 5.0%. Capnometers can be conﬁgured as mainstream or sidestream devices. With the mainstream capnometer, the measurement chamber is placed directly at the airway. With the sidestream capnometer, gas from the airway is aspirated through ﬁne bore tubing to the measurement chamber inside the device. Some devices (e.g., colorimetric capnometers) can only be used as mainstream devices, whereas other devices (e.g., mass and Raman spectrometers) can only be used as sidestream devices. Infrared capnometers can be conﬁgured as either mainstream or sidestream devices. There are advantages and disadvantages of each approach (Table 2). A new capnography technology, Microstream, has recently been introduced (160). Microstream features low ﬂow rates, reduced dead space, and lack of moisture-associated occlusion problems. Microstream technology uses a novel molecular correlation spectroscopy source that operates at room temperature and emits only CO2 speciﬁc radiation. The breath sample is brought to the measuring cell at a ﬂow of 50 mL/min via a specially designed Microstream breath sampling circuit using a miniature diaphragm pump. Carbon dioxide homeostasis is affected by volume of CO2 production (V˙CO2), CO2 transport from the tissues to the lungs, and alveolar ventilation. Conditions that increase V˙CO2 include fever, activity, sepsis, hyperthyroidism, Table 2 Mainstream and Sidestream Capnometers Advantages Mainstream Capnometer Sensor at patient airway Fast response (crisp waveform) Short lag time (real-time readings) No sample ﬂow to reduce tidal volume

Sidestream Capnometer No bulky sensors or heaters at airway Ability to measure N2O Disposable sample line Can be used with nonintubated patients

Disadvantages Secretions and humidity block sensor Sensor heated to prevent condensation Bulky sensor at patient airway Does not measure N2O Difﬁcult to use with non-intubated patients Cleaning and sterilization of reusable sensor Secretions block sample tubing Water trap required Slow response to CO2 changes Sample ﬂow may decrease tidal volume

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trauma and burn injuries, and high carbohydrate intake. Conditions that decrease V˙CO2 include hypothyroidism, hypothermia (if shivering is controlled), sedation, and paralysis. Carbon dioxide from tissue metabolism diffuses into the circulation, producing a mixed venous PCO2 (Pv¯CO2) of about 45 mmHg. The PCO2 of an individual lung unit depends upon the relationship between ventilation ˙ ) (Fig. 5) (161 – 167). With no perfusion (dead space; and perfusion (V˙/Q ˙ ¼ 1), the PaCO2 is the same as the inspired PCO2 (i.e., zero). With a ˙V/Q ˙ , the PACO2 is the same as the arterial PCO2 (i.e., 40 mm Hg). normal V˙/Q ˙ , the PACO2 increases towards the Pv¯CO2 (i.e., 45 mm Hg). With a low V˙/Q The PACO2, and thus the end-tidal PCO2, must always be between zero and ˙ throughout the lungs, the end-tidal PCO2 the Pv¯CO2. With a variety of V˙/Q (PETCO2) is normally several mm Hg less than the PaCO2. However, the relationship between the PaCO2 and PETCO2 will vary depending upon the relative ˙ units of the lungs. contributions of various V˙/Q The volume-based capnogram is displayed with PCO2 on the ordinate and volume on the abscissa (Fig. 6). At the beginning of exhalation, PCO2 remains zero as gas from the anatomic dead space leaves the airway (Phase I). The capnogram then rises sharply as alveolar gas mixes with dead space gas (Phase II). The capnogram then forms a plateau during most of exhalation (Phase III). Phase III represents gas ﬂow from alveoli and is thus called the alveolar plateau. ˙ status of the lung (163,168 – The slope of Phase III is determined by the V˙/Q 171). The slope of Phase III is increased in patients with airway obstruction (e.g., COPD, asthma). The PCO2 at end-exhalation is the PETCO2. Airway dead space volume (anatomic dead space), physiologic dead space fraction (VD/VT), and V˙CO2 can be determined from the volume-based capnogram (Fig. 6). If V˙CO2 is known, it is possible to calculate metabolic rate: _ REE ¼ VCO 2 5:52 1440 where REE is resting energy expenditure (kcal/d), V˙CO2 is in L/min, 5.52 is the caloric equivalent for CO2, and 1440 is the number of minutes in a day. The

Figure 5

˙ , normal V˙/Q ˙ , and high V˙/Q ˙. PETCO2 with low V˙/Q

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% CO2

Alveolar dead space

Carbon dioxide production

VD

VALV Exhaled Tidal Volume

Figure 6 Components of volume-based capnogram. Abbreviations: VD, anatomic dead space; VALV, alveolar gas volume.

mixed exhaled PCO2 (PE¯ CO2) can be calculated from V˙CO2 if the minute ventilation (V˙E) is known: PE¯ CO2 _ _ VCO 2 ¼ VE Pbar

or PE¯ CO2 ¼

_ VCO 2 Pbar V_ E

where Pbar is barometric pressure. The VD/VT can then be calculated if the PaCO2 is known: VD Pa CO2 PE¯ CO2 ¼ VT Pa CO2 Increased VD/VT has been associated with mortality in patients with ARDS (172). Increased VD/VT has also been associated with a lower rate of weaning from mechanical ventilation (173). For critical care applications, the time-based capnogram is often displayed (Fig. 7). Unlike the volume-based capnogram, the time-based capnogram has an inspiratory segment and an expiratory segment. The PCO2 is zero during the inspiratory phase. At the beginning of exhalation, PCO2 remains zero as gas from the anatomic dead space leaves the airway (Phase I). The capnogram then rises sharply as alveolar gas mixes with dead space gas (Phase II). The curve then forms an alveolar plateau during most of exhalation (Phase III). The PCO2 at the end of the alveolar plateau is the PETCO2. Note that Phase I, Phase II, and Phase III are similar for the time –based capnogram and the volume-based capnogram. The capnogram with airﬂow obstruction is characterized by an increased slope of Phase III (Fig. 8). The lack of an alveolar plateau

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III

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end exhalation

II

I time begin exhalation

Figure 7 Time-based capnogram. I, anatomic dead space; II, the transition from anatomic dead space to the alveolar plateau; III, the alveolar plateau.

˙ abnormalities that result from the airﬂow obstruction. occurs because of the V˙/Q In asthmatic patients with acute bronchospasm, the slope of Phase III has been shown to correlate with peak expiratory ﬂow rate, and it normalizes with betaagonist therapy (170,171). The PETCO2 represents alveolar PCO2, and the PACO2 is the result of the ˙ . With a normal V˙/Q ˙ , the PACO2 will approximate the PaCO2. If ventilation V˙/Q is decreased compared with perfusion, there will be more time for equilibration between Pv¯CO2 and PACO2, and thus the PACO2 will rise towards Pv¯CO2. With a ˙ (i.e., dead space), PACO2 will approach the inspired PCO2 (PICO2), high V˙/Q

end exhalation

PCO2

III

II

I time begin exhalation

Figure 8 Capnogram produced with airﬂow obstruction.

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which is usually zero. The PETCO2 is a mixture of gas from millions of alveoli and thus represents the mixture of many potentially different PACO2. Theoretically, PETCO2 could be as low as the PICO2 (zero) or as high as the Pv¯CO2 (but not higher than this). An increase or decrease in PETCO2 can be the result of changes in V˙CO2 and delivery to the lungs (167,174), changes in alveolar ventilation, or an equipment malfunction (Table 3). However, because of homeostasis, compensatory changes may occur so that PETCO2 does not change despite these changes. For example, if V˙CO2 increases (such as with fever) and alveolar ventilation increases proportionately (the normal homeostatic response), then PETCO2 may not change. Thus, PETCO2 is a non-speciﬁc indicator of cardiopulmonary homeostasis and often does not indicate a speciﬁc problem or abnormality. If the PaCO2 is measured, the gradient between PaCO2 and PETCO2 (Pa2ETCO2) can be calculated. This gradient is normally small, being less than ˙ ), the PETCO2 may be 5 mm Hg. With dead space-producing disease (high V˙/Q considerably less than the PaCO2 (Table 4) (174 – 185). Although shunting may result in a large gradient between PAO2 and PaO2, it only has a small effect on the Pa2ETCO2. On occasion, the PETCO2 may be greater than the PaCO2. The reason for a PETCO2 greater than PaCO2 is not well understood (186) and may ˙ regions within the lung. Fletcher and Jonson relate to low (but ﬁnite) V˙/Q (162) have reported that PETCO2 is more often greater than PaCO2 when the tidal volume is high. Tulou and Walsh (187) found that the Pa2ETCO2 decreased signiﬁcantly when measured at maximal exhalation in patients with airway obstruction. With a larger tidal volume, the greater expiratory time may allow Table 3 Causes of Increased and Decreased PETCO2 Increased PETCO2 Increased CO2 production and delivery to the lungs Fever, sepsis, bicarbonate administration, increased metabolic rate, seizures

Decreased alveolar ventilation Respiratory center depression, muscular paralysis, hypoventilation, COPD Equipment malfunction Rebreathing, exhausted CO2 absorber, leak in ventilator circuit

Decreased PETCO2 Decreased CO2 production and delivery to the lungs Hypothermia, pulmonary hypoperfusion, cardiac arrest, pulmonary embolism, hemorrhage, hypotension Increased alveolar ventilation Hyperventilation

Equipment malfunction Ventilator disconnect, esophageal intubation, complete airway obstruction, poor sampling, leak around endotracheal tube cuff

Abbreviation: COPD, chronic obstructive pulmonary disease.

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Table 4 Causes of Increased Pa2ETCO2 Pulmonary hypoperfusion Pulmonary embolism Cardiac arrest Positive pressure ventilation (especially PEEP) High-rate low-tidal volume ventilation Abbreviation: PEEP, positive end-expiratory pressure.

˙ (and thus a longer time constant) to empty (188). Jones lung units with a low V˙/Q et al. (189) found PETCO2 greater than PaCO2 during exercise and attributed this to an increase in PACO2 because of increased CO2 that is emitted into a lung volume becoming smaller during exhalation. Stability of the Pa2ETCO2 is necessary if PaCO2 is to be reliably predicted from PETCO2. Hoffman et al. (178) evaluated PETCO2 in critically ill patients during changes in mechanical ventilation and found that changes in PETCO2 did not correlate well with changes in PaCO2 and that the trends in PETCO2 were opposite of the trends in PaCO2 in some patients. Raemer et al. (181) found that the Pa2ETCO2 was too variable during anesthesia to allow precise prediction of PaCO2 from PETCO2. Russell et al. (182 – 184) found that changes in PaCO2 and PETCO2 were in opposite directions in a sizeable proportion of patients. Because of a ﬂuctuating and unpredictable Pa2ETCO2, caution must be used when predicting PaCO2 from PETCO2. Measurement of PETCO2 is a standard of care to determine proper endotracheal tube position (190 –196). Esophageal PCO2 may be high (5%) after exhaled gas ventilation following inadvertent gastric distention (192), but it drops to ,2% following six ventilations of the stomach. Ingestion of a carbonated beverage also results in an increased esophageal PCO2, but this rapidly decreases following 10 to 15 seconds of gastric ventilation (197). Capnography has also been reported useful to verify feeding tube placement (198). Typically, the onset of cardiac arrest results in a drop of PETCO2 to zero. With the initiation of CPR, there is an increase in PETCO2. PETCO2 correlates with cardiac output (199 – 202) (i.e., pulmonary blood ﬂow) and coronary perfusion pressure (203,204) during CPR. Kalenda (205) observed that PETCO2 decreased when a resuscitator became fatigued and that it increased when resuscitation was continued with another resuscitator. Garnett et al. (206) reported that PETCO2 increased immediately in patients who had a return of spontaneous circulation. Similar results were reported by Falk et al. (207) and Sanders et al. (208). Patients who were resuscitated had a PETCO2 of 15 + 4 mm Hg during resuscitation, whereas patients who were not resuscitated had a PETCO2 of only 7 + 5 mm Hg (208,209). Grmec et al. (210) reported that the initial PETCO2 was greater in patients with asphyxial cardiac arrest than in those with cardiac arrest due to ventricular ﬁbrillation or ventricular tachycardia.

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The relationship between the Pa2ETCO2 and VD/VT has been reported (161,162,185,211 –213). Fletcher et al. (162) reported that patients with increased alveolar dead space had an increased slope of the alveolar plateau on the capnogram. Yamanaka and Sue (185) reported that the Pa2ETCO2 correlated closely with VD/VT. A common clinical cause of increased dead space is pulmonary embolism, and there has been interest in the use of capnography in this setting (214 – 218). In a comparison of capnometry to angiography in the diagnosis of pulmonary embolism in 44 adult patients with chronic obstructive pulmonary disease (COPD), Chopin et al. (217) reported a sensitivity of 100% but a speciﬁcity of only 65% (i.e., a false positive rate of 35%). Although the negative predictive value was 100%, the positive predictive value was only 74%. The Pa2ETCO2 is usually increased when pulmonary embolism is present, but the gradient is also increased for a variety of other causes when pulmonary embolism is not present (e.g., any dead space-producing disease). Hatle (214) reported that Pa2ETCO2 measured at forced exhalation was more useful in the evaluation of acute pulmonary embolism. Eriksson et al. (216) and Verschuren et al. (218) extrapolated phase III of the volumetric capnogram to determine the PCO2 at 15% of the predicted total lung capacity and found that this was useful in the diagnosis of pulmonary embolism (Fig. 9). With maximal exhalation, the

Figure 9 The capnogram in a patient with a diagnosis of pulmonary embolism. This patient has a VT of 612 mL. The PaCO2 was 29 mm Hg, the PETCO2 was 22.7 mm Hg, and 15% of the predicted TLC was calculated to be 699 mL. The PETCO2 at this volume of was 23.5 mm Hg after extrapolation of phase III. This relatively high gradient theoretically separates a patient with pulmonary embolism from a healthy patient or a chronic obstructive pulmonary disease patient. Source: Vershuren F. Liistro G, Coffeng R, et al. Volumetric capnography as a screening test for pulmonary embolism in the emergency department. Chest 2004; 125:841– 850.

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gradient approached zero in patients with obstructive lung disease but remained high in patients with pulmonary embolism. There has been interest in the use of capnometry during weaning from mechanical ventilation (219–227). Most evaluations of the use of capnometry during weaning have been conducted on post-operative patients. It can be argued that the weaning of these patients is usually uncomplicated, that such patients require little monitoring during weaning, and that extrapolation of these data to difﬁcultto-wean patients is not valid. Perhaps more important, hypoventilation is often a late ﬁnding with respiratory muscle fatigue (such as might occur during weaning). Other clinical ﬁndings such as tachypnea, use of accessory muscles of breathing, and thoraco-abdominal paradox may be more sensitive indicators than an increase in PCO2 to indicate fatigue during weaning from mechanical ventilation. On the basis of the available evidence, however, routine capnometry cannot be recommended during weaning from mechanical ventilation. However, the use of capnometry in long-term weaning unit has been reported useful (228). Avoidance of hypercapnia remains a common treatment objective in the care of patients with head injury. Mackersie and Karagianes (229) evaluated the use of PETCO2 in 36 head-injured patients and reported good correlation between PETCO2 and PaCO2. Sharma et al. (230) reported a stable Pa2ETCO2 during neuroanesthesia. In contrast to these ﬁndings, others have reported that PETCO2 is not a useful predictor of PaCO2 in neurosurgical patients (231,232). Because many head – injured patients are young and free of lung disease (at least early in their hospital course), PETCO2 may be useful to monitor PaCO2. However, PETCO2 may not be a very good predictor of PaCO2 in these patients if acute or chronic lung disease is present or if pulmonary blood ﬂow is reduced secondary to hypotension or pulmonary embolism. Kerr et al. (233) found that PETCO2 correlated well with PaCO2 in patients without respiratory complications, but its clinical validity is questionable in patients who have the greatest need for PETCO2 monitoring (those patients with respiratory failure). Palmon et al. (234) reported that PCO2 could be more tightly controlled during transport when PETCO2 was monitored, but their data did not support routine use of capnometry during short transport times. In trauma patients intubated in the ﬁeld, Helm et al. (235) reported tighter control of PCO2 with the use of capnography. In this study, the incidence of normoventilation was greater and the incidence of hypoventilation was less with the use of capnography. Using volume-based capnography, it is possible to noninvasively measure cardiac output with the partial CO2 rebreathing technique (NICO, Novametrix, Wallingford, Connecticut, U.S.) (236,237). V˙CO2 is calculated on a breath-bybreath basis, and the differential Fick equation is applied to establish the relation ˙ ): between V˙CO2 and cardiac output (Q _ _ VCO 2 ¼ Q (Cv CO2 Ca CO2 )

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where Cv¯CO2 represents the CO2 content in mixed venous blood, and CaCO2 represents the CO2 content in arterial blood. CO2 rebreathing is performed for ˙ remains constant 35 seconds every 3 minutes (Fig. 10). Assuming that Q during the rebreathing procedure yields the following: _ _ DVCO 2 ¼ Q (DCv CO2 DCa CO2 ) where DV˙CO2 is the change in V˙CO2 between normal breathing and rebreathing, DCv¯CO2 the change in mixed venous carbon dioxide content, and DCaCO2 the change in arterial carbon dioxide content. If Cv¯CO2 remains constant during rebreathing, the following equation is used: _ _ DVCO 2 ¼ Q (DCa CO2 ) When end-capillary content (CcCO2) is used in place of CaCO2, pulmonary capillary blood ﬂow (PCBF), the blood ﬂow that participates in alveolar gas exchange,

Figure 10 Rebreathing cycle used by NICO to measure cardiac output using the partial rebreathing technique. Source: Courtesy of Novametrix, Wallingford, Connecticut, U.S.A.

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˙ , and the following equation is used: is measured rather than Q _ DVCO 2 ¼ PCBF (Cc CO2 ) Assuming that 2CcCO2 is proportional to DPETCO2, the following equation can be used: _ PCBF ¼ DVCO 2 =(S DPET CO2 ) where DPETCO2 is the change in PETCO2 between normal breathing and rebreathing and S is the slope of the carbon dioxide dissociation curve for hemoglobin. Because cardiac output is the sum of PCBF and intrapulmonary shunt ﬂow: _ ¼ Q

PCBF _ t) _ s =Q (1 Q

˙ s/Q ˙ t is the intrapulmonary shunt fraction. The noninvasive method for where Q ˙ t is adapted from Nunn’s iso-shunt plots, which are a series of con˙ s/Q estimating Q tinuous curves indicating the relation between PaO2 and FIO2 for different levels of shunt. PaO2 is non-invasively determined using a pulse oximeter. There are several potential limitations of partial rebreathing for the measurement of cardiac output. In non-paralyzed patients, rebreathing increases respiratory rate, which reduces the magnitude of the signal and limits the ability to detect changes in PETCO2 and V˙CO2. Noise is increased by respiratory pattern irregularities that produce unstable PETCO2 and V˙CO2 that may impair accuracy. Additional cardiac output not calculated due to shunt fraction is estimated from SpO2 and FIO2, which introduces errors. Several studies have reported mixed results of accuracy of this method for measuring cardiac output (236 –245). X.

Lung Mechanics and Graphics

Pulmonary mechanics is the expression of lung function through measures of pressure and ﬂow (246). From these measurements, a variety of derived indices can be determined, such as volume, compliance, resistance, and workof-breathing. Pulmonary graphics are derived when one of the parameters of pulmonary mechanics is plotted as a function of time or as a function of one of the other parameters. This produces scalar pressure – time, ﬂow – time, and volume– time graphics as well as ﬂow –volume and pressure – volume (PV) loops. Current generation ventilators provide monitoring of pulmonary mechanics and graphics in real time. Bedside monitoring of mechanics and graphics during positive pressure ventilation typically portrays the lungs as a single compartment with a linear response over the range of tidal volume.

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Airway pressure is universally measured during mechanical ventilation. Peak inspiratory pressure (PIP) is predicted mathematically by the Equation of Motion (247,248): PAW þ Pmus ¼

VT þ R V_ þ PEEP C

where PAW is proximal airway pressure, Pmus the pressure generated by the respiratory muscles, C the respiratory system compliance, VT the tidal volume, R the airways resistance, V˙ the inspiratory ﬂow, and PEEP the end-expiratory alveolar pressure set on the ventilator. The Equation of Motion predicts that proximal airway pressure will increase with a higher tidal volume, lower respiratory system compliance, higher airways resistance, higher inspiratory ﬂow, higher PEEP, and the presence of auto-PEEP. Because of the airways resistance, proximal airway pressure will always be greater than alveolar pressure during inspiration if ﬂow is present. During volumecontrolled ventilation, plateau pressure (Pplat) is obtained by applying an endinspiratory breath-hold for 0.5 to 2 seconds, during which pressure equilibrates throughout the system so that the pressure measured at the proximal airway approximates the peak alveolar pressure (Fig. 11) (249,250). Pplat is not valid during active breathing and thus cannot be measured with ventilator modes such as pressure support ventilation. During pressure-controlled ventiation, the ﬂow may decrease to zero before the end of the inspiratory phase, in which case PIP and Pplat are equal. Pplat is determined by tidal volume, PEEP and respiratory system compliance: Pplat ¼ VT/C þ PEEP. Pplat indicates a greater risk of alveolar PIP resistance flow Pplat

compliance tidal volume

PEEP

time

Figure 11 Schematic representation of a pressure waveform during volume-controlled ventilation. The difference between PIP and Pplat is determined primarily by airways resistance and ﬂow. The difference between Pplat and the level of PEEP is determined by compliance and tidal volume. Abbreviations: PEEP, positive end-expiratory pressure; PIP, peak inspiratory pressure; Pplat, plateau pressure.

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over-distension during mechanical ventilation and should be maintained 30 cmH2O (251). However, a higher Pplat may be safe (and necessary) if chest wall compliance is decreased. During volume-controlled ventilation, the alveolar pressure at any time after the initiation of inspiration is determined by the volume delivered by that point in the inspiratory phase and respiratory system compliance: PALV ¼ V/C. For pressure ventilation, PALV at any time after the initiation of inspiration is (247): PALV ¼ (DP) (1 et=t ) where DP is the pressure applied to the airway above PEEP, e the base of the natural logarithm, t the elapsed time after initiation of the inspiratory phase, and t the time constant of the respiratory system. Incomplete emptying of the lungs occurs if the expiratory phase is terminated prematurely (252). When this occurs, alveolar pressure does not equilibrate with proximal airway pressure at end-exhalation, and gas trapping results. The pressure produced by this trapped gas is called auto-PEEP. Auto-PEEP increases end-expiratory lung volume (hyperinﬂation). It is measured by applying an end-expiratory pause for 0.5 to 2 seconds (Fig. 12). The pressure measured at the end of this maneuver that is in excess of the PEEP set on the ventilator is auto-PEEP. For a valid measurement, the patient must be relaxed and breathing in synchrony with the ventilator. Many patients with COPD contract their abdominal muscles during exhalation (253 – 255). This is an important determinant of auto-PEEP in these patients but likely does not produce hyperinﬂation. It has also been shown that the end-expiratory pause method can underestimate auto-PEEP with complete airway closure during expiration, as may occur during mechanical ventilation of patients with severe asthma (256). Auto-PEEP is a function of ventilator settings (tidal volume and expiratory

PIP

pressure

PIP

auto PEEP set PEEP time

Figure 12 Measurement of auto-PEEP with an end-expiratory pause maneuver. The difference between the pause pressure and the set PEEP level is the amount of auto-PEEP. Abbreviations: PEEP, positive end-expiratory pressure; PIP, peak inspiratory pressure.

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time) and lung function (airways resistance and lung compliance). It can be expressed mathematically as (247): auto-PEEP ¼

C

VT K (e x Te

1)

where Kx is the inverse of the expiratory time constant (1/t) and Te is the expiratory time. Note that auto-PEEP is increased with increased resistance and compliance (e.g., chronic obstructive lung disease), increased respiratory rate or increased inspiratory time (both decrease expiratory time), and increased tidal volume. Clinically, auto-PEEP can be decreased by decreasing minute ventilation (rate or tidal volume), increasing expiratory time, or decreasing airways resistance (e.g., bronchodilator administration). Because set-PEEP may counterbalance auto-PEEP in patients with ﬂow limitation, auto-PEEP should be meausured with PEEP ¼ 0. Esophageal pressure is measured from a balloon inﬂated with a small volume of air (,1 mL) placed into the lower esophagus (257). Esophageal pressure changes reﬂect changes in pleural pressure. However, the absolute esophageal pressure does not reﬂect absolute pleural pressure. Changes in esophageal pressure can be used to assess respiratory effort and work-of-breathing during spontaneous breathing, to assess chest wall compliance during full ventilatory support, and to assess auto-PEEP during spontaneous breathing. If an esophageal balloon is not present, changes in pleural pressure can be estimated by observing the respiratory variability of the central venous pressure (Fig. 13) (258). If exhalation is passive, the change in esophageal pressure required to reverse ﬂow at the proximal airway (i.e., trigger the ventilator) reﬂects the amount of auto-PEEP. Negative esophageal pressure changes that produce no ﬂow at the airway indicate failed trigger efforts (Fig. 14). Clinically, this is recognized as a patient respiratory rate that is greater than the trigger rate on the ventilator (observed by inspecting chest wall movement). The airway pressure waveform is affected by active breathing efforts of the patient. Patient – ventilator dyssynchrony results in an airway pressure waveform that varies from breath to breath, particularly during volume-controlled ventilation (250,257). A special form of patient – ventilator dyssynchony can occur during pressure support ventilation, in which the patient actively exhales to terminate the inspiratory phase (259,260). This is seen as a pressure spike at end-inspiration, causing the ventilator to pressure-cycle to the expiratory phase (Fig. 15). During volume-controlled ventilation, the inspiratory ﬂow is that set on the ventilator. During pressure-controlled or pressure-support ventilation, ﬂow is determined by the pressure applied across the lungs, airways resistance, and the time constant (261,262): DP _ V¼ (et=t ) R

Monitoring During Mechanical Ventilation Inhalation

positive pressure ventilation

131 Exhalation

mm Hg

18

Chest wall compliance

10

Inhalation Exhalation

mm Hg

spontaneous breathing

18

Inspiratory muscle effort

10

Figure 13 (Top) During positive pressure ventilation in a relaxed patient, the increase in CVP during the inspiratory phase is determined by chest wall compliance. (Bottom) During spontaneous breathing, the decrease in CVP during the inspiratory phase is determined by inpiratory muscle effort. Abbreviation: CVP, central venous pressure.

1

flow (L/s)

0

0.8

volume (L) 0 30

Paw (cm H2O) Peso (cm H2O)

0 20 0 estimation of auto-PEEP

missed trigger effort

Figure 14 Esophageal pressure measurements in a patient with auto-PEEP. Note that an esophageal pressure drop of about 10 cm H2O is necessary to trigger the ventilator. This represents an auto-PEEP level of about 10 cm H2O. Also note an inspiratory effort that is not great enough to overcome auto-PEEP and trigger the ventilator. It can also be seen that expiratory ﬂow does not return to zero before the subsequent breath is initiated.

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Figure 15 With pressure support ventilation, patients may terminate the inspiratory phase by actively exhaling. This produces an end-inspiratory pressure spike. In this case, the ﬂow does not decrease to the termination ﬂow, as represented by the dashed line. Source: Adapted from Ref. 259.

where DP is the sum of the pressure applied to the airway and the pressure generated by the respiratory muscles, R the airways resistance, t the elapsed time after initiation of the inspiratory phase, e the base of the natural logarithm, and t the product of airways resistance and respiratory system compliance (the time constant of the respiratory system). Expiratory ﬂow is determined by alveolar driving pressure (PALV), airways resistance, the elapsed time since initiation of exhalation, and the time constant of the respiratory system (248): PALV _ V¼ (et=t ) R

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133

A useful application of the airway ﬂow waveform is detection of autoPEEP. If the expiratory ﬂow does not return to baseline, this indicates the presence of auto-PEEP. Although the ﬂow waveform is useful to detect auto-PEEP, it does not quantitatively indicate the amount of auto-PEEP. Dips in expiratory ﬂow during patient-triggered ventilation (e.g., pressure support) indicate trigger efforts in which the patient’s inspiratory effort was insufﬁcient to overcome auto-PEEP to trigger the ventilator (Fig. 14). The use of ﬂow graphics to recognize the presence of auto-PEEP is useful, although the clinical examination can also be used to reliably detect the presence of autoPEEP (263). Critical care ventilators derive volume by integration of ﬂow. Because ﬂow is usually not measured directly at the proximal airway, volume output from the ventilator is less than the volume delivered to the patient due to conditioning of the inspired gas (warming and humidiﬁcation) and gas compression in the circuit. The volume waveform may be useful to detect a leak (e.g., bronchopleural ﬁstula), which results in a difference between the inspiratory and expiratory tidal volume. Respiratory system compliance (CRS) is assessed in mechanically ventilated patients as the tidal volume divided by the pressure required to produce that volume: CRS ¼

DV VT ¼ DP Pplat PEEP

Respiratory system compliance is typically 50 to 100 mL/cm H2O in mechanically ventilated patients and is determined by the compliance of the lungs and chest wall. Chest wall compliance is calculated from the change in esophageal pressure (pleural pressure) during passive inﬂation. Chest wall compliance is normally 200 mL/cm H2O and can be decreased due to abdominal distension, chest wall edema, chest wall burns, thoracic deformities (e.g., kyphoscoliosis), and an increase in muscle tone (e.g., a patient who is bucking the ventilator). Chest wall compliance is increased with ﬂail chest and paralysis. Lung compliance is calculated using the transpulmonary pressure; in other words, the difference between alveolar pressure (Pplat) and pleural pressure (esophageal). Normal lung compliance is 100 mL/cm H2O and is decreased with pulmonary edema (cardiogenic or noncardiogenic), pneumothorax, consolidation, atelectasis, pulmonary ﬁbrosis, pneumonectomy, mainstrem intubation, and hyperinﬂation. Lung compliance is increased with emphysema. During volume-controlled ventilation, inspiratory airways resistance can be estimated: RI ¼

PIP Pplat V_ I

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where V˙I is the end-inspiratory ﬂow. A simple way to make this measurement is to set the ventilator for a constant inspiratory ﬂow of 60 L/min (1 L/sec). Using this approach, the inspiratory airways resistance is PIP– Pplat. Other methods used to measure airways resistance (264) include interrupter techniques, least squares ﬁtting technique, and time constant of the respiratory system. Common causes of an increased airways resistance are bronchospasm, secretions, and a small inner diameter endotracheal tube. For intubated and mechanically ventilated patients, airways resistance should be ,10 cm H2O/(L/sec) at a ﬂow of 1 L/sec. Expiratory airways resistance is typically greater than inspiratory airways resistance. Mean airway pressure is determined by peak inspiratory pressure (PIP), the fraction of time devoted to the inspiratory phase (Ti/Ttot), and PEEP (265,266). For constant ﬂow volume ventilation, in which the airway pressure waveform is triangular, mean airway pressure can be estimated as (267). Ti Mean airway pressure ¼ 0:5 (PIP PEEP) þ PEEP Ttot During pressure ventilation, in which the airway pressure waveform is rectangular, mean airway pressure can be estimated as: Ti Mean airway pressure ¼ (PIP PEEP) þ PEEP Ttot The PV curve represents the static relationship between pressure and volume of the respiratory system (lungs, abdomen, rib cage, and respiratory muscles). It can be constructed using a number of techniques (268) that measure pressure as the lungs are inﬂated or deﬂated. A super-syringe can be used to inﬂate the lungs with step changes in volume, or the lungs can be inﬂated with a constant slow inﬂation (269,270). Volume is plotted as a function of pressure (Fig. 16). This measurement requires a completely relaxed chest wall, and thus the patient must be paralyzed for the best results. The respiratory system PV curve can be separated into the lung and chest wall curves by estimating pleural pressure with an esophageal balloon. In the normal respiratory system, the shape of the PV curve is nearly linear above the resting volume. The inﬂation and deﬂation curves demonstrate differences in their shape and pressure for a given volume (hysteresis). The inﬂation curve with acute lung injury begins with a ﬂat portion followed by a transition to a steeper, more compliant region (Fig. 16). This transition has been called the lower inﬂection point (PFlex). The curve continues with a linear progression and at its upper end undergoes another transition to a ﬂat region. This transition has been called the upper inﬂection point. On deﬂation a similar shape is achieved, but at a lower pressure than the inﬂation curve. In normal lungs, the lower PFlex has been equated with the closing volume, and the upper PFlex has been equated with overdistension (271). Determination of inﬂection points is often arbitrary and inaccurate. Methods have ranged from eyeball approximation to graphical curve-ﬁtting

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135

Figure 16 Pressure – volume curve during mechanical ventilation. Note that the curve is nearly linear in the normal condition. In ARDS, the curve demonstrates a lower inﬂection point and an upper inﬂection point. Abbreviation: ARDS, acute respiratory distress syndrome.

methods. Inter-observer variability in the determination of PFlex has been reported (272,273). Methods based on curve-ﬁtting equations may provide more accurate estimates of the inﬂection points (273,274). There has been enthusiasm for the use of PV curves to optimize ventilator settings with PEEP set above the PFlex and Pplat set below the upper PFlex. Recent observations and analysis of the PV curve in acute respiratory distress syndrome (ARDS) have changed its interpretation and implications for management. Two studies reported that the chest wall affects the PFlex and determination of the upper inﬂection point (275,276). These observations imply that the PV curve should be measured with an esophageal balloon to determine the inﬂection points for the lung alone. Because the PV curve represents the sum behavior of all lung units, and given the heterogeneity of lung injury, it might not be possible to determine an ideal point of recruitment or overdistention. Mathematical modeling data suggest that PEEP settings based on PFlex may not be adequate to ensure an open lung (277,278). XI.

Monitoring in Perspective

How much monitoring is needed? This is an important question for both clinicians and administrators. Clinicians often want to monitor everything possible, with a “more is better” attitude. On the other hand, administrators and managed care providers become justiﬁably concerned with the costs associated with monitoring. The presence of many monitors at the bedside can be very

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distracting to clinicians (279,280). Many monitoring systems beep, buzz, and blink constantly. The most frequent false-positive alarms have been reported from the pulse oximeter (281 – 284). Bentt et al. (283) found that a pulse oximeter alarm was present up to 47% of the time (28 min/hr) in a 10-bed surgical ICU, and many of these were false alarms and required no intervention (283). During anesthesia monitoring, Kestin et al. (284) found that 75% of all alarms that sounded were spurious, and only 3% indicated risk to the patient. In an adult ICU, monitor alarms were present 20% of the time, with an average peak sound level of nearly 80 dBA (the EPA recommends that noise levels in hospitals not exceed 45 dBA). The ﬁnancial impact of monitoring is difﬁcult to assess. For non-invasive monitors such a pulse oximeters, no prospective randomized controlled trials have evaluated cost effectiveness. Using a historical control and a relatively short evaluation period (2 mo), Kellerman et al. (285) reported a reduction in the number of ABGs ordered in an Emergency Department following the introduction of pulse oximetry. However, others have shown an increased number of ABGs when pulse oximetry was used (3). For mixed venous oximetry, Orlando (286) reported a savings of $75/patient. Pearson et al. (287), however, found that monitoring mixed venous saturation added signiﬁcantly to the cost incurred with a routine pulmonary artery catheter. Jastremski et al. (288) also found that mixed venous oximetry may not be cost-effective, particularly in a ﬁxed-payment reimbursement system. Monitoring should not be done just because it is technically feasible. Technical capability must be balanced against clinical usefulness and cost effectiveness. The decision to monitor, like any other clinical decision, should be based on therapeutic objectives.

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Lessard MR, Lofaso F, Brochard L. Expiratory muscle activity increases intrinsic positive end-expiratory pressure independently of dynamic hyperinﬂation in mechanically ventilated patients. Am J Respir Crit Care Med 1995; 151:562 – 569. Ninane V, Yerault J, de Troyer A. Intrinsic PEEP in patients with chronic obstructive pulmonary disease. Role of expiratory muscles. Am Rev Respir Dis 1993; 148:1037 – 1042. Leatherman JW, Ravenscraft SA. Low measured auto-positive end-expiratory pressure during mechanical ventilation of patients with severe asthma: hidden auto-positive end-expiratory pressure. Crit Care Med 1996; 24:541– 546. Truwit JD, Marini JJ. Evaluation of thoracic mechanics in the ventilated patient. Part II: applied mechanics. J Crit Care 1988; 3:199– 213. Chieveley-Williams S, Dinner L, Puddicombe A, et al. Central venous and bladder pressure reﬂect transdiaphragmatic pressure during pressure support ventilation. Chest 2002; 121:533 – 538. Parthasarathy S, Jubran A, Tobin MJ. Cycling of inspiratory and expiratory muscle groups with the ventilator in airﬂow limitation. Am J Respir Crit Care Med 1998; 158:1471 – 1478. Jubran A, Van de Graaff WB, Tobin MJ. Variability of patient-ventilator interaction with pressure support ventilation in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995; 152:129 – 136. Marini JJ, Crooke PS, Truwit JD. Determinants and limits of pressure-preset ventilation: a mathematical model. J Appl Physiol 1989; 67:1081 – 1092. Burke WC, Crooke PS, Marcy TW, et al. Comparison of mathematical and mechanical models of pressure-controlled ventilation. J Appl Physiol 1993; 74:922– 933. Kress JP, O’Connor MF, Schmidt GA. Clinical examination reliably detects intrinsic positive end-expiratory pressure in critically ill, mechanically ventilated patients. Am J Respir Crit Care Med 1999; 159:290 – 294. Hess D, Tabor T. Comparison of six methods to calculate airway resistance during mechanical ventilation. J Clin Monit 1993; 9:275 – 282. Marini JJ, Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance. Part 1: physiologic determinants and measurements. Crit Care Med 1992; 20:1461– 1472. Marini JJ, Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance. Part 2: clinical implications. Crit Care Med 1992; 20:1604 –1616. Primiano FP, Chatburn RL, Lough MD. Mean airway pressure: theoretical considerations. Crit Care Med 1982; 10:378 – 383. Brochard L. Respiratory pressure-volume curves. In: Tobin MJ, ed. Principles and Practice of Intensive Care Monitoring. New York: McGraw-Hill, 1998. Lu Q, Vieira SRR, Richecoeur J, et al. A simple automated method for measuring pressure – volume curves during mechanical ventilation. Am J Respir Crit Care Med 1999; 159:275 – 282. Servillo G, Svantesson C, Beydon L, et al. Pressure – volume curves in acute respiratory failure: automated low ﬂow inﬂation versus occlusion. Am J Respir Crit Care Med 1997; 155:1629 – 1656. Bigatello LM, Hurford WE, Pesenti A. Ventilatory management of severe acute respiratory failure for Y2K. Anesthesiology 1999; 91:1567– 70.

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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 1998; 44:1064 – 1068. Harris RS, Hess DR, Venegas JG. An objective analysis of the pressure– volume curve in the acute respiratory distress syndrome. Am J Respir Crit Care Med. 2000; 161:432 – 439. Venegas JG, Harris RS, Simon BA. A comprehensive equation for pulmonary pressure – volume curve. J Appl Physiol 1998; 84:389– 395. Ranieri VM, Brienza N, Santostasi S, et al. Impairments of lung and chest wall mechanics in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 1997; 156:1082– 1091. Mergoni M, Martelli A, Volpi A, et al. Impact of positive end-expiratory pressure on chest wall and lung pressure – volume curve in acute respiratory failure. Am J Respir Crit Care Med 1997; 156:846 –854. Hickling KG. The pressure-volume curve is greatly modiﬁed by recruitment. Am J Respir Crit Care Med 1998; 158:194 –202. Hickling KG. 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 lungs. Am J Respir Crit Care Med 2001; 163:69 –78. Morrison WE, Haas EC, Shaffner DH, et al. Noise, stress, and annoyance in a pediatric intensive care unit. Crit Care Med 2003; 31:113 – 119. Chambrin MC. Alarms in the intensive care unit: how can the number of false alarms be reduced? Critical Care 2001; 5:184 –188. Lawless ST. Crying wolf: false alarms in a pediatric intensive care unit. Crit Care Med 1994; 22:981 – 985. Tsein CL, Fackler JC. Poor prognosis for existing monitors in the intensive care unit. Crit Care Med 1997; 25:614 – 619. Bentt LR, Santora TA, Laverle BJ, et al. Accuracy and utility of pulse oximetry in the surgical intensive care unit. Curr Surg 1990; 47:267 –268. Kestin IG, Miller BR, Lockhart CH. Auditory alarms during anesthesia monitoring. Anesthesiology 1988; 69:106 – 109. Kellerman AL, Cofer CA, Joseph S, et al. Impact of portable pulse oximetry on arterial blood gas test ordering in an urban emergency department. Ann Emerg Med 1991; 20:130 – 134. Orlando R. Continuous mixed venous oximetry in critically ill patients. ‘High-tech’ cost effectiveness. Arch Surg 1986; 121:470– 471. Pearson KS, Gomez MN, Moyers JR, et al. A cost/beneﬁt analysis of randomized invasive monitoring for patients undergoing cardiac surgery. Anesth Analg 1989; 69:336– 341. Jastremski MS, Chelluri L, Beney KM, et al. Analysis of the effects of continuous on-line monitoring of mixed venous oxygen saturation on patient outcome and cost effectiveness. Crit Care Med 1990; 17:148– 153.

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5 Weaning from Mechanical Ventilation

DANI HACKNER

SHARAD DASS and MICHAEL I. LEWIS

Transitional Critical Care Service Cedars–Sinai Medical Center and Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

Division of Pulmonary and Critical Care Medicine, Cedars– Sinai Medical Center and Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

I.

Introduction

The process of weaning (liberating) patients from mechanical ventilation occupies a considerable portion of the total ventilator time, with estimates ranging from 40% to 60% (1). This chapter provides a comprehensive overview of important key topics related to weaning, such as pathophysiologic insights into weaning failure, predicting and optimizing weaning success, and methods of weaning, including protocol-driven approaches to weaning. A separate section addresses sedation in relation to weaning. Weaning from chronic mechanical ventilation includes the topics of tracheostomy and airway devices. A guide to discussing goals of therapy for the ventilated patient is also addressed. This chapter spans the mechanisms underlying weaning to the practical clinical steps for liberation from ventilation. The ﬁrst section addresses pathophysiologic processes that inform the weaning process and failure to wean. The second section, on “Predicting Weaning Success,” addresses the strengths and weaknesses of indices developed and attempts to place them in a clinical perspective. The third section, “Protocols and Pathways,” describes efforts to systematize the weaning process. The fourth section describes one tested protocol

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for “Weaning from Prolonged Mechanical Ventilation.” The ﬁfth section encompasses topics of comfort, analgesia, sedation, and delirium during weaning, which have great impact on duration of ventilation and patient satisfaction. The sixth and ﬁnal section, “Goals of Therapy: Conversations about Ventilation,” provides a bioethical rubric for initiation or terminating ventilation and weaning.

II.

Pathophysiologic Factors Determining Weaning Success or Failure: An Introductory Overview

A. Functional Force Reserve of the Respiratory Muscles

The concepts underlying a sustainable level of force by the respiratory muscles are keys to appreciating those factors determining the functional force reserve and endurance capacity of the respiratory pump. Skeletal muscles, including the respiratory muscles, can sustain repetitive loads for prolonged periods of time or indeﬁnitely, provided the forces generated during recruitment are below a critical threshold percentage of the maximum force generating capacity of the muscles in question. Transdiaphragmatic pressure (Pdi) is an index of diaphragm strength for which a critical threshold of 40% (Pdi breath/Pdimax) has been determined, above which there is a deﬁnite time limit to fatigue or task failure (2). For maximum inspiratory mouth pressure (an index of global inspiratory muscle strength), the critical ratio is 60%. The pressure (P) generated per breath reﬂects loads imposed, while the maximum pressure reﬂects the maximum “force” reserve. In the critical care arena and in the process of weaning, P breath may be increased, Pmax decreased, or both may co-exist, which can augment the P breath/Pmax ratio to levels at which sustainable ventilation is not possible, with ensuing task failure, unless the level of load is appropriately decreased and the weaning trial terminated. The tension – time index (TTdi) is the product of Pdi/Pdimax and duty cycle (inspiratory time/total respiratory time) and was reported by Bellemare et al. to be strongly related to diaphragm endurance capacity, blood ﬂow, and oxygen consumption (3 – 5). In normal subjects, the resting TTdi was 0.02, with 0.15 to 0.18 representing a fatigue threshold beyond which respiratory muscle fatigue ensued in less than 30 minutes (3). The pressure – time index utilizes inspiratory mouth pressures (in lieu of Pdi), embodies similar concepts, and has been reported in the literature in the context of weaning (6). B. Load vs. Capacity

A delicate balance exists in critically ill patients requiring mechanical ventilation between neuromuscular respiratory capacity and load, alterations of which can severely impact on respiratory pump endurance capacity. Respiratory neuromuscular capacity can be decreased by depressed respiratory drive and conditions or disorders producing weakness of the respiratory muscles. Enhanced loading

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Figure 1 Relationship between the tension-time index of the diaphragm, predicted time to task failure, and duration of trial of spontaneous breathing in weaning failure patients. Note progressive increment in tension-time index of the diaphragm as the weaning trial continued. Overt diaphragm contractile fatigue would likely have ensued if the trial had continued for another 13 minutes. Source: Adapted from Refs. 14,15.

of the respiratory system may be secondary to augmented respiratory drive, increased minute ventilation, and imposed elastic threshold or resistive loads (7) (Fig. 1). C. Respiratory Muscle Fatigue

Issues related to the development of overt contractile (peripheral) muscle fatigue and central fatigue (central reduction in respiratory drive) with ventilatory failure or with weaning failure are not well-deﬁned. Muscle fatigue is deﬁned as a condition in which there is loss in the capacity for developing force and velocity, resulting from muscle activity under load and which is reversible by rest (8). Clinically, respiratory muscle fatigue may be viewed as a condition in which the ability of the respiratory muscles to generate pressure and airﬂow is impaired. The latter is the result of heightened contractile activity of the respiratory muscles relative to strength and a decrease in energy supply. Finally, the impairment of respiratory muscle function would be expected to be improved by rest (i.e., complete unloading). By contrast, “muscle weakness” was deﬁned as “a condition in which the capacity of a rested muscle to generate force is impaired” (8). It should be noted that the fatiguing process may ensue prior to the inability to generate the required

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force; secondly, this point of exhaustion or task failure is dependent on a deﬁned end point which, in turn, depends on the balance between pump capacity and load. From the clinical perspective, task failure of the respiratory muscle pump may be viewed as the onset of ventilatory failure. Respiratory muscle fatigue has been classiﬁed as peripheral fatigue (includes contractile fatigue and neurotransmission fatigue) or central fatigue. Contractile fatigue refers to impaired contractile function of the muscle related to mechanisms occurring within the muscle ﬁbers themselves. These include disturbances in the sarcolemma, metabolic aberrations such as accumulation of Hþ and Pi, critical substrate depletion, and alterations in excitation—contraction coupling mediated by mechanical or chemical factors such as reactive oxygen species, nitric oxide, peroxynitrites, and cytokines, which can produce muscle ﬁber injury including sarcolemmal rupture, sarcomeric disruption, and cellular organelle dysfunction (9 – 11). Fiber injury may be associated with prolonged muscle impairment, peaking at 3– 4 days (12,13). Clinical data are sparse. Efthimiou et al. (14) reported data compatible with contractile fatigue of the sternomastoid muscles in 10% of patients with chronic obstructive pulmonary disease (COPD) admitted with acute exacerbations. With regard to weaning, Zakynthinos et al. (6) reported P breath/ PImax ratios of 0.42 + 0.11 in patients with acute respiratory failure upon discontinuation by mechanical ventilation, with pressure-time indices clustered around or exceeding a critical threshold of 0.15 to 0.18. Similar results have been noted for patients with COPD. Recently, Laghi et al. (15) evaluated diaphragmatic contractile responses non-volitionally (by phrenic nerve stimulation) in patients undergoing spontaneous breathing trials as part of a weaning regimen. Of interest, no change in twitch Pdi was observed in either successful or weaning failure patients, suggesting that in the failure group, no evidence of contractile diaphragm failure occurred at the point of termination of the weaning trial. It was also highlighted in the paper that many of the weaning failure patients had low twitch Pdis (i.e., diaphragm weakness). The data do not exclude a central component, as the increased loads presented to the weaning failure patients were not met with a concomitant increase in diaphragm recruitment. The authors also point out that the reason weaning failure patients did not develop low-frequency contractile fatigue was that mechanical ventilation was instituted prior to this becoming manifest (15). On the basis of some of the considerations summarized above (3), the authors predicted that fatigue would have been evident had the trial of spontaneous breathing continued for a further 13 minutes (14) (Fig. 2). D. Pathophysiology of Weaning Failure

Jubran and Tobin (16) studied respiratory mechanics in ventilated patients with COPD either passing or failing a trial of spontaneous breathing. Rapid shallow respirations were noted in the failure group at the onset of the trial. Further

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Figure 2 Interrelationships between respiratory pump capacity, load, and peripheral and central inﬂuences in relation to weaning from mechanical ventilation. Source: Adapted from Goldstone J and Moxham J. Weaning from mechanical ventilation. Thorax 1991; 46:56 – 62.

progressive increments in elevated inspiratory resistance, elastance, and intrinsic (auto) positive end-expiratory pressure (PEEPi) were noted between onset and end of the trial in the weaning failure patients. This culminated in a signiﬁcant increase in respiratory muscle energy expenditure as noted by a progressive rise in the pressure – time product (the time integral of the difference between esophageal pressure and chest wall recoil pressure). At the conclusion of the weaning trial, 76% of the weaning failure patients developed hypercapnia, which likely reﬂected inefﬁcient clearance of carbon dioxide due to abnormal breathing pattern and worsened pulmonary mechanics. In another study of weaning success or failure following a spontaneous breathing trial in ventilated patients, a progressive fall in mixed venous oxygen saturation (SvO2) was noted in the failure group, but not in those successfully weaned (17). The fall of SvO2 with weaning failure was because of a lack of increase in cardiac index and oxygen delivery (increased right and left ventricular afterload during spontaneous breathing trial), and enhanced oxygen extraction by the tissues.

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Evaluation and Treatment of Reversible Factors

A number of important factors need to be considered when liberation from mechanical ventilation is contemplated or when difﬁculties are encountered with the weaning process. These are outlined in Table 1. While the factors outlined in Table 1 are self-explanatory, a number of key issues will brieﬂy be emphasized. Respiratory muscle weakness and pump dysfunction are discussed in detail in the Chapter 7, Vol. 2 on neuromuscular respiratory failure, as are speciﬁc treatment modalities. PEEPi develops because of insufﬁcient expiratory time for exhalation to the normal relaxation volume of the respiratory system prior to the delivery of the subsequent mechanical breath (18). This results in dynamic hyperinﬂation and positive end-expiratory alveolar pressure. PEEPi increases the work of breathing, as the respiratory muscles must generate sufﬁcient force to overcome positive recoil pressures to initiate airﬂow. The level of PEEPi and imposed work may be reduced by measures that prolong expiratory time. In addition, in certain circumstances, trigger sensitivity may be reduced by the application of external PEEP to levels not exceeding 85% of PEEPi (19). Gottfried (20) provided practical recommendations for the use of external PEEP in patients with PEEPi. Although PEEPi can easily be measured on new generation ventilators, the measurement needs to be made under completely passive conditions, and increased abdominal muscle recruitment can falsely elevate measured levels (21). Further, inappropriate application of external PEEP can result in further dynamic hyperinﬂation and hemodynamic compromise (22). Also, increasing ﬂow rates to increase expiratory time and limit air trapping can result in a tachypneic response negating the positive beneﬁt (23). Dynamic hyperinﬂation secondary to air trapping imposes an increased elastic load on the respiratory system and can alter optimal diaphragm geometric conﬁguration, resulting in inefﬁciency of its action and reduced force generating potential. Thus, efforts to limit PEEPi and air trapping may signiﬁcantly curtail work of breathing. Recent studies have shown that heat and moisture exchanges for airway humidiﬁcation may increase work of breathing, PEEPi, PaCO2, and discomfort, requiring high levels of pressure support to offset (24). The use of a heat and moisture exchanger should, thus, be avoided in patients with borderline reserve and more conventional methods of heated humidiﬁcation employed. The issue of carbohydrate excess as a limiting factor in weaning success is a controversial one. This relates to high CO2 production with diversion of metabolic pathways to fat synthesis in which the RQ for lipogenesis is 8.0. Studies have shown, however, that high caloric feeding was more important than high percentage carbohydrate provision (25). Thus, moderate caloric intake, particularly in patients with limited reserve, is prudent. If necessary, energy requirements can be assessed using indirect calorimetry.

Weaning from Mechanical Ventilation Table 1

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Factors to Consider with Weaning Failure

Depressed respiratory drive Sedatives Analgesics including opiates Signiﬁcant metabolic alkalosis Hypothyroidism Central hypoventilation Obesity—hypoventilation Neurologic damage Respiratory muscle weakness Acute neuromuscular respiratory failure (e.g., Guillain Barre, myasthenic crisis) Chronic neuromuscular respiratory failure (e.g., amyotrophic lateral sclerosis) Critical illness polyneuropathy + myopathy Diaphragm paralysis High cervical cord injury Stressed and unstressed malnutrition/cachexia Electrolyte disorders (e.g., hypophosphatemia, hypomagnesemia, hypokalemia, hypocalcemia) Metabolic disturbances (e.g., respiratory acidosis, metabolic acidosis, compensated metabolic acidosis, hypoxemia, thyroid dysfunction) Drug inﬂuences (e.g., prolonged effects of paralytic agents, drug-induced myopathy or rhabdomyolysis, drug-induced myasthenic syndromes) Resistive loads Conditions associated with airﬂow obstruction Bronchospasm Thick copious secretions Blood clot obstruction Artiﬁcial airway (small endotracheal tube, kinking, biting, balloon herniation, mucus plugs or blood clot) Ventilator circuit and demand valves Elastic loads Reduced lung compliance (e.g., pulmonary edema, consolidation, ﬁbrosis) Reduced chest wall compliance (e.g., kyphoscoliosis, pleural disease, morbid obesity, abdominal distension/ascites) Dynamic hyperinﬂation Threshold loads Intrinsic (auto) PEEP Increased minute ventilation Increased dead space (wasted ventilation) Increased metabolic rate (fever, hypermetabolic states, excess calorie/carbohydrate provision) Pain Psychiatric disorders Anxiety Withdrawal states Cardiac disease LV dysfunction and failure Cardiac ischemia Inadequate reversal of original disease state

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Figure 3 Pathophysiologic inﬂuences impacting on the cardiovascular system upon withdrawal of mechanical ventilatory support in patients with underlying cardiac dysfunction. Abbreviations: PEEPi, intrinsic PEEP; Ppl, pleural pressure; PCWP, pulmonary capillary wedge pressure; VO2, oxygen consumption; MVO2, myocardial oxygen consumption. Source: Adapted from Ref. 7.

Patients with left ventricular dysfunction may beneﬁt from mechanical ventilation, which reduces preload, afterload, and possibly improves contractility. Cardiac compromise and ischemia may ensue upon liberation from mechanical ventilation (26,27). The complex pathophysiologic factors involved are well illustrated in Figure 3. III.

Predicting Weaning Success

The publication of over 400 putative weaning predictors has given way to increasing skepticism regarding the clinical utility of such parameters (28). Indeed, the purported beneﬁts of weaning parameters have recently been highlighted as a myth in an editorial entitled “Weaning the patient or weaning old-fashioned ideas”(29). Over 30 years of publications in this area have not yielded strongly reproducible results. Furthermore, the study groups have been small, and the data have generated unhelpful likelihood ratios (LR) and low predictive power (28). It has been suggested that physicians’ a priori clinical probabilities of success of weaning may affect the selection of patients and in turn the accuracy of the tests (28,29).

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A. Weaning Parameters

“Traditional weaning parameters” have entailed indications of gas exchange and indices of chest mechanics or breathing pattern. Gas exchange criteria have spanned dead space calculations to hypoxemia ratios. In general, the minimal acceptable PaO2 is 60 mmHg on a FIO2 of 0.4 and a PEEP less than 5 cmH2O. Other parameters of oxygenation that can be used include PaO2/PAO2 (.0.35), A2a O2 (,350 mmHg), or PaO2/FIO2 (.200) (30). Although adequate arterial oxygenation is essential to initiate weaning, the predictive value of these indices for the outcome of the weaning trial is usually low (31). Strict adherence to these criteria should not preclude liberating a patient from mechanical ventilation, if deemed clinically appropriate. Historically, indices of chest mechanics and respiratory pattern during spontaneous breathing have included vital capacity (VC) greater than 10 –15 mL/kg, spontaneous tidal volume (VT . 5 mL/kg), respiratory rate (RR , 35/ min), minute ventilation (VE , 10 –15 L/min), maximum voluntary ventilation (MVV) at least twice VE, and maximal inspiratory mouth pressure (PImax using, 215 to 230 cmH2O) (28,32,33). VC reﬂects not only lung and chest wall mechanics, but also respiratory muscle strength, albeit a non-speciﬁc marker particularly of the latter (see chapter 7, vol. 2 on neuromuscular respiratory failure). Pooled data for RR , 38 breaths/min has been analyzed with a LR of 1.1, indicating unchanged post-test probability and thus an unhelpful measure (28,34,35). By contrast, a RR . 38 breaths/min yielded a LR of 0.32, indicating a somewhat reduced probability of weaning success (28,34,35). A high VE may reﬂect an increased dead space, load, and work of breathing. PImax is a measure of global inspiratory muscle strength and is limited by the need for patient cooperation, coordination, inﬂuences of lung volume, and wide inter- and intra-subject variability (see chapter 7, vol. 2 on neuromuscular respiratory failure). While a one-way valve has been utilized to circumvent some of these hindrances, its use has been limited (36). (This valve permits only expiration, while the most negative pressure generated by inspiration against an occluded airway over a 20-second period is recorded as PImax.) Table 2 depicts sensitivity and speciﬁcity for several of these traditional indices. “Newer studies” have attempted to improve the robustness of weaning tests by either grouping variables or by seeking more speciﬁc physiological correlates. Several integrative weaning indices and unique parameters will be brieﬂy discussed. Yang and Tobin developed the commonly employed rapid shallow breathing index (RSBI) after discovering that patients who failed weaning developed tachypnea and decreasing VT almost immediately upon discontinuation of ventilatory support (37). The RSBI was measured after one minute as the ratio of frequency to VT while breathing spontaneously (33). Using 105 (breaths/ min)/L as the threshold, the sensitivity was 97% for predicting weaning success, whereas the speciﬁcity was 64%, indicating that 36% with an RSBI , 105 failed the weaning trial (i.e., false-positives) (33). While pooled

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data from six studies yielded similar sensitivities for RSBI, with a range of 87– 97%, speciﬁcities were generally lower (mean: 47%; range: 33 – 60%) (28). Furthermore, sensitivity for RSBI decreased with increased duration of mechanical ventilation (33), whereas speciﬁcity was inﬂuenced by disease state (38). For example, speciﬁcity of RSBI in patients with COPD was 65%, while in patients with neurologic disease or acute respiratory failure of varying etiology, the speciﬁcity was 26% and 28%, respectively (38). An analysis of extubation failure by Epstein (39) showed that when weaning failed, despite an RSBI ,100 (i.e., falsepositive test), the mechanism was secondary to other comorbid processes and not the underlying respiratory disease alone. RSBI has been reported to be higher in females and patients with smaller endotracheal tubes, suggesting that the index threshold needs appropriate adjustment to speciﬁc patient populations and conditions (40). A threshold of 130 has been suggested as a more appropriate cut point in elderly patients (41). Krieger and Isber suggested that stability of the RSBI when measured serially from the onset of the weaning trial and for the subsequent two to three hours gains sensitivity and speciﬁcity. A number of integrative indices have been reported. The compliance, rate, oxygen, and pressure (CROP) index incorporates gas exchange, chest wall mechanics, and respiratory strength. CROP index ¼ [Dynamic compliance PImax (PaO2/PAO2)]/RR (33). This index had a lower sensitivity and speciﬁcity than the RSBI (Table 2). A weaning index based on ventilatory endurance and efﬁciency of gas exchange by Jabour et al. (42) yielded high predictive value; however, it is cumbersome to calculate and was based on a limited number of patients. With airway occlusion, the ratio of the pressure generated with the ﬁrst breath (PI) to the pressure Table 2 Predictive Indexes of the Outcome of Weaning From Mechanical Ventilation Index Spontaneous minute ventilation (VE) Spontaneous Respiratory frequency (RR) Spontaneous tidal volume (VT) Spontaneous VT/body weight Maximal inspiratory pressure (PImax) Dynamic compliance Static compliance PaO2/PAO2 ratio RR/VT (RSBI) Compliance, rate, oxygen, and pressure (CROP) index Source: Adapted from Ref. 33.

Threshold value

Sensitivity Speciﬁcity

15 L/min

0.78

0.18

38/min

0.92

0.36

325 mL 4 mL/kg 15 cmH2O

0.97 0.94 1.00

0.54 0.39 0.11

22 mL/cmH2O 33 mL/cmH2O 0.35 105 13 mL/(breath/min)

0.72 0.75 0.81 0.97 0.81

0.50 0.36 0.29 0.64 0.57

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generated after 20 seconds of airway occlusion (PImax) has been evaluated as an index of respiratory pump reserve with a threshold value less than 0.3 (43). Combining this index with RSBI, there was improved sensitivity of 81% and speciﬁcity of 93% (43). The occlusion pressure (P0.1), measured as inspiratory pressure 100 milliseconds after airway occlusion, is in part an index of respiratory drive and has been used as a weaning tool (44,45). Several studies in patients with COPD report weaning failure when P0.1 exceeded 6 cmH2O (44,45). The normal value is less than 2 cmH2O. One prospective study showed that P0.1 was a comparable predictor to RSBI and suggested that the combination of RSBI and P0.1 would even provide a better predictor (44). In contrast, Fernandez et al. (46) found bedside P0.1 and P0.1 RSBI of little value in predicting extubation failure. Experimentally, neural networks have been employed with some success (47). B. Novel Approaches Studied

A number of novel approaches have been studied but have not been adopted into common clinical practice. The oxygen cost of breathing (OCB), (deﬁned as the difference in oxygen consumption during spontaneous breathing and on mechanical ventilation), was evaluated with an OCB , 30% deemed a promising indicator (48,49). Evaluation of work of breathing (WOB) is theoretically attractive, with bed-side equipment available (50,51). WOB is fraught with possible errors deriving from assumptions of chest wall compliance, endotracheal tube resistance, and auto-peep. Further, it is invasive, requiring esophageal pressure measurements, and no general or patient population-speciﬁc thresholds are known. A non-invasive indicator of ventilatory load, quantitative assessment of rib cage – abdominal motion, uses respiratory plethysmography and has been studied by Tobin et al. (52) in a cohort of patients weaning from mechanical ventilation. While abdominal paradox was seen in both weaning success and failure patients, combined indices of abnormal rib cage and abdominal motion were elevated in weaning failure patients. A subsequent study suggested that abnormal rib cage and abdominal motion was related to increased load (53). Another somewhat more invasive approach requires an oral- or nasogastric tube. Gastric intra-mural tonometry is well suited to environments such as the intensive care unit. Intra-mural pH (pHi) may be estimated using tonometry devices or analysis of gastric juice (54 –56). With high loads, respiratory work load and blood ﬂow demand is high with blood ﬂow diverted from the splanchnic bed. A fall in pHi , 7.3 or a fall of .0.09 during spontaneous breathing suggests weaning failure (54 –56). VE recovery time has recently been touted as a new potential indicator of extubation outcome in preliminary studies (57). The shorter the recovery time to within 110% of baseline VE upon return to full ventilatory support, the greater the chance of weaning success.

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While weaning parameters are of limited value, especially when applied broadly, there may be a role for selective use of certain parameters. In some cases, diagnosis groups and demographics selection may inform the choice of parameters. Patients with recovering neuromuscular disease may beneﬁt from tracking of vital capacities, whereas these same patients may not beneﬁt from routine application of the rapid shallow breathing index, which lacks speciﬁcity. In contrast, emphysematous patients may beneﬁt from screening for tachypnea (RR . 38) and RSBIs. In some cases, thresholds values may need adjustment, such as RSBIs in women and the elderly. In more selected populations, such as long-term weaning patients, weaning parameters may facilitate non-physician-run protocols. In any application, diligent bedside clinical evaluation cannot be supplanted by current or historical “weaning parameters.”

IV.

Protocols and Pathways

A. Techniques and Best Practice

Attempts at standardization of the weaning process have been touted for over a decade (58). Early reports focused on the best practice techniques in weaning from ventilation. In one prospective, randomized trial of weaning by intermittent mandatory ventilation (IMV), outcomes of time to extubation were similar to Ttube (59). The authors concluded that protocols involving both approaches may be applied to clinically stable patients with success. Despite some early experience in acute surgical populations with IMV trials, weaning protocols involving T-piece trials or pressure support ventilation now appear to be superior to intermittent mandatory and are preferred for acute medical and surgical patients (60). However, for post-ICU long term weaning cohorts, protocols involving synchronized IMV plus pressure support have enjoyed success (61). Similar approaches have achieved promising results in certain special populations, such as spinal cord injury patients, with expected long duration of weaning (62). B. Practice Variation

Personal preference and variability of weaning practice has frequently been reported, and several randomized clinical trials have produced conﬂicting results regarding the best technique for carrying out the weaning process (63). Work done by the Spanish Lung Failure Collaborative Group in the 1980s demonstrated wide variation in regional weaning practice as well as reliance on AC and SIMV techniques during weaning—approaches linked to long durations of weaning (64). Esteban et al.’s analysis of international ventilation practices found remarkable similarity in approaches to maintenance ventilation but wide practice variation around weaning (65). Their group and others have demonstrated the superiority of not one but several approaches over AC or

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SIMV, including daily and multiple daily spontaneous T-tube trials and pressure support weaning (66). Some groups have applied multi-disciplinary processes aimed at the leading factors prolonging ventilator stay, such as ventilator-associated pneumonia (67). In other cases, technology for monitoring weaning progress has also been promoted. In one series, esophageal manometry was used adjunctively to keep patients on protocol (68). No differences in steps to weaning were observed; however, the monitoring technology appeared to give clinicians a greater conﬁdence with staying on protocol without an increase in protocol intolerance. In short, while QI tools, technology, and protocols may reduce variability in practice, a disciplined process and not a particular approach appears to be the salient message. C. To Wean or to Extubate?

Although improvements in time to wean have modestly improved on protocols, overall duration of ventilation has markedly decreased on some protocols (69). One explanation is that protocols enable practitioners to identify patients ready for rapid extubation without weaning. Saura et al. (69) studied the clinical consequences of a protocol that enabled “direct extubation” without a weaning technique, which was applied in 10% of their cohort and resulted in decreased duration of mechanical ventilation and ICU stay. Safe, direct extubation, and not weaning methods per se, appeared to be the factor linked to timely extubation. Similar rapid extubation strategies have been applied with nurse-directed protocols following cardiac surgery, and such protocols under various specialist direction are now standard of care (70). D. Substance over Style

Employing a systematic approach may be more important than the particular technique selected. Protocol-guided weaning usually performed by nonphysicians, with improvements in patient outcomes (durations of mechanical ventilation, incidence of ventilator-associated pneumonia, and frequency of complications), has gained popularity (63). Protocol-guided weaning by nurses and respiratory therapists appears safe and more rapid than physician-directed weaning (71). Respiratory therapists appear to “safely and efﬁciently” wean cardiac surgery patients from mechanical ventilation with a two-hour difference in ventilation time (favoring therapists over physicians) (72). Physicians, including housestaff, appear to accept these protocols when integrated into multidisciplinary practice (73). Protocols do produce dramatic cost reductions (71,74). Nursing care facilities are increasingly interested in such protocols as a regular part of a cost-saving and patient ﬂow strategy (74 – 76). These cost reductions have been achieved by reducing hours of ventilation by 40% to 50%, length of stay by approximately 30%, and acute physiology scores (presumably affecting acuity

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and stafﬁng). Interestingly, protocols do not appear to affect rates of reintubations or mortality (71,74). Nurses and respiratory therapists have been successfully involved in protocols involving educational interventions as well as standing orders for spontaneous breathing trials and pressure support reduction. Medical intensivists have also performed in a manner consistent with successful protocols, but respiratory therapists and nurses were able to implement protocols without physician supervision. In children, one report noted reductions in total ventilation time, weaning time, pre-weaning time, time to extubation, and time on FIO2 . 0.40; even after stratiﬁcation by diagnosis, differences in weaning time remained signiﬁcant (77). As in adults, differences in the incidence of reintubation were not found, and rates of new-onset tracheitis, subglottic stenosis, and pneumonia were not increased in children. Ely et al. identiﬁed common themes to these protocols: stabilization of a patient’s condition should prompt timely spontaneous breathing trials when safe. Strategies for patients who fail a trial of spontaneous breathing should focus on reversible factors, use of a well-monitored mode of mechanical ventilation such as pressure support, and repeat spontaneous trials daily: (1) consideration of all remediable factors (such as electrolyte derangements, bronchospasm, malnutrition, patient positioning, and excess secretions) to enhance the prospects of successful liberation from mechanical ventilation; (2) use of a comfortable, safe, and well-monitored mode of mechanical ventilation (such as pressure support ventilation); and (3) repeating a trial of spontaneous breathing on the following day (78). Through a careful, slow implementation process involving daily reminders, improved compliance with weaning protocols can be achieved (79). Calhoun and Specht describe three phases: optimizing the patient’s condition, assessing and evaluating the patient’s progress, and diagnostic testing (spontaneous breathing trials). In addition, Calhoun and Specht spell out the need for a professional and responsible monitor (nurse or respiratory therapist) (80). Where these elements are present, even without an explicit protocol, respiratory therapist, or nurse monitoring, such as in a closed, well-staffed teaching team run by physicians, outcomes have been reported as equivalent by Krishnan et al. (81). In a counterpoint to the Krishnan article, Tobin argues for caution in studies that compare against “usual care” (82). In contrast to the period when Esteban reported wide practice variation, during the current era, many physicians and other clinicians may have integrated elements of a successful protocol into daily practice. E.

Speciﬁc Approaches and Examples

Several protocols are available that have been shown in well-designed trials to efﬁciently wean most patients. After a spontaneous breathing trial, patients who appear to be doing well by clinical criteria or weaning parameters may be extubated, placed on t-tube, or ventilated with low-level pressure support. Usually the level of pressure support is 7 cmH2O. Trials on t-tube or pressure

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support may last 30 to 120 minutes. Little information is known about the optimal duration of spontaneous breathing trials, and these may safely last from 30 to 120 minutes (83). Many advocate a ﬂexible approach of spontaneous trials of 30 minutes or low-level pressure support (84). Where patients do not tolerate immediate low level pressure support or t-tube, a pressure wean or titration can take place. A pressure support titration can establish the minimal level to provide an adequate respiratory rate, tidal volume, and minute ventilation. Then titration can be followed by gradual reduction by 2 cmH2O every one to two hours. Patients weaned on consecutive days can often return to the last pressure support level tolerated. Two randomized studies found that, in difﬁcult-towean patients, synchronized intermittent mandatory ventilation may be even more effective (85,86). Other studies indicate that patients with prolonged ventilation be placed on a chronic weaning protocol, which usually involves slower, graded IMV reductions followed by pressure support reductions. Non-invasive ventilation has been touted as a means to improve weaning success, and studies have shown improvements in mortality (87). Unfortunately, weaning failures or the duration of mechanical support related to weaning were unimproved (88). One subgroup, chronic obstructive lung disease patients, appeared to demonstrate the greatest mortality reduction (88). In all, given the mixed results on ventilation, the Cochrane group still considers the data on non-invasive ventilation insufﬁcient to recommend its routine use in weaning. Additional detail is described in the AHRQ technology assessment (89). Automated, adaptive support ventilation techniques have been reported to facilitate fewer ventilator manipulations but produced no improvement in outcomes (90). In summary, reduction of practice variation at a single site through the use of protocols may produce reductions in duration of ventilation, despite differences in practitioners and details of protocols. Expert and evidence-based recommendations for acute weaning protocols have been summarized by Ely et al. in Table 3. The group provides guidance on essential content, development strategies, and implementation of protocol. V.

Weaning from Prolonged Ventilation

The long-term acute care (LTAC) setting may be the best setting for protocolized approaches. Scheinhorn et al. (61) reported signiﬁcantly shorter time to weaning than benchmarks and historical controls through therapist-implemented patient-speciﬁc (TIPS) weaning protocols. Scheinhorn’s protocol, trialed in over 250 patients and 9000 ventilator days at Barlow Respiratory Hospital and Research Center, emphasizes adherence with a rigid set of steps, after assessing for patient-speciﬁc issues with “readiness and tolerance screens.” While retaining patient-speciﬁc adaptations, such as undiagnosed hypoxemia (with blood gases), the overall emphasis is a “rigid codes of procedure” and a “mantra: assessment ! intervention ! assessment.” This fusion of process engineering and clinical judgment allows “the expertise of the physicians to be present at the

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Table 3 Weaning Protocol Recommendations Non-physicians should be included in the development and utilization of protocols related to weaning ICU physicians should utilize protocols for liberating patients from mechanical ventilation Clinicians should conduct SBTs at least daily to identify patients ready for liberation When a patient fails SBT, clinicians should consider reversible factors and attempt SBTs at least once daily with head of bed elevated 30 – 458 If faced with recurrent failures, consider early tracheostomy When a patient passes an SBT, prompt extubation should be considered For analgesia, agitation, and delirium, a protocol should be considered, including daily lifting of sedating medications For development of weaning protocols, consider: evidence-based goals, interactive education, audit, reminders, opinion leaders, and feedback Abbreviation: SBT, spontaneous breathing trial. Source: Adapted from Ref. 78.

bedside of weaning patients continuously,” (61,91). The algorithm is shown in Table 4. The algorithm features synchronized IMV weaning, followed by graded pressure support reductions, and increasing duration spontaneous breathing trials. VI.

Sedation

Modern state-of-the-art approaches to weaning include proactive approaches to deal with agitation, delirium and pain, which all affect the efﬁciency of the “weaning process.” Recently much emphasis has been placed on these key issues. Sedation of the ventilated patient is both a goal and process. For the ventilator-dependent patient, adequate oxygenation and safe ventilation can better be achieved with a comfortable and calm patient. Agitation plays a signiﬁcant role in ventilator dyssynchrony, increased oxygen demands, accidental selfextubation, and catheter removals (92,93). Furthermore, the delirium and disorientation, seen in 15% to 20% of general medical –surgical patients and as many as 80% of ventilated intensive care patients, must be resolved in order to adequately ventilate and eventually liberate the patient from the respirator (94,95). Severity of delirium has been associated with duration of ventilation and increased cost, independent of severity of illness, degree of organ dysfunction, admitting diagnosis, or the presence of nosocomial infection (96). Pain and analgesia may also complicate the sedation and weaning plan. In practice, tensions arise between the need to acutely respond to discomfort and the dangers of prolonged ventilation. Prolonged sedation may lead to muscle atrophy, venous stasis and thrombosis, pressure damage to soft tissues, and prolonged obtundation (97). Oversedation may increase duration of ventilation and costs (97,98). Daily reassessment of sedation may be as important as daily

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Table 4 TIPS Long-Term Weaning Protocol Initial ventilator setting If SIMV . 10 or PSV . 20, change to A/C Adjust PSV according to tidal volume measured Daily evaluation for “do not wean” signs Hemodynamic instability Pulse Temperature FIO2 requirement Vasopressor (dopamine) requirement PEEP requirement Other clinical reason Weaning assessment (5 min into each attempt) Respiratory rate Tidal volume O2 saturation Pulse Accessory muscle use Post-weaning RSBI After ﬁrst weaning attempt, For low RSBI (,80), advance to SBTs of increasing duration immediately or Graded SIMV or PSV reduction Graded SIMV reduction ﬁrst Graded PSV reduction Each step with weaning assessment Advance to SBTs of increasing duration Source: Adapted from Ref. 61.

breathing trials to reduce the duration of mechanical ventilation (99,100). Close attention to appropriate dosing intervals of sedatives and re-addressing continuous infusions may avoid prolonged ventilation and escalating drug costs (97). Costeffective “rational use guidelines” may be safely applied in a combination with academic detailing by pharmacists and critical-care consultants (101). A. Establishing a Comfortable Environment

Institutional, and especially ICU-related, causes of agitation should be considered for ventilated patients (93). Noise, light, temperature, insertion of suction catheters, and re-positioning are among the common disruptions for the ventilated patient, and the subsequent loss of contiguous, quality sleep may contribute to patient anxiety and possibly immune function (102). For the ventilated patient, frequent orientation and attempts to control environmental variables have been suggested but have not been well-studied.

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In the uncomfortable patient, after maximizing non-pharmacological approaches, ﬁrst exclude common physiologic causes. Hypoxemia, hypoglycemia, hypotension, pain, ischemia, and arrhythmias can present with non-speciﬁc agitation in the uncommunicative patient and may affect weaning success (93,103). Next, address pain and discomfort, associated with ventilation or other health conditions, prior to initiating sedatives that may preclude a pain assessment. Visual analog scales may be helpful, as family and caregivers may misapprehend patient pain levels (93,104). Unchecked stress responses to pain may also have negative clinical consequences (93). Because “continuous” sedation itself has been linked to poor outcomes, routine lifting or lightening of sedation should be attempted (103). C. Deﬁning the Sedation Goal for the Ventilated Patient

The Task Force of the American College of Critical Care Medicine (ACCM) of the Society of Critical Care Medicine (SCCM), the American Society of HealthSystem Pharmacists (ASHP), and the American College of Chest Physicians (ACCP) recommend goal-oriented therapy for sedation. Keys to success in reaching a sedation goal are frequent assessments and use of common language to describe levels of sedation and anxiety (Table 5) (105). Validated “subjective” scales, such as the Ramsay, Riker Sedation – Agitation Scale (SAS) and the Motor Activity Assessment Scale (MAAS), have been effectively used as part of protocol-driven sedation plans. Figure 4 shows a ﬂow chart with the SCCM/ASHP/ACCP approach. D. Choice of Sedating Agents for Ventilation

Several principles guide the choice of sedating medications. First, analgesics are indicated prior to initiating other agents that impair the expression or assessment of pain. Splinting, guarding, spasm, or rigidity may affect coordinated chest wall, abdominal, and diaphragmatic movement and lead to pulmonary dysfunction (92,93). Appropriate analgesia has been linked to reduced post-operative complications. Second, amnestic agents may prevent recall of painful or traumatic experiences during mechanical ventilation (106). Common ﬁrst line agents include benzodiazepines with excellent anterograde amnestic effects, as well as propofol and haloperidol (Table 4). Midazolam and lorazepam to a lesser extent have the potential for prolonged drug effect in a continuous infusion. Midazolam is rapid acting, but its metabolite may have a prolonged half-life after days of infusion, and lorazepam crystallizes easily and has been associated with acute tubular necrosis. Propofol, in a goal-oriented, protocolized approach, can provide comparable sedation to benzodiazepines and may allow rapid awakening (107). With propofol, clinicians should be on the alert for bradycardia, hypotension, myocardial depression, drops in intracranial

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Table 5 Recommendations for Analgesia, Sedation, and Delirium Analgesia Pain assessment with an appropriate approach on a regular basis Patients who can communicate: Encourage subjective (visual analog) scale Patients who cannot communicate: observe pain-related behaviors and the change in these parameters following analgesia Establish therapeutic plan and communicate to all caregivers Opioid analgesics: fentanyl, hydromorphone, and morphine are the recommended agents Scheduled opioid doses or a continuous infusion is preferred over an “as needed” regimen Fentanyl is preferred for a rapid onset of analgesia in acutely distressed patients Fentanyl or hydromorphone are preferred for patients with hemodynamic instability or renal insufﬁciency Morphine and hydromorphone are preferred for intermittent therapy because of their longer duration of effect NSAIDs or acetaminophen may be used as adjuncts to opioids in selected patients Ketorolac therapy should be limited to a maximum of ﬁve days, with close monitoring for the development of renal insufﬁciency or gastrointestinal bleeding Other NSAIDs may be used via the enteral route in appropriate patients Sedation Sedation of agitated critically ill patients should be started only after providing adequate analgesia and treating reversible physiological causes A sedation goal or endpoint should be established and regularly redeﬁned for each patient Regular assessment and response to therapy should be systematically documented The use of a validated sedation assessment scale (SAS, MAAS, or VICS) is recommended After seven days, consider the potential for opioid, benzodiazepine, and propofol withdrawals Doses should be tapered systematically to prevent withdrawal symptoms Delirium Haloperidol is the preferred agent for the treatment of delirium in critically ill patients Patients should be monitored for electrocardiographic changes when receiving haloperidol (QT interval prolongation and arrhythmias) Sleep Sleep promotion should include optimization of the environment and non-pharmacologic methods to promote relaxation with adjunctive use of hypnotics Source: Adapted from Ref. 93.

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Is patient comfortable or at goal?

Rule out and treat reversible causes

Nonpharmacologic Treatment

Assess pain / analgesia (Visual Analog Scale)

Assess agitation / sedation (Subjective Scale) Assess delirium (CAM-ICU Scale)

Reassess Daily Goal Daily Lifting of Sedation Taper if > 1 week and monitor for withdrawal Consider Continuous Infusion Versus Intravenous Push

Fentanyl, Hydromorphone, Morphine Midazolam, Lorazepam, Propofol Haloperidol UNLESS alcohol-related

Figure 4 Simpliﬁed ﬂow chart for sedation of mechanically ventilated patients. Source: Adapted from Ref. 93.

pressure, and hypertriglyceridemia. Etomidate, a non-benzodiazepine, nonbarbiturate agent used for intubations and anesthesia induction has been associated on repeat use with Addisonian crisis (108). Third, agents that may be used for anxiety and analgesia may precipitate or exacerbate delirium in the young or elderly. In general, clinical status permitting, sedation should be routinely lifted during ventilation to evaluate mental status. E.

Cost Implications of Sedation for the Ventilated Patient

A wide variety of acquisition costs are reported for these sedating medications, but studies on cost are mixed (109,110). On the other hand, sedation guidelines and systematic, multi-disciplinary approaches have been shown to reduce drug costs (from $81.54 to $18.12 per patient per day), ventilator time

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(317 – 167 hr), and the lengths of ICU stay (19.1 – 9.9 days) and total stay without a change in mortality (92). F. Preventing Anticipated Pain and Discomfort and Addressing the Unanticipated

Endotracheal tubes, non-invasive ventilation devices, thoracostomy tubes, catheters, airway suctioning, chest percussive therapy, dressing changes, immobilization, transfers, and re-positioning are all potentially painful and uncomfortable experiences as well. Interventions to improve comfort include: avoidance of endotracheal and thoracostomy tube traction, proper ﬁtting of non-invasive masks/adaptors, avoidance of pressure sores (especially with masks), allowing small leaks on leak compensating non-invasive devices (to avoid tight straps), and catheter infection and clot prevention techniques. Some small studies suggest specialized beds to prevent decubitus ulcers or to facilitate mobility (111). Head of bed elevation to prevent nosocomial pneumonia and acid suppression or mucosal protection for peptic ulcer prevention are now widely accepted to avoid ventilator-associated complications and attendant discomfort (112–114). G. Selection and Titration Analgesic Medications

Analgesics include opioids, non-steroidal anti-inﬂammatory drugs (NSAIDs), and acetaminophen. Agent selection in ventilated patients should be based on side-effects, potency, and cost. Spontaneously breathing patients on non-invasive mechanical ventilation or patients with inadequate mandatory backup rates may have precipitous declines in minute ventilation with opioid analgesia. Without pro-motility agents, patients may not tolerate enteral feeding. Multiple studies have reported the negative consequences of failure to feed early in ventilation. Gastric retention in those being fed may increase the risk of aspiration, especially in patients not placed in a semi-recumbent position. When protocols incorporating daily awakening from analgesia and sedation have been employed, analgesic titration have been more precise, total doses of narcotics were lower, and duration of ventilation and ICU stay were lower (115). H. Tolerance, Withdrawal, and Sedative Reversal

After prolonged ventilation and sedation, adaptation, tolerance, dependence, and withdrawal may occur. One report noted the phenomenon in ARDS patients, who presumably require large doses of sedatives (116). Studies of pediatric patients recommend that small daily opioid decrements may avoid withdrawal in this population. Long-acting agents may also mitigate withdrawal. Subcutaneous infusions have successfully been used for gradual weaning in children (92). Outside of acute respiratory compromise, class-speciﬁc reversal agents, such as naloxone and ﬂumazenil, should be avoided after prolonged treatment, in known analgesic dependence, and in patients prone to dysrhythmias (92).

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Similarly, one should avoid partial opioid agonists, such as butorphanol, buprenorphine, and nalbuphine. In addition to opiate or benzodiazepine withdrawal, clinicians should be vigilant about alcohol withdrawal. Overlooking the diagnosis of alcohol withdrawal and empiric treatment with neuroleptics has been shown to lead to adverse clinical outcomes (117). Vigilance for withdrawal signs and symptoms may avoid costly clinical misadventures, prolonged ventilation in an attempt to resedate, or potentially increased mortality. I.

Delirium

Delirium in the ICU has been associated with fewer “median days alive and without mechanical ventilation” (118). Delirium is also linked to higher incidence of cognitive impairment at hospital discharge and higher six-month mortality, even after adjusting for relevant covariates (118). The condition is also associated with 39% higher ICU costs (94). Long-term neuropsychological impairment is increasingly recognized following mechanical ventilation (119). Severely ill patients, elderly patients, children, and psychotic patients may become more confused with benzodiazepine sedatives. Other risk factors for delirium are listed in Table 6. The need for reliable interdisciplinary measures has led to increasing use of tools such as the Confusion Assessment Method (CAM-ICU) (120) For its treatment, haloperidol is generally well-tolerated and has anxiolytic properties. In patients with prior cardiac disease, the beneﬁts and risks of alternatives should be weighed. In general, patients on prolonged neuroleptics should be monitored for behavioral changes and for electrocardiographic abnormalities. Routine assessment and treatment of delirium, along with sedation and analgesia, should take place for the ventilated patient. VII.

Goals of Therapy: Conversations About Ventilation

Weaning is rarely an immediately successful procedure and should be viewed as a process taking days, weeks, or months. While many patients willingly pursue treatment of reversible causes of respiratory failure over many days or weeks, that sentiment is not universally true. Moreover, clinicians cannot consistently predict whether failure can be reversed or what patients would wish. Even where respiratory dysfunction can be improved, the time and complications attending ventilation and weaning may not be acceptable to all patients. In the end, the weaning process may yield unanticipated low levels of physical function. In order to initiate and continue a course of weaning, it is best practice to address the goals of therapy and the values related to those goals early in the weaning process (or even prior to ventilation if possible). This section provides a rubric to discuss patient wishes and construct clinical plans consistent with patient values. Most patients with known chronic respiratory disease have no discussion of goals of therapy prior to initiation of mechanical support (121). However, one

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Table 6 Risk Factors for Delirium Age over 70 yr Alcohol abuse (within a month) Analgesics or sedatives (benzodiazepines or narcotics) BUN/creatinine ratio .18 Cardiogenic or septic shock Central venous catheters Drug overdose or illicit drug use (within week) History of congestive heart failure History of stroke, epilepsy HIV infection Hypo- or hyperglycemia Hypo- or hypernatremia Hypo- or hyperthermia (fever) Hypo- or hyperthyroidism Liver disease (T-bilirubin .2 mg/dL) Malnutrition Physical restraints (including posey vest) Prior history of deperession Rectal or bladder catheters Renal failure (Cr . 2 mg/dL) Transfer from a nursing home Tube feeding or parenteral nutrition Visual or hearing impairment Source: Adapted from Ref. 95.

study suggests that the vast majority of patients in the inpatient setting do wish to discuss advance directives or goals of therapy (122). Some may have thought carefully about the possibilities but will usually not have had a prior experience with mechanical ventilation (Fig. 5). Moreover, studies report a dissociation between surrogate statements of wishes and those of the patient, especially in cases where a patient wishes not to be intubated/resuscitated (123). One approach to addressing goals is to use a structured approach to discussing goals and values with the patient to elicit speciﬁc values regarding ventilation. In a structured approach, the clinician explores the patient’s health status (baseline), minimal acceptable health status/outcome, willingness to sustain burdensome therapy, and expressed wishes regarding chances of success or duration of therapeutic trials. Then ventilation plans, intubations, extubations, and sedation strategies are adapted to the matrix of values (Table 7). Advance directives can be recommended based on a patient’s goals and values and may change as clinical probabilities or feelings about burden or duration of therapy changes. The ﬁrst concept in laying out goals is the burden of therapy. Prior to initiating mechanical ventilation, a patient should be willing to sustain the burdens of

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Figure 5 Flow chart of patients’ responses to questions about prolonged mechanical ventilation. Shown are the results of patients’ responses to three questions on preferences about prolonged mechanical ventilation. Similar questions asked about resuscitation. Source: Adapted from Hofmann: Ann Intern Med 1997; 127(1):1 –12.

mechanical ventilation for the expected duration of mechanical support. For a patient with late-stage amyotrophic lateral sclerosis, the decision to ventilate may be a lifelong one. On the other hand, with non-invasive options, tracheostomies, and small home ventilators, the option may be favorable for some patients (124,125). For an otherwise healthy young patient with pneumococcal pneumonia, the ventilation may be a brief, reversible occurrence. A second concept, minimal acceptable health status or minimal acceptable outcome, does not depend on a particular therapeutic intervention. For some patients, long-term tracheostomy and mechanical ventilation may be an acceptable and tolerable outcome. For others, nothing short of independence of mechanical devices and independent living is acceptable. For many patients, minimal acceptable health status can be expressed in terms of activities of daily living or as a setting (to be home, in assisted living, in a long-term ventilator facility, etc.). Certain patients may state their wishes in terms of a level of cognitive or neurological function (full cognition, the ability to walk, and the ability to communicate with family or loved ones). If the “minimal” acceptable outcome cannot be achieved, ventilation is not indicated. It is especially important to take into account religious and cultural values, as some patients and families make distinctions on initiating and withdrawing mechanical ventilation. When given the clinical probabilities prior to pursuing a path of mechanical ventilation, even those patients may not choose to embark on ventilation. The clinician’s role in the case of ventilation is to articulate whether the outcomes of ventilation are likely to achieve the health status.

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Table 7 Matrix for Addressing Goals and Values for the Ventilated Patient Concept (Status, goal, value) Baseline: Baseline health status or quality of life

Minimal acceptable outcome: Minimal acceptable health status or quality of life

Maximal burden of therapy: Maximal tolerable pain and suffering and possibly a speciﬁed duration

Common choices Unacceptable according to patient or valid health agent Unacceptable but patient/ proxy express religious belief that distinguishes between initiating and withdrawing Acceptable Declining (e.g., ALS patient)

Ventilation plan

Do not initiate ventilation; encourage Advance Directive Do not initiate; do not withdraw; may be appropriate to place DNAR order and not to initiate other “therapies” Proceed Enter discussions to establish “minimal acceptable outcome” Life at any level of function Proceed only if: medically for any duration achievable, medically LTAC dependence, stable indicated, burden of medically (e.g., end-stage therapy is acceptable along emphysema with dialysis) path to goal; consult Limited ADLs bioethics where futility Cognition, assisted living, considered; unachievable independent living, and outcomes: recommend other choices Advance Directive Freedom from ventilation Discuss ventilation and Comfort is paramount: establish plan for sedation. unwilling to experience If patient or proxy still pain or discomfort expresses unhappiness with plan or experienced trial of ventilation, consider ceasing ventilation/ Advance Directive Proceed with ventilation if Willing to sustain painful, outcome is achievable invasive, or debilitating processes to reach outcome Willing to proceed when Ventilate if clinical odds chances of success are_% exceed patient’s chances of success. Re-evaluate and adjust Advance Directive based on clinical prognosis. Willing to proceed for a Ventilate and meet again to duration of time (days) discuss with patient/proxy

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Thirdly, the concept of a patient baseline informs the discussion of ventilation goals. While a debilitated, end-stage emphysematous patient may recover from an episode of acute respiratory failure, mechanical support may not be acceptable if the baseline itself is unacceptable. For some patients, even a very low level of function, a poor health status, and a declining baseline are acceptable. For these cases, personal values of preservation of life at any cost may place providers in a quandary with respect to futile care and distributive justice. Finally, goals of therapy may change. With more data available to the medical team about clinical prognosis and probabilities of success, or with additional experience available to the patient or proxy about the conditions of mechanical ventilation, both recommendations and decisions may change. It is important to consider that clinical odds of success with ventilation may change bedside decisions. For instance, the cystic ﬁbrosis patient with multiple airway complications, recurrent and resistant nosocomial infections, and requirements for frequent chest physiotherapy may initially pursue all available respiratory support; after experiencing prolonged ventilator dependence and with a reasonable expectation of weeks or months of mechanical ventilation, the patient may now elect palliative care. Over time and with exposure to the medical setting, patients or their spokespersons may decide to forgo or initiate mechanical ventilation with a better understanding of their own values and the interventions clinicians offer.

Acknowledgment Special thanks to Lawrence Maldonado, MD, for his assistance with the “Goals of Therapy: Conversations About Ventilation” section and Table 7.

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6 Prolonged Mechanical Ventilation

SCOTT K. EPSTEIN

MICHAEL L. NEVINS

Department of Medicine Caritas– St. Elizabeth’s Medical Center and Tufts University School of Medicine Boston, Massachusetts, U.S.A.

Division of Pulmonary and Critical Care and Department of Medicine, Group Health Permanente University of Washington School of Medicine Seattle, Washington, U.S.A.

I.

Introduction

Most patients requiring invasive mechanical ventilation for acute respiratory failure are rapidly liberated from the ventilator after improvement or resolution of the acute precipitating illness. Nevertheless, approximately 5% to 20% of patients prove more difﬁcult to liberate taking many weeks to be successfully weaned or, in a smaller number of cases, proving impossible to remove from mechanical ventilation. The deﬁnition of prolonged mechanical ventilation varies whether one refers to those given by regulatory agencies or by investigators publishing in this ﬁeld. In earlier reports, patients with underlying obstructive lung disease, severe chest wall deformities, or neuromuscular disease comprised the majority of patients undergoing prolonged mechanical ventilation. More recently, the demographics have changed, with patients suffering from acute lung injury, prolonged acute hospitalization for multi-organ system failure, or post-operative complications making up the majority requiring prolonged ventilation (1). Prior to 1990, patients needing prolonged mechanical ventilation were almost exclusively cared for in intensive care units (ICUs). Patients requiring prolonged mechanical ventilation comprise a minority of the ICU patient population yet account for a disproportionately high percentage of ICU days, mechanical ventilation days, and ICU costs (2). Up to one quarter of patients requiring prolonged support were eventually discharged home while still needing invasive mechanical ventilation. Beginning in the early 1990s in the United States, the 187

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locus of care began to shift to acute hospital-based long-term weaning units or in free-standing, long-term acute care hospitals. A fundamental principal of these centers is that patients have recovered from their acute illness prior to transfer and thus need a lower intensity of care (including a lower nurse-to-patient stafﬁng ratio) (1). Although some patients are referred for long-term custodial care and some for training in domiciliary mechanical ventilation and airway care prior to their discharge home, most are admitted with a goal of liberation from mechanical ventilation. Therefore, this chapter will principally focus on weaning from prolonged mechanical ventilation. Special emphasis will be placed on the pathophysiology of weaning failure, identifying predictors of weaning outcome, and the techniques used to liberate patients from prolonged mechanical ventilation. This chapter will not examine patients who require prolonged mechanical ventilation for chronic progressive respiratory or neuromuscular disease. Neither will it cover the area of home mechanical ventilation. Recent reviews have expertly covered this important subset of patients requiring prolonged mechanical ventilation.

II.

How Is Prolonged Mechanical Ventilation Deﬁned and How Often Does It Occur?

An essential question concerning patients intubated for acute respiratory failure concerns the time at which a patient shifts from requiring mechanical ventilation as supportive care during the resolution of an acute process to requiring prolonged mechanical ventilation. Authors of earlier reports have deﬁned a period ranging from 24 hours to 29 days (3– 6). Alternatively, DRG 483 (the need for tracheotomy, not for head and neck cancer) has been used to deﬁne prolonged mechanical ventilation. If one excludes trauma patients, it is likely that the vast majority of DRG 483 patients require at least 21 days of mechanical ventilation. Indeed, the majority of experts in the ﬁeld have adopted the deﬁnition employed by the Centers for Medicare & Medicaid Services (CMS); a minimum six hours per day for 21 days (7). The deﬁnition of prolonged mechanical ventilation clearly inﬂuences the incidence of this entity. For example, a large international observational study conducted in 361 ICUs found that 25% of patients required more than seven days of mechanical ventilation (8). It has been estimated that 5% to 20% of all patients who require invasive mechanical ventilation will go on to require more than 21 days of ventilation (9– 12). As an example, in a cohort of nearly 600 medical patients admitted to a tertiary care intensive care unit, approximately 10% remained invasively ventilated at day 21 (13). Another approach to analysis is determining the absolute number of patients requiring prolonged mechanical ventilation. As an example, in 1985 there were 147 patients in Massachusetts who required mechanical ventilation for more than three weeks, which extrapolates to 6800 patients nationwide (14). A study performed a decade later in Massachusetts identiﬁed a similar

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number of patients requiring prolonged mechanical ventilation, subsequently arriving at a national estimate of 7250 patients (15,16). In 1990, the American Association for Respiratory Care and the Gallup Organization conducted a cross-sectional study using a randomly selected sampling of respiratory care directors and pulmonologists to determine the number of patients needing mechanical ventilation for at least six hours a day for 30 or more days (15,16). This study estimated that more than 11,000 patients in the United States required chronic mechanical ventilation. In contrast, the MEDPAR database of Medicare discharges noted .43,000 DRG 483 discharges in the United States in 1998 (17). Indeed, an estimated 88,000 patients (including those under age 65) were coded DRG 483 in an analysis of a National Inpatient Sample database (18). Numerous investigators have developed tools for predicting survival in the acute care setting. Carson and Bach determined APACHE II, SAPS II, MPM II, and the logistic organ dysfunction score in 182 patients with prolonged critical illness admitted to a long-term acute care (LTAC) hospital in the Chicago area. The investigators found that none of the four severity of illness indices distinguished well between patients who lived and those who died (19). In contrast, a retrospective study of four LTACs found that a model containing age and organ failure provided adequate discrimination between survivors and nonsurvivors (20). Examining predictors of one-year survival, Carson et al. (21) found a model containing age and prior functional status identiﬁed a group of patients at very high risk of death. Speciﬁcally, one-year survival was 5% for patients over 75 years old or those older than 65 who also had poor prior functional status. Recent interest has also focused on quality of life for patients with prolonged mechanical ventilation. As an example, 90% of patients with prolonged mechanical ventilation managed in the LTAC setting are not functionally independent at one year (22). Of those who survive and are capable of responding to survey interviews, the reported quality of life is good (23 –25).

III.

Who Requires Prolonged Mechanical Ventilation?

The etiology of acute respiratory failure likely plays a role in determining which patients go on to require prolonged mechanical ventilation. In a study of 183 patients with chronic obstructive pulmonary disease (COPD) and acute respiratory failure admitted to a medical ICU, 10.4% remained mechanical ventilated 21 days after intubation (26). In contrast, in the same ICU, the relative risk of remaining ventilated at day 21 was twice as high in patients intubated for acute lung injury (21 of 107) (27). In a prospective study of 23 long-term acute care hospitals, 1411 patients were admitted after a median of 25 days (range: 0– 273 days) of invasive mechanical ventilation at the referring acute care hospital (28). The average age was 72 years, and 50% were women. Seventy percent of patients were smokers, averaging 57 pack years. In this cohort, 43% had COPD, 54% coronary artery disease or congestive heart failure, and 20% neurologic disease. Among patients with respiratory failure

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secondary to medical illness (61% of the cohort), the precipitating etiology was bacterial pneumonia (34%), sepsis (21%), acute neurological disease (20%), acute exacerbation of COPD (17%), congestive heart failure (14%), and aspiration pneumonia (13%). In 39% of cases, respiratory failure followed a surgical procedure (44% cardiovascular and 22% gastrointestinal). Despite the advanced age of this cohort, other investigators have not found older patients to be at higher risk for prolonged mechanical ventilation compared with younger patients, after controlling for confounding factors (29,30).

IV.

Site of Care for Patients with Prolonged Mechanical Ventilation

Prior to 1990, nearly all patients requiring prolonged mechanical ventilation were cared for in the ICU, with 14% to 25% eventually being discharged home while still requiring mechanical ventilation (14,16). Subsequently, there was a proliferation of centers specializing in the care and weaning of patients with prolonged mechanical ventilation. These have taken the form of specialized units within acute care hospitals and freestanding LTAC or post-acute care hospitals. In a 10-year follow-up study, the percentage of patients receiving prolonged mechanical ventilation in an acute hospital setting decreased (from 62% to 18%), while the number of patients in post-acute care (from 22% to 46%) and long-term care (from 2% to 24%) facilities increased (15). One principle used to support the expansion of these centers is that patients have recovered from their acute illness prior to transfer and therefore require a lower intensity of care. As an example, nurse-to-patient stafﬁng ratios are typically lower in chronic ventilator facilities than in ICUs (31). This may have important implications because appropriate nursing care appears crucial for favorable weaning outcomes in COPD patients on invasive mechanical ventilation in the acute care setting (32). In a European investigation, the duration of mechanical ventilation increased from 7.3 to 38.2 days when the “index of nursing” (a measure of the effective workforce of nurses as deﬁned by both stafﬁng ratios and nursing qualiﬁcations) fell. Indeed, the average duration of mechanical ventilation decreased to 9.9 days when the initial index of nursing was restored. Additionally, patients are now transferred earlier and with a relatively high severity of illness (33). As an example, Scheinhorn et al. (34) originally reported on 421 patients admitted to their regional weaning center, observing a mean duration of mechanical ventilation of 49 days prior to LTAC transfer (34). In subsequent reports, the authors noted a signiﬁcant trend toward shorter duration of pre-admission mechanical ventilation (median: 33 days) and higher admission severity of illness scores (median APS of APACHE III: 32) (33). A recent preliminary update totaling 1600 patients described a continued, rising trend in severity of illness scores in their patients that had become comparable to those reported at the time of ICU admission

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(35). These single-center observations are supported by the ﬁndings in a multi-center observational study, where an average APACHE III acute physiology score of 36 was found at time of admission to the LTAC (28). These APACHE III scores should be interpreted in the context of a study of 116,000 patients admitted to 28 acute care ICUs in the Cleveland area where the median acute physiology score was only slightly higher at 41 (36). As patients with prolonged mechanical ventilation comprise a minority of those in acute ICUs, any one intensivist’s experience may be limited. The fundamental importance of the physician’s role in the care of patients with prolonged mechanical ventilation has been conﬁrmed. Indeed, the high rates of weaning success in certain venues indicate that some experts are adept at identifying patients likely to be successfully liberated (4,37,38). Physicians also inﬂuence many objective outcomes, including the rate of weaning from and the duration of mechanical ventilation, LTAC length of stay, and rates at which care is withdrawn from patients with terminal illness (39). Indeed, with increasing experience, reductions in the time for successful weaning from ventilation, lower mortality, and higher rates of discharge to home can be achieved (40,41). When considering patients transferred with prolonged mechanical ventilation, a minority of patients are referred for long-term custodial care (41), training in domiciliary mechanical ventilation, and airway care prior to their discharge home (37). The overwhelming majority of patients are transferred with a goal of liberation from mechanical ventilation. When full liberation from mechanical ventilation is not feasible, achievement of the alternative goals of nocturnal invasive mechanical ventilation or conversion to non-invasive ventilation may allow for successful discharge to home. Despite all efforts, there remains a small, stable subset of unweanable patients who are transferred home with complete mechanical ventilation.

V.

What Are the Outcomes for Patients Requiring Prolonged Mechanical Ventilation?

The characteristics of individual populations (age, severity of illness, etiology of acute respiratory failure, presence of multiple organ dysfunction, and comorbid conditions) signiﬁcantly affect patient outcomes and must be considered when analyzing this literature. Admission criteria can vary, with many facilities requiring that a patient be on mechanical ventilation for a minimum of three weeks and have failed at least two weaning attempts prior to their transfer to the LTAC (38,42). Various institutions have different levels of care they can administer, and their capabilities may affect their patient selection and outcomes. Some are equipped with operating rooms capable of providing day-surgery level services, whereas others maintain small ICUs with the ability for invasive hemodynamic monitoring should a patient become unstable after transfer. Centers lacking this capability may report a lower mortality if critically ill

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patients are transferred (and die) in an outside acute care facility. There are no randomized controlled trials comparing outcomes for patients cared for in acute ICU versus those managed in an LTAC. Gracey et al. (4,37) compared patients managed in their acute care ICU at the Mayo Clinic to similar patients requiring prolonged mechanical ventilation managed in their chronic ventilator-dependent unit (CVDU). Patients treated in the CVDU had a signiﬁcantly lower mortality rate (9.8% vs. 28.6%, P ¼ 0.001) after excluding patients with multi-organ failure to control for discrepancies between the two populations. Mortality rates range from 7% to 61% in single-center reports depending on the setting (acute care hospital vs. LTAC) and the deﬁnition of prolonged mechanical ventilation (Table 1). In a large multi-center trial of more than 1400 patients admitted to 23 LTACS around the United States, Scheinhorn et al. (28) noted a 26% mortality rate. Some investigators have focused on more long-term outcomes, such as one-year survival, because of the limitations noted above. Indeed, one-year survival ranges from just 23% to 38%, likely a reﬂection of underlying comorbid conditions, an ongoing debilitated state, and vulnerability to recurrent acute disease experienced by “short-term survivors” of prolonged mechanical ventilation (21,33). Other studies found that long-term survival was correlated with younger age and shorter pre-CVDU duration of mechanical ventilation (38). Patients who fail extubation are more likely to require prolonged mechanical ventilation. As an example, 12 additional days of invasive mechanical ventilation were required for a cohort of medical patients who needed reintubation after planned extubation (43). The need for reintubation also identiﬁes patients more likely to need tracheostomy and eventual transfer to a post-acute care facility (43 –45). Weaning success rates vary widely depending on the deﬁnition of success, the population studied, and the admission criteria applied by the unit under investigation. When looking at weaning success at hospital discharge, rates range from 25% to 82% in single-center studies (Table 1). In a prospective multi-center trial, 54% of 1411 patients (73% of hospital survivors) were characterized as successfully liberated from mechanical ventilation at the time of discharge from 23 long-term acute care units (28). Twenty-seven percent of survivors (20% of all patients admitted) remained ventilator-dependent at the time of hospital discharge. VI.

Why Do Patients Become Ventilator-Dependent?

There are numerous factors that may contribute to ventilator dependency in patients intubated for acute respiratory failure (Table 2). A. Systemic Factors

As noted above, patients with prolonged mechanical ventilation have persistently high severity illness (as assessed by APACHE acute physiology scores) and

Outcomes for Patients Requiring Prolonged Mechanical Ventilation

References

Year

Setting

n

Duration of mechanical ventilationb (days)

ICU care Sivak (150) Morganroth et al. (129) Spicher and white (5) Gracey et al. (4)

1980 1984 1987 1992

ICU ICU ICU ICU

15 11 245 104

14 30 10 29

7 27 61 42

Non-ICU care Indihar (41) Cordasco et al. (151) Gracey et al. (4) Scheinhorn et al. (34) Nava et al. (123) Gracey et al. (37) Latriano et al. (59) Gluck (42) Gracey et al. (38) Scheinhorn et al. (33)

1991 1991 1992 1994 1994 1995 1996 1996 1997 1997

PRCU Non-ICU CVDU RWC IICU CVDU RCF LTVF CVDU RWC

Median ¼ 36 ? 21 Mean ¼ 49 21 21 Mean ¼ 23 21 21 Median ¼ 33

33 25 9.5 28 29 9.8 50 38 8 29

171 99 61 421 42 132 224 72 206 1123

Mortality (%)

Weaned at discharge (%) 66 73 ? 53

Prolonged Mechanical Ventilation

Table 1

34 25 82 53 36 78 47 27 (at 42 days) 70 56a (Continued)

193

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Table 1

Outcomes for Patients Requiring Prolonged Mechanical Ventilation (Continued)

References Bagley and Cooney (40) Scalise et al. (152) Bach et al. (39) Carson et al. (21) Dasgupta et al. (58) Gracey et al. (153) Schonhofer et al. (154) Scheinhorn et al. (28)

Year 1997 1997 1998 1999 1999 2000 2002 2003

Setting RWC RWC LTAC LTAC ReSCU CVDU RWC LTAC

n 278 47 86 133 212 549 403 1411a

Duration of mechanical ventilationb (days) ? Mean ¼ 86 ? 14 ? ? Mean ¼ 41 Median ¼ 25

Mortality (%)

Weaned at discharge (%)

48 23 52 50 18 7 24 26c

38 62 34 35 60 60 68 54

a

Multi-center study. Duration of mechanical ventilation ¼ minimum time on ventilation prior to transfer. c Outcomes reported on 1037 patients. Abbreviations: CVDU, chronic ventilator-dependent unit; IICU, Intermediate intensive care unit; LTAC, long-term acute care facility; LTVF, long-term ventilator facility; NIMU, non-invasive monitoring unit; PRCU, prolonged respiratory care unit; RCF, respiratory care ﬂoor; ReSCU, respiratory special care unit; RWC, regional weaning center. b

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Table 2 Potential Causes for Ventilator Dependency Mechanical factors Increased work of breathing Reduced respiratory muscle capacity Critical illness polyneuropathy Steroid myopathy Disuse myopathy Isolated phrenic nerve/diaphragmatic injury (e.g., post-cardiac surgery) Imbalance between increased work of breathing and respiratory muscle capacity Metabolic/systemic factors Chronic comorbid conditions (e.g., malignancy, chronic obstructive pulmonary disease, immunosuppression) Overall severity of illness Non-pulmonary organ failure Poor nutritional status Iatrogenic Factors Imposed work of breathing from tracheotomy tubes Upper airway obstruction (e.g., tracheal stenosis) Recurrent aspiration Infection (e.g., pneumonia, sepsis) Psychological factors Sedation Delirium Depression Anxiety Process of care factors Absence of weaning protocols Inadequate nursing stafﬁng Insufﬁcient physician experience

frequently have important comorbid conditions (e.g., COPD) that likely contribute to persistent weaning failure. Indeed, a large proportion of patients transferred to an LTAC with prolonged mechanical ventilation ultimately require transfer back to acute care (46,47). In one study, of 97 patients (71 with prolonged mechanical ventilation) transferred to LTACs, 23% required readmission to acute care within 30 days of transfer (47). Patients with prolonged mechanical ventilation frequently have non-pulmonary organ failure, the presence of which is associated with poor outcome. In one study of 52 patients with prolonged mechanical ventilation and requiring hemodialysis, none were successfully weaned and only three survived (48). Chao et al. (49) studied 63 patients with severe renal dysfunction (creatinine .2.5 mg/dL) at the time of transfer to their regional weaning center. Forty of these patients were on renal replacement therapy at transfer, and hemodialysis was initiated in another 10 while at the

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LTAC. Patients with severe renal dysfunction were less likely to be successfully weaned (13% vs. 56%), and only four patients requiring renal replacement therapy were liberated from the ventilator. Cardiac disease often limits liberation from mechanical ventilation in the acute setting. Myocardial ischemia (often occult), left ventricular dysfunction, and pulmonary edema have all been documented during trials of spontaneous breathing (50 –55). Systematic examinations of cardiac factors have not been published in patients requiring prolonged mechanical ventilation. In a preliminary report, successful diuresis and weight loss were associated with weaning success in patients transferred to a regional weaning center (56). Poor nutritional status may contribute to prolonged mechanical ventilation by adversely affecting respiratory muscle function and the ventilatory response to gas exchange abnormalities, and by predisposing to infection (57). Indeed, several studies of prolonged mechanical ventilation have noted an association between hypoalbuminemia and weaning failure (58,59). B. Mechanical Factors

An extensive body of research has identiﬁed key mechanical factors related to weaning failure in the acute setting. These factors include abnormalities in respiratory drive, increased work of breathing (resistive, elastic, intrinsic PEEP), decreased respiratory muscle capacity, cardiovascular factors (ischemia, pulmonary edema), and psychological factors. Numerous studies performed in acute hospital settings have shown patients who fail weaning trials will usually have increased, not diminished, central respiratory drive (60 –63). Nevertheless, there are some patients with central nervous system disturbances or who are heavily sedated in whom weaning and extubation may be delayed (64 –66). In the large majority of patients who fail weaning trials, the problem lies in an imbalance between the inspiratory load and the capacity of the respiratory system (60,67,68). Patients failing weaning trials often develop a pattern of rapid, shallow breathing in the face of increased load (63). This pattern of breathing is seen within minutes of disconnection from the ventilator suggesting that diaphragmatic fatigue is not the primary mechanism involved, at least initially (69). Nevertheless, studies demonstrate that weaning failure in the acute setting is associated with a tension – time index (TTI) of .0.15, which is thought to represent the threshold beyond which respiratory muscle fatigue ensues (60,68,70). As in patients with shorter durations of ventilation, patients with a mean of 20 days who failed a trial of spontaneous breathing also developed or maintained values of the TTI in the fatigue zone (67). This possibility that fatigue might occur was further suggested by Cohen et al. (71), who noted EMG evidence suggestive of high-frequency diaphragmatic fatigue during failed weaning trials. Yet, in a study of eight weaning success and 11 weaning failure patients, Laghi et al. (72) measured twitch transdiaphragmatic pressure before and 30 minutes after spontaneous

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breathing trials lasting up to 60 minutes. The weaning failure patients did not develop low-frequency fatigue of the diaphragm despite considerable diaphragmatic weakness, and greater load and diaphragmatic effort. The absence of fatigue may have resulted from increased recruitment of ribcage and expiratory muscles or because of prompt reinstitution of ventilatory support (e.g., before fatigue could ensue). The issue of fatigue is not trivial, as some studies in normals indicate that it can take more than 24 hours to recover full diaphragmatic function (73). There is an emerging literature examining mechanical factors limiting weaning in patients with prolonged mechanical ventilation. Appendini et al. (74) monitored respiratory mechanics and diaphragmatic effort [using pressure – time product (PTP) and diaphragmatic TTI] in eight patients with COPD requiring prolonged mechanical ventilation. Respiratory muscle strength (maximal inspiratory, pleural, and transdiaphragmatic pressures) was found compatible with successful weaning but was countered by excessive load (increased PEEPi, pulmonary resistance, and PTP) (74). Gluck (42) noted that patients with prolonged mechanical ventilation demonstrated a pattern of rapid shallow breathing, increased resistance, increased dead space, elevated dead space, and a decreased compliance. Abnormalities in mechanics may not be overtly detectable. As an example, Reinoso et al. (75), using interrupter mechanics, detected supramaximal ﬂow transients after shutter valve release during passive expiration, indicating occult airways disease in six of 25 patients tested. Purro et al. (76) similarly evaluated 39 patients who had been intubated for more than three weeks, 28 with COPD and 11 who had undergone cardiac surgery [post-cardiac surgery (PCS)] complicated by diaphragmatic dysfunction. Control groups were made up of nine patients with severe, stable COPD (maintained with tracheotomies but not ventilator-dependent), and 11 PCS patients who had been successfully liberated from mechanical ventilation within 48 hours of their surgery. Eight of 28 COPD patients tolerated unsupported breathing for 60 minutes (WS-COPD), while the remaining 20 COPD patients (VD-COPD) and all 11 PCS patients (VD-PCS) failed (mean time to failure: 40 min) and needed reinstitution of ventilatory support. When compared with the stable COPD and WS-COPD patients, the VD-COPD group demonstrated reduced tidal volume, minute ventilation, maximal transdiaphragmatic pressure, and maximal inspiratory pressure. The VD-COPD group demonstrated an increase in central respiratory frequency, airway occlusion pressure at 0.1 seconds (P0.1), PEEPi, and pulmonary resistance. Similarly, when compared with the stable successfully extubated PCS patients, the VD-PCS group had reduced tidal volume and maximum inspiratory pressure (MIP), while demonstrating higher respiratory frequency and P0.1. Initially no differences were noted in the mean respiratory rates between the stable COPD, WS-COPD, and VD-COPD groups. In contrast, analysis of esophageal pressure tracings revealed untriggered breaths (trigger asynchrony) in eight of 20 VD-COPD patients, resulting in a “central respiratory frequency” 40% higher than measured from inspiratory

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ﬂow tracings (28 breaths/min vs. 20 breaths/min). As in investigations in the acute setting, the majority of VD patients, but no weaned or stable patients, had TTI values greater than 0.15 (Fig. 1) (77). The ﬁndings above demonstrate that ventilator dependence in prolonged mechanical ventilation results from of an imbalance between inspiratory load and respiratory capacity, that is, mechanisms similar to those operative in patients failing weaning in the acute setting. Nevertheless, it is uncertain if the underlying mechanisms leading to this imbalance are similar for the two populations. As an example, the potential for disuse atrophy of the diaphragm and other inspiratory muscles may be greater with prolonged mechanical ventilation. In fact, a large number of animal studies document the adverse effect of controlled mechanical ventilation on respiratory muscle function (78 – 82). These adverse effects, which include decreased strength, increased fatigue, alterations in contractile properties, remodeling, and myoﬁbril damage, can occur in less than 24 hours but appear to become more signiﬁcant with increasing duration of controlled mechanical ventilation. Sedated and paralyzed baboons demonstrated a 25% reduction in diaphragmatic strength and 36% in endurance after 11 days of controlled ventilation with large tidal volumes (83).

Figure 1 Plots of respiratory duty cycle (Ti/Ttot) and respiratory muscle effort (mean diaphragmatic pressure generated per breath divided by maximal diaphragmatic pressure, Pdi/Pdimax) for VD, W, and stable patients with either COPD or PCS. The product of the duty cycle and respiratory muscle effort is the TTI. Ventilator dependent patients had higher TTI values, usually greater that the 0.15 threshold thought to represent a fatiguing load on the respiratory system. Abbreviations: COPD, chronic obstructive pulmonary disease; PCS, post-cardiac surgery; TTI; tension time index; VD, ventilatordependent; W, weaned. Source: Adapted from Ref. 76.

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Steroid myopathy, alone (84) or in conjunction with paralytic agents (85,86), delayed reversal of paralysis following the use of neuromuscular blocking agents (87), and critical illness polyneuropathy have all been observed in patients with prolonged mechanical ventilation (88). Critical illness polyneuropathy may involve the diaphragm (89) and typically presents as failure to wean in patients recovering from sepsis and multi-organ system failure (90). Its occurrence has been tied to a higher in-hospital mortality rate and delayed rehabilitation (91). Spitzer et al. (92) prospectively performed electromyographic studies in 21 patients, without known history of neuromuscular disease, with prolonged mechanical ventilation who failed weaning trials. Sixty-two percent had evidence of acquired neuromuscular disease, half of which were consistent with critical illness polyneuropathy or steroid myopathy. Similarly, Coakley et al. (93) found that 95% of patients requiring seven or more days of intensive care had myopathic or neurogenic changes on muscle biopsy. Leitjen et al. (91) colleague studied 50 patients with at least seven days of invasive ventilation. The 58% of patients with EMG evidence of polyneuropathy were more likely to need prolonged mechanical ventilation and post-acute care. De Jonghe et al. (94) measured muscle strength at day 7 using the Medical Research Council Score, considering a score ,48 indicative of ICU-acquired paresis in a prospective clinical study of 95 patients without pre-existing neuromuscular disease (94). Patients with ICU-acquired paralysis took twice as long to wean from mechanical ventilation compared with those who did not acquire neuromuscular disease. The role of respiratory muscle dysfunction is further supported by studies showing an improvement over time in negative inspiratory force or maximal inspiratory pressure when comparing patients failing weaning and then subsequently at the time of weaning success (68,95). C. Iatrogenic Factors

Tracheotomies have been shown to reduce the work of breathing imposed by an artiﬁcial airway when compared with endotracheal tubes, though the impact on weaning success remains unclear (96). Whereas in the acute setting a majority of patients are ventilated through oral or nasal endotracheal tubes, most patients admitted to a chronic ventilator facility have tracheotomies in place (21,41). Indeed, in a large multi-center trial, 95% transferred to 23 LTACs came with a tracheotomy (28). Nevertheless, abnormalities of the upper airway resulting from complications of the artiﬁcial airway can contribute to ventilator dependence. Ten percent of patients with prolonged mechanical ventilation will develop tracheal injury despite the use of artiﬁcial airways with low-pressure, high-volume cuffs (97,98). Tracheal injury at or above the level of the tracheal tube is typically clinically silent until the time of extubation or decannulation. Rumbak et al. (99) identiﬁed 37 of 756 (5%) patients on prolonged mechanical ventilation who had evidence for distal tracheal obstruction contributing to ventilator dependence. All patients had transient elevations in peak airway pressures,

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and difﬁculty passing a suction catheter was uniformly present. Bypassing the obstruction using either a longer tracheal tube or tracheal stent allowed 35 of the 37 patients to be successfully liberated from mechanical ventilation within one week. Tracheostomies can also contribute to swallowing dysfunction and aspiration in patients on prolonged mechanical ventilation. Indeed, 50% of 83 patients had evidence of aspiration when studied using videoﬂouroscopic tapes of modiﬁed barium swallows. The majority of aspiration events were not accompanied by clinical evidence of respiratory distress (100). In another investigation of 35 patients, 83% had swallowing dysfunction by videoﬂouroscopy (101). Using scintigraphy to identify aspiration, Scho¨nhofer et al. (102) found a somewhat lower rate of aspiration (30%) among patients requiring prolonged mechanical ventilation. Aspiration may contribute to weaning failure by compromising lung function, increasing respiratory secretions, predisposing to ventilator-associated pneumonia, and possibly through compromising oral intake of nutrition. In the acute setting, increased duration of mechanical ventilation has been associated with increased risk of complications, including nosocomial infection. In their prospective observation study, Scheinhorn et al. noted that acquired infection was common: urinary tract infection (32%), lower respiratory tract infection (28%), Clostridium difﬁcile infection (18%), and central line infection (12%) (Fig. 2). Importantly, those who acquired lower respiratory tract infection had a longer length of stay, took longer to wean, were less likely to be

Figure 2 Effect of acquisition of lower respiratory tract infection on outcome for patients with prolonged mechanical ventilation. Patients with lower respiratory tract infection (gray bars) were less likely to be successfully weaned (wean %), were more likely to remain ventilator-dependent (vent %), and spent more days on mechanical ventilation and in the hospital than patients without lower respiratory tract infection (black bars). Lower respiratory tract infection occurred in 28% of 1411 patients admitted to 23 long-term acute care facilities. Abbreviation: LOS, length of stay. Source: Adapted from Ref. 103.

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liberated, and were more likely to remain ventilator-dependent at the time of LTAC discharge (103). Increasingly investigators have demonstrated that mechanical ventilation is complicated by psychiatric disturbances, including anxiety, agitation, and delirium (65,66,104– 106). The presence of these entities correlates with increased duration of mechanical ventilation and is frequently present in patients with prolonged mechanical ventilation (107,108). The potential importance of these entities is supported by studies showing that a weaning strategy using biofeedback techniques shortens the duration of mechanical ventilation (109). Rothenhausler et al. (110) treated seven patients with prolonged mechanical ventilation and psychomotor retardation associated with markedly depressed mood (DSM-IV criteria) with methylphenidate, a psychostimulant. Five of the seven patients had marked/moderate improvement in mood within three to four days and were discontinued from ventilatory support within eight to 14 days (110). D. Process of Care Factors

Data from several studies suggest that the ability of a center to liberate patients from mechanical ventilation is related to the caregivers’ skills with patients on prolonged mechanical ventilation (32,40,41). Bach et al. (39) compared outcomes for patients managed by either university- or community-based physicians. Comparable mortality rates were noted, but the duration of mechanical ventilation was reduced (39 days vs. 57 days, P ¼ 0.02), and there was a trend toward higher rates of weaning success (46% vs. 30%, P ¼ 0.14), for patients managed by the university-based physicians. Similarly, some investigators report improving rates of weaning success over time as caregivers gain increasing experience in managing patients with prolonged mechanical ventilation (40,41). Unit nursing and respiratory stafﬁng is important in determining ventilator dependence. As an example, Thorens et al. (32) studied patients with COPD with acute respiratory failure and noted a dramatic increase in the duration of mechanical ventilation (7 – 38 days) when the effective nursing staff decreased. Absence of a structured approach to weaning (a weaning protocol) may increase the number of patients requiring prolonged mechanical ventilation (10,111,112). As an example, Ely et al. (10) found that patients weaned by protocol were less likely to require .21 days of mechanical ventilation when compared to patients weaned by a traditional approach. Efforts to improve bedside communication between healthcare workers (113) and placing a weaning protocol on a handheld computer have also proved beneﬁcial in avoiding prolonged mechanical ventilation (114). Protocols directed at “non-ventilator” aspects of care, including reducing the amount of sedation administered (65,66) and improving glycemic control (115), also reduced the duration of mechanical ventilation in the acute setting.

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What Assessment Tools Are Available to Predict Weaning Outcome for Patients with Prolonged Mechanical Ventilation?

More than 50 distinct weaning predictors have been studied in an effort to foretell the outcome of weaning trials in the acute ICU setting (116,117). The rationale for using objective physiologic parameters is strong as prediction based on clinical gestalt alone is relatively inaccurate (118,119). More importantly, precise predictors would enable physicians to postpone weaning in patients likely to fail. Alternatively, predictors could be used to better identify patients ready to initiate weaning trials with a goal of hastening the process of liberation, thereby reducing the duration of mechanical ventilation. The latter goal is based on the association between increased duration of ventilation and complications (ventilator-associated pneumonia, airway injury, barotrauma, sinusitis, thromboembolism, and gastrointestinal bleeding), which further increase duration of stay, costs, and mortality (120,121). Recent analyses and evidence-based guidelines indicate that weaning predictors are insufﬁciently accurate to adequately inform decisionmaking in the acute ICU (117,122). Studies in patients requiring .21 days of mechanical ventilation have shown that respiratory mechanics used to predict weaning outcomes in acute patients may have some value among patients requiring prolonged mechanical ventilation (76,123). Nava et al. observed that lower maximal inspiratory pressure and higher central drive as measured by the airway occlusion pressure were predictive of weaning success among patients with COPD (76,123). Although the frequency tidal volume ratio was also signiﬁcantly different in patients with weaning success when compared with those of weaning failure, the mean values in the latter group were well below the threshold originally described by Yang and Tobin (69). As suggested by recent work, patients with COPD may be unable to increase their respiratory rates signiﬁcantly because of the mechanical constraints of expiratory-ﬂow limitation and hyperinﬂation. In this setting, a lower f/Vt threshold may yield more accurate predictions (124). Indeed, Scheinhorn et al. (125) used the frequency-to-tidal volume ratio to accelerate weaning progress through a therapist-implement protocol (125). Weaning success was nearly twice as likely when the f/Vt was ,80 compared with .120 (breaths/L)/min (Fig. 3) (126). Failure to appreciate respiratory efforts that do not trigger the ventilator or result in inspiratory ﬂow may lead to an underestimation of the respiratory rate and therefore the f/Vt ratio (76). Indeed, Chao et al. (127) noted an association between patient –ventilator trigger asynchrony and weaning failure in patients requiring prolonged mechanical. Nineteen of the 200 patients screened were noted to have trigger asynchrony. Interventions such as altering trigger sensitivity, changing to ﬂow triggering, and increasing external PEEP were unsuccessful in eliminating the trigger asynchrony. Only decreasing the level of pressure support was successful in

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Figure 3 Percentage of patients with weaning success based on the frequency to tidal volume ratio determined prior to the initiation of weaning efforts. Source: Adapted from Ref. 126.

extinguishing trigger asynchrony, but this maneuver imposed a “fatiguing” respiratory load and was poorly tolerated. Of the 19 patients with trigger asynchrony, only three (16%) were successfully liberated after 70 to 108 days compared with patients without trigger asynchrony who were successfully weaned 56% of the time after a median 33 days. In all likelihood, the presence of trigger asynchrony serves as a marker for severe disease of the respiratory system (abnormal mechanics, increased PEEPi, respiratory muscle weakness, or abnormal control of breathing). As noted earlier, an abnormal mental status has been associated with prolonged mechanical ventilation. Hendra et al., studying a cohort not receiving sedative infusions and half of whom had neurologic diagnoses, found that patients with a modiﬁed Glasgow Coma Scale score of ,8 were 6.5 times more likely to fail weaning (128). Because ventilator dependence may be multi-factorial, an approach that combines a number of factors and parameters (e.g., a scoring system) may prove superior in predicting weaning outcome for patients with prolonged mechanical ventilation. As an example, Morganroth et al. combined a “ventilator score” based upon six simply measured factors (FIO2, PEEP, static and dynamic compliance, set minute ventilation, and triggered respiratory rate) and an “adverse factor score,” calculated using 21 components, including vital signs, quantity and quality of secretions, level of consciousness, emotional state, and medications (129). During 11 episodes of prolonged mechanical ventilation, the investigators demonstrated an improvement in the combined score prior to the initiation of a successful weaning period. In contrast, two patients who died prior to weaning showed no improvements in their scores. To date this score has not been validated and appears cumbersome to determine.

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Gluck and Corrigan (42) studied 20 patients requiring prolonged mechanical ventilation to identify variables in univariate analysis that correlated with weaning outcome and determine threshold values (42). All patients were weaned using a standardized protocol, and patients unable to be weaned from mechanical ventilation after 42 days were classiﬁed as failures. The frequencyto-tidal volume ratio measured ﬁve minutes after removal of the patient from mechanical ventilation, dead space to tidal volume ratio, static compliance, airway resistance, and PaCO2 measured at the end of a trial of spontaneous breathing were integrated into a scoring system. This weaning score was then prospectively studied in an additional 72 patients, correctly classifying weaning outcome 84% of the time. No patient who failed to wean by 42 days on protocol was successfully weaned in the following six months. Scheinhorn et al. tested several scoring system models in a 170-patient validation group and identiﬁed the A þ B þ G score (P(A2a)O2, BUN, and Gender) as most predictive of weaning outcome, correctly classifying patients 70% of the time (6). A group of investigators has suggested that physicians are able to accurately predict both liberation from mechanical ventilation and survival in patients requiring prolonged mechanical ventilation (58). To date, none of these multidimensional approaches to predicting weaning success has been independently validated.

VIII.

What Is the Best Approach to Weaning Patients with Prolonged Mechanical Ventilation?

Fundamental criteria should be satisﬁed prior to weaning a patient from prolonged mechanical ventilation. Speciﬁcally, there should be signiﬁcant recovery from the acute illness that precipitated respiratory failure. The patient must have adequate gas exchange, be hemodynamically stable, and have neurological function that generates spontaneous respiration and airway maintenance. Unlike the acute setting (e.g., when an endotracheal tube is present), the capacity to protect the airway is not a limiting factor in weaning from prolonged mechanical ventilation. Airway integrity becomes crucial when the patient has been liberated from the ventilator and tracheotomy tube decannulation is under consideration. A search for potentially correctable conditions that can contribute to ventilator dependence needs to be undertaken in patients who repeatedly fail to tolerate weaning efforts. In the acute setting, daily spontaneous breathing trials (using T-piece) and pressure support weaning have been shown to be superior to traditional IMV weaning strategies (9,130). Uncontrolled experiences in patients with prolonged mechanical ventilation have noted the successful use of several approaches to weaning. Until recently there were no randomized, controlled trials investigating the use of different weaning modes for patients requiring prolonged mechanical ventilation. Vitacca et al. (131) randomized 52 COPD patients (with a minimum

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duration of mechanical ventilation 15 days, range: 15 –39 days) to weaning by either progressive reduction in pressure support level (PSV) or by tracheotomy trials of increasing duration. The authors found no difference when failure was deﬁned as either death or failure to wean by 30 days. Studies performed in the acute setting have demonstrate that standardization of the weaning process through the use of protocols can shorten the duration of weaning and the time spent on mechanical ventilation (10,111,112,132,133). Of note, the results of this approach in pediatric patients has produced conﬂicting results (134,135). Similarly, protocols shown to be effective in medical ICU patients were not efﬁcacious in neurosurgical patients (136) or in trauma patients (137). Interestingly, a recent study showed no difference between a weaning protocol and a standard approach in an acute ICU where intensivists were on site for a large proportion of the day (138). This scenario is unlikely to occur in the post-acute care setting where nurse- and respiratory therapist-to-patient ratios are lower and on site physician presence is likely to be less. The beneﬁcial effect of protocols may derive more from early identiﬁcation of patients capable of breathing spontaneously rather than an algorithmic reduction in ventilatory support, an observation that may also be applicable to patients with prolonged mechanical ventilation. Vitacca et al. (131) screened 75 COPD patients for their randomized controlled trial by allowing an initial trial of spontaneous breathing (131). Twenty-three (31%) patients did not need a slow process of liberation because they tolerated this initial trial of spontaneous breathing for at least 48 hours. Although several groups have investigated the application of weaning protocols to patients requiring prolonged mechanical ventilation, randomized controlled trials have not been reported. Gluck and Corrigan used a weaning protocol employing sequential reduction in both continuous positive airway pressure and PSV as part of an evaluation of predictors of weaning (42). In an uncontrolled study, Scheinhorn et al. (125) used a respiratory therapist-driven protocol and noted a reduction in the duration of mechanical ventilation (median: 29 days vs. 18 days, P , 0.05) and in the hospital length of stay (median: 53 days vs. 43 days, P , 0.05) after institution of the protocol when compared to historic controls (125). This protocol is notable because the frequency tidal volume ratio was used to identify patients in whom the weaning process could be accelerated. The protocol employed a 19-step gradual reduction of the synchronized intermittent mandatory ventilation rate and PSV level. For patients with a frequency to tidal volume ratio 80 breaths/min/L, the ﬁrst nine steps of weaning were bypassed, with patients advancing directly to a one-hour trial of spontaneous breathing. Vitacca et al. (131) compared 52 patients weaned by protocol (either tracheotomy collar or pressure support) to historic controls and found a higher 30-day weaning success rate and shorter duration of mechanical ventilation in the former (131). The frequent presence of respiratory muscle weakness in patients with prolonged mechanical ventilation has led some to investigate strategies for improving respiratory muscle strength and endurance. Aldrich et al. (95) used

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periods of spontaneous breathing through an adjustable nonlinear resistor with gradually increasing duration and resistance in patients on prolonged mechanical ventilation. Respiratory muscle training resulted in improved mean negative inspiratory force (37 – 46 cmH2O) and vital capacity (561 –901 mL) in 27 patients. Twelve of the patients (44%) were successfully liberated from mechanical ventilation over 10 to 46 days, with another ﬁve weaned to nocturnal ventilation (19%). A similar technique has been reported in the rehabilitation of three high quadriplegic patients who were ventilator-dependent (139). Martin et al. (140) studied 10 patients who had been ventilated for a mean of 34 days and had failed weaning for at least one week (140). Inspiratory muscle training consisting of four sets of six breaths through a threshold resistor were combined with tracheotomy collar trials of increasing duration. Using this approach-nine of 10 patients were liberated from mechanical ventilation after a total of 44 days. These studies did not utilize a control population, so it is difﬁcult to attribute the patients’ improvement to the muscle training where the same number may have been liberated from mechanical ventilation using a more conventional technique. Non-invasive mechanical ventilation has recently been implemented in the acute setting as an adjunct to weaning patients from invasive mechanical ventilation (141 – 143). Several authors have reported their experience with its use in patients requiring prolonged mechanical ventilation because of various etiologies. Udwadia et al. (144) studied 22 patients with weaning failure who had been ventilated for a median of 31 days (range: 2– 219 days) (144). Eighteen patients were successfully liberated from invasive mechanical ventilation and discharged home a median of 11 days (range: 8 –13 days) after starting noninvasive ventilation. Restrick et al. (145) used non-invasive ventilation to successfully wean 13 of 14 patients with prolonged mechanical ventilation. Well-designed randomized controlled trials are needed before this approach can be fully recommended. Approximately 20% of all patients transferred to an LTAC will not be successfully liberated from mechanical ventilation despite surviving the hospitalization (28). In the absence of ongoing but remediable disease, patients with prolonged mechanical ventilation should not be classiﬁed as irreversibly ventilator-dependent before 90 days of failed weaning attempts (122). Efforts shift to determining the need for the tracheotomy tube for patients who are liberated from the ventilator. Assessment of the upper airway becomes crucial because the tracheotomy stoma can close within 48 to 72 hours, making re-establishment of an airway difﬁcult should post-decannulation respiratory distress occur. The initial maneuver is to determine patient response to deﬂation of the cuff (e.g., does the patient aspirate?). If this is tolerated, the response to tube occlusion (capping) is performed after placement of a fenestrated tracheotomy. Once tube occlusion is tolerated for 24 to 48 hours, decannulation may be considered. Alternatively, a strategy of sequential downsizing of tracheotomy tubes may be desirable (146 –148). Ceriana et al. (149) demonstrated that a

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decisional ﬂow chart based on clinical and physiologic principles led to decannulation in 56 of 72 tracheotomized survivors who had been weaned from the ventilator after respiratory failure from a variety of causes. Only 3% of decannulated patients required reintubation within the subsequent three months. The main reasons precluding successful decannulation were either inability to manage secretions or severe glottic stenosis. Fiberoptic bronchoscopy and laryngoscopy should be performed to search for sources of upper airway obstruction (vocal cord injury/dysfunction, granulation tissue, airway strictures) should respiratory distress occur with tracheotomy tube occlusion.

IX.

Conclusion

The need for prolonged mechanical ventilation is multi-factorial in origin, involving abnormalities of respiratory mechanics, respiratory muscle dysfunction, the presence of systemic illness, and complications associated with critical illness. At least in the short-term the majority of patients survive, with slightly more than half being successfully liberated from mechanical ventilation. Although randomized trials are not yet available, strong observational investigations indicate that an organized approach to liberation (e.g., use of a protocol) likely improves weaning success and shortens the duration of ventilation. The literature further demonstrates that satisfactory outcomes can be achieved at long-term acute care facilities with extensive experience in caring for patients with prolonged mechanical ventilation.

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Epstein and Nevins successful extubation in neurosurgical patients. Am J Respir Crit Care Med 2001; 163:658 –664. Duane TM, Riblet JL, Golay D, Cole FJ, Jr., Weireter LJ, Jr., Britt LD. Protocoldriven ventilator management in a trauma intensive care unit population. Arch Surg 2002; 137:1223– 1227. Krishnan JA, Moore D, Robeson C, Rand CS, Fessler HE. A prospective, controlled trial of a protocol-based strategy to discontinue mechanical ventilation. Am J Respir Crit Care Med 2004; 169:673 – 678. Lerman RM, Weiss MS. Progressive resistive exercise in weaning high quadriplegics from the ventilator. Paraplegia 1987; 25:130 – 135. Martin AD, Davenport PD, Franceschi AC, Harman E. Use of inspiratory muscle strength training to facilitate ventilator weaning: a series of 10 consecutive patients. Chest 2002; 122:192 – 196. Ferrer M, Esquinas A, Arancibia F, Bauer TT, Gonzalez G, Carrillo A, Rodriguez-Roisin R, Torres A. Noninvasive ventilation during persistent weaning failure: a randomized controlled trial. Am J Respir Crit Care Med 2003; 168:70 –76. Girault C, Daudenthun I, Chevron V, Tamion F, Leroy J, Bonmarchand G. Noninvasive ventilation as a systematic extubation and weaning technique in acute-on-chronic respiratory failure: a prospective, randomized controlled study. Am J Respir Crit Care Med 1999; 160:86 – 92. Nava S, Ambrosino N, Clini E, Prato M, Orlando G, Vitacca M, Brigada P, Fracchia C, Rubini F. Noninvasive mechanical ventilation in the weaning of patients with respiratory failure due to chronic obstructive pulmonary disease. A randomized, controlled trial. Ann Intern Med 1998; 128:721 –728. Udwadia ZF, Santis GK, Steven MH, Simonds AK. Nasal ventilation to facilitate weaning in patients with chronic respiratory insufﬁciency. Thorax 1992; 47: 715 – 718. Restrick LJ, Scott AD, Ward EM, Feneck RO, Cornwell WE, Wedzicha JA. Nasal intermittent positive-pressure ventilation in weaning intubated patients with chronic respiratory disease from assisted intermittent, positive-pressure ventilation. Respir Med 1993; 87:199 – 204. Heffner JE, Hess D. Tracheostomy management in the chronically ventilated patient. Clin Chest Med 2001; 22:55– 69. Heffner JE. The role of tracheotomy in weaning. Chest 2001; 120:477S – 481S. Heffner JE. Tracheotomy application and timing. Clin Chest Med 2003; 24:389 –398. Ceriana P, Carlucci A, Navalesi P, Rampulla C, Delmastro M, Piaggi G, De Mattia E, Nava S. Weaning from tracheotomy in long-term mechanically ventilated patients: feasibility of a decisional ﬂowchart and clinical outcome. Intensive Care Med 2003; 29:845 –848. Sivak ED. Prolonged mechanical ventilation; an approach to weaning. Cleve Clin Q 1980; 47:89 – 96. Cordasco EM Jr, Sivak ED, Perez-Trepichio A. Demographics of long-term ventilator-dependent patients outside the intensive care unit. Cleve Clin J Med 1991; 58:505 –509.

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Scalise PJ, Gerardi DA, Wollschlager CM, Votto JJ. A regional weaning center for patients requiring mechanical ventilation: an 18-month experience. Conn Med 1997; 61:387 –389. Gracey DR, Hardy DC, Koenig GE. The chronic ventilator-dependent unit: a lowercost alternative to intensive care. Mayo Clin Proc 2000; 75:445– 449. Schonhofer B, Euteneuer S, Nava S, Suchi S, Kohler D. Survival of mechanically ventilated patients admitted to a specialised weaning centre. Intensive Care Med 2002; 28:908 –916.

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7 Procedures in the Intensive Care Unit

SANJAY VADGAMA Pulmonary and Critical Care Section West Los Angeles Healthcare Center VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

I.

JANET AU and NADER KAMANGAR Division of Pulmonary and Critical Care Olive View–UCLA Medical Center and Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

Introduction

This chapter is divided into four sections that focus on major practical principles pertaining to the management of patients with arterial catheters, central venous catheters, pulmonary artery catheters, and chest tubes. Each section carefully reviews the indications, equipment, techniques, and complications of these procedures. II.

Arterial Catheters

A. Background

Arterial catheters are routinely inserted into critically ill patients for monitoring arterial pressure and arterial oxygenation. Indwelling arterial catheters provide a continuous assessment of systolic, diastolic, and mean arterial pressures. As patients become increasingly unstable in the presence of shock, arrhythmias, and vasoactive drug infusions, the traditional cuff pressures lose their accuracy. Non-invasive techniques in these patients have proven to be unreliable (1,2). Arterial catheters provide beat to beat information, allowing for rapid interpretation of therapeutic interactions, helping guide the clinician in providing and assessing the appropriate therapy. 219

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The indications for arterial cannulation are shown in Table 1. The appropriate use limits discomfort caused to the patient and avoids unnecessary complications. C. Equipment

The equipment used varies depending on the artery to be cannulated and the institution’s preference. Commonly used sites for cannulation are the radial, femoral, axillary, and dorsalis pedis artery. The equipment includes a 19- or 20-gauge Teﬂon catheter over a guidewire, 1% lidocaine solution without epinephrine, and 3.0 or 4.0 silk suture. Monitoring equipment consists of the monitor with ampliﬁer, electronic monitoring equipment, oscilloscope display screen and recorder, constant ﬂush device, transducer, and ﬂuid ﬁlled non-compliant tubing with stopcocks. Accurate and reproducible data is dependent upon the absence of technical problems. Management of the most common problems is discussed in the forthcoming section. D. Techniques

As stated earlier, there are many potential sites for the insertion of arterial catheters. The radial and femoral arteries are the most commonly used. When choosing the ideal site for catheter insertion, several factors have to be considered. These include hand dominance, patency of collateral circulation, ease for nursing care, and absence of infection. Radial Artery Cannulation

The radial artery remains the most frequently cannulated artery. Concerns about collateral blood ﬂow stem from studies which have demonstrated incomplete palmar arch anastomosis in 3% to 6% (3) of specimens, that with inadequate or absent ulnar ﬂow in 12% (4). The modiﬁed Allen’s test, ﬁrst described in 1929 (5), has been used to test for collateral ulnar ﬂow. The patient’s hand is elevated with clenched ﬁst, while both radial and ulnar arteries are compressed by the examiner. This allows the blood to be drained from the hand. Once pallor is produced, the hand is lowered and the ﬁst opened. One artery is released and the time Table 1 Indications for Arterial Line Catheters Hemodynamic monitoring

Frequent arterial blood sampling Frequent blood sampling Intra-aortic balloon pump use

In unstable patients (acutely hypotensive or hypertensive), including patients on vasoactive or inotropic drug therapy For blood gas determination, particularly in mechanically ventilated patients In patients with limited venous access

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for color to return to the palm is noted. The procedure is then repeated with the other artery. Color should return to the hand within seconds, indicating a patent ulnar artery and intact superﬁcial arch. There remains some controversy over the validity of Allen’s test. When compared with Doppler examination, it has been shown to have a sensitivity of 87% and speciﬁcity of only 18% (6). In the absence of peripheral vascular disease, Allen’s test does not appear to be a predictor of ischemia of the hand during or after cannulation (7). Doppler ultrasound has been shown to be a safe and rapid method to localize the radial artery in difﬁcult cases (8,9). Once the radial artery is located either by palpation or Doppler ultrasound, the wrist is placed in hyperextension. The skin is prepped and draped using sterile technique. Using a 25-gauge needle, approximately 0.5 mL of the 1% lidocaine is inﬁltrated down to the periosteum on both sides of the radial artery. A 20-gauge non-tapered Teﬂon catheter over needle is advanced into the artery at a 308 to 458 angle to the skin, approximately 3 to 5 cm from the proximal wrist crease. When blood return is noted in the hub, the needle is held in place. The angle is decreased to 258 and the catheter advanced into the artery. When the needle is removed, correct position is conﬁrmed by blood return. Use of the guidewire technique has been shown to be more successful than direct puncture alone (10). Using this method, once the artery is located the guidewire is advanced into the vessel (Fig. 1). The catheter is then advanced over the guidewire into the artery. Upon removal of the guidewire and needle, pulsatile blood return should be seen. The cannula is then connected to the transducer tubing and securely sutured into the skin, and dressing is then applied. Femoral Artery Cannulation

The femoral artery may be the only palpable artery in cases of profound shock. It is a large bore vessel, easily palpable midway between the anteriosuperior iliac

Figure 1 The modiﬁed Seldinger technique of percutaneous arterial line placement. Once the artery is punctured, the tab is used to advance the guidewire into the artery. The cannula is then advanced over the guidewire into the artery; the needle and guidewire are then removed. Source: From Kruse JA, Fink MP, et al. Percutaneous cannulation of the radial artery. Saunders Manual of Critical Care, 2003; 688.

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Table 2

Common Complications of Arterial Cannulation

Hematoma and hemorrhage Limb ischemia Thrombosis and thromboembolism Infections Pseudoaneurysms

spine and the symphasis pubis, lateral to the femoral vein, and medial to the femoral nerve. The artery is cannulated using the Seldinger technique. Difﬁculty in cannulation is normally because of atherosclerosis, or prior vascular procedures. Speciﬁc complications to this site include retroperitoneal hemorrhage and bowel perforation in large inguinal hernias. E.

Complications

Arterial cannulation remains a relatively safe procedure (11), with a small percentage of clinically relevant complications. Complications of arterial cannulation regardless of site are listed in Table 2. Site-speciﬁc complications are listed in Table 3. Thrombosis and Embolization

Thrombosis remains the most common complication of intra-arterial catheters, occurring most frequently in radial and dorsalis pedis arteries and rarely in femoral or axillary artery catheters. The incidence of thrombosis increases with both the size of catheter and duration of cannulation beyond 48 to 72 hours (7,12,13). The risk of thrombosis has been reduced by the use of Teﬂon catheters (14) and the use of continuous or intermittent heparin ﬂush systems (15). Despite the relatively high incidence of thrombosis (up to 10% of 20-gauge radial catheters), it is clinically signiﬁcant in less than 1% of patients (16). Regular examination of the extremity for signs of ischemia and prompt removal of the catheter can minimize thrombotic complications. Distal ischemia can also be caused by embolization of air or atheromatous plaque. Air embolism is caused by gas in the ﬂush solution, the inﬁltrate being under a pressure of 300 mmHg. Depending upon the patient’s size (smaller Table 3 Site Speciﬁc Complications of Arterial Cannulation Radial artery Brachial artery Femoral artery Axillary artery

Cerebral embolization; peripheral neuropathy Median nerve damage; cerebral embolization Retroperitoneal hemorrhage; bowel perforation; arteriovenous ﬁstula Cerebral embolization; brachial plexopathy

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patients) and position (sitting or upright), air embolism may travel in a retrograde direction into the cerebral circulation via the vertebral arteries. Radial artery catheters appear to have a higher incidence of embolization (17). The risk is reduced by ensuring all air is removed from the tubing prior to ﬂushing, and opening the ﬂushing valve for no more than three seconds. Infection

Catheter-related infections are discussed in detail in the “Central Venous Catheters” section. As when placing all intravenous access, thorough site preparation and sterile technique is paramount. The risk of infection increases with duration of cannulation (18,19). The incidence of arterial catheter colonization has been reported to be from 5% to 10%, and it is similar in both radial and femoral catheters (20 – 22). Routine changing of arterial lines has not been shown to lower infection rates. Guidewire exchange is not recommended. Systemic infections may also be caused by contaminated ﬂush solutions or equipment such as stopcocks or transducer domes. Staphylococcus epidermidis remains the most common organism causing line infection (23). Gram-negative organisms and Candida have also been reported, the latter more so in immunocompromised patients. Catheter infections should be treated with the appropriate antibiotic for 7 to 14 days, and complicated cases may require prolonged therapy. Catheters should be removed immediately in suspected or conﬁrmed catheter infections. Most institutions do not replace or relocate arterial catheters routinely for infection control. Transducers and continuous ﬂush devices are replaced at 72 hours, along with intravenous tubing and ﬂush solution. Diagnostic Blood Loss

To avoid contamination when obtaining a sample, 3 to 5 mL of blood is typically wasted with each sample drawn. When frequent samples are required, this can result in a signiﬁcant amount of blood loss over time (24,25) requiring blood transfusion. Methods of minimizing diagnostic blood loss include the use of pediatric tubes, tubing systems that use a reservoir for blood sampling (24,26), and continuous intra-arterial blood gas monitoring (27). F. Technical Sources of Error

Technical problems from the equipment may result in erroneous data collection. The most common problems encountered with the pressure monitoring system are inadequate dynamic response, zeroing drift, and transducer or monitor calibration (28). The dynamic response of the catheter system is determined by the resonant frequency and damping coefﬁcient. Stimulation of the system results in oscillation known as the natural or resonant frequency. The resonant frequency of the monitoring system must be greater than the natural frequency of the input

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signal. This avoids progressive ampliﬁcation of the output signal known as ringing, which may result in exaggeration of systolic peak. The occurrence of resonance is limited by the use of short, wide bore, low compliance catheters and extension tubing. The time taken for an oscillating system to come to rest is known as the damping coefﬁcient. A bedside ﬂush test can be applied to the arterial catheter system to determine the damping coefﬁcient and resonant frequency. Brieﬂy, opening and closing the valve in the continuous ﬂush system produces a square wave displacement in the oscilloscope, followed by ringing and return to baseline. In a normal system, the pressure wave initially seen is followed by a few oscillating waveforms (Fig. 2A). An underdamped system shows lower frequency oscillations resulting in falsely high systolic readings (Fig. 2B). Overdamping is demonstrated by a ﬂush test that does not produce oscillations after the initial pressure release (Fig. 2C). Underdamping can be caused by connecting tubing and stopcocks and patient factors such as tachycardia and high

Figure 2 Square wave testing demonstrating optimal, underdamped, and overdamped frequency responses. (A) Optimally damped. One to two oscillations before returning to tracing. Readings obtained are reliable. (B) Underdamped. .2 oscillations. Overestimates systolic blood pressures. Diastolic pressure may be underestimated. (C) Overdamped. , 1 12 oscillations. Underestimation of systolic blood pressures. Diastolic pressure may not be affected. Source: From Lichtenthal R, ed. Quick Guide to Cardiopulmonary Care, 2002.

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output states. Overdamping may occur with catheter kinking or thrombus occlusion, blood in the transducer dome or line, and air bubbles in the tubing or stopcocks. Improper zeroing is the most common source of error. The transducer can be zeroed by opening the transducer stopcock to air and aligning it at the fourth intercostals space using a level. If the transducer is positioned too high, it will underestimate the true readings, giving falsely low pressures. Conversely, if it is positioned too low, it will record falsely high pressures. This process should be repeated each time the patient’s position is changed; when signiﬁcant changes in blood pressure occur; and routinely every six to eight hours (29).

III.

Central Venous Catheters

A. Background

Central venous catheters are used extensively both in intensive care units (ICUs) and general wards. Knowledge of indications for placement, the appropriate site selection, and complications are essential for all physicians, not only intensive care specialists. It has been estimated that over ﬁve million central venous and pulmonary artery catheters are inserted each year in the U.S.A (30). Their uses include providing secure access to the central circulation for infusion therapy, hemodynamic monitoring, nutritional support, temporary transvenous cardiac pacing, and hemodialysis. The complication rates of venous catheters have been reported to be over 15% (31 – 33), and some have been associated with signiﬁcant morbidity and economic consequences. B. Indications

Common indications for central venous catheter placement are listed in Table 4. The indication for placement and patient-related factors, such as hemodynamic stability, pulmonary problems, and sites of infection, determine the most appropriate site for catheter placement. The most common sites used are the internal

Table 4 Common Indications for Central Venous Catheter Placement Lack of peripheral access, especially in patients requiring rapid volume replacement in the setting of hypovolemic shock Hemodynamic monitoring For the administration of irritant medications or vasopressors Long-term total parental nutrition Acute hemodialysis Temporary transvenous pacing

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jugular, the subclavian, and the femoral veins. Advantages and disadvantages of each site are listed in Table 5.

C. General Technique

Central venous catheter infections remain a major cause of morbidity in critically ill patients. Placement should be performed under strict sterile conditions. The importance of hand washing, aseptic technique, and full barrier precautions cannot be overstated. Central venous catheters are placed by using the Seldinger technique of guidewire dilation. The vein is cannulated with a needle, through which the guidewire is passed. The dilator is then passed over the guidewire,

Table 5 Advantages and Disadvantages of the Internal Jugular, Subclavian, and Femoral Approaches Approach

Advantages

Disadvantages

Internal jugular

Successful cannulation less operator dependent; higher success rate; low risk of pneumothorax; direct path to superior vena cava; easily compressible bleeding vessels

Accidental internal carotid artery puncture; poor landmarks in obese/ edematous patients; difﬁcult access in hypovolemia; difﬁcult access during CPR; left sided thoracic duct injuries; difﬁcult dressing care; uncomfortable for patient; not preferred site for long-term catheterization

Subclavian

Easier landmarks; less infection risk for long-term catheterization; vessels accessible in hypovolemia; easier dressing care; avoids airway

High pneumothorax risk; malposition common; compressibility of bleeding vessels difﬁcult; difﬁcult access during CPR

Femoral

Easy landmarks; high success rate; does not interfere with CPR; no risk of pneumothorax; supine or Trendelenberg is necessary for placement; easily compressible bleeding vessels

High infection rates; increased risk of thrombosis; unreliable drug delivery to the central circulation.

Abbreviation: CPR, cardiopulmonary resuscitation.

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followed by the catheter itself. The wire is then removed, leaving the catheter within the vessel. Triple-lumen catheters are generally used over single-lumen catheters because of their multiple ports. Sites other than the internal jugular vein, subclavian vein, and femoral vein include the external jugular vein and brachiocephalic vein. Insertion techniques at the three most frequently used sites are discussed in the following sections. Internal Jugular Vein

The internal jugular vein provides direct access to the superior vena cava for pulmonary artery catheterization and transvenous pacemakers that enter the right side of the heart. Cannulation of the right internal jugular vein is preferred to the left because it provides direct access to the right heart. The right pleural dome lies lower than the left, thus having a lower theoretical risk of pneumothorax. The right-sided approach also avoids the thoracic duct. Internal jugular vein cannulation generally carries a lower risk of pneumothorax compared with the subclavian approach, with greater ease of compressibility in the event of excessive bleeding or accidental arterial puncture. In the absence of clear anatomic landmarks, cannulation at this site may be difﬁcult without the use of ultrasound localization. When preparing to cannulate the internal jugular vein, the patient should be placed in Trendelenberg’s position both to distend the vein and to prevent the risk of air embolism. The head should be turned to the contralateral side. The operator should be wearing sterile gloves, gown, and a surgical mask. Preparation of the guidewire and catheter is important prior to insertion. All ports of the catheter should be ﬂushed with saline. The skin should be cleaned with 2% chlorhexidine and a sterile ﬁeld established. Cannulation of the internal jugular vein can be achieved by one of three methods: the anterior approach, the median (or central) approach, and the lateral (or posterior) approach. The anterior and median approaches use the carotid artery as a palpable landmark. The landmarks for both these approaches are easily identiﬁed in thinner patients. The lateral (posterior) approach has the highest risk of carotid artery puncture, but the lowest risk of pneumothorax. In the median (central) approach (Fig. 3A), the apex of the triangle formed by the two heads of the stenocleidomastoid muscle and clavicle is identiﬁed. The vein runs beneath this triangle in its medial position prior to entering the superior vena cava. The pulsation of the internal carotid artery is usually felt just medial to the apex of the triangle. With ﬁngers of the left hand on the carotid artery, a 22-gauge needle is used to inﬁltrate 1% lidocaine into the skin at the apex of the triangle. The 22-gauge needle is used to locate the internal jugular vein. This needle is advanced at 308 to 458 in a frontal plane toward the ipsilateral

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Figure 3 (A) Catheterization of the right internal jugular vein. The apex of the triangle formed by the two heads of the sternocliedomastoid and clavicle is identiﬁed. The internal jugular vein lies lateral to the internal carotid artery. (B) Catheterization of the right subclavian vein. The skin is punctured 2 –3 cm caudal to the midpoint of the clavicle. The needle is then advanced in the direction of the sternal notch, hugging the inferior surface of the clavicle. Source: From Mc Gee DC, Gould MK. Pulmonary complications of central venous catheterization. N Engl J Med 2003; 348:1123 –1133.

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nipple applying constant back pressure to the syringe. The vein is normally identiﬁed within 2 to 5 cm from the skin surface. If the vein is not located, the needle should be withdrawn slowly, with continued gentle back pressure as the vein is commonly located during withdrawal of the needle. Repeated attempts should be just medial or lateral to the initial attempt. Once the vein is located with the ﬁnder needle, the operator can either withdraw the ﬁnder needle and insert the larger needle in the same plane or leave the ﬁnder needle in and insert the larger needle alongside it into the vein. Finder needles may not be necessary if the cannulation is performed with ultrasound guidance. The syringe is then removed leaving the hub in place. Backﬂow is checked, ensuring it is not pulsitile, an indication of arterial blood. The J-tip guidewire is then passed through the needle into the vein, where it should pass easily, encountering no resistance. The needle is then removed while maintaining control of the guidewire. A small skin nick contiguous with the guidewire is made using an upward facing scalpel blade. The dilator is then advanced over the wire using a twisting motion; the operator should hold on to the guidewire at all times. The dilator should then be withdrawn, leaving the guidewire in place; gauze is placed at the puncture site to control oozing. The catheter is threaded through the guidewire into the vein 15 – 17 cm. At no point should the operator let go of the actual wire. With the catheter stabilized, the guidewire is removed. Each port of the catheter should be aspirated and then ﬂushed with normal saline. The catheter is securely sutured or stapled into the skin and sterile dressing applied. A chest X-ray is then obtained to check for complications and position of the tip of the catheter. In the anterior approach, the needle is inserted along the medial edge of the sternocleidomastoid muscle at the level of the inferior margin of the thyroid cartilage. The needle is inserted 1 cm lateral to the pulsation of the carotid artery. For the posterior (lateral) approach, the needle is inserted at the posteriolateral margin of the sternocleidomastoid, approximately 5 cm above the sternoclavicular joint. The needle is directed toward the suprasternal notch at a 158 angle to the skin. Venopuncture normally occurs within 5 to 7 cm.

Subclavian Vein

The subclavian vein approach has several advantages. This approach has more easily identiﬁable bony landmarks, a lower incidence of infection, easier dressing care and maintenance, and improved patient comfort. It is the preferred route for long-term total parental nutrition and central access in hypotension when placed by experienced operators. The subclavian vein is a 1 to 2 cm diameter vessel, a continuation of the axillary vein beginning at the lateral border of ﬁrst rib. It is usually ﬁxed by ﬁbrous attachment directly beneath the clavicle for 3 to 4 cm before becoming the brachiocephalic vein. The ﬁbrous attachments prevent the vein from collapsing even in severe

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hypovolemia. The anterior scalene muscle separates the subclavian vein from the subclavian artery. As with the internal jugular approach, the patient is placed in Trendelenberg’s position. Additionally, a small rolled towel is placed between the shoulder blades. There are two basic techniques for inserting the subclavian catheter, the supraclavicular approach and the infraclavicular approach. Catheter malposition and pneumothorax rates may be a little lower using the supraclavicular approach. There is no difference in the success rates between both approaches. With the patient’s head turned towards the contralateral side, the area is prepped with 2% chlorhexidine. Using sterile technique, the area is draped to create a sterile ﬁeld. For the infraclavicular approach, the skin is punctured 2 to 3 cm caudal to the midpoint of the clavicle (Fig. 3B). Following inﬁltration with 1% lidocaine, an 18-gauge needle attached to a 10-mL syringe is advanced in the direction of the sternal notch until the tip of the needle abuts the clavicle. The needle is then “walked” down the clavicle until it slips under its inferior edge. Keeping the bevel pointed cephalad, the needle is advanced towards the suprasternal notch, hugging the inferior surface of the clavicle. If no blood return is seen, the needle is gently withdrawn, maintaining gentle suction. If venopuncture does not occur, the needle should be angled in a slightly more cephalad direction for the next attempt. Once blood return is achieved, the needle is ﬁrmly held, whereas the syringe is detached from the hub. A ﬁnger is placed over the hub to prevent air embolism. The blood return should be non-pulsitile. The guidewire is then passed through the needle, turning the bevel as the guidewire is advanced; the needle is then withdrawn. As with the internal jugular approach, the catheter is passed over the wire following dilatation. The catheter is sutured 16 to 17 cm if placed on the right side of the chest and 18 to 19 cm if placed on the left. A post-procedure chest X-ray is taken. For the supraclavicular approach, the operator is positioned at the head of the patient on the side to be cannulated. The venopuncture site is the claviculosternocleidomastoid angle, found lateral to the insertion of the clavicular head of the sternocleidomastoid muscle, above the clavicle. The needle is advanced underneath the clavicle, at an angle of 158 toward the contralateral nipple. The vein is usually found at a depth of 1 to 4 cm from the surface. Femoral Vein

Cannulation of the femoral vein has several advantages. As the artery is usually easy to palpate, the vein, which lies medially, is usually easy to locate. If the femoral artery is accidentally punctured, it is easily compressible. Patients can be cannulated without being placed in Trendelenberg’s position, important when severe orthopnea may be a problem. It also avoids the risk of pneumothorax. Femoral access is useful during cardiopulmonary resuscitation when chest compressions and airway management may make subclavian and

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internal jugular vein cannulation difﬁcult. Disadvantages of this site include the higher infection rates and unreliable drug delivery to the heart in low ﬂow states. The femoral vein is a continuation of the popliteal vein, becoming the external iliac vein at the inguinal ligament. The femoral vein lies within the femoral sheath, medial to the femoral artery, which is usually easily palpable. If possible, the patient is placed in the supine position. The femoral vein lays approximately 1 to 1.5 cm medial to the femoral artery and 1 to 3 cm below the inguinal ligament. Once again the site is meticulously sterilized and prepped as described earlier. An 18-gauge needle is advanced at a 458 to 608 angle, pointing the needle towards the head. In obese patients it may be necessary to advance the needle up to the hub. Once venous return is conﬁrmed, the syringe is removed. Ensuring non-pulsatile blood ﬂow, the guidewire is passed through the needle and venous catheter placed as described previously. D. Ultrasound-Guided Insertion of Central Venous Catheters

Failure rates for insertion of central venous catheters have been found to be as high as 12%, with a complication rate of 10% (34). Commonest causes of failure or complication include previously difﬁcult catheterization, limited sites, difﬁcult landmarks, and thrombosed vessels. Studies have clearly demonstrated the superiority of using ultrasound guidance over blind landmarkguided techniques in the time taken to place the catheter, the number of attempts, and the complication rate (35 –38). The ultrasound also identiﬁes thrombosed or unusually small vessels, thus avoiding inaccessible sites. Sterile ultrasound probe covers and needle guidance clips allow cannulation of the vessel as it is seen in real-time on the monitor (Fig. 4A). Although helpful, the guidance clips can be cumbersome, and some operators prefer cannulation under real-time conditions. Real-time ultrasound uses high-frequency sound waves (2 – 10 MHz), generating a two-dimensional grey-scale image of the vein and surrounding tissues (Fig. 4B). Fluid such as blood transmits sound completely and is seen as a dark image. Veins are identiﬁed by their non-pulsatile appearance, compressibility, and distension with the patient in Trendelenberg’s position (Fig. 4C). The artery is generally not compressible on application of gentle pressure. Ultrasound-guided catheter placement appears to be the most beneﬁcial for the internal jugular site and should be used whenever available. E.

Complications of Central Venous Catheters

Complications of central venous catheters can be divided into mechanical, embolic, thrombotic, and infectious. Mechanical complications include arterial puncture, hematoma, malposition, and pneumothorax. Accidental arterial puncture is the most frequent complication of the internal jugular site, with rates being reported to be around 3% (39). Bleeding can usually be controlled by the application of local pressure for several minutes. Occasionally a hematoma may form, which can hinder further catheter

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placement attempts. Accidental cannulation of the internal carotid artery has been reported (40), leading to retrograde dissection of the subclavian, innominate artery, and ascending aorta (41). Subclavian artery puncture is less common, usually managed by applying pressure above and below the clavicle. Femoral artery puncture occurs in 5% to 10% of adults (42 – 44); however, this is mostly uncomplicated, controlled by local pressure. Cannulation of the left internal jugular vein has its own complications. These include injury to the left innominate vein and thoracic duct. Because of its anatomy, cannulation of the left innominate vein has a greater risk for perforation. Care should be taken when dilation over the guidewire is attempted, being careful not to force the dilator beyond the internal jugular vein. Damage to the thoracic duct can result in chylothorax and rarely chylopericardium (45). Catheter malposition rates have been reported at 5.3% versus 9.3% for internal jugular versus the subclavian site (39) and lower for the femoral vein. When using the internal jugular and subclavian sites, care should be taken to ensure the catheter tip is not placed too low into the heart. The ideal tip position is 3 to 5 cm proximal to the caval – atrial junction. Fatal tamponade can occur secondary to perforation of the right atrium (RA) or ventricle. Arrhythmias have also been reported (46).

Figure 4 (A) An illustration of the ultrasound probe with needle guide attached. Siterite ultrasound system. Source: C.R. Bard, Inc., (B) Real-time ultrasound demonstrating the internal jugular vein and common carotid artery, with the patient in Trendelenberg’s position. (C) Upon application of gentle downward pressure from the ultrasound probe, the vein collapses but the artery remains clearly seen. (Continued next page.)

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Figure 4 (Continued.)

Malposition of the subclavian catheters into the ipsilateral jugular vein has been well documented (47). Catheters can enter the contralateral brachiocephalic vein more commonly in left-sided insertions. An example of malposition is shown in Figure 5A; the central venous catheter was inserted into the left internal jugular vein and is shown looping back and entering the right internal jugular vein.

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Figure 5 Examples of complications. (A) Anterio-posterior radiograph showing the tip of the central venous catheter, inserted in the left internal jugular vein, entering the right internal jugular vein. (B) Anterio-posterior radiograph showing a complication of femoral artery catheterization, with the guidewire displaced distally into the aortic arch.

Pneumothorax is a recognized complication of both the internal jugular and subclavian approaches. The incidence of pneumothorax ranges from 0.3% to 3.0% (48). The complication rates at these sites increase signiﬁcantly with the number of attempts made at cannulation (34,39). The incidence of pneumothorax

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is higher for the subclavian approach than internal jugular, where pneumothorax only occurs if attempts at catheterization occur close to the clavicle. Treatment of the pneumothorax depends on the patient’s clinical condition, severity of underlying disease, and the size of the pneumothorax. Although most pneumothoracies are immediately apparent, they can also occur as a late complication, occurring several days after subclavian vein catheterization (50). Catheter and wire embolism occur most commonly when they are withdrawn through the needle as a result of the shearing action over the barrel of the needle. The fragments of the catheter can embolize, resulting in potentially serious complications (51). Shearing of the wire is more common than of the catheter. Air embolism occurs most commonly when catheters are accidentally disconnected, becoming open to the atmosphere. Complications range from transient hypoxemia and chest pain, focal cerebral lesions with hemiparesis, or hemianopia (52) to cardiovascular collapse and death (53). Placing the patient in Trendelenberg’s position during catheter insertion and removal is important in the prevention of air embolism and its complications. Infrequently, the operator may lose the guidewire during insertion as is shown in Figure 5B, where the guidewire can be seen in the descending aorta. Thrombosis

Although a high incidence of thrombosis has been reported in central venous catheters, the clinical signiﬁcance is less clear. Catheter associated thrombosis of the femoral vein appears to have more clinical signiﬁcance than either the internal jugular or the subclavian vein (31,54,55) and may be partly responsible for the higher incidence of infection (31,54 – 57) seen at this site. Infection

Intravascular catheters play an essential role in the management of critically and chronically ill patients, with millions purchased by healthcare institutions. Catheter-related infections are associated with increased morbidity, longer duration of hospitalization, and substantial ﬁnancial costs. The incidence of catheter-related infections varies according to the type of catheter used, the site of placement, the conditions under which the catheter was placed, frequency of manipulation, and patient-related factors, such as the severity of their underlying disease (58). The diagnosis of catheter-related infection is often difﬁcult because symptoms of fever, chills, and signs of sepsis may occur from other foci of infection. Catheter-related infection is suggested by several factors. These include inﬂammation or frank pus at the catheter insertion site or exit site, dysfunction of the catheter secondary to intraluminal clot, isolation of coagulase negative staphylococci, corynebacterium species or fungi, and clinical improvement on removal of the catheter. There should also be an absence of infection from other sites, such as the lung and urine. The presence of blood stream infection is conﬁrmed by two

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positive blood cultures drawn from a peripheral vein, not the catheter itself, which may be colonized with contaminants. Catheter-related blood stream infections are unlikely if blood cultures drawn from the catheter are negative (59). Positive cultures of the catheter tip should demonstrate more than 15 colony forming units of the same organism (60). The evaluation and management of catheter-associated infections is discussed in more depth in the chapter on infection control in the ICU. With infection of central venous catheters being such a troublesome cause of nosocomial infections, prevention of infections is paramount. Aseptic technique and strict adherence to hand washing have been found to signiﬁcantly reduce the rates of catheter-related infections (61 –63). Whenever placing a catheter, full barrier precautions are necessary, including sterile gloves, long-sleeved gowns, surgical masks, and sterile drapes (64). Two-percent chlorhexidine has been shown to be a more effective cutaneous disinfectant than povidone – iodine (65). Use of the subclavian vein has been shown to have a lower infection rate compared with both internal jugular and femoral veins (31,66,67). Femoral veins have the highest rate of infection and hence the use of this site is generally discouraged. Chlorhexidine –silver impregnated catheters have been shown to have a lower rate of catheter colonization and catheter-related bacteremia (68), as have minocycline –rifampin bonded catheters (69). At present, antimicrobial impregnated catheters are reserved for use when rates of catheter-related infections remain high despite appropriate prevention measures. Catheters should be removed as soon as they are no longer needed. Infection rates increase after the ﬁfth to seventh day (70 – 72). Routine exchange of catheters over guidewire or new puncture has not been shown to reduce the rates of catheter-related infections (73,74) and carries the risk of mechanical complications. The catheter site should be examined daily for evidence of purulence or erythema, suggestive of infection requiring removal of catheter. The absence of these signs does not exclude the possibility of a catheter-related infection. Antibiotic therapy should be directed by blood and catheter tip cultures, the severity of the patient’s underlying disease, and the hospital’s infection and resistance patterns. Future developments will be aimed at the use of more effective preventative strategies, including more effective antiseptics and catheters made of new polymer-antibiotic systems that will inhibit the formation of a bacterial bioﬁlm.

IV.

Pulmonary Artery Catheters

A. Background

Pulmonary artery (PA) catheterization was introduced in 1929 by a German physician, Werner Forssmann, who guided a urologic catheter through a patient’s vein

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in his arm and into his heart. He took a chest radiograph to conﬁrm the position of the catheter and published the procedure as a brief report (75). In 1947, Dexter et al. measured PA pressure by wedging a catheter in a distal branch of a pulmonary artery. Subsequently, they found that the pressure in the wedge position was the same as the ﬁlling pressure in the left ventricle (LV). By measuring the pressure and oxygen content of blood in the RA, right ventricle (RV), and pulmonary artery, they were able to diagnose congenital heart disease, valvular heart disease, and left ventricular failure (76,77). Bedside catheterization of the pulmonary artery was introduced by Swan et al. in 1970 (78). An inﬂatable balloon at the tip of a ﬂexible catheter enabled the catheter to be directed by blood ﬂow into the pulmonary artery, thus avoiding the need for ﬂuoroscopyguided placement. This ﬂow-directed pulmonary artery catheter, also known as the Swan – Ganz catheter, was originally used to assess and guide therapy of patients following acute myocardial infarction. With subsequent improvements in PA catheter technology, it is now used in both diagnosis and management of a wide range of conditions in critically ill patients. Despite its extensive use over the past 30 years, there has been increasing concern over the use and interpretation of the data obtained by the PA catheter, with some studies suggesting an increased mortality with its use. These controversies will be discussed later.

B. Indications and Contraindications for PA Catheter Placement

Indications for PA catheter can be broadly divided into diagnostic and therapeutic categories (Table 6). Diagnostic indications include differentiating between and assessing different forms of shock, differentiating between cardiogenic and non-cardiogenic pulmonary edema, distinguishing between primary and secondary pulmonary hypertension, and diagnosing cardiac tamponade and intracardiac shunts. Therapeutic indications include the management of shock, complicated myocardial infarctions, guiding ﬂuid management in a variety of conditions, and also guiding pharmacologic therapy. The use and interpretation of data from the PA catheter in speciﬁc clinical scenarios will be discussed later. Contraindications for catheter placement are can be divided into absolute or relative (Table 7) (79). Absolute contraindications include patients with right-sided endocarditis and patients with demonstrated tumor or thrombus within the RA or RV. Catheter placement is also contraindicated in prosthetic tricuspid or pulmonic valves, where there is a danger of the catheter becoming entangled in the valve mechanism, and in patients with terminal illnesses, where aggressive management is futile. The balloons of most catheters are made of latex; therefore, they are contraindicated in patients with a history of latex allergy. Relative contraindications include patients with an underlying

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Table 6 Indications for PA Catheter Use Diagnosis Differentiation and assessment of shock Cardiogenic Hypovolemic Septic Pulmonary embolus Differentiation of pulmonary edema Cardiogenic versus non-cardiogenic (e.g., ARDS) Primary versus secondary pulmonary hypertension Diagnosis of pericardial tamponade Diagnosis of left to right intracardiac shunt Therapeutic Management of complicated myocardial infarction Hypotension unresponsive to volume challenge Hemodynamic instability (cadiogenic shock versus hypovolemia) Ventricular septal rupture versus acute mitral regurgitation Right ventricular infarction Assessment of valvular heart disease Guide to ﬂuid management Gastrointestinal hemorrhage Sepsis Heart failure Acute renal failure Burns Decompensated cirrhosis Guide to pharmacological therapy Afterload and preload reducing agents, inotropics, vasopressors, beta-blockers Management of perioperative cardiac and noncardiac surgical patients with cardiac instability Post-operative management of open heart surgical patients Management of severe pre-eclampsia Ventilator management (assessment of best PEEP for oxygenation) Abbreviations: ARDS, acute respiratory distress syndrome; PEEP, positive end-expiratory pressure.

severe coagulopathy (or receiving anticoagulation) at the time of catheter placement. Fluoroscopic guidance is recommended for patients with temporary pacing wires or recently placed permanent pacemakers or implantable deﬁbrillators, dilated RA or RV, and left bundle branch block. Patients with left bundle branch block are at risk of developing right bundle branch block leading to complete heart block, although the occurrence of this complication in these patients is very low. See the “Complications of PA Catheters” section for more details.

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Table 7 Contraindications for PA Catheter Placement Absolute Right sided endocarditis Mechanical tricuspid (or pulmonic) valve Tumor or thrombus in the right atrium or right ventricle Terminal illness where aggressive is considered futile Latex allergy Relative Coagulopathy (or anticoagulation) Recently placed permanent pacemakers or implantable deﬁbrillators

C. Equipment and Technique PA Catheters and Monitoring Equipment

A variety of catheters are now available. The typical PA catheter is 110 cm in length, having a 1.5 cc balloon located just proximal to its tip. Double lumen catheters allow balloon catheter inﬂation through one lumen, with the distal opening at the catheter tip used to measure intravascular pressures and sample blood. Triple lumen catheters have a proximal port 30 cm from the catheter tip allowing simultaneous measurement of right atrial, PA, and wedge pressures. The four-lumen catheter is the most commonly used PA catheter. It contains a thermistor 4-cm proximal to the tip that allows measurement of the PA blood temperature and calculation of the cardiac output (CO) by thermodilution techniques. Five-lumen catheters have a proximal port at 4 cm allowing delivery of medications and venous blood sampling. PA catheters and electrode on its surface for continuous ECG monitoring or temporary cardiac pacing are also available. Special features in some pulmonary artery catheters allow continuously measurement of mixed venous oxygen saturation (SvO2) via ﬁberoptics, continuous cardiac output (CCO), continuous right ventricular end diastolic volume (RVEDV), right ventricular ejection fraction (RVEF), and pacing. These parameters have the ability to continuously guide the clinician as to the status of oxygen delivery and consumption as well as guide on the assessment of preload, afterload, and contractility. Semi-rigid, non-compliant tubing ﬁlled with isotonic saline and heparin transmits the pressure recorded to a ﬂuid-ﬁlled pressure transducer. Back-up of blood is prevented by a constant infusion device. As the ﬂuid in the non-compliant tubing is non-compressible, changes in intracardiac pressure are accurately transmitted to the transducer membrane, generating an ampliﬁed signal seen on the monitor. Changes in the height of the transducer or the patient will alter the pressure measurements. The system is zeroed to ambient air pressure prior to recording any readings. The reference point is the midpoint of the left atrium, estimated as the fourth intercostal space in the mid axillary line with the patient in the

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supine position. The transducer is ﬁxed at this height, the membrane exposed to atmospheric pressure, and the monitor adjusted to zero. For most catheters, calibration of monitors is not required. It is important for the monitoring system to have an appropriate frequency response. Flicking or gently shaking the catheter tip should elicit a brisk highfrequency response in the waveform. Damped waveforms are caused by air bubbles, long non-compliant tubing, vessel wall impingement, intra catheter debris, and loose connections in the tubing. Following insertion, a rapid ﬂush test is performed similar to that described in the “Arterial Catheters” section. D. Insertion

PA catheters can be inserted through a choice of sites. The risks and beneﬁts of the most popular sites are listed in Table 8. Most physicians prefer the right internal jugular or the left subclavian vein approach. The right internal jugular is the shortest and straightest path to the heart. The curvature of the catheter utilizes the course of the left subclavian vein into the SVC and right heart. A wide sterile procedural ﬁeld is prepared and aseptic technique and full barrier precautions are taken. The catheter is ﬂushed in all ports and the balloon inﬂated to test for leaks. The balloon is then deﬂated. Pressure transducer function is checked by ﬂicking or waving the distal catheter tip gently. Using techniques described in the central lines section, the appropriate site for insertion is identiﬁed, and the vein is located and cannulated using the Seldinger technique. A dilator is passed through the introducer, and together these are advanced over the guidewire into the vein. The guidewire and dilator are then removed simultaneously, leaving the introducer in the vessel. The catheter is introduced through the sterile sheath adapter, which at the end of the procedure is pulled over the catheter. The distal end of the sleeve adapter attaches to the introducer sheath limb. The catheter contains markings spaced 10 cm apart from the distal tip. Using these markings, and continuous pressure monitoring, the catheter is advanced into the RA. Table 8 illustrates the appropriate distances for the three most frequently used venous sites. Table 8 Comparison of the Three Most Frequently Used PA Catheter Insertions Sites Distance (cm) to: Insertion site

RA

RV

PA

Advantages

Disadvantages

Internal jugular

15– 20

30

40

Subclavian

15– 20

30

40

Femoral

30

40

50

Shortest, most direct route to heart Easier to ﬂoat from the left side Easy cannulation, fewer overall complications

Risk of carotid artery puncture, pneumothorax Higher risk of pneumothorax More difﬁcult to ﬂoat, higher infection rate

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The catheter is advanced until it is in the RA; the appropriate right atrial waveform should be seen with characteristic a and v waves. Right atrial blood samples are obtained, if needed, and the pressure recorded. The balloon is then inﬂated with the recommended amount of air (no more than 1.5 mL) until a small amount of resistance is felt. If no resistance is felt, one should suspect balloon rupture and re-examine the catheter immediately. If signiﬁcant resistance is encountered, then one should suspect malposition. The catheter is withdrawn and re-advanced to a new position. With the balloon inﬂated, the catheter is advanced into the RV. As it crosses over the tricuspid valve into the RV, the pressure waveform changes and a rise in systolic pressure is seen (Fig. 6). The pressures within the RV are recorded. The catheter is then advanced until the diastolic pressure increases above that seen in the RV. At this point, the catheter tip has moved across the pulmonary valve into the PA. In this position, the characteristic dicrotic notch appears in the waveform, indicating closure of the pulmonic valve. If the RV tracing is still seen after 40 cm of the catheter is introduced, it is likely that the catheter is coiled within the RV. If this occurs, the balloon is deﬂated and catheter withdrawn until the RA waveform is seen. The balloon can then be inﬂated and advanced again as described. The inﬂated catheter is advanced into the PA until a fall in pressure and a change in waveform is seen. This is the pulmonary capillary wedge pressure (PCWP). The PCWP is recorded as a mean value, not systolic or diastolic, and is measured at the end of expiration. Once this is recorded, the balloon should be deﬂated, at which point the PA tracing should reappear. The balloon inﬂation volume needed to change the PA tracing to the PCWP should be noted. If the volume needed is signiﬁcantly lower than the recommended volume of 1.5 mL or subsequent PCWP readings require smaller volumes, then the catheter tip has migrated too far peripherally and should be pulled back immediately (with the balloon deﬂated). Characteristic waveforms in the right heart chambers, pulmonary artery, and PCWPs are shown in Figure 7. As a rule, the catheter tip should never be advanced until the balloon is inﬂated and must always be deﬂated if the catheter is withdrawn. In patients with an enlarged RA and RV, it may be difﬁcult to advance the PA catheter into PA and wedge position. The catheter softens as it is exposed to body temperature, which makes it more difﬁcult to pass in patients with pulmonary hypertension. The catheter stiffness can be maintained by placing it in a refrigerator or freezer prior to insertion. Alternatively, PA catheters that have a guidewire within one of the lumens to maintain its form may be used. In difﬁcult cases, ﬂuoroscopy is useful in guiding the PA catheter to the appropriate position. Once the optimum position has been located, the catheter is secured by suturing or taping it to the skin. The position of the catheter based on the centimeter markings at the site of insertion is noted. An appropriate dressing is then applied. Finally, a chest X-ray is taken to conﬁrm the catheter position and exclude a pneumothorax. Daily chest X-rays are recommended.

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(B)

(C)

(D)

Figure 6 Posterio-anterior catheter position and the characteristic pressure waveforms in relation to the EKG tracing, from the right atrium to pulmonary artery wedge position. (A) Right atrium. (B) Right ventricle. (C) Pulmonary artery. (D) Pulmonary artery wedge pressure. Abbreviations: a, atrial systole; c, closure of tricuspid valve; v, atrial ﬁlling, ventricular systole. PA, pulmonary artery; PAW, pulmonary artery wedge pressure. Source: From Lichtenthal R, ed. Quick Guide to Cardiopulmonary Care, 2002.

E.

Waveforms and Hemodynamics

Once appropriately inserted and secured, the PA catheter waveforms are measured and calculated parameters can be interpreted.

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Figure 7 Normal pressures and waveforms obtained as the PA catheter is advanced from the right atrium to a pulmonary artery wedge position. Abbreviations: RA, right atrium; RV, right ventricle; PCWP, pulmonary capillary wedge pressure. Source: From Lichtenthal R, ed. Quick Guide to Cardiopulmonary Care, 2002.

The right atrial pressure waveform reﬂects the venous return to the RV and, in the absence of tricuspid valve pathology, is an indicator of right ventricular end diastolic pressure. The normal atrial pressure waveform consists of ﬁve components—three positive deﬂections, the a, c, and v waves, and two negative deﬂections, the x and y descents (Table 9). The normal pressures recorded by the PA catheter are listed in Table 10. Changes in the right atrial pressure waveforms and pressures within the heart in various pathological conditions are discussed later in this section. Using data obtained from the PA catheter, useful hemodynamic parameters can be derived. Table 11 shows how these values are derived and their normal values.

Pulmonary Capillary Wedge Pressure

When the mitral valve is open, there is no barrier between the tip of the catheter and the left heart. Inﬂation and wedging of the balloon closes off ﬂow from the right heart, so the catheter only reﬂects a backward pressure from the left heart. Ideally, left ventricular end diastolic volume (LVEDV) is the desired value for hemodynamic monitoring, but it unfortunately requires cardiac catheterization.

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Table 9 Waveform Presentations Waveform/ descent a wave c wave v wave

x descent y descent

Correlation to EKG and cardiac cycle Atrial systole, it follows P wave (within PR interval) on ECG Bulging of the tricuspid valve into the right atrium (RA) during right ventricular (RV) systole Passive atrial ﬁlling with a closed tricuspid valve, near the end of T wave, correlates with the beginning of QRS and later 1/2 of PR interval on ECG in RA tracing, after T wave in the wedge (PAWP) tracing Atrial diastole (RA relaxation) Atrial emptying by opening of the tricuspid valve with ﬂow of blood into RV

The left ventricular end diastolic pressure (LVEDP) is used as an alternative; however, this value cannot be measured directly. The PA wedge pressure approximates the left atrial pressure, which in turn is usually slightly less than the left ventricular pressure in diastole, or intracavitary LVEDP (ﬁlling pressure) (80 – 95). This relationship allows the PA wedge pressure to be used as a close approximation of the LVEDP. Therefore, the wedge pressure does not directly measure LVEDV but provides an acceptable estimate of the volume in the LV. The relationship between LVEDV or preload (ﬁlling volume) and wedge pressure (ﬁlling pressure) depends on: 1. 2.

Ventricular compliance—meaning the distensibility of the LV. Transmural ventricular distending pressure—equals the intracavitary pressure minus the juxtacardiac pressure.

Changes in juxtacardiac pressure, as with positive end-expiratory pressure (PEEP) or auto-PEEP, or changes in ventricular compliance, as with ischemia or vasoactive agents, can change the values and therefore interpretation of the Table 10

Normal Pressure Values Within the Heart

Measurement from PA catheter Central venous pressure (mmHg) Right arterial pressure (mmHg) Right ventricular pressure, systolic (mmHg) Right ventricular pressure, diastolic (mmHg) Pulmonary artery pressure, systolic (mmHg) Pulmonary artery pressure, diastolic (mmHg) Pulmonary artery pressure, mean (mmHg) Pulmonary artery wedge pressure, mean (mmHg) Cardiac output (L/min)

Normal range ,10 ,10 15 – 30 0–8 15 – 28 5 – 16 10 – 22 6 – 12 4–7

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Table 11 Hemodynamic Parameters Calculated From the PA Catheter and Their Normal Values Parameter CO (Fick Equation) CI SV SI Left ventricular stroke work index Right ventricular stroke work index SVR PVR % Shunt Oxygen uptake

Calculation V˙O2/(CaO2-CvO2) CO/BSA CO/HR CO/HR BSA 0.136 (Stroke volume) (MAP 2 PCWP) 0.0136 (stroke volume) (mean PAP 2 CVP) (MAP 2 CVP/CO) 80

Normal values 4 – 7 L/min 2.8 – 4.2 L/min/m2 50 – 80 mL/beat 30 – 65 mL/beat/m2 43 – 61 g/beat/m2 7 – 12 g/beat/m2

11 – 18 mmHg/L/min 880 –1440 dyne/sec/cm25 (Mean PAP 2 1.5 to 3.0 mmHg/L/min PCWP/CO) 80 150 to 240 dyne/ sec/cm25 (CcO2 2 CaO2)/(CcO2 2 CvO2) ,5% (CaO2 2 CvO2) CO 10 150 – 300 mL O2/min

Abbreviations: BSA, body surface area; CO, cardiac output; CVP, central venous pressure; CaO2, arterial oxygen content; CcO2, pulmonary capillary blood oxygen content; CvO2, venous oxygen content; CvO2, mixed venous oxygen content; HR, heart rate; MAP, mean arterial pressure; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; V˙O2, oxygen consumption.

PCWP. PEEP causes a decrease in LV transmural pressure, so a falsely high PCWP may be obtained. It will overestimate the LVEDP with PEEP or auto-PEEP, but the extent is difﬁcult to determine precisely (94,95). With stiff ventricles, as seen in pericardial effusion, myocardial infarction (MI), and LV hypertrophy, the PCWP may be less than the actual LVEDP. In aortic regurgitation, the LVEDP is higher than the PCWP. Conditions in which the PCWP will overestimate the LVEDP are mitral valve regurgitation, left atrial myxoma, pulmonary embolism, intracardiac left to right shunt, and non-zone 3 catheter position (92). The PA catheter must be in a zone 3 lung segment to provide accurate readings. There are three lung zones depicted by West (92), which are as follows: Zone 1: The least gravity-dependent area of the lung where, theoretically, there is no blood ﬂow because pulmonary artery and venous pressure are less than alveolar pressure. Zone 2: Pulmonary artery systolic pressure is greater than alveolar pressure, but alveolar pressure is greater than pulmonary venous pressure. As pulmonary artery pressure (systolic and diastolic) and alveolar pressure (inspiration and expiration) are phasic, the changing perfusion –ventilation pressures allow only intermittent ﬂow.

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These are not anatomically ﬁxed zones but rather functional zones. Any anatomic part of the lung may take on the characteristics of zone 1, 2, or 3, depending on alterations in hemodynamic (increased or decreased pulmonary blood volume and pressures) and ventilatory status (PEEP, alveolar air trapping).

Relationship Between PCWP and Respiration

There can be considerable variation in the waveform tracings because of respiratory variation. The general pattern may resemble a sine wave. Of course, there may be minimal variation in the waveform baseline and no need to make any adjustments for respiratory variation. By convention, readings are made at the end-expiration, but they will be at different points if the patient is spontaneously breathing or is being mechanically ventilated. At end-expiration, the inﬂuences of pleural pressure during spontaneous breathing or airway pressures during mechanical ventilation are minimized. During spontaneous breathing, pleural pressure usually approximates atmospheric pressure at end-expiration (Fig. 8). This should represent a zero reference point with minimal inﬂuence of external pressures. During mechanical positive pressure breathing, positive airway and intrathoracic pressures are at their lowest at end-expiration (Fig. 9). If there is signiﬁcant inﬂuence due to respiratory effects, end-expiration will occur at the highest portion of the waveform during spontaneous breathing and at the

Figure 8 Ventilatory effect of spontaneous breathing on PCWP. PCWP values should be obtained at end-expiration when intrathoracic pressure inﬂuence is minimal. Abbreviation: PCWP, pulmonary capillary wedge pressure.

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Figure 9 The effect of controlled mechanical ventilation on PCWP. The PCWP is recorded at end-expiration as shown. The positive deﬂections following end-expiration reﬂects positive pressure inspirations. Abbreviation: PCWP, pulmonary capillary wedge pressure. Source: From Lichtenthal R, ed. Quick Guide to Cardiopulmonary Care, 2002.

lowest portion of the waveform during mechanical ventilation. The average of three or more end-expiratory values should be used to minimize variation. These inﬂuences are especially important if the patient is rapid breathing or being mechanically ventilated. In this situation, digital readout devices at bedside are inadequate. These devices do not compensate for changes in waveform baseline, and readings are not reliable and may be inaccurate. In order to correct this error, it is better to read the PCWP at the highest or peak pressure instead of at the average pressures for spontaneously breathing patients. Conversely, the digital readout should be read at the lowest or trough pressures in mechanically ventilated patients. In some patients with severe dyspnea and marked respiratory distress, there can be considerable inﬂuence from actively contracting expiratory muscles, and accurate readings may not be possible without eliminating respiratory muscle activity either with heavy sedation or a short-acting paralytic. In these situations, it is preferable to obtain pressure tracings on calibrated paper and visually identify the pressures at end-expiration. PEEP and PWCP

When a patient is receiving PEEP, the PCWP will increase because PEEP causes a reduction in the left ventricular transmural pressure, as the pleural pressure and juxtacardiac pressure at end-expiration rise more than the intravascular pressure.

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However, this effect is not uniform in all conditions. At end-expiration, pleural pressure will be less than one-half the PEEP in patients with poor lung compliance (e.g., patients with ARDS). The net effect of PEEP is to cause measured PCWP to overestimate transmural LVEDP to an uncertain degree. If the level of PEEP is less than 10 cmH2O, then the effect is negligible. If PEEP is greater than 10 cmH2O, then one can estimate the juxtacardiac pressure by assuming that one half of the PEEP level is transmitted to the pleural and juxtacardiac space, and then subtract that value from the measured PCWP to approximate the real LVEDP. A similar effect on PCWP results when a patient has air-trapping and generates auto-PEEP. It is generally not recommended that patients be disconnected from PEEP for PAWP measurements. Although this will probably eliminate any confounding effects of PEEP, this may further compromise the patient’s respiratory status with loss of alveolar units, and there may also be ﬂuid shifts with the removal of PEEP. It is unlikely that this maneuver provides a clinical beneﬁt in management. In general, it is wise to follow both the hemodynamic and clinical changes that occur with changes in PCWP and not to pay too much signiﬁcance to an isolated PCWP value (96 – 100).

Thermodilution CO

The PA catheter is equipped with a thermistor at the tip, allowing CO to be calculated using differences in ﬂuid temperature in an indicator-dilution technique (90). A bolus of cold (colder than body temperature) ﬂuid can be detected by the thermistor, and the rate of blood ﬂow or CO would be inversely proportional to the change in the amount of cold ﬂuid detected over time. This thermodilution CO measurement produces characteristic curves, with poor CO reﬂected as long, drawn out tracings. In practice, 5 to 10 mL of cold D5W or normal saline is injected into the RA via the proximal port of the PA catheter within two seconds. The ﬂuid can be room temperature or have been placed in ice. If 5 mL of ﬂuid is used, this must be noted for analysis as the CO calculations will need to be adjusted for the smaller ﬂuid bolus. It can be a source of error if this adjustment to the bedside monitoring software program is not made. The solution is rapidly injected, preferably at end-expiration to minimize any variability because of the respiratory cycle (101). Three separate measurements should be obtained at one-minute intervals and reported as an average. The measurements should be consistent within a 10% range, and the curves should be inspected to conﬁrm reproducibility and reliability of readings. Falsely low measurements may be obtained in the presence of tricuspid regurgitation or prolonged injection time exceeding four seconds (102). Falsely high measurements may be noted in the presence of intracardiac shunts and low output states (103).

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Cardiac Output

The PA catheter is equipped with a thermistor at the tip, which allows CO to be calculated using the Fick’s principle (91). In practice, 5 to 10 mL of cold D5W or saline is injected into the RA via the proximal port of the PA catheter. The average of three separate measurements should be obtained at one-minute intervals. The solution is rapidly injected, preferably at end-expiration. Mixed Venous Oxygen Saturation

SvO2 reﬂects the balance between tissue oxygen delivery (DO2) and oxygen consumption or uptake (V˙O2). Hence, it is an indicator of systemic oxygen utilization. It may provide some insight in the management of critically ill patients as changes may signal shifts in this balance, speciﬁcally problems with oxygen delivery or increases in oxygen consumption, which in turn may prompt further interventions. This relationship is further illustrated using the Fick principle in describing CO as calculated by the following equation: CO ¼

_ 2 (mL= min ) VO mixed venous O2 content (Cv O2 ) arterial O2 content (Ca O2 )

CO ¼

_ 2 VO Cv O Ca O2 2

or

Rearranging for CvO2 Cv O2 ¼ Ca O2

_ 2 VO CO

The oxygen content is the sum of both the oxygen bound to hemoglobin and that in solution, therefore Ca O2 ¼ (½Hb Sa O2 1:34) þ Pa O2 0:003 Cv O2 ¼ (½Hb Sv O2 1:34) þ Pv O2 0:003 SaO2 and SvO2 represent arterial oxygen saturations and mixed venous oxygen saturations, respectively. The amount of oxygen (in milliliters) that can bind to 1 g of hemoglobin (Hb) is 1.34. The solubility of oxygen in the blood is 0.003. Under normal conditions this is negligible, therefore Cv O2 ¼ ½Hb Sv O2 1:34 Ca O2 ¼ ½Hb Sa O2 1:34

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Substituting these simpliﬁcations with SvO2 and SaO2 into the Fick equation gives _ 2 VO Sv O2 ¼ Sa O2 CO Hb 1:34 It becomes easy to see that the four factors that can inﬂuence SvO2 are arterial oxygen saturation, oxygen consumption, CO, and hemoglobin level. Therefore changes in SvO2 may reﬂect changes in any or all of these parameters. The normal SvO2 is 75% (range: 60 – 80%). When less than 60%, this suggests anaerobic metabolism (e.g., lactic acidosis), and values below 40% are associated with severely insufﬁcient tissue oxygenation due to shock. When the hemoglobin concentration, oxygen consumption, and arterial oxygen saturation are constant, changes in SvO2 are due to changes in CO. Continuous mixed venous oxygen saturation is possible with PA catheters by the use of ﬁberoptic reﬂectance spectrophotometry. The continuous mixed oxygen saturation reading from the catheter is therefore a useful monitor of CO in hemodynamically unstable patients. Increases in SvO2 would indicate improvement in CO or tissue perfusion, and conversely, a decline would represent further deterioration of hemodynamics and tissue compromise. These changes may be evident prior to other changes in routinely monitored variables (104). In addition, there may be metabolic derangements, such as lactic acidosis, that may be persist despite normal hemodynamics that can be identiﬁed with SvO2 monitoring. Despite the potential beneﬁt of continuous monitoring of SvO2, there remains considerable uncertainty of its role in the management of critically ill patients and advantage over other available monitoring devices (105). The mixed venous oxygen saturation is affected in different clinical conditions as shown in Table 12. F.

Use of the PA Catheter in Speciﬁc Clinical Scenarios

Myocardial Infarction

The PA catheter was initially used in patients with MI complicated by shock. Measurements of CO, preload by obtaining the PAWP, and calculation of systemic vascular resistance allow management of ﬂuids and inotropic or vasopressor medications (106,107). It can also be used for diagnosing and managing complications of MI, such as congestive heart failure, mitral regurgitation, ventricular septal defect, right ventricular infarction, and cardiac tamponade. In 1998, the American College of Cardiology (ACC) published a consensus report stating the indications and recommendations for the use of bedside PA catheter or right-side catheterization in patients with cardiac disease (79). For acute MI, there are six conditions in which PA catheterization is warranted: 1. 2.

To differentiate between cardiogenic and hypovolemic shock. For the management of cardiogenic shock with pharmacologic and mechanical support in patients with and without coronary reperfusion therapy.

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Changes in Mixed Venous Oxygen Saturation in Various Clinical Conditions

Mechanism Increased SvO2 Increased arterial O2 supply by increased cardiac output Decreased tissue demand by decreased V˙O2

Decreased SvO2 Decreased cardiac output Decreased arterial oxygen (CaO2) Decreased Hemoglobin Increased tissue demand by increased V˙O2

Example Sepsis Anesthesia, coma, hypothermia, hypothyroid, cirrhosis, left to right cardiac shunt Hypovolemic shock, acute myocardial infarction Hypoxemia Anemia, hemorrhage Fever, seizures, burns, hyperthyroid, pain, shivering (34 – 37)

3. Short-term guidance of pharmacologic and mechanical management (intra-aortic balloon pump) of acute mitral regurgitation (with or without disruption of the mitral valve) before surgical correction. 4. To diagnose and manage left to right shunt and ventricular septal rupture before surgical correction. 5. Guidance of therapy for right ventricular infarction with hypotension. 6. Guidance of therapy for acute pulmonary edema not responding to treatment with diuretics, nitroglycerin, and other vasodilator agents and low doses of inotropic medications (79). Heart Failure

There are six conditions in patients with heart failure for which PA catheterization is warranted: 1. To differentiate pulmonary edema caused by heart failure or by pulmonary disease or both. 2. To distinguish and guide therapy between cardiogenic and noncardiogenic shock. 3. To guide therapy in patients with concomitant manifestations of “forward” (hypotension, oliguria, and azotemia) and “backward” (dyspnea and hypoxemia) heart failure. 4. To diagnose pericardial tamponade when clinical assessment is inconclusive and echocardiography is unequivocal. 5. To guide perioperative management in selected patients with decompensated heart failure undergoing intermediate or high-risk noncardiac surgery.

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To diagnose pulmonary vasoconstriction and determine its reversibility in patients being considered for heart transplantation (79).

Perioperative Use in Cardiac Surgery

There are four conditions in the management of cardiac surgery patients where PA catheterization is warranted: 1.

2.

3. 4.

To differentiate between causes of low CO (hypovolemia vs. ventricular dysfunction) when clinical and echocardiography is inconclusive. To distinguish between right and left ventricular dysfunction and diagnose pericardial tamponade when clinical and echocardiography is equivocal. To guide management of severely low CO syndromes. To diagnose and guide therapy for pulmonary hypertension in patients with systemic hypotension and evidence of inadequate organ perfusion (79).

Pulmonary Hypertension

There are four conditions for which PA catheterization is warranted in the management of pulmonary hypertension according to the ACC expert consensus: 1. 2. 3. 4.

To exclude postcapillary (elevated PAWP) causes of pulmonary hypertension. To assess the diagnosis and severity of precapillary (normal PAWP) pulmonary hypertension. To determine the safety and efﬁcacy of vasodilator therapy based on acute hemodynamic response. To evaluate different hemodynamic variables before lung transplantation (79).

Although there were no conditions in which right heart catheterization was not warranted, there were conditions in which reasonable differences in opinions between the ACC experts existed. These conditions are the evaluation of the long-term efﬁcacy of vasodilator therapy, in particular prostacycline, and the exclusion of signiﬁcant left to right or right to left intracardiac shunts. Acute Mitral Regurgitation

Acute mitral regurgitation can occur as a complication of acute MI. PA catheterization is very useful when echocardiography with Doppler is inconclusive or unavailable. Elevated left atrial pressure and PAWP are noted and tall peaked “v” waves are seen in the PAWP tracing (Fig. 10). A biﬁd PA waveform composed of the PA systolic wave and the “v” wave can also be seen. A large “v” wave is not diagnostic of acute mitral regurgitation, as it may occur whenever

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Figure 10 The tracing in a patient with mitral regurgitation. The characteristic tall “v” waves are demonstrated.

the LA is distended and non-compliant due to left ventricular failure from any cause, that is, dilated cardiomyopathy (108,109). Tricuspid Regurgitation

Tricuspid regurgitation usually occurs in the setting of pulmonary hypertension and right ventricular dilatation. It is associated with elevated right atrial and right ventricular end-diastolic pressures. It usually represents chronic valvular insufﬁciency. A prominent early right atrial “v” wave with a steep “y” descent is seen. In severe tricuspid regurgitation, the tracings of the right atrial and right ventricular pressures may look similar (110). Cardiac Tamponade

Echocardiography is usually diagnostic for pericardial effusion, and it is widely used to guide the needle for therapeutic measures. In circumstances where the echocardiogram is questionable, PA catheterization may be diagnostic. The characteristic pattern of acute cardiac tamponade is elevation and equalization of right- and left-sided diastolic ﬁlling pressures (RA, RV, PA diastolic, and PAWP). A prominent systolic “x” descent and a blunted “y” descent on the right atrial pressure tracing are seen. The right atrial pressure declines in inspiration in contrast to right ventricular infarction and constrictive pericarditis (111). Right Ventricular Infarction

RV infarction typically occurs in the setting of inferior myocardial infarction. The right atrial pressure is elevated (usually .10 mmHg), and often in the right atrial waveform, prominent “x” and “y” descents are seen. Sometimes the “y” descent may exceed the “x” descent due to a dilated noncompliant RV conﬁned by a non-distensible pericardium (112).

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Chronic ﬁbrous thickening of the pericardium can lead to constrictive pericarditis. Causes of constrictive pericarditis include tuberculosis, malignancy, postchest radiotherapy, and idiopathic causes. Acute or subacute presentations are seen after cardiac surgery. On examination, the jugular venous pressure (JVP) is commonly raised and may rise or fail to fall with inspiration (Kussmal’s sign), which distinguishes this condition from cardiac tamponade, in which there is a decline in the right atrial pressure (JVP) with inspiration. The JVP also shows a prominent y descent. At catheterization, low CO is seen with prominent “x” and “y” descents on the atrial waveform, producing “m” or “w” waveform appearance. The waveforms have a characteristic diastolic dip and plateau pattern (or square root sign) in the ventricular waveform, reﬂecting abrupt termination of the ventricular ﬁlling due to the rigid pericardium. Equilibration of right ventricular and left ventricular end diastolic pressures (,5 mmHg) is often seen, although this can occur in patients with heart failure or acute volume overload. Unlike pericardial tamponade, the PCWP may be as high as 20 to 25 mmHg and similar in appearance to the RA waveform. Acute Respiratory Distress Syndrome

The use of the PA catheter is ARDS is two-fold. These patients may have a chest roentgenogram that suggests cardiogenic pulmonary edema, or it may be difﬁcult to discern whether bilateral diffuse airspace disease is due to congestion or capillary leak. This uncertainty may only be clariﬁed after placement of a PA catheter. The deﬁnition of ARDS includes PAWP readings ,18 mm Hg, thereby excluding a cardiogenic cause of respiratory failure (113). Judicious ﬂuid management is also an integral part of the management of patients with severe respiratory failure and ARDS. There may be a mortality beneﬁt in patients who receive less overall ﬂuid or are treated with a conservative ﬂuid management strategy (114). This may be best managed using a PA catheter. The use of PA catheterization is being intensively investigated in the setting of acute lung injury (ALI) and ARDS (115). A prospective, randomized, multi-center ARDS Network trial comparing PA catheter versus central venous catheter use in the management of ALI and ARDS as well as ﬂuid management strategies entitled Fluid and Catheter Treatment Trial (FACTT) is currently underway. This trial represents two studies designed to compare the use of the PA catheter to a central venous line and also conservative ﬂuid management with liberal ﬂuid management in these patients. It was initiated in July 2000, then suspended in July 2002 because of concerns by the Ofﬁce for Human Research Protection (OHRP), but has since resumed enrollment. Shock States

In clinical practice, speciﬁc conditions are associated with characteristic ﬁndings in the PAWP, CO, systemic, and pulmonary vascular resistance. This can be

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useful in conﬁrming suspected diagnoses and provide guidance in management. Cardiogenic and vasodilatory or septic shock are the two most frequently encountered shock states, and both have characteristic ﬁndings. In cardiogenic shock associated with a myocardial infarction, the primary pathology is that of poor pump function. This is seen as an elevated PAWP, decreased CO and cardiac index, and elevated systemic vascular resistance. Elevated pulmonary artery pressures may be seen as a result of markedly elevated PAWP and a poorly compliant LV. In vasodilatory or septic shock, the PAWP is typically in the normal range or even low, with an increased CO and cardiac index and decreased systemic vascular resistance. Of course these are generalities, but they may be helpful in distinguishing these states from other similar conditions. Acute Pulmonary Embolism

Massive pulmonary embolism may present as cardiogenic shock. At PA catheterization, patients may have decreased CO and cardiac index, but with elevated pulmonary artery diastolic pressures and normal PAWP, which distinguishes massive pulmonary embolism from cardiogenic shock. As much as one-third of a previously normal pulmonary vascular bed may be obstructed, but the mean PA pressure rarely exceeds 50 mmHg unless there is a chronic component of pulmonary hypertension (116). Pulmonary vascular resistance is elevated, and the PA diastolic pressure is signiﬁcantly higher than the mean PAWP (by more than 5 mmHg). The “a” and “v” waves of the PAWP tracing may disappear because of the elevated pulmonary vascular resistance, and the catheter tip may not be able to sense the pressure generated from the LA (117,118). CO may be decreased if more than 60% of the pulmonary vascular bed is being obstructed (116 – 118). Pre- and Post-Operative Monitoring by Using the PA Catheter

This is one of the most controversial areas in the use of the PA catheter. It has never been clear that the placement of a PA catheter will improve the management of high-risk patients undergoing surgery. Sandham et al., in the Canadian Critical Care Clinical Trials Group, examined the use of the PA catheter in high-risk surgical patients in a randomized, controlled trial. Of 3803 eligible patients, 52.4% (1994 patients) underwent randomization, comparing goaldirected therapy with and without a PA catheter (88). The subjects were highrisk according to the American Society of Anesthesiologists (ASA) class III or IV, aged 60 or older, who were scheduled for urgent or elective major surgery, followed by ICU stay. Each group had 997 patients; 78 patients who had a PA catheter died in the hospital, compared with 77 patients without a PA catheter (7.8% vs. 7.7%). There was no signiﬁcant difference in mortality rate between the two groups. But there is a signiﬁcant increase in the incidence of pulmonary embolism in the catheter group (8 events vs. 0 events). More patients in the catheter group received inotropic agents, vasodilators, antihypertensive

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medications, blood transfusions, and colloids. They concluded that routine insertion of the PA catheter perioperatively in high-risk surgical patients is not warranted (88). The ASA, in 2003, published their practice guidelines for PA catheterization (119). They reviewed their old guidelines from 1993 and incorporated information from the American College of Physicians, ACC/American Heart Association, American College of Chest Physicians, American Thoracic Society, and the Society of Critical Care Medicine. They concluded that the appropriateness of PA catheterization depends on the combination of three risk factors: the health status of the patient, the speciﬁc type of surgery, and the practice settings. Patients are stratiﬁed according to the ASA: classes 1 and 2 are patients who are unlikely to have organ dysfunction, class 3 are those with moderate risk, and classes 4 and 5 are those patients who have hemodynamic instability and a greater chance of organ dysfunction or death. Surgery was classiﬁed as low-, moderate-, or high-risk procedures, based on expected morbidity and mortality. Critical features of the practice setting included catheter insertion skills, training, and experience of nursing staff and doctors in interpreting data; technical support; ancillary services; and availability of specialists and equipment (120). In general, PA catheterization is appropriate in moderate to high-risk patients undergoing moderate to high-risk surgery in a moderate to high-risk setting. Patients with moderate to high-risk stratiﬁcation (ASA 3 –5, Table 13) are expected to have a moderate to high predicatability of ﬂuid or hemodynamic changes, increasing the risk of morbidity and mortality. Moderate- to high-risk surgical procedures are those with an increased risk of complications from hemodynamic changes. Examples include surgical patients undergoing elective or urgent major surgery such as coronary artery bypass graft surgery, lung resection,

Table 13

Patient ASA Risk Stratiﬁcation

ASA

Patient stratiﬁcation

1 2

Low Low

3

Moderate

4

High

5

High

Examples Healthy patient Mild systemic disease (e.g., controlled hypertension, diabetes) Severe systemic illness, not incapacitated (e.g., morbid obesity, COPD, angina post, myocardial infarction) Incapacitating systemic illness, constant threat to life (e.g., unstable angina, congestive heart failure, hepatic, or renal failure) Moribund, not expected to survive for 24 hr with or without procedure

Abbreviations: ASA, The American Society of Anesthesiologists; COPD, chronic obstructive pulmonary disease.

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or trauma. These patients usually will be followed by care in the ICU and with the information provided by the PA catheter, intensivists are be able to provide earlier goal-directed therapy. In low-risk patients undergoing low-risk surgery, e.g., knee replacement, the PA catheter is not necessary. Hence, the use of the PA catheter depends on clinician knowledge, patient classiﬁcation, and the severity of the surgery. In summary, there is no absolute requirement for the use of the PA catheter in critically ill patients. Many studies over the last four decades have been done, but none have provided conclusive support or against its routine use. The above examples are suggestions and recommendations for the use of the catheter in speciﬁc clinical situations. Clinician knowledge about the insertion and complications of the catheter, appropriate interpretation of the data, and appropriate application of the data are crucial for the safe use of this device, and this expertise may be lacking by some. Current training, credentialing, and quality improvement issues need to be evaluated at each institution. Clinicians should continue to carefully weigh the risks and beneﬁts of the PA catheterization in management of individual patients before its insertion. G. Complications of PA Catheters

Complications of PA Catheterization are listed in Table 14. These have been separated into complications related to placement of the catheter and complications related to the catheter itself. Dysrhythmias, such as atrial ﬁbrillation and ﬂutter, premature ventricular tachycardia, or ﬁbrillation, may occur during catheter insertion or withdrawal but usually resolve spontaneously after the catheter is advanced or withdrawn through the right heart chambers (121). Dysrhythmias Table 14

Complications of PA Catheterization

Complication related to central venous cannulation (refer to section on “Central Venous Catheters”) Complications related to insertion of the PA catheter Due to catheterization procedure Dysrhythmias Right bundle branch block Complete heart block Catheter knotting Due to catheter presence Thrombosis/embolism Pulmonary infarction PA rupture/perforation Balloon rupture Infection Endocardial damage Abbreviation: PA, pulmonary artery.

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seldom need to be treated with anti-arrhythmic drugs or cardioversion. Risk factors for ventricular tachycardia include hypocalcemia, myocardial ischemia or infarction, hypotension, hypokalemia, hypocalcemia, hypoxemia, and acidosis. Catheter advancement can injure the right bundle branch, with a resultant conduction block. In patients with a pre-existing left bundle branch block, this may precipitate a complete heart block (122 – 128). Although acknowledged as a potential complication, it rarely occurs and should not be considered a contraindication to PA catheter placement (127). Complications of catheter residence inside pulmonary artery include venous thrombosis, thrombophlebitis, pulmonary embolism, and infarction (129 – 134). During the initial years of PA catheterization, pulmonary infarction was thought to be one of the most common serious complications. Foote et al. found a 7.2% incidence of infarction in 1974 (129). In 1983, Boyd et al. found 1.3% of 500 consecutive insertions (56). Sandham et al. (88) in 2003 stated that they had eight events of pulmonary embolism in 78 of 997 patients in whom a PA catheterization was used in the randomization of 1994 patients. Pulmonary infarction can be caused by the persistent wedging of the catheter. Distal migration of the catheter is common (134) and is most likely to occur within 12 to 24 hours of insertion. The catheter should be maintained in such a position that nearly the full recommended balloon inﬂation is required to produce a wedge. Chest roentgenograms should be done daily to assess the position of the tip of the catheter. Since the introduction of heparin-bonded catheters, thromboembolism has been reduced, but other complications such as heparininduced thrombocytopenia and thrombosis remain (135). Fatal pulmonary artery rupture is fortunately rare (136). The major risk factors for rupture or perforation are pulmonary artery hypertension, advanced age of the patient, hypothermia, and anticoagulant therapy. Patients with PA perforation can present with massive hemoptysis. Emergency management includes immediate wedge tamponade followed by arteriogram, bronchoscopy, intubation of the unaffected lung, and consideration of emergency lobectomy (136,137,138). Balloon rupture should be suspected when attempted inﬂation is not met with the usual feeling of resistance (93,94). If the balloon ruptures during catheter insertion, the protective cushioning effect of the balloon will be lost, and it may cause endocardial damage and more arrhythymic complications. Knotting of the catheter can occur when the cardiac chambers are dilated or the catheter is repeatedly withdrawn and re-advanced (128). This can be avoided if care is taken not to advance the catheter signiﬁcantly beyond the distances at which entrance to the ventricle or PA would normally be anticipated. On some occasions, it is advised to perform the PA catheterization under the guidance of ﬂuoroscopy, especially when the RV is dilated. Infection is a potentially serious complication of PA catheter insertion and residence inside the pulmonary artery (139 –142). It may be difﬁcult to determine whether the source of infection is from the catheter or from the patient’s preexisting or concomitant infection. Skin ﬂora is a common source of infection.

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The incidence of catheter-related septicemia increases with prolonged duration of catheter placement (.3 – 4 days) (65). Right-sided septic endocarditis has been reported (141). Incidence of catheter colonization or contamination from skin ﬂora varies from 5% to 20%, depending on the duration of catheter residence and the criteria used to deﬁne colonization (139,143). Aseptic techniques should always be performed during catheter insertion and maintenance. A sterile protective sleeve, antibiotic-bonded catheter, and empiric changing of catheters over a guidewire have been used to reduce the risk of infection (144 – 146). The ASA Task Force concluded that serious complications (PA rupture, serious ventricular dysrhythmias, endocardial lesions) occur in 0.1% to 0.5% of PA catheter-monitored surgical patients (119). However, physicians dealing with other patient populations have different clinical experiences. In a survey of cardiologists and internists, the estimated probability of severe morbidity or death from PA catheterization was noted to be 2% to 5% and 0.5% to 1%, respectively (132). H. Controversy of PA Catheter Use

As PA catheterization is a monitoring device, its clinical utility depends on the appropriate indication, health status of the patient, skill and technical support of the equipment, interpretation of data, and availability of effective treatments. Iberti et al. evaluated 496 physicians’ knowledge of the PA catheter in the U.S.A. and Canada (147). The mean test scores varied independently by training, frequency of insertion and interpretation of data, and whether the respondents’ hospital was a primary medical school afﬁliate. The conclusion was that “physician understanding of the use of the PA catheter is extremely variable and frighteningly low” (148). The main issue in the use of the PA is whether it impacts the mortality and safety of patients. If follows that physicians who use this device should be fully knowledgeable about the intricacies of the catheter. The authors believe that credentialing requirements for PA catheter use should not only include a demonstration of insertion skill, but competence in the interpretation and application of the data. They proposed that 10 insertions would be required to attain the initial mastery and subsequently ﬁve insertions per year would be required to maintain competence. This has not yet been adopted in routine credentialing. Some of the controversy with the use of the PA catheter stems from favorable outcomes noted when it was used to guide therapy to reach normal or supranormal levels. Shoemaker et al. published several papers between 1985 and 1991, using the PA catheter in the perioperative period to evaluate and guide therapy in high-risk surgical patients (80,81,149,150). They optimized the CO and oxygen delivery to supranormal levels with data obtained from the PA catheter. Schultz et al. were able to reproduce similar favorable results in patients with hip fractures (82). In the early treatment of severe sepsis and septic shock in the emergency room, similar success was published by Rivers et al. in a early goal-directed approach to management (83). A higher CO was associated with

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lower mortality in patients in septic shock with the rationale that better tissue perfusion was obtained (81,84). In a meta-analysis of studies published between 1970 and 1996, there was decreased morbidity noted in patients with PA catheters compared with those without, calculating a relative risk ratio of 0.78 (0.65 – 0.94) for the incidence of organ failure (151). However, there are several investigations that are contrary to this experience. Gore et al. reported that the use of the PA catheter was associated with a higher fatality rate in patients with congestive heart failure, 44.8% compared with 25.3% (P , 0.001) (85). In patients with hypotension, the case fatality rate was 48.3% in those with PA catheterization, compared with 32.2% for those without (P , 0.001). Length of hospital stay was signiﬁcantly longer in patients receiving a PA catheter. A study from Israel reported a similar lack of beneﬁt in an observational cohort of 5841 patients with acute myocardial infarction (86). In 1996, Connors et al. (152) performed a post hoc analysis on 5735 critically ill patients in nine disease categories admitted to the ICUs in ﬁve medical centers as part of the SUPPORT study. This was an observational study, and as part of their retrospective analysis, they developed a “propensity score” to adjust for disease severity and other demographic factors. They identiﬁed two groups of patients with similar propensity scores. Patients who underwent PA catheterization had higher mortality rates, longer length of stay in the hospital, and subsequently higher hospital costs than those who did not (87). This suggested that the PA catheter was associated with increased morbidity and mortality and spawned considerable debate about the use of the device in the management of critically ill patients (153). It should be noted that the device was never subject to a prospective evaluation of efﬁcacy prior to its introduction into clinical use. Subsequent, prospective randomized trials have not identiﬁed an increase in mortality associated with the use of the PA catheter. The randomized, controlled trial of PA catheters in high-risk surgical patients by Sandham et al. (88) has been previously outlined. There was no signiﬁcant difference in mortality rate between the two groups, but there is a signiﬁcant increase in the incidence of pulmonary embolism in the catheter group (8 events vs. 0 events). The authors found no beneﬁt to routine insertion of the PA catheter perioperatively in high-risk surgical patients and concluded it was not warranted (88). Richard et al. randomized 676 with shock, ARDS, or both to early use (within 24 hours) of a PA catheter in management. The placement of a PA catheter did not signiﬁcantly affect mortality or morbidity as deﬁned by organ system failure, need for vasoactive agents, duration of mechanical ventilation, ICU, or hospital stay. On day 28, the mortality rate in the PA catheter group was 59.4%, and the control group was 61.0%. They concluded that there was no observed beneﬁt with the insertion of a PA catheter in these patients (89). I.

Ongoing Prospective, Randomized Trials

Subsequent trials addressing the utility of the PA catheter in patient management are in progress. These include the previously described FACTT trial and a U.K.

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sponsored PAC-Man trial (154). The latter trial has now been completed. It enrolled 1041 patients from 65 United Kingdom intensive care units with a broad range of diagnoses. The focus was on critically ill patients with a perceived need for PA catheter placement by their physician. The study demonstrated no difference in hospital mortality in critically ill patients managed with or without pulmonary artery catheters. There were more complications related to catheter insertion and changes in management based on results from the catheter were modest. It is unclear whether PA catheter use improved outcome. Another trial evaluated the utility of the PA catheter in the management of patients with severe congestive heart failure (New York Heart Association classes III and IV) (155). This is the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial, which has completed enrollment and is currently undergoing analysis. The results from these three major studies should further deﬁne the role of the PA catheter in the management of critically ill patients. J.

General Principles in PA Catheter Use

Until the results of these future studies are available, clinicians using the PA catheters for hemodynamic monitoring should carefully assess the risk-to-beneﬁt ratio on an individual patient basis. The indications, insertion techniques, equipment, patient’s health status, and interpretation of data obtained from the catheter should be taken into consideration before the PA catheter is used (156). PA catheterization should only be used as a complementary device to diagnose and guide therapy after clinical evaluation and treatment have been exercised. It is important to recognize that diagnostic tests and monitoring devices do not determine clinical outcomes, but that outcomes are inﬂuenced by therapy directed by information obtained with the catheter. Minimizing the complications associated with its placement and limiting the duration of placement should be the major guiding principles in its use. The PA catheter should be removed as soon as information derived from its placement is no longer clinically useful. In some cases, this may occur within a few hours, and certainly placement should not exceed three to four days in any case. Although there is great hope that pending research studies will further deﬁne the role of the PA catheter in patient management, it is important to recognize that there will remain areas of uncertainty in its use. Even with these trials, there may still be signiﬁcant debate surrounding the use of the PA catheter. It is probably safe to conclude that there will always be a role for this device in the management of critically ill patients. Therefore, it behooves all involved to be cognizant of its potential and limitations.

V.

Chest Tube Thoracostomy

A. Background

Chest tubes are used in many clinical settings, and their placement is one of the most important skills to master in the management of life-threatening conditions.

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Chest tube placement and management is important not only in the ICU but also in Advanced Trauma and Life Support (157). B. Anatomy

The parietal pleura lines the thoracic wall and covers the superior surface of the diaphragm. It can be divided into four sections: the costal pleura, cervical pleura, mediastinal pleura, and the diaphragmatic pleura. The parietal pleura is supplied with blood from the intercostal arteries and branches of the internal thoracic artery. It is innervated by the intercostal nerves and the phrenic nerve. Pain from these nerve ﬁbers may be referred to the thoracic and abdominal walls, neck, and shoulder (phrenic nerve). At the hilum and pulmonary ligament, the pleura becomes the visceral pleura as it is reﬂected and adheres to the surface of the lung. The visceral pleura is mainly perfused by the systemic circulation. The pleural layers are in close opposition to each other, with the potential space between them containing a thin layer of ﬂuid. This ﬂuid acts as a lubricant, allowing the pleural membranes to slide easily against each other. Under normal circumstances, there is a negative intrapleural pressure of 2 to 5 cm of water. Disruption in visceral or parietal pleura results in pneumothorax or hemothorax. Fluid can accumulate in the pleural space because of the changes in hydrostatic or oncotic pressures due to impaired lymphatic drainage or inﬂammatory diseases. C. Indications

Chest tubes are inserted to evacuate air or ﬂuid. The indications for chest tube placement are listed in Table 15 and also discussed in the following sections. Pneumothorax

Pneumothorax is the most common indication for chest tube placement. Patients may present with symptoms of dyspnea, tachypnea, and chest pain. Clinical examination reveals diminished breath sounds and hyper resonance to percussion. The diagnosis is usually conﬁrmed by chest X-ray. Inspiratory and expiratory ﬁlms are helpful in equivocal cases as is chest computed tomographic scanning. Spontaneous or iatrogenic pneumothorax of less than 25% volume in

Table 15

Indications for Chest Tube Placement

Pneumothorax Hemothorax Empyema Pleural effusion Chylothorax Pleurodesis

Spontaneous; traumatic; tension; iatrogenic; bronchopleural ﬁstula Traumatic; iatrogenic; infections; ruptured thoracic aortic aneurysm Parapneumonic; post traumatic; intraabdominal Transudate; exudates — —

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asymptomatic or minimally symptomatic patients without signiﬁcant underlying disease can be observed with serial chest X-rays. Urgent chest tube placement is necessary in patients with severe distress and expanding amounts of intrapleural air, signiﬁcant underlying lung disease, and mechanically ventilation. Tension pneumothorax requires immediate decompression with a 14- or 16-gauge catheter in the second intercostal space, mid clavicular line, while preparations for chest tube placement are being made.

Hemothorax

Hemothorax refers to a collection of blood in the pleural cavity. The pleural ﬂuid hematocrit is greater than or equal to 50% of the blood hematocrit. Etiology of hemothorax can be spontaneous, iatrogenic, or traumatic in origin. Spontaneous hemothorax may result from primary or metastatic malignancy in the lung or pleura, pulmonary infarcts, arteriovenous malformations, and necrotizing pulmonary infections. Common traumatic and iatrogenic causes include rib fractures, attempted thoracentesis, or chest tube placement resulting in damage to intercostal or internal mammary arteries. Large bore drainage tubes in this setting help in the assessment of the degree of blood loss. Evidence of persistent bleeding following trauma, with hemodynamic instability, is an indication for open thoracotomy. Late-stage complications of unresolved hemothorax include empyema and ﬁbrothorax.

Empyema and Parapneumonic Effusions

Pleural ﬂuid secondary to bacterial process in the thoracic cavity is classiﬁed as parapneumonic effusions, complicated parapneumonic effusions, and empyema (158). A parapneumonic effusion is any pleural effusion secondary to a bacterial process, usually treated with antibiotics with or without thoracentesis. A complicated parapneumoic effusion is a parapneumonic effusion that requires chest tube placement for resolution as it is unlikely to clear with antibiotics alone. Empyema is pus in the pleural space. Indications for chest tube placement are a pleural ﬂuid with a pH , 7.20, a glucose level less than 40 mg/dL and a lactate dehydrogenase (LDH) level greater than 1000 U/L, and positive Gram stain or positive pleural ﬂuid cultures. Simple complicated parapneumonic effusions can be managed with relatively small chest tubes placed percutaneously. Complex complicated parapneumonic effusions are multiloculated. CT scans or ultrasound (Fig. 11) are used to help localize the loculated ﬂuid (159). These require larger bore chest tubes and occasionally the addition of a thrombolytic agent, usually streptokinase, urokinase, or alteplase (160,161). Large bore chest tubes (28F or greater) are required for simple empyemas with free-ﬂowing ﬂuid or in a single loculus. Effusions that do not resolve with chest tube placement and thrombolytics require surgical decoritication (162) or open ﬂap drainage.

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Figure 11 Transthoracic sonogram demonstrating a loculated pleural effusion. Fibrin strands are clearly seen.

Pleural Effusion

Fluid can accumulate in the pleural space for a number of reasons. These include changes in hydrostatic and oncotic pressures, increased permeability of the microvasculature by inﬂammatory mediators, and impaired lymphatic drainage. Thoracentesis is usually done to determine whether the effusion is transudative or exudative in origin. Transudates result from imbalances in hydrostatic and oncotic pressures. Causes of transudative effusions include cirrhosis, congestive cardiac failure, and nephrotic syndrome. Management of transudative effusions is aimed at identifying and treating the underlying cause. Chest tubes are usually not indicated in the management of transudates except in selected cases of massive effusions. Exudates are formed by the disruption in the integrity of the endothelial membranes of pleural capillaries and venules. Inﬂammatory processes result in an increased permeability of these membranes with subsequent protein leak. Impaired lymphatic drainage decreases the removal of protein in the pleural space. Fluid from the peritoneum can also cause exudates. Infection, malignancy, and inﬂammatory diseases are all causes of exudative pleural effusions. Chemical analysis of the pleural ﬂuid distinguishes transudative effusions from exudates. Measurement of both serum and pleural ﬂuid protein and LDH is the most practical method of distinguishing the two. Light’s criteria (163), shown in Table 16, are used to distinguish exudative pleural effusions. If one of these three criteria is present, the ﬂuid is almost always an exudate. If none of these three are present, it is virtually always a transudate. If paired testing is not an option, any one of the three tests on a single pleural ﬂuid sample shown in Table 16 will identify an exudate (164).

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Tests Used to Distinguish Between Transudative and Exudative Pleural

Light’s criteria for deﬁning an exudates Pleural ﬂuid protein/serum protein ratio .0.5 Pleural ﬂuid LDH/serum LDH ratio .0.6 Pleural ﬂuid LDH .2/3 of the upper limit of normal of the serum LDH Single pleural ﬂuid testing in deﬁning an exdudate Pleural ﬂuid protein .3.0 g/dL (3 g/L) Pleural ﬂuid cholesterol .45 mg/dL (1.16 mmol/L) Pleural ﬂuid LDH .60% of the upper limit of normal serum value Abbreviation: LDH, lactate dehydrogenase. Source: From Refs. 163 and 164.

Decubitus ﬁlms help determine if the pleural effusion is free ﬂowing. Safe thoracentesis requires at least 1 cm of visible ﬂuid on the decubitus ﬁlm. Ultrasound, as already mentioned, can help determine the most appropriate site for thoracentesis or chest tube placement. In malignant effusions, chest tubes are placed for both symptomatic improvement and, often, subsequent instillation of sclerosing agents for pleurodesis. Sclerosing agents, such as talc, tetracycline derivatives, and bleomycin, are used once the lung has fully re-expanded and pleural ﬂuid drained. Chylothorax

Chyle is lymphatic ﬂuid of intestinal origin carried in the thoracic duct across the chest. It has a high content of triglycerides, typically over 110 mg/dL, and lymphocytes. The thoracic duct enters the mediastinum on the right side of the chest and crosses over to the left at the level of the ﬁfth thoracic vertebrae in most adults. Between 1.5 and 2.4 L of ﬂuid ﬂow through the thoracic duct in a day. The causes of chylothrorax are divided into non-traumatic and traumatic (Table 17). Lymphoma is the most common non-traumatic cause; surgical procedures account for most traumatic cases. Treatment in non-traumatic cases is aimed at the underlying cause. Failure of chemotherapy or radiotherapy or the development of symptoms due to an increasing pleural effusion require chest tube drainage. Symptomatic effusions of idiopathic origin are treated with chest tube drainage and either decreased oral intake or parental nutrition with or without medium chain triglycerides. Most cases resolve within two to three weeks. Treatment options for resistant cases include pleurodesis, pleurectomy, and ligation of the thoracic duct at the hiatus. Prolonged and copious drainage from chest drains can result in weight loss, progressive hypoproteinemia, and immunosuppression. In these cases, earlier surgical intervention is warranted.

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Table 17

Etiologies of Chylothorax

Causes Non-traumatic Malignant Non-malignant Traumatic Surgical Nonsurgical

Lymphomatous, non-Lymphomatous (e.g., pulmonary and mediastinal malignancies) Idiopathic, others (e.g., cirrhosis, tuberculous, venous thrombosis) Cardiovascular, aortic lobectomy, pneumonectomy etc. Penetrating, nonpenetrating trauma to the neck, thorax, upper abdomen

D. Contraindications

There are no absolute contraindications to chest tube placement. Ideally in nonemergent cases, coagulopathies and low platelet counts should be corrected to avoid excessive bleeding. CT imaging or ultrasound-guided location of the placement is helpful in patients with a history of pneumonectomy, lung transplant, or complicated loculated effusions. E.

Equipment

The equipment necessary for chest tube placement is listed in Table 18. This includes the appropriate-size chest tube, a drainage device with or without suction source, connecting hoses with connectors, and a tray with insertion instruments. F.

Drain Size

Modern chest tubes are plastic, pliable, fenestrated tubes made of minimally thrombogenic material. Chest tube sizes range from number 6 to 40 French. Table 18 Equipment for Chest Tube Insertion Povidone – iodine solution Sterile towels and drapes Sterile sponges 2 Kelly clamps 1% lidocaine without epinephrine (40– 50 mL) 1.0 non-absorbable sutures 18, 21, and 25 gauge needles Scalpel, scissors Needle holder 10 mL syringe Sterile gown, gloves, mask, and cape Sterile gauze Chest tube and drainage system

Procedures in the ICU Table 19 French size

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Internal Diameter Correlate to the French Grading System Inch equivalent

Millimeter equivalent

0.053 0.105 0.131 0.210 0.236 0.288 0.341 0.367 0.419 0.471 0.498 0.524

1.35 2.7 3.3 5.3 6.0 7.3 8.7 9.3 10.7 12.0 12.7 13.3

4F 8F 10F 16F 18F 22F 26F 28F 32F 36F 38F 40F

Table 19 lists the internal diameter correlate to the French grading system for a range of chest tube sizes. The use of large bore tubes has previously been recommended (165 – 167) as it was felt they decreased the incidence of blockage, particularly in thick malignant or infected ﬂuid. Most physicians now use smaller tubes (10 – 14 French) as studies have shown these to be as effective as the larger bore tubes (168,169), more comfortable, and better tolerated (170). There remains intense debate over the optimal drain size. The 9 French tubes have been used with success rates of up to 87% in pneumothoracies (171). Ultrasound-guided insertion of small-bore tubes for treatment of malignant pleural effusions for sclerotherapy has been well studied with good effect (169,172,173). Small- and medium-bore chest tubes are usually placed using the Seldinger technique. Complicated parapneumonic effusions not amenable to a single large catheter may require more than one small-bore tube placed under image guidance. Larger bore tubes (32 – 40 French) are recommended for hemothorax, to allow for successful drainage and assessment of continuing blood loss (174). The larger bore tubes are inserted by blunt dissection, which allows the operator to manually break down loculations if necessary. G. Technique

Prior to inserting the chest tube, it is important to place the patient in the correct position. The preferred position is on the bed, slightly rotated with the arm on the side of the lesion behind the patient’s head, exposing the axillary area (166,175). Alternatively, the patient can be sitting upright, leaning on a pillow over a table. Aim for insertion in the triangle of safety (157), which lies between the anterior and posterior axillary lines, through the fourth or ﬁfth intercostal

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space, just above the rib, thus avoiding the intercostal neurovascular bundle. Under sterile conditions, the area is prepped with pivodine –iodine solution. Local anesthesia is inﬁltrated into the site of insertion. A small gauge needle is used to raise a small bleb prior to inﬁltration of the interocostal muscles and pleural surface. Up to 30 – 40 mL of lidocaine may be needed to ensure adequate anesthesia. Thoracentesis is often initially performed to conﬁrm the presence of air or ﬂuid at the site of insertion. Chest tubes can be inserted by either blunt dissection with or without the use of a trochar or the Seldinger technique. Whichever technique is used, the use of substantial force must be avoided to avoid penetration and damage to vital intrathoracic structures. For blunt dissection, a 2-cm incision is made parallel to the intercostal space, immediately above the rib. A Kelly clamp is used for blunt dissection (Fig. 12), creating a subcutaneous tunnel to the intercostal space. The closed clamp is gently inserted through the parietal pleura over the superior aspect of the rib. Once through the parietal pleural, the clamp is gently opened to spread the parietal pleura and intercostal muscles. For a chest tube similar to the size of a ﬁnger, the tract should be gently explored with a ﬁnger, performing a gentle sweep and taking care not to disrupt ﬁrm organized adhesions. The proximal end of the tube, ﬁrmly held

Figure 12 Appropriate angle of penetration into the pleural space during the blunt dissection technique. Source: From Miller, KS, Sahn, SA. Chest tubes, indications, techniques, management and complications. Chest 1987; 91(2):258 – 264.

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by the Kelly clamp, is then inserted into the pleural space. If using a trochar, care must be taken to ensure the sharp point of the trochar is retracted a few centimeters from the chest tube tip. Trochar insertion is relatively fast but runs the risk of impaling the lung or other organs. The position of the tip of the chest tube should ideally be aimed anteriorly towards the apex of the lung in the treatment of a pneumothorax. For free-ﬂowing effusions, chest tubes are aimed downwards and in the posterior direction, into the costovertebral angle. For basal and lateral empyemas or loculated collections, the chest tube is placed in the most dependant region. However, any tube position can be effective at draining air or ﬂuid, and an effective drain should not be repositioned solely because of its radiographic position. The depth of insertion of the chest tube ranges from 5 to 15 cm, ensuring all sideports are within the chest, and the proximal port must be at least 2 cm beyond the rib margin. The centimeter markings on the side of the chest tube start from the most proximal port; therefore, a tube at a 5-cm mark at the skin means it is 5 cm from the most proximal port. The ﬁnal depth is dependant on the ease of aspiration of the pleural ﬂuid and the patient size. Correct insertion of the chest tube is conﬁrmed by visualization of condensation within the tube with respiration or the drainage of pleural ﬂuid. Two simple horizontal mattress sutures are placed on either side of the insertion site to anchor the tube. Complicated purse string sutures should be avoided as they convert a linear incision into a circular wound, which is painful and can leave a prominent scar (176). A sterile dressing is then applied over the site, which is covered and secured with surgical tape. Occlusive petroleum dressings are generally not recommended. Small- and medium-bore catheters are usually inserted with the aid of guide wire by the Seldinger technique (170,177,178) (Fig. 13). This technique is fast and relatively safe, making a smaller incision and insertion, causing less discomfort than the blunt dissection method. It is, however, difﬁcult to control the direction of the tube entry into the pleura, and advancement may be difﬁcult if adhesions are present. Using this technique, the introducer needle is advanced over the superior border of the rib into the pleural space. Air or ﬂuid is aspirated to conﬁrm the correct position. The guide wire is then advanced through the needle into the pleural space without any resistance. The needle is then removed, leaving the guide wire in place. Ensuring adequate analgesia, a series of dilators are passed over the guide wire into the pleural space. Introduction into the pleural space is facilitated by rotating and advancing the dilators in the same plane of the guidewire to prevent kinking. The chest tube assembly is advanced into the pleural space over the guide wire. The guide wire and chest tube inserter are removed, leaving the chest tube in place. All ports of the chest tube should be in the pleural space. Once the chest tube is inserted and secured, it is connected to the pleural drainage system. All connections between the chest tube and its drainage system should be tight and securely taped.

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Figure 13 Percutaneous insertion of a chest tube using the Seldinger technique. Source: Thal-Quick Chest Tube Instruction Manual. Cook Critical Care. Cook Incorporated, 1987. H. Complications

Complications of chest tube placement can be divided into three categories: placement, maintenance, and discontinuation (Table 20). Complication rates from chest tube insertion in blunt trauma have been shown to be between 9% and 21% (179,180). Insertion alone has a complication Table 20

Complications of Chest Tube Placement

Placement

Damage to vital structures (lung, heart, liver, spleen) Hemorrhage (great vessels, heart, intercostal artery) Neurological damage (phrenic nerve) Chylothorax

Maintenance

Re-expansion pulmonary edema Subcutaneous emphysema Lung entrapment Pneumothorax with inadvertent disconnection Empyema

Discontinuation

Recurrence of pneumothorax Pleurocutaneous ﬁstula

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rate of 1% to 2% (179,181). Perforation of the RA, RV, and abdominal organs has also been reported (182 –185), as has chylothorax from thoracic duct injury (186). Perforation of the diaphragm is avoided by inserting the chest tube no lower than the ﬁfth intercostal space. Ipsilateral hemidiaphragmatic palsy from isolated injury to the intrathoracic phrenic nerve has also been reported (187). Subcutaneous emphysema from the thoracostomy site involving the chest wall and extending into the neck can also occur, but this is usually a cosmetic problem. Rapid re-expansion of previously collapsed lung may result in unilateral pulmonary edema (188), which may be fatal (189). It can occur in young patients with pneumothoracies (190) and also following removal of large volumes of ﬂuid or after removal of an obstructive tumor (191 –193). The development of re-expansion pulmonary edema probably correlates with the amount of negative intrathoracic pressure, which in turn is related to the rate of ﬂuid removal. The onset of cough or chest tightness is an important warning sign to end the procedure. Most experts recommend the removal of 1 to 1.5 L at any one time. Supportive treatment is usually sufﬁcient. Secondary infection of the pleural space following chest tube insertion is a rare complication that occurs most frequently following treatment of traumatic hemothorax.

I.

Chest Tube Management

Once secured, the chest tube is attached to a drainage device. Although there are many commercially available devices, they consist of one or more of the following: (1) water seal, (2) drainage tap, (3) pressure control change, and (4) connecting hoses. The water seal prevents air from entering the pleural cavity whilst air or ﬂuid is being drained. Most institutions use a three-chamber system (Fig. 14). The closed water seal is placed under water at 3 cm. This allows the operator to see air bubble out as the lung re-expands in pneumothorax or the ﬂuid evacuation rate in effusions or empyemas. If suction is required, it is performed via the water seal at a level of 15 to 20 cm of water. This water level should be checked daily to ensure an adequate water seal and suction regulator is maintained. If suction is applied, bubbling is seen in the suction control chamber. Periodic milking or stripping of the connecting hoses is generally discouraged because as it has not been shown to increase tube patency (194). If continuous bubbling through the water seal is seen, intermittent clamping of the connecting hoses, starting at the drainage device and moving proximally to the chest wall, should reveal the site of leakage. Connecting sites are common sources of leaks. Persistent air leaks may be due to bronchopleural ﬁstulas. If there is no variation of the water seal with respiration, then occlusion of the chest tube should be suspected. Saline irrigation should initially be attempted. Prolonged clamping of the chest tube should be avoided as this may result in tension pneumothorax. Serial chest X-rays should be obtained to assess tube position, exclude complications

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Figure 14 Example of a three-chamber water seal chest drain. Source: Atrium Ocean Water Seal Chest Drain, Atrium Medical Corporation, 2004.

such as pneumothorax, and evaluate the progress of drainage. Non-functioning tubes should be removed and a new tube placed in a different site.

J.

Chest Tube Removal

Chest tubes are removed when the pneumothorax or pleural ﬂuid has resolved or when they are no longer functional. Although controversial, in the case of pneumothorax, some physicians prefer clamping chest tubes for four to six hours prior to removal in order to identify a persistent leak. Regardless of whether the chest tube is clamped or not, most physicians wait ﬁve to 12 hours after the last evidence of an air leak to repeat a chest X-ray prior to removing the tube. For pleural effusions, chest tubes can be removed when daily output is less than 100 mL on water seal or the tube is no longer functional. Chest tubes are removed at the end of exhalation with the patient performing the Valsalva maneuver. The tube is rapidly removed and an occlusive dressing applied. Indwelling sutures are tightened. A follow-up chest X-ray should be performed.

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8 Bronchoscopy

NIKHIL SHAH

IRAWAN SUSANTO

Pulmonary and Critical Care Section West Los Angeles Healthcare Center VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

UCLA–Santa Monica Specialties Geffen School of Medicine at UCLA Santa Monica, California, U.S.A.

SILVERIO SANTIAGO Pulmonary and Critical Care Section West Los Angeles Healthcare Center VA Greater Los Angeles Healthcare System and Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

I.

Introduction

Bronchoscopy is the most commonly performed procedure by pulmonary physicians today. The history of bronchoscopy dates back to the 19th century and was ﬁrst performed in 1897 by Gustav Killian for extraction of an aspirated piece of bone from a patient’s right main stem bronchus (1). The ﬁrst bronchoscopes developed were rigid and used mostly for extraction of foreign bodies. Modiﬁcations to the rigid bronchoscope now allow for maintenance of ventilation, improved visualization with the use of optical telescopes, and passage of various instruments for diagnostic and therapeutic procedures (2,3). The major disadvantage of rigid bronchoscopy is the inability to access the upper lobes and airways distal to the segmental oriﬁces. The rigid bronchoscope continues to have many important uses today, although its use has subsided with the introduction of the ﬂexible ﬁberoptic bronchoscope. The ﬁrst ﬁberoptic bronchoscope was developed by Ikeda in 1964 (4). The properties of 285

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ﬁberoptics enable the bronchoscope to bend, and this allows for easy navigation throughout the tracheo-bronchial tree. Flexible bronchoscopy currently plays an important role for diagnosis and treatment in both outpatient and inpatient settings. II.

Speciﬁcations, Indications, and Contraindications

Rigid bronchoscopes are straight metal hollow tubes that allow for diagnostic procedures and therapeutic interventions. They have ports that allow for ventilation and administration of anesthetic gases and suction ports for removal of secretions and blood. The hollow tube allows for the introduction of optical telescopes or a ﬂexible ﬁberoptic bronchoscope. Other types of accessory equipment are available, including biopsy forceps, baskets for foreign body removal, introducers for stent placement, and laser ﬁbers for treatment of endobronchial lesions. Rigid bronchoscopy is typically performed under general anesthesia. The indications for rigid bronchoscopy are listed in Table 1. The ﬂexible ﬁberoptic bronchoscope has continued to evolve since its introduction in 1967. The average adult bronchoscope has an external diameter of 4 to 6 mm and a typical viewing radius of 1208. The working channel for introduction of accessory instruments or suction is typically 1 to 3 mm in diameter. Ultrathin bronchoscopes for the evaluation of small distal airways are now available and have an external diameter of 2.7 mm. Another relatively new development is the videoscope that contains a video chip at the distal tip of the bronchoscope. These chips have a lower propensity for damage when compared with ﬁber bundles and also allow for digital processing of images. A wide variety of ancillary equipment may be used with the ﬂexible ﬁberoptic bronchoscope, including biopsy forceps, protected and non-protected brushes for cytologic and microbiologic studies, and devices for transbronchial needle aspiration. Flexible bronchoscopy is usually performed with local anesthesia and may or may not require conscious sedation. The indications for ﬂexible bronchoscopy are listed in Table 2 (5,6). There are relatively few absolute contraindications to both rigid and ﬂexible bronchoscopy. These include lack of consent for the procedure and the presence of malignant cardiac arrhythmias and refractory hypoxemia. Additional absolute contraindications for rigid bronchoscopy include the presence of cervical injury, an unstable neck, and microstomia. Table 1 Indications for Rigid Bronchoscopy Dilatation of strictures/stenosis Placement of airway prostheses (stents) Retrieval of foreign body Massive hemoptysis Resection of bulky tumors Laser therapy Cryotherapy Photodynamic therapy

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Table 2 Indications for Flexible Bronchoscopy Diagnostic indications Abnormal chest roentgenogram Unexplained cough, hemoptysis, wheeze, or stridor Suspected pulmonary infections Refractory lung abscess Determination of the presence and extent of thermal burns Evaluation of the airways for suspected injury after chest trauma Unexplained vocal cord paralysis and diaphragmatic paralysis Abnormal sputum cytology Suspected tracheo-esophageal or broncho-pleural ﬁstulas Carcinoma of the lung Evaluation of problems associated with endotracheal tubes To obtain diagnostic material from patients with non-infectious diffuse lung disease Foreign bodies Assessment of airway patency Evaluation of lung transplant rejection To investigate the etiology of SVC syndrome, chylothorax, or unexplained pleural effusion Therapeutic indications Atelectasis secondary to retained secretions, mucous plugs, or clots not mobilized by non-invasive techniques Debulking of malignant neoplasm Retrieval of foreign bodies Hemoptysis Treatment of Bronchopleural ﬁstula Drainage of bronchogenic cysts Endotracheal tube placement Percutaneous dilatational tracheostomy Electrocautery Cryotherapy Photodynamic therapy Laser therapy Brachytherapy Placement of metal stents Dilatation of strictures and stenosis Therapeutic BAL for Pulmonary Alveolar Proteinosis Abbreviations: SVC, superior vena cava; BAL, Bronchoalveolar lavage.

Conditions involving increased risk for both rigid and ﬂexible bronchoscopy include lack of patient cooperation, recent myocardial infarction, unstable angina, and active bronchospasm. Increased risk of bleeding after transbronchial biopsy is seen in patients with pulmonary hypertension. Similarly, increased risk of bleeding after biopsy is seen in patients with uremia, thrombocytopenia, and coagulopathy. Bleeding and laryngeal edema may also occur in patients with superior vena cava syndrome.

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Patient Preparation, Sedation, and Anesthesia

Bronchoscopies may be performed in endoscopy suites, operating rooms, radiology departments, or at the patient’s bedside. Pre-procedure preparation is similar to that for other procedures. Informed consent should be obtained from the patient. If the patient is unable to consent, the durable power of attorney for healthcare or surrogate should give informed consent on behalf of the patient. Patients should not take anything by mouth for six to eight hours prior to the procedure. Pre-bronchoscopy laboratory tests, including complete blood count, prothrombin time, partial thromboplastin time, and chemistries, are ordered by most physicians. Imaging studies should be available for review, including chest roentgenograms and computerized tomography (CT) scans, especially if transbronchial needle aspiration is to be performed. Patients on anti-coagulant therapy should be transitioned from coumadin to low molecular weight heparin or unfractionated heparin so that coagulopathy can be corrected prior to the procedure. Endocarditis prophylaxis is recommended in susceptible patients undergoing rigid bronchoscopy but not ﬁberoptic bronchoscopy. Nevertheless, each patient should be individualized based on the presence or absence of signiﬁcant infection, prosthetic valves, or prior episodes of endocarditis (7). All patients undergoing bronchoscopy should have an intravenous line. Blood pressure, oxygen saturation, and electrocardiogram should be monitored and oxygen administered to maintain oxygen saturation greater than 90%. Patients who undergo rigid bronchoscopy usually receive general anesthesia under the guidance of an anesthesiologist. On the other hand, ﬂexible ﬁberoptic bronchoscopy can be performed with or without conscious sedation. Most pulmonologists, however, sedate patients for ﬂexible ﬁberoptic bronchoscopy (8). Frequently used agents include benzodiazepines and opiates. The benzodiazepines provide sedation and an amnesic effect, whereas opiates provide sedation and help suppress coughing. Over-sedation with benzodiazepines and opiates can be reversed with ﬂumazenil and naloxone, respectively. Local anesthesia is usually attained with topical agents, such as the amide derivative lidocaine. Lidocaine is one of the safest topical agents for local anesthesia and is applied to the nares, oropharynx, vocal cords, and tracheobronchial tree (9). Caution should be exercised because lidocaine is easily absorbed from the respiratory tract and excess levels can lead to seizures, cardiac arrhythmias, and hypotension. It is, therefore, recommended that the total dose of lidocaine be limited to 8.2 mg/kg in adults (10). As lidocaine is metabolized in large part by the liver, patients with hepatic disease may be at increased risk for developing toxic blood levels. Lidocaine has also been reported to cause methemoglobinemia with hypoxemia (11), but when used judiciously, it provides adequate anesthesia without signiﬁcant risk of adverse effects. The routine use of antisialogogues, such as atropine, has come into question (10).

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Insertion Techniques

The rigid bronchoscope can be inserted through the mouth or through a tracheostomy stoma. On the other hand, the ﬂexible bronchoscope can be introduced through the nose, mouth, tracheostomy, or endotracheal tube. The oral route is preferred for ﬂexible bronchoscopy if frequent removal and reinsertion of the bronchoscope is anticipated or if endotracheal intubation is to be performed. The decision to intubate the patient is dependent on the clinical status of the patient. Patients are frequently intubated over the bronchoscope if their respiratory status is tenuous or if they are at increased risk for bleeding after biopsies. The nasal route avoids the possible complication of damage to the bronchoscope if the patient bites down in the absence of a bite block. In the intensive care unit (ICU), a patient requiring bronchoscopy may already have an endotracheal tube in place. This can pose problems if the tube is too small to accommodate an average bronchoscope. A size 7.5 (mm, inner diameter) endotracheal tube will allow passage of the bronchoscope but can limit adequate ventilation. A size 8.0 or greater endotracheal tube is recommended for ease of passage of the bronchoscope and for adequate ventilation. In patients with signiﬁcant lung disease, the bronchoscope may need to be withdrawn multiple times throughout the procedure to allow the patient to oxygenate and ventilate adequately. Smaller pediatric bronchoscopes can also be used. When compared with larger diameter adult bronchoscopes, use of pediatric bronchoscopes offers advantages in the mechanically ventilated patient, with less signiﬁcant cardiovascular and respiratory side effects while providing comparable cell and microbiological yields (12). When performing bronchoscopy on patients on mechanical ventilation, the FIO2 should be increased to 1.0 and maintained at that level throughout the procedure. V.

Diagnostic Techniques

Bronchoalveolar lavage (BAL) is a frequently utilized diagnostic procedure and is also used occasionally as a therapeutic modality in patients with pulmonary alveolar proteinosis. BAL ﬂuid is a marker for infectious and inﬂammatory processes occurring at the alveolar level. Proper technique of obtaining BAL samples is important in order to ensure diagnostic accuracy. BAL ﬂuid should be obtained prior to performing biopsies or brushings in order to avoid the admixture of signiﬁcant amounts of blood with the sample. This is especially true if bronchoscopy is being performed for diagnosis in patients with interstitial lung disease. Samples should be obtained from localized areas of abnormalities. In the absence of focal abnormalities, samples are usually obtained from the right middle lobe or the lingula. The bronchoscope should be allowed to occlude the airway (usually in the fourth- or ﬁfth-order bronchus) without over-wedging. Sterile saline at room temperature or warmed to body temperature is instilled via the working channel in aliquots of 50 to 60 mL to a total of 150 to 200 mL per BAL site. After a short dwell time, the ﬂuid is suctioned into a sterile

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container, with care being taken not to apply excessive suction to avoid collapse of the airway or suction trauma. It is estimated that this allows for the sampling of approximately one million alveoli. The ﬂuid can then be sent for a variety of analyses, including differential cell counts, cytologic examination, and microbiologic studies (13,14). Complications of BAL are uncommon but include fever, pneumonitis, bleeding, and bronchospasm. Endobronchial brushing is another frequently used technique for obtaining samples for cytology and microbiology. Brushes may be protected (sheathed) or unprotected. When attempting to obtain an uncontaminated material for culture, the protected brush is typically favored. Discrete peripheral lesions suspicious for malignancy can also be brushed to obtain specimens for cytology and is performed under ﬂuoroscopy to ensure that the brush is in the vicinity of the lesion. The most frequent complication seen with brushing is bleeding, which is usually self-limited. Bronchoscopic biopsies can be obtained from both visible endobronchial lesions and distal lesions. Different biopsy forceps are available, including toothed, non-toothed, and spiked forceps. Endobronchial lesions can be biopsied under direct visualization, thus minimizing risk of complications. Spiked forceps with an impaler needle can facilitate biopsies of endobronchial lesions that are difﬁcult to grab. Four to six biopsies are generally recommended to optimize diagnostic yield in bronchogenic carcinoma, although as many as 10 biopsies may be necessary to maximize yield for peripheral carcinomas (15). For more peripheral lung lesions or diffuse lung disease, samples are obtained using the transbronchial approach. Transbronchial biopsy in diffuse lung disease can be performed with or without ﬂuoroscopic guidance. Whether use of ﬂuoroscopy decreases the incidence of pneumothorax after transbronchial biopsy is debated (10,16,17). The other major complication that occurs with bronchoscopic biopsies is bleeding. Bleeding is usually self-limited but may be severe. Thus, it is important to ensure that the patient does not have coagulopathy, thrombocytopenia, signiﬁcant renal failure, or severe pulmonary hypertension prior to proceeding with biopsies. Topical application of 5 mL of 1:20,000 epinephrine prior to biopsy may minimize bleeding (18). Transbronchial needle aspiration is a useful procedure that allows sampling of mediastinal lymph nodes for diagnosis and staging of lung cancer. The bronchoscopist must be familiar with mediastinal anatomy prior to performance of transbronchial needle aspiration. In addition, a CT scan of the chest is required to determine the exact location of adenopathy or tumor. Transbronchial needles come in different sizes, with smaller needles providing cytology specimens and larger ones providing biopsy specimens. Complications from this procedure are rare and include minor bleeding (19). Endobronchial ultrasound (EBUS) is a recent addition in the armamentarium of the interventional pulmonologist. EBUS extends the imaging capability of the bronchoscopist beyond the airway lumen in assessing bronchial wall tumor invasion, locating lymph nodes or tumor for needle biopsy, and locating vascular structures adjacent to the airway. EBUS requires transient occlusion of the airway for 20 to 30 seconds, and it provides a 3608 view of the soft tissues surrounding the airway. It can be used to identify the cause of an extrinsic compression and

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determine if it is a vascular structure or soft tissue. EBUS has been shown to increase the yield of transbronchial needle aspiration of mediastinal lymph nodes (20). Fluorescence bronchoscopy is a diagnostic technique that utilizes characteristic autoﬂuorescence emissions from lung tissues when illuminated by light. When illuminated by a light of a given excitation wavelength, cancerous and pre-cancerous lesions display lower autoﬂuorescence than normal tissue. Fluorescence bronchoscopy is used to enhance the ability to detect and localize dysplastic mucosa (premalignant) or carcinoma in situ. In a multi-center clinical trial, ﬂuorescent bronchoscopy was shown to have a higher sensitivity and a higher negative predictive value than regular white light bronchoscopy for the diagnosis of early lung cancer (21). Mucosal dysplasia or airway cancer is not likely to be present when ﬂuorescence bronchoscopy is negative. The presence of an abnormal ﬂuorescent pattern is, however, non-speciﬁc and requires tissue biopsy for histologic conﬁrmation. Fluorescence bronchoscopy is FDA-approved for patients who present with positive sputum cytology, hemoptysis, unresolved pneumonia, persistent cough of unclear cause, or an abnormal chest X-ray suspicious for lung cancer. Fluorescence bronchoscopy is also useful in the preoperative assessment of lung cancer to determine the extent of endobronchial involvement and the presence of synchronous airway lesions.

VI.

Post-Procedure Care

Prior to discharge, patients should be monitored until sedation has worn off. Post-procedure chest radiographs are routinely recommended after rigid bronchoscopy or after bronchoscopy in patients on mechanical ventilation. This may not be necessary after transbronchial biopsies, particularly if biopsies are performed under ﬂuoroscopic guidance and the patient does not complain of shortness of breath or chest pain. In a large survey, however, the majority of pulmonologists replied that they routinely obtain chest radiographs after transbronchial biopsy (8).

VII.

Complications

When performed with appropriate care, bronchoscopy is a safe procedure. The incidence of major and minor complications range from 0.08% to 0.12% and 0.27% to 6.5%, respectively (8,22 – 25). Mortality rates from surveys and prospective studies range from 0.01% to 0.1% (22 –26). As discussed earlier, common complications include hypoxemia, bronchospasm, cardiovascular events, pneumothoraces, bleeding, fever, pneumonitis, and complications related to anesthesia and pre-medication. The number of major complications was higher with rigid bronchoscopy than with ﬁberoptic bronchoscopy in a comparative study of 3449 rigid bronchoscopies and 1146 ﬂexible bronchoscopies

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(26). In addition, higher rates of complications related to anesthesia were seen for both procedures.

VIII.

Speciﬁc Diagnostic Indications

A. Diagnosis and Staging of Lung Cancer

The utility of bronchoscopy in lung cancer is well established. As a diagnostic tool, the yield is best if bronchoscopic techniques are combined, including forceps biopsy, brush biopsy, BAL, and transbronchial needle aspiration when appropriate. For visible endobronchial lesions, the diagnostic yield is higher than 90% (15). For non-visible peripheral lesions, the yield will vary according to the experience of the bronchoscopist, the location and size of the lesion, and techniques utilized. Reports of diagnostic yield for non-visible lesions range from 27% to 75% (15,27,28). The utility of bronchoscopy is likewise well established in the staging of lung cancer. Again, accuracy will depend on the experience of the operator with transbronchial needle aspiration, the location of the tumor, and the presence or absence of extrinsic compression of the airways. A 73% positive aspiration rate in patients with abnormal mediastinum on chest roentgenograms with high speciﬁcity has been reported by Wang and Terry (19). B. Suspected Pulmonary Infections

Although the etiologic agent of most infections can be determined based on clinical history and non-invasive testing, bronchoscopy often serves as a useful adjunct when therapy is ineffective or when prompt diagnosis is necessary. In addition to providing specimens for microbiologic studies, bronchoscopy provides information regarding the severity of airway inﬂammation and the quantity and nature of secretions. BAL and protected brushings are particularly useful for obtaining specimens for microbiologic studies. It is important to keep in mind that although the isolation of certain organisms is diagnostic for the etiology of disease (e.g., Nocardia), other organisms may be non-pathogenic colonizers (14). All BAL culture results must, therefore, be interpreted in the proper clinical context. Transbronchial biopsy is an additional technique that may add to the diagnostic yield, particularly if invasive fungal or viral disease is suspected (29). Transbronchial biopsies may also help establish the diagnosis of noninfectious processes, such as Kaposi sarcoma or lymphoma, especially in immunocompromised hosts. Although the effect may be negligible, the inhibitory properties of lidocaine on bacterial growth in vitro should be kept in mind when using liberal amounts of lidocaine during diagnostic bronchoscopy for infection (9,30). On the other hand, BAL or brush specimens may be falsely positive if withdrawn through a working channel contaminated with upper airway secretions. Therefore, care must be taken to obtain non-contaminated specimens. In addition, bronchoscopes must

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be thoroughly sterilized prior to use in order to prevent transmission of infection. The latter is an infrequent but real risk (31,32). Bronchoscopy is particularly useful in immunocompromised patients who are susceptible not only to common pathogens, but also to pathogens that do not typically cause illness in immunocompetent hosts. Timely diagnosis is crucial in these patients because of their limited reserve and inability to mount an effective immune response. Among immunocompetent patients with pneumonia, bronchoscopy is reserved for those with persistent or worsening inﬁltrates despite appropriate empiric agents. Bronchoscopy may assist not only in determining the etiologic agent but may also uncover the presence of an obstructing endobronchial lesion or foreign body leading to post-obstructive pneumonia. Bronchoscopy may also assist in determining the cause of rapid deterioration leading to acute respiratory distress syndrome (33). Hospital-acquired (nosocomial) pneumonia is a serious illness with signiﬁcant morbidity and mortality, and it is the leading cause of death from hospital-acquired infections (34,35). It is deﬁned as pneumonia that occurs 48 hours after admission, excluding any infection that is incubating at the time of admission (36). Patients who develop hospital-acquired pneumonia tend to be infected with pathogens different from those associated with community-acquired pneumonias. Typical pathogens include staphylococcus aureus and enteric Gram-negative bacilli. Ventilator-associated pneumonia, a subset of nosocomial pneumonia, is diagnosed based on the appearance of pneumonia .48 hours after intubation. Pneumonia in these patients is difﬁcult to diagnose and is based on radiographic evidence of a new or progressive inﬁltrate with clinical ﬁndings of fever, leukocytosis, and purulent secretions (37,38). Cultures are often obtained from sputum or endotracheal aspirates in intubated patients. These cultures are, however, frequently positive for bacteria that colonize the oropharynx or the endotracheal tube as a bioﬁlm. Bronchoscopy can be performed in these patients utilizing quantitative cultures from BAL or protected brush specimens. The threshold for positive cultures is usually .103 colony forming units (cfu)/mL for brushings and .104 cfu/mL for BAL (39 –41). Controversy exists regarding the impact of invasive testing in patients with nosocomial pneumonia. Results of studies are mixed with regards to the effects of bronchoscopy on outcomes such as mortality (42,43). Additional randomized clinical studies are needed to determine whether bronchoscopy should be routinely performed in patients with suspected nosocomial pneumonia. C. Speciﬁc Pathogens

Pneumocystis jiroveci (previously Pneumocystis carinii) is a common pulmonary pathogen in patients with AIDS and other immunocompromised hosts. The diagnostic yield of BAL for Pneumocystis is as high as 86% to 97% in patients with

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AIDS (44 – 46). Transbronchial biopsy, in addition, increases the diagnostic yield with a reported sensitivity of 100% when combined with BAL (46). The yield tends to be lower, however, in patients receiving aerosolized pentamidine (47) or in patients with disease processes other than HIV. Site-directed multiple lobe BAL combined with the use of indirect ﬂuorescent antibodies have also been reported to increase the diagnostic yield for Pneumocystis (48). Bronchial brushings, on the other hand, do not provide additional value to BAL and transbronchial biopsy (49). Mycobacterial diseases, including those caused by Mycobacterium tuberculosis as well as the many atypical mycobacteria, continue to be a major health concern both in the United States and throughout the world (50). Diagnosis of tuberculosis is typically made by obtaining sputum samples. In patients, however, who cannot produce sputum even with induction, bronchoscopy with BAL may provide the diagnosis. The diagnostic yield from BAL has been reported to be comparable to that from sputum (51 – 53). Additional diagnostic yield has been reported with transbronchial biopsy in conjunction with bronchial brushings (54). Another report, however, did not ﬁnd transbronchial biopsies helpful in establishing diagnosis (55). Following bronchoscopy, patients frequently continue to produce sputum for one to two days. These samples should be collected and sent to the laboratory for analysis as they will often be positive for mycobacteria (56). It should be kept in mind that bronchoscopy in patients with tuberculosis increases the risk of transmission of disease to medical personnel, and appropriate precautions should be taken. Bronchoscopy is also useful in the diagnosis of infection caused by non-tuberculous mycobacteria (NTM). The most frequent pulmonary pathogens include Mycobacterium avium complex, Mycobacterium kansasii, Mycobacterium abscessus, Mycobacterium fortuitum, Mycobacterium xenopi, and Mycobacterium malmoense (57). NTM tend to cause disease in elderly patients, patients with chronic diseases, and immunocompromised hosts. The presence of atypical mycobacteria in bronchoscopic samples is not diagnostic of disease, however, in the absence of radiographic and clinical criteria because of their ubiquitous nature and the high prevalence of colonization (58,59). Fungal infections have also been diagnosed by bronchoscopy. These include histoplasmosis, coccidioidomycosis, blastomycosis, and aspergillosis. In general, the diagnosis of pulmonary histoplasmosis requires a tissue sample obtained via thoracoscopy or open lung biopsy. This is especially true if disease is limited to a solitary pulmonary nodule. However, when utilized in patients with other radiographic features, such as inﬁltrates and cavitary lesions, bronchoscopy samples are associated with a higher diagnostic yield compared with sputum (60). Similarly, bronchoscopy samples are more efﬁcacious in the diagnosis of coccidioidomycosis and blastomycosis compared with sputum. Fungal stains of BAL samples for Coccidioidomycosis immitis tend to have a low yield, but cultures and transbronchial biopsies have high yields. In addition, serologic tests for

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coccidioidomycosis may be positive when BAL cultures are negative. Serologic tests and bronchoscopic studies should, therefore, be considered in unison (61,62). In patients with blastomycosis, the diagnostic yield of cultures from bronchoscopic samples is high, with a higher diagnostic efﬁcacy reported with bronchial washings compared with BAL specimens. The average time for culture conﬁrmation may, however, take up to ﬁve weeks. Use of wet smears and cytologic examination of respiratory specimens should, therefore, be performed. Although lower in yield, KOH smears provide an early diagnosis of blastomycosis when positive (63). Cryptococcus neoformans is a ubiquitous fungal organism that typically causes pulmonary, central nervous system, or disseminated disease in immunocompromised hosts. In cryptococcosis, fungal stains of BAL samples for the organism have a higher sensitivity than transbronchial biopsies. No additive beneﬁt is obtained with biopsy specimens if cryptococcus is suspected as the pathogenic organism (64). Aspergillus species are likewise ubiquitous in the environment. Aspergillus fumigatus, Aspergillus ﬂavus, and Aspergillus niger are the most frequently reported pathogens causing a variety of illnesses of the respiratory tract, including invasive disease, tracheobronchitis, allergic bronchopulmonary aspergillosis, and aspergilloma. Bronchoscopy is particularly useful in diagnosing tracheobronchitis and invasive disease that tend to occur in immunocompromised hosts. Tracheobronchitis is typically evident on inspection of the airways where mucous impaction or pseudomembrane formation is often seen. It is, however, difﬁcult to deﬁnitively ascribe tracheobronchitis to aspergillus infection despite positive cultures of BAL and washings due to the frequent colonization of the airways by aspergillus. Deﬁnitive diagnosis of invasive pulmonary aspergillosis requires a tissue sample. However, these patients frequently have contraindications to transbronchial or open lung biopsy. Variable diagnostic yields are seen with both BAL and transbronchial lung biopsies (65,66). In the appropriate clinical setting (e.g., immunocompromised patient with neutropenia), isolation of aspergillus from BAL cultures in the absence of other pathogens is used as a marker for invasive aspergillosis (65,67). The utility of BAL PCR and detection of galactomannan antigen from BAL samples from patients with invasive aspergillosis has also been reported (68). Herpes viruses and cytomegalic virus (CMV) are pathogenic mostly in immunocompromised hosts. Herpes viruses can rarely cause tracheobronchitis or pneumonia. Lesions may be visualized as vesicles or shallow ulcers during bronchoscopy, and cultures from these lesions may yield positive results (69). CMV isolation from BAL samples is not uncommon. The signiﬁcance of this ﬁnding is, however, controversial as it may represent simple colonization of the lungs (70). In patients with CMV pneumonia, the sensitivity of BAL cultures may be as low as 50% (71). Transbronchial lung biopsy showing evidence of viral inclusions is more speciﬁc for CMV related disease and has a sensitivity of up to 90% (72).

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Bronchoscopy can assist in the diagnosis of various non-infectious diffuse pulmonary diseases. Techniques utilized will vary according to the suspected diagnosis. For example, if sarcoidosis is suspected, transbronchial biopsies are obtained to establish the presence of non-caseating granulomas. If eosinophilic granuloma is suspected, BAL is performed to look for Langerhans cells. Disseminated carcinoma, on the other hand, can be detected by transbronchial biopsy, BAL, or brush biopsy. Although bronchoscopy can assist in the diagnosis of some interstitial lung diseases, thoracoscopic or open lung biopsy remains the standard method for obtaining adequate tissue samples. E.

Suspected Tracheoesophageal Fistula

Tracheoesophageal ﬁstulas most often occur as a result of prolonged intubation with a cuffed endotracheal or tracheostomy tube. Bronchoscopy or esophagoscopy can be performed to diagnose and localize tracheoesophageal ﬁstulas. However, small communications may not be visualized, and the diagnosis may require a barium swallow. F.

Chest Trauma

Blunt chest trauma occasionally results in injury to the tracheobronchial tree. Patients typically complain of dyspnea and hemoptysis and may develop subcutaneous emphysema. Bronchoscopy, in conjunction with radiographic imaging, is the procedure of choice in establishing the presence and extent of traumatic airway injury. G. Thermal Injuries

Thermal injuries are typically the result of exposure to hot smoke from burning material. Edema, inﬂammation, necrosis, and ulceration of the airways lead to upper airway obstruction that can develop rapidly, necessitating emergent intubation. As such, serial bronchoscopy should be considered as edema can be progressive during the ﬁrst 24 hours. However, initial bronchoscopic assessment does not predict the duration or degree of ventilatory support necessary during hospitalization (73,74). In addition to damage caused by direct thermal burns, the lung parenchyma can also be damaged by other products of combustion, leading to pulmonary edema and contributing further to the mortality of patients with inhalation injury. H. Evaluation of Lung Transplant Rejection

Patients who have received lung transplants frequently present with respiratory symptoms and fever that may represent either an infectious complication or acute lung rejection. As these patients are immunocompromised and because

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respiratory failure can evolve rapidly, early diagnostic determination is crucial. The optimal method to make this determination is to perform bronchoscopy and to obtain BAL ﬂuid and transbronchial biopsies (72). Three to ﬁve biopsies may be necessary for establishing the diagnosis of acute rejection (75). IX.

Speciﬁc Diagnostic and Therapeutic Indications

A. Hemoptysis

Bronchoscopy plays an important role in the diagnostic evaluation and treatment of patients with hemoptysis. Both focal and diffuse pulmonary processes may cause hemoptysis, and early diagnosis and treatment are particularly important, especially in patients with massive hemoptysis. Bronchoscopy is useful in localizing the site of bleeding and also allows for suctioning of the airways. In addition, in cases of unilateral bleeding, selective intubation of the uninvolved side can be facilitated using the ﬂexible bronchoscope. Flexible bronchoscopy allows the operator to examine all lobes and segments of the lungs but is somewhat limited with regard to suction capability. The rigid bronchoscope has a larger working channel that allows for improved suctioning and may be preferred in patients with massive hemoptysis. After localizing the site of bleeding and securing the airway, bronchoscopy can also be used as a therapeutic tool. The use of topical epinephrine, balloon tamponade, and laser therapy are various treatment modalities discussed in more detail in other sections of this book. If these modalities are unsuccessful, the bronchoscopist can provide guidance to the interventional radiologist or thoracic surgeon regarding the source of bleeding (76). B. Bronchopleural Fistula

Bronchopleural ﬁstula is a common complication seen in patients requiring mechanical ventilation or following lung resection surgery. In patients with persistent air leak, the bronchoscope can be used for localization of the site of leak and for attempting therapeutic maneuvers. Localization is accomplished by sequential inﬂation and deﬂation of a Fogarty balloon catheter in segmental bronchi and watching for cessation of air leak in the water-seal apparatus. Alternatively, a bronchogram can be performed by injecting contrast material through a catheter in the working channel of the bronchoscope. Various agents have been utilized to seal the airways leading to the ﬁstula, including oxidized regenerated cellulose (Surgicel), ﬁbrin clot, silver nitrate, methyl-2-cyanoacrylate, tetracycline, and doxycycline. In addition, laser therapy has been used to coagulate the site of leak (77 – 80). C. Foreign Bodies

Foreign body aspiration is a common problem seen in pulmonary medicine. Aspiration most often occurs in children with equal prevalence of right and

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left lung aspiration. In adults, the right side is more often involved than the left because of the branch angle of the left main stem bronchus. Patients with foreign bodies in the upper airway may be profoundly symptomatic, whereas those with passage of the foreign body to more distal airways may be asymptomatic. Following imaging studies of the chest, the next diagnostic and treatment modality is bronchoscopy. In the pediatric population, rigid bronchoscopy is preferred. In adults, ﬂexible bronchoscopy is usually attempted ﬁrst and is often successful in removal of the foreign body with use of ancillary equipment, such as forceps and wire baskets. In difﬁcult cases, rigid bronchoscopy may be necessary for extraction of the foreign body and control of the airway (81). D. Endotracheal Tube Placement and Assessment of Placement

Endotracheal intubation is occasionally challenging in patients with difﬁcult airways. Patients with signiﬁcant amounts of redundant upper airway tissue or cervical spine injury precluding extension of the neck are particularly difﬁcult to intubate. In these cases, the bronchoscope serves as an obturator for sliding the endotracheal tube into place. Additionally, bronchoscopic inspection ensures appropriate position of the endotracheal tube above the carina.

X.

Therapeutic Bronchoscopy: Indications and Options

Alleviation of airway obstruction is the primary indication for therapeutic bronchoscopy. Mucus plugs and blood clots in the central airway can be removed using suction and cryotherapy probes, and foreign bodies within the airway can be removed using forceps, snares, or baskets. In addition, central airway obstruction caused by tumors, granulation tissues, or strictures can be managed using laser resection, cryotherapy, electrocautery, photodynamic therapy, and brachytherapy in conjunction with mechanical dilation using balloons, bougies or rigid bronchoscopes, and airway stents. A. Atelectasis

Atelectasis and retained secretions occur commonly among ICU patients. Approximately 50 to 60% of bronchoscopies performed in the ICU are for treatment of atelectasis. The efﬁcacy of bronchoscopy for atelectasis varies in different reports. A recent review found that patients with lobar or segmental atelectasis beneﬁt more from bronchoscopy compared to patients with subsegmental atelectasis or air bronchograms on chest roentgenograms. There are, however, insufﬁcient studies at this time comparing the efﬁcacy of bronchoscopy to non-invasive treatments, such as chest physiotherapy, mucolytic agents, and kinetic beds. The decision to proceed with bronchoscopy for atelectasis must be made on an individual basis (82).

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B. Debulking of Obstructing Neoplasm

With few exceptions, most therapeutic airway interventions can be performed using a ﬂexible bronchoscope. However, bulky lesions obstructing the central airway can be managed much easier and faster using a rigid bronchoscope with less overall risk of complications for the patient. A patient (Fig. 1) had a complete obstruction of the right main stem bronchus by tumor arising out of the right upper lobe. The rigid bronchoscope provided an excellent tool for resecting the tumor in large pieces (Fig. 1D). If a ﬂexible bronchoscope had been used in this patient, it would have taken much longer to evaporate the tumor using laser heat alone, with the additional risk of bleeding, prolonged anesthesia, smoke inhalation, and airway ignition. In many therapeutic airway interventions, however, the ﬂexible and the rigid bronchoscopes are complementary. Although the rigid bronchoscope provides a large ventilating lumen for therapeutic procedures in the central airway, the ﬂexible bronchoscope can aid in interventions involving smaller lobar or segmental airways, especially in the upper lobes. Unfortunately, few practicing pulmonologists routinely perform rigid bronchoscopy. A 1999 survey by the American Association for Bronchology revealed that 96% of the 744 respondents did not perform rigid bronchoscopy (83). Only 8% performed laser airway procedures, and only 5% performed airway stenting. The rigid bronchoscope is a good conduit for Nd:YAG laser photocoagulation and photoevaporation and is an ideal instrument for performing mechanical resection of bulky airway tumors. Nd:YAG laser procedures can also be performed through the ﬂexible bronchoscope. However, resection of bulky tumors using the ﬂexible bronchoscope relies largely on laser photoevaporation, which is time consuming. The prolonged laser time increases the risk of airway ignition and amount of smoke production. An additional disadvantage of the ﬂexible bronchoscope is limited suction capability for evacuation of smoke and blood. Also, metal stents are the only type of stents that can be inserted through the ﬂexible bronchoscope, whereas placement of all types of stents, including silicon and metal stents, are possible with the rigid bronchoscope. Because most rigid bronchoscopy procedures are done with an open bronchoscope, inhalational anesthesia is generally not advisable. General anesthesia is usually accomplished with total intravenous anesthesia. Ventilatory assistance is usually provided by means of positive pressure ventilation using venturi or jet ventilation and, in some cases, assisted spontaneous ventilation. The feasibility and ease of using negative pressure ventilation during rigid bronchoscopy under general anesthesia has also been reported (84). C. Laser Therapy

Laser bronchoscopy can be performed using either a ﬂexible or rigid bronchoscope as described above. For most airway interventions below the vocal cords, the Nd:YAG laser is generally the laser of choice. It is important to

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Figure 1 A 52-year-old man with known metastatic colon carcinoma who presented with worsening dyspnea and on chest roentgenography was found to have complete right lung collapse. (A) Bronchoscopy shows complete obstruction of the right main stem bronchus at the level of the major carina. This tumor was known to arise out of the right upper lobe encroaching into the right main stem bronchus. (B) The chest roentgenogram before tumor resection. (C) The chest roentgenogram immediately following rigid bronchoscopic resection of tumor with opening of the right middle and lower lobes and post obstructive pneumonia. (D) The size of tumor fragments resected from the right main stem bronchus. (Continued.)

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Figure 1 (Continued.)

understand laser physics and the difference between photocoagulation and photoevaporation during airway interventions. Photocoagulation is achieved at low-power density to coagulate blood vessels of the soft tissue or the tumor for prevention of bleeding. This is usually not accompanied by apparent or signiﬁcant tumor shrinkage or smoke production. Photoevaporation, on the other hand, is achieved at high-power density to evaporate the soft tissue, resulting

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in tissue shrinkage and smoke production. Laser photocoagulation is commonly used as a prelude to mechanical tumor resection of the central airway using the rigid bronchoscope. Laser photoevaporation can be used to cut benign strictures and burn small tumors or the residual tumor bed following mechanical resection of bulky tumors. Control of bleeding at any stage of the procedure can be accomplished readily with laser photocoagulation. Because laser photoevaporation results in smoke production, smoke evacuation becomes important during the procedure. The small suction channel of a ﬂexible bronchoscope can be easily overwhelmed by a large amount of smoke if extensive laser photoevaporation is performed. This is generally not a problem with rigid bronchoscopy due to the ability to place a large suction catheter through the rigid bronchoscope. In addition, the risk of ﬁre hazard during a laser airway procedure is higher with the ﬂexible bronchoscope because the outer cover of the bronchoscope itself and many of the common endotracheal tubes used can be ignited by the laser itself. For the most part, bronchoscopic interventions for malignant airway obstruction are used for palliative purposes with a primary objective of improvement in the quality of life of patients with far advanced or end-stage malignancy. In a series of 2008 patients with malignant airway obstruction who underwent laser bronchoscopy, median survival was only several months (85). More recently, bronchoscopic management of tracheobronchial tumor obstruction with curative intent has been reported (86 –88). Not all airway lesions are suitable for bronchoscopic resection. Best results are obtained in patients with proximal or central airway tumors with a signiﬁcant endobronchial component. The presence of airway patency distal to the site of obstruction is necessary. In addition, the obstructed area has to have relatively uncompromised perfusion. Opening an obstructed bronchus subtending an area with limited perfusion because of tumor invasion will only result in dead space ventilation and may potentially worsen hypoxemia. The segment of the obstructed airway should have minimal vascular invasion in order to minimize the risk of bronchovascular ﬁstulas and fatal hemoptysis after the tumor is successfully resected. If laser bronchoscopy is performed with curative intent, the lesion should be small, centrally located, and with limited base and depth of invasion. D. Cryotherapy

Endobronchial cryotherapy works by causing tissue destruction through rapid freezing followed by slow thawing. Nitrous oxide (N20) gas is used to lower the temperature to approximately 2898C. Rapid freezing results in the formation of ice crystals within the cytoplasm that grind and abrade cellular organelles during thawing, resulting in cell death. Cryo-sensitive tissues include skin, mucous membranes, granulation tissues, tumors, and other tissues with a signiﬁcant amount of water content. Cryo-resistant tissues include fat, cartilage, bone,

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and ﬁbrous connective tissue with little water content. The ﬂexible cryotherapy probe can be delivered through a ﬂexible or a rigid bronchoscope. The advantages of endobronchial cryotherapy as opposed to Nd:YAG laser therapy or electrocautery include its safety, low cost, ease of use, and the ability to remove certain foreign bodies and blood clots. The disadvantage is that it is slow in removing tumor or granulation tissue from the airways, with repeat bronchoscopy being generally required within a week. Some success has also been reported with the use of endobronchial cryotherapy with curative intent in the management of airway carcinoma in situ (87). E.

Electrocautery

Endobronchial electrocautery involves the application of heat to the bronchial tissue, resulting in tissue coagulation and vaporization. Electrocautery can be used through either a ﬂexible or rigid bronchoscope, and in experienced hands, results are comparable to that of laser therapy. It can be used as a direct contact agent in the form of probes, snares, and scissors, or as a non-contact agent using argon plasma as a gas conductor within an electrical ﬁeld [argon plasma coagulator, (APC)]. APC’s unique property is its ability to vaporize tumors at an acute angle because the argon plasma burns off the closest tissue within the available electrical ﬁeld, even if the closest tissue is at an angle. This property of the APC is sometimes useful in removing small tumors in the upper lobe bronchi. Endobronchial electrocautery has also been used to treat carcinoid tumors with a curative intent (88). F. Photodynamic Therapy

Photodynamic therapy (PDT) is an effective technique for the management of small endobronchial tumors. It is used primarily in non-surgical candidates with small lesions and early stages of lung cancer, with a reported cure rate of approximately 75% and a recurrence rate of approximately 30% (89). PDT involves intravenous injection of a tumor photosensitizing agent derived from hematoporphyrin, which is retained in tumor cells and cleared from most healthy tissues in six hours except for the lung, reticuloendothelial tissues, and the skin. Airway tumor cells retain the photosensitizer 48 to 72 hours after its administration and undergo selective destruction by photo-activation upon exposure to 630 nm wavelength of laser light introduced in the airway using a ﬂexible bronchoscope. Tumor necrosis occurs as a result of cellular destruction from superoxide and hydroxyl radicals and vascular occlusions related to thromboxane-A2 release (90). A clean-up bronchoscopy two to three days later is required to remove necrotic tumor debris from the airway. Photodynamic therapy makes the skin and eyes sensitive to light for six weeks or more after treatment, and patients are advised to avoid direct sunlight and bright indoor light during this time period.

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Shah, Susanto, and Santiago G. Brachytherapy

Endobronchial brachytherapy involves delivery of radiation therapy from a radioactive source placed within or very near the tumor mass. Direct placement of the radioactive source is accomplished through an airway catheter placed bronchoscopically. When used in early stage endobronchial cancer, brachytherapy produces results comparable to that of photodynamic therapy, with reported cure rates of 75% to 85% (89). In addition, the use of brachytherapy in conjunction with Nd:YAG laser treatment increases survival compared with laser therapy alone (91). H. Placement of Airway Stents

Airway prostheses are used primarily for the treatment of central airway obstructions. These include tracheobronchial stenoses secondary to either extrinsic compressions or intrinsic lesions (tumors and strictures), as well as trachobronchial collapse (tracheomalacia). Although there are several commercially available stents, each has its own advantages and disadvantages. The design and sophistication of airway stents lag behind vascular stents, and the ideal airway stent continues to remain elusive (92). An ideal airway stent should ﬁt the airway lumen snugly and remain in place without external ﬁxation. It should not cause mucosal, cartilage, or vascular injury and should only cause minimal granulation tissue formation. It should create satisfactory expansion of a stricture and should be capable of resisting external compression. Finally, the stent should be easily tailored to ﬁt the entire stricture and should be easy to remove or replace. The common airway stents used in North America are Ultraﬂexw, Wallstentw, Dumonw, Polyﬂexw and Dynamic-Yw. The Ultraﬂex stent and Wallstent are metallic stents that can be deployed using a ﬂexible bronchoscope. The Dumon stents are silicone stents that are placed using a specially designed rigid steel delivery device through a rigid bronchoscope. The Polyﬂex stent is made of a plastic mesh with silicone membrane and is deployed using a plastic tubular delivery device directly into the airway, guided by a rigid laryngoscope. The Dynamic-Y stent is made of silicone with interspersed inverted U-shaped metal struts that mimic the shape of the tracheal cartilage. The Dynamic-Y stent is used in the trachea and is deployed using a special delivery forceps guided by a rigid laryngoscope. The metal stents come as bare stents or covered with a silicone membrane in the middle. Removal of these metal stents usually requires the use of a rigid bronchoscope. Due to the growth of bronchial mucosa over the bare part of these metallic stents, they are considered permanent stents, and they should be used with extreme caution in benign strictures, especially in young patients with long life expectancy. When compared with covered metallic stents or silicone stents, the bare metal stents allow for better mucociliary transport but are more prone to the development of granulation tissue or recurrent tumor growth

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through the wire mesh. Mucostasis and mucus plug formation tend to occur with silicone stents and stents covered with a silicone membrane. The edges of the stents may also elicit formation of granulation tissue, which may potentially cause future obstruction.

XI.

Potential Therapeutic Indications

A. Bronchoscopic Lung Volume Reduction

Advances in our understanding of the physiologic changes associated with lung volume reduction surgery in patients with emphysema have spurred interest in the development of bronchoscopic techniques for achieving lung volume reduction. Ingenito et al. (93) studied bronchoscopic lung volume reduction in an emphysema sheep model. Fibrin-based glue was introduced bronchoscopically to collapse, seal, and scar the target lung tissue. Comparable changes in total lung capacity and residual volume were found between surgical and bronchoscopic methods of lung volume reduction. Several sterile abscesses were seen in some of the treated areas. In a follow-up study by the same group using a modiﬁed agent, sterile abscesses were not found (94). Human studies are now ongoing using bronchoscopically placed one-way valves (Emphasysw and Spirationw valves) in segmental bronchi to achieve lung volume reduction (95). These one-way valves allow air and mucus to exit the lung segment of interest, resulting in passive atelectasis and achievement of lung volume reduction. The valves are removable bronchoscopically. Preliminary human studies using the Emphasys valve to achieve non-surgical lung volume reduction appear encouraging (96). The Spiration valve has been studied only in animals, and pilot human studies are forthcoming.

B. Creation of Extra Anatomical Airway Tract

Because of the increased work of breathing associated with air trapping in patients with emphysema, creation of an artiﬁcial bypass airway tract between a major airway and the emphysematous pulmonary parenchyma may lead to improvements in respiratory mechanics by taking advantage of the extensive collateral ventilation present in the emphysematous lung. In a feasibility human study, lungs of patients scheduled for lobectomy and pneumonectomy were studied for creation of bypass tracts prior to resection (97). Bronchoscopicallyinduced extra anatomical airway tracts were successfully created using a cautery probe, guided by a Doppler catheter to avoid blood vessels in the bronchial wall. An ex vivo study of resected emphysematous lungs showed signiﬁcant improvements in lung mechanics after bypass tracts were successfully formed between the bronchus and the lung parenchyma using a radiofrequency catheter and expandable stents placed through a ﬂexible bronchoscope (98).

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9 Percutaneous Tracheostomy

AMMAR SAKKOUR and IRAWAN SUSANTO UCLA– Santa Monica Specialties Geffen School of Medicine at UCLA Santa Monica, California, U.S.A.

I.

Introduction

Tracheostomy is one of the frequent surgical procedures in critically ill patients. Open surgical tracheostomy (OST) has traditionally been performed by surgeons in the operating room. In the past half-century, several methods of percutaneous tracheostomy have been introduced. Over the last decade, percutaneous tracheostomy has been performed primarily in the intensive care unit (ICU) on patients who require a prolonged artiﬁcial airway because of their critical illness or progressive chronic lung disease. In 1909, Jackson described the standardized surgical technique and indications for open tracheostomy (1). In 1957, Sheldon et al. (2) ﬁrst described percutaneous tracheostomy. He introduced a special slotted needle percutaneously into the trachea. The needle served to direct a three-bladed cutting stylet that was combined with a metal tracheostomy tube. Because of several deaths, the technique was abandoned. In 1969, Toye and Weinstein (3) used the Seldinger technique for tracheostomy placement. After cannulating the trachea with a needle, a tracheostomy tube was loaded onto a stiff wire that contained a recessed blade. The device was advanced into the needle tract until the tracheostomy tube was placed. Because of the high risk of paratracheal insertion, the technique never gained popularity. The most popular technique worldwide today is percutaneous dilatational tracheostomy (PDT), described by Ciaglia et al. in 1985 (4) as a method utilizing serial dilators (later modiﬁed to a single tapered single dilator) over a guidewire 313

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in a modiﬁed Seldinger technique. PDT is most commonly performed at bedside in the ICU with or without bronchoscopic guidance (5). In the past decade, most of the published literature on percutaneous tracheostomy has dealt with this technique. There are also other reported methods for tracheostomy placement. In 1989, Schachner et al. (6) used a dilating tracheostome via the Seldinger technique. The device had blades that slid over the guidewire into the trachea, where they were forced open to make a stoma that would ﬁt a tracheostomy tube (7). This method had a high incidence of posterior tracheal wall tears, which led to its withdrawal from the United States market. In 1990, Griggs et al. (8) described tracheostomy with a grooved Howard– Kelly forceps over a guidewire using the Seldinger technique. Once the tip of the forceps was in the trachea, the forceps were opened to create a stoma. Sviri et al. (9) followed the long-term outcomes of percutaneous tracheostomy using the Griggs technique. Thirty-eight percent of the patients complained of some degree of voice change, 12% of ongoing severe cough, and 31% of shortness of breath, with more than half of these having concomitant heart or lung disease. In 19.5%, there was some evidence of upper airway obstruction on spirometry, but only 5% were symptomatic. Borm and Gleixner (10) found bedside percutaneous tracheostomy with the Griggs system safe and effective in patients with critical neurosurgical disease, if done under bronchoscopic control. They also found no increase in intracranial pressure. Anon et al. (11) observed similar rates of perioperative complications comparing the Ciaglia and Griggs techniques. Van Heurn and Nates (12,13) in separate studies found signiﬁcantly lower rate of complications in the Ciaglia technique. Today, the Griggs technique remains popular in certain parts of the world. In 1993, Fantoni and Ripamonti (14) described a translaryngeal tracheostomy method. In this approach, the endotracheal tube is pulled to the subglottic area. Then, a guidewire needle is placed in the ﬁrst or second tracheal interspace, and a guidewire is passed through the needle and directed to the mouth alongside the endotracheal tube, similar to the technique of retrograde intubation. The endotracheal tube is replaced with a smaller one. The guidewire that exits the mouth is connected to the pointed tip of a special trocar-tracheostomy tube combination. The guidewire is then pulled from the anterior tracheal side, causing the trocar-tracheostomy tube to be pulled through the mouth and the vocal cord. The tube ﬁnally exits the anterior tracheal wall. The relative complexity of this method has kept it from gaining wider acceptance beyond parts of Europe. In 1998, Ciaglia reﬁned his percutaneous dilatational technique to a singlestep dilation instead of multiple dilation using a single-tapered dilator coated with a hydrophilic agent, named the Blue Rhinow. Since its introduction,

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users of the Ciaglia PDT technique have largely adopted this Blue Rhino technique over the serial dilator technique. II.

Indications, Beneﬁts, and Timing of Tracheostomy

Tracheostomy is indicated for critically ill patients who require prolonged mechanical ventilation, for the relief of upper airway obstruction after initial stabilization, or for airway protection from massive aspiration. Converting translaryngeal intubation to tracheostomy in ventilatordependent patients offers several potential advantages (Table 1). It provides a more secure airway and enhances the patient’s mobility, which is limited in patients with translaryngeal intubation because of the risk of inadvertent extubation (15). Patients with tracheostomy have 1% incidence of inadvertent decannulation, compared with 8% to 21% in patients with translaryngeal intubation. Inadvertent extubation may lead to adverse cardiopulmonary and hemodynamic events in a signiﬁcant number of cases (16,17). Because tracheostomy is better tolerated in mentally alert patients, it lessens the need for heavy sedation that has been associated with an increased risk of nosocomial pneumonia (18). It also facilitates airway suctioning, oral hygiene, and oral nutrition. Tracheostomy may also expedite weaning in patients with borderline ventilatory capacity by reducing the airway resistance (19). It facilitates early transfer from ICU before the completion of weaning from mechanical ventilation. In addition, tracheostomy may help avoid some of the complications of prolonged translaryngeal intubation, including vocal cord paralysis, glottic and subglottic stenosis, sinusitis, otitis, and tracheal injury, such as tracheomalacia and tracheal stenosis (20 – 22) (Table 2). The decision on the timing of tracheostomy should be individualized and should take into account the anticipated duration of mechanical ventilation after the initial period of stabilization and therapeutic trial. It should also take into account patient preferences, the likelihood of beneﬁts versus harm, and Table 1 Beneﬁts of Converting Translaryngeal Intubation to Tracheostomy in ICU Patients Sparing further laryngeal injury Facilitating nursing care and airway suctioning Increasing patient mobility by providing a more secure tube Facilitating transfer from the ICU setting Improving comfort Permitting early return of speech Facilitating oral feeding Decreasing airway resistance

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Table 2 Complications of Translaryngeal Intubation Laryngeal injury Vocal cord paralysis Glottic and subglottic stenosis Infectious complications: sinusitis, otitis, pneumonia Tracheal injury (tracheomalacia, tracheal dilation, and tracheal stenosis)

the contraindications at any particular time in the clinical course of the critically ill patient. Some evidence suggests that the risk of long-term airway complications signiﬁcantly increase beyond the 10th day of translaryngeal intubation (23). Many of the studies that compared outcomes of patients converted at various times in their clinical course to tracheostomy vary in design and sampling and suffer from multiple design problems (24). Armstrong et al. (25) found that early use of tracheostomy in blunt trauma patients with ventilator dependence reduces length of stay in ICU and in the hospital with no adverse effect on morbidity and mortality rates. However, Sugerman et al. (26) failed to show any signiﬁcant difference with early tracheostomy. Brook et al. (27) concluded in their study that early tracheostomy was associated with shorter hospital stay, lower hospital cost, shorter length of stay in the ICU, and shorter duration of mechanical ventilation. Kluger et al. (28) found that tracheostomy performed between day 0 and day 3 of mechanical ventilation may decrease the incidence of pneumonia in critically ill trauma patients. A recent prospective randomized study of 120 critically ill medical patients by Rumbak et al. (29) demonstrated that early (within 48 hr) percutaneous tracheostomy was associated with signiﬁcantly lower rates of mortality, pneumonia, and accidental extubations compared with prolonged translaryngeal intubation, in which tracheostomy was performed on day 14 to day 16. The 1989 ACCP consensus conference on artiﬁcial airway in mechanically ventilated patients recommended tracheostomy in patients whose anticipated need for artiﬁcial airway is more than 21 days. It also recommended that once the decision for tracheostomy is made, the procedure should be performed as early as possible to minimize the duration of translaryngeal intubation, based on individual patient factors (30). III.

Contraindications

The relative and absolute contraindications for percutaneous tracheostomy include uncorrectable coagulopathy, infection at the tracheostomy site, previous neck surgery, non-intubated patients, infants, thyromegaly, emergent setting, midline neck mass, positive end-expiratory pressure (PEEP) higher than 10 cmH2O, limited neck extension, poor oxygenation with FIO2 higher than 60%, or hemodynamic instability (Table 3). The line between relative and

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Table 3 Relative Contraindications to Percutaneous Dilatational Tracheostomy in the ICU Immature airway in children Emergency airway access Hemodynamic instability Anatomic abnormality of the trachea (e.g., midline neck mass) Palpable blood vessel over the tracheostomy site Active infection over the planned tracheostomy site Short or obese neck FIO2 .0.6 Positive end-expiratory pressure .10 cmH2O Platelet count ,50,000/mm3 Bleeding time .10 min Serum creatinine .3.0 mg/dL PT or PTT .1.5 times control Limited ability to extend the cervical spine or unstable neck Abbreviations: PT, prothrombin time; PTT, partial thromboplastin time.

absolute, and what is feasible and what is not, becomes less clear with the increasing experience and in the hands of highly skilled operators. Beiderlinden et al. (31) found that bronchoscopically guided PDT in patients on high PEEP did not jeopardize oxygenation one hour and 24 hours following PDT (31). Meyer et al. (32) found that trained physicians can safely perform bedside percutaneous tracheostomy in patients who had undergone previous tracheostomy. Although not considered a standard practice, several studies have reported that emergency percutaneous tracheostomy is feasible and safe (33,34). Morbid obesity has traditionally been a contraindication for percutaneous tracheostomy because of the presumed difﬁculty in identifying landmarks. This assumption was never supported by any trials. In experience, percutaneous tracheostomy in morbidly obese patients can be performed safely as long as proper precautions and adjustments are made, including using a longer tracheostomy tube to accommodate the additional soft tissue of the neck. Mansharamani et al. (35) reported 13 consecutive cases of PDT in patients with a body mass index of 28 to 62. They reported no complications, technical difﬁculty, or failure to place the tracheostomy. Laryngeal mask airway has been shown to be as an effective and reliable alternative to endotracheal intubation as a temporary artiﬁcial airway during percutaneous tracheostomy (36,37). IV.

The Technique of Bedside PDT: How We Do It

The most popular percutaneous tracheostomy technique worldwide is the Ciaglia PDT (Figs. 1 –5). Keep in mind, like any surgical technique, the PDT itself evolves over time, and each practitioner develops and adapts the technique

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Figure 1 A large bore needle with a catheter sheath over it is introduced into the tracheal lumen at the level of the ﬁrst tracheal interspace. Source: Courtesy of Cook Critical Care, Inc., Bloomington, Indiana, U.S.A.

in individual ways. We will focus on describing the Ciaglia PDT the way we do it. The preparatory steps before PDT are just as important as the tracheostomy itself. Proper patient preparation cuts down on the potential complications that may arise during the procedure. The mechanical ventilator settings are adjusted

Figure 2 After the needle is removed, a guidewire is inserted through the catheter sheath into the tracheal lumen. Once the guidewire is in place, the catheter is removed. Source: Courtesy of Cook Critical Care, Inc., Bloomington, Indiana, U.S.A.

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Figure 3 Following dilation of the anterior tracheal wall with an 11 French dilator (not shown), a guiding catheter is introduced over the guidewire. Source: Courtesy of Cook Critical Care, Inc., Bloomington, Indiana, U.S.A.

Figure 4 A dilator is passed over the guiding catheter and guidewire to dilate the anterior tracheal wall. Dilation can be achieved serially using a progressively larger serial dilators or a single tapered dilator (Blue Rhinow). Source: Courtesy of Cook Critical Care, Inc., Bloomington, Indiana, U.S.A.

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Figure 5 A tracheostomy tube preloaded onto a tapered dilator/trocar is inserted over the guiding catheter and guidewire into the trachea. The dilator/trocar, the guiding catheter, and the guidewire are then removed, leaving the tracheostomy tube in place. Source: Courtesy of Cook Critical Care, Inc., Bloomington, Indiana, U.S.A.

to an FIO2 of 1.0, with appropriate alarm settings, and placed on volume control with appropriate rate and tidal volume to maintain adequate basal minute ventilation when a paralytic agent is used. The high-pressure limit is increased to accommodate the increase in peak airway pressure due to the presence of the bronchoscope in the endotracheal tube. Rolled towels are placed behind the patient’s back in a supine position to extend the head and neck. The blood pressure, heart rate, and pulse oximetry are continuously monitored throughout the procedure. The surface markers of the trachea are carefully palpated and marked. The ﬁrst or second tracheal interspace is the preferred tracheostomy site. The subcricoid space may be used in patients with short neck or severe kyphosis. We avoid the space below the third tracheal ring to decrease the risk of accidental erosion into the innominate artery and minimize the potential trauma to the thyroid isthmus. The skin is prepped and draped in a sterile fashion. The patient is premedicated with a combination of intravenous benzodiazepine and opiate analgesics, for example, meperidine, morphine, or fentanyl. Alternatively, the patient could be maintained on intravenous proprofol. A nondepolarizing neuromuscular blocking agent is also used. A 2-cm skin incision is made vertically or transversely at midline over the selected site, at least one ﬁngerbreadth above the suprasternal notch. A blunt dissection is then done using a curved clamp until the pretracheal fascia is felt. The left middle ﬁnger and thumb are used to secure the lateral edges of the trachea, while the index ﬁnger is used to palpate the anterior tracheal wall to select the appropriate tracheal interspace for insertion site. A ﬂexible bronchoscope is introduced into the endotracheal tube. The tip of the bronchoscope is kept inside the tube to prevent damage by the needle. The cuff of the endotracheal tube is then deﬂated, and the tube is slowly withdrawn to the subglottic space, guided by

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the transillumination of the anterior trachea. Alternatively, the proper position of the endotracheal tube can be bronchoscopically estimated by pushing on the anterior tracheal wall using the index ﬁnger of the left hand and visualizing the anterior tracheal lumen wall depression through the bronchoscope. Once the ﬁrst or second tracheal interspace is identiﬁed, the introducer needle is advanced into the tracheal lumen with continuous suction (Fig. 1). This step and all subsequent steps are guided under direct bronchoscopic visualization. The catheter sheath over the needle is then advanced, and the needle is removed. A guidewire is then passed through the catheter (Fig. 2), followed by passage of a short 11 French dilator. An 8 French guiding catheter is then placed over the guidewire (Fig. 3). Dilatation of the stoma is performed either by serial dilators or by using the tapered Blue Rhino single dilator. This dilator has a hydrophilic coating that is activated by wetting the surface prior to use (Fig. 4). The stoma is commonly dilated to 36 or 38 French. Finally, the tracheostomy tube, which is ﬁtted with a curved dilator/trocar, is passed over the guiding catheter and guidewire into the tracheal lumen (Fig. 5). After the dilator/trocar is removed, the intratracheal position of the tracheostomy tube is conﬁrmed by passing the bronchoscope through the tracheostomy tube and observing the normal tracheal anatomy. Any active bleeding into the trachea should be noted and suctioned. It is a good practice to keep the endotracheal tube in position and not remove it until the intratracheal position of the tracheostomy tube has been conﬁrmed. Once the position is conﬁrmed, the tracheostomy tube is connected to the ventilator tubing and the cuff is inﬂated. The tracheostomy tube is then secured with a Velcro neck strap, and the tube is sutured to skin using 2-0 silk. After the tracheostomy tube is successfully placed, we routinely examine the suprastomal area, the subglottic space, and the vocal cords to record the damages and abnormalities associated with the endotracheal intubation. To do this, the bronchoscope is introduced through the endotracheal tube again. The cuff of the endotracheal tube is then deﬂated and the tube is pulled out over the bronchoscope. The bronchoscope is then slowly pulled back from the suprastomal intratracheal position while carefully observing any abnormalities of the proximal trachea, the subglottic space, the vocal cords with particular attention to the posterior commissure, and the supraglottic structures. A chest X-ray is done only if there is suspected pneumothorax or pneumomediastinum in our clinical exam. A recent retrospective study found that routine chest radiography following PDT that had been performed under bronchoscopic visualization was unnecessary in the absence of clinical deterioration or the suspected postoperative complications (38). V.

Complications

In general, the complication rates of PDT compares favorably to that of OST. Mortality of tracheostomy is less than 1% in several large series (39 – 43). The

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most common complications of PDT are bleeding, infection, and tracheal stenosis (Table 4). In a series of 356 patients, Hill et al. (44) reported a mortality rate of 0.3% and a 3.7% rate of symptomatic tracheal stenosis. Marx et al. (45) reported an operative mortality of 0.39%, bleeding of 1.2%, infection of 0.2%, tracheal stenosis of 0.8%, and pneumothorax of 0.4%. On the other end of the spectrum, Friedman and Mayer (46) reported a 5% rate of bleeding, a 3% rate of infection, and a 4% rate of asymptomatic stenosis. The risk of bleeding is low in PDT because of the tamponading effect of the tracheostomy tube and the dilators. Major bleeding complications are rare and can occur if an artery or a vein lies in the tract of the tracheostomy. Also, erosion into the innominate artery may result from low placement of a tracheostomy tube. Minor peristomal oozing can be managed with inﬁltration of the tissue with lidocaine and epinephrine. In our experience, persistent peristomal oozing responds very well to packing of the peristomal area with sterile gelfoam strips soaked in topical thrombin. Platelet transfusion and correction of coagulopathy are also useful in correcting persistent slow peristomal bleeding in the setting of thrombocytopenia and coagulopathy. The rate of infection is between 1.5% and 4% in different series and is usually minor. The rate of infection in PDT is comparable to, if not lower than, that in surgical tracheostomy (47). Routine use of antibiotic prophylaxis is not recommended, except in patients at risk for bacterial endocarditis. Accidental extubation with loss of airway control may happen during tracheostomy. Failure to re-establish a lost airway expediently during tracheostomy can be catastrophic, especially if neuromuscular blockade is used. An intubation tray should be readily available at bedside. The risk of paratracheal placement of the tracheostomy is minimized with the use of bronchoscopic guidance. In case of inadvertent decannulation in the early postoperative period, blind reinsertion of the tracheostomy tube increases the risk of placement of the

Table 4 Complications of Percutaneous Dilatational Tracheostomy Bleeding Infection Accidental extubation Paratracheal insertion Esophageal perforation Subcutaneous emphysema Pneumothorax Tracheal ring fracture Tracheal stenosis Tracheoamalacia

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tracheostomy tube into the paratracheal space, resulting in upper airway obstruction and hypoxemia (48). Inadvertant decannulation in the ﬁrst seven to ten days should ideally be managed by oral intubation and elective reinsertion of the tracheostomy tube with a guidewire and preferably with bronchoscopic guidance. Esophageal perforation should be avoided with bronchoscopic guidance during PDT. Subcutaneous emphysema and pneumomediastinum may occur with dissection of the paratracheal soft tissue through the stoma by the pressured air from the ventilator (49). It is a good practice to inﬂate the tracheostomy tube cuff only after the ventilator has been connected to the tracheostomy tube. The risk of pneumothorax may increase with a low tracheostomy placement (50). Long-term complications of tracheostomy include tracheal stenosis, tracheomalacia, tracheo-esophageal ﬁstula, and tracheo-innominate ﬁstula. Tracheal stenosis can be suprastomal, stomal, or infrastomal in location. Tracheal stenosis may be caused by antecedent injury from endotracheal intubation or from the tracheostomy itself. Distinguishing the cause of the stenosis from the endotracheal tube or from the tracheostomy tube is often difﬁcult and may not be possible; therefore, this issue has to be kept in mind in interpreting the studies on tracheal stenosis. The suprastomal or stomal stenosis can be caused by damage to the tracheal mucosa and cartilage and the presence of the artiﬁcial airway itself, with subsequent granulation tissue formation. Tracheal stenosis at the stoma site can be present one to six months after decannulation (51). The risk of tracheal stenosis ranges in different studies between 0% and 16%. Most of these stenoses are less than 50% and are not symptomatic (41,52 – 57). Infrastomal stenosis could result from pressure and damage exerted by the tracheostomy tip or the excessive cuff pressures. These lead to mucosal degeneration and chondritis that may be exacerbated by pooled secretions and gastro-esophageal reﬂux disease. Patients with tracheal stenosis are often asymptomatic until the actual lumen is reduced by 50% to 70%, especially in patients who are sedentary or bed-bound after a prolonged critical illness and respiratory failure. Tracheo-innominate ﬁstula is a life-threatening complication that requires immediate surgical intervention. The incidence is 0.6% to 0.7%, and it most often occurs within two to four weeks of the tracheostomy. Risk factors include low placement of tracheostomy, high-pressure cuffs, and excessive tracheostomy movement. The injury may be caused by pressure necrosis from any part of the tracheostomy tube. Bleeding is usually the only symptom, with often nondiagnostic angiography or bronchoscopy (58 –60). Tracheo-esophageal ﬁstula is another rare complication and may be due to pressure necrosis or iatrogenic posterior wall puncture by the introducer needle. Symptoms include coughing up feeding or food material, recurrent pulmonary infection, copious secretions, or ventilator air leak. Treatment options include surgical repair or double stenting of the esophagus and the trachea.

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OST vs. PDT

The trend toward minimally invasive surgery and the development of interventional services within the non-surgical specialties has spurred considerable interest in bedside PDT in the ICU. The economic issue was one of the important aspects of PDT that led to its initial popularity. OST has traditionally been performed in the operating room. In many institutions it remains so. However, performing tracheostomy in the ICU avoids the potential hazards of transporting critically ill patients to and from the operating room. When ﬁrst introduced, bedside PDT was touted not only for its ease of performance with safety proﬁle comparable to OST, but also for a signiﬁcant decrease in hospital charges and a more efﬁcient utilization of ICU resources. The latter reﬂects the absence of operating room charges and anesthesia fees associated predominantly with OST performed in the operating room. More recently, there are reports of a comparable safety proﬁle in performing bedside OST (61 –63). Bedside OST is usually performed with a standard reusable tracheostomy tray and electrocautery, without operating room charges and anesthesia fees. The professional fee for tracheostomy is the same, regardless of where or how tracheostomy is performed. The cost of using the surgical instruments at bedside is minimal. PDT is usually performed using disposable kits under bronchoscopic guidance; therefore, there are additional costs and charges for these items, rendering PDT somewhat more costly than OST when both are performed at bedside. Although most studies have reported a shorter operative time for PDT when compared with OST (39,47,62,64,65), this is only an issue when the procedure is performed in the operating room, in which longer operating time entails higher charges. The time from decision to performance of the tracheostomy is shorter in PDT compared with OST (47,66). Whether this faster decision to performance time will reﬂect in overall decreased hospital and ICU days and the overall cost remains to be seen. Some studies also report less hemorrhage and wound infection with PDT, while others have shown no difference (47,65,67– 69). Most of the studies looking at the safety and outcome proﬁle of the two techniques lack the rigorous design for this comparison to be meaningful. Many of the OST in the studies were performed in the operating room, not at bedside. Even the meta-analyses comparing percutaneous tracheostomy and surgical tracheostomy are plagued with inconsistencies, including the heterogeneity of the techniques included under percutaneous tracheostomy and the wide ranging quality of studies included (39,40). In general, the superiority of one procedure over the other has not been established. What has been established in multiple studies is that PDT has a comparable safety proﬁle to OST (70 – 74).

VII.

Care of Patients with Tracheostomy

In the early post-tracheostomy period, care should focus on keeping the wound clean. Dressing changes are indicated twice daily or whenever dressing is

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soiled. The site can be cleaned with a mixture of hydrogen peroxide and saline solution. If the tracheostomy tube is secured with sutures, then sutures can be removed in seven to ten days. The tracheostomy tube can be secured comfortably with a foam-pad Velcrow neck strap. The inner cannula can be changed daily in the early post-operative period. We do not routinely change the tracheostomy tube after placement, unless a different tube is needed or there is a malfunction of the existing tube. Dislodgement of the tracheostomy tube in the ﬁrst seven to ten days before the tract has matured can be problematic. Endotracheal intubation should be performed if the tracheostomy tube cannot be reinserted safely. Bronchoscopic guidance and conﬁrmation of placement is strongly recommended. Routine care for an established tracheostomy generally centers on suctioning, appropriate humidiﬁcation, weekly cleaning of the tube, and daily change of the inner cannula. Cuffed tubes are used when patients are still mechanically ventilated, or when risks of aspiration are high. Cufﬂess tubes promote better clearance of secretions, and less likelihood of infection. The intervals to downsizing of tracheostomy tubes and decannulation should be individualized. Factors to consider include the initial indication for tracheostomy and the current respiratory status, the amount of secretions and the patient’s ability to clear the secretions, and the mental status. Once decannulated, the stoma closes rapidly within days, especially if the stoma has been downsized.

VIII.

Future

Many percutaneous tracheostomy methods have been introduced over the past half-century. Almost two decades since PDT was ﬁrst introduced, a large body of literature has conﬁrmed that in skilled hands, the safety proﬁle of the technique is comparable to OST. PDT comes in the era of cost containment, increasing role of minimally invasive surgery, and the growing intensivist movement, all of which have contributed to the momentum towards its acceptance as a safe and viable bedside technique in the ICU. PDT should not be viewed as a replacement for OST because OST still has its vital role and place. In the future, we will likely see more reﬁnements of percutaneous tracheostomy techniques beyond PDT. In our opinion, PDT will likely be the benchmark to which future percutaneous tracheostomy techniques will be compared.

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10 Radiology in the Intensive Care Unit

BRUCE M. BARACK, C. MATILDA JUDE, and HSIN-YI LEE Department of Imaging VA Greater Los Angeles Healthcare System and Department of Radiological Science Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

I.

ANTOINETTE R. ROTH Department of Radiological Science Geffen School of Medicine at UCLA Los Angeles, California, U.S.A.

Introduction

The care of the intensive care unit (ICU) patient requires frequent radiological consultation. Daily review of radiographs is an integral part of critical care rounds. This chapter will address the role of thoracic radiology in the ICU patient. The indications, technique, interpretation, and limitations of the portable chest radiograph will be discussed. The proper positioning and complications of devices used in the ICU and the radiologic ﬁndings of common thoracic abnormalities encountered will also be described. Lastly, the role of multidetector computed tomography (MDCT) imaging and the role of interventional radiology will be summarized. II.

The Portable Chest Radiograph

A. Indications

The accepted indications for portable chest radiographic examination of the ICU are shown in Table 1.

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Table 1 Indications for Portable Radiographic Examination of the ICU Patient Admission to ICU as baseline Prior to any major diagnostic or surgical procedure in the absence of a previous ﬁlm within 24 hr Immediately following any major diagnostic or surgical procedure Immediately following any tube, line, or pacemaker attempt (insertion or removal) Any rapid clinical deterioration As needed to monitor response to therapy

Although not universally accepted as an indication, the mere presence of the patient in the ICU frequently generates requests for daily portable chest examinations. There is ample evidence in the literature to support this practice in the medical ICU, the respiratory ICU, and intubated, mechanically ventilated patients (1 – 4) when uncomplicated cardiac patients and those without heart or lung disease are excluded. Data for surgical ICU (SICU) patients are mixed with some investigations that support this practice and others that argue against routine daily studies (5 – 7). In support of daily routine examinations, new ﬁndings, including cardiopulmonary abnormalities and line or tube malpositions, led to changes in diagnostic approach or therapeutic measures in 14% to 37% of chest X-rays. Changes in therapy were more frequent in intubated, pulmonary, and unstable cardiac patients (1), patients with two or more catheters and tubes (2), and patients in whom a change in clinical condition prompted the exam (3). In a study of SICU patients arguing against daily routine chest radiography, only 13 of 1028 (1.3%) devices central venous pressure (CVP) lines, endotracheal tubes, etc. required repositioning, and only three of 525 chest X-rays (0.6%) (two pneumothoraces and one effusion) had potential clinical impact (6). In another multivariate analysis of 1003 chest X-rays in SICU patients, only patients with Swan – Ganz catheters were felt to be justiﬁed in having routine daily radiographs (7). The authors recommend that routine daily radiographs be obtained only on admission to the SICU and after placement of an invasive device. The American College of Radiology recommends daily portable chest radiographs on patients with acute cardiopulmonary problems and those receiving mechanical ventilation (8). B. Technique Portable Antero-Posterior View

Portable chest radiography accounts for 50% of all chest radiographs performed in hospitals (9). The key to obtaining optimal repeat portable chest radiographs on the same ICU patient is to minimize variation in the technical parameters of successive radiographs (10 –12). At our institution, all portable ICU chest radiographs are performed at a 50 in. source image distance (SID), with the

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patient in the supine position, during peak inspiration with 85 kVp. The exposure is timed with respect to peak inspiratory pressure if the patient is on mechanical ventilation. The technique is recorded on an adhesive label, which is placed at the patient’s bedside for use on all subsequent examinations. It has been found that the supine position minimizes position errors secondary to rotation, distortion errors secondary to kyphosis, and unwanted body artifacts secondary to head or extremity obscuring the thoracic anatomy. Portable chest radiographs result in the patient receiving two to four times the radiation dose of a radiograph obtained with stationary equipment, primarily because of increased scatter radiation (12). Scatter radiation at ICU nursing stations has been demonstrated to be signiﬁcantly below the maximal permissible dose for non-occupational workers (13,14). Special Views

Special portable views that may be useful in the ICU patient include lateral, transthoracic lateral, and lateral decubitus views of the chest, left lateral decubitus view of the abdomen, and an antero-posterior (AP) view of the lower chest and upper abdomen. In one series, the portable lateral chest radiograph yielded an 11% incidence of either unexpected conditions, such as catheter or tube malpositions, or improved interpretation on the AP radiograph (15). The transthoracic lateral view may conclusively demonstrate a pneumothorax. The lateral decubitus view also demonstrates a pneumothorax and differentiates free from loculated pleural ﬂuid and pneumothorax from pneumomediastinum. The left lateral decubitus view of the abdomen is frequently used to demonstrate free intraperitoneal air, which collects superiorly to the liver. An AP view of the lower chest and upper abdomen is useful in localizing the tip of a nasoenteric tube. Oral Contrast

Oral contrast may be used to diagnose a tracheoesophageal ﬁstula or an esophageal perforation in conjunction with a portable chest radiograph in an ICU patient too unstable to be transported to the radiology department. It may also be used to localize the tip of a nasoenteric or gastrostomy tube. The choice of oral contrast agent is dictated by the site of the suspected pathology. Barium provokes an extensive inﬂammatory reaction in the mediastinum and hinders surgical exploration. It should not be used when mediastinal extravasation is a possibility. On the other hand, barium is relatively inert in the airway and lung parenchyma. Water soluble contrast is better tolerated in the mediastinum than barium. However, water soluble contrast results in a severe inﬂammatory response in the lungs. Furthermore, hypertonic water soluble contrast may result in ﬂuid shifts between compartments. Barium should be used in cases of suspected tracheoesophageal ﬁstula (Fig. 1) and water soluble contrast in suspected esophageal rupture or perforation

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Figure 1 Tracheoesophageal ﬁstula. Antero-posterior view of barium swallow in a patient with a bulky tumor in the upper mid esophagus demonstrates opaciﬁcation of the distal trachea, left main stem bronchus, and left lower lobe bronchus (black arrowheads), indicating the presence of a tracheoesophageal ﬁstula. The proximal and distal esophagus are well coated with barium (white arrowheads).

(Fig. 2). Because of the compromised condition of the ICU patient, isoosmolar water soluble contrast is used to avoid possible ﬂuid compartmental shifts. Advantages of Digital Film and PACS

A digital radiograph is any radiographic image acquired without the use of photographic ﬁlm. Digital radiography includes computed radiography (CR), direct digital radiography (DR), indirect digital radiography, and optically coupled direct radiography. At present, CR is the only system used for bedside chest radiographs. DR systems offer high image quality and the potential for dose reduction when compared with images obtained with conventional ﬁlm-screen systems (16). Advantages of a CR system over conventional ﬁlm-screen systems are the inherent wide latitude of the CR system with relatively constant image

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Figure 2 Esophageal perforation. Axial computed tomography image (mediastinal window) in a patient post-dilatation of an esophageal stricture demonstrates evidence of perforation with extravasation (arrows) of oral contrast from the distal esophagus through the mediastinum into the right pleural space.

quality over a wide range of exposures, the ability to postprocess the image, and advanced imaging processing algorithms that minimize scatter and reduce radiation dose. The major disadvantages of slightly higher image noise and lower spatial resolution are not signiﬁcant problems with portable chest radiographs (17). Although the classic technical errors of patient motion and malpositioning, incorrect patient identiﬁcation, incorrect examination, and double exposure occur with the same frequency as with conventional ﬁlm-screen systems (18), repeat rates of less than 1% are reported with CR systems (19). This is primarily attributed to fewer repeat examinations because of under and overexposure. Digital radiography is usually an integral part of an information system called picture archiving and communications system (PACS). At present, the majority of radiographic images are acquired in a digital format, and it is estimated that by the end of this decade, over half of all radiology departments in medical centers will be completely or almost completely digital (20). Major advantages of PACS include elimination of lost studies, marked reduction in ﬁlm costs, fewer repeat examinations, improved image quality, rapid availability of images, rapid viewing of large studies such as MDCT or magnetic resonance imaging (MRI), and improved efﬁciency of radiology personnel and clinicians.

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Accurate interpretation of the portable chest radiograph demands a careful, systematic evaluation, which requires discipline and practice. The following approach is intended as a guide, although individual approaches may vary. The initial observation should include the technical quality of the radiograph for exposure factors and patient positioning, and insure that the lung bases and apices have been included on the ﬁlm. The radiograph should then be inspected for any tubes, lines, or catheters, and any malposition, complication, or change from the prior radiograph noted. Examination of the osseous structures, the mediastinum (including the vascular pedicle), the heart, the pulmonary vessels, and the lungs should follow. An attempt should be made to form a preliminary impression and a relevant differential diagnosis. There are ﬁve additional factors to consider when interpreting a portable chest radiograph. First, patients are expected to inspire to the same lung volumes on successive radiographs in the absence of intra-abdominal changes, cardio-respiratory problems, or cardiac decompensation (10). Then, lower lung volumes are only because of a decrease in lung, chest wall, or abdominal compliance. Second, the heart size does not change when the patient goes from the erect to the supine position. The apparent increase in heart size on a supine ﬁlm is because of magniﬁcation. As the heart is an anterior structure within the chest, it will be magniﬁed on an AP view when the cassette is placed behind the patient, as opposed to a postero-anterior (PA) view when the cassette is closer to the heart. The upper limit of normal for the cardiothoracic ratio in supine patients with a normal heart is 0.57 to 0.58 (10,21). Third, the vascular pedicle extends from thoracic inlet to the superior aspect of the heart. The right border is formed by the right brachiocephalic vein superiorly and the superior vena cava inferiorly. The left border is usually formed by the left subclavian artery above the aortic arch. Therefore, the right side of the vascular pedicle is venous and the left side arterial. As veins are more compliant than arteries, changes in intravascular volume will be reﬂected by a larger change in the right side of the vascular pedicle than the left side. The width of the vascular pedicle is measured horizontally from where the right mainstem bronchus crosses the superior vena cava to a perpendicular line drawn from where the left subclavian artery arises from the aorta (22). Fourth, the size of the azygous vein changes linearly with the width of the vascular pedicle, and both closely correlate with changes in intravascular systemic blood volume (10). Assuming the supine position, rotation to the right, ﬂuid overload, acute right heart failure, and pericardial tamponade (Fig. 3) will increase the width of the vascular pedicle, whereas increasing ventilatory pressure, decreasing intravascular volume, and rotation to the left will decrease the width of the vascular pedicle (10, 22). The vascular pedicle width (VPW) varies according to the patient’s body habitus. The normal VPW is 48 + 5.0 mm on a 72-in.

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Figure 3 Pericardial tamponade. Antero-posterior radiograph in a patient with pericardial tamponade demonstrates enlarged heart (reﬂecting pericardial effusion), wide vascular pedicle (reﬂecting decreased systemic venous return and increased systemic blood volume), and markedly decreased pulmonary vascularity (reﬂecting decreased cardiac output). Subsegmental atelectasis is present in the right lower lung zone.

PA radiograph. On an AP supine radiograph obtained at 40 in., there is an approximate 5% geometric increase in the VPW over the value obtained in a 72-in. PA radiograph (22). Finally in the supine patient, the effect of gravity on vessels in the upper and lower lobes is equal. Therefore, the ratio of the diameter of the pulmonary veins in the upper lobes to the lower lobes is 1:1 and not 1:2 as is seen in the upright chest radiograph. D. Limitations of the Portable Chest Radiograph

The limitations of the portable chest radiograph are listed in Table 2. Table 2 Limitations of the Portable Chest Radiograph Lack of lobar localization Inability to determine content of vascular lumen (e.g., clot) or integrity of vessel wall (e.g., intimal ﬂap) Limited ability to differentiate parenchymal opacities Limited ability to characterize and localize pleural effusions and pneumothorax Limited ability to diagnose lung abscess and empyema, and to differentiate lung abscess from empyema

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Devices Used in the ICU

A. Proper Position, Malposition, and Complications

Familiarity with the proper position, malposition, and potential complications of the multiple devices used in patients admitted to the ICU is essential as malpositions and complications associated with both insertion and use of such devices may be life-threatening. The optimal positions of commonly utilized medical devices are summarized in Table 3. Tubes Endotracheal Tube

The tip of the endotracheal tube should ideally be located 3 –7 cm above the carina with the head in neutral position (23,24). This position allows for maximal excursion of the endotracheal tube within the airway, with changing head position preventing the possibility of subsequent malposition. Neutral head position is best insured with the patient supine, and this is the recommended position for the immediate post-intubation radiograph. When the carina is not identiﬁed on the immediate post-intubation radiograph, a repeat radiograph is recommended. The method of estimating the location of the carina from the projection of the tip of the endotracheal tube in Table 3 Optimal Position of Commonly Utilized Medical Devices in Critically Ill Patients Device Endotracheal tube Changes with head position Flexion Extension Lateral movement

Cuff inﬂation Tracheostomy tube Nasoenteric tube Chest tube Central venous catheter Pulmonary artery catheter

Radiographic location 3 – 7 cm above the carina Mean: 5.5 mm inward; maximum range: 23 mm in/19 mm out Mean: 6.3 mm outward; maximum range: 21 mm in/33 mm out Mean: insigniﬁcant; maximum range: right—19 mm in/17 mm out left—22 mm in/18 mm out Cuff diameter: tube diameter ,1.5: 1 Tip 1/2 to 1/3 of the distance between tracheal stoma and carina 10 cm from the gastroesophageal junction Proximal port .3 cm from the lateral chest wall Superior vena cava 2 – 3 cm distal to bifurcation of main pulmonary artery Less than 2 cm lateral to the hilum Not beyond the proximal interlobar artery

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relation to the thoracic vertebral bodies is unreliable (24), as is the practice of estimating the location of the carina by comparing its location on a previous portable radiograph (23). The inward and outward movement of the tip of the endotracheal tube with head ﬂexion, extension, and rotation has been reported and is shown in Table 3 (25,26). The portable chest radiograph is an unreliable predicator of unsafe endotracheal tube cuff pressures (27). When balloon overinﬂation results in the cuff diameter/tracheal lumen ratio of greater than 1.5, tracheal damage is likely to occur (28). Excessive cuff pressure requirements (19%) and inability to seal the airway (11%) are the frequent adverse consequences of endotracheal tube intubation (29). Complications from overinﬂation of the endotracheal tube are unusual as most endotracheal tubes used today have high-volume, low-pressure cuffs (23). Tube malposition occurs in 10% to 20% of intubations (29 –33). The right mainstem bronchus is the most common location of malposition because the left mainstem bronchus arises from the carina at a more acute angle (Fig. 4). Complications of persistent right mainstem bronchus intubation are inadequate ventilation, left lung collapse with gradual leftward mediastinal shift, and increasing risk of a right-sided pneumothorax (23). Malposition of an endotracheal tube into the esophagus is uncommon and may not be immediately apparent clinically. Such malposition is difﬁcult to detect on routine portable AP radiographs because the tube may be projected over the trachea. Radiographic ﬁndings seen in decreasing frequency on routine portable AP ﬁlms include projection of the tube lateral to the trachea,

Figure 4 Endotracheal tube in the bronchus intermedius. Antero-posterior radiograph demonstrates the tip of the endotracheal tube (arrowhead) extending into the bronchus intermedius well below the carina (arrow).

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gastric distention, esophageal air, and deviation of the trachea by the balloon cuff. Examination of the patient in a 258 right posterior oblique projection accurately demonstrates the endotracheal tube position in 92% of radiographs (34). Tracheal rupture is a serious, less common complication of endotracheal tube intubation. Early radiographic ﬁndings are orientation of the distal portion of the tube to the right of the tracheal air column with overdistention of the tube cuff towards the endotracheal tube tip and subsequent development of pneumomediastinum, subcutaneous air, and pneumothorax (35). Aspiration pneumonitis has been reported to occur in 8% of endotracheal tube intubations (29,36). It is usually easily identiﬁed on the post-intubation radiograph and frequently becomes more apparent on subsequent examinations. Fillings, teeth, and dentures may also be aspirated or swallowed secondary to dislodgment during intubation (37). Tracheostomy Tube

Tracheostomy is performed on patients with upper airway obstruction or on patients who require long-term ventilator support (23). The tracheostomy tube is inserted between the ﬁrst and second tracheal ring or second and third tracheal ring. The tip of the tracheostomy tube should be one-half to two-thirds of the distance between the tracheal stoma and the carina at the level of the third thoracic vertebral body. Neither head ﬂexion nor extension affects the location of the tip of the tracheostomy tube (12). The lumen of the tube should be onehalf to two-thirds the diameter of the trachea, and the cuff should not distend the tracheal wall. A post-tracheostomy ﬁlm showing the internal and external ends of the tube in the same plane may indicate that the tracheostomy tube has not distended properly into the trachea, which can be conﬁrmed on a portable lateral radiograph (38). A small amount of subcutaneous air in the neck and a small pneumomediastinum are frequent ﬁndings on the post-tracheostomy radiograph (39). However, fascial plane disruption may result in a large amount of air in the neck, with a larger pneumomediastinum and a pneumothorax frequently seen following injuries to the lung apex. Pneumothorax may also be seen in tracheal perforation. Late complications include tracheo-innominate artery ﬁstulas or tracheoesophageal ﬁstula (40 – 42). The ﬁstulas are usually secondary to prolonged hyperinﬂation of the cuff and occur at the level of the cuff with erosion anteriorly (tracheo-innominate artery) or posteriorly (tracheoesophageal). In tracheoesophageal ﬁstulas above the cuff, gastric contents may accumulate in the upper trachea. With ﬁstulas below the cuff, aspiration of gastric contents into the lungs is a routine occurrence. Other late complications include stricture, tracheomalacia, and tracheal stenosis. Nasoenteric Tubes

Nasoenteric tubes are commonly used in ICU patients for gastric decompression or feeding. Sideholes are present along the distal 10 cm of nasogastric tubes.

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Therefore, the tip of the tube should extend at least 10 cm beyond thegastroesophageal junction. A more proximal position may result in obstruction of the distal esophagus with applied suction or may allow contents entering the distal portion of the tube to exit into the distal esophagus and predispose to aspiration (23). Incorrect placement was seen in 4.4% of nasogastric tube insertions in one series of 340 patients (43). Similarly, the most proximal sidehole of the tube should be placed inferior to the anastomotic site in postoperative esophagectomy patients. Feeding tubes are used for nutritional support as an alternative to intravenous feeding. Ideally, they should be positioned distal to the gastric pylorus to reduce gastroesophageal reﬂux. A post-placement radiograph should always be obtained, as malpositions are common following insertion (44,45) (Fig. 5). Malpositioned tubes may be coiled in the pharynx, esophagus, or stomach. In intubated or obtunded patients, or patients lacking a gag reﬂex, tubes may pass into the trachea and preferentially enter the right mainstem bronchus. Immediate complications of nasoenteric tube insertion include traumatic esophageal perforation with pneumomediastinum or, more rarely, bronchial perforation and pneumothorax (23). Parietal pleural perforation may also result from malposition of the tube within the esophagus and should be suspected when a pleural effusion, pneumomediastinum, mediastinal widening, or mediastinal air ﬂuid levels appear rapidly after beginning tube feedings (36,46).

Figure 5 Feeding tube in the left lower lobe bronchus. Antero-posterior post-insertion radiograph demonstrates the tip of the feeding tube in the left lower lobe bronchus (arrowhead). The tube was subsequently removed and reinserted without complication.

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Late complications of insertion include esophagitis and esophageal stricture formation. Late complications of unrecognized malposition include inadvertent infusion of feeding solutions into the lungs and entry into the visceral pleural space causing a pneumothorax. If the feeding tube is noted within the tracheobronchial tree, an immediate post-removal radiograph should be obtained to exclude the possibility of a pneumothorax (47,48). Sengstaken –Blakemore (SB) tubes are used as a temporary measure to control esophageal variceal bleeding. These tubes contain two inﬂatable balloons. The larger, more distal spherical balloon is inﬂated only in the stomach to a volume of 250 cc. After inﬂation, it is retracted back to the gastric cardia, insuring correct positioning of the more proximal cylindrical balloon within the esophagus, which is inﬂated to a pressure of 15 to 30 mmHg (49,50). The incidence of esophageal perforation following placement of SB tubes is reported as high as 15% to 30%, and a post-placement radiograph of the chest and upper abdomen is essential to ensure proper positioning (51). Esophageal perforation may result from either inﬂation of the distal balloon within the esophagus or retraction of the inﬂated distal balloon into the esophagus by an agitated patient or unintentionally by the physician. Findings suggesting perforation of the esophagus on the post-placement radiograph include mediastinal widening, pneumomediastinum, and subcutaneous emphysema. Thoracostomy Tube

Thoracostomy tubes are commonly used in ICU patients to drain pleural ﬂuid collections and pneumothoraces. In the supine patient, mobile pleural ﬂuid collects posteriorly and pleural air anteriorly. A pleural drainage tube for mobile ﬂuid collection should therefore be positioned postero-inferiorly through the sixth to eighth intercostal space at the level of the mid axillary line, preferably guided by ultrasonic localization (52). If there is uncertainty about the potential for injury to abdominal structures, placement through the ﬁfth intercostal space provides a margin of safety. A thoracostomy tube for pneumothorax treatment should be positioned near the lung apex at the level of the anterior axillary line and be directed antero-superiorly. Loculated pleural ﬂuid collections, as seen in empyemas, require precise localization with ultrasonography or computerized axial tomography (23). Rapid improvement is expected on post-drainage radiographs if the tube is properly positioned. Conversely, a persistent pneumothorax or undrained pleural ﬂuid collection suggests a malpositioned or malfunctioning tube. A malfunctioning tube may result from kinking or plugging by debris (12). Improper tube position may be appreciated on the AP radiograph. However, a lateral radiograph or computerized axial tomography may be required to determine the exact tube position (15,53). A malpositioned tube may be in the subcutaneous or extrapleural soft tissues, within an interlobar ﬁssure (Fig. 6) or within the lung parenchyma (Fig. 7). The proximal side hole of the chest tube should be medial to the inner margin of the ribs and can be identiﬁed along the radio-opaque edge of the

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Figure 6 Tip of right chest tube in the right major ﬁssure. Sagittal computed tomography reformation (mediastinal window) in a patient with a non-draining chest tube demonstrates the tip of the right chest tube within the right major ﬁssure (arrow). A large empyema (E) is present in the right posterior hemithorax, causing anterior displacement and compression of the right lower lobe (arrowheads).

tube (54). Malposition of the tube in the subcutaneous tissue may result in subcutaneous emphysema and occurs more frequently in patients with excessive subcutaneous fat (44). Malpositioned tubes within an interlobar ﬁssure are associated with a 29% rate of unsatisfactory drainage (55). Malposition within the lung parenchyma may be associated with bronchopleural ﬁstula, pulmonary laceration, and hematoma (36). Pulmonary laceration and hematoma are particularly seen in patients with pleural adhesions or decreased lung compliance. Complications of drainage tubes because of tube insertion include bleeding secondary to laceration of an intercostal artery, laceration of the diaphragm with associated splenic, hepatic, and gastric injuries, and mediastinal and parenchymal lung injury (56). A delayed complication of thoracostomy tubes is unilateral pulmonary edema on the side of tube placement due to rapid pulmonary

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Figure 7 Tip of the right chest tube in the right middle lobe. Axial computed tomography image (mediastinal window) in a patient with a right empyema and a non-functioning right chest tube demonstrates the tip of the right chest tube within the lateral segment of the right middle lobe (arrow). The right major ﬁssure is clearly visualized (arrowhead). The tube was removed without complications.

re-expansion after removal of a large amount of ﬂuid or air from the pleural space (36). A less common delayed complication is pulmonary infarction due to suctioning of lung tissue by the chest tube even at low suction pressures (57). After a thoracostomy tube has been removed, a tubular structure containing air or ﬂuid may persist in the position previously occupied by the thoracostomy tube. Because of a local inﬂammatory response and associated pleural thickening, free communication between this tubular tract and the rest of the pleural space may not exist and the isolated tube tract may simulate a localized pneumothorax or abscess on the chest radiograph (52). Such tracts usually decrease and disappear within a few days and rarely become infected.

Catheters Central Venous Catheters

Approximately 38% of patients in the ICU have central venous catheters (58). The most proximal port is 5 cm from the tip. The ideal location of the tip of the central venous catheter is the superior vena cava at or slightly above the entrance of the azygous vein. This location assures that all ports of the central venous catheter are beyond the most proximal venous valves. Below the azygous vein, the superior vena cava becomes intrapericardial, and caval perforation is associated with a pericardial effusion and eventual tamponade (11).

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If the catheter is to be used to monitor central venous pressure, the tip of the pressure monitoring port must be proximal to any competent valve. The last valve in the subclavian vein occurs 2 cm distal to the junction of the subclavian and internal jugular veins at about the level of the ﬁrst anterior rib (59). Therefore, the tip of the pressure monitoring port should be visualized medial to the anterior portion of the ﬁrst rib at the level of the ﬁrst anterior intercostal space. The right and left brachiocephalic veins join to form the superior vena cava at this level (23). Neither the brachiocephalic veins nor the superior vena cava contains valves. Malposition of central venous lines occurs in approximately one-third of catheter insertions, and most malpositions are not clinically suspected (60). The subclavian vein is the most often used site for central venous placement. A retrospective study of 500 subclavian vein catheterizations revealed only 68% to be properly positioned, with 21.4% to be positioned in the right atrium and 0.4% in the right ventricle. Cardiac malposition was more common with a right-sided approach (30.1%) than a left-sided approach (61). The average safe insertion length of the central venous catheter from either the right or left subclavian or internal jugular vein is 16.5 cm in most adults, and no central venous catheter should be inserted greater than 20 cm from these access sites (62). The most common venous malposition of the subclavian venous catheter is the ipsilateral internal jugular vein (Fig. 8), which is reported to occur in 15% of such central venous insertions (36). A malpositioned catheter in this location may produce abnormal sensations in the ear or severe headache (63). Retrograde infusion of intravenous ﬂuids into the internal jugular vein in this malposition may result in thrombosis, erosion of the vein, and pooling of infused solutions near the brain in the supine patient (64). Another common venous malposition occurs when the catheter enters the contralateral brachiocephalic vein (Fig. 9). This is more common when the junction of the brachiocephalic veins is higher and at a less acute angle and more common with left-sided insertions. Malposition of the catheter in the azygous vein occurs occasionally. Rarely, a catheter may be positioned in the right superior intercostal vein, the internal mammary vein, the pericardiophrenic vein, the left superior intercostal vein, and an inferior thyroid vein. The coronary sinus, which drains the cardiac veins and empties into the posterior aspect of the right atrium near the entry of the inferior vena cava, may be entered by a malpositioned catheter in the right atrium, as may the hepatic veins and inferior vena cava (23). Catheter malposition within the superior vena cava may occur in left-sided catheter insertions when the catheter tip abuts perpendicularly upon the right lateral wall of the superior vena cava. This position causes the tip to repeatedly hit the lateral caval wall with inspiratory movements or with head and neck movements with left internal jugular catheters. This can eventually damage the caval epithelium and cause caval rupture hours or days after insertion (65).

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Figure 8 Tip of right subclavian venous catheter in the right internal jugular vein. Antero-posterior radiograph obtained after insertion demonstrates right subclavian venous catheter extending into the right internal jugular vein (arrow).

A gentle curve of the tip of the catheter may be seen when the catheter tip is in contact with the lateral caval wall, and the catheter should promptly be repositioned (66). A simulated catheter malposition occurs in the presence of a persistent left superior vena cava, which is the most common anomaly of systemic venous drainage (Fig. 10). This anomaly occurs in 0.3% of the normal population and 4.3% of patients with congenital heart lesions when the left anterior and common cardinal veins fail to regress normally (67,68). This vein courses inferiorly along the left side of the mediastinum and drains into the coronary sinus. Most patients with this anomaly also have a right-sided superior vena cava, which may be smaller than normal (23). The most common complication of central venous line placement is pneumothorax, which has been reported in 5.6% of patients with any central line placement (3) and 6% of subclavian venous insertions (69). The latter is explained by the 1 cm or less proximity of the apical pleura to the subclavian vein. Therefore, a radiograph is recommended following any unsuccessful subclavian venous insertion to exclude a pneumothorax before contralateral

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Figure 9 Tip of right subclavian catheter in the left brachiocephalic vein. Anteroposterior radiograph demonstrates the right subclavian catheter extending into the left brachiocephalic vein (arrow).

insertion is attempted. A pneumothorax may become apparent hours to days after central line insertion because of slow accumulation of pleural air (70,71). The typical location of the pneumothorax in the upright ﬁlm is apicolateral. However, the most non-dependent aspect of the thorax in a supine patient is the anteromedial aspect of the thorax and the subpulmonic recesses. Air collections in these regions should be carefully looked for on both the immediate and subsequent delayed post-insertion radiographs (52). Puncture of the subclavian artery is not uncommon and usually produces bright red, pulsatile backﬂow of blood. However, arterial blood may be nonpulsatile and dark, stimulating venous blood in hypoxic and hypotensive patients (72). Extrapleural collections of blood may be suggested by a mass in the soft tissues of the neck or a focal mediastinal bulge on the unsuccessful post-insertion radiograph following an arterial puncture (44). Unrecognized vessel perforation is one of the most dangerous complications of catheter insertion. Radiographic ﬁndings of this potentially fatal complication include identiﬁcation of the catheter or parts of catheter lateral to the normal mediastinal shadow outside the anatomic position of the vena cava coursing in an abnormal direction (44) and the rapid accumulation of pleural or mediastinal ﬂuid after catheter insertion

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Figure 10 Pulmonary artery catheter in the left superior vena cava. Antero-posterior radiograph demonstrates the tip of the pulmonary artery catheter in the right interlobar pulmonary artery. The catheter was inserted into the right subclavian vein and coursed through the right brachiocephalic vein, a left superior vena cava (arrow), the coronary sinus, right atrium, right ventricle, and main pulmonary artery to reach the ﬁnal location.

(23). A correct AP projection is mandatory as normal anatomic landmarks may be lost in a rotated ﬁlm. Fragmentation of the catheter at the time of insertion is an uncommon but potentially serious complication. The fragmented catheter may embolize to the superior vena cava, right atrium, right ventricle, or pulmonary artery. Sepsis, pulmonary embolization, arrhythmias, or perforation may follow. Most fragments can be successfully removed percutaneously (23). Knotting of the catheter, which may result in vessel thrombosis, arrhythmia, and vascular injury, is rare and usually successfully treated percutaneously (52). Mediastinal enlargement appearing days or weeks after catheter insertion may indicate superior vena cava thrombosis (44). However, patients with superior vena caval thrombosis may have a normal radiograph even in the presence of sepsis, superior vena cava syndrome, and loss of central venous access (73). When superior vena caval thrombosis is suspected, contrast computerized tomography should be performed with bilateral arm injections to determine if thrombosis exists and to delineate the extent of the obstruction. In general, the type and frequency of the malposition and complication are strictly dependent on the site of catheter insertion (44). The more curves a catheter has to pass through to reach the superior vena cava, the greater the risk for malposition and vascular damage. Because the left brachiocephalic vein has a

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more acute and curvaceous course than the right before joining to form the superior vena cava, closer scrutiny for malpositions and complications is required when left-sided insertions are reported. On the right side, the internal jugular insertion is safer than the subclavian insertion because of the higher rate of pneumothorax with the latter approach. Peripherally Inserted Central Catheters

Peripherally inserted central catheters (PICC) are small caliber catheters inserted in the superﬁcial veins of the arm. The major advantage of PICCs is that they can be left in place for weeks to complete a course of intravenous therapy (12) or for total parenteral nutrition (74,75). The ideal location of the tip of the PICC catheter is the superior vena cava (76,77). Successful bedside insertion rates by specially trained nurses have been reported at 82.6% (327 insertions), with rates as high as 98.2% (869 insertions) (78). Radiologists use a venographic – ﬂuoroscopic direct puncture and sheath technique for difﬁcult insertions, PICC salvage, and PICC exchanges. The service length for a given PICC is 28.1 days (78,79). Peripheral malpositions, including coiling, are easily recognized clinically or by the absence of visualization of the PICC catheter on the post-insertion chest radiograph. The central malpositions are similar to those associated with central venous catheters. Pulmonary Artery Catheters (Swan – Ganz Catheters)

Pulmonary artery catheters are 2 –3 lumen catheters used to measure right-sided cardiovascular parameters and infer left sided parameters. The smallest of the lumens is situated close to the catheter tip and connected to an inﬂatable balloon. When the balloon is temporarily inﬂated, the catheter ﬂoats peripherally and wedges. When the balloon is deﬂated, the catheter tip recoils proximally. The ideal position of the catheter tip is 2 to 3 cm distal to the bifurcation of the main pulmonary artery, less than 2 cm lateral to the hilum, and not beyond the proximal interlobar artery (12). Approximately 24% of Swan – Ganz catheters are malpositioned on the post-insertion radiograph (59). Catheter migration after initial placement is common probably because of catheter warming (80). This is due to increased catheter compliance, shortening of the loop of the catheter through the right ventricle, and subsequent distal malposition. The incidence of pneumothorax is the same as with any upper chest central line placement (5 – 6%). Rapid insertion of the catheter in a patient with right ventricular dilatation may result in intracardiac knotting (39). The most common complication of distal malposition is pulmonary infarction. This can result from peripheral position of the catheter tip obstructing ﬂow, persistent balloon inﬂation in a peripheral pulmonary artery, or clot formation around the catheter (52). The size of the infarct depends upon the size and distribution of the occluded vessel. Radiographically, one may see a patchy area of consolidation peripheral to the Swan – Ganz catheter or a more classic,

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wedge-shaped pleural-based opacity (53) (Fig. 11) or no evidence of infarction. Other rare complications include thromboembolism, hemorrhage, and pulmonary arterial pseudoaneurysm formation, which can present as a new solitary pulmonary nodule months after discharge (81,82). Dialysis Catheters

The types of dialysis catheters used in the ICU are acute dialysis catheters (83), cuffed tunneled catheters (84), and subcutaneous vascular port catheters. Acute dialysis catheters are primarily used as short-term access in patients with malfunction of permanent access or in bed-bound patients with acute renal failure. Most acute dialysis catheters are non-cuffed, non-tunneled, dual lumen catheters composed of polyurethane. Polyurethane is quite sturdy, permitting a larger internal lumen for a given outer diameter, and is less thrombogenic than silicone (83). Bedside ultrasound to localize the vein reduces the number of needle passes, failed placements, and insertion-related complications and increases the success rate of inexperienced operators to 95% (85). In addition, 28% to 35% of dialysis patients have demonstrated signiﬁcant vein abnormalities, such as total occlusion, non-occlusive thrombus, stenosis, and anatomic variation (86,87). The tip of acute dialysis catheters placed in the internal jugular vein should lie in the superior vena cava. Catheters placed in the femoral vein should be long enough to insure that their tip lies in the inferior vena cava to prevent excessive recirculation. Right internal jugular placement provides superior blood ﬂow and is less likely to malfunction than left internal jugular or femoral placement. High complications rates temper subclavian vein placement of these catheters (83). Complications of acute dialysis catheters are both immediate insertion related and delayed (83) and similar to those associated with central venous catheter placement. Because acute dialysis catheters are relatively stiff, they are associated with a higher incidence of vessel and right atrial perforation than cuffed, tunneled catheters. Late complications include central vein stenosis/thrombosis, vessel perforation, cardiac tamponade, hemomediastinum, and infection. Stenosis/thrombosis has been reported in up to 28% of subclavian dialysis catheters with infection, increasing the risk in such insertions (88). Because of the high rate of complication, subclavian insertions should be avoided and are contraindicated in patients expected to receive permanent access on the same side. In contrast, internal jugular insertions are associated with only a 2% to 3% thrombosis/stenosis rate (89 – 92). Because cuffed, tunneled catheters are softer and less rigid than acute dialysis catheters, vessel and atrial perforation is not a major complication. The optional location of the tip of cuffed, tunneled catheters is the mid right atrium (84), as opposed to the superior vena cava. The right internal jugular site is the preferred site for catheter placement because it has a lower rate of complication during and after insertion than other locations (93).

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Figure 11 Pulmonary infarction (the Hampton’s hump). (A) Antero-posterior arrow radiograph demonstrates the tip of the pulmonary artery catheter extending more than 2 cm beyond the origin of the right interlobar artery into the right mid lung zone (arrow). (B) Radiograph obtained four days later demonstrates a homogeneous pleural based opacity with convex medial contour towards hilum (the Hampton’s hump) in a subsegment of the lateral segment of the right middle lobe (arrowheads). The pulmonary artery catheter has been withdrawn, and the tip is now in good position (arrow).

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The value of the post-insertion chest radiograph has been questioned when a cuffed tunneled catheter is inserted under ﬂuoroscopy (94). Only seven procedural complications were identiﬁed in 937 consecutive central venous access procedures, and all were identiﬁed at ﬂuoroscopy. No procedural complication was detected on post-procedure chest radiography that was not detected on ﬂuoroscopy, and only one malpositioned catheter was detected by chest radiography. The most common acute complications are inadvertent carotid artery puncture, air embolism, hemothorax, and pneumothorax (95 – 97). Late malfunctions of cuffed, tunneled catheters are primarily associated with thrombosis, which may be either extrinsic or intrinsic (96). Other Devices Intra-Aortic Balloon Pump

The intra-aortic counterpulsation balloon pump is used in patients in cardiogenic shock or with severe ventricular dysfunction and patients who undergo high-risk cardiac surgical procedures (53). The pump is composed of a catheter surrounded by a long balloon. The catheter is placed in the descending thoracic aorta with its tip immediately distal to the origin of the left subclavian artery (23). The balloon is inﬂated during systole, increasing coronary artery perfusion, and forcibly deﬂated during diastole, facilitating aortic blood ﬂow and decreasing ventricular afterload (98). On the portable chest X-ray, the radio-opaque tip is identiﬁed within the aortic knob (Fig. 12). The inﬂated balloon is a long radiolucent

Figure 12 Intra-aortic counterpulsation balloon pump. Antero-posterior radiograph demonstrates the radio-opaque tip of the intra-aortic counterpulsation balloon pump in the inferior aspect of the aortic arch (arrow), in good position.

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tubular structure extending the length of the descending thoracic aorta (11), and the deﬂated balloon cannot be visualized on the radiograph. The location of the tip should be noted on daily radiographs to avoid complications. Advancement of the catheter too far may result in cerebral embolization or occlusion or dissection of the left subclavian or vertebral artery. If the balloon tip is positioned more distally in the descending thoracic aorta, counterpulsation is less effective, and potential occlusion of the major branches of the abdominal aorta, including the renal arteries, may occur (99). Dissection of the aorta at the time of insertion is a rarely reported complication (100). This is accompanied by clinical symptoms and may be suggested by loss of deﬁnition of the descending aorta or widening of the para-aortic line on the portable radiograph. The diagnosis may be conﬁrmed by either contrast enhanced computerized tomography (CT) or magnetic resonance angiography (MRA). Transvenous Pacing Devices

Transvenous endocardial pacing is used for patients with heart block or bradyarrhythmias. The pacer is usually inserted into the subclavian or internal jugular vein and manipulated into the apex of the right ventricle under ﬂuoroscopy where it is wedged into the trabeculae. Malposition is the most common complication (53). On the post-insertion radiograph, the catheter tip should be projected over the right ventricle with the lead wire directed downward and toward the left. Superior deﬂection of the tip of the wire is suggestive of coronary sinus malposition and should be conﬁrmed on a portable lateral view, which will demonstrate a posterior course of the pacing wire, as opposed to an anterior position in the apex of the right ventricle (12,23). Over time, approximately 20% of pacing wires will change position, migrating to the right atrium, pulmonary artery, or coronary sinus. Cardiac perforation has been reported in 5% to 7% of placements (101). This complication should be suspected when the tip of the pacing wire projects beyond the border of the myocardium into the epicardial fat or when the cardiac silhouette rapidly enlarges after pacing wire placement. The former is best appreciated on a portable lateral radiograph. Cardiac perforation can be conﬁrmed with multidetector CT. Failure to pace properly may be the result of pacing wire malposition, lead fracture, or myocardial perforation. Lead fracture has been reported in 3% of cases and may be the result of a sharp bend in the wire or may be caused by compression of the lead between the clavicle and the ﬁrst rib, called pinch-off syndrome, which has also been documented with cardiac pacemaker leads (102). Lead fracture may be difﬁcult to visualize on a portable radiograph and is sometimes more apparent on ﬂuoroscopy. Automatic Implantable Cardioverter-Deﬁbrillator Devices

Automatic implantable cardioverter-deﬁbrillator devices are used in patients to control potentially fatal arrhythmias. These devices may be inserted via

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thoracotomy or transvenously and may consist of additional wire leads in the superior vena cava or wires or patches placed over the pericardium (103,104). A post-insertion radiograph should be obtained to check for lead placement and possible complications, including pneumothorax. Knowledge of the exact type of device is mandatory as many combinations of transvenous sensing and deﬁbrillator catheters have additional subcutaneous and pericardial patches (12,53). Temporary Epicardial Wire Electrodes

Temporary epicardial pacemaker electrodes are commonly attached to the right atrium and right ventricle following cardiac surgery. These electrodes are commonly secured to the right atrium and right ventricle and are usually removed prior to discharge (53). Reported rare complications associated with removal of such electrodes include pneumothorax and hemorrhage (100). Another rare complication associated with removal is rupture of the epicardial wire electrode at the point of electrode attachment to the right atrium and ventricle (Fig. 13). The retained epicardial electrode must be removed surgically under general anesthesia. B. Complications of Mechanical Ventilation (Barotrauma)

The term “barotrauma” refers to the adverse consequences of mechanical ventilation in the lungs. The major adverse consequences of positive pressure ventilation

Figure 13 Retained epicardial pacing electrode. Overpenetrated antero-posterior radiograph status post-CABG demonstrates a retained right epicardial electrode (arrow), which fractured from the pacing wire during attempted removal.

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have been divided into three categories: (1) physiologic effects on the heart and pulmonary vasculature, (2) direct lung injury, and (3) air leak phenomena (105). Positive pressure ventilation (PPV) may affect cardiopulmonary function, particularly when used with positive end-expiratory pressure (PEEP). Cardiac output may be diminished by PPV with PEEP in patients with suboptimal volume status, resulting in further reduction in cardiac blood volume. The diminished cardiac output and reduction in cardiac blood volume may be manifest radiographically as a decrease in heart size. However, the decrease in heart size does not necessarily indicate an improvement in the cardiovascular status of the patient. Conversely, the increase in heart size, which may occur when PPV and PEEP are discontinued or decreased to lower levels, does not necessarily indicate cardiac disease or ﬂuid overload. Therefore, changes in heart size in patients receiving mechanical ventilation should be carefully interpreted along with information on current ventilator settings and changes in settings from the time of the previous radiograph. The effect of PPV and PEEP on pulmonary vasculature is complex, and large radiographically visible pulmonary vessels can either increase or decrease in size depending on lung volume, inﬂation pressures, and pre-existing pulmonary vascular tone (105). Because the air to tissue ratio increases when the patient is placed on PPV or PEEP, the post-PPV or -PEEP chest radiograph may show signiﬁcant apparent improvement despite the presence of severe residual underlying disease (106 – 110). Additional lung injury, manifest as non-cardiogenic pulmonary edema or diffuse alveolar damage, may occur with PPV and PEEP. Experimentally, the threshold peak inspiratory pressures (PIP) that cause lung injury appear to be approximately 25 to 30 cmH2O (111), that is, the same PIP at which perivascular interstitial emphysema (PIE) occurs (110). Further increases in PIP produce more severe lung injury (112). On the basis of the experimental studies, it has been recommended that maximum transalveolar pressure should not exceed 30 to 35 cmH2O, which usually corresponds to 45 cmH2O end-inspiratory pressure (110). The other major complication of mechanical ventilation is air-leak phenomena, PIE and its sequellae, commonly recognized manifestations of barotrauma and oxygen toxicity. The incidence of barotrauma in the general population of ventilator dependent patients varies from 4% to 15% (113,114) and rises to as high as 60% when underlying lung disease, such as pneumonia or acute respiratory distress syndrom (ARDS), is present (115). Although PIE may be seen in any age, the majority of severe cases have been reported in infants, children, and adults under 40, suggesting that perivascular and connective tissues in older adults are less easily dissected than in younger patients (105). Ventilator-related risk factors for development of air leak include large tidal volumes, PIP greater than 40 cmH2O, plateau pressures greater than 35 cmH2O, high levels and long-term duration of PEEP, and higher minute ventilation. A PIP of 40 cmH2O or greater is usually required to

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produce radiographically visible PIE (116,117). While many studies imply an association of high-peak airway pressures and the development of PIE, other studies suggest that alveolar overdistension or volutrauma may be a more important factor than PIP in the development of PIE (118 –120). PIE occurs when pressure in the air spaces exceeds tension in the adjacent perivascular connective tissues and interlobular septa, resulting in alveolar rupture and air entering the adjacent interstitium producing interstitial emphysema (121). Air then dissects centrally to the hilum along the vascular sheaths and interlobular septa, resulting in pneumomediastinum. As there is no gradient between alveoli and bronchi, peribronchial air dissection does not occur. PIE has not been identiﬁed in alveolar septal walls or in the bronchial walls (105). The progressive dissection of air from the interlobular septa into the contiguous subpleural connective tissues results in subpleural air cyst formation. The subpleural air collections can become much larger than the air collections within the lung interior because of the larger potential size of the subpleural space. Air cysts greater than 1 cm in diameter are sometimes called pneumatoceles. Extensive PIE can signiﬁcantly impact cardiopulmonary function by producing progressive collapse of pulmonary vessels, resulting in increased vascular resistance and vascular shunting (122). Veins are more compressed than arteries because of their thinner walls and less distending pressure. The preferential location of PIE in larger interlobular septa, hilar regions, and the mediastinum and the greater compression of central veins than arteries result in decreased pulmonary venous return to the heart. This may explain the atypical acute pulmonary edema pattern that may be observed in cases of severe PIE (105). In this setting, the peripheral portions of the lungs demonstrate marked increased radio-opacity, resulting in a reversal of the usual central perihilar or bat wing pattern of acute pulmonary edema (Fig. 14). Rapid clearing of the peripheral edema is observed when the acute “air-block” is removed (123) by either decreasing the pressures used during PPV or by sudden decompression of air into the soft tissues of the neck, pleural space, mediastinum, or abdomen (124). The diminished functioning lung volume, a consequence of the part of the lung volume occupied by PIE, is usually only clinically signiﬁcant in patients whose pulmonary function is already severely compromised or in cases of severe, extensive PIE. However, the stiffening of the lungs or diminished lung compliance that occurs because of the distended interstitial air pockets may have far more clinical signiﬁcance. The increased lung stiffness or diminished lung compliance increases resistance to both inspiration and expiration (121). Thus, a repetitive cycle may be created in which PIE increases airway resistance, requiring higher peak pressures, which forces more air into the interstitial compartments, mediastinum, and soft tissues, further increasing airway resistance. This results in progressively stiffer and severely hyperexpanded lungs (105). The radiographic recognition of PIE usually occurs before its clinical recognition because deterioration of gas exchange, lung compliance, and

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Figure 14 Pulmonary edema in pulmonary interstitial emphysema. Antero-posterior radiograph in a patient with severe pulmonary interstitial emphysema demonstrates bilaterally symmetric peripheral airspace disease consistent with acute pulmonary edema. The peripheral distribution is the reversal of the usual central perihilar or bat-wing pattern seen in acute cardiogenic pulmonary edema.

vascular resistance may be due to causes other than barotrauma (124). The early stage of PIE prior to formation of large air cysts is easier to recognize in the presence of signiﬁcant concomitant alveolar consolidation. A mottled increase in radiolucency of the lung anteriorly and medially around the heart and surface of the diaphragm is the ﬁrst chest radiograph abnormality detected in adults (105) (Fig. 15). This corresponds to the hyperinﬂated pulmonary lobules and interstitial and subpleural linear and cystic air collections demonstrated on CT scans (125,126). These lucencies are extremely difﬁcult to recognize in patients with underlying emphysema or subcutaneous emphysema in the absence of consolidated lung. However, without CT correlation, the plain ﬁlm diagnosis of PIE is difﬁcult at this stage because of similar ﬁndings in microabscesses, hyperinﬂated acini, honeycombing, and emphysema. Streaky, non-branching, ﬁxed caliber radiolucencies radiating from the hila to the lung periphery corresponding to air in the perivascular connective tissue also may be identiﬁed as an early radiographic sign of PIE and are more suggestive of its diagnosis. The non-branching, ﬁxed caliber appearance of these lucencies distinguishes them from the branching, peripherally tapering appearance of air bronchograms. Rarely, perivascular halos, which are pathognomonic for PIE, may be seen (127). Other, more disorganized streaky

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Figure 15 Early pulmonary interstitial emphysema. Antero-posterior radiograph in a patient, who subsequently developed a tension pneumothorax as a manifestation of barotrauma, demonstrates a mottled increased radiolucency medially around the heart and hila (arrowheads). This ﬁnding, although non-speciﬁc, has been described as one of the earliest plain ﬁlm ﬁndings in pulmonary interstitial emphysema.

radiolucencies probably correspond to air within the interlobular septa (105). The subpleural cystic air collections that can be seen on CT scans in patients with ARDS may originate in the interlobular septa. The presence of subpleural air cysts is the most frequent plain ﬁlm radiographic ﬁnding in PIE and often precedes a pneumothorax (124,128). Subpleural air cysts may become large and may be effectively treated by percutaneous catheter drainage (129). They also may become secondarily infected, demonstrating progressive thickening of the cyst wall or an air – ﬂuid level, with subsequent rupture producing either a pneumothorax or tension pneumothorax (105,128). Pneumomediastinum has been found in 37% of patients with PIE (117) and has been reported to precede the appearance of pneumothorax in 50% of patients with ARDS (115). On a supine radiograph, pneumomediastinum may be difﬁcult to distinguish from pneumopericardium, anteromedial pneumothorax, and an optical illusion, the Mach effect, which is an apparent line of contrasting density bordering a soft tissue shadow (130). All of these entities may produce a sharp outline of the heart on the supine radiograph. The radiographic differentiation of these four entities is mandatory given the potentially life threatening complication of evolution to a tension pneumothorax in mechanically ventilated patients.

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Pneumopericardium is more commonly observed in the pediatric than the adult population as a complication of barotrauma (131). It is easily diagnosed when the superior pericardial reﬂection around the great vessels is outlined by air and may also be diagnosed when the main pulmonary artery and undivided right pulmonary artery are outlined by air, which is uncommonly seen (105). When pneumopericardium cannot be differentiated from pneumomediastinum on the supine radiograph, pericardial air may be distinguished from mediastinal air by a change in the position of pericardial air on radiographs exposed in different body positions (132). Pericardial air will rise on upright or decubitus ﬁlms, whereas mediastinal air will remain ﬁxed. Pneumomediastinum can be differentiated from the Mach effect by visualizing air in regions of the mediastinum not enhanced by the Mach effect. Similarly, pneumomediastinum may be distinguished from pneumothorax when air outlines the borders of anatomical structures not normally visible in the presence of a pneumothorax (133,134). Rarely, decubitus ﬁlms or CT may be required to differentiate these two conditions (105). Pathognomonic signs of pneumomediastinum include air dissecting along the medial border of the superior vena cava, left subclavian artery, common carotid artery and right innominate artery, and the continuation of these air dissections into the neck (105). Air also can be seen around the central pulmonary arteries, the ring around the artery sign (135) (Fig. 16), and the ascending aorta and dissecting the pericardial fat pads. Because of the continuity of the right and left sides of the mediastinum, air interposed between the heart and diaphragm may permit identiﬁcation of the central portion of the diaphragm in continuity with its lateral portions, the continuous diaphragm sign (133). This will not be seen in the presence of a subpulmonic pneumothorax, as the latter will not cross the midline. A pneumopericardium may permit visualization of the central portion of the diaphragm. However, as pneumopericardium is almost always associated with the presence of pericardial ﬂuid, the ﬂuid will silhouette the central portion of the diaphragm on an upright ﬁlm, allowing it to be differentiated from a pneumomediastinum. The incidence of pneumothorax in all patients on mechanical ventilation varies from 4% to 15% (105). The incidence in patients with ARDS varies from 25% to 87% (105,136). The incidence of pneumothorax in patients with PIE has been reported to be 77% (117). In mechanically ventilated patients, pneumothoraces tend to increase rapidly and progress to tension in 60% to 90% of cases (107,137,138). Pneumothorax is associated with increased mortality in patients with ARDS (121,136). The radiographic diagnosis of pneumothorax in a supine radiograph requires a detailed knowledge of anatomy of pleural recesses and mediastinal structures (139,140) and a thorough understanding of gravity and lung compliance, which determine the movement of pleural air (141,142). Therefore, pleural air is usually not visualized in the apicolateral position as occurs in an upright ﬁlm, but more likely occurs anteromedially, as this represents the

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Figure 16 Pneumomediastinum—the ring around the artery sign. (A) Close-up posteroanterior view of the left hilum demonstrates the left main pulmonary artery outlined by air (arrows), the ring around the artery sign, and a small amount of air inferiorly within the mediastinum (arrowhead). (B) Lateral radiograph demonstrates air surrounding the left main pulmonary artery (arrows).

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highest position in the hemithorax of supine patients. The size of a pneumothorax in an ICU patient has poor correlation with its clinical signiﬁcance. Therefore, it is not relevant that the size of a pneumothorax cannot be calculated on a supine radiograph. In a study of supine radiographs in 88 ICU patients, anteromedial and subpulmonic pneumothoraces predominated, with apicolateral pneumothoraces being relatively uncommon (140). Because air preferentially accumulates in front of the lung surrounding the anterior mediastinal structures in the supine position (143), sharp visualization of the superior vena cava and azygous vein on the right and left subclavian artery as it curves over the apex of the left lung are the initial signs of anteromedial pneumothorax. The only signs of a small pneumothorax conﬁned to the medial pleural space may be sharp visualization of the left superior intercostal vein and the superior pulmonary veins (105). Bilateral anteromedial pneumothoraces result in a sharply outlined anterior junction line (144). Infrahilar anteromedial air collections result in sharp delineation of the heart border, a lucent cardiophrenic sulcus, a well-outlined pericardial fat pad which may simulate a mass or segmental collapse (145), and sharp delineation of the inferior vena cava as it enters the right atrium (105). A hyperlucent upper quadrant of the abdomen, with visualization of the superior aspect of the diaphragm to the midline, is seen in subpulmonic pneumothorax (146). Other signs of subpulmonic pneumothorax include abnormal deepening and lucency of the lateral costophrenic angle, the deep sulcus sign (147), a sharp depressed ipsilateral hemidiaphragm, and visualization of the inferior edge of a collapsed or consolidated lower lobe (Fig. 17). When subpulmonic air occupies the anterior subpulmonic space, the superior position of the anterior diaphragmatic sulcus in relation to the more inferior position of the posterior diaphragmatic sulcus is easily appreciated (148). Occasionally, one may see both the anterior surface and the dome of the diaphragm sharply outlined by air, the double-diaphragm sign (145) (Fig. 18). The presence of an apicolateral pneumothorax in a supine radiograph implies that a large volume of pleural air has already accumulated and has displaced the visceral pleura medially (143). The ﬁrst sign of an apicolateral pneumothorax in the presence of a small amount of air is lack of contact of the minor ﬁssure with the chest wall (105). As air progressively accumulates, the visceral pleura is further displaced medially and eventually becomes tangential to the X-ray beam, and the pneumothorax becomes easier to diagnose (143). The concomitant presence of subpleural consolidated lung and apicolateral pleural ﬂuid may mask the presence of an apicolateral pneumothorax (105). In this instance, the pleural line, which requires contiguous normal aerated lung and pleural air to be seen, is obscured by the subpleurally contiguous consolidated lung, and the pleural surface of the consolidated lung is silhouetted by the pleural ﬂuid. In posteromedial pneumothorax, the posterior mediastinal structures, paraspinal line, descending aorta, and the costovertebral sulcus may become outlined

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Figure 17 Subpulmonic pneumothorax in supine radiograph—the deep sulcus sign. Antero-posterior supine radiograph in a patient with barotrauma demonstrates a deepened, lucent left costophrenic angle (arrows), the deep sulcus sign, consistent with a subpulmonic pneumothorax. The inferior edge of the left lower lobe is visualized (small arrowheads).

by air, and the medial surface of the lower lobe may be displaced laterally (Fig. 19). Posteromedial pneumothorax is associated with lower lobe volume loss and parenchymal disease, both of which are common in the ICU patient. As air preferentially surrounds the surface of abnormal lung in lobar collapse, the air in a posteromedial pneumothorax continues to surround the abnormal collapsed lower lobe and fails to rise to less dependent pleural surfaces, even when it is not loculated. When the pressure in the pleural space exceeds atmospheric pressure, a pneumothorax is considered to be under tension. Both a simple and a tension pneumothorax may result in lung collapse and mediastinal shift (149). However, both lung collapse and mediastinal shift may be absent in a tension pneumothorax because of pleural adhesions and because of the stiffness of the lungs in ARDS (150). Hence, a residual small loculated collection of air can cause a tension pneumothorax even when the ipsilateral hemithorax is drained by a thoracostomy tube.

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Figure 18 Pneumothorax in supine radiograph—the double diaphragm sign. Anteroposterior radiograph in a patient with barotrauma and a right pneumothorax demonstrates the anterior aspect (black arrows) and the dome (black arrowheads) of the right hemidiaphragm, the double diaphragm sign. The presence of air in the apicolateral region (white arrows) indicates that a large amount of air has already accumulated in the right hemithorax, displacing the visceral pleural medially.

Simple pneumothoraces in mechanically ventilated patients progress to tension in 60% to 90% of cases (105). Signs of tension include inversion of the diaphragm, contralateral shift of the heart and mediastinum, contralateral displacement of the anterior junction line, and displacement of the azygoesophageal recess. Flattening of the heart border and other vascular structures including the superior and inferior vena cava, the radiographic reﬂection of diminished venous return to the right heart (140), has been considered to be the most speciﬁc sign of tension and correlates with the clinical ﬁndings (105) (Fig. 20). As a result of pneumomediastinum and pneumothorax, air may be found within the interlobar ﬁssures, subcutaneously, and in the peritoneal and retroperitoneal spaces. Air may collect within the interlobar ﬁssures with or without pleural ﬂuid, resulting in apparent air ﬂuid levels or pneumatoceles (126,151). Subcutaneous emphysema is a benign complication of pneumomediastinum and pneumothorax, which resolves as the latter improves (105). Pneumoperitoneum and pneumoretroperitoneum may occur with either pneumomediastinum (152) or pneumothorax (153). In patients with other signs of air leak, pneumoperitoneum may be assumed to be due to the air leak (124) rather than a perforated viscus (154).

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Figure 19 Left posteromedial hydropneumothorax. (A) Antero-posterior radiograph in a patient with a left chest tube for treatment of a pneumothorax complicating barotrauma demonstrates a persistent left posteromedial pneumothorax (P). The medial aspect of the consolidated left lower lobe (arrowheads) is displaced laterally. (B) Axial computed tomography image (lung window) demonstrates left posteromedial hydropneumothorax (P) displacing the consolidated left lower lobe laterally.

IV.

Common Thoracic Abnormalities Encountered in the ICU

Common thoracic abnormalities encountered in the ICU include those of cardiovascular, pulmonary, and pleural origin and those associated with trauma. Chest radiographic abnormalities may be present at the time of ICU admission or may

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Figure 20 Tension pneumothorax. Antero-posterior radiograph in a patient with barotrauma and clinical signs and symptoms of tension demonstrates a large left pneumothorax with shift of the heart and mediastinum to the right and inversion of the left hemidiaphragm. There is incomplete collapse of the left upper lobe (white arrows) and the left lower lobe (white arrowheads), reﬂecting the decreased lung compliance seen in barotrauma. Flattening of the left heart border (black arrowheads) is demonstrated. This is considered to be the most speciﬁc radiographic sign of tension and correlates with the clinical ﬁndings.

develop during the course of the ICU stay. The etiology of any abnormality should be interpreted in conjunction with the clinical history and the prior radiographs (11). A. Atelectasis

Atelectasis by deﬁnition means incomplete expansion, and it is used to describe any condition where lung volume loss occurs. Atelectasis is a common radiographic ﬁnding in ICU patients for a multitude of reasons including, but not limited to, an impaired cough reﬂex, supine position, and hypoventilation. Most frequently, atelectasis is observed in the left lower lobe where the heart causes mass effect on the left lower lobe bronchus in the supine position (155). The radiographic appearance of atelectasis varies from undetectable in the mildest cases to complete opaciﬁcation of the affected hemithorax in cases of total lung collapse. The latter represents the most extreme form of atelectasis. Atelectasis can be described as subsegmental, segmental, or lobar, each of which has characteristic radiographic ﬁndings. Subsegmental atelectasis manifests as linear, plate-like opacities, predominantly at the lung bases or lower lung zones. Segmental atelectasis has a

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triangular or wedge-shaped appearance. Lobar atelectasis, or lobar collapse, is a common occurrence in the ICU due to mucous plugging. The appearance of lobar collapse depends on the affected lobe. The hallmark of lobar collapse is the displacement of the interlobar ﬁssures. Important secondary signs of collapse include displacement of the hila, shift of the mediastinum, compensatory hyperinﬂation of the normal lung, and elevation of the hemidiaphragm (156 –159). Right upper lobe collapse causes a homogeneous opacity extending from an elevated hilum towards the apex. There is mild shift of the trachea to the right, a preserved tracheal stripe, and elevation of the minor ﬁssure. Right middle lobe collapse can be subtle in the anterior –posterior projection, resulting in a vague opacity in the right lower lung zone, which silhouettes the right heart border. In addition, there is inferomedial displacement of the minor ﬁssure. Right lower lobe collapse causes a homogeneous opacity in the right retrocardiac region, which silhouettes the medial aspect of the right hemidiaphragm. The right hilum appears small secondary to incorporation of the right interlobar artery within the collapsed lobe. The right heart border is preserved because the right middle lobe is normally aerated (158). Left upper lobe collapse is recognized by a poorly deﬁned left perihilar opacity, the veil sign, extending upward along the medial aspect of the left upper lung zone. Because the left upper lobe collapses antero-medially, the aortic arch and left hilum are visualized through the opacity since they are middle mediastinal structures. Occasionally, herniation of the superior segment of the left lower lobe between the collapsed upper lobe and the mediastinum produces an air crescent that highlights the aortic arch, the Luftsichel sign. Left lower lobe collapse results in a sharply marginated retrocardiac opacity, which silhouettes the medial aspect of the left hemidiaphragm (158). Atelectasis is difﬁcult to differentiate from pneumonia. Although the signs of volume loss discussed earlier are suggestive of atelectasis, they are often not apparent, or they may co-exist with pneumonia. In the ICU, changing appearance and rapid clearing of parenchymal opacities followed by their recurrence suggests the diagnosis of atelectasis (12).

B. Pneumonia Types

Pneumonia is a frequent cause of ICU admission, as well as a complication of hospitalization (nosocomial). The radiological ﬁndings in pneumonia are varied. The unilateral and focal airspace opaciﬁcation of pneumonia may be difﬁcult to distinguish from atelectasis, pulmonary edema, or hemorrhage. These entities comprise the differential of airspace disease. In one study, the accuracy of bedside radiography in diagnosing pneumonia in ventilated patients was only 50% (160). Generally, pulmonary opacities due to infection appear later and resolve slower than do those seen with aspiration or atelectasis (161).

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Lobar pneumonia classically appears as a homogeneous, conﬂuent opacity, delineated by ﬁssures, which may be expansile. However, the lobar stage is less commonly seen today due to the early institution of antimicrobial therapy. Air bronchograms are a common ﬁnding. The expansile pattern is most frequently observed in pneumonia due to Klebsiella (162). Bronchopneumonia, or lobular pneumonia, presents with multiple small, indistinct nodules, corresponding to peribronchiolar inﬂammation. Subsequently, these nodules enlarge to form multifocal, ill-deﬁned opacities (163). As the pattern coalesces, it may difﬁcult to differentiate from lobar pneumonia. The incidence of nosocomial bacterial infections of the respiratory tract in inpatients is 0.5% to 5% (164 –167). Over 15% of patients hospitalized for treatment of pneumonia acquire bronchopulmonary superinfections, some of which prove fatal (168). A multilobar pattern of involvement is frequently seen, particularly in patients with an altered immune system. Aspiration

Predisposing factors for aspiration pneumonitis include vomiting, gastroesophageal reﬂux, altered mental status, intubation, and tracheostomy. Radiographic ﬁndings develop within 24 hours and commonly occur in the dependent portions of the lung with a basilar distribution. However, in the supine patient, airspace opacities may be seen in the upper lung zones due to aspiration into the posterior segments of the upper lobes or the superior segments of the lower lobes. The radiographic ﬁndings of simple toxic aspiration begin to clear within 48 hours (169). Persistence of opacities beyond this period suggests a complicating infection. Complications of Pneumonia

Two of the more serious complications of pneumonia include lung abscess and empyema. These entities may be difﬁcult to diagnose and to differentiate by plain chest radiography. Lung Abscess

Lung abscess most frequently develops in pneumonias associated with infectious aspiration, bronchial obstruction, and an immunocompromised state. A lung abscess may also be a complication of septic emboli. Lung abscesses typically develop one to two weeks after pneumonia. Approximately 20% are not apparent on plain chest radiographs because a cavity is not evident (170). The plain ﬁlm radiographic ﬁndings of lung abscess are single or multiple cavities, isolated or within areas of consolidation. In one study, 88% of cavities demonstrated a smooth internal margin, and 72% of cavities contained air – ﬂuid levels (170). The wall thickness varies from 4 to 15 mm (171). Abscesses demonstrating irregular margins and thick walls may simulate cavitary tumors radiographically and cannot be differentiated by MDCT. Lung abscesses may result in formation of pneumatoceles, which can either resolve or persist indeﬁnitely

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(170). A rare and more serious complication of lung abscess is the development of a bronchopleural ﬁstula (Fig. 21). Empyema

Empyema is a collection of pus in the pleural space. Empyemas often progress from parapneumonic effusions or may occur as a consequence of hematogenous spread of infection, penetrating trauma, or any procedure disrupting the pleural space. Neither the plain ﬁlm nor the CT ﬁndings of empyema are speciﬁc. Thickening and enhancement of the visceral and parietal pleura, the split pleura sign, may be seen in empyema and parapneumonic and malignant pleural effusion (170). An air – ﬂuid level may be present in an infection resulting from a gas-forming organism. CT may be necessary to demonstrate the location of the air – ﬂuid level. In an empyema or a bronchopleural ﬁstula, the air – ﬂuid level will be in the pleural space. In contrast, the air –ﬂuid level will be in the lung parenchyma in a lung abscess. CT may also be useful in delineating pleural ﬂuid loculations prior to drainage. Rare and more serious complications of empyema include the spontaneous drainage through the chest wall (empyema necessitans) or the development of a bronchopleural ﬁstula, which occurs secondary to erosion into the tracheobronchial tree.

Figure 21 Bronchopleural ﬁstula. Axial computed tomography image (lung window) demonstrates a bronchopleural ﬁstula (white arrow) between a subsegmental branch of the superior segmental bronchus of the right lower lobe and the pleural space. A hydropneumothorax is clearly visible.

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C. Pulmonary Edema Introduction

Pulmonary edema represents an abnormal increase in extravascular water in the lung and is commonly classiﬁed into two major categories, hydrostatic edema and increased permeability edema (172). However, it is not possible to group all patients into these two categories because many patients have pulmonary edema resulting from both hydrostatic and increased permeability mechanisms. Therefore, a third category, mixed pulmonary edema, has been created (173). The three major categories of pulmonary edema and their subcategories with disease groups are shown in Table 4. Hydrostatic pulmonary edema can be further divided into cardiogenic edema, decreased capillary osmotic pressure edema, and edema associated with disease of the pulmonary veins. The subcategory of cardiogenic edema includes patients whose edema results from left ventricular failure and mitral valve disease. The subcategory of decreased capillary osmotic pressure edema includes patients whose edema results from renal failure, ﬂuid overload, or hypoproteinemia (cirrhosis and nephrotic syndrome). A decrease in serum osmotic pressure can contribute to hydrostatic edema. Edema secondary to disease of the pulmonary veins occurs with pulmonary veno-occlusive disease and ﬁbrosing mediastinitis. This form of edema is primarily hydrostatic but is incompletely understood. Although this subclassiﬁcation is useful for further grouping patients according to the pathophysiology of the edema, these three subcategories of hydrostatic pulmonary edema cannot be differentiated radiographically. Similarly, the category of increased permeability edema may be subdivided into two subcategories, increased permeability edema with diffuse alveolar damage (DAD) and increased permeability edema without DAD. The subcategory of increased permeability edema with DAD includes ARDS. The subcategory of increased permeability edema without DAD includes the edema associated with cytokine administration, high altitude, and heroin overdose. These two subcategories of increased permeability edema also cannot be radiographically differentiated from each other. Acute lung injury (ALI) refers to the spectrum of acute diffuse pulmonary injury characterized by acute onset, gas exchange abnormalities (PaO2/ FIO2 , 300 mmHg regardless of PEEP level), and diffuse bilateral opacities in the absence of an elevated pulmonary wedge pressure (172). For practical purposes and discussion, increased permeability edema and the edema associated with ALI are synonymous with non-cardiogenic pulmonary edema. Hydrostatic Pulmonary Edema

The most common causes of hydrostatic pulmonary edema are cardiogenic edema as a result of left ventricular failure and mitral valve disease.

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Table 4

Pulmonary Edema in ICU Patient Increased hydrostatic pressure

Cardiogenic Left ventricular failure Mitral valve disease Asymmetric

Other Disease of pulmonary veins

Decreased capillary osmotic pressure Hypervolemia (ﬂuid overload) Renal failure Hypoproteinemia (cirrhosis, nephrotic syndrome)

COPD Patient position Mitral regurgitation

With diffuse alveolar damage Acute respiratory distress syndrome

Without diffuse alveolar damage

Mixed edema

Cytokines

Acute and chronic pulmonary emboli

High altitude Heroin overdose

Near drowning Neurogenic

Reperfusion Lung transplantation Reexpansion Post pneumonectomy or lung reduction Air embolism

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Abbreviation: COPD, chronic obstructive pulmonary disease.

Increased permeability edema (acute lung injury, non-cardiogenic edema)

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Cardiogenic Pulmonary Edema

The radiographic appearance of cardiogenic edema is dependent upon the severity of pulmonary venous hypertension, reﬂected by the pulmonary capillary wedge pressure (PCWP) (174). There is often a time lag between the elevation of PCWP and the subsequent development of radiographic ﬁndings (175). In addition, the radiologic ﬁndings due to an elevated PCWP usually persist after the PCWP has returned to normal (176). These two observations may explain the all too common discrepancy between the radiographic appearance and the clinical appearance of the patient at any given moment. On the portable supine radiograph, the earliest radiographic sign of pulmonary venous hypertension is redistribution of blood ﬂow from the lower to the upper lung zones, manifested by an increase in caliber of the upper lobe vessels. This ﬁnding is difﬁcult to appreciate in the supine position (177,178) and begins to become apparent when the PCWP exceeds 12 mmHg. Assessment of redistribution is performed by comparing the number and size of the upper lobe vessels to lower zone vessels at an equal distance from the hila (179,180). A more objective assessment is direct measurement of the diameter of the bronchi and adjacent pulmonary arteries visualized end-on. In the supine position, the ratio of the artery to bronchus is 1.01 (SD: 0.31). With redistribution in left ventricular failure, the ratio is 1.49 (SD: 0.31) (181). Interstitial pulmonary edema develops when the PCWP exceeds 17 to 20 mmHg (179). This results in ﬂuid accumulation in the perivascular, interlobular septal, and parenchymal interstitial tissue (173). Radiographic ﬁndings of interstitial pulmonary edema are loss of the normal sharp deﬁnition of subsegmental and segmental pulmonary vessels, thickening of the interlobular septa and of the ﬁssures, peribronchial cufﬁng, pleural effusions, and perihilar and lower lobe haziness. Interlobular septal thickening is manifested on the chest radiograph as Kerley B lines, which are short lines perpendicular to the pleura. Kerley B lines are most commonly observed in the costophrenic angles (Fig. 22). Alveolar edema, or ﬂuid accumulation in air spaces, results from a further increase in pulmonary venous pressure and occurs when PCWP exceeds 25 mmHg. Characteristic radiographic ﬁndings are bilaterally symmetric patchy or conﬂuent opacities with a perihilar and lower lung zone distribution. Air bronchograms can be seen in 10% to 30% of patients (182). An uncommon manifestation of cardiogenic pulmonary edema is the bat-wing or butterﬂy pattern (Fig. 23). This appearance has been reported in 5% of the patients with edema of varying etiology and is most commonly associated with acute left ventricular failure (173). Radiographically, there is perihilar opaciﬁcation with sparring of the lung periphery. Asymmetric cardiogenic edema may be caused by chronic obstructive pulmonary disease (COPD), patient positioning, and mitral regurgitation. COPD results in asymmetric pulmonary edema depending on the degree of the underlying lung parenchymal disease. The edema is more evident in regions

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Figure 22 Cardiogenic pulmonary edema—Kerley B lines. Close-up postero-anterior view of the right lower lung zone in a patient with cardiomegaly, pulmonary venous hypertension, and interstitial edema clearly demonstrates the Kerley B lines (arrowheads).

containing normal lung parenchyma in comparison to diseased lung parenchyma (173). Asymmetric cardiogenic edema is a manifestation of the effect of gravity on the patient and reﬂects patient position with increased edema in the dependent portion of the lungs. Mitral regurgitation causes a right upper lobe distribution of abnormalities because of reﬂux directed towards the right upper lobe pulmonary vein (183,184). The CT ﬁndings of cardiogenic edema substantiate the ﬁndings seen on plain ﬁlms. Additionally, enlarged mediastinal lymph nodes have been reported in 80% of patients and inhomogeneous attenuation of the mediastinal fat in 59% (185).

Increased Permeability Pulmonary Edema (Non-cardiogenic Pulmonary Edema) ARDS

ARDS is a clinical entity characterized by acute onset, gas exchange abnormalities (PaO2/FIO2 , 200 mmHg regardless of PEEP level), and diffuse bilateral opacities compatible with pulmonary edema in the absence of an elevated pulmonary capillary wedge pressure (172). ARDS represents the most severe end of the spectrum of ALI or increased permeability edema with DAD.

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Figure 23 Acute cardiogenic pulmonary edema—the bat-wing pattern. Anteroposterior radiograph in a patient with acute myocardial infarction demonstrates bilateral perihilar air space opaciﬁcation, the bat-wing pattern, characteristic of acute pulmonary edema.

Pathologically, ARDS is characterized by three phases. The ﬁrst, or exudative, phase begins with the leakage of protein-rich ﬂuid into the alveoli and is associated with hemorrhage, type II pneumocytes proliferation, and hyaline membrane formation. The second, or proliferative, phase of ARDS is characterized by formation of ﬁbrinous exudate with thickening of the alveolar septa. The third, or reparative, phase demonstrates either complete recovery, varying degrees of ﬁbrosis resulting from ARDS, and ﬁbrosis and lung cysts as a complication of mechanical ventilation (173). Radiographically, the earliest ﬁndings in the exudative phase are seen approximately 12 hours after the clinical onset of respiratory failure. These ﬁndings consist of patchy, ill-deﬁned opacities throughout both lungs (172). Interstitial edema may be present and tends to have a more peripheral distribution than the edema of cardiac origin (186 – 188). The heart size is usually normal. Within 24– 72 hours, there is rapid coalescence of the patchy opacities into diffuse air space consolidation, which extends from the lung apex to the lung base and into the lung periphery. Air bronchograms are frequent, but pleural effusions are typically not seen (189). The proliferative and ﬁbrotic phases become apparent in approximately one week. The lungs remain diffusely abnormal but begin to demonstrate a

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reticular pattern (186,188) corresponding to the beginning of interstitial and airspace ﬁbrosis. Similar to the exudative phase, pleural effusions are not typically seen. The appearance of pleural effusion at any time on a supine radiograph suggests a complication such as pneumonia or pulmonary infarction. In general, the radiograph shows improvement within 10 to 14 days in those patients who survive. Failure to improve suggests a superimposed process (pneumonia) and has a poor prognosis (190 –191). The radiologic course of ARDS differs from other entities, causing diffuse, coalescent opacities. Speciﬁcally, the radiologic abnormalities persist for a longer period of time or may resolve completely. In those cases with incomplete resolution, scarring, atelectasis, or traction bronchiectasis may be evident. Complications of mechanical ventilation such as subpleural and intrapulmonary lung cysts are also frequently noted. As emphasized in the section on Complications of Mechanical Ventilation (Barotrauma), mechanical ventilation and PEEP can dramatically alter the radiographic appearance of diffuse airspace consolidation. This is particularly true during the exudative phase of ARDS. Diffuse airspace consolidation may clear within minutes following the institution of PEEP despite obvious clinical deterioration. The CT ﬁndings in ARDS have been extensively described and depend on the stage of ARDS (192 –195). They are non-speciﬁc and cannot be used to differentiate ARDS from severe cardiogenic pulmonary edema or widespread bacterial pneumonia. Radiographic Distinction Between Cardiogenic and Non-Cardiogenic Edema

Although non-cardiogenic and cardiogenic pulmonary edema have distinct radiographic characteristics, it may be difﬁcult to distinguish between them. In the ICU patient, this distinction is even more difﬁcult because of the patient’s supine position. In the supine patient, the distribution of blood ﬂow has not been found to be helpful in distinguishing between these two entities (177,178). The distinction is further complicated in the ICU patient with ARDS who may have associated cardiac failure and ﬂuid overload and therefore demonstrate the characteristics of mixed edema. In general, it is easier to distinguish between cardiogenic and non-cardiogenic edema in patients who have mild to moderate edema, on erect radiographs, and when serial radiographs are available for comparison. The most useful radiographic ﬁndings in distinguishing between cardiogenic and non-cardiogenic edema are shown in Table 5. While no one ﬁnding allows reliable distinction between cardiogenic and non-cardiogenic edema, and imaging ﬁndings overlap, the combination of ﬁndings as summarized in Table 5 has been reported to correctly distinguish the two in most instances. Cardiogenic or hydrostatic pulmonary edema has been accurately diagnosed radiographically in 80% to 90% of patients and permeability pulmonary edema in 60% to 90% (178,182,196).

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Table 5 Useful Radiographic Findings in Differentiating Non-cardiogenic or Increased Permeability Edema in ARDS from Cardiogenic or Increased Hydrostatic Edema in the ICU Patient Non-cardiogenic edema

Finding Heart size

Normal

Septal lines Vascular pedicle

Uncommon Normal

Air bronchograms Pleural effusion

Common Uncommonly seen in supine radiograph Peripheral or diffuse

Distribution of edema

Upper lobe vessels on erect ﬁlm Thickening of interlobar ﬁssures

Normal Ratio upper: lower ¼ 1:2 Absent

Cardiogenic edema Commonly enlarged Cardiothoracic ratio .0.58 on supine radiograph Common Widened in chronic congestive heart failure with left ventricular failure; normal in acute left ventricular failure Uncommon Small effusions common Perihilar or diffuse (perihilar more common in renal failure, bat-wing in acute left ventricular failure) Increased caliber Ratio upper:lower .1:2 Present

Source: From Ref. 172.

D. Pleural Effusion

Pleural effusion represents an abnormal increase in the quantity of ﬂuid in the pleural space. Normally, the pleural space contains 5 to 15 mL of ﬂuid. On the basis of the composition of the ﬂuid, pleural effusions are classiﬁed as transudates or exudates. Transudative pleural effusions are non-inﬂammatory and develop as a result of increased venous pressure and decreased plasma oncotic pressure, as in congestive heart failure, liver cirrhosis, or nephrotic syndrome. Exudative pleural effusions are caused by pleural inﬂammation or impaired lymphatic drainage and are most commonly seen with infection and neoplasm (197). Pleural effusions are a common occurrence in the medical ICU and are found in up to 62% of patients (198). Common causes of pleural effusion in the ICU are cardiac failure, pneumonia, and ascites. Less common causes include pulmonary embolism, postpericardiotomy syndrome (Dressler’s syndrome), post-thoracic and abdominal surgery, and intra-abdominal processes such as pancreatitis or subdiaphragmatic abscess.

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Initially, free pleural ﬂuid accumulates in the most dependent aspect of the thorax, which is located postero-inferiorly in the supine patient. With increasing volume, pleural ﬂuid tracks into the subpulmonic space and along the convexity of the lung postero-laterally, resulting in silhouetting of the diaphragm, obliteration of the lateral costophrenic angle, and formation of a lateral meniscus sign. Fluid tracks into the posterior superior aspect of the major ﬁssures and the lateral aspect of the minor ﬁssure as it accumulates. With a large pleural effusion, an apical cap develops. In one study, the reported sensitivity and speciﬁcity for detecting pleural effusions on supine radiographs were 67% and 70%, respectively (199). In a prospective study, the minimum amount of pleural ﬂuid necessary for radiographic visualization on the supine radiograph was 175 mL (200). Radiographic signs associated with the presence of small pleural effusions (175 – 525 mL) included increased homogeneous density in the lower lung zone in 91% of cases and silhouetting of the diaphragm in 45% of cases. Moderate pleural effusions (.525 mL) demonstrated increased homogenous density in the lower lung zones in all cases, silhouetting of the diaphragm in 71% of cases, and blunting of the lateral costophrenic angle in 25% of cases. Large pleural effusions showed increased homogenous density in the lower lung zones in all cases, silhouetting of the diaphragm in 68% of cases, blunting of the lateral costophrenic angle in 41% of cases, and apical capping in 54% of cases. Thickening of the minor ﬁssure was present in 48% of cases (200). Other radiographic ﬁndings of free pleural ﬂuid on supine radiographs include apparent elevation of the hemidiaphragm, which is caused by subpulmonic ﬂuid accumulation, and decreased visualization of the pulmonary vessels below the apparent dome of the hemidiaphragm because of the added density of subpulmonic ﬂuid. However, these ﬁndings are difﬁcult to appreciate due to the frequent presence of bilateral effusions silhouetting both hemidiaphragms and simulating low lung volumes and insufﬁcient penetration of the upper abdominal structures on the supine radiograph (200). A subpulmonic pleural effusion is characterized by apparent lateral displacement of the dome of the hemidiaphragm and a more acute lateral costophrenic angle. On the supine radiograph, pleural effusion may be difﬁcult to recognize because of overlying breast tissue, an enlarged heart, or a prominent epicardial fat pad. Pleural effusion may be simulated by any condition resulting in an increase or decrease in the density of a hemithorax. Conditions resulting in increased density, such as chest wall or pleural masses, may simulate an ipsilateral pleural effusion. Conditions causing decreased density, such as prior mastectomy, unilateral emphysema, or bullous disease, and anterior pneumothorax or atrophy of the pectoralis muscle may simulate a contralateral effusion (201). The lateral decubitus ﬁlm is the most sensitive technique for detecting free pleural ﬂuid, with a sensitivity threshold of 5 mL (202). It may be performed to identify the presence of pleural ﬂuid and to distinguish free from loculated pleural effusions. Bilateral decubitus views are preferred as the contralateral decubitus view often yields additional important information.

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An unusual appearance of pleural effusion results from localization of ﬂuid within an interlobar ﬁssure. This has been termed a pseudotumor because it may simulate a lung mass. A localized interlobar pleural effusion is most commonly seen in heart failure. It appears spontaneously and is usually self-limited. It is more common in the right hemithorax and more often in the minor than the major ﬁssure. On the frontal chest radiograph, the pseudotumor has a characteristic elliptical conﬁguration and is sharply circumscribed. If the X-ray beam is not tangential to the entire margin of the pseudotumor, a portion of the margin may appear indistinct, the incomplete border sign (203,204). CT demonstrates the ﬂuid attenuation of the pseudotumor as well as its mobile nature, which changes with different patient position (Fig. 24). Pleural ﬂuid may loculate against the chest wall or within the ﬁssures (Fig. 25). Such loculations may occur following episodes of pleuritis, including empyema and hemothorax. E.

Embolic Disease

Pulmonary Embolism

Pulmonary embolism results from occlusion of a pulmonary arterial branch by an embolus. The most frequent source of emboli is the deep systemic veins. Predisposing factors for the development of pulmonary embolism include prolonged immobilization, surgery, trauma, and hypercoagulable states.

Figure 24 Pseudotumor in the major ﬁssure. Postero-anterior radiograph demonstrates a homogeneous opacity (arrows) in the right lower lung zone with blunting of the right costophrenic angle. The superior margin of the opacity is indistinct, the incomplete border sign.

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Figure 25 Pseudotumor in the minor and upper portion of the major ﬁssures. (A) Antero-posterior radiograph demonstrates a sharply circumscribed, homogeneous, horizontally oriented opacity in the right mid lung zone lateral to the right hilum (arrowheads) and a second obliquely oriented opacity extending medial and superior to the right hilum (arrows). Subpulmonic ﬂuid spills into the lateral costophrenic sulcus and extends upward along the lateral chest wall. (B) Lateral view of chest demonstrates the horizontally oriented opacity to lie in the minor ﬁssure (arrowheads) and the obliquely oriented opacity to lie in the superior aspect of the right major ﬁssure (arrows). Subpulmonic ﬂuid spills into the anterior and posterior costophrenic sulci and extends upward along the anterior and posterior chest wall.

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The chest radiograph is reported to be 33% sensitive and 59% speciﬁc for diagnosing pulmonary embolism (205). In a large prospective study, the most common radiographic abnormalities associated with pulmonary embolism were cardiomegaly (27%), pleural effusion (23%), elevated hemidiaphragm (20%), pulmonary artery enlargement (19%), atelectasis (18%), and parenchymal opacity (17%). The chest radiograph was normal in 24% of the cases (206). Radiographic ﬁndings classically associated with pulmonary embolism are hyperlucency of the lung distal to the occluded arterial segment because of regional oligemia, the Westermark’s sign (207), a prominent central pulmonary artery, the Fleischner sign, and an abrupt cutoff of the interlobar pulmonary artery, the knuckle sign (208) (Fig. 26). These ﬁndings are highly speciﬁc but insensitive for the diagnosis of pulmonary embolism (209). Pulmonary embolism can also cause segmental and lobar consolidation secondary to edema and hemorrhage, mimicking the radiologic appearance of pneumonia (210). Pulmonary infarction is uncommon and is present in only 15% of pulmonary embolisms because of the dual pulmonary arterial and bronchial blood supply of the lung. Pulmonary infarction is more likely to occur in patients with heart failure or severe hypotension. The characteristic radiographic appearance of infarction is a homogeneous pleural-based opacity with convex medial contour towards the hilum, the Hampton’s hump (211). At institutions where MDCT is available, CT pulmonary angiography is the study of choice for suspected pulmonary embolism. Studies have shown that MDCT pulmonary angiography is highly sensitive and speciﬁc for the diagnosis of pulmonary embolism. Discrepancies with conventional angiography are mainly at the subsegmental level, where even angiographers have poor inter-observer variability (212 – 214). The newer scanners have thinner slice acquisition, higher resolution, faster scanning times, and less motion artifact, resulting in superior visualization of the peripheral pulmonary arteries. All these factors improve detection of pulmonary emboli. In a prospective study comparing the effect of different slice thickness on study interpretation, MDCT at 1.25 mm collimation has been found to signiﬁcantly improve visualization of the segmental and subsegmental arteries. In this study, 96% of lobar, 90% of segmental, and 75% of subsegmental arteries were well visualized using 1.25 mm slice thickness. Inter-observer agreement for detection of pulmonary embolism at the segmental and subsegmental level was also improved when these parameters were used (215). Animal studies have demonstrated no difference in the sensitivity of MDCT at 1.25 mm collimation and pulmonary angiography in the detection of subsegmental emboli. Speciﬁcity was reported to be slightly higher for angiography, 88% versus 81% for MDCT (216). Clinical studies have shown that a negative MDCT pulmonary angiogram has high negative predictive value for subsequent development of a pulmonary embolism. The risk of pulmonary embolism in patients with a negative MDCT pulmonary angiography is less than 1% at six months (217) and nine months

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Figure 26 Pulmonary embolism without infarction—the Westermark sign. (A) Posteroanterior radiograph with magniﬁcation of the right hilum and right lower lung zone (insert) demonstrates normal tapering of the right interlobar artery with normal branching vessels in the right lower lung zone. (B) Postero-anterior radiograph with magniﬁcation of the right hilum and right lower lung zone (insert) obtained two years later demonstrates an enlarged, bulging right main pulmonary artery, the Fleischner sign. The right interlobar pulmonary artery demonstrates an abrupt cutoff, the knuckle sign. Increased lucency is seen in the right lower lung zone, the Westermark sign, in comparison to the left due to decreased blood ﬂow. (C) Axial computed tomography pulmonary angiogram demonstrates a large acute clot (C) expanding the right main pulmonary artery.

after the study (218), and less than 2% at 12-month follow-up (219). Additionally, a large prospective study has shown that MDCT reveals additional potentially signiﬁcant ﬁndings in up to 76% of patients, with 47% of these ﬁndings not suspected on chest radiography (218).

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On CT, a pulmonary embolus appears as a central or eccentric ﬁlling defect within an opaciﬁed pulmonary arterial branch, which may partially or totally occlude the vessel. Expansion of the lumen may be seen in acute thromboembolism. Additional ﬁndings include consolidation, pleural-based opacities, and pleural effusion (220). Eighty percent of pulmonary emboli are associated with deep venous thrombosis. A positive Duplex ultrasound identiﬁes patients at risk for development of pulmonary emboli. However, a negative Duplex ultrasound evaluation does not exclude the diagnosis of pulmonary embolism (221). Pulmonary angiography has been the gold standard in the diagnosis of pulmonary embolism (222,223). Its role today is still being deﬁned. It will continue to be the gold standard in those institutions where MDCT is not available. However, in those institutions in which MDCT is available, the use of pulmonary angiography should be reserved for the small subset of patients with a high clinical probability of pulmonary embolism, a negative CT pulmonary angiogram, and a negative lower extremity Duplex ultrasound examination and the rare case of acute massive embolism where thromboembolic therapy is being considered (224 – 227). Selective pulmonary angiography may also be performed in those patients with compromised renal function and an increased risk of nephropathy from the amount of contrast necessary for a CT pulmonary angiogram (228), recognizing that the interpretation of a digital substraction image is more susceptible to motion artifact. Septic Emboli

Septic emboli result from the hematogenous dissemination of infection to the lung parenchyma. Septic emboli occur more often in people under the age of 40 (229). The most common sources of emboli are the heart in association with tricuspid endocarditis, or a ventricular septal defect, or the peripheral veins secondary to septic thrombophlebitis or an indwelling vascular catheter (230,231). Common predisposing factors associated with septic emboli include drug addiction, alcoholism, infections in immunocompromised patients, congenital heart disease, and dermal infections (232). The most common causative organisms are Staphylococcus aureus, Streptococcus viridans, and Streptococcus pneumoniae (229). On chest radiography, the diagnosis of septic emboli should be considered when multifocal, peripheral, ill-deﬁned, round or wedge-shaped opacities are seen in the setting of a febrile patient (233). The opacities have a basilar predilection reﬂecting greater blood ﬂow. They may be uniform or variable in size, reﬂecting recurrent showers of emboli. Cavitation is frequent and early. The cavities are usually thin-walled and occasionally contain a central loose body, the target sign (234), which may simulate a fungus ball (234,235). The central loose body represents a piece of necrotic lung. Air – ﬂuid levels are conspicuously absent in many of the cavities. Invasive aspergillosis is the major radiologic differential diagnosis in the immunocompromised patient (233).

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CT demonstrates abnormalities before radiography in 30% of cases and more extensive disease in 44% of cases (236). On CT examination, subpleural peripheral nodules and wedge-shaped peripheral lesions less than 3 cm in size are the most common ﬁnding (237). Cavitation is a common feature and is seen in varying degrees in 50% of the lesions imaged. A feeding vessel leading into the parenchymal opacity may be identiﬁed, suggesting a hematogenous origin (236). F.

Pulmonary Hemorrhage

Pulmonary hemorrhage can result from trauma, bleeding diatheses, infections, pulmonary embolism, penicillamine therapy, and autoimmune diseases. The most common autoimmune disease causing pulmonary hemorrhage is Goodpasture’s syndrome (238). Radiographically, pulmonary hemorrhage manifests as coalescent airspace opaciﬁcation. Unless there is recurrent bleeding, the airspace opaciﬁcation clears rapidly within two to three days. The chest radiograph ﬁndings are nonspeciﬁc and indistinguishable from pulmonary edema and pneumonia, and deﬁnitive diagnosis is based on clinical, laboratory, and bronchoscopic ﬁndings, if necessary. G. Dissecting Hematoma of the Aorta

Dissecting hematoma of the aorta results from an intimal tear followed by formation of an intramural hematoma and the formation of a false lumen. Aortic dissection has a male predominance. Predisposing factors include hypertension, connective tissue disease, congenital valve abnormalities, and coarctation (239). Rapid diagnosis of dissecting hematoma is paramount because mortality in untreated patients is 50% in the ﬁrst 48 hours (240). Therefore, suspected acute aortic dissection is one of the indications for emergent radiographic evaluation. MDCT, if available, is the imaging modality of choice when renal function is normal. In those patients with compromised renal function, MRI is the imaging modality of choice. The sensitivity and speciﬁcity of CT and MRI for diagnosing dissecting hematoma are similar (241,242). The radiographic ﬁndings of dissecting hematoma on MRI and CT are an intimal ﬂap and a false lumen (Fig. 27). Aortography has long been considered to be the gold standard in evaluation of aortic dissection (243). Aortography has essentially been replaced by CT and MRI in the evaluation of dissecting hematoma when these imaging modalities are available. Two important entities that should be distinguished from dissecting hematoma are aortic intramural hematoma and penetrating atherosclerotic ulcer. Aortic intramural hematoma represents blood within the aortic wall without intimal disruption. Aortic intramural hematoma occurs primarily in elderly hypertensive patients. Recognition is important because it may progress to

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Figure 27 Stanford A aortic dissection (dissecting hematoma). Sagittal reconstruction (mediastinal window) demonstrates Stanford A dissecting hematoma with intimal tear extending into the proximal left subclavian artery (white arrow) and into the descending thoracic aorta (white arrowheads). Abbreviations: A, aortic root; RV, right ventricle; PA, main pulmonary artery; LA, left atrium; T, true lumen; F, false lumen.

dissecting hematoma. Diagnosis is made by non-contrast CT examination where it appears as a hyperdense, crescentic collection located eccentrically within the aortic wall, with or without signiﬁcant narrowing of the lumen (244). Penetrating atherosclerotic ulcer of the aorta is a lesion caused by ulceration of an atheromatous plaque with disruption of the internal elastic lamina. It is found in elderly, hypertensive patients. The most common sites of penetrating atherosclerotic ulcer are the mid to distal descending thoracic aorta and the upper abdominal aorta. The ulcer may remain stable or progress to form an aortic pseudoaneurysm in 25% to 35% of cases (245,246) or may rupture. CT and MRI demonstrate a localized outpouching of the aortic wall corresponding to the ulcer and thickening of the wall secondary to subintimal bleeding (247,248). H. Traumatic Abnormalities Aortic Injury

Rupture of the thoracic aorta is a common cause of death following blunt chest trauma. Death occurs at the accident site in more than 80% of aortic ruptures. Patients (60 – 70%) who reach the hospital survive if prompt treatment is instituted. Ninety percent of aortic injuries occur at the level of the ligamentum arteriosum. Less common sites of involvement are the aortic root and the diaphragmatic hiatus (249).

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Types of aortic injury seen in patients who survive include dissecting hematoma, pseudoaneurysm, and partially contained rupture. The radiographic ﬁndings in aortic injury are due to the presence of mediastinal hematoma. The radiographic ﬁndings of dissecting hematoma have been previously described. The ﬁndings of a pseudoaneurysm at the level of the ligamentum arteriosum on the frontal radiograph are a smooth convex lateral soft tissue opacity silhouetting the distal aortic arch and proximal descending aorta (Fig. 28). A negative frontal chest radiograph has a 98% negative predictive value in excluding aortic injury (250). On non-contrast CT, an acute pseudoaneurysm appears as a homogeneous, hyperdense (.40 HU) collection within the wall of the aorta, which does not enhance following the administration of intravenous contrast. On MR, this collection follows intensity characteristics of acute blood. On occasion, the distal extension of the pseudoaneurysm may result in marked narrowing of the aortic lumen, which is termed pseudocoarctation. In a partially contained rupture, there is active extravasation of contrast. Esophageal Rupture

Esophageal rupture can be secondary to Boerhaave’s syndrome, iatrogenic causes, or blunt trauma. Boerhaave’s syndrome is spontaneous perforation of the thoracic esophagus due to sudden increase in intraluminal pressure.

Figure 28 Traumatic pseudoaneurysm of the aortic arch. Postero-anterior radiograph in a patient two hours after blunt chest trauma demonstrates smooth convex lateral soft tissue opacity silhouetting the distal aortic arch and proximal descending aorta (white and black arrows). A traumatic pseudoaneurysm distal to the origin of left subclavian artery was demonstrated at computed tomography aortography.

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Iatrogenic esophageal perforation can occur during lung and cardiovascular surgery, placement of an intraluminal tube for esophageal variceal bleeding, esophageal dilatation, and endoscopy. Traumatic esophageal injuries are rare. When present, they occur in the cervical and upper thoracic esophagus or just above the gastroesophageal junction. The mortality rate for esophageal tears complicated by mediastinitis is 38% (251). The prognosis is markedly improved if the injury is identiﬁed within 24 hours of occurrence (252). Therefore, in suspected cases of esophageal perforation, diagnostic imaging should be performed promptly. An esophageal perforation may ﬁrst be evaluated with a portable esophagram as in the section on Oral Contrast. If clinically indicated, CT with oral and intravenous contrast may be performed. Extravasation of contrast from the lumen of the esophagus is diagnostic of perforation. However, this may not be seen. Other suggestive ﬁndings are extraluminal periesophageal air, pleural effusion, and periesophageal inﬂammation with wall thickening (252,253). Other

Any sequellae of trauma can result in admission to the ICU if severe enough to require mechanical ventilation and close hemodynamic monitoring. Such conditions include severe mediastinal and parenchymal hematoma, cardiac contusion, osseous injuries (Fig. 29), and tracheobronchial rupture. The latter should be suspected in a trauma patient following chest tube placement for a pneumothorax with a persistent air leak.

V.

Computerized Tomography

A. Indications

CT is the imaging modality of choice for the evaluation of pulmonary embolism, acute aortic syndromes (dissecting hematoma, intramural hematoma, and penetrating aortic ulcer), and traumatic aortic injury. Other clinical situations where CT may be indicated include: (1) persistent pulmonary opacities unresponsive to treatment, (2) further deﬁnition of pneumothorax or pleural effusion for interventional treatment, (3) prior to bronchoscopy or biopsy, (4) differentiating lung abscess from empyema for interventional treatment, (5) assessment of patency of bypass grafts and deﬁning anatomy prior to further thoracic surgery, (6) suspected esophageal rupture, (7) differentiating unilateral bullous disease or emphysema from pneumothorax, and (8) suspected bronchopleural ﬁstula. B. Technique

The VA Greater Los Angeles Health Care System Hospital at West Los Angeles performs all thoracic imaging on a 16-row multidetector Toshiba scanner. Routinely, axial images are acquired with 1-mm collimation. The 1-mm axial

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Figure 29 Traumatic left apical pneumothorax. Postero-anterior radiograph demonstrates fracture of the left clavicle (black arrowhead), fracture of the left third rib (arrow), and traumatic left apical pneumothorax (white arrowheads) in an elderly patient post-fall.

images with 3-mm axial reformations and 1.5-mm coronal and sagittal reformations are then sent to PACS for interpretation. Nonionic contrast is administered when indicated and when renal function permits (creatinine within 0– 45 days of exam 1.5). When serum creatinine is between 1.5 and 2.0 and in patients susceptible to developing nephrotoxicity, contrast is administered depending upon the clinical situation and only after close clinical consultation. Such patients are adequately hydrated and given oral N-acetylcysteine 600 mg twice daily the day before and the day of the exam. Isoosmolar nonionic contrast is used exclusively in this subset of patients, and the volume of contrast administered is carefully tailored to the clinical situation. The creatinine is closely monitored after the examination. Intravenous contrast is not administered to patients whose serum creatinine is 2.0 unless the patient is on dialysis. In these patients, contrast is administered on the day of dialysis prior to the procedure. If the patient is on glucophage, the drug is withheld on the day of the examination and for two days thereafter. Radiation exposure is always a concern in these patients. Assuming a 2-mm helical mode continuous axial acquisition is obtained on an average patient over a 30-cm length (lung apex to lung base) with a 16-row multidetector CT using the following parameters (120 kVp, 360 mA, 0.5 sec gantry rotation, 1.25 effective

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pitch, 16:1 acquisition, and 40% automatic dose reduction), the effective dose equivalent given to the patient roughly corresponds to an effective dose of 120 PA chest radiographs obtained in a 70-kg patient using a technique of 110 kVp and 3 mAs. It should be noted that variation among CT scanners, scanning parameters, and actual patient size may result in considerable variation in this number (Christopher H. Cagnon, Ph.D., Radiology Physicist, Department of Radiological Science, David Geffen School of Medicine at U.C.L.A.). C. Problems Unique to the ICU Patient

CT scanning of the ICU patient presents unique problems, including an inability to suspend respiration (produces motion artifact), renal disease limiting contrast utilization, and the risks associated with transporting the mechanically ventilated patient. The newer scanners have partially overcome the problem of motion artifact. With a 16-row MDCT scanner and a pitch of 20, a 1-mm contiguous axial acquisition can be obtained on a 30-cm average thorax (apex to base) in approximately 9.5 seconds. This time can be reduced to approximately six seconds with a 2-mm axial acquisition. The problems associated with transporting ICU patients remain unaddressed. When considering a CT examination on the ICU patient, one must weigh the potential of identifying a potentially treatable condition against the risks associated with transferring a critically ill patient. These problems are partially reduced when CT and MRI scanners are placed in closer proximity to the ICU. Future hospital design may include a dedicated radiographic suite adjacent to the ICU. VI.

Image-Guided Interventional Procedures in the ICU

A. Venous Access

Central venous catheters are important in critically ill patients for purposes of pressure monitoring, blood sampling, and administration of medications and blood products. It has become increasingly apparent that both success and safety are enhanced by central venous catheter placement under image guidance. Venous Evaluation

Before catheter placement, it is important to delineate the anatomy and patency of the venous structures involved. Venography used to be the gold standard to determine the patency of a venous segment. As ultrasound and MR techniques become more reﬁned, they largely replaced the need for venography, which can cause patient discomfort because of needle puncture and contrast administration. MRA (most frequently using contrast-enhanced and time of ﬂight techniques) can reliably delineate the central venous anatomy. Ultrasound complemented by spectral and color Doppler analysis allows convenient assessment of the venous system. Although ultrasound cannot provide direct visualization of

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the central veins [i.e., central subclavian and innominate veins], patency can be inferred by evaluation of the spectral waveform for the presence of respiratory phasicity and cardiac periodicity. Central Line Placement

Central line placement performed under ultrasound and ﬂuoroscopy guidance offers signiﬁcant advantages over blind placement because the chance for successful placement is increased. Venous systems that are inaccessible to blind puncture due to anatomic variation or obesity can be easily accessed, and the safety proﬁle is increased with decreased incidence of pneumothorax or arterial puncture. For ultrasound-guided procedures, high-frequency linear array transducers are optimal (i.e., 7.5 or 5 MHz). The target vessel should be evaluated carefully in transverse and longitudinal planes for its suitability for catheterization and its proximity to structures to be avoided. Once the vessel is accessed, ﬂuoroscopy is generally used for proper catheter position. A steerable wire or contrast injection may be required. Peripheral Venous Access: PICCs and Arm Ports

PICC line placement has become a preferred alternative to central line placement because of favorable long-term complication rates. In a series of 404 PICC placements, Cardella et al. (254) reported a 2% infection rate and 1% thrombophlebitis rate. In patients with a paucity of obvious peripheral veins, image guidance is often required for line placement. The procedure is typically performed using ultrasound or venography guidance to obtain access. Micropuncture needles and .018-inch wires should be utilized for initial punctures as these smaller systems are less traumatic and result in the least amount of venospasm. Tourniquets can be used to distend upper arm veins, and nitroglycerin may be injected through a peripheral intravenous line in aliquots of 100 mcg to help relieve spasm. The use of a hydrophilic vascular wire allows greater torque control to negotiate through venous varients and collaterals, markedly enhancing the success rate for PICC line placement in the angiography suite. In the study by Cardella et al. (254), a 98.7% success rate with 100% optimal placement was demonstrated in the angiography suite compared with 74% and 92.8%, respectively, with bedside placement. Venous arm ports are smaller single-lumen versions of products that have been available for placement on the chest wall. Port placement requires strict adherence to sterile technique, although prophylactic antibiotics are not necessary. The catheter is placed in a similar fashion as described with a PICC. A skin incision is made, and a small subcutaneous pocket is created using blunt dissection for port placement. Finally, the port and the infusion catheter are attached securely together.

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Alternative Central Vein Access

When conventional means of access is not possible for central catheter placement, interventional radiologists and clinicians should be aware of alternative access. This usually occurs in patients who have had multiple prior catheterizations. Translumbar and transhepatic approaches are the two main alternative options. After conﬁrming normal anatomy, the translumbar approach can usually be performed with ﬂuoroscopy guidance, although CT may be required for initial access. Transhepatic access can be performed under ultrasound guidance. The middle hepatic vein is the largest and the primary choice. Other possible venous access includes hypertrophied collateral veins, azygous and hemiazygous veins, and intercostal veins. Furthermore, access can be achieved in occluded veins after they are recanalized with wire, angioplasty, and stenting techniques. Malpositioned Catheters

Interventional radiologists are frequently consulted to salvage a malpositioned central line. For non-tunneled catheters, repositioning of the catheters is easily done over a guidewire. However, when a cuffed or implanted catheter tip is malpositioned, various snares or catheter and wire techniques allow manipulation and repositioning of the catheters. This is commonly done via a femoral approach. Pigtail catheters, tip deﬂecting wires, or Amplatz snares have been used with great success to pull catheters back into position. Occluded Catheters

Catheter occlusions secondary to ﬁbrin sheath formation or improper ﬂushing resulting in intraluminal clots are often treated with instillation of thrombolytic agents (i.e., TPA or urokinase). Fibrin sheaths and clots at the tips of the catheters can be treated by disruption with a curled heavy-duty wire, or even with a large angioplasty balloon. However, resistant pericatheter ﬁbrin sheaths require a different approach. A non-cuffed catheter can be easily replaced over a guidewire. For cuffed or implanted catheters, exchange over a wire is usually not feasible. A technique of catheter ﬁbrin sheath stripping has been described by Mewissen et al. (255) with an Amplatz snare from the femoral venous approach for failing hemodialysis catheters. Fibrin sheath typically acts as a ball valve, allowing infusion but occluding side holes upon negative pressure application, therefore hindering catheter aspiration. Its diagnosis is conﬁrmed by venography. Once the ﬁbrin sheath is demonstrated, a guidewire is passed through the distal port of the central line and manipulated through an open Amplatz snare (15, 25, or 35 mm) deployed from the femoral approach. The loop is then guided around the catheter and ﬁrmly snugged against it. As the snare is withdrawn, the ﬁbrin sheath is removed. Thirty-day patency rates are on the order of 30% to 50%. Repeated stripping is necessary in maintaining long-term patency.

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Interventional radiological techniques are now routinely incorporated into the management of critically ill patients with thoracic ﬂuid collections. The currently available radiologically guided procedures to diagnose and treat chest diseases are discussed in the following paragraphs, with emphasis on indications, techniques, potential complications, and post-procedural patient management. Radiologically Guided Thoracentesis

Large pleural effusions may be safely aspirated at the bedside without imaging guidance. However, guided thoracentesis is necessary in cases when the volume of the ﬂuid is small, the effusion is loculated, and the patient has severely compromised respiratory status or is dependent on respirator. Guidance improves the success rate for obtaining ﬂuid and minimizes the risks of pneumothorax and hepatic or splenic injury. Ultrasound is the most versatile modality to guide initial access. It allows characterization of ﬂuid by accessing the echogenicity of the ﬂuid and the degree of septations. Its portability enables procedures to be done at the bedside. If a collection is severely loculated or has a particularly difﬁcult access route, CT may be utilized. Pleural Collections

The common etiologies for pleural collections that require drainage include complicated parapneumonic effusions and post-traumatic or post-surgical collections. It is important to identify the collections that would beneﬁt from drainage early in the course, as delays in drainage allow the collection to organize and ultimately diminish the speed and efﬁcacy of percutaneous drainage. Three stages have been described in the natural history of parapneumonic effusions. Stage I (exudative) is characterized by a sterile exudative effusion with a pH .7.30, glucose .60 mg/dL, and LDH ,500 U/L. In stage II (ﬁbrinopurulent), bacteria enter the pleural space, polymorphonuclear cells increase, and glucose decreases to ,40 mg/dL, pH ,7.10, and LDH . 1000 U/L. As ﬂuid protein increases, intrapleural ﬁbrinolytic activity diminishes, and coagulation of the ﬂuid can occur. Fibrin deposition and ﬁbroblastic activity are initiated. Stage III (organizational) is characterized by formation of a thick, ﬁbrotic pleural peel (256,257). Radiologically placed tubes (8 –14 French) are relatively small compared with the traditional, surgically placed tubes (24 – 38 French). Percutaneous drainage catheters can be inserted under ultrasound and ﬂuoroscopy guidance most of the time. However, if the ﬂuid collection is loculated, poorly accessible (e.g., overlying scapula, brachial plexus, or subclavian vessels) or close to vital structures, CT guidance may be necessary for more precise localization. In severely complex collections, multiple drainage catheters may be necessary. The combination of a glide catheter and wires can be used to disturb septations

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in a complex collection. Thrombolytics have been utilized to break up loculations and to increase the ﬂuidity of the collection. Various protocols with different agents (urokinase, TPA, streptokinase) have been reported, demonstrating an overall promising result. Gentle irrigation of the catheters with normal saline may be performed every eight hours to maintain tube patency. Catheter output should be monitored closely. If the output decreases, and there is signiﬁcant residual ﬂuid, catheter reposition or upsizing may be necessary. Guided catheter drainage of pleural collection has a success rate in the 70% range with a low incidence of complications (258 – 261). Lung Abscess

Lung abscesses are usually treated conservatively with antibiotics, postural drainage, and occasionally bronchoscopy to clear bronchial obstruction. In patients failing conservative treatment, catheter drainage has been shown to be effective and safe (262 – 265). CT is the modality of choice for initial needle access. The patient should be placed with the normal lung in a non-dependent position to avoid spillage of purulent material into the normal lung. Such a complication can lead to overwhelming sepsis and death. An 8 to 14 French catheter with a retention lock is commonly used. The catheter is ﬂushed two to three times a day and placed on water seal for suction. The catheter can be removed when clinical parameters improve, drainage volume decreases, and the radiographic abnormality resolves. Mediastinal and Pericardial Abscess

Acute mediastinitis complicated by abscess formation can result from esophageal perforation (penetrating or blunt trauma, instrumentation, anastomotic leak) or from infections of the neck, spine, lung, or pleura. Median sternotomy, usually performed for cardiac surgery, is the most common cause of mediastinitis (255). Percutaneous drainage may be curative or may temporize and improve the patient’s condition, allowing deﬁnite repair at a later date. CT guidance is necessary on account of the proximity of the heart and great vessels. The catheters are cared for in the same manner as a pleural chest catheter with Pleuro-Vac suction. Pericardial abscess or other ﬂuid collections can be effectively treated by guided aspiration or percutaneous catheter drainage. Ultrasound, and less commonly CT, is utilized. Both aspiration and drainage have been shown to be safer when performed with guidance than when performed blindly (266). Both subxyphoid and intercostal approaches are utilized. C. Management of Pulmonary Embolism and Deep Vein Thrombosis

Acute pulmonary embolism represents the most severe end of the spectrum of the venous thromboembolic disease. The majority of the patients with

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thromboembolic disease are successfully treated with anticoagulation. However, in those patients in whom anticoagulation is not feasible, fails, or results in complications, placement of an IVC ﬁlter is required. IVC ﬁlters have been placed prophylactically in patients who have not had, but are at increased risks for the development of, a thromboembolic event. However, this practice remains controversial. All ﬁlters currently available in the United States can be inserted safely and quickly using percutaneous methods, with an approximate recurrent PE rate of 4% to 5% (267). IVC ﬁlters are placed via the femoral or jugular approach. An IVC venogram is necessary to evaluate the size of the cava and to assess for the level of renal veins and for possible venous variants. Ideally, ﬁlters should be positioned below the level of the renal veins to avoid thrombus propagation compromising renal function. Overall, IVC ﬁlters are safe and effective devices. For patients who are hemodynamically unstable as a result of an acute massive pulmonary embolism, an emergent pulmonary angiogram, and possibly thrombolytic therapy, should be considered. Catheter-directed thrombolysis technique is performed with multisidehole infusion catheters to deliver the thrombolytic agent directly into the thrombus. More recently, endovascular thromboembolectomy has been promoted with mechanical devices. D. Conclusion

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Index

ABG (arterial blood gases) oxygen saturation, 107 surgical ICU and, 107 spontaneous variability, 107 Abscess, mediastinal and pericardial, 391 Acute asthma, 12 Acute respiratory failure, management of, 33 – 34 Air-entrainment mask, oxygen administration devices, 9 Airway assessment, 14 Airway management, 13– 24 airway assessment, 14 direct laryngoscopy visualization, 15 endotracheal intubation, 13 indications for, 13– 14 laryngeal visualization, 15 Mallampati classiﬁcation, 14 nasotracheal vs. orotracheal intubation, 14 oxygen therapy and, 1 – 24 predicting difﬁcult mask ventilation, 14 predicting difﬁcult tracheal intubation, 14 – 15 thyromental distance, 15 Airway pressure waveform, patientventilator dyssynchrony, 130

Airway stents, insertion techniques, 304 – 305 Airway trauma, 33 – 34 barotrauma, 33 – 34 nosocomial sinusitis, 33 – 34 pneumonia, 33 – 34 tracheal stenosis, 33 – 34 Alveolar gas equation, 2 American Society of Anesthesiologists, difﬁcult airway algorithm, 23 Anaerobic infections, oxygen therapy, 3 Analgesics, in ventilator weaning, 170, 171 Aortic injury, 383 – 384 ARDS, 372 – 374 Arm ports, 388 Arterial blood gas analysis, problems with, 106 Arterial blood gases. See ABG. Arterial catheters complications, 222 – 223 equipment, 220 ICU procedures and, 219 –225 indications, 220 technical errors, 223 – 225 techniques, 220 Arterialized capillary, blood gases, 108

407

408 Aspergillus ﬂavus, 295 Aspergillus fumigatus, 295 Aspergillus niger, 295 Aspergillus species, 295 Aspiration pneumonia, 367 Assist/control ventilator, 98– 99 Atelectasis, 365– 366 insertion techniques, 298 “BACK” maneuver, laryngoscopy visualization, 16 BAL ﬂuid as marker, 289, 292 Barium portable antero-posterior view, 333 tracheoesophageal ﬁstula, 333 Barotrauma, 34, 65, 354– 363 Bat-wing pattern in pulmonary edema, 373 Benzodiazepines, over-sedation with, 288 Blood gas analyzers, cost of, 110 Blood gas monitors, mechanical ventilation and, 109– 110 Blood gases, arterialized capillary, 108 Boerhaave’s syndrome, 384 Brachytherapy, 304 Breath, deﬁnition of, 78 Breath patterns/modes, 94– 99 assist/control ventilator, 98– 99 continuous positive airway pressure, 99 intermittent mandatory ventilation, 98 –99 Breath phases, 78– 79 cycle phase, 83– 84 primary cycling mechanisms, 83 secondary cycling mechanisms, 84 expiratory phase, 84–87 FiO2:PEEP relationship, 85–86 open lung approach, 86– 87 pressure – volume curve, 86 limit phase, volume control ventilation, 81 pressure control ventilation, 81– 83 trigger phase, 79– 80 patient triggering, 79– 80 time triggering, 79

Index Breath types, 87 – 94 closed-loop control systems, 93 – 94 equipment and special features, 95 – 97 machine breath, 87 – 91 adapted support ventilation, 90 airway pressure-release ventilation, 90 bi-level ventilation, 89 pressure control ventilation, 88 – 89 pressure-regulated volume control vendilation, 90 volume-assured pressure support ventilation, 90– 91 volume-control ventilation, 87 – 88 spontaneous breath, 91 pressure support breath, 91 – 92 proportional assist ventilation breath, 93 tube compensation breath, 92 –93 volume support breath, 92 Bronchoalveolar lavage (BAL) as diagnostic procedure, 289 Bronchopleural ﬁstula, insertion techniques, 297 Bronchopneumonia, 367 Bronchoscope ﬂexible ﬁberoptic, 286 ultrathin, 286 Bronchoscopic biopsies, 290 Bronchoscopic lung volume reduction, insertion techniques, 305 Bronchoscopy, 285 – 306 contraindications, 286 – 287 history of, 285 immunocompetent patients, 293 indications for ﬂexible, 287 indications for rigid, 286 laser, 299 therapeutic, indications and options, 298 – 305 Bronchospasm, 291 “BURP” maneuver, laryngoscopy visualization, 16 Capnogram airﬂow obstruction and, 121 pulmonary embolism, 124

Index time-based, 120– 121 volume-based, 119–120 Capnography, mechanical ventilation, 117 – 127 Capnometers conﬁguration of, 118 mainstream and sidestream, 118 Capnometry microstream, 118 weaning from mechanical ventilation, 125 Carbon monoxide poisoning, oxygen therapy, 3 Carboxyhemoglobin, half-life of, 3 Cardiogenic edema, radiographic ﬁndings, 375 Cardiogenic pulmonary edema (CPAP), 38 – 41 APACHE II scores, 39 beneﬁts of, 38– 39 comparison to NPPV, 40– 41 randomized trials, 39– 41 performance in, 38– 39 positive intrathoracic pressure, beneﬁts of, 38 respiratory failure, reversibility, 38 Cardiogenic edema vs. non-cardiogenic edema, 374 vs. pulmonary edema, 371– 375 Catheter fragmentation of, 348 malpositioned, 389 in ICU, 344– 352 occluded, 389 Catheter drainage, percutaneous, 390–391 Catheter insertion, mediastinal enlargement, 348 Central vein access, 389 Central venous catheters complications, 231– 236 general technique, 226– 231 ICU procedures and, 225– 226, 344 – 349 indications, 225– 226 ultrasound-guided insertions, 231 Chest radiograph, portable, 331– 337 Chest trauma, insertion techniques, 296

409 Chest tube thoracostomy anatomy, 262 complications, 270 – 271 contraindications, 266 drain size, 266 – 267 equipment, 266 ICU procedures and, 261 –272 indications, 262 –266 technique, 267 – 269 tube management, 271 – 272 tube removal, 272 Chronic obstructive pulmonary disease (COPD) BiPAP deﬁnition of, 36 use of, 36 exacerbations of, acute, 35 intubation rate, 37 – 38 length of stay, 37 – 38 mortality, 37 – 38 randomized trials, 35 –36 Ciaglia PDT technique, 314, 317 Closed-loop control systems, 93 – 94 Clostridium difﬁcile infection, ventilator-dependency, 200 CO2 detector, single-use, 21 CO2 rebreathing technique, 125 Coccidioidomycosis immitis, 294 Common thoracic abnormalities, in the ICU, 364 – 385 Compliance, rate, oxygen, and pressure (CROP) index, 162 – 163 Computed radiography (CR), 334 in the ICU, 387 indications, 385 technique, 385 – 387 Coumadin, and bronchoscopy, 288 Cricothyrotomy, 22 Cryptococcus neoformans, 295 Cystic ﬁbrosis, 50 Cytomegalic virus (CMV), 295 Decompensated obstructive sleep apnea, 50 Deep vein thrombosis, management of, 391 – 392 Deﬁnition of oxygen (O2), 1

410 Delirium, from weaning, 171– 175 recommendation to treat, 171 risk factors, 175 Demand oxygen conservers, 8 Dialysis catheters, in the ICU, 350 –352 Difﬁcult airway, ETT and, 22 Difﬁcult airway algorithm, American Society of Anesthesiologists, 23 Diffuse alveolar damage (DAD), 369 Diffuse non-infectious pulmonary disease, 296 Digital radiography (DR), 334 Dissecting hematoma, 383 of the aorta, 382– 383 Double diaphragm sign, 363 Dumon, 304 Dynamic-Y, 304 Dyshemoglobinemias, in pulse oximetry, 113 Electrocautery, insertion techniques, 303 Embolic disease, 377– 382 Empyema, 368 End-expiratory pause maneuver, measurement of auto-PEEP, 129 End-inspiratory pressure spike, active exhalation, 132 Endobronchial brushing, 290 Endobronchial ultrasound (EBUS), 290 Endotracheal intubation airway management, 13 equipment for, 16 etomidate, 17 medications to facilitate, 17 propofol, 17 rocuronium, 17 succinylcholine, 17 vecuronium, 17 Endotracheal tube placement in ICU, 338– 340 insertion techniques, 298 Esophageal pressure, measurement of, 130 with auto-PEEP, 131 Esophageal rupture, 384– 385

Index ETT care of, 22 – 23 cricothyrotomy, 22 difﬁcult airway and, 22 laryngeal mask airway (LMA), 22 placement, conﬁrmation of proper, 20 – 21 Extubation, weaning vs., 165 Eye irritation, 65 Fasciitis, oxygen therapy for, 3 Feeding tube. See nasoenteric tubes, 341 Fick equation, 110 FiO2:PEEP relationship, in breath phases, 85 – 86 Fleischner sign, 379 Flexible ﬁberoptic bronchoscopy, sedation for, 288 Flexible bronchoscopy, insertion techniques, 289 Flexible ﬁberoptic ancillary equipment, 286 bronchoscope, 286 Flumazenil, 288 Fluorescence bronchoscopy, 291 Foreign bodies, insertion techniques, 297 – 298 Functional force reserve of respiratory muscles, in weaning from mechanical ventilation, 154 Galvanic cell analyzers, 3 Gas exchange, as weaning parameter, 161 Gastric distension, 65 Gastric tonometer conﬁguration, 117 mechanical ventilation, 116 – 117 Hampton’s hump, 351 Heliox, 10 – 13 acute asthma, 12 administration of, 12 stridot, 10 Hematoma of the aorta, dissecting, 382 – 383 Hemodynamic instability, 52 Hemodynamics, of pulmonary artery catheters, 242 – 250

Index Hemoglobin oxygen saturation, gold standard for measurement of, 107 Hemoptysis, insertion techniques, 297 Hemorrhage, pulmonary, 382 Heparin and bronchoscopy, 288 Herpes viruses, 295 High-ﬂow delivery system, 11 oxygen administration devices, 6, 9 – 10 Hydropneumothorax, 364 Hydrostatic pulmonary edema, 369 Hypercapnia in patients with head injury, 125 Hypoxemia, 291 oxygen therapy, 2, 3 ICU procedures, 219– 272 arterial catheters, 219– 225 catheters, 344– 352 central line placement, 388 central venous catheters, 225– 236, 344 – 349 chest tube thoracostomy, 261– 272 devices used in, 338– 364 dialysis catheters, 350– 352 endotracheal tube in, 338– 340 image-guided interventional procedures, 387– 392 implantable cardioverter-deﬁbrillator devices, 353– 354 intra-aortic balloon pump, 352– 353 nasoenteric tubes, 340– 342 peripherally inserted central catheters (PICC), 349 pulmonary artery catheters, 236– 261, 349 – 350 pulmonary edema, 370 Swan-Ganz catheters, 349– 350 thoracostomy tube, 342– 344 tracheostomy tube, 340 transvenous pacing devices, 353 venous access, 387– 389 venous evaluation, 387– 388 Image-guided interventional procedures, ICU, 387– 392 Immunocompromised patients, 45–50 acute respiratory distress syndrome, 49

411 asthmatics, 47 – 48 asphyxia in, 47 chest/wall trauma, rib fractures, 48 – 49 atelectasis in, 48 ineffective cough in, 48 pneumonia in, 48 pulmonary contusion in, 48 COPD patients, and, 49 – 50 cystic ﬁbrosis, 50 decompensated obstructive sleep apnea, 50 do not intubate status, 49 – 50 end-stage-disease patients, 49 – 50 intubation relief, 49 – 50 kyphoscoliosis, 50 lung cancer patients, post-operative, 48 neuromuscular disease, 50 Pneumocystis carinii pneumonia, 50 post-operative lung cancer mucus plugging in, 48 post-pneumonia in, 48 pulmonary edema, non-cardiogenic in, 48 respiratory distress syndrome, acute, 49 rib fractures, chest/wall trauma, 48 – 49 Indirect digital radiography, 334 Insertion techniques airway stents, 304 –305 atelectasis, 298 bronchopleural ﬁstula, 297 bronchoscopic lung volume reduction, 305 chest trauma, 296 complications, 291 – 292 cryotherapy, 302 – 303 electrocautery, 303 endotracheal tube placement, 298 extraanatomical airway tract, 305 foreign bodies, 297 –298 hemoptysis, 297 lung cancer, 292 lung transplant rejection, 296 – 297 neoplasm, debulking of obstructing, 299 photodynamic therapy (PDT), 303

412 Insertion techniques (Contd.) post-procedure care, 291 suspected pulmonary infections, 292 –293 thermal injuries, 296 tracheoesophageal ﬁstula, 296 Inspiratory airways resistance estimation, 133 Intermittent mandatory ventilation (IMV), 98– 99, 164 Intra-aortic balloon pump, ICU, 352– 353 Intramural tonometry, as weaning parameter, 163 Jaw thrust maneuver, in laryngoscopic visualization, 16 Kaposi sarcoma, 292 Knuckle sign, 379 Kyphoscoliosis, 50 Laryngeal mask airway (LMA), 22, 24 Laryngoscopic visualization “BACK” maneuver, 16 “BURP” maneuver, 16 jaw thrust maneuver, 16 maneuvers to improve, 15– 16 Laser, bronchoscopy, 299 Lidocaine, 288, 292 Lobar pneumonia, 367 Lorazepam, in ventilator weaning, 170 LTAC, prolonged mechanical ventilation and, 190 Lung abscess, 391 pneumonia and, 367–368 Lung mechanics, mechanical ventilation, 127 –135 Lung transplant rejection, insertion techniques, 296– 297 Mach effect, 359 Machine breath, 87–91 adapted support ventilation, 90 airway pressure-release ventilation, 90 bi-level ventilation, 89 pressure control ventilation, 88– 89 pressure-regulated volume control vendilation, 90

Index volume control ventilation, 87 – 88 volume-assured pressure support ventilation (VAPS), 90 – 91 Mallampati class I airway, example of, 15 Mallampati classiﬁcation, airway management, 14 Mask air-entrainment, 6 Mask non-rebreathing, 6 Masks claustrophobia, 55 comparison of, 55 compliance, 55 face, 54 mouth breathing, 55 oronasal, 54 patient cooperation, 55 simple, as oxygen administration devices, 6 ventilation, efﬁcacy, 55 Mean airway pressure, determination of, 134 Mechanical ventilation arterial blood gases, 105 – 108 blood gas monitors, 109 – 110 breath patterns, 78 capnography, 117 –127 classiﬁcation scheme, 77 complications of, 354 – 363 ﬁnancial impact of, 136 gastric tonometry, 116 – 117 goals and values matrix, 177 lung mechanics and graphics, 127 – 135 manufacturers terminology, 77 mixed venous blood gases, 110 –112 modes of, 77 –100 monitoring during, 105 – 136 physiologic parameters, 106 point-of-care testing (POC), 108 – 109 prolonged, 187 – 207 patient response, 176 pulse oximetry, 112 – 116 sublingual PCO2, 116 –117 weaning from, 153 – 178. See also Weaning, from mechanical ventilation. Midazolam, in ventilator weaning, 170 Mixed venous oxygen saturation, measurement of, 111

Index Monitoring, of oxygen therapy, 3 – 4 Monitoring response to treatment complications, 64– 65 COPD, 62 erosion of nasal cartilage or bone, 65 eye irritation, 65 failure predictors, 63 disease conditions, 63 late failure, 63 level of consciousness, 63 severity of illness, 63 time frame for failure requiring intubation, 63 gastric distension, 65 nasal congestion, 65 nosocomial pneumonia, 65 patient cooperation, 61 sepsis, 65 sinusitis, 65 skin necrosis, 65 success vs. failure, 61– 64 Mycobacterial disease, 294 Mycobacterium abscessus, 294 Mycobacterium avium complex, 294 Mycobacterium fortuitum, 294 Mycobacterium kansasii, 294 Mycobacterium malmoense, 294 Mycobacterium tuberculosis, 294 Mycobacterium xenopi, 294 Naloxone, 288 Nasal cannula, as oxygen administration devices, 6 Nasal congestion, 65 Nasal O2 cannula, 5 – 7 Nasoenteric tubes, in the ICU, 340 – 342 Nasotracheal vs. orotracheal intubation, 14 Neoplasm, debulking of, insertion techniques, 299 Neuromuscular disease, 50 NICO, rebreathing cycle, 125– 126 NIMV clinical aspects of, 50– 61 co-morbidities, 52– 53 efﬁcacy, 67 helium-oxygen mix, 60– 61

413 humidiﬁcation, 60 limitations, 50 – 51, 54 – 56 mask leaks, 50, 53 – 54 nosocomial pneumonia, 43 post-extubation period, 41 – 46 potential of, 67 pressure support to patient, 60 upper airway obstruction, 42 ventilators, types of, 55, 56 – 57 Nocardia, 292 Non-invasive ventilation, 33 –67 Non-cardiogenic pulmonary edema, 372 – 374 Non-rebreathing mask, 8 Non-tuberculosis mycobacteria (NTM), 294 Nosocomial pneumonia, 65, 293 Open lung approach, in breath phases, 86 – 87 Open surgical tracheostomy (OST), 313 Opiates, over-sedation with, 288 Optically coupled direct radiography, 334 Optimal position of medical devices in, ICU, 338 Orotracheal intubation, complications of, 24 Orotracheal intubation preparation for, 16 – 18 technique for, 18 – 20 Oximetric methodology, to measure mixed venous oxygen saturation, 111 Oxygen administration devices, 5 – 8 air-entrainment mask, 9 high-ﬂow devices, 6, 9 –10 mask air-entrainment, 6 mask non-rebreathing, 6 mask simple, 6, 8 nasal O2 cannula, 5 – 7 non-rebreathing mask, 8 Oxygen analyzers, 3 galvanic cell analyzers, 3 polarographic, 3 zirconium analyzer, 3 Oxygen cost of breathing (OCB), 163

414 Oxygen therapy airway management and, 1 –24 anaerobic infections, 3 carbon monoxide poisoning, 3 fasciitis, 3 haldane effect, 4 hypoxemia, 2, 3 indications for, 2 – 3 monitoring of, 3 – 4 physiologic complications of, 4– 5 technical hazards of, 5 Oxyhemoglobin dissociation curve, 113 PACS, advantages of, 335 Patient synchrony, 50– 51 Patient triggering “ﬂow trigger,” in breath phases, 79 mechanical ventilation, 79– 80 “pressure trigger,” 79 PDT complication rates of, 321 esophageal perforation, 323 OST vs., 324 technique, 317– 321 Peak airway pressure (PAP), and equation of motion, 128 Penumbra effect, in pulse oximetry, 113 Percutaneous catheter drainage, 390 –391 Percutaneous dilatational tracheostomy (PDT), 313 complications of, 322 in the ICU, contraindications to, 317 Percutaneous tracheostomy, 313– 325 Pericardial tamponade, 337 Peripheral venous access, 388 Peripherally inserted central catheters (PICC), ICU, 349 Perivascular interstitial emphysema (PIE), 355 PETCO2, causes of increases/decreases, 122 Photocoagulation, laser, 302 Photodynamic therapy (PDT), insertion techniques, 303 Photoevaporation, laser, 302 PICCS, 388 Pleural collections, 390– 391

Index Pleural effusion, 375 – 377 Pneumocystis carinii pneumonia, 50, 293 Pneumocytis jiroveci, 293 Pneumomediastinum, 359, 360 Pneumonia, 34, 65, 366 – 368 complications, 367 lung abscess, 367 – 368 types of, 366 Pneumonitis, 291 Pneumopericardium, 359 Pneumothorax, 346, 359 apicolateral, 361 posteromedial, 361 simple, 363 Polarographic oxygen analyzers, 3 Polyﬂex, 304 Portable antero-posterior view barium, 333 interpretation of, 336 – 337 oral contrast, 333 portable chest radiography, 332 radiation dose level, 333 special views, 333 Portable chest radiography, 331 – 337 limitations of, 337 indications of, 332 Positive end-expiratory pressure (PEEP), 355 Positive pressure ventilation (PPV), 355 in relaxed patient, 131 Post-extubation period, 41 – 45 Pre-bronchoscopy, laboratory tests, 288 Pressure control ventilation, in breath phases, 81 – 83 “Pressure trigger,” in breath phases, 79 Pressure – volume curve in breath phases, 86 during mechanical ventilation, 135 Primary cycling mechanisms, in breath phases, 83 Prolonged mechanical ventilation, 187 – 204 chronic obstructive pulmonary disease, (COPD), 189 deﬁnition of, 188 – 189 frequency of, 188 history of, 187 in ICU, 190

Index indications for, 189 LTAC or post-acute care hospitals, 190 patient outcomes, 191–192 pneumonia, 190 site of care for patients with, 190 – 191 surgical procedure, 190 weaning patients, 204– 207 Propofol, in ventilator weaning, 170 Pulmonary angiography, 381 Pulmonary artery catheters complications of, 257– 259 controversy re usage, 259– 261 equipment and techniques, 239– 240 ICU procedures and, 236– 261, 349 – 350 indications/contraindications, 237 – 239 insertion of, 240– 242 principles of, 261 speciﬁc clinical scenarios, 250– 257 trials of, 261 waveforms, 242– 250 Pulmonary disease, diffuse non-infectious, 296 Pulmonary edema, 269–375 cardiogenic, 371– 375 in ICU, 370 increased permeability, 372– 374 non-cardiogenic, 372– 374 pulmonary interstitial emphysema, 357 Pulmonary embolism, 377– 381 computerized tomography, 385 – 387 management of, 391– 392 radiographic ﬁndings, 379 Pulmonary hemorrhage, 382 Pulmonary infarction, 351, 379 Pulmonary interstitial emphysema, 358 pulmonary edema in, 357 Pulmonary mechanics, 127 Pulse oximetry limitations of, 112 impact on patient outcomes, 115 mechanical ventilation, 112–116 PV curve, 134

415 Radiology, in the intensive care unit, 331 – 392 Rapid shallow breathing index (RSBI), 161 – 162 Reservoir O2 cannula (moustache and pendant types), 8 Respiratory failure acute, management of, 33 – 34 airway trauma, 33 – 34 barotrauma, 33 – 34 intubation, 33 – 34 nosocomial sinusitis, 33 – 34 pneumonia, 33 – 34 tracheal stenosis, 33 – 34 Respiratory system compliance (Crs), 133 Respiratory therapy, duration of, 50 –51 Rigid bronchoscope, insertion techniques, 289 Ruptured thoracic aorta, 383 Secondary cycling mechanisms, in breath phases, 84 Sedation benzodiazepines, 170 – 172 cost implications for ventilated patient, 172 – 174 weaning and, 168 – 169, 170, 171 Sepsis, 65 Septic emboli, 381 – 382 causative organisms, 381 diagnosis of, 381 Sinusitis, 6 Skin necrosis, 65 Spiration, 305 Spontaneous breath pressure support breath, 91 – 92 proportional assist ventilation breath, 93 tube compensation breath, 92 – 93 volume support breath, 92 Stanford aortic dissection, 383 Subclavian artery, puncture of, 347 Subclavian venous catheter, venous malposition of, 344 Sublingual PCO2, mechanical ventilation, 116 – 117 Superior vena cava thrombosis, 348 Swan– Ganz catheters, in the ICU, 349 – 350

416 Tension pneumothorax, 362, 365 Thermal injuries, insertion techniques, 296 Thoracentesis, radiologically guided, 390 Thoracostomy tube, in the ICU, 342– 344 Time triggering, mechanical ventilation, 79 TIPS long-term weaning protocol, 169 Tracheal stenosis, 34 Tracheoesophageal ﬁstula, 296, 323, 334 Tracheo-innominate ﬁstula, 323 Tracheostomy complications of, 323 contraindications, 316– 317 in the ICU, 340 patient care, 324– 325 percutaneous, 313– 325 placement, methods for, 314 timing of, 315 translaryngeal intubation, 315 ventilator-dependency, 199 Transbronchial biopsy, 290 Transbronchial needle aspiration, 290 Translaryngeal intubation, 315– 316 Translaryngeal tracheostomy method, 314 Transtracheal O2 catheter, 8 Transvenous pacing devices, 353 Treatment, monitoring response to, 61 –67. See also Monitoring response of treatment. Ultraﬂex, 304 Ultrasound-guided insertions, central venous catheters and, 231 Ultrathin, bronchoscopes, 286 VE recovery time, as weaning parameter, 163 Venous access, in the ICU, 387– 389 Venous oxygenation, mixed, 110 Ventilation, non-invasive, critical care, 33 –68 Ventilator breath, ﬁne tuning of, 99– 100 Ventilator efﬁciency, 50–51 Ventilator modes, 78. See also Breath phases.

Index Ventilator-dependency assessment tools to predict outcome, 202 – 204 care factors, 201 Clostridium difﬁcile infection, 200 iatrogenic factors, 199 – 201 mechanical factors, 196 – 199 non-invasive mechanical ventilation, as adjunct to weaning, 206 potential causes for, 195 reasons for, 192 – 202 respiratory muscle weakness, 205 spontaneous breathing trials, 204 standardization protocols, 205 systemic failures, 192 – 196 tracheotomies, 199 weaning from prolonged mechanical ventilation, 197 weaning protocols, 205 Ventilatory support deﬁnition of, 34 efﬁcacy, 34 – 35 general guidelines, 35 rationale for use, 34 – 35 Volume control ventilation, in breath phases, 81 Volume-assured pressure support ventilation (VAPS), 90 – 91 Volume-based capnography, and cardiac output, 125 Wallstent, 304 Waveforms, pulmonary artery catheters and, 242 – 250 Weaning agitated patient, 170 analgesics, 170 selection of, 173 best practices, 164 intermittent mandatory ventilation (IMV), 164 delirium from, 174 environment, importance of, 168 extubation vs., 165 from mechanical ventilation, 153 – 178 compliance, rate, oxygen, and pressure (CROP) index, 162 – 163

Index criteria of success/failure, 154– 160 functional force reserve of respiratory muscles, 154 intra-mural tonometry, 163 load vs. capacity, 154– 155 oxygen cost of breathing (OCB), 163 parameters, 161– 163 pathophysiology of failure, 156– 157 rapid shallow breathing index (RSBI), 161– 162 respiratory muscle fatigue, 155– 156 reversible factors, 158 – 160 rib cage-abdominal motion, 163 success prediction, 160– 164 VE recovery time, 163

417 parameters, 161 –163 preventing pain and discomfort, 173 prolonged ventilation, 167 – 168 protocol recommendations, 168 TIPS, 169 protocol-guided, 165 – 167 recommendations for delirium, 171 sedation, 168 –169, 170 benzodiazepines, 170 – 172 sedative reversal, 173 – 174 Weaning failure, causes of, 159 Westermark sign, 379 – 280 Zirconium analyzer, 3

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