Surgical intensive care medicine 2016

Surgical intensive care medicine 2016 Sách cập nhật những kiến thức mới nhất về hồi sức cấp cứu tổng quát và đặc biệt là hồi sức ngoại khoa. sách cần thiết cho các bác sĩ hồi sức ngoại, bác sĩ cấp cứu và các bác sĩ đa khoa.

Third Edition

1 3

Surgical Intensive Care Medicine

John M O’Donnell • Flávio E Nácul

Editors

Surgical Intensive Care Medicine

Third Edition

Editors

John M O’Donnell, MD

Division of Surgery

Department of Surgical Critical Care

Lahey Hospital and Medical Center

Burlington , MA , USA

Flávio E Nácul, MD, PhD Critical Care Medicine University Hospital Federal University of Rio de Janeiro Surgical Critical Care Medicine Pró-Cardíaco Hospital

Rio de Janeiro , RJ , Brazil

DOI 10.1007/978-3-319-19668-8

Library of Congress Control Number: 2016943138

Springer Cham Heidelberg New York Dordrecht London

© Springer Science+Business Media New York 2001

© Springer Science+Business Media, LLC 2010

© Springer International Publishing Switzerland 2016

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Springer International Publishing AG Switzerland is part of Springer Science+Business Media ( www.springer.com )

me purpose; to my beloved parents, Kay and Frank “Shorty” O’Donnell, who never lost faith; to my mentors, medical students, and residents,

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 Hospital and Medical Center

John M O’Donnell, MD

To my parents Lilian and Jacob, for showing me that possibilities are infi nite;

To my wife Alessandra, for her unconditional love;

To my children Mariana and Rafael, for enriching my life and making

everything worthwhile;

And to my brother Luis and my uncle Sabino, for showing me that medical practice should be guided by kindness, knowledge, ethics, and common sense; with admiration

Flávio E Nácul, MD, PhD

We are honored to present the third edition of Surgical Intensive Care Medicine and we are

very grateful for the enthusiastic reception with which the academic community received the

fi rst two editions Most considered them to be important contributions to the critical care ture Although the basic organization of our new book remains unchanged, being composed of

litera-63 carefully selected chapters divided into 11 parts, the chapters have been largely rewritten to include the many important advances that have been made and the controversies that have arisen over the past few years While the chapters discuss defi nitions, pathophysiology, clinical course, complications, and prognosis, the primary emphasis is devoted to patient management

We have been extremely fortunate to attract a truly exceptional group of contributors, many of whom are nationally and internationally recognized researchers, speakers, and practitioners in the fi eld of critical care medicine An important feature of this edition is the geographical diversity of authors Most are based in the USA but colleagues from Australia, Belgium, Brazil, Canada, Denmark, France, Germany, Italy, The Netherlands, Norway, Portugal, Sweden, and the UK have also made notable contributions The book is written for medical students, residents, fellows, practitioners, and for all health care professionals involved in the care of the critically ill surgical patient We are 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 it is our hope that both our readers and their patients will benefi t

Burlington, MA, USA Rio de Janeiro, RJ, Brazil

We would fi rst like to thank Springer Publishing Company for giving us the opportunity and providing the support necessary to develop the third edition of Surgical Intensive Care Medicine We are forever grateful to Barbara Murphy, Melissa Ramondetta, and Paula Callaghan for helping us with the publications of our fi rst two editions It is diffi cult to ade-quately express our appreciation and thanks to Lorraine Coffey, to whom we are indebted for her assistance, advice, and friendship during the preparation of this present text Without her dedicated help, completion of this project would not have been possible Lastly, we are espe-cially grateful to the many colleagues who helped us by offering recommendations for improv-ing the content and format of our textbook

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

Part I Resuscitation and General Topics

1 Supplemental Oxygen Therapy 3 Andrew G Villanueva , Sohail K Mahboobi , and Sana Ata

2 Airway Management in the Intensive Care Unit 15 Catherine Kuza , Elifçe O Cosar , and Stephen O Heard

3 Vascular Cannulation 37 Monique Espinosa , Shawn E Banks , and Albert J Varon

4 Fluid Resuscitation 47

N E Hammond , M K Saxena , and J A Myburgh

5 Vasopressors and Inotropes 55 Flávio E Nácul

6 Shock 61

Joshua M Glazer , Emanuel P Rivers , and Kyle J Gunnerson

7 Oxygen Transport 81 Michael B Maron

8 Evaluation of Tissue Oxygenation 91 Daniel de Backer and Katia Donadello

9 Hemodynamic Monitoring 99 Flávio E Nácul and John M O’Donnell

10 Acid–Base 109

Paul Elbers , Victor van Bochove , Pieter Roel Tuinman, and Rainer Gatz

11 Analgesia and Sedation 119

Shaan Alli and Ruben J Azocar

12 Neuromuscular Blocking Agents 131

Gerardo Rodríguez , Ruben J Azocar , and Rafael A Ortega

13 Optimisation of the High-Risk Surgical Patient 143

Hollmann D Aya and Andrew Rhodes

14 Cardiopulmonary Resuscitation 153

Andreas Schneider , Erik Popp , and Bernd W Böttiger

Part II Neurocritical Care

15 Management of Closed Head Injury 169

Jason P Rahal , Steven W Hwang , and Peter K Dempsey

16 Spinal Cord Injuries 181

Zarina S Ali and Robert G Whitmore

17 Malignant Ischemic Infarction 195

Bjoern Weiss , Alawi Lütz , and Claudia Spies

Part III Cardiology

21 Management of Perioperative Hypertension 271

Daniela M Darrah and Robert N Sladen

22 Postoperative Myocardial Infarction 283

Glynne D Stanley and Sundara K Rengasamy

23 Postoperative Arrhythmias: Diagnosis and Management 295

Eugene H Chung and David T Martin

Part IV Pulmonary Medicine

24 Acute Respiratory Failure 319

Luca M Bigatello and Rae M Allain

25 Mechanical Ventilation 335

Virginia Radcliff and Neil MacIntyre

26 Fat Embolism Syndrome 349

Patricia Mello , Dimitri Gusmao-Flores , and R Phillip Dellinger

29 Vascular Catheter-Related Bloodstream Infections 389

Donald E Craven and Kathleen A Craven

30 Pneumonia 407

Jana Hudcova , Kathleen A Craven , and Donald E Craven

31 Intra-abdominal Sepsis 427

Reuben D Shin and Peter W Marcello

32 Evaluation of the Febrile Patient in the Intensive Care Unit 437

François Philippart , Alexis Tabah , and Jean Carlet

33 Antimicrobial Use in Surgical Intensive Care 449

Robert A Duncan

Contents

Part VI Hematology

34 Coagulation Abnormalities in Critically Ill Patients 463

Marcel Levi and Steven M Opal

35 Blood Products 473

Leanne Clifford and Daryl J Kor

Part VII Metabolism and Nutrition

36 Hyperglycemia in the Surgical Intensive Care Unit 497

Steven Thiessen , Ilse Vanhorebeek , and Greet Van den Berghe

37 Adrenal Insufficiency 507

Bala Venkatesh and Jeremy Cohen

38 Nutrition Support in Intensive Care 517

Jan Wernerman

Part VIII Nephrology

39 Acute Kidney Injury 529

Rashid Alobaidi and Sean M Bagshaw

Sara A Mansfi eld and Larry M Jones

46 Intra-Abdominal Hypertension and the Abdominal Compartment Syndrome 621

Derek J Roberts , Jan J De Waele , Andrew W Kirkpatrick , and Manu L N G Malbrain

47 Rhabdomyolysis 645

Genevra L Stone , Flávio E Nácul , and John M O’Donnell

48 Postoperative Care of the Cardiac Surgical Patient 653

Joshua C Grimm and Glenn J R Whitman

49 Postoperative Care Following Major Vascular Surgery 669

Elrasheed S Osman and Thomas F Lindsay

50 Postoperative Care After Bariatric Surgery 679

Fredric M Pieracci , Alfons Pomp , and Philip S Barie

51 Care of the Organ Donor 693

Marie R Baldisseri and Younghoon Kwon

52 Postoperative Care of the Heart Transplant Patient 701

Aida Suarez Barrientos , Georgios Karagiannis , and Nicholas R Banner

53 Postoperative Care of the Lung- Transplant Patient 731

Wickii T Vigneswaran and Sangeeta M Bhorade

Part XI Additional Topics

54 Management of the Critically Ill Geriatric Patient 743

Paul E Marik

55 Critical Care Issues in Oncologic Surgery Patients 759

Kunal P Patel , Kaye Hale , and Stephen M Pastores

56 Echocardiography in the Critically Ill 771

Viviane G Nasr , Anam Pal , Mario Montealegre-Gallegos ,

and Robina Matyal

57 Point-of-Care Ultrasound 787

Peter E Croft and Vicki E Noble

58 Scoring Systems and Outcome Prediction 817

Rui P Moreno , Susana Afonso , and Bruno Maia

59 Long-Term Outcomes After Intensive Care 825

Hans Flaatten

60 Ethics in the Intensive Care Unit 837

Dan R Thompson

61 Triage of Surgical Patients for Intensive Care 851

Julia Sobol and Hannah Wunsch

62 Improving the Quality of Care in the ICU 861

Asad Latif , Bradford Winters , Sean M Berenholtz , and Christine Holzmueller

63 Continuing Education in Critical Care Medicine 873

Todd Dorman and Michael C Banks

Index 883

Contents

Susana Afonso , MD Neurointensive Care Unit, Hospital de São José , Centro Hospitalar de

Lisboa Central, E.P.E , Lisbon , Portugal

Zarina S Ali , MD Department of Neurosurgery , Hospital of the University of Pennsylvania ,

Philadelphia , PA , USA

Rae M Allain , MD Department of Anesthesiology, Critical Care, and Pain Medicine, St

Elizabeth’s Medical Center , Tufts University School of Medicine , Boston , MA , USA

Shaan Alli , MD Department of Anesthesiology , Tufts Medical Center , Boston , MA , USA Rashid Alobaidi , MD Department of Pediatrics and Critical Care Medicine, Faculty of Medicine and Dentistry , University of Alberta , Edmonton , Alberta , Canada

Sana Ata , MD Department of Anesthesiology and Interventional Pain Management , Lahey

Hospital and Medical Center , Burlington , MA , USA

Hollmann D Aya , MD, EDIC Adult Intensive Care Directorate, St George’s University

Hospital , NHS Foundation Trust and University of London , London , UK

Ruben J Azocar , MD, FCCM Department of Anesthesiology , Tufts Medical Center , Boston ,

MA , USA

Daniel de Backer , MD, PhD Department of Intensive Care, CHIREC Hospitals , Univerisité

Libre de Bruxelles (ULB) 35 rue Wayez 1420 , Braine L’Alleud , Belgium

Sean M Bagshaw , MD, MSc Department of Critical Care Medicine, Faculty of Medicine

and Dentistry , University of Alberta , Edmonton , AB , Canada

Marie R Baldisseri , MD, MPH, FCCM University of Pittsburgh Medical Center , Pittsburgh ,

PA , USA

Michael C Banks , MD Department of Anesthesiology & Critical Care Medicine , Johns

Hopkins University School of Medicine , Baltimore , MD , USA

Shawn E Banks , MD Department of Anesthesiology , University of Miami Miller School of

Medicine , Miami , FL , USA

Nicholas R Banner , MD, FRCP Harefi eld Hospital , Royal Brompton and Harefi eld Hospital

NHS Foundation , Middlesex , UK

Philip S Barie , MD, MBA, Master CCM, FIDSA, FACS New York-Presbyterian Hospital/

Weill Cornell Medical Center , New York , NY , USA

Aida Suarez Barrientos , MD Royal Brompton and Harefi eld Hospital NHS Foundation ,

Harefi eld Hospital , Middlesex , UK

Sean M Berenholtz , MD MHS FCCM Department of Anesthesiology and Critical Care

Medicine , Johns Hopkins University School of Medicine, Armstrong Institute for Patient

Safety and Quality , Baltimore , MD , USA

Greet Van den Berghe , MD, PhD Clinical Division and Laboratory of Intensive Care

Medicine, Department of Cellular and Molecular Medicine , University Hospital KU Leuven ,

Leuven , Belgium

Sangeeta M Bhorade , MD Section of Pulmonary and Critical Care Medicine, Division of

Medicine , Northwestern Memorial Hospital , Chicago , IL , USA

Luca M Bigatello , MD Department of Anesthesiology, Critical Care, and Pain Medicine, St

Elizabeth’s Medical Center , Tufts University School of Medicine , Boston , MA , USA

Thomas P Bleck , MD, MCCM, FNSC Rush Medical College , Chicago , IL , USA

Victor A van Bochove , MSc Department of Anesthesiology , Erasmus University Medical

Center , Rotterdam , The Netherlands

Carl J Borromeo , MD Department of Anesthesiology , Lahey Hospital and Medical Center ,

Burlington , MA , USA

Bernd W Böttiger , MD Department of Anesthesiology and Intensive Care Medicine ,

University Hospital of Cologne , Köln , Germany

Jean Carlet , MD Department of Medical-Surgical Intensive Care Medicine , Groupe

Hospitalier Paris Saint Joseph , Paris , France

Eugene H Chung , MD, MSc Division of Cardiology, Cardiac Electrophysiology, Department

of Medicine , University of North Carolina at Chapel Hill , Chapel Hill , NC , USA

Leanne Clifford , BM, MSc Department of Anesthesiology , Mayo Clinic , Rochester , MN ,

USA

Jeremy Cohen , MBBS, MD(Int.Med), FRCA, FFARCSI Burns, Trauma and Critical Care

Research Centre , University of Queensland , St Lucia , QLD , Australia

Royal Brisbane Hospital , Brisbane , QLD , Australia

Elifçe O Cosar , MD Department of Anesthesiology , UMass Memorial Medical Center ,

Worcester , MA , USA

Donald E Craven , MD, FACP, FIDSA, FRCP(C) Infectious Diseases Research &

Prevention , Lahey Health Medical Center & Hospital , Burlington , MA , USA

Tufts University School of Medicine , Boston , MA , USA

Visiting Scientist, Harvard T H Chen School of Public Health , Boston , MA , USA

Kathleen A Craven , RN, BS, MPH Preventionist and Public Health Consultant , Wellesley ,

MA , USA

Peter E Croft , BA, MD Department of Emergency Medicine , Massachusetts General

Hospital , Boston , MA , USA

Daniela M Darrah , MD Division of Critical Care Medicine, Department of Anesthesiology ,

Columbia University Medical Center , New York , NY , USA

R Phillip Dellinger , MD Department of Medicine, Cooper Medical School of Rowan

University , Cooper University Hospital , Camden , NJ , USA

Theodore R Delmonico , MD Department of General Surgery , Lahey Hospital and Medical

Center , Burlington , MA , USA

Contributors

Peter K Dempsey , MD Department of Neurosurgery , Lahey Hospital & Medical Center ,

Burlington , MA , USA

Katia Donadello , MD Department of Intensive Care , Azienda Ospedaliera Universitaria Integrata (AOUI) di Verona , Verona , Italy

Dipartimento ad Attività Integrata (DAI) di Emergenza e Terapie Intensive , U.O.C Anestesia

e Rianimazione B , Verona , Italy

Todd Dorman , MD Department of Anesthesiology and Critical Care Medicine, Surgery and

the School of Nursing , Johns Hopkins University School of Medicine , Baltimore , MD , USA

Robert A Duncan , MD, MPH Tufts University School of Medicine , Boston , MA , USA

Center for Infectious Diseases & Prevention , Lahey Hospital & Medical Center , Burlington ,

MA , USA

Paul W.G Elbers , MD, PhD Department of Intensive Care Medicine , VU University Medical

Center , Amsterdam , The Netherlands

Monique Espinosa , MD Department of Anesthesiology , University of Miami Miller School

of Medicine , Miami , FL , USA

Hans Flaatten , MD, PhD General Intensive Care Unit , Haukeland University Hospital ,

Joshua C Grimm , MD Division of Cardiac Surgery, Department of Surgery , The Johns

Hopkins Hospital , Baltimore , MD , USA

Kyle J Gunnerson , MD Department of Emergency Medicine, Division of Emergency Critical Care , University of Michigan Health System , Ann Arbor , MI , USA

Dimitri Gusmao-Flores , MD Hospital Universitário Prof Edgar Santos , Universidade Federal da Bahia , Salvador , Bahia , Brazil

Kaye Hale , MD Department of Anesthesiology and Critical Care Medicine , Memorial Sloan-

Kettering Cancer Center , New York , NY , USA

Naomi E Hammond , BN, MN (Crit Care), MPH Malcolm Fisher Department of Intensive

Care , Royal North Shore Hospital , St Leonards , NSW , Australia

Stephen O Heard , MD Department of Anesthesiology , UMass Memorial Medical Center ,

Worcester , MA , USA

Christine Holzmueller , BLA Department of Anesthesiology and Critical Care Medicine,

Armstrong Institute for Patient Safety and Quality , Johns Hopkins University School of Medicine , Baltimore , MD , USA

Jana Hudcova , MD Department of Surgical Critical Care , Lahey Hospital and Medical

Center , Burlington , MA , USA

Steven W Hwang , MD Department of Neurosurgery , Tufts Medical Center , Boston , MA , USA Larry M Jones , MD Department of Surgery , The Ohio State University Wexner Medical

Center , Columbus , OH , USA

Georgios Karagiannis , MD Royal Brompton and Harefi eld Hospital NHS Foundation , Harefi eld Hospital , Middlesex , UK

Andrew W Kirkpatrick , MD, MHSc Department of Surgery and the Regional Trauma

Program , University of Calgary and the Foothills Medical Centre , Calgary , Alberta , Canada

Daryl J Kor , MD Department of Anesthesiology , Mayo Clinic , Rochester , MN , USA

Andreas H Kramer , MD, MSc, FRCPC Department of Critical Care Medicine & Clinical

Neurosciences , University of Calgary, Foothills Medical Center , Calgary , AB , Canada

Catherine Kuza , MD Department of Anesthesiology , UMass Memorial Medical Center ,

Worcester , MA , USA

Younghoon Kwon , MD Division of Cardiology, Department of Medicine , University of

Minnesota , Minneapolis , MN , USA

Asad Latif , MD, MPH Department of Anesthesiology and Critical Care Medicine , Johns

Hopkins University School of Medicine, Armstrong Institute for Patient Safety and Quality ,

Baltimore , MD , USA

Marcel Levi , MD, PhD Department of Medicine , Academic Medical Center , Amsterdam ,

The Netherlands

Thomas F Lindsay , MDCM, MSc, FRCS, FACS Division of Vascular Surgery, Department

of Surgery , University of Toronto , Toronto , ON , Canada

R Fraser Elliot Chair in Vascular Surgery, Peter Munk Cardiac Centre , Toronto General

Hospital, University Health Network , Toronto , ON , Canada

Alawi Lüetz , MD Department of Anesthesiology and Intensive Care Medicine , Charité-

Universitaetsmedizin Berlin , Berlin , Germany

Neil MacIntyre , MD Duke University Medical Center , Durham , NC , USA

Sohail K Mahboobi , MD Department of Anesthesiology , Lahey Hospital and Medical

Center , Burlington , MA , USA

Tufts University School of Medicine , Boston , MA , USA

Bruno Maia , MD Neurointensive Care Unit, Hospital de São José , Centro Hospitalar de

Lisboa Central, E.P.E , Lisbon , Portugal

Manu L.N.G Malbrain , MD, PhD Department of Intensive Care , Ziekenhuis Netwerk

Antwerpen , Antwerpen , Belgium

Sara A Mansfi eld , MD Department of General Surgery , The Ohio State University ,

Columbus , OH , USA

Peter W Marcello , MD Department of Colon and Rectal Surgery , Lahey Hospital & Medical

Center , Burlington , MA , USA

Paul E Marik , MD, FCCM Department of Medicine , Eastern Virginia Medical School ,

Norfolk , VA , USA

Michael B Maron , PhD Department of Integrative Medical Sciences , Northeast Ohio

Medical University , Rootstown , OH , USA

David T Martin , MD, FRCP, FACP, FACC, FHRS Lahey Hospital and Medical Center ,

Tufts University School of Medicine , Burlington , MA , USA

Robina Matyal , MD Department of Anesthesia , Critical Care, and Pain Medicine, Beth Israel

Deaconess Medical Center , Boston , MA , USA

Mario Montealegre-Gallegos , MD Department of Anesthesia , Critical Care and Pain

Medicine , Beth Israel Deaconess Medical Center , Boston , MA , USA

Contributors

Rui P Moreno , MD, PhD Neurointensive Care Unit, Hospital de São José , Centro Hospitalar

de Lisboa Central, E.P.E , Lisbon , Portugal

John A Myburgh , AO, MBBCh, PhD, FCICM Department of Intensive Care Medicine , St

George Hospital , Sydney , New South Wales , Australia

Flávio E Nácul , MD, PhD Critical Care Medicine, University Hospital, Federal University

of Rio de Janeiro ; Surgical Critical Care Medicine, Pró-Cardíaco Hospital , Rio de Janeiro , RJ , Brazil

Viviane G Nasr , MD Department of Anesthesiology and Critical Care , Boston Children’s

Hospital , Boston , MA , USA

Vicki E Noble , MD Department of Emergency Medicine , Massachusetts General Hospital ,

Boston , MA , USA

John M O’Donnell , MD Division of Surgery, Department of Surgical Critical Care , Lahey

Hospital and Medical Center , Burlington , MA , USA

Steven M Opal , MD Division of Infectious Diseases , The Memorial Hospital of Rhode

Island-Brown University , Pawtucket , RI , USA

Rafael A Ortega , MD Department of Anesthesiology , Boston Medical Center , Boston , MA ,

USA

Elrasheed S Osman , MBBS, FRCSI Division of Vascular Surgery, Department of Surgery ,

Toronto General Hospital , Toronto , ON , Canada

Anam Pal , MD Division of Cardiac Surgery, Department of Surgery , Beth Israel Deaconess

Medical Center, Harvard Medical School , Boston , MA , USA

Stephen M Pastores , MD Department of Anesthesiology and Critical Care Medicine , Memorial Sloan-Kettering Cancer Center , New York , NY , USA

Kunal P Patel , MD Department of Critical Care Medicine , Memorial Sloan Kettering Medical Center , New York , NY , USA

François Philippart , MD, PhD Department of Medical-Surgical Intensive Care Medicine ,

Groupe Hospitalier Paris Saint Joseph , Paris , France

Frank M Phillips , BSc, MBBS, MRCP Department of Gastroenterology , Royal Derby

Hospital , Derby , UK

Fredric M Pieracci , MD, MPH University of Colorado School of Medicine , Denver , CO ,

USA

Martijn Poeze , MD, PhD Department of Surgery and Intensive Care Medicine , Maastricht

University Medical Center , Maastricht , The Netherlands

Alfons Pomp , MD Weill Cornell Medical Center , New York Presbyterian Hospital , New

Tony M Rahman , MA, DIC, PhD, FFICM, FRCP, FRACP Department of Gastroenterology

& Hepatology , The Prince Charles Hospital , Brisbane , QLD , Australia

Sundara K Rengasamy , MD Department of Anesthesiology , Boston University Medical

Center , Boston , MA , USA

Andrew Rhodes, MD, FRCA, FRCP, FFICM Adult Critical Care, St George’s University

Hospital , NHS Foundation Trust and University of London , London , UK

Emanuel P Rivers , MD, MPH Department of Emergency Medicine and Surgical Critical

Care, Henry Ford Hospital , Wayne State University , Detroit , Michigan , USA

Derek J Roberts , BSc(Pharm), MD, PhD(Cand) Departments of Surgery and Community

Health Sciences (Division of Epidemiology) , Intensive Care Unit Administration, Foothills

Medical Centre, University of Calgary , Calgary , Alberta , Canada

Gerardo Rodriguez , MD Department of Anesthesiology , Boston Medical Center , Boston ,

MA , USA

Michael S Rosenblatt , MD, MPH, MBA Department of General Surgery , Lahey Hospital

and Medical Center , Burlington , MA , USA

Manoj Saxena , MBBChir, BSc Department of Intensive Care Medicine , St George Hospital ,

Kogarah , NSW , Australia

Andreas Schneider , MD Department of Anesthesiology and Intensive Care Medicine ,

University Hospital of Cologne , Köln , Germany

Reuben D Shin , MD Department of General Surgery , Lahey Hospital and Medical Center ,

Burlington , MA , USA

Robert N Sladen , MBChB, MRCP(UK), FRCP[C] Department of Anesthesiology ,

Columbia University Medical Center , New York , NY , USA

Julia Sobol , MD, MPH Department of Anesthesiology , Columbia University Medical Center ,

New York , NY , USA

Claudia Spies , MD Department of Anesthesiology and Intensive Care Medicine , Charité

Campus Mitte and Charité Virchow Klinikum, Charité-Universitätsmedizin , Berlin , Germany

Glynne D Stanley , MBChB, FRCA Plexus Anesthesia Services Management , Westwood ,

MA , USA

Genevra L Stone , MD Graduate of Tufts University School of Medicine Class of 2014 ,

Boston , MA , USA

Alexis Tabah , MD Burns Trauma and Critical Care Research Centre , The University of

Queensland , St Lucia , QLD , Australia

Royal Brisbane and Women’s Hospital , Brisbane , QLD , Australia

Steven Thiessen , MD Clinical Division and Laboratory of Intensive Care Medicine,

Department of Cellular and Molecular Medicine , University Hospital KU Leuven , Leuven ,

Belgium

Dan R Thompson , MD, MA, MCCM Department of Surgery , Albany Medical College ,

Albany , NY , USA

Sam Thomson , MD, MBBS, MRCP Department of Gastroenterology & Hepatology ,

Western Sussex Hospitals NHS Foundation Trust, Worthing Hospital , West Sussex , UK

Pieter Roel Tuinman, MD, PhD Department of Intensive Care Medicine, VU University

Medical Center, The Netherlands

Contributors

Ilse Vanhorebeek , MEng, PhD Clinical Division and Laboratory of Intensive Care Medicine,

Department of Cellular and Molecular Medicine , University Hospital KU Leuven , Leuven , Belgium

Albert J Varon , MD, MHPE, FCCM Department of Anesthesiology , University of Miami

Miller School of Medicine , Miami , FL , USA

Patricia Mello , MD Hospital Getulio Vargas , Universidade Federal do Piauí , Teresina , Brazil Bala Venkatesh , MBBS, MD(Int.Med), FRCA, FFARCSI Wesley Hospital , Auchenfl ower ,

QLD , Australia Princess Alexandra Hospital , Harlow , UK University of Quensland , Brisbane , QLD , Australia University of Sydney , Sydney , Australia

José Mauro Vieira Jr , MD, PhD Critical Care Medicine , Hospital Sírio Libanês , São Paulo ,

SP , Brazil

Wickii T Vigneswaran , MD Department of Surgery , University of Chicago Medicine ,

Chicago , IL , USA

Andrew G Villanueva , MD Department of Pulmonary and Critical Care Medicine , Lahey

Hospital and Medical Center , Burlington , MA , USA

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

Ghent , Belgium

Katja E Wartenberg , MD, PhD Neurointensive Care Unit , Department of Neurology,

Martin- Luther- University , Halle , Germany

Bjoern Weiss , MD Department of Anesthesiology and Intensive Care Medicine , Charité

Campus Mitte and Charité Virchow Klinikum, Charité-Universitätsmedizin , Berlin , Germany

Jan Wernerman , MD, PhD Department of Anesthesia and Intensive Care Medicine , Karolinska University Hospital Huddinge , Stockholm , Sweden

Glenn J.R Whitman , MD Division of Cardiac Surgery, Department of Surgery , Johns Hopkins Hospital , Baltimore , MD , USA

Robert G Whitmore , MD Department of Neurosurgery, Lahey Hospital and Health System ,

Tufts University School of Medicine , Burlington , MA , USA

Bradford Winters , MD, PhD Department of Anesthesiology and Critical Care Medicine ,

Johns Hopkins University School of Medicine, Armstrong Institute for Patient Safety and Quality , Baltimore , MD , USA

Hannah Wunsch , MD, MSc Department of Critical Care Medicine, Sunnybrook Health

Sciences Centre and Department of Anesthesia , University of Toronto , Toronto , ON , Canada

Part I Resuscitation and General Topics

© Springer International Publishing Switzerland 2016

J.M O’Donnell, F.E Nácul (eds.), Surgical Intensive Care Medicine, DOI 10.1007/978-3-319-19668-8_1

Supplemental Oxygen Therapy

Andrew G Villanueva, Sohail K Mahboobi, and Sana Ata

A.G Villanueva, MD

Department of Pulmonary and Critical Care Medicine,

Lahey Hospital and Medical Center, Burlington, MA, USA

S.K Mahboobi, MD ( * )

Department of Anesthesiology, Lahey Hospital and Medical

Center, 41 Mall Road, Burlington, MA 01805, USA

Tufts University School of Medicine, Boston, MA, USA

e-mail: Sohail.mahboobi@lahey.org

S Ata, MD

Department of Anesthesiology and Interventional Pain

Management, Lahey Hospital and Medical Center,

Burlington, MA, USA

e-mail: sana.ata@lahey.org

1

Oxygen is the most commonly used medication in intensive

care units Intensivists caring for critically ill patients in a

surgical intensive care unit continually face multiple diverse

and challenging problems regarding adequacy of oxygen

therapy A fundamental goal is to provide adequate cellular

respiration and thereby maintain sufficient tissue

oxygen-ation and normal organ function Routinely supplemental

oxygen is being used in settings of normal oxygen saturation

believing it will increase oxygen delivery to the tissues

Hyperoxia in the setting of decrease perfusion can result in

hyperoxia-induced tissue injury, and this narrow margin of

safety makes it important for intensivists to understand all

aspects of oxygen therapy Successful cellular oxygenation

depends on the maintenance of several factors, including

adequate alveolar ventilation, a functioning gas-exchange

surface, the capacity to transport oxygen to the tissue, and

intact tissue respiration (the mitochondrial cytochrome

oxi-dase 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 ventilation and how to use supplemental oxygen

therapy to improve arterial oxygenation in patients who are

hypoxemic but do not require mechanical ventilation

Indications of Oxygen Therapy

The most common and important indication of oxygenation therapy is the prevention and correction of hypoxemia aiming

to avoidance or treatment of tissue hypoxia Other indications for oxygen therapy include suspected hypoxemia, acute myo-cardial infarction, severe trauma, and postoperative recovery from anesthesia 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 hypoxemia Severe hypoxemia is associated with slow and irregular respirations, bradycardia, hypotension, convulsions, and coma

Pathophysiology of Hypoxemia

Hypoxemia and hypoxia are not synonymous Hypoxemia is defined as a relative deficiency of oxygen in the arterial blood as measured by arterial oxygen tension (PaO2) Hypoxia is defined as inadequate oxygen tension at the cel-lular 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 Patients may have hypoxia without hypoxemia, but patients cannot have sus-tained severe hypoxemia without developing hypoxia It is thus imperative to promptly treat patients who have signifi-cant 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 mecha-nisms of hypoxemia are (1) decreased ambient fraction of inspired oxygen (FiO2), (2) alveolar hypoventilation, (3) dif-fusion limitation across the alveolar–capillary membrane, (4) shunt, and (5) V/Q mismatch [1] Decreased ambient FiO2 is generally not a cause, unless the altitude is very high

Pure alveolar hypoventilation is often related to drug

overdose, the excess use of medications that suppress the

respiratory drive such as opiates or benzodiazepines, or

cata-strophic events of the central nervous system such as head

trauma, stroke, subarachnoid hemorrhage, subdural

hema-toma, or cerebral edema The hypoxemia is caused by a

decrease in the alveolar oxygen tension (PAO2), which can be

measured using the alveolar gas equation:

P OA 2=FiO2(PB-47)-PaCO R2/

where FiO2 is the fraction of inspired oxygen (expressed as a

decimal), (PB − 47) is the barometric pressure minus water

vapor pressure, PaCO2 is the arterial carbon dioxide tension,

and R is the respiratory quotient (usually 0.8) Clinically,

hypoventilation results in a decreased PaO2 and an elevated

PaCO2 With hypoventilation, however, the alveolar–arterial

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

(PaO2/PAO2) are normal (2.5 + [0.21 × age] mmHg, and 0.77–

0.82, respectively) Diffusion limitation across the alveolar–

capillary membrane, shunt, and V/Q mismatch all causes an

abnormal [A − a]O2 and PaO2/PAO2

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

capil-lary 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 PAO2 using supplemental oxygen therapy

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 collapse due to retained respiratory

secre-tions, pulmonary arterial-venous malformasecre-tions, and

pulmo-nary capillary dilatation, as is sometimes seen in liver disease

(the so-called hepatopulmonary syndrome) [2] Oxygen

ther-apy is of limited benefit with significantly increased shunt

because, regardless of the FiO2, oxygen transfer cannot occur

when blood does not come into contact with functional

alve-olar 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 collapse

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 alveolar ventilation and pulmonary capillary blood flow

A detailed explanation of why V/Q mismatch results in hypoxemia is beyond the scope of this chapter (see Chap

7), but this mechanism is believed to be the most common cause of hypoxemia [3 4] V/Q mismatching can result from an array of disorders such as bronchospasm, chronic obstructive pulmonary disease (COPD), bronchial secre-tions, mild pulmonary edema, interstitial lung disease, venous thromboembolism, pleural effusion, pulmonary contusion, 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 con-trast to shunt, an increase in the FiO2 causes a substantial increase in PaO2

Goals of Supplemental Oxygen Therapy

A constant supply of oxygen is required for proper tissue function as it is not stored An adequately functioning car-diovascular system is required for adequate delivery of oxy-gen to the tissues Oxygen supply must match the metabolic demand by tissues; otherwise organ dysfunction may occur Oxygen delivery is the total amount of oxygen delivered to tissues and is described by the equation:

DO2 =CaO CO2´where DO2 is oxygen delivery in ml/m, CaO2 is arterial oxy-gen content, and CO is cardiac output Arterial oxygen con-tent can be calculated by following equation:

CaO2 =SaO2´Hg´1 39 +PaO2´0 003.where SaO2 is arterial oxygen saturation, Hg is hemoglobin, 1.39 is oxygen carrying capacity of hemoglobin, PaO2 is arterial partial pressure of oxygen, and 0.003 is solubility coefficient of oxygen in plasma In healthy persons DO2 is more than oxygen consumption, but in critical illness, the ability of tissues to extract oxygen is not efficient The pur-pose of oxygen therapy is to correct hypoxemia by achieving

a PaO2≥ 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, val-ues that define hypoxemia are PaO2 of 50–55 mmHg, corre-sponding to arterial oxygen saturation 88–90 % [6] These target values for PaO2 or arterial oxygen saturation assume the presence of normally functioning hemoglobin In situa-tions with abnormal hemoglobins that cannot effectively bind oxygen, such as methemoglobinemia or carbon monox-ide poisoning, even supranormal PaO values may be

A.G Villanueva et al.

associated with a reduction in available hemoglobin and

resultant lower oxygen content [7 9]

Oxygen Delivery Systems

Oxygen delivery systems can be classified as low-flow (or

variable performance) and high-flow (or fixed

perfor-mance) systems Low-flow systems provide small amounts

of 100 % oxygen as a supplement, with FiO2 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

pro-vide the patient’s total ventilatory requirements An

advan-tage of high-flow systems is that the level of FiO2 remains

constant regardless of any changes that may occur in the

ventilatory pattern [10] In this section these two types of

oxygen 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 noninvasive

ventilation (NIV)

Low-Flow Systems

Low-flow oxygen devices are the most commonly used because of their simplicity and ease of use, healthcare pro-viders’ familiarity with the system, low cost, and patient acceptance

4 L/min, the gases should be humidified to prevent drying of the nasal mucosa As a rule, FiO2 increases by approximately 0.03–0.04 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 variations in individual patients’ breathing patterns To be effective, the patient’s nasal pas-sages must be patent to allow filling of the anatomic reser-voir The patient, however, does not need to breathe through the nose, because oxygen is entrained from the anatomic res-ervoir even in the presence of mouth breathing

The nasal cannula is advantageous because of the comfort 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

50 10

0

02 tension (mm Hg)

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 characteristic

sig-moid shape, the affinity for O 2 progressively increases as successive

molecules of O 2 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

arte-rial PaO 2 (60–100 mmHg), and the middle steep segment enables large

quantities of O 2 to be released at the PaO 2 prevailing in the peripheral

chemical components of the tubing, cannulas are well

tolerated The physiologic disadvantage of cannula use is that

FiO2 varies with the patient’s breathing pattern, and

calcula-tions requiring accurate FiO2 data cannot be made In most

patients with mild hypoxemia, precise knowledge of FiO2 is

unnecessary and clinical improvement occurs rapidly

Simple Face Mask

A simple oxygen mask is a low-flow system that delivers

approximately 35–50 % oxygen at flow rates of 5 L/min or

greater The mask provides a reservoir (100–200 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

[12] Flow rates greater than 8 L/min do not increase the

FiO2 significantly above 0.6 (Table 1.1) The disadvantages

of using this device include the resultant variable FiO2 and

the fact that it must be removed for eating or drinking

Partial Rebreathing Mask

Partial rebreathing and nonrebreathing masks with 600–

1000-mL reservoir bags (Fig 1.2) can deliver high inspired

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 FiO2 should occur (Table 1.1) The

rebreathing capacity of this system allows some degree of

oxygen conservation, which may be useful while

transport-ing patients with portable oxygen supplies [11]

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 FiO2 [11] 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 FiO2, masks should fit snugly on the face, but excessive 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 FiO2 masks include the risk of absorption atelectasis and the potential for oxygen toxicity if they are used for longer than 24–48 h 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 sub-sequent ventilatory failure

Tracheostomy Collars

Tracheostomy collars primarily are used to deliver humidity

to patients with artificial airways Oxygen may be delivered

Fig 1.2 Rebreathing mask with reservoir bag With permission from

Lahey Hospital & Medical Center

A.G Villanueva et al.

with these devices, but as with other low-flow systems, the

FiO2 is unpredictable and inconsistent and depends on the

patient’s ventilatory pattern

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

temperature of the inspired gases, and maintain a fixed

inspired oxygen concentration despite changes in the

venti-latory pattern

High-Flow Oxygen with Nasal Cannula

As discussed earlier, nasal cannula is usually categorized as low-flow oxygen delivery device Not long ago high-flow nasal cannula oxygen therapy concept was introduced It consists of a patient interface (nasal prongs), a gas delivery device for FiO2, and a humidifier (Fig 1.5) Heated humidi-fication system is added to avoid drying of upper airway mucosa because of high flows and for patient comfort and greater tolerance Humidification also decreases the energy cost of conditioning of inspired gases by upper respiratory tract High flows of oxygen can be used from 15 to 60 L/m range [14] The nasal prongs are designed to minimize sec-ondary room air entrainment Nasopharynx and oropharynx serve as natural reservoirs for oxygen Delivered high flows reduce nasopharyngeal dead space and result in improved alveolar ventilation [15, 16] The nasopharyngeal gas flows are usually higher than the peak inspiratory flow and thus decrease resistance and improve the work of breathing and compliance There is a CPAP effect due to high flows, which

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 % oxygen Reprinted from Shapiro

BA, Kacmarek RM, Cane RD, et al Clinical application of respiratory

care 4th edition St Louis: Mosby Year Book 1991 [ 13 ] Copyright

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 % oxygen Reprinted from Shapiro BA, Kacmarek RM, Cane RD, et al Clinical application of respiratory care 4th edition St Louis: Mosby Year Book

1991 [ 13 ] Copyright Elsevier

not only decreases atelectasis but also improves ventilation–

perfusion ratio of the lungs This CPAP effect is dependent

on the leak and in turn the size of nasal prongs to the nose

Recent data supports the use of this technique in patients

with persistent hypoxemia after receiving oxygen with other

low-flow delivery systems Because oxygen flow can be

titrated on a wide range depending on patient response, it can

be used as an initial measure in settings like ER This

deliv-ery system is particularly useful in situations where

remov-ing mask to speak, eat, drink, or cough and clearremov-ing of

secretions can cause hypoxemia

Air-Entrainment (Venturi) Mask

Air-entrainment masks (Fig 1.6), commonly called “Venturi

masks,” entrain air using the Bernoulli principal and

con-stant pressure-jet mixing [17] A jet of oxygen is forced

through a small opening that because of viscous shearing

forces creates a subatmospheric pressure gradient

down-stream relative to the surrounding gases (Fig 1.7) The

pro-portion of oxygen 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 FiO2 increases, the air/oxygen-entrainment ratio

decreases with a net reduction in total gas flow Therefore,

the probability of the patient’s ventilatory needs exceeding

the total flow capabilities of the device increases with higher

FiO2 settings [11]

Venturi masks are available in various colors The colors

specify delivered oxygen concentration and the required gas

flow Another type of Venturi mask has a dialed setting on

the apparatus In order to change delivered oxygen concentration in these masks, flow is increased and desired concentration is dialed on the apparatus The dial will change

Fig 1.5 High-flow oxygen

delivery system with nasal

cannula by Fisher and Paykel

With permission from Lahey

Hospital & Medical Center

Fig 1.6 Air-entrainment (Venturi) mask With permission from Lahey

Hospital & Medical Center

A.G Villanueva et al.

the diameter of the aperture responsible for air entrainment

and result in the delivery of dialed concentration of oxygen

through the mask (Fig 1.8)

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 humidifier should be used [11]

The major indication for the use of Venturi masks is the

need for precise control of the FiO2 between 0.24 and 0.40

when providing oxygen therapy to patients with COPD who

are hypercarbic (Table 1.2) [18] For patients with COPD

who have a PaCO2 greater than 45 mmHg, it is generally

rec-ommended that the FiO2 be low initially (0.24–0.28) and then

adjusted upward to maintain an oxygen saturation of 88–90 %

Using devices that deliver a high FiO2 to patients with COPD

and elevated PaCO2 can result in a high PaO2, which can lead

to further elevations in PaCO2 and worsening respiratory

aci-dosis (see section “Complications of Oxygen Therapy”)

Aerosol Mask

An FiO2 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 neb-ulizers or air/oxygen blends, can deliver a consistent and predictable FiO2 regardless of the patient’s ventilatory pattern

An air-entrainment nebulizer can deliver an FiO2 of 0.35–1.0, produce an aerosol, and generate flow rates of 14–16 L/min Air/oxygen blenders can deliver a consistent FiO2 ranging from 0.21 to 1.0, with flows up to 100 L/min These devices are generally used in conjunction with humidifiers [11]

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 mix-ture known as “heliox.” Heliox reduces the density of the delivered gas, thereby reducing the work of breathing and improving ventilation in the presence of airway obstruction [19–21] 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 lami-nar flow does and is inversely proportional to the density of the gas being inspired Clinically, a 60:40 or 70:30 ratio of helium to oxygen is generally recommended The combina-tion is administered through a well-fitted nonrebreathing mask with a complete set of one-way valves The reported

Air

Air Air

o 2

Fig 1.7 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 proportion of oxygen can be controlled by enlarging or

reducing the size of the injection port A smaller opening creates

pres-sure of oxygen flow, resulting in more room air entrained and a lower

percentage of inspired oxygen

Fig 1.8 Dialable Venturi masks

with components shown on left and

complete assembly on right With

permission from Lahey Hospital &

Medical Center

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 rate [22, 23] 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 FiO2 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 ventilation via

an endotracheal tube to treat patients with hypoxemic or

hypercarbic respiratory insufficiency is 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 1.9)

Continuous Positive Airway Pressure

A continuous positive pressure is delivered throughout the

respiratory cycle, either by a portable compressor or from a

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 FiO2 delivered by the

mechanical ventilator The major use of CPAP, particularly

when delivered 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

col-lapsed alveoli and reduce the work of breathing by

increas-ing functional residual capacity, thus movincreas-ing the patient onto

the more compliant portion of the pressure volume curve

[24–26] Mask CPAP is also an effective treatment for

car-diogenic pulmonary edema, because positive intrathoracic pressure reduces both cardiac preload and afterload; it has been shown to decrease the need for intubation [27–29] Typically, pressures of 5–15 cm H2O 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 stud-ies comparing mask CPAP and NIV in the treatment of car-diogenic pulmonary edema showed that while both modalities reduced intubation rates [30], there may be more rapid improvement in gas exchange with NIV than with CPAP alone [31, 32] NIV may therefore be preferable for patients with persisting dyspnea or hypercapnia after the ini-tiation of mask CPAP

Noninvasive Ventilation

NIV is defined as the delivery of mechanically assisted or generated breaths without placement of an artificial airway (endotracheal or tracheostomy tube) The benefits are similar

to those of mechanical ventilation delivered through an ficial airway without the risks associated with endotracheal

arti-Fig 1.9 Full-face mask used for noninvasive positive pressure

ventila-tion With permission from Lahey Hospital & Medical Center

Table 1.2 Air-entrainment ratios and total gas outflows of

commer-cially available Venturi masks [ 18 ]

O2 concentration

of delivered gas O2 Flow (L)

Liters of air entrained per liter O2

Total gas outflow (l/min)

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

A.G Villanueva et al.

intubation, including the risk of ventilator-associated

pneu-monia 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 FiO2 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,

deliv-ered either in the pressure support mode or with bi-level

positive airway pressure ventilation [33] Bi-level positive

airway pressure ventilation delivers both inspiratory

pres-sure support and an expiratory prespres-sure “BiPAP” refers to a

specific bi-level positive airway pressure ventilator

manu-factured 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

conven-tional ventilators

Prospective, randomized, controlled trials over the last

two decades have shown that the technique is efficacious in

the treatment of many forms of acute respiratory failure

There is strong evidence for its use in COPD exacerbations

[34–36], acute cardiogenic pulmonary edema [31],

immuno-compromised patients, and the facilitation of weaning in

COPD patients [37–39] Recent reviews on the use of NIV

for COPD exacerbations have summarized the benefits of

reduced intubation rate, mortality, and hospital length of stay

[40, 41] and suggest that the use of NIV in many of these

patients should be the standard of care [42] NIV produces

few complications other than local damage related to

pres-sure effects of the mask and straps [43] Cushioning the

fore-head and the bridge of the nose before attaching the mask

can decrease the likelihood of these problems Mild gastric

distention occurs with some frequency but is rarely

signifi-cant at routinely applied levels of inspiratory pressure

sup-port (10–25 cm H2O), and the routine use of a nasogastric

tube is not warranted Ocular irritation and sinus pain or

con-gestion 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 PaO2≥ 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

measurement of pH, PaO2, PaCO2, and O2 saturation of

hemoglobin in arterial blood While oxygenation cannot be

continuously monitored with this method, the measurement

of pH and PaCO2 helps determine a patient’s acid–base status and the adequacy of the alveolar ventilation, because the PaCO2 is inversely proportional 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 FiO2 being administered to the patient and the patient’s PaCO2 and PaO2, the alveolar gas equation can be used to measure the alveolar–arterial oxygen gradient (see section “Pathophysiology of Hypoxemia”) The normal (A − a) O2 gradient varies with age and ranges from 7 to 14 mmHg when the patient is breathing room air; the gradient increases in cases of diffu-sion impairment, right-to-left shunt, and V/Q mismatch The following equation can be used to estimate the expected (A − a) O2 gradient [44]:

( ) 2=2 5 0 21 + ´The measurement of the (A − a) O2 is most useful when the patient is breathing room air, because it increases with higher inspired oxygen concentrations [45] Another useful index for measuring arterial oxygenation is the ratio of PaO2

to PAO2 (PaO2/PAO2), which also can be calculated using data from arterial blood gas measurements [46, 47] Lower limit

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–

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 Photodiodes are switched on and off several 100 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 [49–51]

Pulse oximetry has been shown to be accurate to within

3–4 % in the range of 70–100 % saturation [52] Loss of

pul-sation, which can occur with hypotension, hypothermia, or

vasoconstriction, causes a loss of signal Because pulse

oximetry is dependent on perfusion, it works well during

pri-mary respiratory arrest but is unreliable during cardiac arrest

Pulse oximetry is more accurate in light-skinned than in

dark-skinned patients For light-skinned patients, a less

con-servative target SaO2 of 90–92 % is recommended for

oxy-gen titration For dark-skinned patients, a target value of

95 % should be adequate [53]

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

hemoglo-bin of susceptible patients from its ferrous to its ferric state

[52] 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

gravi-tate toward 85 % If the actual oxygen saturation of a patient

with methemoglobinemia is over 85 %, the pulse oximeter

underestimates it; if it is less than 85 %, the pulse oximeter

overestimates it [52]

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 technique does not assess arterial pH or PaCO2 and

that marked changes in PaO2 can occur with only modest

changes in SaO2 if the latter is above 90 % Pulse oximetry,

therefore, does not eliminate the need for arterial blood gas

determinations in acutely ill patients

Weaning of Oxygen Therapy

Weaning of oxygen therapy should be considered once the

disease process is established, and the evaluation of patient’s

respiratory rate, heart rate, blood pressure, oximetry, and

blood gases shows improvement Weaning can be done

gradually by lowering oxygen concentration for a period and reevaluation of the abovementioned clinical parameters If there is no deterioration, oxygen concentration can be further lowered and process continues till oxygen is no more required

Complications of Oxygen Therapy

While the benefits of supplemental oxygen therapy for hypoxemic patients heavily outweigh the risks in most cases, there are potential problems of which the intensivist should

character-57], increased V/Q inequality in the lung caused by release

of hypoxic vasoconstriction [58–60], and the effect of gen on the hemoglobin–carbon dioxide dissociation curve of blood [59], the so-called Haldane effect There is still ongo-ing debate as to which of these mechanisms is most impor-tant [61, 62] in causing the hypercarbia, but it is now accepted that supplemental oxygen does not cause these patients to

oxy-“stop breathing” [63] If worsening respiratory acidosis occurs with the initiation of oxygen therapy in a patient with severe hypoxemia, treatment choices include decreasing the FiO2 to achieve a lower but acceptable SaO2, noninvasive positive pressure ventilation to improve oxygenation while maintaining 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 gen 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 encountered in spontaneously breathing patients who are given oxygen in concentrations greater than 0.70

oxy-A.G Villanueva et al.

Oxygen Toxicity

In spite of known advantages of oxygen therapy, one major

limiting factor in its liberal use is narrow margin of safety

between its effective and toxic doses A high FiO2 level can

be injurious to the tissues depending on dose and duration of

exposure The mechanism of oxygen toxicity is related to a

significantly higher production rate of oxygen free radicals

such as superoxide anions, hydroxyl radicals, hydrogen

per-oxide, 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 hyperoxia, the normal oxygen-radical-

scavenging mechanisms are overwhelmed, and toxicity

results [64, 65] The FiO2 at which oxygen toxicity becomes

important is controversial and varies depending on the

ani-mal species, degree of underlying lung injury, ambient

baro-metric pressure, and duration Two most obvious systems

affected by toxicity are lungs and central nervous system

Lungs are the first organs to have injury from reactive

oxy-gen species Initially there is a latent period with no clinical

symptoms and it is inversely proportional to inspired

con-centration of oxygen Initial symptoms can vary from

inspi-ratory pain, substernal distress to tenacious secretions, and

persistent cough Long-term exposure of higher oxygen

con-centration can lead to diffuse alveolar damage with signs and

symptoms mimicking ARDS Central nervous system

toxic-ity occurs in long-term hyperbaric treatment with oxygen

and is rare to see in surgical intensive care units [66, 67]

Symptoms include nausea, dizziness, headache,

disorienta-tion, blurred vision, and ultimately tonic–clonic seizures

A higher pCO2 decreases threshold of nervous system

toxic-ity In general, it is best to avoid exposure to an FiO2 greater

than 0.6 for more than 24 h, if possible However, correction

of severe hypoxemia takes precedence over the potential of

oxygen toxicity

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oxim-50 Tremper KK, Barker SJ Pulse oximetry Anesthesiology 1989;70:98–108.

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© Springer International Publishing Switzerland 2016

J.M O’Donnell, F.E Nácul (eds.), Surgical Intensive Care Medicine, DOI 10.1007/978-3-319-19668-8_2

Introduction

Intubation of the trachea in the patient with acute respiratory

failure or for airway protection in the intensive care unit

(ICU) is a relatively common occurrence Although efforts to

avoid intubation should be undertaken, many times these

interventions fail and intubation becomes necessary The

inci-dence of complications associated with intubation is high

Severe complications include hypoxemia, esophageal

intuba-tion, hypotension, aspiraintuba-tion, cardiac arrest, and death [ 1 ],

whereas mild to moderate complications include diffi cult

intubation, cardiac arrhythmias, and dental injury Intubation

of these patients can be challenging, and the number of

attempts at intubation increases the risk of subsequent

com-plications [ 2 ] Consequently, only clinicians skilled at

intuba-tion should attempt tracheal intubaintuba-tion However, many

times, there is not enough time to wait for the arrival of an

airway specialist, and an intervention must be made by the

bedside clinician This chapter reviews the anatomy and

eval-uation of the airway, methods to establish an airway,

tech-niques of tracheal intubation, and extubation of the trachea

Obtaining hospital privileges for airway management is

important Usually these privileges are requested by the

pro-vider and approved by the chair of the department and

cre-dentials committee of the hospital Demonstration of

profi ciency is through the successful completion of a

resi-dency or fellowship where these skills are taught and learned

For those providers who have not obtained these skills

dur-ing postgraduate traindur-ing, the necessary skills for airway

management can be obtained by attending postgraduate

courses, undergoing simulation training, and proctoring by

credentialed providers in the ICU and operating room

Anatomy

A detailed description of the anatomy of the airway is beyond the scope of this chapter; however, a basic knowledge of air-way anatomy is important when a provider is involved in airway management

The nose and the mouth are the airway apertures which lead to the nasopharynx and oropharynx, respectively Their function is to fi lter and humidify inspired air The soft palate separates the nasopharynx from the oropharynx The naso-pharynx and oropharynx join posteriorly in the pharynx The epiglottis separates the oropharynx from the hypopharynx The hypopharynx begins at the epiglottis and ends just distal (approximately 1 cm) to the cricoid cartilage The hypophar-ynx is attached to the cricoid by a series of ligaments and muscles [ 3 ] and contains the piriform recesses where foreign bodies may be lodged [ 4 ]

The larynx lies inferior to the pharynx and superior to the trachea and is composed of a number of cartilaginous struc-tures (cricoid, thyroid, epiglottic, arytenoid, corniculate, and cuneiform) supported by ligaments and muscles (Fig 2.1a,

b ) Its primary function is phonation [ 4 ] The muscles of the larynx are innervated by the recurrent laryngeal nerve except for the cricothyroid muscle , which is innervated by the exter-nal branch of the superior laryngeal nerve Sensation below the epiglottis and above the vocal cords is provided by the internal branch of the superior laryngeal nerve Innervation below the vocal cords is provided by the recurrent laryngeal nerve The glossopharyngeal nerve provides sensation to the posterior third of the tongue, the vallecula, the anterior sur-face of the epiglottis (lingual branch), walls of the pharynx (pharyngeal branch), and the tonsils (tonsillar branch)

The trachea begins at the cricoid cartilage (C6) and branches into the right and left bronchus at the carina (located

at the sternal angle at T4-5) It is 9–15-cm long and has about

20 incomplete hyaline cartilaginous rings that open orly toward the esophagus and prevent the trachea from col-lapsing [ 4 ] The right main bronchus is shorter, wider, and

Airway Management in the Intensive Care Unit

Catherine Kuza , Elifçe O Cosar , and Stephen O Heard

C Kuza , MD • E.O Cosar , MD • S O Heard , MD ( * )

Department of Anesthesiology , UMass Memorial Medical Center ,

55 Lake Avenue North , Worcester , MA 01655 , USA

e-mail: catherine.kuza@umassmemorial.org ; elifce.cosar@

umassmemorial.org ; stephen.heard@umassmed.edu

2

more vertical than the left and continues as the bronchus

intermedius after the takeoff of the right upper lobe It has

three branches to the upper (located 1.5–2 cm from the

carina), middle, and lower lobe The left main bronchus

diverges from the carina at a 45° angle and has branches to

the left upper and lower lobes The distance from the carina

to the bifurcation of the left upper and left lower lobe is

approximately 4.5–5 cm [ 5 ]

Indication for Intubation

Indications for intubation include respiratory failure, airway

protection, pulmonary toilet, and airway obstruction

(Table 2.1 )

Evaluation of the Airway

Even in the most urgent situations, a rapid assessment of the

airway anatomy can decrease the likelihood of

complica-tions or alert the clinician to a possible diffi cult airway An

airway exam is important in assessing the patient’s airway It

will provide information on factors which may affect the

ability to ventilate and intubate the patient The face should

be examined for abnormal features associated with certain

syndromes (Pierre Robin, Treacher Collins, Apert’s, and

Klippel-Feil) which may make ventilation and intubation

challenging Mouth opening and jaw mobility should be examined Normal mouth opening is between 40 and 60 mm

If the mouth opening is <30 mm, laryngeal visualization ing laryngoscopy will be diffi cult The inability of the patient

dur-to protrude the mandible (with the lower teeth in front of the upper ones) is associated with diffi cult laryngoscopy and ventilation Protruding teeth may hinder the visualization of the airway and may be damaged during laryngoscopy The Mallampati classifi cation assesses the oral structures visible upon mouth opening The patient sits in a neutral position, opens the mouth widely, and protrudes the tongue as far as possible without phonation The modifi ed Mallampati clas-sifi cation is shown in Fig 2.2 Mallampati classes III and IV are associated with diffi cult intubation

The neck and cervical stability should be examined

A history of rheumatoid arthritis, Down’s syndrome, and ankylosing spondylitis should alert the provider to abnormal neck anatomy Patients with reduced cervical spine mobility are more likely to have diffi cult airways Neck circumfer-ence >40 cm may also predict a diffi cult intubation [ 6 ] Most tests for evaluation of diffi cult intubation suffer from low sensitivity (<50 %) but have reasonable specifi city (>85 %) [ 7 ] Furthermore, most of these tests require patient cooperation, something that is frequently lacking in the ICU Recently, investigators developed a multimodal scoring system (MACOCHA) to predict a diffi cult intubation (Fig 2.3a ) [ 8 ] Factors included in the score were Mallampati class III or IV, presence of obstructive sleep apnea, reduced

Hyoid bone, body

Hyoid bone, lesser

Hyoid bone, greater

Lateral thyrohyoid

Cartilago triticea

superior laryngeal Thyroid cartilage, superior comu Superior thyroid

Laryageal

Epiglottis

Hyoid bone, greater comu

Thyrohyoid membrane Quadrangular membrane Saccule of larynx Thyroid cartilage laryngeal ventricle

Thyroarytenoid Cricoid cartilage

Aryepiglottic fold

Tubercle of epiglottis

Vestibular fold

Vocal fold Conus elasticus;

cricovocal membrane

Vestibule;

Supraglottic cavity

Laryngeal ventricle

Infraglottic cavity

tubercle Oblique line Inferior thyroid tubercle Lateral cricothyroid ligament

Thyroid cartilage inferior comu Articular capsule of Cricothyroid joint

Fig 2.1 ( a ) Anterolateral view of the larynx ( b ) Coronal view (posterior) of the larynx This fi gure was published in Standring S (editor in chief)

Gray’s Anatomy, 40th Edition Copyright Elsevier [ 59 ]

C Kuza et al.

cervical spine movement, reduced mouth opening,

underly-ing condition of the patient (e.g., coma or severe

hypox-emia), and an operator other than an anesthesiologist A

maximum score of 12 could be achieved As the MACOCHA

score increased, the diffi culty in intubation also increased

(Fig 2.3b ) Although this scoring system may prove to be

useful in the future, elements of the system still require

patient cooperation

Airway Equipment

The equipment and supplies needed for intubation are depicted in Table 2.2 Ideally, these should be housed in a bag or cart (Fig 2.4a–c ) The cart should be locked and contents checked on a scheduled basis, particularly battery life to ensure proper function of the laryngoscope

A supply of 100 % oxygen and a face mask bag valve device (FMBVD) or BiPAP machine should be available In addition, suctioning equipment with a tonsillar suction device is necessary In areas of the hospital where suction is not readily available, handheld suction devices can be used Adequate lighting is important, and the bed should be at a comfortable height with the backboard removed Raising the head of the bed to at least 30° will also reduce the risk of passive regurgitation of stomach contents, but a step stool may be required for the operator

Laryngoscopes

Rigid laryngoscopes are composed of two pieces: a handle that houses the battery and a blade with a bulb or fi ber-optic bundle that will illuminate when properly attached to the handle The two most common types of blades are the MacIntosh (curved) and Miller (straight) The choice of blade is a matter of personal preference; however, some data suggest that less force and neck extension are required when the straight blade is used [ 9 ]

Videolaryngoscopes have gained widespread popularity

in recent years These devices contain a small camera near the tip of the rigid plastic laryngoscope blade thereby allow-ing an indirect view of the glottis that is often better than that obtained with direct laryngoscopy

Laryngeal Mask Airway (LMA)

The laryngeal mask airway is a supraglottic airway which can be used during diffi cult ventilation or intubation It is composed of a shallow pliable mask with an infl atable rim that is attached to a hollow plastic tube (Fig 2.5a ) There are special types of LMAs One allows for a higher seal pressure and an orifi ce to drain fl uids regurgitating up the esophagus and/or to allow the insertion of gastric tube (Fig 2.5b ) This LMA reduces the risk of pulmonary aspiration of gastric contents and allows positive pressure ventilation at higher infl ation pressures The other supraglottic device is an intu-bating LMA (Fig 2.5c) which enables blind and bronchoscopy- assisted endotracheal tube placement through

it With proper placement, the cuff borders the base of the tongue superiorly, the upper esophageal sphincter inferiorly, and the piriform sinuses laterally

Table 2.1 Indications for endotracheal intubation

Acute airway obstruction

Laryngeal spasm (anaphylactic response)

Access for suctioning

Used with permission from Wolters Kluwer Health: Walz JM, Kaur S,

Heard SO Airway management and endotracheal intubation In: Irwin

RS, Rippe JM, Lisbon A, Heard SO, editors Irwin and Rippe’s

Procedures, Techniques and Minimally Invasive Monitoring in Intensive

Care Medicine [ 10 ]

Endotracheal Tube (ETT)

Endotracheal tubes (ETT) are made from polyvinyl chloride

The internal diameter of the tube is measured in millimeters

or French units [3 × internal diameter (in mm)] The former is

stamped on the tube while the latter is noted on the proximal

adapter of the tube The length (in cm) is also stamped

begin-ning at the distal end [ 10 ] The tube has a high-volume low-

pressure cuff which is infl ated to create a seal allowing

positive pressure ventilation The normal tracheal capillary

pressure is 32 mmHg If cuff pressure is >32 mmHg,

emic damage can occur The complications related to

isch-emia include tracheal-innominate artery fi stula,

tracheoesophageal fi stula, tracheomalacia, or tracheal

steno-sis [ 10] It is important to remember that high-volume

low- pressure cuffs can be converted into high-pressure cuffs

if they are infl ated with enough air thereby increasing the

risk of mucosal damage The dimensions of the tubes and

suggested size based on age are seen in Table 2.3

Medications for Intubation

When an emergent airway is needed during nary arrest, typically no anesthetics are required In the ICU setting, little medication is usually necessary as patients often have a decreased level of consciousness If a patient is awake or responds to stimulation from mask ventilation or during laryngoscopy, sedation or general anesthesia may be required Laryngoscopy in an inadequately sedated or anes-thetized patient can cause tachycardia and hypertension which may be poorly tolerated in the patient with coronary artery disease or intracranial hypertension NPO status, comorbid medical conditions, and risk of aspiration should

cardiopulmo-be established prior to medicating the patient Table 2.4 delineates commonly used medications used for intubation Midazolam , a short-acting benzodiazepine, acts as a seda-tive and amnestic agent The usual dose is 0.5–2 mg IV It causes respiratory depression and hypotension and abolishes protective airway refl exes

Fig 2.2 Modifi ed Mallampati classifi cation Class I: the soft palate,

uvula, fauces, and pillars are visible Class II: the soft palate, uvula, and

fauces are visible Class III: the soft palate and base of uvula are visible

Class IV: only the hard palate is visible Reproduced with permission

from BioMed Central, Huang H-H, Lee M-S, Shih Y-L, Chu H-C, Huang T-Y, Hsieh T-Y Modifi ed Mallampati classifi cation as a clinical predictor of peroral esophagogastroduodenoscopy tolerance BMC Gastroenterology 2011; 11: 12 [ 60 ]

C Kuza et al.

Opioids may also be used to sedate the patient and blunt

the hypertensive response associated with laryngoscopy

Fentanyl is a commonly used synthetic opioid Its potency is

100 times that of morphine and has a shorter duration of

action The typical dose is 25–100 mcg IV

Other commonly used anesthetics include propofol,

etomidate, and ketamine The patient’s hemodynamic status

must be considered when deciding which agent to use

Propofol decreases systemic vascular resistance and causes

myocardial depression and is not an ideal agent in patients who have congestive heart failure, hypovolemia, or hypoten-sion Phenylephrine (40–120 mcg IV) may be used prior to propofol administration to optimize the patient’s blood pressure The dose of propofol is 1–2.5 mg/kg Lower doses should be administered if midazolam and fentanyl are used concomitantly Ketamine and etomidate provide more hemo-dynamic stability The intubating dose for etomidate is 0.2–0.3 mg/kg IV Although it has minimal effects on the

100 90 80 70 60

50 40 30 20 10 0

50 40 30 20 10 0

Fig 2.3 Percentage of diffi cult intubations in the original cohort ( a )

and validation cohort ( b ) Point system (total possible—12): Mallampati

score III or IV [5 points], obstructive sleep apnea [2 points], reduced

mobility of cervical spine [1 point], limited mouth opening <3 cm [1

point], coma [1 point], sere hypoxemia [1 point] nonanesthesiologist

performing intubation [1 point] Reprinted with permission from the

American Thoracic Society Copyright © American Thoracic Society

De Jong A, Molinari N, Terzi N, et al Early identifi cation of patients at risk for diffi cult intubation in the intensive care unit: development and validation of the MACOCHA score in a multicenter cohort study Am J Respir Crit Care Med 2013;187(8):832–839 [ 8 ]