Surgical Intensive Care Medicine

Second Edition

Surgical Intensive Care MedicineSecond Edition

Edited by

John M. O’DonnellDirector, Surgical Intensive Care UnitChairman, Department of Surgical Critical CareDivision of SurgeryThe Lahey Clinic Medical Center Burlington, MAUSA

Flávio E. NáculIntensive Care Medicine University HospitalFederal University of Rio de JaneiroRio de Janeiro, RJBrazil

EditorsJohn M. O’DonnellDirector, Surgical Intensive Care Unit Chairman, Department of Surgical Critical CareDivision of SurgeryThe Lahey Clinic Medical Center Burlington, MA, USA

Flávio E. NáculUniversity HospitalIntensive Care MedicineFederal University of Rio de JaneiroRio de Janeiro - RJBrazil

ISBN 978-0-387-77892-1 e-ISBN 978-0-387-77893-8DOI 10.1007/978-0-387-77893-8

Library of Congress Control Number: 2009930636

© Springer Science + Business Media, LLC 2010All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science + Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden.The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identifi ed as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein.

Printed on acid-free paper

Springer is part of Springer Science+Business Media (www.springer.com)

This book is dedicated to my wife, Rocky, and daughter, Jacquelyn, who give me purpose; to my beloved parents, Kay and Frank “Shorty” O’Donnell, who never lost faith; to my mentors, whose patience was tested every day; and to all of the nurses who have ever cared for patients in the surgical intensive care unit at the Lahey Clinic Medical Center.

John M. O’Donnell, M.D.

To my parents Lilian and Jacob, and my wife Alessandra, for their uncondi-tional love; to my daughter Mariana, for the joy she brings to my life; and to my brother Luis and my uncle Sabino, for their support.

Flávio Eduardo Nácul, M.D.

Preface to the Second Edition

We are honored to present the second edition of Surgical Intensive Care Medicine . Our first edition was considered to be an important contribution to the critical care literature and received excellent reviews from Critical Care Medicine , Chest , and Anesthesiology . In the second edition, the basic organization of the book remains unchanged, being composed of 60 carefully selected chapters divided into 11 sections. The book begins with general topics in primary intensive care, such as airway management and vascular cannulation, followed by categories based on medical and surgical subspecialties. While the chapters discuss definitions, pathophysiology, clinical course, complications, and prognosis, the primary emphasis is devoted to patient management. The contents of the current edition have been comprehensively upgraded and the chapters retained from the first edition have been thoroughly updated, revised, or rewritten.

In this second edition, some new topics have been added including Postoperative Care of the Obese Patient, Postoperative Care of the Pancreas Transplant Patient, Optimization of High-Risk Surgical Patients, Postop-erative Alcohol Withdrawal Syndrome, Ethics and End of Life Issues, Improving the ICU, and Continuous Medical Education in Intensive Care Medicine. We are extremely fortunate to have high-quality contributors, many of whom are nationally and internationally recognized researchers, speakers, and practitioners in Criti-cal Care Medicine. An important feature of this latest edition is the geographical diversity of its authors. Most are based in the United States, but colleagues from Canada, England, Ireland, Germany, Belgium, Holland, France, Italy, Portugal, and Australia have also made notable contributions.

The book is written for medical students, residents, and critical care fellows in training, and its purpose is to educate, stimulate, and serve as a resource for all professionals caring for the critically ill. Those who are not involved in the daily care of the acutely ill patient but who seek information will also find this book a valuable resource. We are very fortunate to have Springer as our publisher and we are especially thankful to our chapter authors and their families. We anticipate that our book will be both educational and enjoyable and we hope that both our readers and their patients will benefit.

Flávio E. Nácul, MD John M. O’Donnell, MD

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Acknowledgements

We would first and foremost like to thank Paula Callaghan and Springer Publishing Company for giving us the opportunity and providing the support necessary to develop the second edition of Surgical Intensive Care Medicine . We are forever grateful to Barbara Murphy and Melissa Ramondetta for giving us the opportunity to publish the first edition of our book. We are indebted to Maureen Pierce for her knowledge, enthusiasm, patience, and meticulous attention to detail while formatting and organizing the entire manuscript. We thank Kathy McQueen who was extremely helpful reviewing and editing the chapters. We thank Carol Spencer, the Lahey Clinic librarian, for without her tireless efforts, this text would not be possible. We are indebted to Roger Jenkins, MD, Sanford Kurtz, MD, and David Barrett, MD for their ongoing department support during the organizing, writing, and editing of this textbook. Lastly, we are especially grateful to the following col-leagues for sharing their expertise and for their very useful comments on the chapters of this book: Fernando Afonso, MD, Luciano Azevedo, MD, Carlos Ferrari, MD, Maria Giaquinto, MD, Fernando Gutierrez MD, PhD, Jana Hudcova, MD, Jean Hurynowicz, RN, Alexandre Isola MD, Sara Lenherr, MD, Luciano Lisboa, MD, A. Lucy Querino, Denise Medeiros, MD, PhD, Carina Ruiz, MD and Patricia Toledo.

John M. O’Donnell, MD Flávio E. Nácul, MD

Bruno Zawadzki, MD

ix

Contents

Preface to the Second Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . viiAcknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix

Part I Resuscitation and General Topics

1 Supplemental Oxygen Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Andrew G. Villanueva

2 Airway Management in the Intensive Care Unit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13Denis H. Jablonka and William Rosenblatt

3 Vascular Cannulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25Shawn E. Banks and Albert J. Varon

4 Fluid Resuscitation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35Joachim Boldt

5 Vasoactive Amines and Inotropic Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45Keith P. Lewis, R. Mauricio Gonzalez, and Konstantin Balonov

6 Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53Kyle J. Gunnerson and Emanuel P. Rivers

7 Hemodynamic Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67Flávio E. Nácul and John M. O’Donnell

8 Acid–Base Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75Philip M. Alapat and Janice L. Zimmerman

9 Analgesia and Sedation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85Ruben J. Azocar, Pouneh Taghizadeh, and Ishaq Lat

10 Neuromuscular Blocking Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97Rafael A. Ortega, Gerardo Rodríguez, and Rubén Azocar

11 Optimization of the High-Risk Surgical Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107Nawaf Al-Subaie and Andrew Rhodes

12 Cardiopulmonary Resuscitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113Andreas Schneider, Erik Popp, and Bernd W. Böttiger

Part II Neurocritical Care

13 Management of Closed Head Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129Peter K. Dempsey and Steven W. Hwang

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14 Spinal Cord Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137Fred H. Geisler and William P. Coleman

15 Ischemic Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149Jamary Oliveira-Filho and Walter J. Koroshetz

16 Hemorrhagic Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163Jamary Oliveira-Filho and Walter J. Koroshetz

17 Status Epilepticus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173Andreas H. Kramer and Thomas P. Bleck

18 Critical Illness Polyneuropathy and Myopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185Galen V. Henderson

Part III Cardiology

19 Management of Hypertension in the Perioperative Period . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191Nicholas P. Tsapatsaris and Durathun Farha

20 Postoperative Myocardial Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199Glynne D. Stanley and Sundara K. Rengasamy

21 Management of Postoperative Arrhythmias. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209Eugene H. Chung and David T. Martin

Part IV Pulmonary Medicine

22 Acute Respiratory Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231Luciano Gattinoni, Eleonora Carlesso, and Federico Polli

23 Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241Peter Rock and Vadivelu Sivaraman

24 Venous Thromboembolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255Andrew G. Villanueva and Nicholas P. Tsapatsaris

25 Fat Embolism Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277John M. O’Donnell

26 Venous Air Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285Carl J. Borromeo

Part V Infectious Diseases, Sepsis, MODS

27 Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297Patricia Mello and R. Phillip Dellinger

28 Vascular Catheter-Related Bloodstream Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311Nikolaos Zias, Alexandra Chroneou, John F. Beamis, and Donald E. Craven

29 Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325Alexandra Chroneou, Nikolaos Zias, Anthony Gray, and Donald E. Craven

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30 Intra-abdominal Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343Marc E. Brozovich and Peter W. Marcello

31 Evaluation of the Febrile Patient in the ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349Alexis Tabah, François Philippart, and Jean Carlet

32 Antimicrobial Use in Surgical Intensive Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 361Robert A. Duncan

Part VI Hematology

33 Coagulation Abnormalities in the Critically Ill . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371Marcel Levi and Steven M. Opal

34 Blood Products . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379Kurt F. Heim

Part VII Metabolism and Nutrition

35 Hyperglycemia in the Surgical Intensive Care Unit. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391Gary W. Cushing

36 Adrenal Insufficiency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399Bala Venkatesh and Jeremy Cohen

37 Nutrition Support in Intensive Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407Susan E. Schaefer and David L. Burns

Part VIII Nephrology and Electrolytes

38 Acute Kidney Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421Paolo Calzavacca, Elisa Licari, and Rinaldo Bellomo

39 Renal Replacement Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 431Elisa Licari, Paolo Calzavacca, and Rinaldo Bellomo

40 Disorders of Electrolytes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 439Flávio Eduardo Nácul

Part IX Gastroenterology

41 Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455Sam J. Thomson, Matthew L. Cowan, Robert Morgan, and Tony M. Rahman

42 Acute Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471Jan J. De Waele

Part X Surgery, Trauma, and Transplantation

43 Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 489Michael S. Rosenblatt

44 Burns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497Larry M. Jones, Alain C. Corcos, and Amarjit D. Peter

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45 The Abdominal Compartment Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 507Manu L. Malbrain, Michael Cheatham, Michael Sugrue, and Rao Ivatury

46 Rhabdomyolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529Flávio E. Nácul and John M. O’Donnell

47 Postoperative Care of the Cardiac Surgical Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535Ross F. Dimarco Jr.

48 Postoperative Care Following Major Vascular Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 567Giuseppe Papia and Thomas F. Lindsay

49 Postoperative Care After Bariatric Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 577Fredric M. Pieracci, Alfons Pomp, and Philip S. Barie

50 Care of the Organ Donor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 591Younghoon Kwon and Marie R. Baldisseri

51 Postoperative Care of the Heart Transplant Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 599Nicholas R. Banner, Iman Hamour, Haifa Lyster, Margaret Burke, Michael J. Boscoe, and Gilles Dreyfus

52 Postoperative Care of the Lung-Transplant Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 621Wickii T. Vigneswaran and Sangeeta M. Bhorade

53 Postoperative Care of the Liver-Transplant Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 629Philip A. Berry, Hector Vilca Melendez, and Julia A. Wendon

54 Postoperative Care of the Pancreas-Transplant Recipient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 639Shimul A. Shah and Rodney J. Taylor

Part XI Additional Topics

55 Management of the Critically Ill Geriatric Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 649Paul E. Marik

56 Alcohol Withdrawal in the Surgical Patient: Prevention and Treatment . . . . . . . . . . . . . . . . . . . 659Anja Heymann, Irit Nachtigall, Anton Goldmann, and Claudia Spies

57 Ethics and the End-of-Life Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 667Dan R. Thompson

58 Scoring Systems and Outcome Prediction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 679Rui Moreno and Isabel Miranda

59 Improving the Intensive Care Unit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 685Allan Garland

60 Continuing Education in Critical Care Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 705Elizabeth H. Sinz

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 711

Erratum to Chapters 2, 3 and 11 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 723

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Contributors

Philip Alapat, MD Assistant Professor, Department of Pulmonary, Critical Care and Sleep Medicine, Baylor College of Medicine, Ben Taub General Hospital, Houston, TX, USA

Nawaf Al-Subaie, MD, FRCA, MBChB Anaesthesia and Intensive Care Medicine, St. George’s Hospital London, UK

Ruben J. Azocar, MD Assistant Professor and Residency Program Director, Department of Anesthesiology, Boston University School of Medicine, Boston, MA, USA

Marie R. Baldisseri, MD, FCCM Associate Professor of Critical Care Medicine, Department of Critical Care Medicine, University of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, PA, USA

Konstantin Balonov, MD Resident, Department of Anesthesiology, Boston University Medical Center, Boston, MA, USA

Shawn E. Banks, MD Assistant Professor of Anesthesiology, Department of Anesthesiology, Jackson Memorial Hospital, University of Miami Miller School of Medicine, Miami, FL, USA

Nicholas R. Banner, MD, FRCP Consultant and Senior Lecturer, Royal Brompton and Harefield NHS Trust, Cardiology and Transplant Medicine, Imperial College University of London, Middlesex, UK

Philip S. Barie, MD, MBA, FCCM, FACS Professor of Surgery and Public Health, Department of Surgery and Public Health, Weill Cornell Medical Center, New York, NY, USA

John F. Beamis Jr, MD Associate Professor of Medicine, Tufts University School of MedicineChairman, Division of Internal Medicine, Department of Pulmonary and Critical Care Medicine,Lahey Clinic Medical Center, Burlington, MA, USA

Rinaldo Bellomo, MD, FRACP, FJFICM Professor, Department of Intensive Care, Austin Hospital, Victoria, Australia

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xvi Contributors

Philip A. Berry, MD, MBChB, MRCP Institute of Liver Studies, King’s College Hospital, King’s College London, London, UK

Sangeeta M. Bhorade, MD Associate Professor of Medicine, Medical Director of Lung Transplantation, Department of Medicine, University of Chicago Hospitals, University of Chicago, Chicago, IL, USA

Thomas P. Bleck, MD, FCCM Professor of Neurological Sciences, Neurosurgery, Medicine, and AnesthesiologyAssistant Dean, Rush Medical College, Associate Chief Medical Officer (Critical Care) Rush University Medical Center, Chicago, IL, USA

Joachim Boldt, MD Professor, Klinikum Ludwigshafen, Department of Anesthesiology and Intensive Care Medicine, Ludwisgshafen, Germany

Carl J. Borromeo, MD Assistant Clinical Professor of Anesthesiology, Tufts University School of Medicine,Staff Anesthesiologist, Department of Anesthesiology, Lahey Clinic Medical Center, Burlington, MA, USA

Michael J. Boscoe, MD, MBBS, FRCA Consultant Anaesthetist, Royal Brompton and Harefield NHS Trust, Department of Anaesthetics, Middlesex, UK

Bernd W. Böttiger, MD Professor, Department of Anesthesiology and Postoperative Intensive Care Medicine, University of Cologne, Cologne, Germany

Marc E. Brozovich, MD Assistant Professor of Surgery, Department of Surgical Oncology, University of Pittsburgh Medical Center, Wexford, PA, USA

Margaret Burke, MD, MB FRCPath Department of Histopathology, Royal Brompton and Harefield NHS Trust, Middlesex, UK

David L. Burns, MD, CNSP, FACG Assistant Clinical Professor of Medicine, Tufts University School of Medicine;Director of Nutritional Support, Lahey Clinic Medical Center, Burlington, MA, USA

Paolo Calzavacca, MD Research Fellow, Department of Intensive Care, Austin Hospital, Victoria, Australia

Eleonora Carlesso, MSc Dipartimento di Anestesiologia e Terapia Intensiva, Università degli Studi di Milano, Milan, Italy

Jean Carlet, MD Head Medical/Surgical ICU, Department of Réanimation, Groupe Hospitalier Paris – St. Joseph, Paris, France

Michael L. Cheatham, MD, FACS, FCCM Director, Surgical Intensive Care Units, Department of Surgical Education, Orlando Regional Medical Center, Orlando, FL, USA

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Contributors xvii

Alexandra Chroneou, MD Research Fellow, Department of Pulmonary and Critical Care Medicine, Lahey Clinic Medical Center, Burlington, MA, USA

Eugene H. Chung, MD Assistant Professor of Medicine, Division of Cardiology, Cardiac Electrophysiology Service, The University of North Carolina School of Medicine, Chapel Hill, NC, USA

Jeremy Cohen, MBBS, MRCP, FRCA, FJFICM Critical Care Endocrinology and Metabolism Research Unit, Division of Anesthesiology and Critical Care, Princess Alexandra and Wesley Hospitals, University of Queensland, Brisbane, Australia

William P. Coleman, PhD Biostatistician, WPCMath, Buffalo, NY, USA

Alain C. Corcos, MD, FACS Assistant Director, Trauma and Burn Services, UPMC Mercy, Department of Trauma Services, Pittsburgh, PA, USA

Matthew Cowan, BSc, MRCP Clinical Research Fellow, Department of Gastroenterology, St. George’s Hospital, London, UK

Donald E. Craven, MD Professor of Medicine, Tufts University School of Medicine,Chair, Department of Infectious Diseases, Lahey Clinic Medical Center, Burlington, MA, USA

Gary W. Cushing, MD, FACE Associate Clinical Professor of Medicine, Tufts University School of Medicine,Chairman, Department of Endocrinology, Lahey Clinic Medical Center,Burlington, MA, USA

R. Phillip Dellinger, MD Professor of Medicine, Head, Division of Critical Care Medicine, Robert Wood Johnson Medical School, Cooper University Hospital, University of Medicine and Dentistry of New Jersey, Camden, NJ, USA

Peter K. Dempsey, MD Assistant Clinical Professor, Tufts University School of Medicine,Senior Staff Physician, Department of Neurosurgery, Lahey Clinic Medical Center;Burlington, MA, USA

Jan J. De Waele, MD, PhD Intensivist, Department of Critical Care Medicine, Ghent University Hospital, Ghent, Belgium

Ross F. DiMarco Jr., MD Chief, Cardiovascular Thoracic Surgery, Department of Surgery, UPMC Mercy Hospital of Pittsburgh, Pittsburgh, PA, USA

Gilles D. Dreyfus, MD, FRCS Professor of Cardiac Surgery, NHLI, Department of Cardiac Surgery, Imperial College, London,Royal Brompton and Harefield NHS Trust, Harefield Hospital, Harefield, Middlesex, UK

Robert A. Duncan, MD, MPH Associate Professor of Medicine, Tufts University School of Medicine; Hospital Epidemiologist, Department for Infectious Diseases, Lahey Clinic Medical Center, Burlington, MA, USA

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xviii Contributors

Durathun Farha, MD Vascular Medicine Fellow, Department of Vascular Medicine, Lahey Clinic Medical Center, Burlington, MA, USA

Allan Garland, MD, MA Associate Professor, Department of Medicine, University of Manitoba, Manitoba, Canada

Luciano Gattinoni, MD, FRCP Professor of Anesthesia and Intensive Care, Dipartimento di Anestesiologia e Terapia Intensiva,Università degli Studi di MilanoDipartimento di Anestesia, Rianimazione e Terapia del Dolore, Fondazione IRCCS, Ospedale Maggiore Policlinico, Mangiagalli, Regina Elena di Milano, Milan, Italy

Fred H. Geisler, MD, PhD Founder, Department of Neurosurgery, Illinois Neuro-Spine Center, Rush Copley Medical Center, Aurora, IL, USA

Anton Goldmann, MD Department of Anesthesiology and Intensive Care Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany

R. Mauricio Gonzalez, MD Vice Chairman, Department of Anesthesiology, Boston Medical Center, Boston, MA, USA

Anthony W. Gray Jr., MD Assistant Professor of Medicine, Tufts University School of Medicine; Director, Medical Intensive Care Unit, Department of Pulmonary and Critical Care Medicine, Lahey Clinic Medical Center, Burlington, MA, USA

Kyle J. Gunnerson, MD Associate Professor and Director of Critical Care Anesthesiology, Virginia Commonwealth University Medical Center, VCURES Laboratory, Richmond, VA, USA

Iman M. Hamour, MD, MBBS, MRCP Department of Cardiology and Transplant Medicine, The Royal Brompton and Harefield NHS Trust, Harefield Hospital, Middlesex, UK

Kurt F. Heim, MD, PhD Director, Transfusion Medicine, Department of Laboratory Medicine, Lahey Clinic Medical Center, Burlington, MA, USA

Galen V. Henderson, MD Director of Neurocritical Care and Neuroscience ICU, Department of Neurology, Harvard Medical School, Brigham and Womens Hospital, Boston, MA, USA

Anja Heymann, MD Resident, Department of Anesthesiology, Charité – Universitätsmedizin Berlin, Berlin, Germany

Steven W. Hwang, MD Resident, Department of Neurosurgery, Tufts Medical Center, Boston, MA, USA

xviii

Contributors xix

Rao R. Ivatury, MD, FACS Chair, Division of Trauma, Critical Care and Emergency General Surgery, Virginia Commonwealth University Medical Center, Richmond, VA, USA

Denis H. Jablonka, MD Assistant Professor, Department of Anesthesiology, Yale University, Yale – New Haven Hospital, New Haven, CT, USA

Larry M. Jones, MD, FACS Medical Director, Burn Center, The Western Pennsylvania Hospital, Pittsburgh, PA, USA

Walter J. Koroshetz, MD Deputy Director, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA

Andreas H. Kramer, MD, MSc FRCPC Clinical Assistant Professor, Department of Critical Care Medicine and Clinical Nuerosciences, University of Calgary, Alberta, Canada

Younghoon Kwon, MD HealthEast Care System, St. Joseph’s Hospital, Saint Paul, MN, USA

Ishaq Lat, PharmD Clinical Pharmacist - Critical Care, Pharmacy Department, University of Chicago Medical Center, Chicago, IL, USA

Marcel Levi, MD, PhD Professor of Medicine, Chairman, Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands

Keith P. Lewis, RPh, MD Chairman, Department of Anesthesiology, Boston Medical Center, Boston, MA, USA

Elisa Licari, MD Research Fellow, Department of Intensive Care, Austin Hospital, Victoria, Australia

Thomas F. Lindsay, MDCM, MSc, FRCSC, FACS Professor, Department of Surgery, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada

Haifa Lyster, BPharm(Hons), MSc Principal Pharmacist, Transplantation, Royal Brompton and Harefield NHS Trust, Pharmacy Department, Harefield Hospital, Middlesex, UK

Manu L. N. G. Malbrain, MD, PhD Director, Intensive Care Unit, ZNA Stuivenberg, Intensive Care Unit, Lange, Antwerpen, Belgium

Peter W. Marcello, MD, FACS, FASCRS Vice Chairman, Department of Colon and Rectal Surgery, Lahey Clinic Medical Center, Burlington, MA, USA

Paul E. Marik, MD, MBBCh, FCP(SA), FRCP(c), FCCM, FCCP Professor of Medicine, Chief of Pulmonary and Critical Care Medicine, Eastern Virginia Medial School, Norfolk, VA, USA

xix

xx Contributors

David T. Martin, MD, FRCP Associate Professor of Medicine, Tufts University School of Medicine; Director, Cardiac Arrhythmia Service, Department of Cardiovascular Medicine, Lahey Clinic Medical Center, Burlington, MA, USA

Patricia Mello, MD Director, Intensive Care Unit, Department of Critical Care, Hospital de Terapia Intensiva, Universidade Estadual Do Piauí, Teresina, PI, Brazil

Isabel Miranda, MD, MSc Intensive Care Unit, Centro Hospitalar de Lisboa Central, E.P.E., Hospital de St. António dos Capuchos, Lisboa, Portugal

Rui Moreno, MD, PhD Director, Intensive Care Unit, Centro Hospitalar de Lisboa Central, E.P.E., Hospital de St. António dos Capuchos, Lisboa, Portugal

Robert Morgan, MCChB, MRCP, FRCR Consultant Vascular and Interventional Radiologist, Department of Radiology, St. George’s Hospital, London, UK

Irit Nachtigall, MD Department of Anesthesiology, Charité – Universitätsmedizin Berlin, Berlin, Germany

Flávio Eduardo Nácul, MD, MSc Intensive Care Medicine, University Hospital of the Federal University of Rio de Janeiro, Rio de Janeiro - RJ, Brazil

John Merritt O’Donnell, MD Director, Surgical Intensive Care Unit, Chairman, Department of Surgical Critical Care, Division of Surgery, The Lahey Clinic Medical Center, Burlington, MA, USA

Jamary Oliveira-Filho, MD, PhD Chief, Neurology Service and Neurocritical Care Unit, Hospital Espanhol;Associate Professor, Federal University of Bahia, Salvador, BA, Brazil

Steven M. Opal, MD, PhD Professor, Division of Infectious Diseases , The Memorial Hospital of Rhode Island, Brown University, Pawtucket, RI, USA

Rafael Ortega, MD Professor of Anesthesiology, Department of Anesthesiology, Boston Medical Center, Boston University, Boston, MA, USA

Giuseppe Papia, MD, MSc, FRCSC Assistant Professor, Division of Cardiac and Vascular Surgery, University of Toronto, Department of Critical Care Medicine, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada

A. David Peter, MD Surgical Resident, UPMC Mercy, Department of Surgery, Pittsburgh, PA, USA

François Philippart, MSc, MD Department of Intensive Care Medicine, Groupe Hospitalier Paris Saint Joseph, Paris, France

Fredric M. Pieracci, MD, MPH Resident, Department of Surgery and Public Health, Weill Cornell Medical Center, New York, NY, USA

xx

Contributors xxi

Federico Polli, MD Resident, Dipartimento di Anestesiologia eTerapia Intensiva, Università degli Studi di Milano, Milan, Italy

Alfons Pomp, MD, FRCSC, FACS Professor of Surgery, Department of Surgery, Weill Cornell Medical College, New York, NY, USA

Erik Popp, MD Department of Anesthesiology, University of Heidelberg,Heidelberg, Germany

Tony M. Rahman, MD, BMBCh, MA DIC, PhD, FRCP Consultant Gastroenterologist and ICU Physician, Departments of Intensive Care and Gastroenterology, St. George’s Hospital, London, UK

Sundara K. Rengasamy, MD Cardio Thoracic and Vascular Anesthesiologist, Department of Anesthesiology, Boston University, Boston, MA, USA

Andrew Rhodes, FRCP, FRCA Department of Intensive Care Medicine, St. George’s Hospital, London, UK

Emanuel P. Rivers, MD, MPH Vice Chairman and Research Director, Department of Emergency Medicine and Surgery, Henry Ford Hospital, Detroit, MI, USA

Peter Rock, MD, MBA, FCCM Professor and Martin Helrich Chairman of Anesthesiology, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, ML, USA

Gerardo Rodriguez, MD Resident, Department of Anesthesiology, Boston Medical Center, Boston University, Boston, MA, USA

Michael S. Rosenblatt, MD, MPH, MBA, FACS Clinical Associate Professor of Surgery, Tufts University School of Medicine;Director, Trauma Service, Lahey Clinic Medical Center, Burlington, MA, USA

William H. Rosenblatt, MD Professor of Anesthesiology, Yale University School of Medicine, New Haven, CT, USA

Susan E. Schaefer, MS, RD, CNSD Nutrition Support Specialist, Department of Nutrition Service, Lahey Clinic Medical Center, Burlington, MA, USA

Andreas Schneider Department of Anesthesiology and Postoperative Intensive Care Medicine, University of Cologne, Cologne, Germany

Shimul A. Shah, MD Assistant Professor of Surgery, Department of Surgery, University of Massachusetts Medical School, Worcester, MA, USA

xxi

xxii Contributors

Elizabeth H. Sinz, MD Professor of Anesthesiology and Neurosurgery, Medical Director, Simulation Development and Cognitive Science Laboratory, Department of Anesthesiology, Penn State Milton S. Hershey Medical Center, The Pennsylvania State University College of Medicine, Hershey, PA, USA

Vadivelu Sivaraman, MD, MBBS Assistant Professor, Anesthesiology and Critical Care, Department of Anesthesiology, University of Maryland Medical System, Baltimore, MD, USA

Claudia Spies, MD Professor, Department of Anesthesiology and Intensive Care Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany

Glynne D. Stanley, MD, MB, ChB, FRCA Chairman, Department of Anesthesia, North Shore Medical Center, Salem, MA, USA

Michael Sugrue, MB BCh, BAO, MD, FRCSI FRACS Department of Surgery, Letterkenny General and Galway University Hospitals, Letterkenny General Hospital, Letterkenny, Donegal, Ireland

Alexis Tabah, MD Medical Intensive Care Medicine, Michallon Teaching Hospital, La Tronche, France

Pouneh Taghizadeh, MD Department of Anesthesiology, Boston University Medical Center, Boston, MA, USA

Rodney J. Taylor, MD Director of Kidney/Pancreas Transplant, Department of Surgery, University of Massachusetts Medical School, Worcester, MA, USA

Dan R. Thompson, MD, MA Professor of Surgery and Anesthesiology, Department of Surgery, Alden March Bioethics Institute, Albany Medical College, Albany, NY, USA

Sam J. Thomson, MBBS, MRCP Clinical Research Fellow, Department of Gastroenterology, St. George’s Hospital, London, UK

Nicholas P. Tsapatsaris, MD Associate Section Head, Department of Cardiovascular Medicine, Lahey Clinic Medical Center, Burlington, MA, USA

Albert J. Varon, MD Professor and Vice Chairman for Education, Department of Anesthesiology, University of Miami Miller School of Medicine, Jackson Memorial Hospital, Miami, FL, USA

Bala Venkatesh, MBBS, MD, FRCA, FFARCSI, FJFICM Professor, Critical Care Endocrinology and Metabolism Research Unit, Division of Anesthesiology and Critical Care, Princess Alexandra and Wesley Hospitals, University of Queensland, Brisbane, Queensland, Australia

Wickii T. Vigneswaran, MD, FACS, FRCSC, FRCS(CTh) Professor of Surgery, Associate Chief of Cardiac and Thoracic Surgery, Director of Lung and Heart-Lung Transplantation, Department of Surgery, University of Chicago Hospitals, University of Chicago, Chicago, IL, USA

xxii

Contributors xxiii

Hector Vilca-Melendez, MD, PhD Institute of Liver Studies, King’s College Hospital, King’s College London, London, UK

Andrew G. Villanueva, MD Chairman, Department of Pulmonary and Critical Care Medicine,Lahey Clinic Medical Center, Burlington, MA, USA

Julia Wendon, MBChB, FRCP Institute of Liver Studies, King’s College Hospital, King’s College London, London, UK

Bruno Zawadzki, MD

Nikolaos Zias, MD Research Fellow, Department of Pulmonary and Critical Care Medicine, Lahey Clinic Medical Center, Burlington, MA, USA

Janice L. Zimmerman, MD Professor of Clinical Medicine, Weill Cornell Medical College, Head, Critical Care Division, Department of Medicine, Director of MICU, The Methodist Hospital, Houston, TX, USA

xxiii

Part IResuscitation and General Topics

1Supplemental Oxygen TherapyAndrew G. Villanueva

Intensivists caring for critically ill patients in a surgical intensive care unit continually face multiple diverse and challenging problems. While the specific disease processes in these patients are myriad, a fundamental goal is to provide adequate cellular respiration and thereby maintain sufficient tissue oxygenation and normal organ function. Successful cellular respiration depends on the maintenance of several factors, including ade-quate alveolar ventilation, a functioning gas-exchange surface, the capacity to transport oxygen to the tissue, and intact tissue respiration (the mitochondrial cytochrome oxidase system). Subsequent chapters in this textbook describe problems with each of these factors and how intensivists should approach and manage them. This chapter focuses on alveolar ventila-tion and how to use supplemental oxygen therapy to improve arterial oxygenation in patients who are hypoxemic but do not require mechanical ventilation.

Pathophysiology of Hypoxemia

Hypoxemia is defined as a relative deficiency of oxygen in the arterial blood as measured by arterial oxygen tension (PaO

2).

Hypoxia is defined as inadequate oxygen tension at the cellular level. Currently, there is no way for clinicians to directly measure hypoxia and the diagnosis must be made indirectly based on the assessment of organ function, oxygen delivery, and mixed venous oxygen tension. Hypoxemia and hypoxia are therefore not syn-onymous—patients may have hypoxia without hypoxemia, but patients cannot have sustained severe hypoxemia without devel-oping hypoxia. It is thus imperative to promptly treat patients who have significant hypoxemia with supplemental oxygen.

The PaO2 is determined by the inspired oxygen tension, the

alveolar ventilation, and the distribution of ventilation and perfusion (V/Q) in the lungs. The five major mechanisms of

hypoxemia are (1) decreased ambient fraction of inspired oxygen (FiO

2), (2) alveolar hypoventilation, (3) diffusion lim-

itation across the alveolar-capillary membrane, (4) shunt, and (5) V/Q mismatch1. Decreased ambient FiO

2 is generally not a

cause, unless the altitude is very high.Pure alveolar hypoventilation in critically ill patients is

often related to drug overdose; the excess use of medications that suppress the respiratory drive such as opiates or benzodi-azepines; or catastrophic events of the central nervous system such as head trauma, stroke, subarachnoid hemorrhage, sub-dural hematoma, or cerebral edema. The hypoxemia is caused by a decrease in the alveolar oxygen tension (P

AO

2), which can

be measured using the alveolar gas equation:

PAO

2 = F

IO

2 (PB – 47) – PaCO

2/R

where FIO

2 is the fraction of inspired oxygen (expressed as a

decimal), (PB – 47) is the barometric pressure minus water vapor pressure, PaCO

2 is the arterial carbon dioxide tension,

and R is the respiratory quotient (usually 0.8). Clinically, hypoventilation results in a decreased PaO

2 and an elevated

PaCO2. With hypoventilation, however, the alveolar-arterial

oxygen gradient ([A-a]O2) and the arterial-alveolar ratio

(PaO2/P

AO

2) are normal (2.5 + [0.21 x age] mmHg, and 0.77-

0.82, respectively). Diffusion limitation across the alveolar-capillary membrane, shunt, and V/Q mismatch all cause an abnormal [A-a]O

2 and PaO

2/P

AO

2.

Diffusion limitation across the alveolar-capillary mem-brane can be caused by pulmonary edema fluid or interstitial fibrotic tissue between the alveolar epithelium and the cap-illary endothelium. This impaired oxygen exchange is wors-ened as blood transit time through the pulmonary capillaries decreases, such as during exercise. Arterial hypoxemia sec-ondary to diffusion defects is not common but is responsive to an increase in P

AO

2 using supplemental oxygen therapy.

Pathophysiology of Hypoxemia ..................................................................................... 3

Goals of Supplemental Oxygen Therapy ....................................................................... 4

Oxygen Delivery Systems .............................................................................................. 4

Bedside Monitoring of Oxygenation ............................................................................. 9

Complications of Oxygen Therapy ................................................................................ 10

J.M. O’Donnell and F.E. Nácul (eds.), Surgical Intensive Care Medicine, 3DOI 10.1007/978-0-387-77893-8_1, © Springer Science + Business Media, LLC 2010

4 A.G. Villanueva

True shunt occurs when right-heart blood enters the left heart without an increase in oxygen content because the blood does not interact with alveolar gas (zero V/Q). The shunt can be intracardiac (e.g., atrial septal defect, patent foramen ovale) or intrapulmonary. Causes of intrapulmonary shunting include alveolar collapse, which occurs with acute lung injury or acute respiratory distress syndrome (ARDS); complete lobar col-lapse due to retained respiratory secretions; pulmonary arterial-venous malformations; and pulmonary-capillary dilatation, as is sometime seen in liver disease (the so-called “hepatopulmo-nary syndrome”).2 Oxygen therapy is of limited benefit with significantly increased shunt because, regardless of the F

IO

2,

oxygen transfer cannot occur when blood does not come into contact with functional alveolar units. Therefore, true shunt pathology is refractory to oxygen therapy. The shunt, however, can be improved if the cause is lobar or alveolar collapse. Lobar lung collapse can often be reversed with appropriate bronchial hygiene or removal of the source of obstruction. Alveolar col-lapse resulting from destabilization of the alveolar architecture due to disruption of the surfactant layer, such as with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), can improve with the use of positive end expiratory pressure (PEEP), but this requires mechanical ventilation.

V/Q mismatch is defined as an imbalance between alveo-lar ventilation and pulmonary capillary blood flow. A detailed explanation of why V/Q mismatch results in hypoxemia is beyond the scope of this chapter, but this mechanism is believed to be the most common cause of hypoxemia.3,4 V/Q mismatch-ing can result from an array of disorders such as bronchospasm, chronic obstructive pulmonary disease (COPD), bronchial secretions, mild pulmonary edema, interstitial lung disease, venous thromboembolism, pleural effusion, pulmonary contu-sion, aspiration of gastric contents, and pneumonia, to name just a few. The hallmark of hypoxemia due to V/Q mismatch is that it improves with oxygen therapy. In contrast to shunt, an increase in the F

IO

2 causes a substantial increase in PaO

2.

Goals of Supplemental Oxygen Therapy

In general, the purpose of oxygen therapy is to correct hypox-emia by achieving a PaO

2 > 60 mmHg or an arterial oxygen

saturation of > 90%.5 Little additional benefit is gained from further increases because of the functional characteristics of hemoglobin (Fig. 1.1). Different criteria are used for patients with COPD and chronic carbon dioxide retention. In these patients, values that define hypoxemia are PaO

2 of 50 to 55

mmHg, corresponding to an arterial oxygen saturation 88% to 90%.6 These target values for PaO

2 or arterial oxygen satu-

ration assume the presence of normally functioning hemo-globin. In situations with abnormal hemoglobins that cannot effectively bind oxygen, such as methemoglobinemia or car-bon monoxide poisoning, even supranormal PaO

2 values may

be associated with a reduction in available hemoglobin and resultant lower oxygen content.7,8,9

Other indications for oxygen therapy include suspected hypoxemia, acute myocardial infarction, severe trauma, and postoperative recovery from anesthesia.5 Early clinical findings associated with hypoxemia include tachycardia, tachypnea, increased blood pressure, restlessness, disorientation, headache, impaired judgment, and confusion. Some patients may become euphoric and lack the classic signs and symptoms of hypox-emia. Severe hypoxemia is associated with slow, irregular respi-rations, bradycardia, hypotension, convulsions and coma.

Oxygen Delivery Systems

Oxygen delivery systems can be classified as low-flow (or vari-able-performance) and high-flow (or fixed performance) sys-tems. Low-flow systems provide small amounts of 100% oxygen as a supplement, with F

IO

2 determined by the patient’s pattern

of breathing and minute ventilation. The greater portion of the inspired volume is obtained from room air. High-flow systems, on the other hand, are designed to supply premixed oxygen in volumes that provide the patient’s total ventilatory requirements. An advantage of high-flow systems is that the level of F

IO

2

remains constant regardless of any changes that may occur in the ventilatory pattern.10 In this section these two types of oxygen

Fig. 1.1. The normal oxyhemoglobin dissociation curve for humans. The reversible chemical reaction between O

2 and hemoglobin is

defined by the oxyhemoglobin equilibrium curve, which relates the percent saturation of hemoglobin to the PaO

2. Because of the char-

acteristic sigmoid shape, the affinity for O2 progressively increases

as successive molecules of O2 combine with hemoglobin. There are

physiologic advantages in that the flat upper portion allows arterial O

2 content to remain high and virtually constant (>90%) despite

fluctuations in arterial PaO2 (60-100 mmHg), and the middle steep

segment enables large quantities of O2 to be released at the PaO

2 pre-

vailing in the peripheral capillaries. Illustrations by Paul Singh-Roy reprinted from the Journal of Critical Illness Vol. 4, No. 6 June 1989 with permission from CMP Medica.

1. Supplemental Oxygen Therapy 5

delivery systems will be discussed, as well as delivery systems for helium-oxygen gas mixtures and for oxygen via positive pressure devices using a mask device instead of an endotracheal tube—so-called non-invasive ventilation (NIV).

Low-Flow Systems

Low-flow oxygen devices are the most commonly used because of their simplicity and ease of use, healthcare providers’ famil-iarity with the system, low cost, and patient acceptance.

Nasal Cannula

The most frequently used low-flow oxygen delivery system con-sists of a pronged nasal cannula to deliver 100% oxygen at flow rates of 0.5 to 6 L/min, delivering an F

IO

2 ranging from 0.24

to 0.40. Patients generally cannot tolerate an oxygen flow rate of more than 6 L/min from the nasal cannula because of nasal discomfort. If the oxygen flow rate exceeds 4 L/min, the gases should be humidified to prevent drying of the nasal mucosa. As a rule, F

IO

2 increases by approximately 0.03 to 0.04 for each

increase of 1 L/min in the oxygen flow rate, up to about 0.40 at 6 L/min (Table 1.1). However, in clinical practice this rule of thumb cannot be applied with confidence, because of varia-tions in individual patients’ breathing patterns. To be effective, the patient’s nasal passages must be patent to allow filling of the anatomic reservoir. The patient, however, does not need to breathe through the nose, because oxygen is entrained from the anatomic reservoir even in the presence of mouth breathing.

The nasal cannula is advantageous because of the com-fort and convenience it affords—the patient may eat, speak, and cough with it in place. Except for irritation of the nasal mucosa at higher flow rates and an occasional reaction to chemical components of the tubing, cannulas are well tolerated.

The physiologic disadvantage of cannula use is that FIO

2 varies

with the patient’s breathing pattern, and calculations requiring accurate F

IO

2 data cannot be made. In most patients with mild

hypoxemia, precise knowledge of FIO

2 is unnecessary and

clinical improvement occurs rapidly.

Simple Face Mask

A simple oxygen mask is a low-flow system that delivers approximately 35% to 50% oxygen at flow rates of 5 L/min or greater. The mask provides a reservoir (100 to 200 mL) next to the patient’s face to increase the fraction of oxygen in the tidal volume. The open ports in the sides of the mask allow entrainment of room air and venting of exhaled gases. Because the mask fits over the nose and mouth, the volume it contains may increase ventilatory dead space; flow rates of 5 L/min or greater are required to keep the mask flushed.11 Flow rates greater than 8 L/min do not increase the F

IO

2 signifi-

cantly above 0.6 (Table 1.1). The disadvantages of using this device include the resultant variable F

IO

2 and the fact that it

must be removed for eating or drinking.

Partial-Rebreathing Mask

Partial rebreathing and nonrebreathing masks with 600- to 1,000-mL reservoir bags (Fig. 1.2) can deliver high inspired

Table 1.1. Flow rates and FIO

2 with low-flow oxygen-delivery devices.

Predicted FIO

2 values for low-flow systems assume a normal and

stable pattern of ventilation.12

Low-flow system Oxygen flow rates (L) FIO

2

Nasal cannula 1 0.242 0.283 0.324 0.365 0.406 0.44

Simple fa ce mask 5-6 0.406-7 0.507-8 0.60

Partial-rebreathing mask 6 0.607 0.708 0.809 0.80+10 0.80+

Nonrebreathing mask 10 0.80+15 0.90+

Fig. 1.2. Rebreathing mask with reservoir bag.

6 A.G. Villanueva

oxygen concentrations of greater than 50% with low flow rates.6 In partial rebreathing masks, the first one-third of the patient’s exhaled gas fills the reservoir bag (Fig. 1.3). Because this gas is primarily from anatomic dead space, it contains little carbon dioxide. With the next breath, the patient inhales a mixture of the exhaled gas and fresh gas. If the fresh gas flows are equal to or greater than 8 L/min and the reservoir bag remains inflated throughout the entire respiratory cycle, adequate carbon dioxide evacuation and the highest possible F

IO

2 should occur (Table 1.1).

The rebreathing capacity of this system allows some degree of oxygen conservation, which may be useful while transporting patients with portable oxygen supplies.12

Nonrebreathing Mask

A nonrebreathing mask is similar to a partial-rebreathing mask but with the addition of three unidirectional valves (Fig. 1.4). Two of the valves are located on opposite sides of the mask; they permit venting of exhaled gas and prevent entrainment of room air. The remaining unidirectional valve is located between the mask and the reservoir bag and pre-vents exhaled gases from entering the fresh gas reservoir. As with the partial-rebreathing mask, the reservoir bag should be inflated throughout the entire ventilatory cycle to ensure

adequate carbon dioxide clearance from the system and the highest possible F

IO

2.12 Because its bag is continuously filled

with 100% oxygen and expired gases do not enter the reservoir, the tidal volume should be nearly 100% oxygen (Table 1.1). To avoid air entrainment around the mask and dilution of the delivered FIO

2, masks should fit snugly on the face, but exces-

sive pressure should be avoided. If the mask is fitted properly, the reservoir bag should partially deflate and inflate with the patient’s inspiratory efforts.

The disadvantages of high FIO

2 masks include the risk of

absorption atelectasis and the potential for oxygen toxicity if they are used for longer than 24 to 48 hours. Therefore, these masks are only recommended for short-term treatment. Critically ill patients with profound hypoxemia usually require ventilatory assistance as well, because pure hypoxic respiratory failure rarely occurs without concomitant or subsequent ventilatory failure.

Tracheostomy Collars

Tracheostomy collars primarily are used to deliver humid-ity to patients with artificial airways. Oxygen may be deliv-ered with these devices, but as with other low-flow systems the F

IO

2 is unpredictable, inconsistent, and depends on the

patient’s ventilatory pattern.

Fig. 1.3. Partial-rebreathing mask. The mask captures the first portion of exhaled gas (dead-space gas) in the reservoir bag. The remainder of the reservoir bag is filled with 100 percent oxygen. Reprinted from Shapiro BA, Kacmarek RM, Cane RD, et al. Clinical application of respiratory care. 4th edition. St. Louis: Mosby Year Book 1991 with permission from Elsevier.

Fig. 1.4. Nonrebreathing mask. The one-way valves of the nonre-breathing mask prevent expired gases from reentering the reservoir bag. The tidal volume with this device should be nearly 100% oxy-gen. Reprinted from Shapiro BA, Kacmarek RM, Cane RD, et al. Clinical application of respiratory care. 4th edition. St. Louis: Mosby Year Book 1991 with permission from Elsevier.

1. Supplemental Oxygen Therapy 7

High-Flow Systems

In contrast to low-flow systems, high-flow systems are designed to deliver a large volume of premixed gas. Because the patient is breathing only gas applied by the system, the flow rate must exceed the patient’s minute ventilation and meet the patient’s peak inspiratory demand. The advantages of a high-flow system include the ability to deliver relatively precise oxygen concentrations, control the humidity and tem-perature of the inspired gases, and maintain a fixed inspired oxygen concentration despite changes in the ventilatory pattern.

Air-entrainment (Venturi) Mask

Air-entrainment masks (Fig. 1.5), commonly called “Venturi masks,” entrain air using the Bernoulli principal and con-stant pressure-jet mixing.13 A jet of oxygen is forced through a small opening that because of viscous shearing forces cre-ates a subatmospheric pressure gradient downstream relative to the surrounding gases (Fig. 1.6). The proportion of oxy-gen can be controlled by enlarging or reducing the size of the injection port. A smaller opening creates greater pressure of oxygen flow, resulting in more room air entrained and a lower percentage of inspired oxygen. As the desired F

IO

2

increases, the air-to-oxygen-entrainment ratio decreases with a net reduction in total gas flow. Therefore, the probability of

Fig. 1.5. Air-entrainment (Venturi) mask.

Fig. 1.6. Air-entrainment (Venturi) mask and the Bernoulli principal. A jet of oxygen is forced through a small opening, which creates a low-pressure area around it and entrains ambient air. The propor-tion of oxygen can be controlled by enlarging or reducing the size of the injection port. A smaller opening creates pressure of oxygen flow, resulting in more room air entrained and a lower percentage of inspired oxygen. Illustrations by Paul Singh-Roy reprinted from The Journal of Critical Illness Vol. 4, No. 6 June 1989 with permission from CMP Medica.

the patient’s ventilatory needs exceeding the total flow capa-bilities of the device increases with higher F

IO

2 settings.12

Occlusion of or impingement on the exhalation ports of the mask can cause back-pressure and alter gas flow. The oxygen-injector port also can become clogged, especially with water droplets. Aerosol devices should therefore not be used with Venturi masks; if humidity is necessary, a vapor-type humidi-fier should be used.12

The major indication for the use of Venturi masks is the need for precise control of the F

IO

2 between 0.24 and 0.40

when providing oxygen therapy to patients with COPD who are hypercarbic (Table 1.2). For patients with COPD who have a PaCO

2 greater than 45 mmHg, it is generally recom-

mended that the FIO

2 be low initially (0.24 to 0.28) and then

adjusted upward to maintain an oxygen saturation of 88% to 90%. Using devices that deliver a high F

IO

2 to patients with

8 A.G. Villanueva

COPD and elevated PaCO2 can result in a high PaO

2, which

can lead to further elevations in PaCO2 and worsening respira-

tory acidosis. (See “Complications of Oxygen Therapy.”)

Aerosol Mask

An FIO

2 greater than 0.40 with a high-flow system is best

provided with a large-volume nebulizer and wide-bore tub-ing. Aerosol masks, in conjunction with air-entrainment nebulizers or air/oxygen blends, can deliver a consistent and predictable F

IO

2 regardless of the patient’s ventilatory

pattern. An air-entrainment nebulizer can deliver an FIO

2 of

0.35 to 1.0, produce an aerosol, and generate flow rates of 14 to 16 L/min. Air/oxygen blenders can deliver a consis-tent F

IO

2 ranging from 0.21 to 1.0, with flows up to 100 L/

min. These devices are generally used in conjunction with humidifiers.12

Helium-Oxygen Therapy

There are situations in which it may be beneficial to combine oxygen with a gas other than nitrogen. Helium and oxygen, for instance, can be combined to form a therapeutic gas mixture known as “heliox.” Heliox reduces the density of the delivered gas, thereby reducing the work of breathing and improving ven-tilation in the presence of airway obstruction.15,16,17 When there is airflow obstruction due either to an obstructing lesion in the central airways or narrowing of the peripheral airways from bronchospasm, turbulent flow of the airway gases predominates over the usual laminar flow. Turbulent flow requires a greater driving pressure than laminar flow does and is inversely pro-portional to the density of the gas being inspired. Clinically, a 60:40 or 70:30 ratio of helium to oxygen is generally recom-mended. The combination is administered through a well-fitted nonrebreathing mask with a complete set of one-way valves. The reported clinical benefits of administering heliox to patients with severe asthma include improved ventilation, avoidance of mechanical ventilation, decreased paradoxical pulse, and increased peak expiratory flow rates.18,19 Because the benefits of heliox dissipate if the ratio for helium to oxygen is less than

60:40, it should not be used if a high FIO

2 is required to treat the

patient’s hypoxemia.

Noninvasive Ventilation

All of the oxygen delivery devices previously mentioned are used in patients who are spontaneously breathing and require no assisted ventilation. The use of mechanical venti-lation via an endotracheal tube to treat patients with hypox-emic or hypercarbic respiratory insufficiency are described elsewhere in this text. Oxygen also can be delivered using mechanical ventilators via a mask strapped to the patient’s face, without the need for tracheal intubation. The mask can either be a nasal mask, which fits snugly around the nose, or a full facial mask, which covers both the nose and mouth. Success for this mode of oxygen delivery depends in large part on the patient’s acceptance and tolerance to the tight-fitting mask (Fig. 1.7).

Continuous Positive Airway Pressure (CPAP)

A continuous positive pressure is delivered throughout the respiratory cycle, either by a portable compressor or from a

Table 1.2. Air entrainment ratios and total gas outflows of com-mercially available Venturi masks.14

O2 concentration

of delivered gasLiters of air entrained per liter O

2

Total gas outflow (liter/min)

24 25.3 105(DF=4)28 10.3 68 (DF=6)31 6.9 63 (DF=8)35 4.6 56 (DF=10)40 3.2 50 (DF=12)50 1.7 33 (DF=12)

DF, highest driving flow of oxygen, in liters per minute, recommended by the manufacturer for a given concentration. In general, the highest driving flow should be used to provide the highest total gas outflow.

Fig. 1.7. Full-face mask used for noninvasive positive pressure ventilation.

1. Supplemental Oxygen Therapy 9

flow generator in conjunction with a high-pressure gas source. Oxygen can be delivered by attaching a low-flow system to the mask or by adjusting the F

IO

2 delivered by the mechani-

cal ventilator. The major use of CPAP, particularly when deliv-ered by a nasal mask, is to treat obstructive sleep apnea. It does, however, also have a role in the critically ill patient because it can improve oxygenation by opening collapsed alveoli and reduce the work of breathing by increasing functional residual capacity, thus moving the patient onto the more compliant por-tion of the pressure volume curve.20,21,22 Mask CPAP is also an effective treatment for cardiogenic pulmonary edema, because positive intrathoracic pressure reduces both cardiac preload and afterload; it has been shown to decrease the need for intuba-tion.23,24,25 Typically, pressures of 5 to 15 cm H

2O of CPAP are

applied, depending on the effect on oxygenation and patient comfort. Mask CPAP can only be used in patients who are breathing spontaneously, and is contraindicated in those who are hypoventilating. For these patients, noninvasive ventilation (NIV) may be a treatment option. Indeed, some recent studies comparing mask CPAP and NIV in the treatment of cardiogenic pulmonary edema showed that while both modalities reduced intubation rates26, there may be more rapid improvement in gas exchange with NIV than with CPAP alone.27,28 NIV may there-fore be preferable for patients with persisting dyspnea or hyper-capnia after the initiation of mask CPAP.

Noninvasive Ventilation (NIV)

NIV is defined as the delivery of mechanically assisted or gen-erated breaths without placement of an artificial airway (endo-tracheal or tracheostomy tube). The benefits are similar to those of mechanical ventilation delivered through an artificial airway without the risks associated with endotracheal intubation, includ-ing the risk of ventilator-associated pneumonia. As with mask CPAP, oxygen can be delivered via a low-flow device attached to a nasal or full facial mask, or by adjusting the F

IO

2 delivered

by the mechanical ventilator. Several early studies of NIV in acute respiratory failure used volume-controlled ventilators, but most clinical trials have been performed with pressure-controlled ventilation, delivered either in the pressure support mode or with bi-level positive airway pressure ventilation.29 Bi-level positive airway pressure ventilation delivers both inspiratory pressure support and an expiratory pressure. “BiPAP” refers to a specific bi-level positive airway pressure ventilator manufactured by the Respironics Corporation, which has been used in some trials. The term BiPAP is often erroneously used interchangeably with bi-level positive airway pressure ventilation, which can also be delivered by most conventional ventilators.

Prospective, randomized, controlled trials over the last two decades have shown that the technique is efficacious in the treat-ment of many forms of acute respiratory failure. There is strong evidence for its use in COPD exacerbations30,31,32, acute cardio-genic pulmonary edema33, immunocompromised patients, and for the facilitation of weaning in COPD patients.34,35,36 Recent reviews on the use of NIV for COPD exacerbations have

summarized the benefits of reduced intubation rate, mortality, and hospital length of stay37,38 and suggest that the use of NIV in many of these patients should be the standard of care.39 NIV produces few complications other than local damage related to pressure effects of the mask and straps.40 Cushioning the forehead and the bridge of the nose before attaching the mask can decrease the likelihood of these problems. Mild gastric dis-tention occurs with some frequency but is rarely significant at routinely applied levels of inspiratory pressure support (10-25 cm H

2O), and the routine use of a nasogastric tube is not war-

ranted. Ocular irritation and sinus pain or congestion may occur and require lower inspiratory pressure or the use of a face mask rather than a nasal mask.

Bedside Monitoring of Oxygenation

As mentioned previously, the purpose of oxygen therapy is to correct hypoxemia by achieving a PaO

2 > 60 mmHg or an

arterial oxygen saturation > 90%.5 The readily available tools to measure oxygenation of arterial blood are arterial blood gas analysis and pulse oximetry.

Arterial Blood Gas Analysis

Arterial blood gas analysis allows the intermittent, direct mea-surement of pH, PaO

2, PaCO

2, and O

2 saturation of hemoglobin

in arterial blood. While oxygenation cannot be continuously monitored with this method, the measurement of pH and PaCO

2

helps determine a patient’s acid-base status and the adequacy of the alveolar ventilation, because the PaCO

2 is inversely pro-

portional to the alveolar ventilation. Arterial blood gas analysis also allows a more sensitive means to detect subtle degrees of hypoxemia, compared with pulse oximetry. By knowing the F

IO

2 being administered to the patient and the patient’s PaCO

2

and PaO2, the alveolar gas equation can be used to measure

the alveolar-arterial oxygen gradient (see “Pathophysiology of Hypoxemia”). The normal (A-a)O

2 gradient varies with age and

ranges from 7 to 14 mmHg when the patient is breathing room air; the gradient increases in cases of diffusion impairment, right-to-left shunt, and V/Q mismatch. The following equation can be used to estimate the expected (A-a)O

2 gradient41:

(A-a)O2 = 2.5 + 0.21 x age in years

Measurement of the (A-a)O2 is most useful when the patient is

breathing room air, because it increases with higher inspired oxy-gen concentrations.42 Another useful index for measuring arterial oxygenation is the ratio of PaO

2 to P

AO

2 (PaO

2/P

AO

2), which also

can be calculated using data from arterial blood gas measure-ments.43,44 The lower limit of normal PaO

2/P

AO

2 is 0.77 to 0.82.43

Pulse Oximetry

The use of pulse oximetry is now considered the standard of care when monitoring patients being treated for hypoxemia.

10 A.G. Villanueva

It is noninvasive, inexpensive, and simple, and requires only the placement of a probe on a finger, toe, or ear. The conve-nience of pulse oximetry measurements may improve patient monitoring and reduce the number of samples that must be obtained for arterial blood gas analysis. However, PaO

2 and

arterial oxygen saturation (SaO2) should always be measured

directly via arterial blood gas analysis at the inception of pulse oximetry monitoring of critically ill patients. SaO

2 is mea-

sured by CO-oximetry, a technique that quantifies four species of hemoglobin in arterial blood: oxyhemoglobin, deoxyhe-moglobin, carboxyhemoglobin, and methemoglobin.45 Pulse oximeters can detect only two hemoglobin species: oxyhemo-globin and deoxyhemoglobin.46,47,48

The pulse oximeter functions when any pulsating arterial vascular bed is positioned between a dual-wavelength light-emitting diode (LED) and a detector. The LED emits red light (wavelength, 660 nm) and infrared light (wavelength, 900 to 940 nm). As the pulsating bed expands and relaxes, it creates a change in the length of the light path, modifying the amount of light detected. A plethysmographic waveform results. Pho-todiodes are switched on and off several hundred times per second by a microprocessor, while the photodetector records changes in the amount of red and infrared light absorbed. The pulsatile component (reflecting absorption by pulsatile arte-rial blood) is divided by the baseline component (reflecting absorption by nonpulsatile arterial blood, venous and capil-lary blood, and tissue) for both wavelengths. Ratios are used to obtain a signal that is related to saturation.46,47,48

Pulse oximetry has been shown to be accurate to within 3% to 4% in the range of 70% to 100% saturation.49 Loss of pulsa-tion, which can occur with hypotension, hypothermia, or vaso-constriction, causes a loss of signal. Because pulse oximetry is dependent on perfusion, it works well during primary respira-tory arrest but is unreliable during cardiac arrest. Pulse oxi-metry is more accurate in light-skinned than in dark-skinned patients. For light-skinned patients, a less conservative target SaO

2 of 90% to 92% is recommended for oxygen titration.

For dark-skinned patients, a target value of 95% should be adequate.50

Carbon monoxide is not detected by pulse oximetry, so that pulse oximetry overestimates oxygen saturation in patients who have been exposed to smoke or who actively smoke cigarettes. Pulse oximetry is also inaccurate in the presence of methemoglobinemia, which results from expo-sure to chemicals or drugs (such as dapsone, benzocaine, nitrates, and sulfonamides) that oxidize the iron in hemo-globin of susceptible patients from its ferrous to its ferric state.49 Oxyhemoglobin absorbs more light at 940 nm than at 660 nm, reduced hemoglobin has the opposite property, and methemoglobin absorbs light equally at both wavelengths. These facts underlie the miscalculation of oxygen saturation in the presence of methemoglobin. When light absorption at both wavelengths is equal, the pulse oximeter records an oxygen saturation of 85%. Therefore, increasing levels of methemoglobin cause the pulse oximetry reading to gravitate

toward 85%. If the actual oxygen saturation of a patient with methemoglobinemia is over 85%, the pulse oximeter under-estimates it; if it is less than 85%, the pulse oximeter over-estimates it.49

Despite these potential problems, pulse oximetry is extremely useful when monitoring hypoxemic patients being treated in the intensive care unit. It should be remembered that the tech-nique does not assess arterial pH or PaCO

2 and that marked

changes in PaO2 can occur with only modest changes in SaO

2

if the latter is above 90%. Pulse oximetry, therefore, does not eliminate the need for arterial blood gas determinations in acutely ill patients.

Complications of Oxygen Therapy

While the benefits of supplemental oxygen therapy for hypox-emic patients heavily outweigh the risks in most cases, there are potential problems of which the intensivist should be aware.

Worsening Acute on Chronic Respiratory Acidosis

Acute respiratory failure in patients with COPD is charac-terized by increased PaCO

2 and severe hypoxemia. When

oxygen is administered to these patients, their PaCO2 lev-

els commonly increase.51,52 Hypothesized mechanisms for oxygen-induced hypercarbia include a decrease in minute ventilation caused by removal of the hypoxic stimulus53,54, increased V/Q inequality in the lung caused by release of hypoxic vasoconstriction55,56,57, and the effect of oxygen on the hemoglobin-carbon dioxide dissociation curve of blood56, the so-called “Haldane effect.” There is still ongo-ing debate as to which of these mechanisms is most impor-tant58,59 in causing the hypercarbia, but it is now accepted that supplemental oxygen does not cause these patients to “stop breathing.”60 If worsening respiratory acidosis occurs with the initiation of oxygen therapy in a patient with severe hypoxemia, treatment choices include decreasing the F

IO

2

to achieve a lower but acceptable SaO2, noninvasive positive

pressure ventilation to improve oxygenation while maintain-ing a satisfactory minute ventilation, and tracheal intubation for assisted ventilation.

Absorption Atelectasis

Absorption atelectasis occurs when high alveolar oxygen concentrations cause alveolar collapse. Ambient nitrogen, an inert gas, remains within the alveoli and splints alveoli open. When a high FIO2 is administered, nitrogen is “washed out” of the alveoli, and the alveoli are filled primarily with oxygen. In areas of the lung with reduced V/Q ratios, oxygen is absorbed into the blood faster than ventilation can replace it. The affected alveoli then become progressively smaller until they reach the critical volume at which surface-tension forces cause alveolar collapse. This problem is most frequently

1. Supplemental Oxygen Therapy 11

encountered in spontaneously breathing patients who are given oxygen in concentrations greater than 0.70.

Oxygen Toxicity

A high FIO

2 level can be injurious to the lungs. The mecha-

nism of oxygen toxicity is related to a significantly higher production rate of oxygen free radicals such as superoxide anions, hydroxyl radicals, hydrogen peroxide, and singlet oxygen. These radicals affect cell function by inactivating sulfhydryl enzymes, interfering with DNA synthesis, and disrupting the integrity of cell membranes. During period of lung-tissue hyperoxia, the normal oxygen-radical-scavenging mechanisms are overwhelmed, and toxicity results.61,62 The F

IO

2 at which oxygen toxicity becomes important is contro-

versial and varies depending on the animal species, degree of underlying lung injury, ambient barometric pressure, and duration of exposure. In general, it is best to avoid exposure to an F

IO

2 greater than 0.6 for more than 24 hours, if possible.

However, correction of severe hypoxemia takes precedence over the potential of oxygen toxicity.

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