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Section I - The Respiratory System

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Chapter 1 - Asthma and Chronic Obstructive Pulmonary Disease


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Chapter 2 - Bronchoscopy, Mediastinoscopy, and Thoracotomy


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Chapter 3 - Aspiration Pneumonitis and Acute Respiratory Failure


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Chapter 4 - Lung Transplantation


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Chapter 5 - Tracheoesophageal Fistula


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Chapter 6 - Congenital Diaphragmatic Hernia


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Section II - The Cardiovascular System


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Chapter 7 - Ischemic Heart Disease and Coronary Artery Bypass Grafting


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Chapter 8 - Valvular Heart Disease


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Chapter 9 - Pacemakers and Implantable Cardioverter-Defibrillators


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Chapter 10 - Thoracoabdominal Aortic Aneurysms


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Chapter 11 - Abdominal Aortic Aneurysm Repair


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Chapter 12 - Hypertension

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Chapter 13 - Cardiac Tamponade


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Chapter 14 - Heart Transplantation and Subsequent Noncardiac Surgery


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Chapter 15 - Ischemic Heart Disease and Noncardiac Surgery


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Chapter 16 - Tetralogy of Fallot


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Chapter 17 - Transposition of the Great Arteries


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Chapter 18 - Patent Ductus Arteriosus and Prematurity


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Section III - The Gastrointestinal System


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Chapter 19 - Intestinal Obstruction


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Chapter 20 - Liver Transplantation


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Chapter 21 - Pyloric Stenosis


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Section IV - The Endocrine System


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Chapter 22 - Brain Tumor and Craniotomy


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Chapter 23 - Carotid Endarterectomy


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Chapter 24 - Awake Craniotomy for Deep Brain Stimulation


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Chapter 25 - Management of Head Injury


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Chapter 26 - Cerebral Aneurysm


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Section V - Pain Management and Neuraxial Blocks


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Chapter 27 - Brachial Plexus Block


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Chapter 28 - Nerve Blocks of the Lower Extremity


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Chapter 29 - Complex Regional Pain Syndromes


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Chapter 30 - Cancer Pain


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Chapter 31 - Low Back Pain and Sciatica


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Chapter 32 - Perioperative Pain Management


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Chapter 33 - Acupuncture
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Section VI - The Endocrine System


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Chapter 34 - Thyrotoxicosis
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Chapter 35 - Pheochromocytomas

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Chapter 36 - Diabetes Mellitus


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Section VII - The Genitourinary System


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Chapter 37 - Transurethral Resection of the Prostate


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Chapter 38 - Kidney Transplant


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Chapter 39 - Laparoscopic Surgery


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Section VIII - The Reproductive System


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Chapter 40 - Peripartum Hemorrhage


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Chapter 41 - Hypertensive Disorders of Pregnancy


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Chapter 42 - Transverse Lie, Fetal Distress, and Mitral Stenosis


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Chapter 43 - Appendectomy for a Pregnant Patient


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SECTION IX - The Hematologic System


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Chapter 44 - Hemophilia and Coagulation Disorders


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Chapter 45 - Sickle Cell Disease


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SECTION X - Eye, Ear, Nose, and Throat


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Chapter 46 - Airway Trauma


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Chapter 47 - Open-Eye Injury


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Chapter 48 - Laser Treatment for Laryngeal Lesions


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Chapter 49 - Airway Obstruction in Childhood: Stridor and Croup Syndromes


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Chapter 50 - Cleft Palate


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Chapter 51 - Congenital Heart Disease with a Cervical Mass in Infancy


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SECTION XI - Miscellaneous
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Chapter 52 - Myasthenia Gravis


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Chapter 53 - Malignant Hyperthermia


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Chapter 54 - Prolonged Postoperative Apnea


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Chapter 55 - Burns
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Chapter 56 - Trauma
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Chapter 57 - Scoliosis

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Chapter 58 - Hypoxia and Equipment Failure


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Chapter 59 - Electroconvulsive Therapy


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Chapter 60 - Ambulatory Surgery


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Chapter 61 - Magnetic Resonance Imaging


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Chapter 62 - Morbid Obesity

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Editor-in-Chief
Fun-Sun F. Yao MD Professor Department of Anesthesiology, Weill Medical College of Cornell University; Attending Anesthesiologist, New York Presbyterian Hospital, New York

Associate Editors
Vinod Malhotra MD Professor Department of Anesthesiology, Weill Medical College of Cornell University; Vice-Chair for Clinical Affairs, Clinical Director of Operating Rooms, Department of Anesthesiology, New York Presbyterian Hospital, New York

Manuel L. Fontes MD Associate Professor of Anesthesiology and Critical Care Weill Medical College of Cornell University; Co-Director of Cardiothoracic Intensive Care Unit, Associate Attending Anesthesiologist, Department of Anesthesiology, New York Presbyterian Hospital, New York

Contributors List
Sharon Abramovitz MD Associate Attending Physician Department of Anesthesiology, New York Presbyterian Hospital, New York

Shakil Ahmed MD, MB, BS, FRCS (RCS Glasgow) Assistant Professor of Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University; Attending A n e s t h e s i o l o g i s t , D e p a r t m e n t o f A n e st h e s i o l o g y , N e w Y o r k P r e s b y t e r i a n H o s p i t a l , N e w York

Rae M. Allain MD Instructor in Anesthesia Department of Anesthesia and Critical Care, Harvard University; Assistant in Anesthesia, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts

Paul Barash MD Professor Department of Anesthesiology, Yale University School of Medicine; Attending Anesthesiologist, Yale-New Haven Hospital, New Haven, Connecticut.

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Matthew R. Belmont MD Associate Professor of Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University; Associate Attending Anesthesiologist, Department of Anesthesiology, New York, Presbyterian Hospital, New York

Jeffery S. Berger MD Assistant Professor of Anesthesiology New York University Medical School; Attending Anesthesiologist, New York University Hospital, New York

Rajesh Bhat MB, BS Assistant Professor D e p a r t m e n t o f A n e s t h e s i o l o g y , U n i v e r s i t y o f C a l i f o r n i a , S a n F r a n ci s c o , S c h o o l o f Medicine; Attending Anesthesiologist, Moffit Hospital, San Francisco, California

Eric Cappiello MD Instructor in Aneasthesia Harvard Medical School, Brighan and Women's Hospital, Boston, Massachusetts

Alan Cheng MD Assistant Professor of Medicine Department of Medicine, Division of Cardiovascular Diseases, Johns Hopkins School of Medicine; Cardiac Electrophysiologist, Department of Medicine, Division of Cardiovascular Diseases, Johns Hopkins Hospital, Baltimore, Maryland

Philip S.L. Chan MD Fellow of Pain Medicine, Weill Medical College of Cornell University; New York Presbyterian Hospital, New York

Davy C. H Cheng MD, MSc, FRCPC Professor and Chair Department(s) of Anesthesia and Preoperative Medicine, The University of Western Ontario; Department(s) of Anesthesia and Preoperative Medicine, London Health Sciences Center, London

Charles D. Collard MD Division of Cardiovascular Anesthesia, Texas Heart Institute; Associate Professor, Division of Cardiovascular Anesthesia, Baylor College of Medicine at the Texas Heart Institute, St. Luke's Episcopal Hospital, Houston, Texas

Panchali Dhar MD Assistant Professor of Clinical Anesthesiology Weill Medical College of Cornell University; Assistant Attending Anesthesiologist, New

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York Presbyterian Hospital, New York

James A. DiNardo MD Associate Professor of Anaesthesia Department of Anesthesia, Children's Hospital Boston, Harvard Medical School; Senior Associate in Cardiac Anesthesia, Cardiac Anesthesia Fellowship Director, Children's Hospital Boston, Boston, Massachusetts

Miles Dinner MD Professor of Clinical Anesthesiology C o r n e l l U n i ve r s i t y M e d i c a l C o l l e g e , N e w Y o r k P r e s b y t e r i a n H o s p i t a l , N e w Y o r k

Sudhir Diwan MD, MS Director Division of Pain Medicine, New York Presbyterian Hospital; Associate Professor of C l i n i c a l A n e s t h e s i o l o g y , D e p a r t m e n t o f A n e s t h e s i o l o g y, W e i l l M e d i c a l C o l l e g e o f C o r n e l l University, New York

Richard P. Dutton MD, MBA Associate Professor Department of Anesthesiology, University of Maryland School of Medicine; Director of Trauma Anesthesiology, R Adams Cowley Shock Trauma Center, University of Maryland Medical System, Baltimore

Chris Edmonds MD C l i n i ca l A s s i s t a n t P r o f e s s o r o f A n e s t h e s i o l o g y Weill Medical College of Cornell University; Assistant Attending Anesthesiologist, Hospital for Special Surgery, New York

James B. Eisenkraft MD Professor Department of Anesthesiology, Mount Sinai School of Medicine of New York University; Attending Anesthesiologist, Department of Anesthesiology, The Mount Sinai Medical Center, New York

Jill Fong MD Associate Professor of Clinical Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University, New York

Manuel L. Fontes MD Associate Professor of Anesthesiology and Critical Care Department of Anesthesiology, Weill Medical College of Cornell University; Co-Director Cardiothoracic Intensive Care Unit, Department of Anesthesiology, New York

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Presbyterian Hospital, New York

Elizabeth A.M. Frost MD Professor D e p t o f A n e s t h e s i o l o g y , M o u n t S i n a i M e d i ca l C e n t e r ; A t t e n d i n g p r o f e s s o r , D e p t o f Anesthesiology, Mount Sinai Medical Center, New York

Eugene S. Fu MD Associate Professor Department of Anesthesiology, University of Miami; Chief of Neuroanesthesia, D e p a r t m e n t o f A n e s t h e s i o l o g y, J a c k s o n M e m o r i a l H o s p i t a l , M i a m i , F l o r i d a

Farida Gadalla MD Professor of Clinical Anesthesiology Department of Anesthesiology, Weill Cornell Medical College, New York Presbyterian Hospital, New York

Matthew C. Gomillion MD Associate Professor of Clinical Anesthesiology Weill Medical College of Cornell University, New York

Marbelia Gonzalez MD Staff Anesthesiologist Department of Anesthesia, Hartford Hospital, Hartford, Connecticut

Jeff T. Granton MD, FRCPC Assistant Professor Anesthesia and Perioperative Medicine, University of Western Ontario; Cardiac Anesthesiologist and Intensivist, Anesthesia and Perioperative Medicine, London Health Sciences Centre, London, Ontario, Canada

Dana L. Gurvitch MD Assistant Professor Department of Anesthesia, Weill Medical College of Cornell University; Department of Anesthesia, New York Presbyterian Hospital, New York

Marcus Gutzler MD Instructor in Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University; Assistant Attending Anesthesiologist, Department of Anesthesiology, New York Presbyterian Hospital, New York

Jung Hee Han MD

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Clinical Instructor Department of Anesthesiology, Weill Medical College of Cornell University; Assistant Attending, Department of Anesthesiology, New York Presbyterian Hospital, New York

Leo T. Harris MPH Physician Assistant Department of Neurosurgery, University of Miami; Physician Assistant, Department of Neurosurgery, Jackson Memorial Hospital, Miami, Florida

Gregg S. Hartman MD Professor Department of Anesthesiology, Dartmouth-Hitchcock Medical Center, Lebanon

Paul M. Heerdt MD, PhD Professor Department of Anesthesiology and Pharmacology, Weill Medical College of Cornell University, New York

Hugh C. Hemmings Jr. MD, PhD Professor and Vice Chair of Research Department of Anesthesiology and Pharmacology, Weill Medical College of Cornell University, New York

Charles W. Hogue Jr. MD Associate Professor of Anesthesiology Johns Hopkins School of Medicine; Attending Anesthesiologist, Johns Hopkins Hospital, Baltimore, Maryland

Jagid Jonathan R. MD Assistant Professor of Neurological Surgery D e p a r t m e n t o f N e u r o s u r g e r y , U n i v e r s i t y o f M ia m i ; A s s i s t a n t P r o f e s s o r o f N e u r o l o g i c a l Surgery, Department of Neurosurgery, Jackson Memorial Hospital, Miami, Florida

Robert E. Kelly MD Professor Clinical Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University; Attending Anesthesiologist, Department Anesthesiology, New York Presbyterian Hospital, New York

Gregory E. Kerr MD Associate Professor of Anesthesiology Weill Medical College of Cornell University; Associate Attending Anesthesiologist, D i r e c t o r , C a r d i a c A n e s t h e si a , N e w Y o r k P r e s b y t e r i a n H o s p i t a l , N e w Y o r k

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Klaus Kjaer-Pedersen MD Assistant Professor of Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University; Attending A n e s t h e s i o l o g i s t , D e p a r t m e n t o f A n e st h e s i o l o g y , N e w Y o r k P r e s b y t e r i a n H o s p i t a l , N e w York

Theresa T. Kudlak MD Attending Anesthesiologist Maine Medical Center, Portland, Maine Clinical Associate Professor, University of Vermont College of Medicine, Burlington, Vermont

J. Lance LaFleur MD Department of Anesthesiology, University of Texas Medical School at Houston

Jonathan Leff MD Assistant Professor of Anesthesiology Mount Sinai Medical College, Montefoire Medical Center, Bronx, New York

Wilton C. Levine MD Instructor of Anesthesiology Harvard Medical School; Massachusetts General Hospital, Department of Anesthesia and Critical Care, Boston, Massachusetts

Andrew B. Leibowitz MD Associate Professor Department of Anesthesiology and Surgery, Mount Sinai School of Medicine of New York University; Executive Vice Chair, Department of Anesthesiology, Mount Sinai Hospital, New York

Barbara Leighton MD Professor of Anesthesiology, Professor of Obstetrics and Gynecology W a s h i n g t o n U n i v e r s i t y S c h o o l o f M e d i c i n e i n S t . L o u i s ; A t t e n d i n g A n e st h e s i o l o g i s t , Chief, Division of Obstetric Anesthesia, Barnes Jewish Hospital, St. Louis, Missouri

Cynthia A. Lien MD Professor of Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University

Yuan-Chi Lin MD, MPH Associate Professor of Anaesthesia and Pediatrics Department of Anaesthesia, Harvard Medical School; Director, Medical Acupuncture Service, Department of Anesthesiology, Perioperative and Pain Medicine, Children's Hospital Boston, Boston, Massachusetts

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Jaideep K. Malhotra MD Assistant Professor of Clinic Anesthesiology Weill Medical College of Cornell University; Assistant Attending Anesthesiologist, New York Presbyterian Hospital, New York

Vinod Malhotra MD Professor Department of Anesthesiology, Weill Medical College of Cornell University; Vice-Chair for Clinical Affairs, Clinical Director of Operating Rooms, Department of Anesthesiology, New York Presbyterian Hospital, New York

Kathryn E. McGoldrick MD Professor and Chair Department of Anesthesiology, New York Medical College; Director, Department of Anesthesiology, Westchester Medical Center, Valhalla, New York

Jeffrey Y. Ngeow MBBS Clinical Associate Professor Department of Anesthesiology, Weill Medical College of Cornell University; Attending A n e s t h e s i o l o g i s t , D e p a r t m e n t o f A n e st h e s i o l o g y , H o s p i t a l f o r S p e c i a l S u r g e r y , N e w Y o r k

James Albert Osorio MD Assistant Professor Anesthesiology and Critical Care, Department of Anesthesiology, Weill Medical College o f C o r n e l l U n i v e r s i t y ; A s s i s t a n t A t t e n d i n g A n e st h e s i o l o g i s t , A n e s t h e s i o l o g y a n d C r i t i c a l Care, Department of Anesthesiology, New York Presbyterian Hospital, New York

Alessia C. Pedoto MD Assistant Member Level I, Memorial Sloane-Kettering Cancer Center; Assistant Attending Anesthesiologist, Anesthesiology and Critical Care Medicine, Memorial Hospital for Cancer and Allied Diseases, New York

Robert A. Peterfreund MD, PhD Associate Professor of Anesthesia Department of Anesthesia, Harvard Medical School; Anesthetist, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts

Kane O. Pryor MD Assistant Professor Department of Anesthesiology, Weill Medical College of Cornell University; Assistant Attending Anesthesiologist, Department of Anesthesiology, New York Presbyterian Hospital, New York

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Narinder Rawal MD, PhD Professor Dept of Anesthesiology and Intensive Care, rebro University Hospital, Grev Rosengatan, Sweden

Henry Rosenberg MD Professor Department of Anesthesiology, Mount Sinai School of Medicine, New York; Director, Department of Medical Education and Clinical Research, Saint Barnabas Medical Center, Livingston, New Jersey

Lori A. Rubin MD Assistant Professor of Anesthesiology New York Presbyterian Hospital, Weill Medical College of Cornell University, New York

Isobel Russell MD, PhD, FACC Professor Department of Anesthesia, University of California, San Francisco; Chief of Cardiac Anesthesia, University of California, San Francisco Medical Center, San Francisco, California

Jon D. Samuels MD Assistant Professor Department of Anesthesiology, Weill Medical College of Cornell University; Attending A n e s t h e s i o l o g i s t , D e p a r t m e n t o f A n e st h e s i o l o g y , N e w Y o r k P r e s b y t e r i a n H o s p i t a l , N e w York

John J. Savarese MD Professor and Chair Department of Anesthesiology, Weill Medical College of Cornell University; Anesthesiologist-in-Chief, New York Presbyterian Hospital, New York

Jacques H. Scharoun MD Assistant Professor Department of Anesthesiology, Weill Medical College of Cornell University; Attending P r o f e s s o r , D e p a r t m e n t o f A n e s t h e s i o l o g y , N e w Y o r k P r e sb y t e r i a n H o s p i t a l , N e w Y o r k

Manu Sethi MD Division of Cardiovascular Anesthesia, Texas Heart Institute; Assistant Professor, Division of Cardiovascular Anesthesia, Baylor College of Medicine at the Texas Heart Institute, St. Luke's Episcopal Hospital, Houston, Texas

Aarti Sharma MD

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Assistant Professor Department of Anesthesia, Weill Medical College of Cornell University; Assistant Attending, Department of Anesthesia, New York Presbyterian Hospital, New York

Linda Shore-Lesserson MD Associate Professor of Anesthesiology Mount Sinai Medical College; Chief, Division of Cardiothoracic Anesthesiology, Montefoire Medical Center, Bronx, New York

Vijayendra Sudheendra MD Clinical Assistant Professor Department of Surgery and Anesthesiology, Brown University School of Medicine, Providence, Rhode Island; Director of Cardiothoracic Anesthesia, Miriam Hospital, Providence, Rhode Island; Medical Director, Southern New England Surgicenter, Attleboro, Massachusetts

Nikolaos Skubas MD Assistant Professor Department of Anesthesiology, Weill Medical College of Cornell University; Director, Perioperative Echocardiography, Department of Anesthesiology, New York Hospital, New York

Ralph L. Slepian MD Associate Professor of Clinical Anesthesiology Weill Medical College of Cornell University; Associate Attending Anesthesiologist, New York Presbyterian Hospital, New York

David G. Stein MD Assistant Professor of Anesthesiology Department of Anesthesiology, Weill Medical College of Cornell University; Attending A n e s t h e s i o l o g i s t , D e p a r t m e n t o f A n e st h e s i o l o g y , N e w Y o r k P r e s b y t e r i a n H o s p i t a l , N e w York

Cephas P. Swamidoss MD, MS, MPH Associate Professor of Clinical Anesthesia Department of Anesthesiology, Weill Medical College of Cornell University; Associate Attending Anesthesiologist, Department of Anesthesiology, New York Presbyterian Hospital, New York

Stephen J. Thomas MD Topkins Van Poznak Professor Department of Anesthesiology, Weill Medical College of Cornell University; Vice Chair, Department of Anesthesiology, New York Presbyterian Hospital, New York

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Joseph Tjan MD Assistant Professor Department of Anesthesiology, Weill Medical College of Cornell University, New York

Michael Tjeuw MD Senior Consultant Department of Anesthesia, Westmead Hospital, University of Sydney, Sydney, NSW, Australia; Honorary Professor of Anesthesiology, Burn center, South West hospital, The Third Military Medical University, Chongqing, China

David Wang MD Clinical Assistant Professor Department of Anesthesiology, Weill Medical College of Cornell University; Attending Physician, Department of Anesthesiology, Hospital for Special Surgery, New York

Judith Weingram MD Assistant Professor Department of Anesthesiology, Weill Medical College of Cornell University; Attending A n e s t h e s i o l o g i s t , D e p a r t m e n t o f A n e st h e s i o l o g y , N e w Y o r k P r e s b y t e r i a n H o s p i t a l , N e w York

Fun-Sun F. Yao MD Professor Department of Anesthesiology, Weill Medical College of Cornell University; Attending Anesthesiologist, New York Presbyterian Hospital, New York

Victor M. Zayas MD Clinical Assistant Professor of Anesthesiology and Pediatrics Department of Anesthesiology and Pediatrics, Weill Medical College of Cornell University; Director, Pediatric Anesthesiology, Department of Anesthesiology, Hospital for Special Surgery, New York

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Chapter 1 Asthma and Chronic Obstructive Pulmonary Disease


Fun-Sun F. Yao P.2 P.3

A 55-Year-Old Man
w ith cholelithiasis was schedul ed for cholecystectomy. He had a long history of asthma a nd deve lo pe d dysp ne a wi th on ly mod era te e xerti on . He sl ep t on two pi l lo ws. Th ere w as no per ip her al ede ma . Arteri al b lo od g ase s show ed th e following : pH 7.3 6; PCO 2 , 60 mm Hg; PO 2 , 70 mm H g; CO 2 co nten t, 36 mEq p er L .

A. Medical Disease and Differential Diagnosis A.1. What differential diagnosis is compatible with these symptoms?
The differential diagnosis of wheezing and dyspnea includes bronchial asthma, acute left ventricular failure (cardiac asthma), upper airway obstruction by tumor or laryngeal edema, endobronchial disease such as foreign body aspiration, neoplasms, bronchial stenosis, carcinoid tumors, recurrent pulmonary emboli, chronic bronchitis, eosinophilic pneumonias, chemical pneumonias, and occasionally polyarteritis. To differentiate asthma from other diseases with wheezing and dyspnea is usually not difficult. The triad of dyspnea, coughing, and wheezing, in addition to a history of periodic attacks, is quite characteristic. A personal or family history of allergic diseases is valuable contributory evidence. A patient with long-standing asthma may develop chronic obstructive lung disease and suffer from exertional dyspnea and orthopnea. Cardiac asthma is a misnomer and refers to acute left ventricular failure. Although the primary lesion is cardiac, the disease manifests itself in the lungs. The symptoms and signs may mimic bronchial asthma, but the findings of moist basilar rales, gallop rhythms, blood-tinged sputum, peripheral edema, and a history of heart disease allow the appropriate diagnosis to be reached. Gould BE. Pathophysiology for the health professions, 3rd ed. Philadelphia: Saunders Elsevier, 2006:393398. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15081516.

A.2. What is the prevalence of asthma?


Approximately 4% to 5% of adults and 7% to 10% of children in the United States and Australia have asthma. It occurs at all ages but is predominant in early life. Approximately half the number of the patients develop asthma before age 10 and another one third of them before age 40. In childhood, there is a 2:1 male/female preponderance, which equalizes by age 30. P.4 Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15081516. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:194.

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A.3. What is the etiology of asthma?


Asthma is a heterogeneous disease, the etiology of which is difficult to define. The common denominator that underlies the asthmatic diathesis is a nonspecific hyperirritability of the tracheobronchial tree. Clinically, asthma is classified into two groups: allergic (extrinsic) and idiosyncratic (intrinsic). Allergic asthma is usually associated with a personal or a family history of allergic diseases, positive skin reactions to extracts of airborne antigens, and increased levels of immunoglobulin E (IgE) in the serum. Immunologic mechanisms appear to be causally r e l a t e d t o 2 5 % t o 3 5% o f a l l c a s e s a n d c o n t r i b u t o r y i n a n o t h e r o n e t h i r d o f t h e m . I d i o s y n c r a t i c asthma cannot be classified on the basis of immunologic mechanisms, and it is probably due to abnormality of the parasympathetic nervous system. Bronchospasm is provoked when certain agents stimulate tracheobronchial receptors. Intraoperative bronchospasm is probably usually cholinergically mediated. Afferent receptors in the bronchial mucosa can be an initiating event although such an event is not always identifiable. Efferent parasympathetic fibers travel to bronchial smooth muscle and can then result in bronchoconstriction by stimulation of the M3 cholinergic receptors on bronchial smooth muscle. Following release of acetylcholine (Ach) at the M3 receptor, the Ach will stimulate the M2 muscarinic receptor, which is an inhibitory receptor that limits further release of Ach. Alterations of M2 receptor function may contribute to bronchospasm. Brusse WW, Lemanske RF. Asthma. N Engl J Med 2001;344:350362. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15081516.

A.4. Discuss the pathogenesis of asthma


Asthma is a chronic disease characterized by chronic airway inflammation, reversible expiratory airflow obstruction resulting from narrowing of the airways in response to various stimuli, and airway hyperreactivity. The common denominator underlying the asthmatic diathesis is a nonspecific hyperirritability of the tracheobronchial tree. The basic mechanism of the persistent subacute airway hyperirritability remains unknown. The most popular hypothesis is that of subacute airway inflammation. Even when asthmatics are in remission, bronchial biopsy reveals infiltration by inflammatory cells and epithelial shedding from the mucosa. After exposure to an initiating stimulus, mast cells, eosinophils, lymphocytes, epithelial cells, and macrophages can be activated to release various mediators that lead to contraction of airway smooth muscle (bronchospasm), vascular congestion, increased capillary permeability (edema of bronchial mucosa), and thick tenacious secretions, thereby evoking an intense inflammatory reaction (Fig. 1.1). The net result is a reduction in airway diameter, an increase in airway resistance, decreased forced expiratory volumes and flow rates, hyperinflation of the lungs and thorax, increased work of breathing, alterations in respiratory tract muscle function, mismatched ventilation/perfusion, and altered blood gases. Brusse WW, Lemanske RF. Asthma. N Engl J Med 2001;344:350362. Djukanvic R, Roche WR, Wilson JW, et al. State of the art: mucosal inflammation in asthma. Am Rev Respir Dis 1990;142:434457. P.5 Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15151516.

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Figure 1.1 The pathogenesis of bronchial asthma. IgE, immunoglobulin E.

A.5. What are the predisposing factors of asthmatic attacks?


Allergens. Airborne allergens are the most common. Pharmacologic stimuli. The drugs most commonly associated with the induction of acute a s t h m a t i c a t t a c k s a r e a sp i r i n , c o l o r i n g a g e n t s s u c h a s t a r t r a z i n e , - a d r e n e r g i c antagonists, and sulfiting agents. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin, mefenamic acid, ibuprofen, fenoprofen, flufenamic acid, naproxen, and phenylbutazone make the asthma worse because of inhibition of prostaglandin G/H synthase 1 (cyclooxygenase type 1).

Environment and air pollution. Some types of asthma, such as Tokyo-Yokohama or New Orleans asthma, tend to occur in individuals who live in heavy industrial or dense urban

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areas.

Occupational factors. Various compounds used in industry can cause asthma in susceptible individuals. Various names have been applied to this condition, such as meat wrapper's asthma, baker's asthma, and woodworker's asthma.

Infections. Respiratory tract infections are among the most common stimuli that evoke acute asthmatic attacks.

Exercise. Asthma can be induced or made worse by physical exertion. Emotional stress is also a factor.

P.6 Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15151516. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:196198.

A.6. What is the universal finding in arterial blood gases during asthmatic attacks: Hypoxemia or CO 2 retention?
Hypoxemia is a universal finding during asthmatic attacks. However, frank ventilatory failure with CO2 retention is relatively uncommon because CO2 has a diffusion capacity that is 20 times higher than that of oxygen. During acute asthmatic attacks, most patients try to overcome airway obstruction and hypoxia by hyperventilation. This results in hypocarbia and respiratory alkalosis. CO2 retention is a late finding and indicates severe and prolonged airway obstruction, as in status asthmaticus. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15151516.

A.7. What changes are seen in spirometry, lung volumes, and lung capacities during an asthmatic attack?
The forced vital capacity (FVC) is usually normal but may be decreased during a severe attack. The forced expiratory volume at 1 second (FEV1) is sharply reduced, usually to less than 50% of the FVC, typically less than 40% of that predicted. The maximum midexpiratory flow rate (MMEFR) and maximum breathing capacity (MBC) are sharply reduced as well. Residual volume (RV) is markedly increased, frequently approaching 400% of normal, and expiratory reserve volume (ERV) is moderately decreased. Therefore, FRC and total lung capacity (TLC) are increased. FRC frequently doubles. Gold MI, Han YH, Helrich M. Pulmonary mechanics and blood gas tensions during anesthesia in asthmatics. Anesthesiology 1966;27:216. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15151516. Kingston HGG, Hirshman CA. Perioperative management of the patient with asthma. Anesth Analg 1984;63:844.

B. Preoperative Evaluation and Preparation B.1. What preoperative workup would you order?

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The goal of preoperative evaluation is to formulate an anesthesia plan that prevents or blunts obstruction to expiratory airflow. In addition to routine tests such as complete blood cell count; serum electrolytes; urinalysis; electrocardiogram; and coagulation screening; special attention s h o u l d b e p a i d t o c a r d i o p u l m o n a r y f u n c t i o n ; c h e s t x - r a y f i l m ; p u l m o n a r y f un c t i o n t e s t r e s u l t s , including response to bronchodilator; and baseline arterial blood gases. A history of allergy and symptoms and signs of cardiac or respiratory failure must be checked carefully. P.7 Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:200.

B.2. How would you distinguish obstructive lung disease from restrictive lung disease by spirometry?
Table 1.1 summarizes the distinctions between the two types of lung diseases. In restrictive lung disease (e.g., pulmonary fibrosis and ankylosing spondylitis), the FVC is low because of limited expansion of the lungs or chest wall. However, the FEV1 is often not reduced proportionately, because airway resistance is normal. Therefore, the FEV1/FVC percentage is normal or high. In obstructive lung disease (e.g., emphysema), the FEV1/FVC is grossly reduced because the airway resistance is high. MBC and MMEFR are reduced early in small airway obstruction. MMEFR is also called FEF25%75% (forced expiratory flow). MMEFR is obtained by dividing the volume between 75% and 25% of the vital capacity (VC) by the corresponding elapsed time. Unlike FEV1, MMEFR is independent of patient effort. Normally, FEV1 is more than 80% of FVC and VC should be more than 80% of predicted value. The predicted values depend on body size, age, and sex. The TLC is increased in obstructive lung disease and decreased in restrictive lung disease. However, TLC cannot be obtained by routine screening spirometry. Normal MBC is more than 125 L per minute and normal MMEFR is more than 300 L per minute. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:807. Crapo RO. Pulmonary function testing. N Engl J Med 1994;331:2530. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:14991500.

B.3. Define normal lung volumes and lung capacities and their normal values in the average adult male
There are four basic volumes and four derived capacities that are combinations of these volumes (Fig. 1.2). Tidal volume (VT) is the volume of air inhaled or exhaled during normal breathing. Normal VT is 500 mL or approximately 6 to 8 mL per kg. Inspiratory reserve volume (IRV) is the maximum volume of gas that can be inhaled after a normal inspiration while at rest. Normal IRV is 2,000 to 3,000 mL.

Table 1.1 Differences between Obstructive and Restrictive Lung Diseases. OBSTRUCTIVE Vital capacity N or RESTRICTIVE

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Total lung capacity Residual volume FEV1/FVC Maximum midexpiratory flow rate Maximum breathing capacity

N or

N or N N

N, normal; , decreased; , increased; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity.

P.8

Figure 1.2 Lung volumes and lung capacities.

Expiratory reserve volume (ERV) is the maximum volume of gas that can be exhaled after a normal expiration. Normal ERV is 1,000 mL. R e s i d u a l v o l u m e ( R V ) i s t h e v o l u m e o f g a s r em a i n i n g i n t h e l u n g s a f t e r a f o r c e d e x h a l a t i o n . Normal RV is 1,500 mL.

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Vital capacity (VC) is the maximum amount of gas that can be exhaled after a maximum inhalation. VC is the sum of VT, ERV, and IRV. Normal VC is approximately 60 mL per kg. Inspiratory capacity (IC) is the maximum amount of gas that can be inhaled from the resting expiratory position after a normal exhalation. It is the sum of VT and IRV. Normal IC is 3,500 mL. Functional residual capacity (FRC) is the remaining lung volume at the end of a normal quiet expiration. It is the sum of RV and ERV. Normal FRC is 2,500mL. Total lung capacity (TLC) is the lung volume at the end of a maximum inspiration. It is the sum of VC and RV. Normal TLC is 5,000 to 6,000 mL. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:804805 Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:3335.

B.4. What are flowvolume loops? Draw flowvolume loops in a healthy subject, in a patient with COPD, and in a patient with restrictive lung disease
Flowvolume loops provide a graphic analysis of flow at various lung volumes. Both flow and volume are plotted simultaneously on an XY recorder as subjects inspire fully to TLC and then perform an FVC maneuver. This is immediately followed by maximum inhalation as fast as possible back to TLC (Fig. 1.3). The entire inspiratory portion of the loop and the expiratory curve near TLC are highly effort dependent, and the expiratory flow at 75% to 25% of VC is effort independent. The normal expiratory flow/inspiratory flow ratio at 50% of VC (mid-VC flow ratio) is approximately 1.0. This ratio is particularly useful in identifying the presence of upper airway obstruction. In patients with restrictive lung disease such as pulmonary fibrosis and scoliosis, P.9 a reduction is seen in FVC, with a relatively normal FEV1. The TLC is markedly reduced, and FEF25%75% and mid-VC flow ratio are usually normal (Fig. 1.4). In patients with obstructive lung disease, peak expiratory flow rate, FEF25%75%, and mid-VC flow ratio are reduced, but TLC is increased secondary to the increase in RV, as shown in Fig. 1.4.

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Figure 1.3 Flowvolume loop in a healthy subject. V75, V50, and V25 represent flow at 75%, 50%, and 25% of vital capacity, respectively. RV, residual volume. (From Goudsouzian N, Karamanian A. Physiology for the anesthesiologist, 2nd ed. Norwalk, CT: Appleton-Century-Crofts, 1984, with permission.)

A variable obstruction is defined as a lesion with influence that varies with the phase of respiration. In variable extrathoracic obstructions such as vocal cord paralysis or tracheal stenosis, during forced inspiration the respiratory flow is reduced because the negative transmural pressure inside the airway tends to collapse the airway. During expiration, the expiratory flow is reduced far less and may be normal because the positive pressure inside the airway tends to decrease the obstruction (Fig. 1.4). On the contrary, in variable intrathoracic obstruction, the expiratory flow is markedly reduced because the high positive intrapleural pressures during forced expiration decrease airway diameter, and the inspiratory flow is far less reduced because the negative intrapleural pressure tends to increase the diameter of the airway. (Also see Fig. 34.1 in Chapter 34.) Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:806. Goudsouzian N, Karamanian A. Physiology for the anesthesiologist, 3rd ed. Norwalk, CT: Appleton-Century-Crofts, 1984:212213. Miller RD, ed. Miller's anesthesia, 6th ed. Philadelphia: Elsevier Churchill Livingstone, 2005:10081009. P.10

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Figure 1.4 Flowvolume loops relative to lung volumes in a healthy subject, a patient with chronic obstructive pulmonary disease (COPD), a patient with fixed obstruction (tracheal stenosis), and a patient with pulmonary fibrosis (restrictive defect). Note the concave expiratory form in the patient with COPD and the flat inspiratory curve in the patient with a fixed obstruction. (From Goudsouzian N, Karamanian A. Physiology for the anesthesiologist, 2nd ed. Norwalk, CT: AppletonCentury-Crofts, 1984, with permission.)

B.5. Define closing capacity (CC) and closing volume (CV). What is the normal value of CV?
CC is the lung volume at which the small airways in the dependent parts of the lung begin to close. CC is the sum of CV and residual volume (RV). CV is the gas volume expelled during phase IV of the single-breath nitrogen test; it denotes the lung volume from the beginning of airway closure to the end of maximum expiration. Therefore, CV = CCRV (Fig. 1.5). In healthy young people, CV is approximately 10% of the VC, or 400 to 500 mL. CV and CC increase with age. CV is increased in patients with small airway disease and in chronic smokers. Buist AS. The single-breath nitrogen test. N Engl J Med 1975;293:438. Closing volume [Editorial]. Lancet 1972;2:908. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:44.

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B.6. What are the effects of age and posture on FRC and CC?
FRC is either independent of age in adults or increases very slightly with age, increasing by around 16 mL per year. CC, however, increases with age. Normally, CC becomes equal to FRC at the age of 66 in the upright position and at the age of 44 in the supine position. P.11

Figure 1.5 Closing volume measurement by single-breath nitrogen test. CC, closing capacity; CV, closing volume; RV, residual volume; TLC, total lung capacity.

FRC increases by approximately 30% by changing from the supine position to the upright position. CC, on the other hand, is independent of body position. It is important to remember that the effects of age on CC and posture on FRC determine whether airway closure exists. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:34, 44. Rehder K, Marsh HM, Rodarte JR, et al. Airway closure. Anesthesiology 1977;47:40.

B.7. What are the effects of anesthesia on FRC and closing capacity (CC)?
During anesthesia, FRC is reduced by approximately 20% with spontaneous breathing and by approximately 16% with artificial ventilation. This is due to changes in the chest wall shape and diaphragm position. After induction of general anesthesia, a reduction occurs in the crosssectional area of the rib cage corresponding to a decrease in lung volume of approximately 200 mL. Recent studies have consistently shown a cephalad movement of the dependent regions of the diaphragm, with little or no movement of the nondependent regions. However, the change in FRC that can be ascribed to changes in diaphragm is on average less than 30 mL. CC was previously reported to be unchanged during anesthesia, but later studies concluded that CC reduced in parallel to FRC during anesthesia. Bergman NA, Tien YK. Contribution of the closure of pulmonary units to impaired oxygenation

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during anesthesia. Anesthesiology 1983;59:395. Gilmour I, Burnham M, Craig DB. Closing capacity measurements during general anesthesia. Anesthesiology 1976;45:477. Juno P, Marsh HM, Knopp TJ, et al. Closing capacity in awake and anesthetized-paralyzed man. J Appl Physiol 1978;44:238. P.12 Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:304.

B.8. Why is the FRC important in oxygenation?


First, when FRC is decreased to below CC, airways close in the dependent parts of the lung during certain periods of normal tidal ventilation. Airway closure results in shunting of pulmonary blood flow through the unventilated alveoli. Therefore, QS/QT is increased and arterial oxygenation is decreased. Second, pulmonary circulation and alveolar gas exchange are continuous during both inspiratory and expiratory phases of respiration. Irrespective of whether there is airway closure or not, blood oxygenation during the expiratory phase is mainly dependent on the remaining lung volume, which is FRC. Therefore, when the FRC is high, blood oxygenation is better and there is more time for oxygenation before hypoxemia occurs during apnea. FRC is decreased in the supine position during general anesthesia and in patients with acute respiratory distress syndrome. Positive end-expiratory pressure (PEEP) increases FRC and decreases airway closure. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:34, 44.

B.9. Are there methods to measure FRC and closing volume?


FRC may be measured by helium dilution, nitrogen washout, and body plethysmography. CV may be determined by two techniques, the single-breath nitrogen test (residual gas technique) and the bolus technique with an inert tracer gas such as helium, xenon, or argon. Buist AS. The single-breath nitrogen test. N Engl J Med 1975;293:438. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:3637, 5253.

B.10. Give the equations for shunt (QS/QT) and dead space/tidal volume (VD/VT). What are their normal values?

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Normal QS/QT is 4% to 5% and VD/VT is approximately 0.3. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:803804. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:3335.

B.11. Interpret the following arterial blood gases: pH, 7.36; PCO 2 , 60 mm Hg; PO 2 , 70 mmHg; CO 2 content, 36 mEq per L
taken while the patient is breathing room air. The blood gases show mild hypoxemia and

The fraction of inspired oxygen (FIO2) is essential to evaluate PaO2. We assume the blood is respiratory acidosis, compensated by metabolic alkalosis. The blood gases are compatible with COPD. P.13

B.12. What are the common physiologic causes of hypoxemia?


From the shunt equation, arterial oxygen content is related to the change in pulmonary capillary oxygen content, venous oxygen content, and venous admixture. It is easier to classify hypoxemia into the following three categories.

Decreased Pulmonary Capillary Oxygen Tension


Hypoventilation Low FIO2 Ventilation/perfusion abnormalities from pulmonary parenchymal change Diffusion abnormality (rare)

Increased Shunting, Either Intrapulmonary or Cardiac Reduced Venous Oxygen Content


Congestive heart failurelow cardiac output Increased metabolismfever, hyperthyroidism, shivering

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Decreased arterial oxygen contentanemia

Braunwald E, Fauci AS, Kasper DL, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15031504. Malley WJ. Clinical blood gases, assessment and intervention, 2nd ed. St. Louis: Elsevier Saunders, 2005:236239. Shapiro BA, Peruzzi WT, Templin R. Clinical application of blood gases, 5th ed. Chicago: Year Book Medical Publishers, 1994:4752.

B.13. Would you order any special preoperative preparations for asthmatic patients with COPD?
Yes. The preoperative preparation should include the following:

Eradication of acute and chronic infection with appropriate antibiotics Relief of bronchial spasm with a bronchodilator Chest physiotherapy to improve sputum clearance and bronchial drainage Reversal of uncompensated or borderline cor pulmonale with diuretics, digitalis, improved oxygenation, and correction of acidemia by more efficient ventilation

Correction of dehydration and electrolyte imbalance Familiarization with respiratory therapy equipment likely to be used in the postoperative period

Cessation of smoking, if possible for 2 months, to improve mucociliary clearance and to decrease sputum production

Abstinence from smoking for 2 days (at least 12 hours), to reduce carboxyhemoglobin levels, resulting in improvement of blood oxygen content and increasing the release of oxygen in hemoglobin

Continuation of prophylactic cromolyn inhalation up to the time of surgery to prevent the degranulation of mast cells and the subsequent release of chemical mediators responsible for bronchoconstriction

Initiation of a tapered steroid therapy in the week before surgery for patients with ongoing wheezing and scheduled elective surgery

Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:484. P.14 Bishop MJ. Bronchospasm, avoiding an anesthetic disaster. In: Barash PG, ed. ASA refresher courses in anesthesiology. Park Ridge, IL: American Society of Anesthesiologists, 1991: 1527. Miller RD, ed. Miller's anesthesia, 6th ed. Philadelphia: Elsevier Churchill Livingstone, 2005:18581859.

B.14. How long would you postpone elective surgery if the patient had a recent URI?
Respiratory tract infections are the most common stimuli that evoke acute exacerbations of

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asthma. The airway responsiveness of even healthy subjects to nonspecific stimuli is transiently increased after a viral infection. Increased airway responsiveness can last from 2 to 8 weeks after the infection in both healthy subjects and asthmatics. Recently Cohen and Cameron reported that if a child had a URI and had endotracheal anesthesia, the risk of a respiratory complication increased 11-fold. In addition, Tait and Knight found that laryngospasm and bronchospasm were significantly increased even in healthy children 2 weeks after a URI. Therefore, it has been recommended to wait for 2 to 3 weeks after clinical recovery from a URI in asthmatics even if clinical symptoms are not present. Bishop MJ. Bronchospasm, avoiding an anesthetic disaster. In: Barash PG, ed. ASA refresher courses in anesthesiology. American Society of Anesthesiologists, 1991:1527. Cohen MM, Cameron CB. Should you cancel the operation when a child has an upper respiratory infection? Anesth Analg 1991;72:282288. Tait AR, Knight PR. Intraoperative respiratory complications in patients with upper respiratory tract infections. Can J Anaesth 1987;34:300303.

B.15. What medicines would you expect the patient to have taken in the past or to be taking at the present time?
The asthmatic patient might take bronchodilators such as methylxanthines and sympathomimetics. Special attention is required if the patient has taken systemic glucocorticoids. Recently, aerosol therapy has become quite popular because it provides optimal local therapeutic effects and minimizes the systemic side effects. Various relatively selective 2agonists (albuterol, fenoterol, terbutaline, and bitolterol), anticholinergic bronchodilators (ipratropium bromide and methylatropine nitrate), mast cell stabilizer (cromolyn), leukotriene receptor antagonists such as zafirlukast (Accolate) and montelukast (Singulair) and various steroids are now available as aerosols and are frequently able to control most cases of chronic asthma. Brusse WW, Lemanske RF. Asthma. N Engl J Med 2001;344:350362. Gould BE. Pathophysiology for the health professions, 3rd ed. Philadelphia: Saunders Elsevier, 2006:393398. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15081516. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:198199.

B.16. Would you order preoperative steroid preparation? Why?


It is recommended that preoperative glucocorticoid replacement therapy be given to all patients with known or suspected adrenal insufficiency. Patients who have been treated with high-dose P.15 glucocorticoids within the previous year should also be assumed to have an unknown element of adrenocortical suppression that should be treated with full replacement therapy. The human adrenal glands normally secrete approximately 30 mg of hydrocortisone (cortisol) per day under baseline conditions; however, under stress up to 200 to 500 mg a day may be secreted. It is reasonable to replace 300 mg of hydrocortisone per day during perioperative periods. The night before surgery, 100 mg of hydrocortisone acetate may be given intramuscularly. In addition, a 100-mg dose of hydrocortisone phosphate is given intravenously before induction and during surgery. Postoperatively, hydrocortisone phosphate, 100 mg intravenously, is given every 8 hours for 48 hours and then the steroid therapy is tapered. The biologic half-life of hydrocortisone is 8 to 12 hours. If the patient had less than 1 week of systemic steroid therapy

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more than 6 months previously and there are no signs of adrenal insufficiency, routine steroid preparation is not advised. However, intravenous steroid preparations should be available in the operating room in case intractable hypotension from adrenal insufficiency occurs during surgery. The increasing emphasis on reactive airways as an inflammatory disease has led to greater appreciation of the importance of steroids in controlling the incidence of attacks and in aborting acute attacks. It has been recommended that systemic steroid preparation be used preoperatively in patients with moderate to severe asthma and a history of a need for steroids in the past. One day of high-dose steroids should not significantly affect wound healing. In the face of ongoing wheezing and scheduled elective surgery, a steroid course in the week or weeks before surgery may be useful. The concern that steroids will increase the rate of wound-healing problems or infection are not well founded. A recent study of asthmatics treated with steroids preoperatively found no increase in the incidence of wound infections or wound-healing problems. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:484. Bishop MJ. Editorial views: preoperative corticosteroids for reactive airway. Anesthesiology 2004;100:10471048. Bishop MJ. Bronchospasm: successful management. In: ASA annual meeting refresher course lectures, Park Ridge, IL: American Society of Anesthesiologists, 2005:408. Kabalin CS, Yarnold PR, Grammer LC. Low complication rate of corticosteroid-treated asthmatics undergoing surgical procedures. Arch Intern Med 1995;155:13791384. Sheffer AL. Expert panel on the management of asthma. J Allergy Clin Immunol 1991;88: 425 534. Silvanus M-T, Groeben H, Peters J. Corticosteroids and inhaled salbutamol in patients with reversible airway obstruction markedly decrease the incidence of bronchospasm after tracheal intubation. Anesthesiology 2004;100:10521057.

B.17. What is the onset of action of intravenous steroid therapy in asthma?


The bronchial effects of intravenous steroids are not immediate and may not be seen for 6 to 12 hours after the initial administration. When severe bronchospasm does not resolve despite intense optimal bronchodilator therapy, intravenous corticosteroid administration is indicated. A loading dose of hydrocortisone, 4 mg per kg, is given to achieve plasma cortisol levels above 100 g per dL, followed by 3 mg per kg every 6 hours. Alternatively, methylprednisolone, 60 to 125 mg, may be given every 6 hours. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15081516. P.16 Parker SD, Brown RH, Darowski MJ, et al. Time related decrease in airway reactivity by corticosteroids [Abstract]. Anesthesiology 1989;71:A1077. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:194.

B.18. What are the effects of cimetidine on asthmatic patients?


Cimetidine is an H2-receptor antagonist. Nathan et al. found that histamine mediates bronchoconstriction through the H1-receptor (blocked by chlorpheniramine), and bronchodilation

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is mediated by H2-receptor agonists (blocked by cimetidine). H2-receptors are thought to be responsible for inhibitory feedback control of mediator release. Cimetidine may potentiate histamine H1-receptor bronchoconstrictions. It should be avoided in asthmatic patients. Cimetidine also slows clearing of theophylline by inhibiting microsomal metabolism. Therefore, theophylline dosage should be decreased to avoid toxicity. Nathan R, Segall N, Schocket A. A comparison of the actions of H1 and H2 antihistamines on histamine-induced bronchoconstriction and cutaneous wheal response in asthmatic patients. J Allergy Clin Immunol 1981;67:171. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:201.

B.19. How would you premedicate the patient? Why?


No good controlled studies have been performed on premedication used in asthmatic patients. The asthmatic patient may be premedicated with atropine and diphenhydramine alone or in combination with droperidol. Atropine is an anticholinergic drug. It decreases airway resistance, and diminishes secretion-initiated airway reactivity. Diphenhydramine is an H1-receptor blocking drug. It inhibits histamine-mediated bronchoconstriction and possesses a sedative effect. The sedative effect of diphenhydramine may prevent bronchospasm induced by psychologic stress. Hydroxyzine hydrochloride (Vistaril) is a frequently used alternative because of its sedative, antihistaminic, and bronchodilating effects. Inhaled or systemic steroids may be given to patients with moderate to severe asthma to decrease the incidence of asthmatic attacks. Inhaled 2-agonists, cromolyn, or steroids should be continued up to the time of surgery. Bishop MJ. Bronchospasm, avoiding an anesthetic disaster. In: Barash PG, ed. ASA refresher courses in anesthesiology. Park Ridge, IL: American Society of Anesthesiologists, 1991:1527. Stoelting RK, Dierdorf SF. Anesthesia And co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:200201.

C. Intraoperative Management C.1. What are the disadvantages of administering atropine to the asthmatic patient?
Some physicians consider atropine relatively contraindicated because it causes drying of secretions, further plugging, and perhaps the initiation of a severe attack of asthma. This P.17 assumption has proved more theoretic than real in the reasonably well-managed asthmatic patient. However, atropine blocks the formation of cyclic guanosine monophosphate (GMP) and therefore has a bronchodilation effect. Inhaled atropine improves FEV1 in 85% of patients with COPD. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:819. Barrett JP. Editorial views: clinical epilog on bronchomotor tone. Anesthesiology 1975;42: 13.

C.2. If the patient had a severe asthmatic attack in the operating room before the induction of anesthesia, would you put the patient to sleep or postpone the surgery?

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First of all, medical treatment should be given to relieve the asthmatic attack. Elective surgery should be postponed and the patient should be reevaluated carefully and better prepared preoperatively. In case of emergency surgery such as acute appendicitis, the surgery can be performed after the asthmatic attack is terminated with medical treatment. During surgery, the medical treatment should be continued.

C.3. The patient did not have an asthmatic attack in the operating room. How would you induce anesthesia? Would you use an LMA instead of an endotracheal tube?
The principles of anesthetic management for the asthmatic patient are threefold: to block airway reflexes before laryngoscopy and intubation, to relax airway smooth muscle, and to prevent release of biochemical mediators. Before induction of anesthesia, I would like to ask the patient to take two to three puffs of albuterol from a metered-dose inhaler (MDI). Methohexital is used for induction. Then oxygen and a potent inhalation agent, such as halothane, sevoflurane, or isoflurane, are administered by mask to achieve adequate depth of anesthesia before endotracheal intubation after injection of succinylcholine or other muscle relaxants. Topical endotracheal spray of 80 to 120 mg of lidocaine through a laryngotracheal anesthesia (LTA) kit may be used before intubation to suppress the cough reflex induced by intubation, but the introduction of lidocaine itself may cause the cough reflex when the depth of anesthesia is light. As a supraglottic airway, the LMA seems to be suitable for asthmatic patients. The LMA provides a unique opportunity for the clinician to control the airway without having to introduce a foreign body into the trachea. Therefore, it may be an ideal airway tool in the asthmatic patient who is not at risk of reflux and aspiration. However, the patient is undergoing cholecystectomy, which may need manipulating and packing of stomach and bowels; the patient is at risk of regurgitation and aspiration. Meanwhile, the patient may need a nasogastric tube for decompression of gastrointestinal tract. The classic LMA device (except LMA-ProSeal) is not compatible with the use of a nasogastric tube intraoperatively. I would not choose a classic LMA instead of an endotracheal tube for this procedure. However, the introduction of the LMA-ProSeal with a gastric drain tube and larger cuff reduces both the risk of gastric inflation and the risk of aspiration of refluxed gastric contents. The LMA-ProSeal has been successfully used for laparoscopic cholecystectomy in obese patients. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:605607. Malthy JR, Beriault MT, Watson NC, et al. The LMA ProSeal is an effective alternative to tracheal intubation in laparoscopic cholecystectomy. Can J Anaesth 2002;49:857. P.18

C.4. Why would you use methohexital instead of thiopental?


Hirshman et al., using human skin mast cell preparations, demonstrated histamine release by thiopental and thiamylal, but not by methohexital and pentobarbital. Thiopental and thiamylal are thiobarbiturates, and methohexital and pentobarbital are oxybarbiturates. This suggests that the sulfur atom is important in barbiturate-induced histamine release. Moreover, they further found that thiobarbiturates, but not oxybarbiturates, constricted guinea pig tracheas and that this constriction was mediated by thromboxane. Therefore, methohexital may be preferred as the induction agent in patients showing extreme sensitivity to histamine (asthmatics) or increased histamine releasability (atopics). However, thiopental itself does not cause bronchospasm. Because it provides only a light plane of anesthesia, airway instrumentation under thiopental anesthesia alone may trigger bronchospasm. Therefore, clinically, both barbiturates have been used successfully in the asthmatic patient, provided that an adequate depth of anesthesia is

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achieved before stimulating the airway. Bishop MJ. Bronchospasm: successful management. In: ASA annual meeting refresher course lectures. Park Ridge, IL: American Society of Anesthesiologists, 2005:408. Curry C, Lenox WC, Spannhake EW, et al. Contractile responses of guinea pig trachea to oxybarbiturates and thiobarbiturates. Anesthesiology 1991;75:679683. Lorenz W, Doenicke A. Editorial views: anaphylactoid reactions and histamine release by barbiturate induction agents: clinical relevance and pathomechanisms. Anesthesiology 1985;63:351. Hirshman CA, Edelstein RA, Ebertz JM, et al. Thiobarbiturate-induced histamine release. Anesthesiology 1985;63:353.

C.5. Would you use propofol, etomidate, or ketamine for induction?


Propofol may be the induction agent of choice for the patient with reactive airways who was hemodynamically stable. A recent report found that induction of asthmatics with 2.5 mg per kg of propofol per kg of body weight resulted in a significantly lower incidence of wheezing after tracheal intubation when compared with induction with 5 mg per kg of thiopental or thiamylal or with 1.75 mg per kg of methohexital per kg of body weight. The incidence of wheezing was 0%, 45%, and 26% in patients who received propofol, a thiobarbiturate, and oxybarbiturate, respectively. Another study found that in unselected patients, propofol resulted in a significantly lower respiratory resistance after tracheal intubation than induction with thiopental or etomidate. Etomidate does not depress myocardial function. Therefore, it provides hemodynamic stability in critically ill patients. Although it was advertised as an ideal agent for asthmatic patients, little evidence supports the claim except that etomidate does not release histamine. A recent study suggests that neither etomidate nor thiopental prevents wheezing after intubation, as opposed to the marked protection afforded by propofol. Ketamine produces bronchodilation both through neural mechanisms and through release of catecholamines. In an actively wheezing patient, ketamine is the induction agent of choice, particularly when hemodynamics are unstable. Bishop MJ. Bronchospasm: successful management. In: ASA annual meeting refresher course lectures. Park Ridge, IL: American Society of Anesthesiologists, 2005:408. Eames WO, Rooke GA, Wu RS, et al. Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance following tracheal intubation. Anesthesiology 1996;84:1307 1311. P.19 Pizov R, Brown RH, Weis YS, et al. Wheezing during induction of general anesthesia in patients with and without asthma. A randomized, blind trial. Anesthesiology 1995;82: 11111116. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:194.

C.6. Would you use lidocaine for intubation?


Intravenous lidocaine, 1 mg per kg, may be given 1 to 2 minutes before intubation to prevent reflex-induced bronchospasm. Topical endotracheal spray of lidocaine must be used cautiously because it may provoke reflex bronchoconstriction if adequate depth of anesthesia has not been achieved. Lidocaine infusion, 1 to 2 mg per kg per hour, may be used in cardiac or elderly patients with COPD whose airways need more anesthesia than their cardiovascular system can

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tolerate. Hirshman CA. Anesthesia and bronchospastic disease. In: Barash PG, ed. ASA refresher courses in anesthesiology. Chicago: American Society of Anesthesiologists, 1985:8195. McAlpine LG, Thomson NC. Lidocaine-induced bronchoconstriction in asthmatic patients. Relation to histamine airway responsiveness and effect of preservative. Chest 1989; 96:1012 1015.

C.7. If this is emergency surgery and rapid sequence induction is indicated, how would you induce anesthesia in this patient?
All the precautions to prevent aspiration of gastric contents and asthmatic attack must be considered simultaneously. Rapid sequence induction and tracheal intubation using propofol, thiopental or methohexital, and succinylcholine are necessary to prevent aspiration, but light anesthesia may precipitate severe bronchospasm. Ketamine, 2 mg per kg, may be the induction agent of choice in noncardiac asthmatic patients, because ketamine increases catecholamine release with resultant bronchodilation. In asthmatic patients who have ischemic heart disease, we give a moderate dose of fentanyl, 5 g per kg, 2 to 3 minutes before the administration of propofol, 1.5 mg per kg, or methohexital, 1.5 mg per kg, to suppress airway reflexes and prevent tachycardia and hypertension caused by intubation. Intravenous lidocaine, 1 to 2 mg per kg, given immediately before the administration of ketamine or fentanyl, and succinylcholine, are useful adjunct drugs to prevent reflex bronchospasm, particularly in an emergency situation when deep anesthesia cannot be achieved before intubation. A full stomach should be emptied by a functioning nasogastric tube. The patient should be denitrogenated with 100% oxygen by mask. Cisatracurium or vecuronium, 1 mg, should be given 3 minutes before administration of succinylcholine. If the patient has a wheezing attack before anesthesia, inhalation of sympathomimetics such as albuterol may be used as the first-line therapy for acute asthmatic attacks. Bishop MJ. Bronchospasm, avoiding an anesthetic disaster. In: Barash PG, ed. ASA refresher courses in anesthesiology. Park Ridge, IL: American Society of Anesthesiologists, 1991: 1527. Kingston HGG, Hirshman CA. Perioperative management of the patient with asthma. Anesth Analg 1984;63:844. P.20 Martin DE, Rosenberg H, Aukburg SJ, et al. Low-dose fentanyl blunts circulatory responses to tracheal intubation. Anesth Analg 1982;61:680.

C.8. What is your choice of agents for maintenance of anesthesia? Why?


We use inhalation agents such as sevoflurane, halothane, and isoflurane with nitrous oxide and oxygen. Sevoflurane, enflurane, and isoflurane are preferable to halothane, because halothane sensitizes the myocardium to arrhythmic effects of circulating catecholamines more than sevoflurane, enflurane, and isoflurane. However, some authorities prefer halothane and sevoflurane to isoflurane and desflurane because the latter anesthetics have a pungent odor that may cause airway irritation and trigger bronchospasm. At lower doses (<1.0 minimum alveolar concentration [MAC]), the inhaled anesthetics inhibit chemically induced tracheal contractions in the order: halothane > enflurane isoflurane > sevoflurane. However, more

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recent clinical observations in humans indicate that sevoflurane at 1.1 MAC may be the most effective agent, particularly in the presence of airway instrumentation. In addition, sevoflurane may have a more rapid onset of bronchodilation than isoflurane or halothane. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:408. Rock GA, Choi JH, Bishop MJ. The effect of isoflurane, halothane, sevoflurane and thiopental nitrous oxide on respiratory system resistance after tracheal intubation. Anesthesiology 1997;86:12941299. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:202.

C.9. What are the mechanisms of halothane that produce bronchodilation?


The major component of bronchodilation elicited by halothane is mediated through -adrenergic receptor stimulation, which is decreased by -blocking agents. The -agonistic effect works through two intracellular mechanisms. The first mechanism is direct relaxation of bronchial musculature mediated by an increase in intracellular cyclic 3,5-adenosine monophosphate (cAMP). Increased cAMP may bind free calcium within bronchial myoplasm and thereby promote relaxation by a negative feedback mechanism. The second mechanism may arise from the first inasmuch as elevated levels of cAMP seem to impede antigen-/antibody-mediated enzyme production and release of histamine from leukocytes. However, a study by Hirshman et al. suggests that the mechanism of action involves the depression of airway reflexes and direct effects on airway smooth muscle. Halothane may also have protective effects by acting on bronchial epithelium through a nonadrenergic, noncholinergic mechanism, possibly involving the nitric oxide pathway. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:408. Hirshman CA, Edelstein G, Peetz S, et al. Mechanism of action of inhalational anesthesia on airways. Anesthesiology 1982;56:107. Linderman KS, Baker SG, Hirshman CA. Interaction between halothane and the nonadrenergic, noncholinergic inhibitory system in porcine trachealis muscle. Anesthesiology 1994;81:641. P.21

C.10. Why would you choose an inhalational instead of an intravenous technique?


First, inhalation agents such as sevoflurane, halothane, enflurane, and isoflurane have doser e l a t e d d i r e c t b r o n c h o d i l a t o r e f f e c t s . K e t a m i n e h a s a n i n d i r e c t b r o n c h o d i l a t o r e f f e c t , w hi c h i s n o t dose related and not predictable. Large doses of morphine produce bronchoconstriction because morphine increases central vagal tone and releases histamine. Droperidol has an -blocking effect that may relieve bronchospasm induced by stimulation. Meperidine was shown to have a spasmolytic effect in asthmatic patients, but not in experimental dogs. Fentanyl does not have a significant effect on bronchial tone. Second, cholinesterase inhibitors can induce bronchospasm. Inhalation agents potentiate muscle relaxants; therefore, lower doses of relaxants are needed for surgery. The use of cholinesterase inhibitors to reverse the effect of muscle relaxants may be avoided or decreased. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:408.

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Kingston HGG, Hirshman CA. Perioperative management of the patient with asthma. Anesth Analg 1984;63:844.

C.11. Is regional anesthesia better than general anesthesia in this situation?


This issue is controversial. The use of regional anesthesia avoids the possibility of bronchospasm that may be induced by endotracheal tube stimulation. However, if high levels of sensory and motor block are required, they may produce severe anxiety and actually incite bronchospasm. Another concern is the associated blockade of sympathetic input to the lungs. Some case reports have speculated about a resultant increase in airway resistance. Respiratory complications were reported to be quite common (83%) in patients undergoing intraperitoneal s u r g e r y w h o h a d r e l a t i v e l y h i g h s p i n a l a n e s t h e s i a ( T6 - 4 ) . L o w s p i n a l , e p i d u r a l , a n d c a u d a l anesthesia for surgery of the perineum, lower extremities, and pelvic extraperitoneal organs resulted in fewer respiratory complications than did general anesthesia. A study of patients with asthma demonstrated no differences between those anesthetized with high epidurals (T2-4) and those undergoing general anesthesia with ketamine and isoflurane. Endotracheal general anesthesia is advantageous because it provides a controlled airway to deliver the desirable oxygen concentration, but the endotracheal tube may also induce bronchospasm during light anesthesia. Bishop MJ. Bronchospasm: successful management. In: ASA annual refresher course lectures. Park Ridge, IL: American Society of Anesthesiologists, 2005:408. Gold MI, Helrich M. A study of the complications related to anesthesia in asthmatic patients. Anesth Analg 1963;42:283293. Ramanathan J, Osborne B, Sibai B. Epidural anesthesia in asthmatic patients. Anesth Analg 1990;70:S317S318.

C.12. Which muscle relaxants would you use? Why?


Muscle relaxants that cause histamine release should be avoided (Table 1.2). Pancuronium, rocuronium, cisatracurium, and vecuronium are the preferred relaxants because the histamine released is insignificant. Vecuronium, rocuronium, and cisatracurium may be better choices of relaxant because of their intermediate action durations, allowing early recovery without reversal P.22 with an anticholinesterase, which may precipitate bronchospasm. D-Tubocurarine can cause bronchospasm by histamine release. Metocurine and succinylcholine also cause histamine release, but to a lesser extent. Gallamine has minimal histamine release but has been reported to cause bronchospasm in patients. Atracurium, mivacurium, and doxacurium in high doses increase histamine release. Therefore, they are not the relaxants of choice.

Table 1.2 Histamine Release from Nondepolarizing Muscle Relaxants. MUSCLE RELAXANT Benzylisoquinolinium compounds D-Tubocurarine Metocurine 0.6 2.0 HISTAMINE RELEASEa

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Doxacurium Mivacurium Atracurium Cisatracurium Steroidal compounds Pancuronium Vecuronium Pipecuronium Rocuronium Others Alcuronium Gallamine
aDefined

>4.0 3.0 2.5 None

None None None None

None None

as the number of multiples of the ED95 for neuromuscular blockade required to produce histamine release.

Basta SJ. Modulation of histamine release by neuromuscular blocking drugs. Curr Opin Anesth 1992;5:572. Caldwell JE, Lau M, Fisher DM. Atracurium versus vecuronium in asthmatic patients. A blinded, randomized comparison of adverse events. Anesthesiology 1995;83:985991. Mehr EH, Hirshman CA, Lindeman KS. Mechanism of action of atracurium on airways. Anesthesiology 1992;76:448454. Miller RD, ed. Miller's anesthesia, 6th ed. Philadelphia: Elsevier Churchill Livingstone, 2005:511512.

C.13. In the middle of surgery, the patient developed a severe wheezing attack. How do you manage it?

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First, deepen the level of anesthesia and increase FIO2. Remember that the patient is under anesthesia and surgery. Therefore, medical intervention, such as -agonist administration, is not the first choice of treatment. The most common cause of asthmatic attack during surgery is inadequate anesthesia. The asthmatic patient has an extremely sensitive tracheobronchial tree. When the level of anesthesia is too light, he may develop bucking, straining, or coughing as a result of the foreign body (endotracheal tube) in his trachea and go on to develop bronchospasm. First the blood pressure is taken to ensure it is normal or high, and then anesthesia is deepened by increasing the concentration of inhalation agents, such as sevoflurane, halothane, enflurane, or isoflurane, which are direct bronchodilators as well. An incremental dose of ketamine may be a quick way P.23 of maintaining blood pressure, rapidly deepening anesthesia, achieving bronchodilation, and avoiding the problem of delivering an inhaled anesthetic to a patient with poor ventilation. At the same time, oxygenation can be improved by increasing the oxygen concentration and decreasing the nitrous oxide. The patient should be continuously ventilated with a volume-cycled ventilator. Second, relieve mechanical stimulation. Pass a catheter through the endotracheal tube to suction secretions and to determine whether there is any obstruction or kinking of the tube. The cuff of the endotracheal tube can be deflated, the tube moved back 1 to 2 cm, and the cuff reinflated. Occasionally, the endotracheal tube slips down and stimulates the carina of the trachea, causing severe bronchospasm during light anesthesia. Surgical stimulation, such as traction on the mesentery, intestine, or stomach, should be stopped temporarily, because it causes vagal reflex and can cause bronchospasm. Third, medical intervention is necessary if the previously mentioned treatment cannot break the bronchospasm or the anesthesia cannot be increased because of hypotension. The cornerstone of the treatment of the intraoperative bronchospasm is inhalation of 2-agonists such as albuterol, which induce further bronchodilation even in the presence of adequate inhalational anesthesia. 2-Agonists produce more rapid and effective bronchodilation than intravenous aminophylline. When severe bronchospasm is not resolving despite intense optimal bronchodilation therapy, intravenous corticosteroid is indicated (see sections B.16 and B.17). Fourth, bring in an intensive care unit (ICU) ventilator. Anesthesia ventilators are not designed for patients with high airway resistance. It is impossible to deliver adequate alveolar ventilation because the anesthesia circuit has too much compressible volume (tubing compliance) and the anesthesia ventilator does not have enough driving power. An ICU ventilator can generate inspiratory pressures as high as 120 cm H2O. With low tubing compliance, little ventilation is wasted into the circuit. High inspiratory flow rate allows for shorter inspiratory time with adequate time for expiration and lower auto-PEEP. The major disadvantage of an ICU ventilator is its inability to use inhalational anesthetics. However, the Siemens 900D anesthesia machine incorporates an ICU-type ventilator with vaporizers and oxygen mixers. It may be ideal for this situation. Bishop MJ. Bronchospasm: successful management. In: ASA annual refresher course lectures. Park Ridge, IL: American Society of Anesthesiologists, 2002:411. Brusse WW, Lemanske RF. Asthma. N Engl J Med 2001;344:350362. Tobias JD, Hirshman CA. Attenuation of histamine-induced airway constriction by albuterol during halothane anesthesia. Anesthesiology 1990;72:105110.

C.14. How would you give 2 -agonists? What problems may arise when isoproterenol is given during halothane anesthesia? What is its mechanism of action on asthma?
In the past it was fashionable to treat episodes of severe asthma with intravenous

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sympathomimetics such as isoproterenol. This approach no longer appears justifiable. Isoproterenol infusions can induce ventricular arrhythmias during halothane anesthesia. In addition, isoproterenol infusion can clearly cause myocardial damage, and even the 2-selective agents such as terbutaline and albuterol when given intravenously offer no advantages over the inhaled route. 2-Agonists such as albuterol, terbutaline, fenoterol, and pirbuterol may be administered through MDI adapters or small-volume jet nebulizers to the anesthetic circuit. Because MDI adapters are not very efficient in the intubated patient, more than two puffs are needed to break acute bronchospasms. Adrenergic stimulants produce bronchodilation through action on -adrenergic receptors. Agonists increase intracellular cAMP by activating adenyl cyclase, which produces cAMP from adenosine triphosphate (ATP). Increased cAMP promotes bronchial relaxation and inhibits the release of mediators from mast cells (Fig. 1.6). P.24

Figure 1.6 Cyclic adenosine monophosphate (cAMP) pathways involved in bronchodilator action. 3_, 5_ cAMP, cyclic 3_,5_-adenosine monophosphate; AMP, adenosine monophosphate; ATP, adenosine triphosphate; PDE, phosphodiesterase. (From Hirshman C. Airway reactivity in humans: anesthetic implications. Anesthesiology 1983;58:170, with permission.)

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Barnes PJ. A new approach to the treatment of asthma. N Engl J Med 1989;321:15171527. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15081516. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:199.

C.15. Would you administer aminophylline? How does aminophylline relieve bronchospasm? What is the mechanism of action? What are the therapeutic blood levels of aminophylline? What are the toxic effects of aminophylline?
Currently, aminophylline is rarely used for acute bronchospasm because of its narrow therapeutictoxic window and its relatively weak bronchodilating effect. In addition, aminophylline does not add to the bronchodilating efficacy of inhaled halothane. The usual intravenous loading dose is 6.0 mg per kg given slowly, followed by a continuous infusion of 1.0 mg per kg per hour for smokers, 0.5 mg per kg per hour for nonsmokers, P.25 and 0.3 mg per kg per hour for severely ill patients, such as those with congestive heart failure, pneumonia, and liver disease. Maintenance doses must also be reduced to 0.3 mg per kg per hour for patients taking cimetidine, which interferes with hepatic microsomal enzymes. It was formerly thought that aminophylline increases intracellular cAMP through inhibition of the enzyme phosphodiesterase (PDE), which inactivates cAMP (Fig. 1.6). However, the available evidence does not support this concept. The therapeutic plasma levels of aminophylline range from 5 to 15 g per mL. The common side effects of aminophylline include nervousness, nausea, vomiting, anorexia, and headache; cardiac arrhythmias and seizures occur with high plasma levels. Hirshman CA. Airway reactivity in humans: anesthetic implications. Anesthesiology 1983;58:170. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New York: McGraw-Hill, 2005:15081516. Tobias JD, Kubos KL, Hirshman CA. Aminophylline does not attenuate histamineinduced airway constriction during halothane anesthesia. Anesthesiology 1989;71:723729.

C.16. If the patient does not respond to the aforementioned treatment and becomes cyanotic, what would you do?
The values of arterial blood gases should be determined immediately. In a severe, prolonged asthmatic attack, there will be combined respiratory and metabolic acidosis resulting from CO2 retention and lactic acidosis from tissue hypoxia. NaHCO3 should be given to correct the acidosis, because aminophylline and -agonists are not effective in severe acidosis. At the same time, bronchodilator therapy should be continued or increased. Consultation with senior staff or a physician in pulmonary medicine may be necessary. Kampschulte S, March J, Safar P. Simplified physiologic management of status asthmaticus in children. Crit Care Med 1973;1:6974.

C.17. What are the differential diagnoses of intraoperative bronchospasm?


The causes of wheezing and increased airway pressure include the following:

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Kinked endotracheal tube Solidified secretions or blood Pulmonary edema Tension pneumothorax Aspiration pneumonitis Pulmonary embolism Endobronchial intubation Persistent coughing and straining Negative pressure expiration

Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:203. P.26

C.18. The asthmatic attack was finally relieved and the surgery was completed. The patient was found to be hypoventilating. What are the common causes of hypoventilation? Would you like to reverse the muscle relaxant?
The following are common causes of apnea or hypoventilation at the end of surgery:

Respiratory center depression by inhalational anesthetics, narcotics, or hyperventilation (low PaCO2) Peripheral blockade by muscle relaxants

Because the patient is a severe asthmatic, it is better to avoid the use of an anticholinesterase, such as neostigmine, to reverse a nondepolarizing relaxant. Neostigmine may trigger bronchospasm by a cholinergic mechanism. Although atropine given simultaneously with neostigmine may prevent bronchospasm, the action duration of neostigmine is longer than that of atropine. If reversal is required, it appears prudent to administer larger than customary doses of glycopyrrolate (>0.5 mg) or atropine (>1.0 mg) to minimize the possibility of bronchospasm. It is advisable to use inhalation agents to potentiate relaxants and to use smaller amounts of intermediate-acting relaxants for surgery. If spontaneous respiration is not adequate, artificial ventilation should be continued. Gal TJ. Reactive airway disease: anesthetic perspectives. In: International anesthesia research society review course lectures. Cleveland, OH: International Anesthesia Research Society, 2002:4553. Hazizai A, Hatija A. Bronchospasm caused by neostigmine. Eur J Anaesthesiol 2006;23: 8586.

D. Postoperative Management D.1. Would you extubate the asthmatic patient while he or she was deeply anesthetized?
To avoid bronchospasm triggered by coughing and bucking caused by laryngeal and pharyngeal reflexes during emergence and extubation, patients may be extubated at surgical (deep) levels

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of anesthesia. However, the risks of aspiration, airway obstruction, and hypoventilation should be weighed against the benefits. With a history of severe COPD, chronic hypoxemia, and CO2 retention, the patient was not a good candidate for extubation while deeply anesthetized. A systematic approach for emergence and extubation is illustrated in Fig. 1.7. However, the guidelines do not include all possible patient-surgical-anesthetic conditions. Certainly the practitioner's clinical judgment is of utmost importance in the decision about whether to extubate the patient. Lien CA, Koff H, Malhotra V, et al. Emergence and extubation: a systemic approach. Anesth Analg 1997;85:1177. Miller KH, Harkin CP, Bailey PL. Postoperative tracheal extubation. Anesth Analg 1995; 80:148 172.

D.2. When the patient cannot be extubated early in the recovery room, how would you keep the endotracheal tube in place without causing bronchoconstriction?
Loading doses of lidocaine or aminophylline, followed by continuous infusion, as described in the sections C.6 and C.15, may be administered intravenously to prevent bronchoconstriction induced by stimulation of the endotracheal tube. 2-Agonists such as albuterol may be administered P.27 through MDI adapter to prevent bronchospasm. Alternatively, an LMA may be used to replace the endotracheal tube for control of ventilation and to avoid tracheal stimulation.

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Figure 1.7 A systemic approach to emergence and extubation. COPD, chronic obstructive pulmonary disease; ESRD, end-stage renal disease.

Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:604605.

D.3. In asthmatic patients, are narcotics contraindicated for postoperative pain control?
Narcotics should be used very carefully because prolonged respiratory depression may further compromise the airway. Morphine is avoided because of possible histamine release and increased P.28 central vagal tone, which may cause bronchospasm. Meperidine may be a better choice for postoperative analgesia because of its spasmolytic action. Narcotics should be titrated carefully to control pain and not depress respiration. Poor pain control may compromise respiration

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because of splinting of the thoracic cage and decreased ability to cough. Paravertebral or intercostal nerve blocks, epidural analgesia, or transcutaneous electrical nerve stimulation (TENS) may be used to control postoperative pain without depressing respiration. NSAIDs precipitate acute bronchospasm in an estimated 8% to 20% of adult asthmatics. NSAIDs block the cyclooxygenase-mediated conversion of arachidonic acid to prostaglandins, thereby shunting arachidonic acid toward the formation of bronchoconstrictor leukotrienes. Therefore, it may be prudent to avoid NSAIDs for postoperative pain control. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:358361. Marsh HM. Anesthesia for patients with chronic pulmonary disease. In: Hershey SG, ed. ASA refresher courses in anesthesiology. Park Ridge, IL: American Society of Anesthesiologists, 1984:133. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:197, 201.

D.4. The patient was breathing well and was extubated. How much oxygen would you give to this asthmatic patient with COPD in the recovery room?
Forty percent oxygen by mask is usually used postoperatively in the recovery room. However, for a small proportion of patients with COPD, the hypoxic drive might be taken away by increased FIO2. Moreover, oxygen therapy may abolish hypoxic pulmonary vasoconstriction in poorly ventilated areas, increasing blood flow to these areas and so decreasing blood flow to other lung regions with normal or high ventilation/perfusion ratios. These regions will then contribute to alveolar dead space and thereby cause an increase in PaCO2. It is important to monitor the patient's respiration, oxygenation, and PaCO2 very carefully during oxygen therapy. Venturi masks with FIO2 of 0.24 to 0.4 may be used for patients with COPD. Nevertheless, adequate oxygen concentration must be used in the presence of hypoxemia. Hypoventilation can be assisted or controlled by artificial ventilation. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:191, 381.

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Chapter 2 Bronchoscopy, Mediastinoscopy, and Thoracotomy


Alessia Pedoto Paul M. Heerdt Fun-Sun F. Yao

A 60-Year-Old Man
has s uffered from cough, intermittent h emopty s is, and weight loss for 2 mon ths. He has been smok ing one pack of cigarettes per day for 40 years . A c hest x-ray 1 month ago r evealed a right middle lobe infiltrate t hat w as treated with antibiotic s, without improv ement. Subsequent evaluation revealed a carcinoma. He is now s cheduled for fiberoptic bronc hoscopy (FOB), mediastinosc opy, and poss ible th oracotomy for lobectomy or pneumonec tomy.

P.30

A. Medical Disease and Differential Diagnosis A.1. How are lung carcinomas diagnosed, and what is your prediction for the most likely type of malignancy?
Symptoms of nonproductive cough and hemoptysis, along with unresolved lung infiltrate, usually suggest carcinoma. The diagnosis and extent of the disease are confirmed with sputum cytology, bronchoscopy and brush biopsy, biopsy of palpable lymph nodes in the neck or axilla, needle aspiration biopsy, mediastinoscopy, and possibly exploratory thoracotomy. Prior to thoracotomy, an extensive work up is aimed to diagnose metastases that would contraindicate surgery. Cancers of the lung comprise 16% of all malignancies and account for approximately 30% of cancer deaths worldwide. Bronchogenic carcinomas comprise the vast majority of lung cancers presenting for surgical resection and can be classified into four major types: small cell, large cell, squamous cell, and adenocarcinoma. For surgical purposes, small cell tumors are kept distinct and the others grouped into a nonsmall cell category. In general, nonsmall cell carcinomas are amenable to surgical resection whereas small cell tumors tend to be nonresectable and are treated medically. Further subclassification of tumors involves the TNM system where T represents tumor site, size, and local extent; N represents presence and location of regional lymph node involvement; and M represents presence of distal metastases beyond the ipsilateral hemithorax. The TNM classification is used in the staging of bronchogenic carcinomas and helps predict response to therapy. In general, small cell carcinomas that spread beyond the bounds of possible resection by the time of presentation are primarily managed with chemotherapy, with or without radiation. The 5-year survival after chemotherapy and radiation is approximately 3% to 8%. In contrast, nonsmall cell cancers found to be localized at the time of presentation should be considered for resection. The 5-year survival after primary resection is dependent on tumor staging, but can be as high as 85% for small tumors without regional lymph node involvement or P.31 m e t a s t a s e s ( s t a g e I ) . A p p r o x i m a t e l y 4 5 % o f p a t i e n t s p r e s e n t wi t h c i r c u m s c r i b e d e x t r a p u l m o n a r y extension and/or lymphatic spread to the ipsilateral mediastinal or subcarinal lymph nodes (stage IIIA) and exhibit a 5-year postresection survival of less than 20%. Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New Y o r k : M c G r a w - Hi l l , 2 0 0 5 : 5 0 6 5 1 5 . Shibutani HC. Pulmonary resection. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:639659.

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A.2. What are the less common manifestations of bronchogenic carcinoma?


Other manifestations of lung tumors are primarily related to mass effects or altered metabolism. In addition to bronchial obstruction (evident in this patient), mass effects include invasion into the chest wall, compression of great vessels (e.g., superior vena cava syndrome), tracheobronchial displacement, paresis of the recurrent laryngeal or phrenic nerves, and Pancoast's syndrome (pain and upper extremity weakness secondary to invasion of the brachial plexus, first and second thoracic and eighth cervical nerve roots). Recognized metabolic manifestations of lung tumors include symptoms that resemble those of myasthenia gravis, peripheral neuritis involving both motor and sensory components, Cushing's syndrome, carcinoid syndrome, hypercalcemia and hypophosphatemia (from ectopic secretion of parathyroid hormone [PTH]/PTH-related peptide by epidermoid cancer), hypokalemia (from ectopic secretion of adrenocorticotropic hormone [ACTH] by small cell cancer), and hyponatremia (from inappropriate secretion of antidiuretic hormone or possibly atrial natriuretic factor by small cell cancer). Kasper DL, Braunwald E, Fauci AS, et al. eds. Harrison's principles of internal medicine, 16th ed. New Y o r k : M c G r a w - Hi l l , 2 0 0 5 : 5 0 8 5 0 9 . Slinger PD, Johnston MR. Preoperative assessment for pulmonary resection. J Cardiothorac Vasc Anesth 2000; 14:202211. Wirtz PW, Wintzen AR, Verschuuren JJ. Lambert-Eaton myasthenic syndrome has a more progressive course in patients with lung cancer. Muscle Nerve 2005; 32(2):226229.

A.3. The patient has a long history of cigarette smoking. What is the significance of this finding?
Cigarette smoking promotes the development of chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema. Evidence of chronic changes can be found in preoperative pulmonary function testing. Pulmonary hypertension and cor pulmonale are also more common in this patient population. Patients who continue to smoke until surgery are at greater risk for postoperative pulmonary complications such as atelectasis and hypoxemia. Although carboxyhemoglobin concentrations decline substantially within 12 hours of smoking cessation, it remains unclear as to how long smoking must be discontinued to see a significant reduction of post-thoracotomy complications. In cardiac surgery patients, smoking must be discontinued for 2 months before an impact upon postoperative pulmonary function, mainly related to improved mucociliary function. Licker MJ, Widikker I, Robert J, et al. Operative mortality and respiratory complications after lung resection for cancer: impact of chronic obstructive pulmonary disease and time trends. Ann Thorac Surg 2006;81(5):18301837. P.32 Slinger PD, Johnston MR. Preoperative assessment for pulmonary resection. J Cardiothorac Vasc Anesth 2000;14:202211. T i s i G M . P r e o p e r a t i v e e v a l u a t i o n o f p u l m o n a r y f u n c t i o n : v a l i d i t y , i n d i c a t i o n s , a n d b e n e f i t s . A m Re v Respir Dis 1979;119:293.

B. Preoperative Evaluation and Preparation B.1. How would you evaluate the patient preoperatively?
Preoperative evaluation should include a complete history, physical examination, and laboratory tests (e.g., complete blood count, SMA7, coagulation as well as electrocardiogram and chest x-ray). A history of smoking, cough, sputum production, orthopnea, and dyspnea are hallmarks of cardiopulmonary disease and should be further investigated. Abnormal exercise tolerance (such as inability to climb at least three flights of stairs) can be helpful in anticipating the patient's response to the stress of anesthesia and surgery. Most patients are admitted to the hospital on the day of surgery. A brief review of symptoms, physical limitations, interval changes, and airway anatomy should be performed at this

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time. In addition to routine electrocardiogram and blood analysis, patients should have preoperative pulmonary function testing to help define the relative risks for the magnitude of planned resection. Respiratory function can be assessed using the following parameters:

Respiratory mechanics. Forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), maximum voluntary ventilation (MVV), and the residual volume (RV)/total lung capacity (TLC) ratio Cardiopulmonary reserve. Maximal oxygen uptake (VO2max), stair climbing, 6-minute walk Lung parenchymal function. Diffusing capacity (DLCO) and arterial PaO2 and PaCO2

Datta D, Lahiri B. Preoperative evaluation of patients undergoing lung resection surgery. Chest 2003; 123:20962103. Slinger PD, Johnston MR. Preoperative assessment for pulmonary resection. J Cardiothorac Vasc Anesth 2000; 14:202211.

B.2. What are the pulmonary function guidelines that indicate increased risk of morbidity and mortality?
The reported mortality from lung resection is between 2% and 4%, mainly due to pneumonia, respiratory failure, bronchopleural fistula, empyema, and pulmonary embolism. Respiratory insufficiency occurs in approximately 5% of patients following lung resection, which is associated with a 50% mortality rate. Advanced age and a relatively high incidence of concomitant nonpulmonary disease seem to contribute to this outcome. An increased risk of postoperative complications can be predicted by the following parameters:

Spirometry

FVC less than 50% of predicted value FEV1 less than 50% of FVC or 2 L MVV less than 50% of predicted value or 50 L per minute Diffusion capacity less than 50% of predicted value RV/TLC greater than 50%

P.33

Table 2.1 Minimal Pulmonary Function Test Criteria for Various-Sized Pulmonary Resections. TEST MBC UNIT Liters/minute (L/min) Percentage (%) predicted NORMAL PNEUMONECTOMYLOBECTOMYBIOPSY OR SEGMENTAL >100 >50 >40 >25

MBC

100

>50

>40

>25

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FEV 1 FEV 1

Liters (L) Percentage (%) Liters (L)

>4 >80% FVC >2

>2.11.7 >50% FVC

>1.21.0 >40% FVC >0.61.6

>0.60.9 >40% FVC >0.6

FEV25% 75%

> 1.6

FEV1, forced expiratory volume in the first second; FEV25%75%, forced expiratory volume from 25% to 75% of forced vital capacity; MBC, maximum breathing capacity.

Arterial Blood Gases


PaCO2 greater than 45 mm Hg PaO2 less than 50 mm Hg

In addition, the location of the tumor, the extent of the proposed resection and the presence of preoperative induction chemotherapy seem to be associated with further risks (Table 2.1). Better preoperative evaluation and care has contributed to improved outcome, especially in patients with severe emphysematous disease undergoing lung volume reduction surgery (i.e. FEV1 < 1/min). The development of minimally invasive techniques for pulmonary resection-including pneumonectomy - has helped lessen perioperative morbidity and mortality. Therefore, the evaluation of risk factors for pulmonary resection has changed with time. Pulmonary function tests are valid indices of physiologic performance, but the actual predictive use of a range of values for a single parameter is poorly defined. Emphasis has now been directed toward the integration of various aspect of preoperative evaluation (e.g. respirometry, ventilation-perfusion scanning, and the extent of planned resection) to estimate postoperative function. With this technique, the utility of FEV1 as a predictor of pulmonary complications is substantially improved. Patients shown to have a predicted postoperative FEV1 less than 40% of the predicted value are now considered to be at increased risk for the more sophisticated regimen of thrombosis prophylaxis of postoperative complications. Even so, continuing refinements of intraoperative and postoperative management, the use of goal-specific analgesia techniques, and more sophisticated thrombosis prevention regimens have probably attenuated the incidence of complications in the high-risk group. Hartigan PM, Pedoto A. Anesthetic considerations for lung volume reduction surgery and lung transplantation. Thorac Surg Clin 2005;15(1):143157. Matsubara Y, Takeda S, Mashimo T. Risk stratification for lung cancer surgery: impact of induction therapy and extended resection. Chest 2005;128(5):35193525. M i l l e r R D , e d . M i l l e r ' s a n e s t h e s i a , 5 t h e d . N e w Y o r k : Ch u r c h i l l L i v i n g s t o n e , 2 0 0 5 : 1 8 5 3 . Slinger PD, Johnston MR. Preoperative evaluation of the thoracic surgery patient. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia, 3rd ed. Philadelphia: Churchill Livingstone, 2003:123. P.34 T i s i G M . P r e o p e r a t i v e e v a l u a t i o n o f p u l m o n a r y f u n c t i o n : v a l i d i t y , i n d i c a t i o n s , a n d b e n e f i t s . A m Re v Respir Dis 1979;119:293. T r i a n t a f i l l o u A N. A n e s t h e t i c m a n a g e m e n t f o r b i l a t e r a l v o l u m e r e d u c t i o n s u r g e r y . S e m i n T h o r a c Cardiovasc Surg 1996;8(1):9498.

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C. Intraoperative Management C.1. How would you premedicate, monitor, and anesthetize this patient?
Current practice at most institutions dictates that patients arrive at the hospital the day of surgery, thereby rendering largely obsolete the traditional oral or parenteral premedication before transport to the operating suite. Bronchoscopy and mediastinoscopy are generally ambulatory procedures, necessitating relatively rapid hospital discharge. Because bronchoscopy followed by mediastinoscopy and thoracotomy in this patient is only a possibility, intravenous midazolam immediately upon entry into the operating room is sufficient for anxiolysis and subsequent amnesia. In addition, a small intravenous dose (0.2 mg) of glycopyrrolate can be useful as an antisialagogue, particularly in patients who smoke. However, the potential of tachycardia should be considered, especially in patients with coronary artery disease (CAD) or atrial fibrillation. During mediastinoscopy, intermittent compression or occlusion of the innominate artery can occur. The blood pressure cuff should, therefore, be placed on the left arm and the pulse oximeter on the right hand. In case of innominate artery compression, a dampening of the pulse oximetry trace will be evident while blood pressure measurements remain accurate. Finally, along with the electrocardiogram (ECG), t e m p e r a t u r e s h o u l d b e m o n i t o r e d a n d a wa r m i n g b l a n k e t a p p l i e d ; d e s p i t e t h e p o t e n t i a l f o r a s h o r t procedure, elderly patients, in particular, can become hypothermic. Induction, maintenance of anesthesia, and muscle relaxation can be achieved with relatively short-acting agents. Propofol is u s u a l l y u s e d f o r i n d u c t i o n f o l l o we d b y r o c u r o n i u m , v e c u r o n i u m , o r c i s a t r a c u r i u m t o f a c i l i t a t e t r a c h e a l i n t u b a t i o n t h r o u g h a s i n g l e - l u m e n E T T . A n e s t h e s i a i s m a i n t a i n e d wi t h a p o t e n t i n h a l a t i o n a l a g e n t i n oxygen/air, if oxygen saturation tolerates it, and 3 to 4 g per kg of fentanyl often provides sufficient analgesia for the procedure. In addition, a local anesthetic can be infiltrated in the wound. Many clinicians choose to avoid nitrous oxide because of the potential for the mediastinoscope to enter the pleural space and create a pneumothorax. Ehrenwerth J, Brull SJ. Anesthesia for thoracic diagnostic procedures. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia, 3rd ed. Philadelphia: Churchill Livingstone, 2003: 174195. Molins L, Fibla JJ, Perez J, et al. Outpatient thoracic surgical programme in 300 patients: clinical results and economic impact. Eur J Cardiothorac Surg 2006;29(3):271275. Wilson RS. Anesthesia for bronchoscopy and mediastinoscopy. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:660669.

C.2. How many types of bronchoscopes are available and what are the intraoperative considerations of each one?
There are three types of bronchoscopes currently in use: flexible fiberoptic, rigid ventilating, and rigid venturi. The flexible FOB can be used in sedated patients either under local anesthesia (allowing examination of vocal cords movements), or under general anesthesia with laryngeal mask airway P.35 (LMA) or endotracheal intubation. For awake sedated examination, local anesthesia of the upper airway can be accomplished by gargling 4% viscous lidocaine. Lower airway anesthesia can be produced with 4% lidocaine administered through an atomizer with a long nozzle or a nebulizer mask. Bilateral superior laryngeal nerve blocks and/or transtracheal block can be added. Intravenous sedation is supplemented with 0.5-mg increments of midazolam and/or 10 g of remifentanyl boluses, until the patient is calm and cooperative but not obtunded. If the oropharynx is adequately anesthetized, an LMA can be inserted without discomfort and used to assist ventilation and provide higher FIO2 concentrations. In contrast, rigid bronchoscopy usually necessitates general anesthesia and muscle relaxation to avoid coughing or moving, which could cause tracheal trauma. The rigid ventilating bronchoscope has a sidearm adapter that can be attached to the anesthesia machine. A variable air leak usually exists around

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the bronchoscope, so high flow rates of inspired gases and/or packing of the oropharynx are needed. Volatile anesthetics can leak and contaminate the operating room, therefore total IV anesthesia is a valid alternative. The rigid Venturi-effect bronchoscope relies on an intermittent (10 to 12 times/minute) high-pressure oxygen jet to entrain air and insufflate the lungs. The jet is delivered through a reducing valve into a 16or 18-gauge needle inside and parallel to the lumen. Major disadvantages of this bronchoscope are lack of control of the inspired oxygen concentration and inability to administer inhaled anesthetics. Accordingly, anesthesia must be maintained by intravenous techniques. Bronchoscopic procedures can be relatively short, therefore continuous succinlycholine infusion still remains an option. If not contraindicated, mivacurium is also a valid alternative for muscle relaxation. When followed by another procedure (such as the mediastinoscopy scheduled for this patient), an intermediate duration nondepolarizing muscle relaxant is often desirable. Ehrenwerth J, Brull SJ. Anesthesia for thoracic diagnostic procedures. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia, 3rd ed. Philadelphia: Churchill Livingstone, 2003: 174195. Wilson RS. Anesthesia for bronchoscopy and mediastinoscopy. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:660669.

C.3. What are the indications for mediastinoscopy? Are there potential complications?
Mediastinoscopy is usually performed to establish diagnosis of specific lesions within the mediastinum or as a staging procedure for malignancy to determine mediastinal lymph node spread. If lymph nodes are positive for malignancy on frozen section, the patient is probably not a candidate for surgery and the planned lung resection is aborted. Conventional cervical mediastinoscopy involves a small incision at the sternal notch for introduction of the scope and sampling of lymph nodes within the mediastinum. The pleural space is generally not entered intentionally and therefore, a chest tube is not indicated. However, occult pneumothorax can occur. Examination of the intrapleural space can be performed either with a mediastinoscope inserted through an extension of a cervical incision or through a small anterior thoracotomy. In this case, the chest may be evacuated through a catheter after closure or after a chest tube is inserted. Complications during mediastinoscopy are relatively rare (1% to 2%) and generally result from nerve injury (recurrent laryngeal or phrenic) or trauma to adjacent structures (pleura, trachea, esophagus, superior vena cava, azygous vein innominate artery, pulmonary artery, and aorta). Should a major vascular structure be perforated, blood loss can be rapid and profound, necessitating emergent sternotomy. Because packing or vascular clamps P.36 may be applied to the superior vena cava, clinicians should always have a plan for establishing venous access in the lower extremity. Ehrenwerth J, Brull SJ. Anesthesia for thoracic diagnostic procedures. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia, 3rd ed. Philadelphia: Churchill Livingstone, 2003: 174195. Wilson RS. Anesthesia for bronchoscopy and mediastinoscopy. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:660669.

C.4. The decision was made to proceed with thoracotomy and right middle lobectomy. How would you alter your management?
Although not uniformly regarded as necessary for lung resection, an arterial catheter will be placed in the left (dependent) radial artery and the single-lumen ETT replaced with a left-sided double-lumen tube. Although right middle lobectomy is not an absolute indication for lung isolation, this has become common practice because of improved surgical exposure. Nonetheless, OLV is associated with certain disadvantages and complications. The most notable is the large and variable alveolar-to-arterial oxygen tension difference (PAO2PaO2) that occurs as a result of continued perfusion to the nondependent, nonventilated lung. The incidence of severe hypoxemia and hypercarbia, however, is relatively small

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and primarily results from incorrect positioning of the DLT. Other complications include traumatic laryngitis and tracheobronchial rupture. Brodsky JB, Fitzmaurice B. Modern anesthetic techniques for thoracic operations. World J Surg 2001; 25 (2):162166. C a m p o s J A . L u n g s e p a r a t i o n t e c h n i q u e s . I n : K a p l a n J A , S l i n g e r P D, e d s . T h o r a c i c a n e s t h e s i a , 3 r d e d . Philadelphia: Churchill Livingstone, 2003:159173. Shibutani HC. Pulmonary resection. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:639659.

C.5. What are the indications for OLV and how can it be accomplished?
Absolute Indications

Isolation from spillage or contamination


Infectionbronchiectasis and lung abscess Massive hemorrhage

To control the distribution of ventilation


Bronchopleural fistula Bronchopleural cutaneous fistula Giant unilateral lung cyst or bulla Tracheobronchial tree disruption/trauma Surgical procedures on major conducting airway Life-threatening hypoxemia due to unilateral lung disease Unilateral bronchopulmonary lavage (pulmonary alveolar proteinosis)

To facilitate surgical exposure

Video and robotic-assisted thoracoscopic surgery (VATS)

P.37

Relative Indications

Facilitation of surgical exposurehigh priority


Thoracic aortic aneurysm Pneumonectomy Upper lobectomy Mediastinal exposure Pulmonary resection through median sternotomy

Facilitation of surgical exposurelow priority Esophageal resection Middle and lower lobectomies and segmental resection Procedures on the thoracic spine

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Postcardiopulmonary bypass status after removal of totally occluding chronic unilateral pulmonary emboli

Severe hypoxemia due to unilateral lung disease

Several techniques can be used to provide OLV: conventional ETTs passed endobronchially, special single-lumen ETTs with incorporated bronchial blocking catheters (Univent endotracheal tube), bronchial blocking catheters passed outside or inside the ETT, and double-lumen endobronchial tubes. Currently, the use of DLTs remains the most common method for achieving lung isolation. Although DLTs of variant design and material have been used clinically (e.g., Robertshaw, Carlens, and White), the models most commonly used now are disposable and are made of polyvinylchloride (PVC). Such a tube was chosen for this procedure. Double-lumen ETTs are available in five sizes: 28, 35, 37, 39, and 41 French catheter gauge (size in French equals 3.14 times external diameter in millimeters or 4 times the internal diameter plus 2). Choosing the size of a DLT is an important step in decreasing the likelihood of airway trauma or malposition. Although there is a general rule that average-sized men usually accommodate a No. 39 ETT and average-sized women a No. 37 ETT, there is apparently no clear correlation between age, height, weight, and DLT size. A variety of techniques have been described on the basis of measurements of airway size derived from radiographic or computed tomographic (CT) imaging, but these have been questioned across gender and ethnic lines. Ultimately, a properly sized DLT should pass atraumatically through the glottis, advance easily into the trachea and bronchus, and exhibit any air leak when the bronchial cuff is deflated. C a m p o s J A . L u n g s e p a r a t i o n t e c h n i q u e s . I n : K a p l a n J A , S l i n g e r P D, e d s . T h o r a c i c a n e s t h e s i a , 3 r d e d . Philadelphia: Churchill Livingstone, 2003:159173. M i l l e r R D , e d . M i l l e r ' s a n e s t h e s i a , 5 t h e d . N e w Y o r k : Ch u r c h i l l L i v i n g s t o n e , 2 0 0 5 : 1 8 7 3 1 8 7 5 . Slinger PD. Lung isolation. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:660669.

C.6. What are the contraindications to the use of double-lumen ETTs?


Placement of a double-lumen ETT should be carefully considered in the following situations:

Patients whose upper airway anatomy may preclude safe insertion of the tube (recessed jaw, prominent teeth, bull neck, anterior larynx)

Patients with lesions present somewhere along the pathway of the tube that could be traumatized such as airway stricture or endoluminal tumors

Small patients for whom a 35 French tube is too large to fit comfortably through the larynx and a 28 French tube is considered too small P.38

Critically ill patients who have a single-lumen tube already in place and who cannot tolerate cessation of mechanical ventilation and positive end-expiratory pressure (PEEP) ventilation for a short period of time

Under these circumstances, OLV can be achieved through an endobronchial blocker or endobronchial tube placed into a mainstem bronchus. Brodsky JB, Fitzmaurice B. Modern anesthetic techniques for thoracic operations. World J Surg 2001; 25 (2):162166. C a m p o s J A . L u n g s e p a r a t i o n t e c h n i q u e s . I n : K a p l a n J A , S l i n g e r P D, e d s . T h o r a c i c a n e s t h e s i a , 3 r d e d . Philadelphia: Churchill Livingstone, 2003:159173. M i l l e r R D , e d . M i l l e r ' s a n e s t h e s i a , 5 t h e d . N e w Y o r k : Ch u r c h i l l L i v i n g s t o n e , 2 0 0 5 : 1 8 8 3 . Slinger PD. Lung isolation. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic

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anesthesia. New York: Churchill Livingstone, 2000:660669.

C.7. Would you use a right- or left-sided DLT?


A left-sided DLT is preferable for most procedures because the origin of the right upper lobe (RUL) approximately 0.5 to 1.0 cm below the carina complicates placement of a right-sided tube. The left mainstem bronchus is much longer than the right one (approximately 5055 mm vs. 1520 mm), thereby providing a greater margin for error in positioning. A right-sided DLT is indicated in case of large exophytic lesions within the left mainstem bronchial, tight left mainstem bronchus stenosis, distortion of the left mainstem bronchus by an adjacent tumor or a thoracoabdominal aneurysm, and tracheobronchial disruption. Relative indications are left pneumonectomy or lung transplantation because the surgical field is not encumbered by a foreign body that could be included into the staple line. At the end of the procedure, the stump or bronchial anastomosis can be protected from positive pressure ventilation. Right DLTs are contraindicated in case of anomalous takeoff of the right upper bronchus above tracheal carina. Brodsky JB, Fitzmaurice B. Modern anesthetic techniques for thoracic operations. World J Surg 2001;25 (2):162166. C a m p o s J A . L u n g s e p a r a t i o n t e c h n i q u e s . I n : K a p l a n J A , S l i n g e r P D, e d s . T h o r a c i c a n e s t h e s i a , 3 r d e d . Philadelphia: Churchill Livingstone, 2003:159173. Slinger PD. Lung isolation. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:660669.

C.8. How do you know that the tube is in the correct position?
The DLT position may be confirmed by listening to breath sounds of each lung while clamping each lumen of the DLT. However, in emphysematous patients breath sounds may be decreased, making auscultation difficult and unreliable; therefore, FOB is often helpful before placing the patient in lateral decubitus position. During bronchoscopy, the tracheal cartilaginous rings are anterior and the tracheal membrane is posterior. Therefore, the right and left sides can be discerned by the relation of the mainstem bronchi to the anterior cartilaginous ring and the posterior membrane (Fig. 2.1A). In addition, looking for the RUL takeoff (which usually arises from the lateral aspect of right mainstem bronchus just below the tracheal carina) is a useful landmark when the airway anatomy has been obscured by bleeding, edema, or radiation-induced changes, or it has been distorted by extrinsic compression. Left DLT position and depth are confirmed by inserting the FOB in the tracheal lumen. The entire right mainstem bronchus P.39 should be visible and the tracheal lumen orifice should be 1 to 2 cm above the tracheal carina. When properly positioned, the upper surface of the blue endobronchial cuff is visualized just below the tracheal carina in the left mainstem bronchus (Fig. 2.1B). If a right DLT is used, correct positioning is c o n f i r m e d b o t h b y v i s u a l i z a t i o n o f t h e b r o n c h i a l c u f f i n t h e r i g h t m a i n b r o n c h u s ( F i g . 2 . 1 C) a n d b y visualization of the RUL orifice through a port on the lateral surface of the DLT (Fig. 2.1D). For both left and right tubes, the bronchoscope should also be inserted in the bronchial lumen to evaluate the distance between the tip of the tube and distal bifurcation of the bronchus. Position should be reconfirmed after the patient is laterally positioned.

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Figure 2.1 Representative bronchoscopic images of a bronchial blocker and double-lumen endotracheal tube placement. A: Depicts normal tracheal anatomy with cartilaginous rings anteriorly and membranous trachea posteriorly; this helps define left versus right sides. A bronchial blocking catheter is seen in the right main bronchus. B: Depicts placement of a left-sided double-lumen tube; upper portion of endobronchial cuff is evident as is the orifice of the right upper lobe just below the tracheal carina. C: Depicts placement of a right-sided double-lumen tube; the upper portion of the endobronchial cuff is evident. D: Depicts the orifice of the right upper lobe visualized through the port on the lateral aspect of a rightsided double-lumen tube.

C a m p o s J A . L u n g s e p a r a t i o n t e c h n i q u e s . I n : K a p l a n J A , S l i n g e r P D, e d s . T h o r a c i c a n e s t h e s i a , 3 r d e d . Philadelphia: Churchill Livingstone, 2003:159173. P.40 Slinger PD. Lung isolation. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:660669.

C.9. How many types of bronchial blockers are available? What are the advantages and disadvantages of bronchial blockers?
The bronchial blockers most often used for adults are the Fogarty occlusion catheter or the Arndt catheter (wire-guided endobronchial blocker). Fogarty catheters come with either a 12- or a 20-mL high pressure, low volume balloon in both latex and nonlatex models. They have a metallic stylet that can be bent into shape to facilitate endobronchial placement. In case of dislodgment, the stylet can be reinserted and the blocker repositioned. Fogarty catheters have no communicating central channel, therefore continuous positive airway pressure (CPAP) or suction cannot occur. They are usually placed

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outside a single-lumen ETT and positioned with FOB (Fig. 2.1A). If placed inside the ETT, a connector such as two swivel adaptors in series is needed to facilitate insertion of both the catheter and the bronchoscope. Arndt bronchial blockers are available in different sizes with elliptical or spherical cuffs (low pressure, high volume), and are particularly advantageous to isolate the RUL. They are usually inserted through the ETT via a three-way connector (catheter, bronchoscopy, ventilation circuit) and are made with a guide suture loop at the tip that can be placed around a bronchoscope to facilitate p o s i t i o n i n g . T h i s s u t u r e l o o p i s t h e n r e m o v e d , l e a vi n g a n i n n e r l u m e n t h a t a l l o w s f o r s u c t i o n i n g , C P A P , or jet ventilation. Other devices made for endobronchial placement of a blocking cuff through a catheter within the ETT include the Univent tube (a blocker built inside an ETT) and the Cohen endobronchial blocker that is similar to the Arndt catheter but includes a device for mechanically moving the catheter tip. In addition, the use of gauze tampons, a Magill balloon-tipped luminal blocker, and Foley catheters have been reported.

A d v a n t a g e s . B r o n c h i a l b l o c k e r s a r e r e l a t i v e l y s i m p l e a n d c a n b e u s e d i n c h i l d r e n a n d a d u l t s wh o are too small for DLTs. Also, they can


facilitate OLV in patients with a difficult airway or where a DLT is contraindicated; be placed through an existing single-lumen ETT in emergent situations; eliminate the need to change ETTs for postoperative mechanical ventilation.

Disadvantages. In comparison to DLTs, bronchial blockers present

inability to suction efficiently or intermittently ventilate the lung distal to the blocker without deflating the balloon;

the need for bronchoscopic positioning; difficulty in maintaining position in the right mainstem/isolating the RUL efficiently if the takeoff is close to carina

obstruction of the trachea if the bronchial blocker dislodges proximally or bilateral lung ventilation if the cuff is not inflated properly;

potential risk of being stapled in the bronchial stump if not retracted at an appropriate time.

A r n d t G A , De L e s s i o S T , K r a n n e r P W , e t a l . O n e - l u n g v e n t i l a t i o n w h e n i n t u b a t i o n i s d i f f i c u l t presentation of a new endobronchial blocker. Acta Anaesthesiol Scand 1999; 43(3):356358. Campos JH. An update on bronchial blockers during lung separation techniques in adults. Anesth Analg 2003;97:12661274. Ginsberg RJ. New technique for one-lung anesthesia using an endobronchial blocker. J Thorac Cardiovasc Surg 1981;82(4):542546. P.41 Miller RD. Miller's anesthesia, 5th ed. New York: Churchill Livingstone, 2005:1853. Slinger PD. Lung isolation. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:660669.

C.10. How will systemic oxygenation be monitored during OLV? What is the mechanism of oxymetry?
Pulse oximetry has become the hallmark for monitoring arterial oxygenation during lung resection, decreasing the need for repeated measurements of arterial blood gases. This technique uses spectrophotoelectric oximetric principles to determine oxygen saturation. Pulse oximeters are multiple wavelength plethysmographs. The amplitude of the pulse is a function of arterial distension, hemoglobin oxygen saturation of arterial blood inflow, and light wavelength. Hemoglobin saturation in the arterial blood is the result of the ratio between the pulse amplitude of red (660 nm = deoxyhemoglobin) and infrared light (940 nm = oxyhemoglobin). Because pulsatile waveform is a characteristic of arterial blood

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flow, there is no interference from surrounding venous blood, skin, connective tissue, or bone. Arterial pulsations cause changes in light absorption, which are used to calculate oxygen saturation. Adequate finger pulsation is generally lost with hypothermia of a few degrees, hypotension (mean blood pressure < 50 mm Hg), and infusion of vasoconstrictive drugs. Dyshemoglobinemias (such as carboxyhemoglobin, methemoglobin, and sulfhemoglobin) and intravenous dye injection can also affect the oximeter accuracy. Other methods include transcutaneous oxygen tension (PtcO2) and arterial oxygen tension using an indwelling electrode. PtcO2 requires special site preparation, airtight probe mantling, and a potentially harmful local source of heat to induce arterialization. Moreover, PtcO2 fails to perfectly reflect true arterial oxygenation. An indwelling arterial oxygen electrode is inserted into the arterial line and may increase the incidence of thromboembolism. Brodsky JB, Fitzmaurice B. Modern anesthetic techniques for thoracic operations. World J Surg 2001;25 (2):162166. Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology 1989;70:98108.

C.11. The patient was placed in the lateral decubitus position for thoracotomy. Describe the effects of lateral positioning on pulmonary blood flow and respiration
In both upright and supine positions, the right lung receives approximately 55% of the total blood flow, whereas the left lung receives the remaining 45%. Gravity causes a vertical gradient in the distribution of blood flow in the lateral decubitus. Therefore, blood flow to the dependent lung is significantly greater than that to the nondependent lung. When the right lung is nondependent, it receives 45% of the total blood flow, whereas 55% perfuses the dependent left lung. When the left lung is nondependent, it receives 35% of the total blood flow, whereas the dependent right lung receives 65%. Therefore, the average blood flow of the nondependent lung is approximately 40% of the total blood flow, whereas the dependent lung is perfused with the remaining 60%.

Respiratory effects
Lateral decubitus position causes mechanical interference with chest wall movement, decreasing lung expansion. The dependent chest wall is constricted by the operating room table, and lateral movements are limited by the bolsters or bean-bags used to hold the patient in position. In addition, the increase in i n t r a - a b d o m i n a l p r e s s u r e t h a t o c c u r s wi t h g e n e r a l a n e s t h e s i a , d e c r e a s e s d i a p h r a g m a t i c m o v e m e n t s . Mismatching of ventilation and perfusion in the lateral position P.42 is the result of (a) gravity, with redistribution of blood flow toward the dependent lung, and (b) compression of the dependent lung by the mediastinum and abdominal contents. In awake, spontaneously breathing subjects the lower (dependent) diaphragm is still able to contract more efficiently, maintaining ventilation to the dependent lung and matching increased perfusion. In contrast, when the patient is anesthetized, with or without paralysis, most ventilation is preferentially switched to the upper lung, because of an increase in compliance in these areas. The preferential ventilation of the upper lung, coupled with greater perfusion of the lower lung, results in an increased degree of ventilationperfusion mismatch. Rehder K, Hatch DJ, Sessler AD, et al. The function of each lung of anesthetized and paralyzed man during mechanical ventilation. Anesthesiology 1972;37:16. Shibutani HC. Pulmonary resection. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:639659. Walff KE, Aulin I. The regional lung function in the lateral decubitus position during anesthesia and operations. Acta Anesthesiol Scand 1972;16:195205.

C.12. What is HPV?


HPV is an autoregulatory mechanism to prevent ventilationperfusion mismatch and improve arterial

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oxygenation. HPV involves a redox-based O2 sensor within pulmonary artery smooth muscle cells and is triggered by decreased PaO2 within the lung from low FIO2, hypoventilation, or atelectasis. The s e l e c t i v e i n c r e a s e o f v a s c u l a r r e s i s t a n c e i n t h e h y p o x i c p a r e n c h y m a d i v e r t s b l o o d a wa y t o t h e b e t t e r ventilated normoxic lung, decreasing the amount of shunt flow. Brimioulle S, LeJeune P, Naeije R. Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange. Appl Physiol 1996; 81(4):15351543. Nagendran J, Stewart K, Hoskinson M, et al. An anesthesiologist's guide to hypoxic pulmonary vasoconstriction: implications for managing single-lung anesthesia and atelectasis. Curr Opin Anaesthesiol 2006;19(1):3443.

C.13. What are the effects of anesthetic agents on HPV and what are their clinical implications?
Several clinical studies have failed to demonstrate a decrease in HPV during one-lung ventilation and total intravenous anesthesia (TIVA). Intravenous anesthetics, such as thiopental, ketamine, morphine, and fentanyl, have no direct effect on HPV. In contrast, inhalational anesthetics have been shown to inhibit HPV in a dose-related manner but usually at concentrations much higher than those used clinically. Other nonanesthetic drugs such as -agonists and antagonists, calcium channel blockers, nitrovasodilators and theophylline may influence the effects of inhalation anesthetics on shunting and arterial oxygenation during OLV.

The effect of increased shunt on PaO2 depends on the absolute level of the initial shunt and the inspired oxygen concentration. In practice, almost 100% oxygen is used during OLV. Even when shunt is increased, PaO2 usually remains well above 100 mm Hg, and oxygen saturation and oxygen content hardly change. The direct inhibition of HPV due to inhaled anesthetics can be antagonized by their secondary effects, such as a decrease in cardiac output, mixed venous oxygen tension and pulmonary pressure. All these can intensify HPV in the nondependent lung. Furthermore, the presence of chronic, irreversible disease in the vessels of the nondependent lung may impair HPV response. P.43 The presence of disease in the dependent lung will decrease the ability of accepting redistribution of blood flow, thereby decreasing the HPV effect of the nondependent lung. Surgical interference with blood flow to the nondependent lung also decreases the anesthetic effect on HPV.

Boldt J, Mller M, Uphus D, et al. Cardiorespiratory changes in patients undergoing pulmonary resection using different anesthetic management techniques. J Cardiothorac Vasc Anesth 1996;10:854859. Nagendran J, Stewart K, Hoskinson M, et al. An anesthesiologist's guide to hypoxic pulmonary vasoconstriction: implications for managing single-lung anesthesia and atelectasis. Curr Opin Anaesthesiol 2006;19(1):3443. Reid CW, Slinger PD, Lewis S. A comparison of the effects of propofol-alfentanil versus isoflurane anesthesia on arterial oxygenation during one-lung ventilation. J Cardiothorac Vasc Anesth 1996;10:860863.

C.14. Discuss pulmonary blood flow distribution, shunt flow, and PaO 2 (FIO 2 = 1.0) during OLV
When the nondependent lung is collapsed, HPV will increase pulmonary vascular resistance and decrease lung blood flow in this area. If no complicating factors exist, HPV should decrease blood flow to that lung by approximately 50%. Consequently, the nondependent lung should be able to reduce its blood flow from 40% to 20% of the total, and the nondependent/dependent lung blood flow ratio during OLV should be 20%/80%.

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In atelactasis, all the blood flow to the nonventilated lung is shunt flow. Therefore, OLV creates an o b l i g a t o r y r i g h t - t o - l e f t t r a n s p u l m o n a r y s h u n t t h a t w a s n o t p r e s e n t d u r i n g t wo - l u n g v e n t i l a t i o n . I f n o s h u n t e x i s t e d d u r i n g t wo - l u n g v e n t i l a t i o n ( i g n o r i n g t h e n o r m a l 1 % t o 3 % s h u n t f l o w d u e t o t h e b r o n c h i a l , pleural, and the besian circulation), an ideal total shunt flow of 20% would be expected during OLV. PaO2 with fractional inspired O2 concentration (FIO2) equal to 1 should be approximately 280 mm Hg if hemodynamic and metabolic states are normal. Clinically, PaO2 (FIO2 = 1) ranges from 150 to 250 mm Hg. Marshall BE, Marshall C. Continuity of response to hypoxic pulmonary vasoconstriction. J Appl Physiol 1980;59:189196. Shibutani HC. Pulmonary resection. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:639659.

C.15. How could you improve oxygenation during OLV?


The following interventions can be used to improve oxygenation:

Use 100% oxygen. Check the position of the DLT with an FOB. Ventilate manually to determine whether higher or lower tidal volumes/inspiratory pressures are beneficial.

S e t m i n u t e v e n t i l a t i o n t o m a i n t a i n P a C O 2 a t 4 0 m m H g ( h y p o c a p n i a m a y i n h i b i t HP V i n t h e nondependent lung; hyperventilation may increase airway pressure and promote blood flow to the nonventilated lung).

Insufflate oxygen to the nonventilated lunga flow of approximately 3 L per minute allowed to circulate freely will often increase arterial oxygen saturation by 3% to 4%. P.44

Apply PEEP of 5 cm H2O to the dependent lungit may be beneficial if larger tidal volumes delivered manually improved arterial saturation (i.e., recruitable alveoli). Alternatively, if tidal volumes are too large, adding PEEP may overdistend alveoli that are already open and compress blood vessels, diverting blood to the nonventilated lung and worsening the shunt.

Partially re-expand the nonventilated lung and then cease ventilation but keep the lumen to the nonventilated side closed. This could interfere with surgical exposure.

Use differential lung CPAP/PEEP. Use CPAP to the nonventilated lung alone or in combination with PEEP to the ventilated lung in the effort of matching shunt with ventilation (rarely necessary): Add CPAP of 5 cm H2O to the nondependent lung during the deflation phase of a large tidal volume breath to overcome critical opening pressure in the atelectatic lung. Disadvantage of this maneuver is that although the lung is not ventilated, it may remain distended. Apply PEEP of 5 cm H2O to the dependent lung. Increase the nondependent lung CPAP to 10 cm H2O whereas the dependent lung is maintained at PEEP of 5 cm H2O. Increase dependent lung PEEP to 10 cm H2O to match the nondependent lung CPAP. The differential lung CPAP/PEEP search discussed in the preceding text is conducted in this way to find the optimal (best) end-expiratory pressure for each lung and minimum QS/QT for the patient as a whole.

Use two-lung ventilation intermittently. Clamp the pulmonary artery of the nondependent lung temporarily (rarely necessary).

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Benumof JL. Anesthesia for thoracic surgery, 2nd ed. Philadelphia: WB Saunders, 1995: 408428. Brodsky JB, Fitzmaurice B. Modern anesthetic techniques for thoracic operations. World J Surg 2001;25 (2):162166. M i l l e r R D , e d . M i l l e r ' s a n e s t h e s i a , 5 t h e d . N e w Y o r k : Ch u r c h i l l L i v i n g s t o n e , 2 0 0 5 : 1 8 9 4 1 8 9 9 . Shibutani HC. Pulmonary resection. In: Youngberg JA, Lake CL, Wilson RS, eds. Cardiac, vascular and thoracic anesthesia. New York: Churchill Livingstone, 2000:639659.

C.16. Right middle lobectomy was performed. Would you extubate the trachea at the end of the procedure?
After routine lung resection, the trachea can be extubated as long as the patient meets all criteria and has adequate analgesia. If the patient cannot maintain adequate oxygenation and ventilation, postoperative mechanical support is indicated. Under most circumstances, when patients require postoperative ventilatory support, it is advantageous to change the DLT to a single-lumen ETT. Since spontaneous ventilation avoids the potential hazards of positive pressure on the suture lines of the new bronchial stump or parenchymal air leaks, the combination of modest CPAP and pressure support ventilation is usually preferable to controlled intermittent mandatory ventilation.

D. Postoperative Management D.1. What are the immediate life-threatening complications that follow lobectomy or pneumonectomy?
Serious complications after lobectomy include lobar collapse, massive hemorrhage caused by loosening of a ligature from a pulmonary vessel, bronchopleural fistula from disruption of a bronchial stump, and pulmonary torsion due to increased mobility of a lobe. P.45 Pneumonectomy can be complicated by herniation of the heart (in case of intrapericardial approach), acute right heart failure, right-to-left shunting across a patent foramen ovale due to increased pulmonary vascular resistance and right ventricular pressure, nerve injuries (phrenic, vagus, or recurrent laryngeal) during radical hilar dissection or excision of mediastinal tumors, and acute respiratory insufficiency. Higgins TL. Postthoracotomy complications. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia, 3rd ed. Philadelphia: Churchill Livingstone, 2003:159173. Reed CE. Physiologic consequences of pneumonectomy. Consequences on the pulmonary function. Chest Surg Clin N Am 1999;9(2):449457.

D.2. Why is it important to control postoperative pain? How would you achieve this?
Postoperative pain control is important not only for patient comfort but also to minimize pulmonary complications, allowing the patient to breathe deeply, cough effectively, and ambulate. Systemic administration of opiates is often used alone or in combination with other modalities to control postoperative pain. Morphine in 2-mg increments can be titrated during emergence from anesthesia to a c h i e v e a d e q u a t e p a i n r e l i e f , a v o i d i n g r e s p i r a t o r y d e p r e s s i o n . T h i s c a n b e f o l l o we d p o s t o p e r a t i v e l y b y patient-controlled analgesia (PCA), often in combination with nonsteroidal anti-inflammatory drugs (NSAIDs). However, when used as a single modality, systemic opioids require plasma concentrations that are usually associated with sedation and potential respiratory depression. Even when used with PCA, pain control is often suboptimal, because of fluctuations in the drug plasma concentration. NSAIDs such as ketorolac, diclofenac, ketoprofen, and indomethacin are usually used as adjuvants to parenteral opiates, particularly for the treatment of shoulder pain associated with chest tube placement. The main short-term concerns for NSAIDs are the potential for exacerbating renal insufficiency and inducing platelet dysfunction. Alternative methods for pain control include epidural local anesthetic with or without opiate, intrathecal opiates, intercostal or paravertebral nerve block, cryoanalgesia, interpleural

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regional analgesia, and transcutaneous electrical nerve stimulation (TENS).

Epidural and intrathecal analgesia


Thoracic or lumbar epidural analgesia may be achieved by a single injection or a continuous infusion of local anesthetic, alone or in combination with an opiate. In order to reduce the volume required to produce an effect and lessen the chance of hypotension and motor weakness, the catheter should be placed as close as possible to the dermatomes to be covered. A low concentration of local anesthetic such as 0.1% or 0.05% bupivacaine combined with an opiate (e.g., fentanyl 10 g/mL or sufentanil 0.1 g/mL) produces synergistic effects that help reduce the sympathetic blockade that may occur with more concentrated local anesthetic alone. In addition, the presence of local anesthetics seems to increase the affinity of the narcotic for the opioid receptors. The use of thoracic epidural analgesia with local anesthetic plus opiate has been shown to improve postoperative pulmonary function. Potential complications of the thoracic epidural technique include inadvertent dural puncture, trauma to the spinal cord, and intravascular injection of local anesthetics with resultant cardiovascular and central nervous system toxicity. Intrathecal injection of opiates has been successfully used preoperatively or intraoperatively to provide postoperative pain relief for 18 to 24 hours. However, in comparison to epidural injection, intrathecal opiate (in particular morphine) is associated with an increased incidence of late respiratory depression ( 4 % t o 7 % a s c o m p a r e d wi t h < 1 % f o r e p i d u r a l a d m i n i s t r a t i o n ) . T h e a d v a n t a g e s o f n e u r a x i a l o p i a t e s a s compared with systemic opiates include selective blockade of spinal pain with minimal sympathetic blockade and no loss of motor function, and greater P.46 predictability of pain relief. Epidural analgesia and opiates in combination with local anesthetics block the presynaptic and postsynaptic neuron cells of the substantia gelatinosa of the spinal cord by passive diffusion across the dura into the cerebrospinal fluid. The lipophilic narcotics, such as fentanyl, methadone, and meperidine, in doses of 0.1mg, 5mg, and 30mg to 100 mg, respectively, have a relatively short onset of action of less than 12 minutes. They provide significant pain relief in 20 to 30 minutes and have a duration of action of 6 to 7 hours. In contrast, a lipophobic narcotic, such as morphine, in a 5-mg dose, has a relatively slow onset of action of 15 to 30 minutes, provides maximal pain relief in 40 to 60 minutes, and has a duration of action of more than 12 hours. The most serious complications of epidural narcotics are early and late respiratory depression. The other side effects include urinary retention, pruritus, and nausea and vomiting. The narcotic antagonist, naloxone, can reverse all the earlier side effects but will reverse the analgesic effect as well, and therefore must be used cautiously.

Intercostal or paravertebral nerve block


Intercostal nerve blocks with long-acting local anesthetics can be used to control pain after thoracoscopy or thoracotomy and can be done by the surgeon intraoperatively. The blocks to the intercostal nerves are placed at the level of the incision and two or three interspaces above and below this level. Catheters that can be injected postoperatively when pain occurs may be placed in the appropriate intercostal grooves at the time of thoracotomy closure. Paravertebral blocks in combination with parenteral opiates and NSAIDs are an alternative to thoracic epidural analgesia. However, the failure rate for this technique is relatively high (6% to 10%). Pneumothorax (especially if bilateral blocks are attempted), hypotension, local anesthetic toxicity due to the high vascularization of the area, and inadvertent total spinal block are the potential risks.

Cryoanalgesia
Long-lasting (3 to 4 weeks up to 6 months) intercostal nerve block can be obtained by cryoablation. Two 30-second freeze cycles (-60C), separated by a 5-second thaw period, are applied to each of the nerves selected. Although cryoanalgesia was initially shown to effectively relieve pain and improve postoperative pulmonary function, a more detailed study has revealed a significant incidence of paresthesia and postthoracotomy pain syndrome.

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Interpleural regional analgesia


This technique involves percutaneous introduction of a catheter into the thoracic cage between the parietal and visceral pleura for injection of local anesthetic. Analgesia is thought to occur as a result of (a) diffusion of local anesthetic through the parietal pleura and the innermost intercostal muscle to the intercostal nerves (where the block occurs), (b) block of the intrathoracic sympathetic chain, and (c) direct action of local anesthetic on nerve endings within the pleura. However, efficacy is not uniform because of the loss of anesthetic through thoracotomy drainage, the presence of extravasated blood and tissue fluid in the pleural space diluting the local anesthetic, and possible sequestration and channeling of local anesthetic by the decreased movements of the operated lung. Moreover, in the sitting position, the local anesthetic pools in the costophrenic angle, limiting the quality of analgesia. The use of multiple or fenestrated catheters may achieve more even distribution of local anesthetic over the pleura and improve the quality of analgesia.

Transcutaneous electrical nerve stimulation


The advantages of TENS include low cost, ease of application, and lack of undesirable side effects. H o w e v e r , T E NS h a s a we a k a n a l g e s i c e f f e c t . I t i s g e n e r a l l y r e s e r v e d f o r a d j u n c t i v e u s e w i t h n a r c o t i c s t o relieve postthoracotomy pain if mild to moderate. It is ineffective if the pain is severe. Ali J, Yaffe CS, Serrette C. The effect of transcutaneous electric nerve stimulation in treatment of postoperative pain. Surgery 1981;89:507512. P.47 Brodsky JB, Fitzmaurice B. Modern anesthetic techniques for thoracic operations. World J Surg 2001;25 (2):162166. Cousins MJ, Mather LE, Wilson PR. Intrathecal and epidural administration of opioid analgesic. Anesthesiology 1984;61:276. Ferrante FM, Chan VWS, Arthur R, et al. Interpleural analgesia after thoracotomy. Anesth Analg 1991;72:105109. Kaplan JA, Slinger PD. Thoracic anesthesia, 3rd ed. New York: Churchill Livingstone, 2003: 445456. Kavanagh BP, Katz J, Sandler AN. Pain control after thoracic surgery. A review of current techniques. Anesthesiology 1994;81:737759. Maiwand MO, Makey AR, Rees A. Cryoanalgesia after thoracotomy: improvement of technique and review of 600 cases. J Thorac Cardiovasc Surg 1986;92:291. M i l l e r R D , e d . M i l l e r ' s a n e s t h e s i a , 5 t h e d . N e w Y o r k : Ch u r c h i l l L i v i n g s t o n e , 2 0 0 5 : 1 9 0 6 1 9 0 9 .

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Chapter 3 Aspiration Pneumonitis and Acute Respiratory Failure


M a n u e l L. F o n t e s Jeffrey S. Berger Fun-Sun F. Yao

A 20-Year-Old Full-Term Pregnant Woman


w as ru shed to the op erati n g ro om fo r emerg en cy cesa rea n sectio n be caus e of fe tal d is tress. Du ri ng e me rge nce fr om gen era l a nes thesi a, th e pa ti ent vo mi ted and a spi ra ted.

P.49 P.50

A. Management of Aspiration A.1. Delineate the risk factors for aspiration pneumonitis
Aspiration pneumonitis arises most often from aspiration of gastric content that is both acidic and voluminous. It can also occur from aspiration of oropharyngeal content. Several patient characteristics lead to the development of aspiration. These include:

Neurologic dysphagia Disruption of gastroesophageal junction Anatomic abnormalities of the upper aerodigestive tract General anesthesia Pharmacologic agents that alter consciousness (e.g., sedatives, antipsychotics, antidepressants, narcotics). Extremes of age (elderly, neonates)

The risk of aspiration pneumonitis is approximately 10% in patients presenting to the hospital after a drug overdose. This condition used to be very common in general anesthesia and accounted for most obstetric morbidity and mortality. The most recent report suggests an incidence of 1 in 3,000 patients receiving general anesthetics; however, the mortality remains very high and accounts for 10% to 30% of all deaths related to anesthesia. The elderly, particularly the nursing home population, is at increased risk of aspiration secondary to both an increased incidence of pharyngeal dysmotility and gastroesophageal reflux. Aspiration pneumonia and pneumonitis are the most common causes of death in patients with dysphagia caused by neurologic disorders, a condition that affects approximately 300,000 to 600,000 people yearly in the United States. Irwin RS. Aspiration. In: Irwin RS, Cerra FB, Rippe JM, eds. Irwin and Rippe's intensive care medicine, 4th ed. Vol. 1. Philadelphia: Lippincott-Raven Publishers, 1999:685692. Janssens JP. Pneumonia in the elderly (geriatric) population. Curr Opin Pulm Med 2005;11 (3):226230. Jaovisidha K, Csuka ME, Almagro UA, et al. Severe gastrointestinal involvement in systemic

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sclerosis: report of five cases and review of the literature. Semin Arthritis Rheum 2005; 34 (4):689702. Marik P. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001;344:665671. Ng A, Smith G. Gastroesophageal reflux and aspiration of gastric contents in anesthetic practice. Anesth Analg 2001;93:494513.

A.2. What is Mendelson syndrome?


Mendelson first described acute chemical aspiration pneumonitis in 1946. The triphasic sequence beginning with immediate respiratory distress, bronchospasm, cyanosis, tachycardia, and dyspnea, following with partial recovery, and concluding with a final phase of gradual respiratory recovery is characteristic of Mendelson syndrome. No signs of mediastinal shift are seen, but chest x-ray films usually show irregular mottled densities. This syndrome is due to the irritation of bronchioles by gastric hydrochloric acid, producing bronchiolar spasm, a peribronchiolar exudates, and congestion. James CF, Modell JH, Gibbs CP, et al. Pulmonary aspirationeffects of volume and pH in the rat. Anesth Analg 1984;63:665668. P.51 Knight PR, Rutter T, Tait AR, et al. Pathogenesis of gastric particulate lung injury: a comparison and interaction with acidic pneumonitis. Anesth Analg 1993;77:754760. Mendelson CC. The aspiration of stomach contents into the lungs during obstetric anesthesia. Am J Obstet Gynecol 1946;52:191205. Schwartz DJ, Wynne JW, Gibbs CP, et al. The pulmonary consequences of aspiration of gastric contents at pH values greater than 2.5. Am Rev Respir Dis 1980;121:119126. Teabeault JR. Aspiration of gastric contents: experimental study. Am J Pathol 1952;28:5167.

A.3. What is the critical pH value and volume of aspirate to cause Mendelson syndrome?
The critical pH value is 2.5. At a pH value higher than 2.5, the response is similar to that of distilled water. Maximal pulmonary damage is achieved at an aspirate pH value of 1.5. A patient is thought to be at risk when there is more than 25 mL (0.4 mL/kg) of gastric contents and the pH value of the gastric contents is less than 2.5. Hong JY, Oh JI. Effects of preoperative anxiety on gastric fluid acidity and volume. J Korean Med Sci 2005;20(2):232235. Pisegna JR, Martindale RG. Acid suppression in the perioperative period. J Clin Gastroenterol 2005;39(1):1016. Teabeault JR. Aspiration of gastric contents: experimental study. Am J Pathol 1952;28:5167.

A.4. How does aspiration pneumonitis differ from aspiration pneumonia?


Aspiration pneumonitis is generally attributed to a chemical injury of the lungs from aspiration of gastric content. The more acidic the pH value and the more voluminous the gastric content, the more severe the chemical burn. Food particles, independent of the acidity, can also cause a chemical injury. Aspiration pneumonitis consists of two phases: the first stage peaks within the first few hours after the aspiration and is mostly related to the caustic effect of the low pH value of the aspirate on the cells lining the alveolar-capillary interface; the second phase generally

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peaks at approximately 6 hours and is characterized both by infiltration of neutrophils into the a l v e o l i a n d t h e l u n g i n t e r s t i t i u m a n d b y a n i n f l a m m a t o r y p r o c e s s i d e n t i c a l t o t h a t o bs e r v e d i n other types of acute lung injury. Aspiration pneumonia, on the other hand, differs from aspiration pneumonitis on the basis of microbiology. The latter is sterile, and the former contains bacterial agents. As such, the incidence of aspiration pneumonia in the population at risk (see section A.1) is much greater because a small amount of either oropharyngeal or gastric content that is colonized with bacteria is sufficient to cause injury, particularly in the elderly and the immunocompromised host. In the community, both Haemophilus influenzae and Streptococcus pneumoniae first colonize the oropharynx and access the tracheobronchial tree and alveoli after aspiration to cause community-acquired pneumonia. The term aspiration pneumonia is used specifically to describe radiographic evidence of infiltrate in a patient who is at risk of oropharyngeal aspiration. More than 50% of adults aspirate some amount of oropharyngeal secretion during sleep; however, very little sequelae arise from this for several reasons: first, the burden of virulent bacteria in normal pharyngeal secretions is low; second, the host is able to clear the aspirate through ciliary transport and cough reflexes; and third, the status of the immune system is noncompromised. Cassiere HA, Niederman MS. Aspiration pneumonia, lipoid pneumonia, and lung abscess. In: Baum GL, Crapo JD, Celli BR, et al, eds. Textbook of pulmonary diseases, 6th ed. Vol. 1. Philadelphia: Lippincott-Raven Publishers, 1998:645655. P.52 Irwin RS. Aspiration. In: Irwin RS, Cerra FB, Rippe JM, eds. Irwin and Rippe's intensive care medicine, 4th ed. Vol. 1. Philadelphia: Lippincott-Raven Publishers, 1999:685692. Marik P. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001;344:665671. Mylotte JM, Goodnough S, Gould M. Pneumonia versus aspiration pneumonitis in nursing home residents: prospective application of a clinical algorithm. J Am Geriatr Soc 2005; 53(5):755761.

A.5. You suspect the patient has aspirated. What is your initial management strategy?
Rapidly tilt the operating table to a 30-degree head-down position to have the larynx at a higher level than the pharynx and to allow gastric content to drain to the outside. While an assistant maintains cricoid pressure, suction the mouth and pharynx as rapidly as possible. Next, endotracheal intubation should be performed (if the patient had been extubated) with immediate inflation of the endotracheal cuff to prevent further aspiration. Quickly suction through the endotracheal tube before administering 100% oxygen by PPV. This is to prevent pushing aspirated material beyond your reach. Suction should be brief to avoid cardiac arrest from hypoxia. Give 100% oxygen before and after suctioning. An orogastric tube should be inserted to empty the stomach. The pH value of the gastric content should be determined. Tracheobronchial aspirate is collected for culture and sensitivity tests. Auscultation of the chest will determine whether diminished breathing sounds, wheezing, rales, and rhonchi are present. If bronchospasm is noted, 2-agonists such as albuterol or terbutaline may be administered through metered-dose inhaler adapters to the anesthetic circuit. The earliest and most reliable sign of aspiration is hypoxemia, which follows aspiration of even the mildest and most benign aspirate. Therefore, analysis of arterial blood gases should be performed to determine the severity of hypoxemia. Early application of PEEP is recommended to improve pulmonary function.

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Abouleish E, Grenvik A. Vomiting, regurgitation, and aspiration in obstetrics. Pa Med 1974; 77:4558. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:13931395. d'Escrivan T, Guery B. Prevention and treatment of aspiration pneumonia in intensive care units. Treat Respir Med 2005;4(5):317324. Stoelting RK, Dierdorf SP. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:580581.

A.6. Would you give prophylactic antibiotics?


The initial aspirate, excluding feculent aspirate, is usually sterile and remains so for the first 24 hours. Thereafter, the aspiration pneumonitis can become aspiration pneumonia either from contamination of the initial aspirate or secondarily from aspiration of a colonized oropharyngeal secretion in a host that now has tracheobronchial and alveolar damage. Colonization cultures may demonstrate gram-positive or gram-negative superinfection or both, usually with Escherichia, Klebsiella, Staphylococcus, Pseudomonas, and Bacteroides or with anaerobes. Prophylactic antibiotic has not been shown to improve mortality or reduce secondary infection r a t e s . C u l t u r e s m u s t b e t a k e n a s s o o n a s p o s s i b l e af t e r a s p i r a t i o n a n d t h e r e a f t e r a s c l i n i c a l l y indicated. The antibiotic therapy is given according to the sensitivity test result. Prophylactic use of broad-spectrum antibiotics P.53 may lead to drug-resistant bacterial and fungal superinfection. However, if intestinal obstruction is a possibility, antimicrobial therapy for the possibility of anaerobic and gram-negative infection may be warranted. Although data supporting the use of prophylactic antibiotics are lacking, it is not unusual for clinicians to prescribe such therapy in settings in which the host is considered immunocompromised (e.g., elderly and critically ill patients). If one or several antibiotics have been administered, prompt withdrawal should occur with laboratory or clinical evidence of no infection. In contrast, the use of antibiotics in aspiration pneumonia is unequivocally indicated (e.g., third-generation cephalosporins, fluoroquinolones, or piperacillin). Allewelt M, Schuler P, Bolcskei PL, et al. Study Group on Aspiration Pneumonia. Ampicillin + sulbactam vs clindamycin +/- cephalosporin for the treatment of aspiration pneumonia and primary lung abscess. Clin Microbiol Infect 2004;10(2):163170. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:13931395. Genne D, Sommer R, Kaiser L, et al. Analysis of factors that contribute to treatment failure in patients with community-acquired pneumonia. Eur J Clin Microbiol Infect Dis 2006;25(3):159 166. Rebuck JA, Rasmussen JR, Olsen KM. Clinical aspiration-related practice patterns in the intensive care unit: a physician survey. Crit Care Med 2001;29(12):22392244.

A.7. Would you give steroid therapy?


The value of systemic corticosteroids is controversial. The rationale for immediate use of corticosteroids is to reduce inflammation and stabilize lysosomal membranes. In addition, they have been shown to prevent pulmonary cellular damage by protecting type II alveolar pneumocytes and to attenuate agglutination of leukocytes and platelets. I n e x p e r i m e n t a l s t u d i e s , t h e e f f e c ti v e n e s s o f c o r t i c o s t e r o i d t h e r a p y a p p e a r e d t o b e r e l a t e d t o t h e pH value of aspirates. When the pH value of the aspirate was in the narrow range of 1.5 to 2.5,

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corticosteroid therapy was beneficial in treating acid-aspiration pneumonitis. Dexamethasone, given 0.08 mg per kg every 6 hours, decreased pulmonary water content significantly starting at 24 hours, with return to the normal range by 72 hours. When the pH value of the aspirate was less than 1.5, the pulmonary parenchymal damage was maximal. Therefore, the steroid therapy was not effective. When the pH value of the aspirate was higher than 2.5, the response was similar to that of water. Wolfe, Bone, and Ruth found that pneumonia caused by gram-negative bacteria was more frequent after aspiration in patients treated with corticosteroids than in those who were not. Similarly, studies in animals have failed to demonstrate a beneficial effect of corticosteroids on pulmonary function, lung injury, alveolar-capillary permeability, or outcome after acid aspiration. Furthermore, because of the failure of two multicenter, randomized, controlled trials to demonstrate a benefit of high-dose corticosteroids in patients with ARDS, the administration of corticosteroids cannot be recommended. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:1395. Bernard GR, Luce JM, Sprung CL, et al. High-dose corticosteroids in patients with the adult respiratory distress syndrome. N Engl J Med 1987;317:15651570. Downs JB, Chapman RL Jr, Modell JH, et al. An evaluation of steroid therapy in aspiration pneumonitis. Anesthesiology 1974;40:129135. P.54 Dudley WR, Marshall BE. Steroid treatment for acid-aspiration pneumonitis. Anesthesiology 1974;40:136141. Lee M, Sukumaran M, Berger HW, et al. Influence of corticosteroid treatment on pulmonary function after recovery from aspiration of gastric contents. Mt Sinai J Med 1980;47:341346. Lowrey LD, Anderson M, Calhoun J, et al. Failure of corticosteroid therapy for experimental acid aspiration. J Surg Res 1982;32:168172. Miller RD, ed. Anesthesia, 5th ed. New York: Churchill Livingstone, 2000:2222. Sukumaran M, Granada MJ, Berger HW, et al. Evaluation of corticosteroid treatment in aspiration of gastric contents: a controlled clinical trial. Mt Sinai J Med 1980;47:335340. Wolfe JE, Bone RC, Ruth WE. Effects of corticosteroids in the treatment of patients with gastric aspiration. Am J Med 1997;63:719722. Wynne JW, DeMarco FJ, Hood CI. Physiological effects of corticosteroids in foodstuff aspiration. Arch Surg 1981;116:4649.

A.8. Would you irrigate the bronchial tree with bicarbonate or saline solution?
No. In acid-aspiration pneumonitis, Bannister, Sattilaro, and Otis demonstrated that pulmonary lesions were aggravated by irrigation with sodium bicarbonate, normal saline, and sodium hydroxide. This was explained on the basis that (a) the large volume of fluid served to push the hydrochloric acid deeper into the lungs; (b)mixing of the acid and treatment solution was impossible because of the minute size of the interface; (c) hydrochloric acid probably causes damage within a very short time; (d) if equal volumes of hydrochloric acid (e.g., with a pH value of 1.6) and sodium chloride are mixed, the pH value increases only to 1.8; and (e) neutralization of hydrochloric acid with sodium bicarbonate produces heat, and a thermal burn of the bronchial mucosa may occur. Bronchial irrigation is indicated only in the obstructive type of aspiration. Five to ten milliliters of

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normal saline is instilled into the tracheobronchial tree, followed immediately by suction. Bronchial irrigation is preceded and followed by oxygenation. The sequence is repeated until the aspirate fluid is clear. Bannister WK, Sattilaro AJ, Otis RD. Therapeutic aspects of aspiration pneumonitis in experimental animals. Anesthesiology 1961;22:440443. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:1395.

A.9. How would you prevent aspiration during emergency surgery?


An ounce of prevention is worth a pound of cure. The following principles of preoperative preparation are of extreme importance:

Application of gastric decompression by a wide-bore orogastric tube Use of regional anesthesia whenever possible Preoperative administration of a clear antacid, such as 30 mL of 0.3-M. sodium citrate Premedication with anticholinergic agents, such as atropine or glycopyrrolate Administration of metoclopramide to stimulate gastric emptying and to increase lower esophageal sphincter tone

Preoperative administration of an H2-receptor antagonist or proton inhibitors (pantoprazole sodium) to decrease further secretion of additional acid Extubation only when the patient is fully awake

P.55 Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:10551056, 1234, 1395. DiSario JA. Future considerations in aspiration pneumonia in the critically ill patient: what is not known, areas for future research, and experimental methods. JPEN J Parenter Enteral Nutr 2002;26(6 Suppl):S75S78; discussion S79. Miller RD, ed. Miller's anesthesia, 6th ed. New York: Churchill Livingstone, 2005:25992601. Pisegna JR, Martindale RG. Acid suppression in the perioperative period. J Clin Gastroenterol 2005;39(1):1016. Smith G, Ng A. Gastric reflux and pulmonary aspiration in anaesthesia. Minerva Anestesiol 2003;69(5):402406.

B. Acute Lung Injury


T h e p a t i e n t w a s e x t ub a t e d i n t h e r e c o v e r y r o o m . C h e s t x - r a y f i l m s s h o w e d q u e s t i o n a b l e m o t t l e d density in the posterior segments of the right upper lobe. Six hours after being transferred to the floor, she was found to be dyspneic and cyanotic. On auscultation of the chest, significant wheezing was noted and the results of the most recent analysis of arterial blood gases showed the following: pH, 7.26; PaCO2, 55 mm Hg; PaO2, 55 mm Hg; and HCO3, 20 mEq per L on room air.

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B.1. Define ALI and ARDS


ARDS is the most severe form of ALI. To standardize definitions, a consensus panel of experts developed a set of criteria characterizing ARDS and ALI. The criteria include onset that is acute, bilateral infiltrates on chest radiography, hypoxemia, and no evidence of cardiogenic failure (i.e., pulmonary artery occlusion pressure, < 18 mm Hg). Additionally, this group defined hypoxemia in ALI as a PaO2/FIO2 ratio of less than 300 mm Hg and selected a threshold ratio of PaO2/FIO2 of less than 200 mm for ARDS, reflecting the more severe nature of the disease. Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference of ARDS: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994;149:818824. Murray JF, Matthay MA, Luce JM, et al. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis 1988;138:720723. Putensen C, Wrigge H. Ventilator-associated inflammation in acute lung injury. Intensive Care Med 2000;26:15151522. Tobin MJ. Advances in mechanical ventilation. N Engl J Med 2001;344:19861996.

B.2. What are the common causes of ARDS?


ARDS can occur as a result of pulmonary injury arising primarily from the lung pathology or secondarily from extrapulmonary processes. These include multiple trauma, massive blood transfusion, septic shock, fat or air embolism, disseminated intravascular coagulation, aspiration pneumonitis, fluid overload, burns, smoke or gas inhalation, and viral and mycobacterial pneumonia. The following conditions are also associated with ARDS: acute renal failure, oxygen toxicity, drug overdose, radiation, immunosuppression, neurogenic pulmonary edema, acute vasculitis, pancreatitis, cardioversion, cardiopulmonary bypass, and Goodpasture syndrome. P.56 Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:14851486. Stoelting RK, Dierdorf SP. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:225. Tobin MJ. Advances in mechanical ventilation. N Engl J Med 2001;344:19861996.

B.3. Describe the pathogenesis of acute lung injury


The histopathology reveals areas of hyaline membrane, alveolar hemorrhage, increased endothelial and epithelial permeability, and neutrophilic infiltration. Increased permeability allows passage of protein-rich plasma both in the alveolar and in the interstitial spaces, resulting in poor lung compliance and ineffective gas exchange. As the injury process progresses, dependent lung regions beneath the diseased and edematous lung become collapsed, worsening oxygenation. Additionally, alveolar surfactant content diminishes, and its space becomes filled with fibrin and other cellular materials. Ultimately, a fibroproliferative phase is entered whereby further destruction of the lungs occurs with varying degrees of collagen deposition and pulmonary fibrosis. Complement activation may also play a major role in the pathogenesis of ARDS. Activation of the complement cascade through the alternative pathway by endotoxin or lipopolysaccharides results in the production of C5a complement. C5a complement causes microvascular occlusion and pulmonary granulocyte aggregation and embolization. The resultant damage to the endothelium leads to capillary leakage and pulmonary interstitial edema, ultimately producing

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terminal airway and alveolar edema and collapse. However, studies have shown limitations of the complement-neutrophil theory. Complement activation does not necessarily correlate with the development or severity of ARDS. ARDS can develop in patients with neutropenia, and pulmonary sequestration of neutrophils may not produce lung injury. As a result, the complement-neutrophil theory of ARDS has been expanded to include central roles for additional humoral mediators (such as endotoxin, tumor necrosis factor, interleukins, and thromboxane) and cellular mediators (e.g., the macrophage-monocyte system). The lung in patients with ARDS is now viewed as one of the organs involved in the multiorgan system dysfunction that occurs as a result of the systemic inflammatory response syndrome. Increased mediator levels are found in bronchoalveolar lavage fluid from patients with ARDS. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:14851486. Parsons PE. Mediators and mechanism of acute lung injury. Clin Chest Med 2000;21:467476. Raghavendran K, Davidson BA, Mullan BA, et al. Acid and particulate-induced aspiration lung injury in mice: importance of MCP-1. Am J Physiol 2005;289(1):L134L143. v a n We s t e r l o o D J , K n a p p S , v a n ' t V e e r C , e t a l . A s p i r a t i o n p n e u m o n i t i s p r i m e s t h e h o s t f o r a n exaggerated inflammatory response during pneumonia. Crit Care Med 2005;33(8): 17701778.

B.4. What are the radiographic findings in ARDS?


The chest radiograph typically shows bilateral, fluffy involvement that initially led clinicians to think the pathology was homogenous. Now, however, pulmonary imaging techniques have provided convincing evidence that the injury is segmental. Although the vascular permeability is widespread and homogenous in all lung regions, both total and extravascular lung water is P.57 greatest in the dependent lung region. The computed tomography (CT) scans of patients with ARDS are several folds more dense than those of healthy individuals and in severe cases can involve up to 80% of lung fields. Based on the findings of Gattinoni et al., the lungs in patients with ARDS may be divided in thirds, wherein one third represents a completely consolidated, nonventilated region; one third is healthy with normal ventilation/perfusion matching; and one third is a region that is hyperdistended with bullae formation. Contrary to previous belief, the compliance of the lung in patients with ARDS is normal for one third of the lung parenchyma and stiff for the rest. The healthy portion is frequently referred to as baby lung and is subject to injury because of injudicious assignment of tidal volume. By selecting tidal volume on the basis of body weight (>10 mL/kg), clinicians have overlooked the important fact that only a small fraction of the total lung in patients with ARDS participates in gas exchange. Therefore, a disproportionate share of the tidal volume will travel to the better compliant baby lung, subjecting it to overdistention and injury. Proponents of using lower tidal volume in ALI and in ARDS stress that utilizing a larger tidal volume in such settings is as inappropriate as ventilating an infant's lung with a tidal volume equivalent to that of an adult. Gattinoni L, Bombino M, Lissoni A, et al. Lung structure and function in different stages of severe adult respiratory distress syndrome. JAMA 1994;271:17721779. Gattinoni L, Pesenti A, Bombino M, et al. Relationships between lung computed tomographic density, gas exchange, and PEEP in acute respiratory failure. Anesthesiology 1988;69:824832. Puybasset L, Cluzel P, Chao N, et al. A computed tomography scan assessment of regional lung volume in acute lung injury. Am J Respir Crit Care Med 1998;158:16441655. Rossi UG, Owens CM. The radiology of chronic lung disease in children. Arch Dis Child 2005;90 (6):601607.

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B.5. Describe protective-ventilation strategy in acute lung injury (ALI) and ARDS
Many investigators have demonstrated a direct association between mechanical ventilation and lung injury that is independent of barotrauma and functionally and histoanatomically identical to injury observed in ARDS. ALI can occur at both low and high lung volumes (Fig. 3.1). At the lower end (below functional residual capacity [FRC]), cyclical opening and closure of alveolar units during tidal breathing may lead to lung injury from generated sheer forces. The regions most subject to this type of injury are at the interface between lung units that are edematous and nonfunctional with regions that are recruitable and mildly affected by the ARDS process. At the other extreme of lung volume, high airway pressure can cause segmental alveolar overdistention. During the 1990s, use of a protective-ventilation strategy in patients with ALI or ARDS was shown to improve survival rates. Hickling, Henderson, and Jackson were the first to report a 60% reduction in the expected mortality for patients with ARDS. In a subsequent prospective randomized trial of patients with ARDS treated by a protective lung strategy versus a conventional approach, Amato et al. also demonstrated significant survival improvement in the experimental group. The basic principles of the lung protection strategy include: maintenance of lower inspiratory driving pressures (< 20 cm H2O above PEEP); use of lower tidal volumes (6 mL/kg); acceptance of permissive hypercapnia over higher airway pressures; providing liberal sedation to improve patient-ventilator synchronization; and circumvention of alveolar collapse through judicious use of PEEP. PEEP maintains the end-expiratory pressure above the lower inflexion point on the static pressurevolume curve of the respiratory system (Fig. 3.1). This contrasts to management by the conventional approach employing a tidal volume of 12 mL per kg; selection of lowest PEEP to achieve adequate oxygenation; and keeping the arterial carbon dioxide levels P.58 between 35 and 38 mm Hg. Fifty-three patients were enrolled in Amato's study (29 were assigned to a protective strategy and 24 were assigned to conventional management). After 28 days, the mortality in the protective-ventilation group was significantly reduced (38% vs. 71%). Further, the rates of weaning from mechanical ventilation were 66% and 29% for the protectiveventilation group and conventional group, respectively.

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Figure 3.1 Static pressurevolume curve depicting low inflexion point and high inflexion point. On the basis of the concept of a protective-ventilation strategy in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), there are two critical regions in which pulmonary compliance is very poor. The first region is slightly above the residual volume and denotes a critical opening volume whereby recruitable alveoli have the propensity to collapse during tidal breathing. Cyclic opening and closing of these alveolar units has been implicated as a cause of ventilator-induced lung injury. On a static pressure-volume curve, the determination of this lower inflexion point (LIP) allows the clinician to set the positive end-expiratory pressure (PEEP) to 2 cm H2O above this critical opening volume to prevent alveolar collapse and promote recruitment. The compliance of the lung markedly improves beyond this point until it reaches higher lung volumes, labeled upper inflexion point (UIP). The ideal tidal volume can be extracted from this exercise as the volume contained between the LIP and the UIP. Similarly, ideal compliance can be derived from the slope of this steep portion (region between LIP and UIP). FRC, functional residual capacity.

Following the work of Amato et al., a multicenter study sponsored by the National Institutes of Health (NIH), the Acute Respiratory Distress Syndrome Network, which included 861 patients, reported the same results. Briefly, 432 patients were ventilated with 6 mL per kg of tidal volume, and 429 patients received 12 mL per kg of tidal volume. The mean airway pressures were 25 6 P.59 and 33 8 cm H2O. The trial was stopped prematurely after an interim analysis revealed an overall mortality reduction of 22% in the protective-ventilation group (31% vs. 39%, p = 0.01). This trial measured plasma level of interleukin-6 at days 0 through 3 and found it to be markedly

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r e d u c e d i n t h e l o w e r t i d a l v o l u m e g r o u p , s u g g e s t i n g f e w e r s ys t e m i c i n f l a m m a t o r y p r o c e s s e s associated with the protective approach. Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:13011308. Amato MB, Barbas CS, Medeiros DM, et al. Beneficial effects of the open lung approach with low distending pressures in acute respiratory distress syndrome: a prospective randomized study on mechanical ventilation. Am J Respir Crit Care Med 1995;152: 18351846. Amato MBP, Barbas CSV, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338:347354. Fontes ML. Progress in mechanical ventilation. Curr Opin Anesthesiol 2002;15:4551. Hickling KG, Henderson SJ, Jackson R. Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med 1990;16:372377. Stewart TE, Meade MO, Cook DJ, et al. Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. N Engl J Med 1998;338:355361.

B.6. Define pulmonary compliance


Lung compliance is defined as the change in lung volume per unit change in trasmural pressure gradient, (i.e. between the alveolus and pleural space). Compliance is measured by adding a known amount of volume to a system and recording the pressure change. The ratio between this volume change and the respective pressure change defines compliance. The reciprocal of this relationship is called elastance. The lungs are said to be compliant or noncompliance depending on the pressure change that occurs after a given volume (tidal volume) is delivered. The overall lung compliance is rarely measured during clinical practice; rather, inspiratory pressures (peak airway and plateau pressures) are used to infer the status of overall compliance (lungs and thoracic). In actuality, assessing lung compliance is very difficult because different regions of the lungs exhibit different states of compliance, reflecting the heterogeneity of alveolar compliance. For example, in the upright position, the upper lung fields have the poorest compliance relative to the middle and lower lung segments. Evolutionarily speaking, blood flow is directed to lung regions that have the best compliance (i.e., the dependent regions). As described in the previous section, pulmonary compliance changes as the lung volume is increased from residual volume to total lung volume. At the extremes of volume, compliance becomes reduced. Therefore, the ideal compliance occurs at a lung volume between FRC and the resultant lung volume contributed by a normal tidal volume (7 mL/kg). Pulmonary compliance changes with aging. Compliance is worse at the extremes of age. In addition, several disease states can compromise pulmonary compliance such as ALI, ARDS, congestive heart failure, barotraumas, neuromuscular disease, obesity, and pregnancy. Gropper MA, Wiener-Kronish JP. Acute lung injury and acute respiratory distress syndrome. In: Murray MJ, Coursin DB, Pearl RG, et al, eds. Critical care medicine: perioperative management. Philadelphia: Lippincott-Raven Publishers, 1997. P.60 Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:2533.

C. Mechanical Ventilation

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The patient did not improve after receiving 50% oxygen through a face mask. A second arterial blood gas analysis showed the following: pH value, 7.25; PaCO2, 50mm; PaO2, 55 mm; and CO2 content, 22 mEq per L. The respiratory rate was 40 breaths per minute.

C.1. Interpret the blood gases


The patient is demonstrating significant signs of respiratory failure. She is hypoxemic, hypercarbic, and dyspneic, and has an acid-base disturbance marked by a combined respiratory and metabolic acidosis. A 10 mm rise in PaCO2 should have reduced the pH value by 0.08 (pH D 7.32). Therefore, a component of metabolic acidosis is present, lowering the pH value to 7.25.

C.2. What is your clinical plan?


Several approaches can be used for the initial management of this patient. A noninvasive approach using PPV by nasal or face bilevel positive airway pressure (BiPAP) is a temporary measure. BiPAP is typically reserved for patients who are experiencing mild to moderate respiratory failure and who are not at increased risk of aspiration. Given this patient's presentation, the severity of respiratory failure will likely not improve rapidly. In fact, the clinical picture suggests that the patient has suffered ALI resulting in transpulmonary shunting and ineffective ventilation. The safest approach is to electively intubate the trachea and provide mechanical ventilation. Once successfully intubated, sedation can be given to allow for better patient-ventilator synchronization and comfort. If the pulmonary compliance is poor, as is commonly the case in the setting of ALI and ARDS, deep sedation may be required as well as muscle relaxation to facilitate gas exchange and to reduce barotrauma.

C.3. What are the criteria for mechanical ventilation?


The physiologic criteria for mechanical ventilation are as follows:

Mechanics

Respiratory rate of more than 35 breaths per minute Vital capacity of less than 15 mL per kg Rapid shallow breathing index (respiratory rate/tidal volume) more than 200 breaths per minute per L

Oxygenation

PaO2 less than 70 mm on mask oxygen PaO2PaO2 more than 350 mm on 100% FIO2 or QS/QT more than 20%

Ventilation

PaCO2 more than 55 mm, except in patients with chronic hypercarbia VD/VT more than 0.60

The trend of values and clinical state is important. The numerical guidelines should not be

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followed to the exclusion of clinical judgment. Also, frequently, the blood gas analysis results P.61 reflect what the patient's status had been at the time the sample was obtained. Depending on the time interval required to perform the analysis and to receive the result, there can be significant exacerbation or resolution in both oxygenation and ventilation, emphasizing the role of clinical judgment. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the adult. N Engl J Med 1972;287:743751. Stoelting RK, Dierdorf SP. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:224.

C.4. Describe the basic modes of mechanical ventilation. Discuss the advantages and disadvantages of pressurecontrolled and volume-controlled modes?
Fundamentally, the various modes of mechanical ventilation, both new and old, share the following variables: trigger, control, limit, cycle, and baseline.

Trigger mode
The trigger is the first and most important component of the inspiratory phase, marking the end of exhalation. Examples of triggering mechanisms include time, flow, and pressure. In the nonparalyzed and nonanesthetized state, the patient triggers a mechanical or assisted breath by generating negative transpulmonary pressure that is sensed by the ventilator as a pressure change in the airway (the ventilator circuit including the endotracheal tube). The threshold for triggering a breath (i.e., the set sensitivity) can be altered depending on the clinical setting; however, the greatest challenge in mechanical ventilation is determining the level at which sensitivity pressure should be set (usually at 1 to 2 cm H2O). If the threshold is set too low, the ventilator will be triggered by any process that causes the airway pressure to surpass the set threshold. These include patient motion, external compression, gastric suctioning, and air leaks in the circuit or in the chest tubes. Conversely, if the threshold is set too high, the work of breathing increases; that is, to trigger every breath, the patient must make a significant effort to overcome the threshold limit for inspiratory flow to occur. At high levels of ventilatory assistance, as much as one third of the patient's inspiratory efforts may be insufficient to trigger the ventilator. In a 2001 review, Tobin explained that breaths that do not reach the threshold for triggering the ventilator have higher tidal volumes and shorter expiratory times than do b r e a t h s t h a t d o t r i g g e r t h e v e n t i l a t o r . I n t h e s e t t i n g o f a c u t e r e s pi r a t o r y f a i l u r e , t h e i n s p i r a t o r y effort exhausted by the patient is approximately four to six times the normal value. This level of respiratory work frequently causes breath stacking, generating intrinsic PEEP, which in turn imposes a tremendous burden on inspiratory muscle and if sustained can result in muscle fatigue and cardiopulmonary collapse.

Control mode
The delivered breath can be either pressure regulated (pressure control) or volume targeted (volume control). In the pressure-controlled mode, the amount of volume delivered is inversely related to the resistance encountered.When the resistive forces are low (i.e., normal compliance), the tidal volume for a given pressure will be relatively larger than if compliance were poor. For adults, the recommended upper limit of pressure control is 35 cm H2O. Higher pressures may directly cause ALI or delay healing of the already injured lung. When the resistive forces are high, the resultant tidal volume may be inadequate for ventilation or oxygenation, even at high levels of inspiratory pressures. Typically, these patients have ARDS, and lower levels of arterial oxygen tension (PaO2) are tolerated along with higher levels of

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arterial carbon dioxide tension (permissive hypercapnia). P.62 Volume-controlled mode is the most common control mode used to ventilate patients mechanically. Examples include assist-control ventilation and synchronous intermittent mandatory ventilation (SIMV). The ventilator will attempt to deliver a preset volume regardless of the pressure generated. For patients with poorly compliant lungs, volume-controlled mode may promote barotrauma and acute lung injury (ALI).

Limit mode
The limit is an essential feature in mechanical ventilation. Its variables include volume, pressure, and flow. The upper and lower limits of these variables should be preselected for each patient and adjusted in a manner consistent with the goals of the protective lung strategy employed.

Cycle mode
As discussed in the previous section, cycling has several variables: time, flow, and pressure. As such, the inspiratory phase and the expiratory phase becomes controlled. The challenge faced is in synchronizing the machine's cycling of inspiration and exhalation with the patient's neural respiratory cycle. Although pressure, flow, and time can be used to affect cycling, the manipulation of one or all three variables, both intrabreath and interbreath, to coincide precisely with the demands of the patient is virtually impossible (Fig. 3.2).

Baseline mode
The baseline variable is the function that is controlled during exhalation and generally indicates the level of PEEP. Fontes ML. Progress in mechanical ventilation. Curr Opin Anesthesiol 2002;15:4551. Hess D, Branson R. Ventilators and weaning modes. Respir Care Clin N Am 2000;6:407435. Tobin MJ. Advances in mechanical ventilation. N Engl J Med 2001;344:19861996.

C.5. What control mode would you select for this patient?
For adult patients, volume-controlled mode is most often chosen for ventilatory management. Examples include assist-control ventilation, SIMV, and PSV. A targeted tidal volume is selected (7 to 12 mL/kg), and the ventilator will attempt to deliver this volume regardless of the pressure generated. If the resistance to ventilation is great, the pressure change can be excessive, resulting in barotrauma and ALI. Occasionally, the pressure increase is acute, reflecting some reversible condition, such as mucous plugging, bronchospasm, and patient anxiety. These conditions can be treated appropriately without having to switch to a different ventilatory mode. Alternatively, patients with ALI may have very poor compliance for which volume-controlled mode may be ineffective or prohibitive. Some alternative modes of mechanical ventilation combine pressure control that is volume compensated or vice versa. Examples include pressure-regulated volume-controlled (PRVC) ventilation, proportional assist ventilation, adaptive support ventilation, and many other combinations of volume control, volume support, pressure support, and pressure control. These alternative modes attempt to improve patient comfort and synchronization with the ventilator. Older modes were overly simplistic, and incorrect assumptions were made regarding the role of ventilatory assistance. The concept was to make the ventilator the boss and allow it to drive the respiratory cycles. The important insight gained from today's clinical research is that the

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ventilator should be a helper aimed at assisting the patient in a manner determined by the patient. P.63

Figure 3.2 Activation of expiratory muscle during a mechanical inspiratory cycle. The airway flow, pressure, and electromyogram recording of two mechanically assisted respiratory cycles are illustrated. The start of inspiration is reflected by diaphragmatic activity that begins before the commencement of the inspiratory flow or airway pressure. The diaphragm stops contracting, marking the end of inspiratory effort. The expiratory muscle activity begins with contraction of the transversus abdominis muscle (lower panel); however, the ventilator continued to deliver inspiratory flow while the patient was attempting to exhale. This illustrates a common problem with all ventilation modes that cannot fully adapt and synchronize with the patient's neuronal timing of inspiration and expiration. In the case mentioned earlier, the ventilator's inspiratory time exceeded the patient's inspiratory cycle, resulting in dyssynchrony and in some instances high airway pressure, predisposing to barotrauma. (From Tobin MJ. Advances in medical ventilation. N Engl J Med 2001;344:19861996, with permission.)

Brochard L. Pressure support ventilation. In: Tobin MJ, ed. Principles and practice of mechanical ventilation. New York: McGraw-Hill, 1994:239257. Esteban A, Anzueto A, Alia I, et al. How is mechanical ventilation employed in the intensive care

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unit? An international utilization review. Am J Respir Crit Care Med 2000;161: 14501458. S a s s o o n C S H . I n t e r m i t t e n t m a n d a t o ry v e n t i l a t i o n . I n : T o b i n J M , e d . P r i n c i p l e s a n d p r a c t i c e o f mechanical ventilation. New York: McGraw-Hill, 1994:221237. Tobin MJ. Mechanical ventilation. N Engl J Med 1994;330:10561061. P.64

C.6. What initial ventilator settings will you prescribe for this patient (tidal volume, respiratory frequency, inspiratory oxygen fraction, etc.)?
Initially, an attempt will be made to ventilate the patient with a volume-controlled mode. The tidal volume will be set at 5 to 8 mL/kg, respiratory frequency at 10 breaths per minute, FIO2 of 70%, PEEP of 10 cm H2O. The limits for alarming will be standard. After this initial setting, an arterial blood gas analysis should be performed to determine the adequacy of ventilation and oxygenation. Should lung compliance be poor, large tidal volumes must be avoided, which will predispose the lungs to barotrauma. The patient should be adequately sedated, and both the patient and the ventilator should be examined to rule out correctable causes of elevated inspiratory pressures. Alternatively, a pressure-controlled mode can be selected to ensure the driving pressure (plateau or mean airway pressure) does not exceed 35 cm H2O. The PEEP level should be adjusted to improve oxygenation. A PaO2 level of more than 60 mm Hg is acceptable, and the level of PaCO2 can rise in excess of 60 or 70mm (permissive hypercapnia). Treating the ensuing acidemia, particularly, respiratory acidemia is no longer recommended, unless the pH value becomes less than 7.20. The use of sodium bicarbonate is reserved for profound acidemia. Once administered, this agent is chemically converted to byproducts that include H2O and CO2. The latter can diffuse easily through the cell membrane to make the intercellular milieu more acidotic. Cuhaci B, Lee J, Ahmed Z. Sodium bicarbonate and intracellular acidosis: myth or reality? Crit Care Med 2001;29(5):10882090. Levraut J, Giunti C, Ciebiera JP, et al. Initial effect of sodium bicarbonate on intracellular pH depends on the extracellular nonbicarbonate buffering capacity. Crit Care Med 2001;29(5):1033 1039.

C.7. Describe the potential hemodynamic effects of positive pressure ventilation (PPV)
During spontaneous inspiration, air is delivered to the lungs by generating a pressure gradient between pleural (negative pressure) and atmospheric pressures (1 atmospheric pressure). During exhalation, the reverse process occurs and air is expelled as pleural pressure increases (never positive) and the rib cage recoils returning lung volume to FRC. The hemodynamic consequence of physiologic breathing is minor but is associated with alterations in systemic blood pressure. For example, during inspiration, blood flow to the right ventricle is promoted and blood flow to the left side of the heart is diminished. This results in a decrease in stroke volume and systemic systolic pressure (approximately 5 to 10 mm Hg). In contrast, during positive pressure inspiration, the ventilator applies positive pressure to overcome alveolar pressure. Overall, transthoracic pressure increases, impeding or diminishing venous return to the heart. Both the right and the left ventricular output can decrease depending on the thoracic compliance, intravascular volume status, and biventricular function; that is, PPV will cause a decrease in cardiac output and blood pressure when the overall lung compliance is poor, the intravascular volume is inadequate, and/or ventricular function is compromised. The hemodynamic consequences of both spontaneous pressure ventilation and PPV may be profound and may have opposite effects on cardiovascular stability in different patient

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populations. Therefore, no firm rules apply about the specific response that will be seen in all patients and under all conditions. Some generalities, however, are probably reasonable. In patients with markedly increased work of breathing, hypervolemia, or impaired left ventricular pump function, the institution of mechanical ventilatory support can be life saving because of its ability to support the cardiovascular system, independent of any beneficial effects that mechanical ventilation may have on gas exchange. In patients with decreased pulmonary elastic recoil, increased pulmonary vascular resistance, hypovolemic, or airflow obstruction, the institution of mechanical P.65 ventilatory support may induce cardiovascular instability, which if not corrected can lead to total cardiovascular collapse. The initiation of intermittent positive pressure ventilation (IPPV) is associated with a decrease in cardiac output and in arterial blood pressure in patients without significant lung consolidation. Cardiac output and stroke volume decrease as the peak airway pressure increases. There is also a decrease in cardiac output with increasing inspiratory/expiratory ratios. IPPV increases intrathoracic pressure, resulting in decreased venous return and cardiac output. Patients with healthy lungs behave differently from patients with significant cardiopulmonary disease. When pulmonary compliance decreases, the transmission of airway pressure to intrathoracic pressure decreases. Patients with more rigid lungs can tolerate higher airway pressures. IPPV decreases transmural pulmonary artery pressure as well. There is no change in pulmonary vascular resistance. The systemic vascular resistance increases slightly when IPPV is begun. The decrease in cardiac output during IPPV is rarely of any clinical significance because it is compensated by an increase in peripheral vascular resistance in nonanesthetized patients. When patients are hypovolemic, the decrease in blood pressure can be significant. Pinsky MP. Cardiovascular effects of ventilatory support and withdrawal. Anesth Analg 1995;79:567576. Shapiro BA, Kacmarek RM, Cane RD, et al. eds. Clinical application of respiratory care. St. Louis: Mosby-Year Book, 1991:285286.

C.8. What are the adverse effects of mechanical ventilation?


Physiologic Complications

Decreased cardiac output resulting from increased intrathoracic pressure Respiratory alkalosis from hyperventilation Increased venous admixture (QS/QT) from prolonged low tidal volume ventilation

Pulmonary Complications

Infection Acute lung injury Barotrauma/pneumothorax, mediastinal, interstitial, and subcutaneous emphysema in 10% to 15% of adults

Oxygen toxicity if the inspired oxygen concentration is more than 60%

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Atelectasis caused by immobilization and ineffective humidification

Complications from Endotracheal Intubation


Endobronchial intubation, kinking or obstruction, leaking cuffs Nasal damage from nasal intubation, nose bleeding, fractured turbinates, septal perforation, partial loss of alae nasi, nasal synechiae

Laryngeal damage and edema, vocal cord paresis and granulomas, laryngotracheal membranes, subglottic fibrotic stenosis

Tracheal damage and tracheal erosion, tracheoesophageal fistula, tracheomalacia, tracheal stenosis

Complications from mechanical device malfunction

Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med 1998;157:294323. P.66 Pierson DJ. Barotrauma and bronchopleural fistula. In: Tobin MJ, ed. Principles and practice of mechanical ventilation. New York: McGraw-Hill, 1994:813836. Pinsky MP. Cardiovascular effects of ventilatory support and withdrawal. Anesth Analg 1995; 79:567576. Puybasset L, Cluzel P, Chao N, et al. A computed tomography scan assessment of regional lung volume in acute lung injury. Am J Respir Crit Care Med 1998;158:16441655. Stoelting RK, Dierdorf SP. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:221222.

D. Therapeutic Approaches for Ventilatory Support


After intubation and mechanical ventilation, the oxygenation did not improve. On FIO2 0.7, the arterial blood gas analysis showed the following: pH, 7.30; PaCO2, 40 mm Hg; PaO2, 57 mm Hg; and CO2 content, 18 mEq per L.

D.1. What factors determine oxygen delivery?


Oxygen delivery is dependent on blood flow (cardiac output) and the content of oxygen carried in blood (hemoglobin and dissolved oxygen). The actual amount is reflected by the following formula: oxygen delivery = CO[(Hgb x 1.39)SaO2 C PaO2 x 0.003], where CO is cardiac output; Hgb, hemoglobin content in blood; SaO2, percent arterial oxygen saturation; and PaO2, partial pressure of oxygen dissolved in blood. Based on this formula, oxygenation can be improved by several modalities. First, it is important to determine where the physiologic derangement lies. If the cardiac output is inadequate, the appropriate therapy should be to improve the elements of cardiac output (rate and rhythm, preload, contractility, and afterload); next, should the hemoglobin content be too low, the patient should undergo a transfusion with red blood cells; last, oxygen delivery to the lungs and uptake should be maximized. The latter can be accomplished by increasing the inspired oxygen

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concentration, increasing the level of PEEP, and by other maneuvers that will improve ventilation/perfusion matching and decrease intrapulmonary shunting (e.g., chest physiotherapy, prone position, bronchodilators, and diuresis). Ginosa Y, Pizov R, Sprung C. Arterial and pulmonary artery catheters. In: Parrillo J, Bone R, eds. Critical care medicine, principles of diagnosis and management. St Louis: Mosby-Year Book, 1995:2749.

D.2. How will you treat the hypoxemia?


The arterial blood gas analyses suggest that the patient is hypoxemic but is adequately ventilated and has a component of metabolic acidosis. As discussed previously, it is not appropriate to correct this level of metabolic acidosis with sodium bicarbonate or to attempt to hyperventilate the patient and induce respiratory alkalosis. The underlying problem producing the hypoxemia is lung injury from the aspiration pneumonitis, whose effect has led to significant intrapulmonary shunting. The FIO2 is set at 0.7. The most appropriate maneuver is to increase the PEEP level, ensure good patient-ventilator synchronization (i.e., the patient is not fighting the ventilator), and avoid excessive tidal volumes or inspiratory driving pressures. Other ventilatory modalities P.67 that can be applied include IRV, pressure-controlled ventilation, prone position, use of NO, jet ventilation, and partial liquid ventilation (PLV).

D.3. What are the major factors governing oxygen toxicity?


Oxygen toxicity is governed by the duration of exposure, the partial pressure of oxygen, and the susceptibility of the individual to pulmonary oxygen injury. The degree of toxicity is related to the partial pressure, but not to the percentage of oxygen inspired, as demonstrated during U.S. space flights, where astronauts tolerate 100% oxygen for 2 to 4 weeks at a tension of 250 mm. Systemic oxygen toxicity is related to arterial oxygen tension, whereas pulmonary oxygen toxicity depends on alveolar oxygen tension. Retrolental fibroplasia (retinopathy of prematurity) in the premature neonate has been reported after exposure to PaO2 at more than 80 to 150 mm for a few hours. Pulmonary toxicity can develop after prolonged exposure to oxygen at concentrations between 0.5 and 1.0 atmospheres. It must be emphasized that the adult patient can generally tolerate 1 atmosphere of oxygen partial pressure for at least 24 hours. Moreover, there is no evidence that clinically relevant pulmonary oxygen toxicity occurs in humans at inspired partial pressures less than 0.5 atmosphere. Lastly, no patients should ever experience life-threatening levels of hypoxemia to avoid possible oxygen toxicity. Deneke SM, Fanburg BL. Normobaric oxygen toxicity of the lung. N Engl J Med 1980; 303:7686. Frank L, Massaro D. Oxygen toxicity. Am J Med 1980;69:117. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:348358.

D.4. What is the mechanism of oxygen toxicity?


The so-called free-radical theory of oxygen toxicity proposed in the early 1960s has garnered a great deal of recent experimental support and is now accepted as the most probable molecularlevel explanation for oxygen toxicity. Various highly reactive and potentially cytotoxic freeradical products of oxygen are generated metabolically in the cell. These short-lived O2 metabolites, including superoxide anion (O-2), hydroxyl radical (OH.), hydrogen peroxide (H2O2), and singlet oxygen (O-), have been shown to be capable of effects such as inactivation of sulfhydryl enzymes, interaction with and disruption of DNA, and peroxidation of unsaturated membrane lipids with resultant loss of membrane integrity. The cell is also equipped with an

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array of antioxidant defenses, including the enzymes superoxide dismutase (SOD), catalase, glutathione peroxidase, vitamin E, and ascorbate. Under hyperoxia, the intracellular generation and influx of free radicals is believed to increase markedly and may overwhelm the detoxifying capacity of the normal complement of antioxidant defenses, with resultant cytotoxicity. The pathology of oxygen toxicity is nonspecific and consists of atelectasis, edema, alveolar hemorrhage, inflammation, fibrin deposition, and thickening and hyalinization of alveolar membranes. There are exudative and proliferative phases. Capillary endothelium is damaged early and plasma leaks into interstitial and alveolar spaces. Pulmonary surfactant may be altered. Type I alveolar lining cells are injured early, and bronchiolar and tracheal ciliated cells can be damaged by 80% to 100% oxygen. Resolution of exudative changes, hyperplasia of alveolar type II cells, fibroplastic proliferation, and interstitial fibrosis occur with recovery or with the development of tolerance to oxygen. Total resolution is possible if the initial hyperoxia is not overwhelming. Deneke SM, Fanbarg BL. Normobaric oxygen toxicity of the lung. N Engl J Med 1980; 303:7686. P.68 Frank L, Massaro D. The lung and oxygen toxicity. Arch Intern Med 1979;139:347350. Freeman BA, Crapo JD. Free radicals and tissue injury. Lab Invest 1982;47:412. Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:348358.

D.5. What is your criteria to start PEEP?


The role of PEEP in mechanical ventilation is evolving. Previously, it was reserved for patients who had significant pulmonary pathology and hypoxemia. Either in apparently healthy lungs or in disease lungs, there can be significant heterogeneity in alveolar compliance and ventilation. Therefore, at normal levels of PEEP (physiologic), while in the supine position, alveolar components can collapse during tidal breathing, particularly, when there exist underlying comorbid states (e.g., ALI, ARDS, chronic obstructive pulmonary disease [COPD], congestive heart failure, obesity, and general anesthesia). To prevent cyclical closure of alveolar units and to ensure that the lung volume is maintained at or slightly above FRC, PEEP should be instituted accordingly. One should not wait for physiologic or laboratory evidence of inadequate gas e x c h a n g e t o i n i t i a t e P E E P . F i v e t o 1 0 c m H 2 O i s o f t e n s u f f i c ie n t a n d i s n o t a s s o c i a t e d w i t h hemodynamic disturbances. In the setting of ALI and ARDS, application of PEEP is essential for achieving adequate oxygenation. Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:13011308. Amato MB, Barbas CS, Medeiros DM, et al. Beneficial effects of the open lung approach with low distending pressures in acute respiratory distress syndrome: a prospective randomized study on mechanical ventilation. Am J Respir Crit Care Med 1995;152: 18351846. Amato MBP, Barbas CSV, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J 1998;338:347354. Gattinoni L, Pesenti A, Bombino M, et al. Relationships between lung computed tomographic density, gas exchange, and PEEP in acute respiratory failure. Anesthesiology 1988;69:824832.

D.6. How does PEEP improve arterial oxygenation?


The mechanism is related to an increase in the FRC and redistribution of extravascular lung water. The FRC expands linearly with increases in the end-expiratory pressure, usually at a rate

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of 400 mL or more for each 5 cm H2O of end-expiratory pressure; however, recruitment of alveolar units is both variable and unpredictable in patients with ARDS. This increase in FRC represents alveoli that remain open and available for gas exchange during all phases of the respiratory cycle. The increase in FRC improves the relationship between FRC and closing capacity and therefore decreases intrapulmonary shunt or venous admixture. PEEP therapy changes the distribution of interstitial lung water but does not directly decrease lung water. PEEP facilitates the movement of water from the less compliant interstitial spaces (between the alveolar epithelium and capillary endothelium, where gas exchange occurs) to the more compliant interstitial spaces (toward the peribronchial and hilar areas). This redistribution of interstitial lung water improves oxygen diffusion across the alveolar-capillary membrane, resulting in increased arterial oxygenation. Approximately 25% of patients with ARDS are unresponsive to increases in PEEP as measured by an increase in PaO2. P.69 Abbound N, Rehder K, Rodarte JR, et al. Lung volume and closing capacity with continuous positive airway pressure. Anesthesiology 1975;42:138142. Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:13011308. Miller WC, Rice DL, Unger KM, et al. Effect of PEEP on lung water content in experimental noncardiogenic pulmonary edema. Crit Care Med 1981;9:7. Pare PD, Warriner B, Baile M, et al. Redistribution of pulmonary extravascular water with positive and expiratory pressure in canine pulmonary edema. Am Rev Respir Dis 1983;127:590.

D.7. How would you determine the best PEEP and the optimal PEEP?
Suter, Fairley, and Isenberg described best conventional PEEP in 1975. The best PEEP is defined as the level of PEEP with the highest oxygen transport, which is the product of cardiac output and oxygen content. This PEEP correlates with the highest total respiratory compliance, the highest mixed venous oxygen tension, and the lowest VD/VT (Fig. 3.3). Arterial oxygen tension and intrapulmonary shunt are not good indicators of the best conventional PEEP. They continue to improve even after this level has been reached. Oxygen transport decreases after the best PEEP is reached, because the cardiac output decreases. Civetta, Barnes, and Smith described optimal high PEEP in 1975. It is defined as the level of PEEP with the lowest intrapulmonary shunt and without compromising cardiac output. The PEEP used in this report is so-called high or super PEEP, more than 25 cm H2O, whereas the PEEP in the article by Suter, Fairley, and Isenberg is conventional PEEP, ranging from 5 to 20 cm H2O. However, the concept of best or optimal PEEP has evolved over the years.More recently, the endpoint for PEEP application is the lowest level of PEEP that provides an adequate PaO2 at an FIO2 of less than 0.5. Increasing PEEP beyond this level to obtain optimum values for various other endpoints, such as the production of maximum oxygen transport, maximum static pulmonary compliance, shunt less than 15% to 20%, minimal arterial end-tidal CO2 gradient, decreased mixed venous oxygen tension, and minimum FIO2 will not be clinically helpful and may be harmful. Albert RK. Least PEEP: primum non nocere. Chest 1985;87:23. Benumof JL. Anesthesia for thoracic surgery, 2nd ed. Philadelphia: WB Saunders, 1995:725. Carrol GC, Tuman KJ, Braverman B, et al. Minimal positive end-expiratory pressure (PEEP) may be best PEEP. Chest 1988;93:10201025.

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Civetta JM, Barnes TA, Smith LO. Optimal PEEP and intermittent mandatory ventilation in the treatment of acute respiratory failure. Respir Care 1975;20:551557. Pelosi P. DVD: vertical gradient of regional lung inflation in adult respiratory distress syndrome. Am J Respir Crit Care Med 1994;149:8. Suter PM, Fairley HB, Isenberg MD. Optimum end-expiratory airway pressure in patients with acute pulmonary failure. N Engl J 1975;292:284288.

D.8. What are the cardiovascular effects of PEEP?


The cardiovascular effects of PEEP depend on the severity of respiratory failure, the level of PEEP, the intravascular volume, the contractility of the heart, and the pulmonary vasculature. P.70 In healthy subjects without respiratory failure, PEEP decreases cardiac output mainly because of increased intrathoracic pressure resulting in decreased venous return. PEEP also causes pulmonary parenchymal overdistention, which makes the lung come in close contact with the left ventricle, changing compliance and interfering with ventricular function. In addition, PEEP increases pulmonary pressure and resistance, resulting in right ventricular dilation, which causes an intraventricular septum shift toward the left ventricle. The leftward septal shift decreases P.71 left ventricular diastolic filling, resulting in decreased stroke volume and cardiac output. Also, unilateral pulmonary hyperinflation may cause neural reflex, resulting in a decreased cardiac output and heart rate. Moreover, humoral depression of myocardial contractility may also be a factor. The aforementioned deleterious effect of PEEP is more apparent in individuals with limited cardiovascular reserve. Although PEEP is applied only at the end of expiration, in actuality, the alveolar and transpulmonary pressures are highest during inspiration (driving pressures exceeding 20 to 30 cm H2O in some patients) and are associated with the greatest negative hemodynamic effects.

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Figure 3.3 Best positive end-expiratory pressure. (From Suter PM, Fairley HB, Isenberg MD. Optimal end-expiratory airway pressure in patients with acute pulmonary failure. N Engl J Med 1975;292:284288, with permission.)

In persons with respiratory failure, PEEP, up to optimum levels, usually increases or does not change cardiac output because of an increase in oxygenation with resultant improvement of cardiac performance. Cardiac output decreases when PEEP exceeds the individual's optimum

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PEEP. Hypotension during PEEP therapy may be exacerbated by hypovolemia. In patients with underlying left ventricular failure and filling pressure more than 18 mm, PEEP may increase cardiac output by increasing coronary arterial oxygen content, augmenting systolic function, or reducing venous return. The decreased venous return may produce a shift in the Starling curve to filling pressures associated with better myocardial function. Pinsky MP. Cardiovascular effects of ventilatory support and withdrawal. Anesth Analg 1995;79:567576. Robotham JL, Lixfeld W, Holland L, et al. The effects of positive end-expiratory pressure on right and left ventricular performance. Am Rev Respir Dis 1980;121:677683.

D.9. What is pressure support ventilation (PSV)? Discuss its advantages


PSV is pressure-limited, flow-controlled PPV during which each spontaneous inspiratory effort is assisted by mechanically maintaining a predetermined inspiratory pressure plateau throughout inspiration. Whereas PSV is most often flow cycled, both pressure and time can be secondary cycling mechanisms. That is, pressure support can cycle to the exhalation phase when flow decelerates to a ventilator-determined level or to a pressure-determined level and/or when the inspiratory time has reached a predetermined level. PSV can be used for patients who are breathing completely spontaneously or who are being supported with IMV, and it can be used for patients receiving CPAP (Fig. 3.4). PSV, which is an adjunct form of ventilatory support, is controlled with a microprocessor incorporated into the mechanical ventilator's circuit. When the patient makes the initial inspiratory effort, a very sensitive pressure transducer detects the slight negative pressure change and application of a constant support pressure is begun. Pressure is applied continuously throughout inspiration at the value selected by the operator. The advantages of PSV are as follows:

Achieving larger tidal volumes with lower airway pressures Decreasing work of breathing Improving spontaneous breathing patterns, including decreased respiratory rate, longer expiratory phase, and better synchrony with mechanical ventilation

Promoting weaning from mechanical ventilation because of decreased respiratory muscle fatigue

Although theoretic advantages and safety of the mode in appropriately monitored patients support its use, few clinical studies have documented the efficacy of PSV. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:1470. P.72 Berger KI, Barry Sorkin I, Norman RG, et al. Mechanism of relief of tachypnea during pressure support ventilation. Chest 1996;109:13201327. Braun NMT, Faulkner J, Hughes RL, et al. When should respiratory muscles be rested? Chest 1986;84:7684. Hess D, Branson R. Ventilators and weaning modes. Respir Care Clin N Am 2000;6:407435.

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MacIntyre NR. Respiratory function during pressure support ventilation. Chest 1986;89: 677 683.

D.10. What is inverse-ratio ventilation (IRV)?


During the normal respiratory cycle, the duration of inspiration is one half to one third shorter than the duration of exhalation. In IRV, the inspiratory cycle time is increased to two or more times greater than expiratory cycle time. This mode of ventilation can be applied during pressure-controlled ventilation (pressure controlled, time cycled) or in volume-controlled ventilation (by decreasing the inspiratory flow rate and applying a decelerating waveform). The intended benefits of IRV in ARDS are several: (a) lower peak airway pressures are generated; (b) improved gas exchange as a result of allowing greater time for exchange and mixing to take place; (c) sustained elevation of airway pressure and maintenance of higher mean airway pressure can both prevent alveolar collapse and improve alveolar recruitment; and (d) reduction in dead space with improvement in carbon dioxide elimination. By shortening the exhalation cycle, several problems can arise. First, the propensity for gas trapping increases, resulting in a n i n c r e a s e i n i n t r i n s i c P E E P . W i t h t h e d e v e l o p m e n t o f i n t r i n s ic P E E P , t h e w o r k o f b r e a t h i n g becomes excessive, along with patient-ventilator dyssynchrony. Consequently, most patients require heavy sedation and paralysis while on IRV mode. The proposed improvement in gas exchange and possibly in alveolar recruitment may come solely from the effects of intrinsic PEEP. In fact, Zavala et al. investigated the effect of gas exchange during four ventilator settings: (a) volume-controlled mechanical ventilation (VC-MV) without PEEP; (b) VC-MV with PEEP; (c) volume-controlled IRV (VC-IRV); and (d) pressure-controlled IRV (PC-IRV). In each mode of ventilation, the level of PEEP (8 cm H2O) was assigned equally, whereas the tidal volume, respiratory rate, and inspired oxygen fraction P.73 were maintained unchanged from baseline values. The following observations were made: (a) The peak airway pressure was lower during IRV than VC-MV PEEP; however, the plateau pressure was similar for all three modes (VC-MV PEEP, VC-IRV, and PC-IRV); (b) the mean airway pressure was higher in the IRV group, particularly, in the PC-IRV; (c) the arterial PaO2 improved with the addition of PEEP in VC-MV and VC-IRV but not in PC-IRV; and (d) the level of PaCO2 significantly decreased and the pH increased in IRV mode as compared with the controlled mechanical ventilation modes. These findings suggest that in IRV mode, whether in pressure-controlled or volume-controlled mode, there is no short-term benefit in gas exchange relative to controlled mechanical ventilation when the same level of PEEP is applied. Whereas the peak airway pressures were lower in the IRV than in the VC-MV PEEP mode, the lack of differences in plateau pressure between these ventilator modalities can be explained by the resistive pressure decrease (differences in peak airway pressure and plateau pressure) that is predominantly determined by the endotracheal tube. At present, no prospective randomized trial has been conducted to assess the beneficial effect of IRV compared with conventional ventilation on outcome in ARDS; consequently, opposing opinions exist regarding the application of IRV in the management of ALI and ARDS.

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Figure 3.4 Airway pressure tracings of pressure-support ventilation (solid line) and spontaneous ventilation (dotted line). CYC, cycle; IN, initiation; LIM, limit;. (From Shapiro BA, Kacmarek RM, Cane RD, et al. Clinical application of respiratory care, 4th ed. St. Louis; Mosby-Year Book, 1991:317, with permission.)

Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:1471. Fontes ML. Progress in mechanical ventilation. Curr Opin Anesthesiol 2002;15:4551. McIntyre RC Jr, Pulido EJ, Bensard DD, et al. Thirty years of clinical trials in acute respiratory distress syndrome. Crit Care Med 2000;28(9):33143331. Smith RP, Fletcher R. Pressure-controlled inverse ratio ventilation after cardiac surgery. Eur J Anaesthesiol 2001;18(6):401406. Zavala E, Ferrer M, Polese G, et al. E ratio ventilation on pulmonary gas exchange in acute respiratory distress syndrome. Anesthesiology 1998;88:3542.

D.11. Describe the rationale for prone-position ventilation and its effect on oxygenation
The concept of improving oxygenation and gas exchange in patients with ARDS was proposed more than 20 years ago. The mechanisms for improvement in oxygenation in the prone position are unclear, and whether such physiologic benefit alters outcome is equally unknown. For gas exchange to improve, several respiratory processes must occur: (a) better matching of ventilation and perfusion in those lung regions affected by either too little perfusion but normal ventilation or normal perfusion but inadequate ventilation; (b) improvement in pulmonary diffusion capacity of oxygen and carbon dioxide (i.e., reduced interstitial edema and inflammation); (c) improvement in mobilization and delivery of these gases from the tissues to the lungs (better cardiac output and end-organ function); and (d) reduction in ventilator-induced lung injury in the prone position as compared with supine. In ARDS, the whole lung is affected by endothelial and epithelial hyperper-meability with resulting edema. In the supine position, dependent lung regions are subjected to a relatively greater regional pleural pressure gradient secondary to the forces of gravity acting on the ribcage, the diaphragm, the abdomen, the heart, and the mediastinal structures. Such increases in transpulmonary pressures overstretch normal

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alveoli, cause epithelial and endothelial disruption, and induce a state of pulmonary edema. Studies of animal models of ALI have shown that while in the supine position, high levels of PEEP are required to maintain the injured and surfactant-depleted alveoli open. Failure to do this promotes ventilator-related lung injury. Additionally, perfusion of these dependent regions may be reduced from regional compression by the weight of the edematous upper lung units and from the effects of hypoxic pulmonary vasoconstriction. In contrast, positioning the patient prone allows for a more uniform gravitational gradient for alveolar P.74 ventilation and redistribution of alveolar ventilation to dorsal lung regions. Several other processes may account for the observed improvement in physiologic parameters in the prone position:

The airway orientation is such that it tends to promote drainage of airway liquids toward the airway opening while in prone position and toward the dorsal regions when lying supine

Redistribution of perfusion along a gravitational gradient to less injured lung regions Increased FRC Change in regional diaphragm motion

Pelosi et al. measured the change in thoracoabdominal compliance in the supine versus the prone position and compared this to changes in oxygenation. They found a direct correlation between improvement in compliance in the prone position and improvement in oxygenation that was most likely attributed to positioning the more rigid ribcage and vertebrae in the superior position while splinting the mobile anterior chest by the mattress. This maneuver favored redistribution of ventilation to the dorsal lung segments and alveolar recruitment. Clinical improvement in oxygenation is reported in up to 90% of patients after transition from the supine to the prone position. Jolliet et al. studied the effects of 12 hours of prone positioning in 19 patients with ARDS who were heavily sedated and paralyzed. Patients were defined as responders if an increase in PaO2 of greater than or equal to 10 mm or in PaO2/FIO2 ratio of greater than or equal to 20 was observed in the prone position. Fifty-seven percent of the subjects in this study responded to prone placement. At the end of 12 hours, the patients were repositioned supine and had repeated measurements of respiratory parameters. Interestingly, the measures of oxygenation did not change after the first 30 minutes of resuming supine ventilation as compared with the previous prone position. In fact, oxygenation was improved from the baseline value. Jolliet et al. also reported that repeated trials of supine-to-prone and prone-to-supine maneuvers revealed a positive response in 71% of the initial responders versus a 25% positive response in the former nonresponders. Unfortunately, the study could not identify patient characteristics that predicted positive response, magnitude of positive or negative response, or the effect of positive response on survival and outcome. Others have also reported similar findings. Voggenreiter compared the effects of intermittent prone ventilation in 22 patients (11 of whom had severe and moderate posttraumatic lung injury and 11 had ARDS). Statistically significant improvements in respiratory parameters were observed in the prone position relative to the supine position for the following variables: (a) oxygenation; (b) PaO2PaO2 and QS/QT; (c) total static lung compliance; and (d) reduction in pulmonary densities. Although the advantages of the prone position have been shown in many case reports and in animal studies of ALI, the definitive study (large, randomized, and prospective) has not been done. The risks of proning patients also need to be tested prospectively. Several of the known risks include accidental extubation, inadvertent removal of intravenous lines and central venous

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catheters, and pressure injury of soft tissues. Albert RK, Hubmayr RD. The prone position eliminates compression of the lungs by the heart. Am J Respir Crit Care Med 2000;161:16601665. Fontes ML. Progress in mechanical ventilation. Curr Opin Anesthesiol 2002;15:4551. Gattinoni L, Bombino M, Lissoni A, et al. Lung structure and function in different stages of severe adult respiratory distress syndrome. JAMA 1994;271:17721779. Gattinoni L, Pelosi P, Vitale G, et al. Body position changes redistribute lung computedtomographic density in patients with acute respiratory failure. Anesthesiology 1991;74: 1523. Jolliet P, Bulpa P, Chevrolet JC, et al. Effects of the prone position on gas exchange and hemodynamics in severe acute respiratory distress syndrome. Crit Care Med 1998;26: 1977 1985. P.75 Mure M, Domino KB, Lindahl SG, et al. Regional ventilation-perfusion distribution is more uniform in the prone position. J Appl Physiol 2000;88:10761083. Mutoh T, Guest RJ, Lamm WJ, et al. Prone position alters the effect of volume overload on regional pleural pressures and improves hypoxemia in pigs in vivo. Am Rev Respir Dis 1992;146:300306. Pelosi P, Tubiolo D, Mascheroni D, et al. Effects of the prone position on respiratory mechanics and gas exchange during acute lung injury. Am J Respir Crit Care Med 1998;157: 387393. Voggenreiter G, Neudeck F, Aufmkok M, et al. Intermittent prone positioning in the treatment of severe and moderate posttraumatic lung injury. Crit Care Med 1999;27: 23752382.

D.12. How is liquid ventilation accomplished?


Kylstra, who demonstrated that salt solutions could be saturated with oxygen at high pressures, first introduced the concept of fluid breathing in the 1960s. In 1966, Leland Clark uncovered that both oxygen and carbon dioxide were soluble in fluorocarbon liquids. The earlier methods of liquid ventilation with fluorocarbons met limited success as a result of impurities and chemical compositions of the fluorocarbons that caused ALI. Advances in perfluorocarbon (PFC) technology, however, have led to the development of improved generations of oxygen carriers that incorporated nontoxic carriers. The PFC compounds are inert organic chemicals produced by replacement of fluorine for hydrogen in specific sites within the carbon chain. These agents do not undergo metabolism in the body and are eliminated through the pulmonary, gastrointestinal and renal systems. The proposed mechanisms for both improvement in oxygenation and hastening of recovery from ALI include a high solubility coefficient for oxygen and carbon dioxide relative to hemoglobin and a density that is twice that of water. As such, replacement of the FRC by PFC eliminates the alveolar membrane-air-liquid interface, reduces surface tension in the surfactant-depleted lung, and physically maintains the alveoli open. Because of its high density, it tends to gravitate toward the more dependent lung region that is most affected by lung edema and ALI. This effect stabilizes alveolar units in these regions and aids in alveolar recruitment. The use of partial liquid ventilation (PLV) with PFC may alter regional blood flow by diverting blood from dependent to nondependent lung regions, thereby improving ventilation/perfusion matching (i.e., fluid PEEP). An additional benefit of PLV is the displacement of alveolar proteinaceous edema, inflammatory cells, debris, and other mediators from the alveolar spaces that are less dense. Several clinical trials investigating the effect of PFC for PLV have shown a dose-dependent improvement in oxygenation. Leach et al. studied the efficacy of PLV using perflubronan eight

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carbon PFCin 13 premature infants with severe ARDS in whom conventional therapy using various modalities, including surfactant replacement, had failed. An amount of PFC equaling the infant's FRC was infused endotracheally while standard mechanical ventilation was maintained. Within 1 hour after installation of PFC, the PaO2 increased by 138% and the dynamic compliance improved by 61%. Whereas the duration of PLV was 24 to 72 hours and no direct complications occurred during the trial, the overall mortality rate was 50%. In 2001, Schuster et al. investigated whether or not the distribution of PFC in PLV is inhomogeneous, resulting in either inadequate improvement or deterioration in oxygenation, particularly during the first 24 hours after initiation of PLV. Inhomogeneity in distribution may arise from regional obstruction of airway components by (a) cellular debris, edema, and inflammatory factors; (b) local destruction of lung parenchyma; and (c) regional uptake of the PFC by blood. In this study, the chest radiograph of 16 patients who had received PLV for 48 hours were reviewed. The best predictor of inhomogeneous filling was the initial dose of PFC (10 mL/kg as compared with 20 mL/kg). Although other investigators P.76 have shown a dose-dependent improvement in oxygenation, several others have confirmed the findings of Schuster et al. PLV has been combined with several ventilatory approaches to maximize oxygen delivery. Suh et al. showed, in an animal model of ALI, that PLV has a dose-dependent increase in PaO2 with PEEP or proning as compared with volume-controlled mechanical ventilation mode. Additionally, lung histology revealed significantly less hyaline membrane formation in the PLV group, suggesting that this modality of ventilation allows the lungs to heal after an acute injury process. Relative to lungs from conventionally ventilated animals, similar histologic findings have been described whereby the use of PLV resulted in less alveolar hemorrhage, decreased lung fluid a c c u m u l a t i o n , a n d d i m i n i s h e d n e u t r o p h i l i c i n f i l t r a t i o n . T h i s a n t i i n f l a mm a t o r y b e n e f i t m a y b e attributed to the mechanical lavage of alveolar debris by the PFC and by a direct effect on alveolar macrophages. Despite these proven benefits, the use of PFC for PLV remains investigative for management of ARDS and ALI. Additional larger randomized clinical trials addressing the efficacy and safety of PLV need to be performed before any definitive recommendation can be made. Leach CL, Greenspan JS, Rubenstein SD, et al. Partial liquid ventilation with perflubron in premature infants with severe respiratory distress syndrome. N Engl J Med 1996; 335:761767. Lewis DA, Colton D, Johnson K, et al. Prevention of ventilator-induced lung injury with partial liquid ventilation. J Pediatr Surg 2001;36(9):13331336. Ricard JD, Lemaire F. Liquid ventilation. Curr Opin Crit Care 2001;7(1):814. Schuster DP, Lange NR, Tutuncu A, et al. Study group: clinical correlation with changing radiographic appearance during partial liquid ventilation. Chest 2001;119(5):15031509. Suh GY, Chung MP, Park SJ, et al. Partial liquid ventilation shows dose-dependent increase in oxygenation with PEEP and decreases lung injury associated with mechanical ventilation. J Crit Care 2000;15:103112. Valls-I-Soler A, Alvarez FJ, Gastiasoro E. Liquid ventilation: from experimental use to clinical application. Biol Neonate 2001;80(Suppl 1):2933.

D.13. What are the indications and contraindications for extracorporeal membrane oxygenation? How many ways can it be used? What are its results?
Extracorporeal membrane oxygenation (ECMO) should be used for patients in severe acute respiratory failure with reversible lung disease, who are dying of severe hypoxemia despite

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maximal conventional ventilatory care (e.g., tracheal intubation, mechanical ventilation with 10 to 15 cm H2O PEEP, diuresis, chest physical therapy, antibiotics, normothermia or mild hypothermia, sedation, paralysis, and increased oxygen concentration). Indications for ECMO by the NIH are as follows: PaO2 less than 50 mm for more than 2 hours with FIO2 of 1.0 and conventional PEEP; and a PaO2 less than 50 mm for more than 12 hours with FIO2 of more than 0.6 and conventional PEEP. Active bleeding is the only absolute contraindication to use of the artificial lung. The three routes for ECMO are as follows: venovenous perfusion from the inferior vena cava by way of the femoral vein to the oxygenator and then to the superior vena cava; venoarterial perfusion from the femoral vein to the oxygenator and then to the femoral artery; and venovenous arterial perfusion from the femoral vein to the oxygenator and then to both the internal jugular vein and the femoral artery. A collaborative study on ECMO has been completed under the auspices of the National Heart, Lung, and Blood Institute of the NIH. The results of this controlled study are as follows:

Compared with the control group of conventional respiratory therapy, ECMO did not improve mortality (90%), and the predominant cause of death was still progressive respiratory failure. P.77 ECMO did not affect the progress of disease (or lung pathology in those patients who died) any differently from conventional respiratory therapy. Although ECMO is an effective means of short-term life support, its clinical application for the treatment of ARDS is not appropriate or economically justified.

However, data analyzed from a national registry series of 715 neonatal ECMO patients (1980 to 1987) demonstrated an overall survival of 81%, which in earlier series had been the overall mortality rate with conventional therapy. As neonatal ECMO has evolved, entry criteria have been used, and experience with ECMO technology has been shown to improve survival. ECMO is now a proven support modality for neonatal respiratory failure that is due to several causes, such as meconium aspiration syndrome, persistent pulmonary hypertension of the newborn, congenital diaphragmatic hernia, and infant respiratory distress syndrome. Kirshbom PM, Bridges ND, Myung RJ, et al. Use of extracorporeal membrane oxygenation in pediatric thoracic organ transplantation. J Thorac Cardiovasc Surg 2002; 123(1):130136. Mamprin F, Pesenti A, Fumagalli R. Extracorporeal circulation for acute respiratory failure. Intensive Care Med 2001;27(5):934936. National Heart, Lung, and Blood Institute. Extracorporeal support for respiratory insufficiency. A collaborative study. Bethesda, MD: US Department of Health, Education and Welfare, 1979. Schumacher RE, Baumgart S. Extracorporeal membrane oxygenation 2001. The odyssey continues. Clin Perinatol 2001;28(3):629653. Taghavi S, Ankersmit HJ, Wieselthaler G, et al. Extracorporeal membrane oxygenation for graft failure after heart transplantation: recent Vienna experience. J Thorac Cardiovasc Surg 2001;122(4):819820.

D.14. What is high frequency positive pressure ventilation (HFPPV)? What are its characteristics?
HFV was originally used as a technique to provide adequate oxygenation and alveolar ventilation for rigid bronchoscopy and laryngeal surgery. Since that time, the literature is replete with clinical applications of HFV. The major characteristics of the ventilatory pattern of volume-

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controlled HFPPV are as follows:

A ventilatory frequency of approximately 60 to 100 per min and an inspiration/expiration ratio of less than 0.3

Smaller tidal volumes and therefore lower maximum and mean airway and transpulmonary pressures, yet a higher FRC than in conventional PPV

Positive intratracheal and negative intrapleural pressures throughout the ventilatory cycle Less circulatory interference than in IPPV and/or continuous positive pressure ventilation (CPPV)

Reflex suppression of spontaneous respiratory rhythmicity during normoventilation Decelerating inspiratory flow without an end-inspiratory plateau More efficient pulmonary gas distribution than in IPPV and/or CPPV

Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:1471. Sjostrand U. High frequency positive-pressure ventilation (HFPPV): a review. Crit Care Med 1980;8:345364. P.78

D.15. What are the frequencies used in HFV? How are they classified?
HFV is a generic term encompassing any form of mechanical ventilation operating at a frequency at least four times higher than the natural breathing frequency of the subject being ventilated. Smith categorized HFV into three groups:

HFPPV, 60 to 110 per minute High-frequency jet ventilation (HFJV), 110 to 400 per minute High-frequency oscillatory ventilation (HFOV), 400 to 2,400 per minute

Froese summarized HFV into five groups as shown in Fig. 3.5. Sjostrand, in Sweden, first introduced HFPPV. It was administered with a very low compliant ventilator with high gas flow rates. This produces a flow profile with rapid upstroke to a high peak flow rate, followed by a passive expiration. Because it is a closed circuit, there was no entrainment of additional gas during inspiration. HFJV delivers a small tidal volume at a high flow rate by means of a narrow orifice at an adjustable drive pressure, rate, and inspiratory time or I/E ratio. Gas is regulated by a solenoid P.79 or fluidic mechanism. Because jet flow is delivered to a small-lumen tube, entrainment occurs due to subambient pressure created at the distal end of a cannula. Exhalation occurs around the tube or through another lumen and is passive. Frequencies are commonly 100 to 200 per minute, occasionally up to 400 per minute.

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Figure 3.5 Summary of features of several commonly encountered high-frequency modalities. See text for details. CHFV, combined high-frequency ventilation; HFJV, high-frequency jet ventilation; HFOV, high-frequency oscillatory ventilation; HFPPV, high-frequency positive pressure ventilation; HIFI, high fidelity. (From Froese AB. High-frequency ventilation; uses and abuses. ASA refresher courses in anesthesiology. Park Ridge, IL: American Society of Anesthesiologists, 1986:127 138, with permission.)

High-frequency flow interrupters (HFFI) are closely related to jet ventilators. Gas from a highpressure source is chopped into pulses by a rotating ball valve and directed into the lung. The frequencies are usually 100 to 200 per minute in adults and 300 to 1,200 per minute in infants. CHFV means combined high-frequency ventilation. Combined approaches usually superimpose some form of HFV onto backup conventional mechanical ventilation. The reported combinations vary considerably, with the slow component ranging from 1 to 60 per minute, and the fast component being delivered at 100 to 3,000 per minute. HFOV is delivered by an oscillator-type ventilator consisting of a rotary-driven piston to produce to-and-fro movement of gas within the airway. Unlike all the other modalities, during HFOV the ventilator actively drives both inspiratory and expiratory flows. Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:11721173.

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Butler WJ, Bohn DJ, Bryan AC, et al. Ventilation by high frequency oscillation in humans. Anesth Analg 1980;59:577584. Carlon GC, Kahn RC, Howland WS, et al. Clinical experience with high frequency jet ventilation. Crit Care Med 1981;9:16. El-Baz N, Faber LP, Doolas A. Combined high frequency ventilation for management of terminal respiratory failure: a new technique. Anesth Analg 1983;62:3949. Froese AB. High frequency ventilation: uses and abuses. In: Barash PG, ed. ASA refresher courses in anesthesiology. Park Ridge, IL: American Society of Anesthesiologists, 1986: 127 138. Smith RB. Ventilation at high respiratory frequencies. Anaesthesia 1983;37:1011.

D.16. What are the indications and precautions for high frequency ventilation (HFV)?
The indications for HFV include the following:

Respiratory failure with bronchopleural fistula, tracheoesophageal or bronchoesophageal fistula, barotrauma, pulmonary fibrosis, and pulmonary hemorrhage, because of low airway pressure with HFV. Anesthesia for special procedures, such as bronchoscopy, laryngoscopy, tracheal reconstruction over a T-tube, and laser resection of a bronchial lesion, because HFV uses a small cannula for ventilation, leaving adequate room for surgeons to operate. Anesthesia for open thoracic surgery because of a moderately expanded lung and minimal respiratory movement with HFV. Improving oxygenation in adult and infant respiratory distress syndrome when hypoxemia persists in spite of maximal conventional ventilatory support. Enhancement of CO2 elimination when conventional mechanical ventilation has been unable to support adequate CO2 elimination despite multiple adjustments of ventilator settings in situations such as persistent fetal circulation in the neonate. HFV could prove advantageous in achieving a respiratory alkalosis by hyperventilation at low peak and mean airway pressures.

The precautions with HFV include the following:

HFV must never be used in a situation in which expiratory outflow of gas from the lung is impeded. Under such circumstances, lethal barotrauma can occur. P.80 HFV should never be used with inadequate humidification, because serious tracheal injury may occur. HFV system pressure should be accurately and appropriately sampled and monitored in order to drive an automatic shutoff mechanism so gas entry into the lungs can be terminated immediately if an overpressure situation occurs. HFV should never be used without adequate training.

Borg U, Eriksson I, Sjostrand U. High frequency positive pressure ventilation (HFPPV): a review

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based upon its use during bronchoscopy and for laryngoscopy and microlaryngeal surgery under general anesthesia. Anesth Analg 1980;59:594603. Carlon GC, Howland WS, Ray C, et al. High frequency jet ventilation. A prospective randomized evaluation. Chest 1983;84:551559. Carlon GC, Kahn RC, Howland WS, et al. Clinical experience with high frequency jet ventilation. Crit Care Med 1981;9:16. Cartotto R, Cooper AB, Esmond JR, et al. Early clinical experience with high-frequency oscillatory ventilation for ARDS in adult burn patients. J Burn Care Rehabil 2001;22(5): 325 333. Dalton HJ. Lung volume measurement during high-frequency ventilation: a new role for an old technique? Crit Care Med 2001;29(12):23942395. El-Baz N, Holinger L, El-Ganzouri A, et al. High frequency positive-pressure ventilation for tracheal reconstruction supported by tracheal T-tube. Anesth Analg 1982;61:796800. Froese AB. High frequency ventilation: uses and abuses. In: Barash PG, ed. ASA refresher courses in anesthesiology. Park Ridge, IL: American Society of Anesthesiologists, 1986: 127 138. Fujino Y, Kacmarek RM, Hess DR. Nitric oxide delivery during high-frequency oscillatory ventilation. Respir Care 2000;45(9):10971104. Imai Y, Nakagawa S, Ito Y, et al. Comparison of lung protection strategies using conventional and high-frequency oscillatory ventilation. J Appl Physiol 2001;91(4):18361844. Keszler M, Durand DJ. Neonatal high-frequency ventilation. Past, present, and future. Clin Perinatol 2001;28(3):579607. Varkul MD, Stewart TE, Lapinsky SE, et al. Successful use of combined high-frequency oscillatory ventilation, inhaled nitric oxide, and prone positioning in the acute respiratory distress syndrome. Anesthesiology 2001;95(3):797799. Whitwam JG, Chakrabarti MK, Cody M, et al. Intermittent high frequency ventilation. Clinical evaluation of a new mode of ventilation. Anaesthesiol Scand 1990;34(6): 447451.

D.17. What is nitric oxide (NO)? What is the role of inhaled NO in the treatment of ARDS?
In 1987, endothelium-derived relaxing factor was identified as NO. NO produced by the endothelium diffuses into vascular smooth muscle where NO activates soluble guanylate cyclase. The subsequent increase in intracellular cyclic guanosine monophosphate (cGMP) causes smooth muscle vasodilation. Endothelium-independent nitrovasodilators such as nitroglycerin and nitroprusside also act through guanylate cyclase activation to directly release NO. Inhaled NO is a selective pulmonary vasodilator. NO is not effective during systemic administration because it is rapidly inactivated by hemoglobin. Therefore, inhaled NO may diffuse from the alveoli to pulmonary vascular smooth muscle and produce pulmonary vasodilation P.81 without systemic vasodilation because any NO that diffuses into blood will be inactivated by hemoglobin. Inhaled NO has been shown to be effective in treating primary pulmonary hypertension, as well as decreasing pulmonary hypertension and improving oxygenation after mitral valve replacement and in the newborn with persistent pulmonary hypertension.

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Pulmonary hypertension and hypoxemia universally occur in ARDS. Pulmonary hypertension in ARDS may be due to active vasoconstriction from local alveolar hypoxic pulmonary vasoconstriction and other vasoconstrictor mediators. Hypoxemia in ARDS is due to ventilation/perfusion mismatch, intrapulmonary shunting, or anatomic shunting. Intravenous pulmonary vasodilator therapy with agents such as nitroglycerin, nitroprusside, prostaglandin E, prostacyclin, adenosine, and nifedipine produces small reduction in pulmonary artery pressure but large reduction in systemic blood pressure and arterial oxygenation. The adverse effect on oxygenation is primarily due to reversal of hypoxic pulmonary vasoconstriction. On the contrary, inhaled NO may decrease pulmonary hypertension and improve oxygenation in patients with ARDS because inhaled NO may be distributed according to ventilation so the associated vasodilation increases blood flow to well-ventilated alveoli. Rossaint et al. published the first major report of the use of inhaled NO in patients with ARDS. They found that inhaled NO (5 to 20 parts per million [ppm]) effectively decreased pulmonary hypertension and improved oxygenation. In a subsequent study, they showed that inhaled concentrations of only 60 to 250 parts per billion could increase PaO2 by 30%. These concentrations had little or no effect on pulmonary artery pressure. The other major study by Bigatello et al. demonstrated that inhaled NO produced dose-related decreases in pulmonary artery pressure with 50% of the maximal effect occurring at 5 ppm. Inhaled NO also increased oxygenation, but dose-response effects could not be demonstrated. Inhaled NO has been effective on ARDS in combination with other therapies. The combination of inhaled NO (5 to 10 ppm) and almitrine bismesylate, a potentiator of hypoxic pulmonary vasoconstrictor, had additive effects on improving oxygenation in ARDS and simultaneously decreased pulmonary hypertension. Dcering et al. studied intravenous phenylephrine, 50 to 200 g per minute, titrated to a 20% increase in mean arterial pressure; inhaled NO, 40 ppm; and the combination of phenylephrine and NO. They found that phenylephrine alone can improve PaO2 in patients with ARDS. In phenylephrine-responsive patients, phenylephrine augments the improvement in PaO2 seen with inhaled NO. These results may reflect selective enhancement of hypoxic pulmonary vasoconstriction by phenylephrine, which complements selective vasodilation by inhaled NO However, an important unsolved issue is the potential pulmonary toxicity of inhaled NO. Toxicity may be due to NO itself, or to its reactive metabolite, NO2. NO can combine with superoxide anion to produce peroxynitrite anion, which is a powerful oxidizing agent. The effects of NO and NO2 on repair versus fibrosis in injured lung and on pulmonary host defenses are unknown. Therefore, the effects of inhaled NO on outcome in patients with ARDS are not predictable. Overall, the data on NO therapy in the setting of ARDS demonstrate that it can improve oxygenation in some patients, but this is limited over time and it does not improve survival. Currently, NO is not recommended for use in the setting of ARDS. Bigatello LM, Hurford WE, Kacmarek RM, et al. Prolonged inhalation of low concentrations of nitric oxide in patients with severe adult respiratory distress syndrome. Effect on pulmonary hemodynamics and oxygenation. Anesthesiology 1994;80:761770. Dcering EB, Hanson CW III, Reily DJ, et al. Improvement in oxygenation by phenylephrine and nitric oxide in patients with adult respiratory distress syndrome. Anesthesiology 1997;87:1825. Ferguson ND, Granton JT. Inhaled nitric oxide for hypoxemic respiratory failure: passing bad gas? Can Med Assoc J 2000;162(1):8586. P.82 Finer NN, Sun JW, Rich W, et al. Randomized, prospective study of low-dose versus high-dose inhaled nitric oxide in the neonate with hypoxic respiratory failure. Pediatrics 2001;108(4):949 955.

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Gerlach H, Pappert D, Lewandowski K, et al. Long-term inhalation with evaluated low doses of nitric oxide for selective improvement of oxygenation in patients with adult respiratory distress syndrome. Intensive Care Med 1993;19:443449. Hurfold WE. Inhaled nitric oxidecurrent concepts. In: ASA annual meeting refresher course lectures, Park Ridge, IL, American Society of Anesthesiologists, 2001;431. Matthews BD, Noviski N. Management of oxygenation in pediatric acute hypoxemic respiratory failure. Pediatr Pulmonol 2001;32(6):459470. Mercier JC. Franco-Belgium Neonatal Study Group on Inhaled NO. Uncertainties about the use of inhaled nitric oxide in preterm infants. Acta Paediatr Suppl 2001;90(436): 1518. Rossaint R, Falke KJ, Lopez F, et al. Inhaled nitric oxide for the adult respiratory disease syndrome. N Engl J Med 1993;328:399405. Weinacker AB, Vaszar LT. Acute respiratory distress syndrome: physiology and new management strategies. Annu Rev Med 2001;52:221237. Zwissler B, Welte M, Habler O, et al. Effects of inhaled prostacyclin as compared with inhaled nitric oxide in a canine model of pulmonary microembolism and oleic acid edema. J Cardiothorac Vasc Anesth 1995;9:634640.

E. Weaning from Ventilatory Support


The patient's condition improved after respiratory support with 20 cm H2O PEEP. Arterial blood gases showed pH, 7.45; PaCO2, 35 mm Hg; PaO2, 150 mm; FIO20.75.

E.1. What would you do now?


The arterial blood gas analysis suggests that the oxygenation has improved markedly; nevertheless, there continues to be significant intrapulmonary shunting and the level of PEEP remains high. Before making any drastic changes, it is important to examine the patient thoroughly to determine that in fact the lung injury is resolving and that there is no evidence of infection, systemic inflammatory involvement, and metabolic derangements. The most appropriate ventilatory change is to lower the FIO2 to less than 0.5 or 0.6. This should be well tolerated. Next, the PEEP should be lowered gradually. The suggested criteria to lower PEEP level are a stable, nonseptic patient; PaO2/FIO2 more than 200 mm; effective compliance, more than 25 mL per cm H2O; PaO2_ PaO2, less than 200 mm at FIO20.5. PEEP should not be decreased by more than 5 cm H2O during a trial. At least 6 hours should elapse before undertaking a further attempt at lowering the PEEP level. Esteban A, Alia I, Tobin MJ, et al. Effect of spontaneous breathing trial duration on outcome of attempts to discontinue mechanical ventilation. Am J Respir Crit Care Med 1999;159:512518. Luterman A, Hororvitz JH, Carrico CJ, et al. Withdrawal from PEEP. Surgery 1978;39: 328332. Tobin MJ. 1999 Donald F Egan scientific lecture: weaning from mechanical ventilation: what have we learned? Respir Care 2000;45:417431. P.83

E.2. The patient continued to improve. When would you consider weaning the patient from the respirator? Discuss the criteria for weaning
The criteria for discontinuance of mechanical ventilation are essentially the converse of the criteria for the institution of mechanical support and are as follows:

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Clear consciousness with adequate gag and cough reflex Cardiovascular stability Stable metabolic state without hypothermia, hyperpyrexia, metabolic acidosis, or alkalosis Adequate pulmonary function

Mechanics

A vital capacity of more than 10 mL per kg or more than twice the normal tidal volume Rapid shallow breathing index (respiratory frequency/tidal volume) of less than 100 breaths per minute per L

A maximum inspiratory force of at least _20 to _30 cm H2O

Oxygenation

PaO2 more than 80 mm with FIO2 at 0.4 PaO2_ PaO2 less than 300 mm with FIO2 at 1.0 QS/QT less than 15%

Ventilation

PaCO2 less than 45 mm VD/VT less than 0.6

Lumb AB. Nunn's applied respiratory physiology, 6th ed. Philadelphia: Elsevier ButterworthHeinemann, 2005:430431.

E.3. Describe weaning by synchronized IMV, pressure support, CPAP, and T-piece
Mechanical ventilatory assistance is often an obligatory step during management of critically ill patients; however, complete withdrawal from this support represents a significant clinical problem in approximately 25% of intubated patients. Frequently employed weaning techniques have included PSV, T-piece, CPAP, and SIMV. Several studies have compared these various weaning approaches, but the results have been conflicting. Brochard et al. compared weaning by PSV, T-piece, and SIMV and found weaning by PSV to be superior to weaning by T-piece and by SIMV. In contrast, in a large multicenter trial of nonsurgical patients with diverse medical problems, Esteban et al. demonstrated that the duration of weaning by T-piece once a day was significantly less than weaning by PSV, which in turn was less than weaning by SIMV. Recently, Kollef et al. showed that a protocol-guided weaning by nurses and respiratory therapists was safe and led to extubation more rapidly than physician-directed weaning. Therefore, in addition to differences in study design, weaning modalities, and weaning techniques, there are selection and physician biases that interfere with the process of weaning. Although employment of protocol-driven weaning may control for physician bias, it is also data driven, time consuming,

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and costly.

Conventional T-piece technique


When the patient meets the criteria for weaning, a T-piece adapter and heated nebulizer are connected to the patient's endotracheal tube. The patient should be in a semisitting or sitting position. The inspired oxygen concentration is set at a level 5% to 10% higher than what the P.84 patient was receiving during mechanical ventilation. The vital signs and cardiac rhythm are monitored carefully every 5 to 10 minutes. Arterial blood gases are determined 15 minutes after weaning is begun and then every hour. The patient who tolerates the T-piece very well is extubated after 2 to 4 hours. Oxygen is then administered through a face mask with a heated nebulizer, at the same inspired oxygen concentration as during the T-piece trial. The high success associated with T-piece weaning is related primarily to the fact that the clinician biases are removed from the process. In other words, the patient becomes the sole controller of his or her weaning and readiness for extubation. No guessing is involved. One is either ready or not for weaning, and the best way to determine this is to apply no support. The weaning process is very difficult because the patient's need varies on a breath-by-breath basis, such that the clinician is incapable of predicting such changes. The common error is to be too conservative, thereby prolonging the weaning process.

Synchronized intermittent mandatory ventilation technique


Weaning is accomplished by a gradual decrease in the SIMV rate that the ventilator delivers, allowing the patient slowly to take over spontaneous ventilation. This system allows the patient to breathe spontaneously between the preset mechanical ventilation. This system ensures intermittent hyperinflation of the lung. Weaning by SIMV is the least effective approach in terms of weaning time. It promotes dependence on the ventilator and can be confusing to the respiratory center. The delivery of the mechanical breath must coincide with the central inspiratory time. The same rule applies during exhalation. Prolonging the mechanical breath will overlap with the neural start of exhalation; that is, although the neural input is telling the patient to exhale, the ventilator continues to inflate the lungs. This is frequently seen in patients with COPD whose airway flow changes more slowly and the expiratory muscle becomes active during ventilator-induced inflation. A mismatch can also occur if the patient's inspiratory drive occurs before exhalation is complete, leading to breath stacking. Another important aspect of synchronization during PPV is the flow rate that changes on an intrabreath and an interbreath basis. Frequently, patients will show signs of air hunger and tachypnea if the inspiratory flow rate is inadequate. In most ventilators, the flow rate is set at 60 L per minute. Too much flow is also problematic. Occasionally, the flow rate is increased to lower the inspiratory time while increasing the exhalation time. Unfortunately, the patient may respond adversely by becoming tachypneic, resulting in shortened expiratory times, which then potentiates dynamic hyperinflation (intrinsic PEEP). Several studies have shown a flow-related inspiratory termination reflex. Activating such reflexes can result in curtailing the neural inspiration producing shallow inspiratory efforts. Overall, the consequences of poor synchronization include increase in work of breathing, anxiety, patient discomfort, ineffective ventilation, and increased morbidity and mortality.

Pressure-support weaning
Pressure-support weaning can be combined with IMV and with CPAP weaning. Its proposed advantages include reducing the work of breathing, improving synchronization between the

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patient and the ventilator, reducing inspiratory pressures, and facilitating weaning. While on IMV, once the patient has been weaned to a minimum rate (i.e., IMV of 4 to 6 breaths per minute), the level of pressure support is gradually reduced (2 to 3 cm H2O at a time). In some cases, this level of change is performed only once a day, whereas in other cases, the changes may be made several times a day. When the pressure-support level is at a minimum (< 8 cm H2O), weaning parameters are obtained in preparation for complete withdrawal from the mechanical ventilation. Attention to the pressurevolume and flow waveforms, which are available in most mechanical ventilators, can facilitate the weaning process and help determine other important aspects of respiratory mechanics (Fig. 3.6). P.85

Figure 3.6 Airway pressure waveforms. ACV, assist/control ventilation; APRV, airway pressure-release ventilation; CMV, controlled mechanical ventilation; EMMV, extended mandatory minute ventilation; HFV, high-frequency ventilation; IMV, intermittent mandatory ventilation; PCIRV, pressure-controlled inverse-ratio ventilation; PCV, pressure-controlled ventilation; PSV, pressure-support ventilation. (From Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:1470, with permission.)

As with IMV, the inherent problem with pressure-support weaning is the clinical biases that exist. Once again, the technology and the knowledge that allow for minute-to-minute assessment and adjustment of the dynamic environment of the patient's physiology needs are lacking. Consequently, we make predictions about the level of support the patient needs and await clinical and laboratory signs of problems or success. Overall, difficulties with weaning can be ascribed in part to the heterogeneity of underlying

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pulmonary diseases and to inconsistencies in clinical practice. Data-driven approaches to weaning are often nonpredictive of outcome and may fail to provide clinicians with signs of impending respiratory muscle fatigue. The patient's respiratory demand can vary considerably, requiring appropriate and timely ventilatory adjustments. A potential solution to this laborintensive and costly task is to employ a computer-driven automated weaning process. Benumof JL. Anesthesia for thoracic surgery, 2nd ed. Philadelphia: WB Saunders, 1995:738 740. Brochard L, Rauss A, Benito S, et al. Comparison of three methods of gradual withdrawing from ventilatory support during weaning from mechanical ventilation. Am J Respir Crit Care Med 1994;150:896903. P.86 Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods of weaning patients from mechanical ventilation. N Engl J Med 1995;332:345350. Kollef MH, Shapiro SD, Silver P, et al. A randomized, controlled trial of protocol-directed versus physician-directed weaning from mechanical ventilation. Crit Care Med 1997;25:567574.

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Chapter 4 Lung Transplantation


Paul M. Heerdt Charles W. Hogue Jr.

A 52-Year-Old Man
with progressively worsening dyspnea on exerti on, limitation of daily activity des pite su pp le me ntal oxy gen , and rad io gra phi c a nd sp ir ometri c evi de nce of sev ere obstr ucti ve p ulmo nar y disea se wa s sche duled for sing le-lun g tra nsplan tation . Histo ry wa s r emarka bl e for a on e pa ck pe r da y for 3 0 yea rs smoki ng hi story ( al thou gh non e for 10 ye ars ) and mi l d h yper tensi on .

P.88

A. Medical Disease and Differential Diagnosis A.1. What were the expected manifestations of severe obstructive pulmonary disease in this patient, and why was he a transplant candidate?
This patient suffered from increased airway resistance, reduced expiratory flow rates, and high residual lung volumes. When expiratory airway obstruction and lung hyperinflation become so severe that the chest cannot physically expand to accommodate a normal tidal volume, restrictive physiology becomes superimposed on obstructive disease. This condition is usually refractory to medical management and substantially limits daily activity. This patient's age and lack of other major systemic illness allowed him to be considered a transplant candidate. Chronic obstructive pulmonary disease (COPD) (often secondary to smoking), emphysema secondary to 1-antitrypsin deficiency, and cystic fibrosis are the most common obstructive disorders in adults undergoing lung transplantation. At one time, concerns about mediastinal displacement and profound ventilation/perfusion mismatch secondary to hyperinflation of the remaining native lung prevented surgeons from attempting single-lung transplantation for emphysema. However, clinical experience has demonstrated that many emphysemic patients can be successfully treated by single-lung transplantation. Because of the severe shortage of organs for transplant, single-lung procedures have been advocated as a means to increase the number of recipients. However, increasing experience suggests that bilateral lung transplantation for COPD is associated with improved functional outcomes and perhaps improved long-term survival compared with single-lung transplantation. Nonetheless, although transplantation may improve the quality of life for patients with severe COPD, recent data question whether either single or bilateral lung transplant has significant survival benefit. Stavem K, Bjortuft O, Borgan O, et al. Lung transplantation in patients with chronic obstructive pulmonary disease in a national cohort is without obvious survival benefit. J Heart Lung Transplant 2006;25(1):7584. Sundaresan RS, Shiraishi Y, Trulock EP, et al. Single or bilateral lung transplantation for emphysema? J Thorac Cardiovasc Surg 1996;112:1485.

A.2. What other end-stage lung diseases can also be treated with transplantation?

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The first successful (i.e., the patient left the hospital) single-lung transplantations were performed in 1983 for idiopathic pulmonary fibrosis. Since that time, the procedure has been applied P.89 to patients suffering from various end-stage pulmonary diseases (Table 4.1). In general, the underlying disease processes produce lung dysfunction that can be broadly characterized as o b s t r u c t i v e , r e s t r i c t i v e , i n f e c t i o u s ( e . g . , c y s t i c f i b r o si s a n d b r o n c h i e c t a s i s ) , o r v a s c u l a r . A s o f 2005, most single-lung transplantations have been performed for obstructive lung disease, followed by idiopathic pulmonary fibrosis. The most common indications for bilateral lung transplantation are cystic fibrosis and obstructive lung disease.

Table 4.1 Lung Transplants Categorized by Disease. END-STAGE LUNG DISEASE Cystic fibrosis Retransplant Primary pulmonary hypertension a1-Antitrypsin deficiency Miscellaneous Idiopathic pulmonary fibrosis Emphysema SINGLE-LUNG TRANSPLANT (% OF TOTAL) 3 3 4 BILATERAL/DOUBLE-LUNG TRANSPLANT (% OF TOTAL) 33 2 9

11

10

11 21

18 8

47

20

Reflecting a loss of lung parenchymal elasticity and compliance, end-stage restrictive disease is characterized by profoundly reduced lung volumes and diffusing capacity but relative preservation of ventilatory flow rates. Comparison of flowvolume loops representing obstructive and restrictive diseases is shown in Fig. 4.1. The underlying disease process also tends to obliterate P.90 pulmonary microvasculature, thereby chronically increasing vascular resistance, producing pulmonary hypertension, and predisposing to cor pulmonale. Most patients with restrictive disease are good candidates for a single-lung transplantation because the stiff, vasoconstricted native lung will receive relatively little ventilation and perfusion and can therefore usually be left without compromising the transplanted lung.

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Figure 4.1 Representative tracings of flowvolume loops from a healthy subject, a patient with parenchymal obstructive disease, a patient with tracheal stenosis, and a patient with restrictive disease from parenchymal fibrosis. (From Goudsouzian N, Karamanian A. Physiology for the anesthesiologist, 2nd ed. Norwalk: AppletonCentury-Crofts, 1984:213, with permission.)

Infectious lung disease such as cystic fibrosis is the most frequent indication for lung transplantation in patients younger than 18 years. Characterized by chronic infection and the production of copious purulent secretions, patients with cystic fibrosis primarily exhibit functional abnormalities that are obstructive with increased airway reactivity. Undermost circumstances, residual volumes and functional residual capacity are increased and bronchodilators have little effect on expiratory flow rates. Because of potential infectious crosscontamination of the transplanted lung, chronic infectious disease represents a contraindication to single-lung transplantation. However, single-lung transplantation with contralateral pneumonectomy has been performed and suggested as an alternative solution. Pulmonary vascular disease with severe pulmonary hypertension and right ventricular dysfunction has also emerged as an indication for transplantation. Pathologically, severe PA hypertension can result from idiopathic proximal vascular processes such as persistent pulmonary hypertension (PPH) or secondary to chronically increased pulmonary blood flow (e.g., left-to-right intracardiac shunt, leading to Eisenmenger's syndrome) or pulmonary venous hypertension. Pulmonary hypertension may precipitate chronic hypoxemia if it is associated with an intracardiac defect that allows for development of a right-to-left shunt. Because a native lung can usually be left intact without compromising a transplanted lung (which will receive most of blood flow), some patients with pulmonary vascular disease may be reasonable candidates for single-lung transplantation, with concurrent repair of any cardiac anomalies. Early reports indicated poorer functional recovery and higher mortality after single versus bilateral lung transplantation for PPH. Subsequent studies, however, have failed to show differences in outcome. In addition, improved medical therapy for PPH, particularly with continuous long-term intravenous prostacyclin infusions, has affected the numbers of patients undergoing lung

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transplantation for this disease at some centers. Gammie JS, Keenan RJ, Pham SM, et al. Single-versus double-lung transplantation for pulmonary hypertension. J Thorac Cardiovasc Surg 1998;115:397402. Hinson KFW. Diffuse pulmonary fibrosis. Hum Pathol 1970;1:825847. Pasque MK, Kaiser LR, Dresler CM, et al. Single lung transplantation for pulmonary hypertension. Technical aspects and immediate hemodynamic results. J Thorac Cardiovasc Surg 1992;130(3):475482. Shennib H, Massard G, Gauthier R, et al. Single lung transplantation for cystic fibrosis: is it an option? J Heart Lung Transplant 1993;12(2):288293. Trulock EP, Edwards LB, Taylor DO, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-second official adult lung and heart-lung transplant report2005. J Heart Lung Transplant 2005;24(8):956967. Voelkel NF, Weir EK. Etiologic mechanisms in primary pulmonary hypertension. In: Weir EK, Reeves JT, eds. Pulmonary vascular physiology and pathophysiology. New York: Marcel Dekker Inc, 1989:513539.

A.3. How many lung transplantations have been performed?


Although the first human lung allograft was performed in 1963, transplantation of one or both lungs did not emerge as a viable therapeutic option for patients with end-stage lung disease until the 1980s. The ultimate emergence of this procedure can be largely attributed to advances in the P.91 prevention and treatment of airway complications, infections, and rejection. Since initiation of an international registry for lung transplantation in the mid-1980s, the number of procedures reported yearly rose sharply, until beginning to slow in 1993. To date, the highest yearly total was 1,767 in 2002. Despite this volume, the number of patients awaiting lung transplantation continues to exceed the limited donor supply. As of the 2005 international registry, 19,197 lung transplantations had been reported. Hardy JD, Webb WR, Dalton ML, et al. Lung homotransplantation in man. JAMA 1963;186: 1065 1074. Trulock EP, Edwards LB, Taylor DO, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-second official adult lung and heart-lung transplant report2005. J Heart Lung Transplant 2005;24(8):956967. Trulock EP. Lung transplantation. Am J Respir Crit Care Med 1997;155:789818.

A.4. What are the selection criteria for recipients?


In general, patients with severe end-stage lung disease are considered candidates for transplantation when their life expectancy is less than 2 to 3 years, they have minimal disease of other organ systems, and they are mentally and psychologically capable of following strict regimens for rehabilitation and immunosuppressive therapy. Specific criteria, including age, are dependent on the type of lung disease and whether the planned procedure is single or bilateral lung transplantation. Recent data reveal that the age of lung transplant recipients is increasing with approximately 20% now 60 years of age and above. In contrast to criteria formulated when lung transplantation was in its infancy, concomitant steroid therapy, previous intrathoracic surgery, mechanical ventilation, and right ventricular failure are no longer considered absolute contraindications.

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Bigham M, Dickstein ML, Hogue CW Jr. Cardiac and lung transplantation. In: Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia. Philadelphia: Lippincott Williams & Wilkins, 2001:636. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Trulock EP, Edwards LB, Taylor DO, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-second official adult lung and heart-lung transplant report2005. J Heart Lung Transplant 2005;24(8):956967.

A.5. How is the decision made to transplant one or both lungs, and does this influence preoperative management?
Single-lung transplantation is often preferred because of the extreme shortage of donor organs. The only absolute contraindication to single-lung transplantation is infectious lung disease (e.g., cystic fibrosis and bronchiectasis), with which leaving the native lung could endanger long-term viability of the transplanted lung. As noted earlier, severe emphysema was once thought of as a contraindication to single-lung transplantation because of the probability of mediastinal shift and marked ventilation mismatch between the highly dispensable native lung and the graft. This is only rarely of clinical significance, and it is now accepted that single-lung transplantation can be successfully performed in patients with obstructive disease. Although single-lung transplantation is technically easier and advocated for more difficult recipients, such as those with prior thoracic surgery or coexisting illnesses, functional improvements are often better with bilateral lung transplantation. In addition, the status of the donor lungs further influences the decision of P.92 whether to perform a single or bilateral procedure. Finally, transplantation of two lobes from two living related donors for patients with inflammatory disease who are unlikely to survive the wait for a cadaver donor is gaining acceptance. From a practical standpoint, the decision to perform a single-lung or a bilateral lung transplant has little impact on preoperative management because both procedures necessitate the same level of preparation. Date H, Tanimoto Y, Goto K, et al. A new treatment strategy for advanced idiopathic interstitial pneumonia: living-donor lobar lung transplantation. Chest 2005;128(3):13641370. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Sundaresan RS, Shiraishi Y, Trulock EP, et al. Single or bilateral lung transplantation for emphysema? J Thorac Cardiovasc Surg 1996;112:1485.

A.6. How does a single-lung transplantation differ technically from a double-lung transplantation?
It is extremely important that anesthesiologists be broadly familiar with the surgical methods, because manipulation of the heart and lungs at specific points during the transplantation can produce marked cardiopulmonary disturbances. Ideally, the anesthesiologist will anticipate these changes and adapt the anesthetic management accordingly. Description of the detailed technical aspects of lung transplantation are readily available. Single-lung transplantation is usually performed in the lateral decubitus position through a thoracotomy incision, often with the upper leg and pelvis angled to allow groin exposure for potential femoral cannulation and CPB. In contrast, bilateral sequential lung transplantation is usually performed with the patient supine through a clamshell incision (bilateral anterior thoracotomies with or without transverse sternotomy). For both single-lung and bilateral lung transplantation, intermittent single-lung ventilation is required during dissection of the native

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lung to be removed and implantation of the graft. Once stable single-lung ventilation is established, dissection of the lung to be transplanted is initiated with isolation of the PA. To assess the cardiopulmonary response to diverting the entire cardiac output through one lung, progressive temporary occlusion of the vessel is first performed manually; if well tolerated, the vessel is then clamped and stapled. After ligation of the PA, the pneumonectomy is completed. Implantation of the graft begins with anastomosis of the airway. In the past, the bronchial anastomosis was wrapped with an omental pedicle, mobilized through a small abdominal incision in an effort to improve blood supply to the airway and promote healing. However, the use of a telescoping bronchial anastomosis has now largely obviated the need for omental wrapping. The PA branch is then attached to the graft, followed by anastomosis of a cuff of the left atrium containing the pulmonary veins. The implanted lung is then partially inflated, the left atrial cuff and pulmonary veins de-aired, and circulation to the organ restored. Patients presenting for single-lung transplantation with chronic persistent pulmonary hypertension (PPH) of primary or secondary etiology often exhibit severe functional compromise of the right ventricle. To avoid additional right ventricular stress, many institutions choose to institute partial normothermic CPB during single-lung transplantation for PPH or in patients with severe pulmonary hypertension and right ventricular dysfunction secondary to restrictive or obstructive disease. Cannulation is typically through the femoral artery and the right atrium unless simultaneous correction of an intracardiac defect is planned. In such patients, conventional aortic and single- or double-stage atrial cannulation are performed. Implantation of the lung is otherwise performed in the same manner as described earlier. Double-lung transplantation was first described by the Toronto Lung Transplant Group in the mid-1980s as en bloc implantation of both lungs simultaneously. The procedure is P.93 performed through a median sternotomy using hypothermic CPB, cardioplegic cardiac arrest, and single tracheal (or double bronchial) anastomosis of the trachea and main PA. Although the procedure initially produced encouraging results, considerable limitations related to technical complexity, morbidity, mortality, and application to many patients with end-stage lung disease soon became apparent. Not surprisingly, use of the procedure declined sharply and has now been largely replaced by the bilateral sequential implantation technique, which does not uniformly require hypothermic CPB. Introduced in 1990, bilateral sequential (or bilateral single) lung transplantation has become the surgical procedure of choice when replacement of both lungs is necessary. As noted earlier, in contrast to single-lung transplantation, bilateral sequential lung transplantation procedures are performed in the supine position. In general, the procedure can be regarded as having two phases. First, the most severely compromised lung (as determined by preoperative ventilation/perfusion lung scanning) is removed during ventilation of the good contralateral lung. Implantation is achieved through a bronchial anastomosis as with a single-lung transplantation. The second lung is then removed and transplanted during ventilation of the new lung alone. Kaiser LR, Cooper JD. Adult lung transplantation. In: Flye MW, ed. Atlas of organ transplantation. Philadelphia: WB Saunders, 1995:296312. Pasque MK, Cooper JD, Kaiser LK, et al. An improved technique for bilateral single lung transplantation; rationale and clinical experience. Ann Thorac Surg 1990;49:785789.

B. Preoperative Evaluation and Preparation B.1. What preoperative evaluation is desirable?


At most centers, an extensive physical examination, psychologic evaluation, and numerous tests of cardiopulmonary function are performed before acceptance into the transplant program. This f a c i l i t a t e s t h e p r e a n e s t h et i c e v a l u a t i o n t h a t i d e a l l y i s p e r f o r m e d w h e n t h e p a t i e n t i s f i r s t

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accepted into the transplant program. Familiarity with pulmonary function tests, ventilation/perfusion lung scan results, heart catheterization, echocardiographic data (including evidence of intracardiac shunts), exercise tolerance, oxygen use, and dependence on continuous pulmonary vasodilator infusion (i.e., prostacyclin) are beneficial for formulating an anesthetic plan. Although many of these parameters are regularly reassessed, the interval between evaluation and transplantation necessitates that a careful history and physical examination be performed before the procedure, focusing on signs of pulmonary hypertension and cardiac dysfunction. Bigham M, Dickstein ML, Hogue CW Jr. Cardiac and lung transplantation. In: Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia. Philadelphia: Lippincott Williams & Wilkins, 2001:636. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314.

B.2. How would you premedicate this patient?


As with all critically ill patients, considerations regarding preoperative sedation are governed primarily by the functional limitations imposed by the underlying disease. Consideration must also be given to the possibility that the donor lungs will be deemed unacceptable at final inspection, and therefore, the procedure canceled and the patient discharged from the hospital. When indicated, parenteral sedation is usually chosen because of insufficient time to effectively P.94 administer oral anxiolytics. Midazolam alone or with diphenhydramine (potentially protecting the lung against drug-induced histamine release) is often sufficient. Clinically, most patients with end-stage restrictive, obstructive, or infectious lung disease are tachypneic while breathing room air and cannot be aggressively sedated. In contrast, patients with persistent pulmonary hypertension and no intracardiac defect often appear reasonably normal and will benefit from sedation because of the potential for stress-related increases in pulmonary vascular resistance. Alternatively, patients with pulmonary hypertension and significant right-to-left intracardiac shunting (i.e., Eisenmenger physiology) are often cyanotic despite oxygen supplementation and may not tolerate sedation well. In addition, consideration needs be given to immunosuppression protocols, and in appropriate patients supplemental bronchodilator therapy. Hartigan PM, Pedoto A. Anesthetic considerations for lung volume reduction surgery and lung transplantation. Thorac Surg Clin 2005;15(1):143157. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314.

B.3. What vascular access is required?


Typically, a large-bore intravenous catheter and central venous access for PA catheter placement are secured before surgery. In many centers, additional central venous cannulation is performed with a multiple-lumen catheter to provide intraoperative and postoperative venous access. For patients with chronic infectious lung disease or a history of previous intrathoracic procedures, a second large-bore intravenous catheter is often started because of the potential for brisk blood loss during dissection of pulmonary adhesions. Meticulous removal of air from venous infusion lines should be performed, particularly in patents with known or suspected rightto-left shunts. At many institutions, cannulation of a femoral artery, instead of the radial artery, is performed under local anesthesia in the operating room, because radial arterial pressures may become damped during the procedure secondary to positioning of the arms. Hartigan PM, Pedoto A. Anesthetic considerations for lung volume reduction surgery and lung

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transplantation. Thorac Surg Clin 2005;15(1):143157. Heerdt PM, Triantafillou AN. Anesthesia for lung transplantation. In: Flye MW, ed. Atlas of organ transplantation. Philadelphia: WB Saunders, 1995:313318.

B.4. Is preoperative epidural catheter placement advantageous?


Pain control after lung transplantation can be critical in facilitating patient extubation and rehabilitation. Both lumbar and thoracic epidural catheters have been used for postoperative pain management. At many institutions, catheters are placed immediately before the procedure inmost patients, despite the rare possibility of anticoagulation and CPB during the transplantation procedure. This practice is supported by data indicating no adverse sequelae to preoperatively placed epidural catheters, including patients who required emergent heparinization and CPB. Obvious exceptions to this approach are patients anticoagulated preoperatively or those in whom CPB is planned. Delaying placement of the epidural catheter until the postoperative period may actually increase the potential risk of complications, because both hemodilution and immunosuppression tend to promote a coagulopathy. Hartigan PM, Pedoto A. Anesthetic considerations for lung volume reduction surgery and lung transplantation. Thorac Surg Clin 2005;15(1):143157. P.95 Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314.

C. Intraoperative Management C.1. What special equipment is necessary?


Items advantageous for lung transplantation procedures include an anesthesia machine with a ventilator capable of delivering a wide range of inspiratory/expiratory (I : E) ratios, differing ventilatory modes, and efficacy at higher airway pressures. Apparatus to deliver continuous positive airway pressure (CPAP) should be readily available, as should a fiberoptic bronchoscope to confirm double-lumen tube (DLT) positioning, to provide guided airway suctioning, and for inspecting anastomosis. Access to transesophageal echocardiography (TEE) is often beneficial and a CPB machine should always be immediately available for lung transplantation. Though not specifically approved for this indication, a nitric oxide (NO) delivery system is highly desirable during lung transplantation.

C.2. How would you monitor this patient?


Intraoperatively, hemodynamic, and respiratory changes are often acute and profound, so extensive monitoring is imperative. In addition to the electrocardiogram, arterial blood pressure, and peripheral arterial oxygen saturation, PA catheter placement is routine for lung transplantation at most institutions because of the profound changes in pulmonary and systemic hemodynamics that often occur. During single-lung transplantations, PA catheters often migrate to the operative side after the patient has been laterally positioned even when radiographically confirmed to be in the nonoperative lung. Therefore, the surgeon should be reminded to palpate the PA and withdraw the catheter if necessary before cross-clamping the vessel. PA catheters capable of measuring mixed venous oxygen saturation have become widely used. TEE is often employed during lung transplantation to evaluate right ventricular function, particularly during clamping of the PA, to assess for intracardiac shunts, and to evaluate vascular anastomosis. Bigham M, Dickstein ML, Hogue CW Jr. Cardiac and lung transplantation. In: Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia. Philadelphia: Lippincott Williams & Wilkins,

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2001:636. Miyaji K, Matsubara H, Nakamura K, et al. Equivalence of flow velocities through bilateral pulmonary vein anastomoses in bilateral living-donor lobar lung transplantation. J Heart Lung Transplant 2005;24(7):860864. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Schenk P, Globits S, Koller J, et al. Accuracy of echocardiographic right ventricular parameters in patients with different end-stage lung prior to lung transplantation. J Heart Lung Transplant 2000;19(2):145154.

C.3. How would you induce anesthesia in this patient?


As with induction of anesthesia in any critically ill patent, multiple techniques have been safely used for patients undergoing lung transplantation. The only general rule is that induction be relatively gradual, because abrupt withdrawal of sympathetic tone in these patients with high sympathetic activity can result in marked cardiovascular compromise, particularly during the P.96 transition from spontaneous to mechanical ventilation. For this reason, injecting an epidural catheter with local anesthetic before induction of anesthesia can be problematic. Because effective alveolar ventilation and nitrogen washout are poor in the patient with severe obstructive lung disease and high residual volumes, prolonged (i.e., 15 to 20 minutes) preoxygenation is worthwhile, followed by a rapid-acting induction agent to shorten the excitement stage, expedite airway management, and prevent opiate-induced truncal rigidity. Thiopental, etomidate, propofol, and ketamine have all been used safely, but specific properties of each drug in the setting of the patient's underlying disease should be considered. Thiopental, for example, may not be desirable for patients with bronchospasm or pulmonary hypertension because of a propensity for histamine release. Alternatively, the sympathomimetic properties of ketamine may preclude use in the presence of pulmonary hypertension, whereas its bronchodilating effects may be beneficial in the setting of bronchospasm. After administration of the hypnotic, either fentanyl, 10 to 15 g per kg, or sufentanil, 1 to 2 g per kg, has been commonly used with either succinylcholine or a nondepolarizing muscle relaxant to complete induction. Benzodiazepines, scopolamine, and/or volatile anesthetic agents are frequently administered after induction to promote amnesia and in the case of volatile agents to promote bronchodilation. Bigham M, Dickstein ML, Hogue CW Jr. Cardiac and lung transplantation. In: Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia. Philadelphia: Lippincott Williams & Wilkins, 2001:636. Hartigan PM, Pedoto A. Anesthetic considerations for lung volume reduction surgery and lung transplantation. Thorac Surg Clin 2005;15(1):143157.

C.4. How would you ventilate this patient? What kind of endotracheal tube would you use?
After induction, the trachea is usually intubated with a left endobronchial double-lumen tube (DLT) for both single-lung and bilateral lung transplantation. Use of a single-lumen endotracheal tube with either an external or an internal bronchial blocking catheter has been described but does not appear to be clearly superior to the left endobronchial tube for most procedures. Furthermore, an endobronchial tube allows for differential lung ventilation if required postoperatively. One exception to this approach has been in patients with cystic fibrosis who exhibit thick tenacious secretions that are difficult to suction through the small-lumen suction catheters necessary for DLTs. In these patients, it is often helpful to first place a large single-

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lumen tube and perform extensive bronchoscopic-directed bronchial lavage and suctioning before placement of the DLT. The transition from spontaneous to mechanical ventilation invariably produces hemodynamic alterations resulting from acute changes in intrathoracic pressure and chest wall compliance. With obstructive lung disease, mechanical ventilation magnifies airtrapping, leading to pulmonary tamponade. Varying degrees of this phenomenon should be expected during anesthesia induction. The treatment consists of intermittent apnea with an open ventilator circuit, adjustment of the ventilatory pattern to an I : E ratio of 1 : 5 or less with moderate tidal volumes, and administration of bronchodilating drugs. Prompt restoration of blood pressure usually ensues. If hypotension persists, other causes of circulatory compromise must be excluded including pneumothorax. With restrictive disease, higher inflation pressures and positive end-expiratory pressure (PEEP) are often required. In both patients with obstructive and patients with restrictive disease, optimal balance of ventilation with hemodynamic stability often necessitates tolerating a degree of hypercapnia. In pulmonary hypertensive patients, mechanical ventilation usually produces less cardiovascular disturbance if caution is exercised not to increase pulmonary vascular resistance (e.g., from hypoxia, hypercarbia, or lung hyperinflation). Because lung recipients have little pulmonary reserve, ventilation with 100% oxygen is commonly used intraoperatively. Although this approach is somewhat controversial, few data P.97 suggest acute oxygen toxicity to a transplanted lung. High PaO2 may also directly promote pulmonary vasodilation and therefore be beneficial in reducing right ventricular afterload. Hartigan PM, Pedoto A. Anesthetic considerations for lung volume reduction surgery and lung transplantation. Thorac Surg Clin 2005;15(1):143157. Triantafillou AN, Heerdt PM, Patterson GA. Lung transplantation. In: Youngberg JA, Lake CA, Roizen MF, et al. eds. Cardiac, thoracic and vascular anesthesia. New York: Churchill Livingstone, 2000:703. Weir EK, Reeves JT, eds. Pulmonary vascular physiology and pathophysiology. New York: Marcel Dekker Inc, 1989:241290.

C.5. How does the physiology of single-lung ventilation influence the procedure?
In laterally positioned patients, gravity helps redistribute blood away from the nonventilated lung during single-lung ventilation and lessen intrapulmonary shunt. In supine patients, this benefit is obviously lost and single-lung ventilation may not be well tolerated. In general, because of large residual lung volumes that will become filled with a high concentration of oxygen content during the initial stages of the procedure, lung recipients with severe obstructive lung disease may initially maintain oxygenation for the first 10 to 15 minutes of single-lung ventilation. However, rapid arterial desaturation may then occur once a substantial portion of the residual volume is absorbed. Alternatively, patients with restrictive lung disease and a low functional residual capacity may rapidly exhibit both hypoxia and hypercarbia. Multiple steps can be taken to improve oxygenation including insufflation of oxygen or CPAP to the nonventilated lung, bronchoscopic-guided suctioning of the ventilated lung, careful manipulation of the ventilatory pattern, and PEEP to the ventilated lung. Differential PEEP/CPAP should be done cautiously, however, because increased airway pressure in the ventilated lung can divert blood toward the nonventilated side. In some patients, intermittent ventilation of the operative lung may have to be performed before pneumonectomy. In general, oxygenation improves after the clamping of the PA supplying the nonventilated lung. For desaturation not responding to the usual maneuvers, tourniquets can be placed around the PA by the surgeon as a temporizing step until dissection permits proper stapling of this vessel.

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Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Triantafillou AN, Heerdt PM, Patterson GA. Lung transplantation. In: Youngberg JA, Lake CA, Roizen MF, et al. eds. Cardiac, thoracic and vascular anesthesia. New York: Churchill Livingstone, 2000:703.

C.6. Should volatile anesthetics be avoided during single-lung ventilation?


Because of experimental evidence demonstrating inhibition of hypoxic pulmonary vasoconstriction (HPV) by the volatile anesthetic agents, some authors have suggested that these drugs be avoided in the anesthetic management of patients with end-stage lung disease requiring single-lung ventilation. However, true clinical significance of these experimental observations remains somewhat controversial. From a clinical standpoint, commonly used doses o f i s o f l u r a n e ( e . g . , e n d -t i d a l c o n c e n t r a t i o n s o f 1 . 0 ) h a v e n o t b e e n e m p i r i c a l l y a s s o c i a t e d w i t h worsening of intrapulmonary shunt and hypoxia. Therefore, isoflurane remains widely used in these patients and may actually benefit some lung recipients because of its bronchodilating properties. (See Chapter 2, section C.13.) P.98 B e n u m o f J L . A n e s t h e si a f o r o n e - l u n g v e n t i l a t i o n [ R e p l y ] . A n e s t h e s i o l o g y 1 9 8 8 ; 6 9 : 6 3 1 . Bjertnaes J, Hauge A, Torgrinson T. The pulmonary vasoconstrictor response to hypoxia: the hypoxia sensitive site studied with a volatile inhibitor. Acta Physiol Scand 1980; 109:447462. Hartigan PM, Pedoto A. Anesthetic considerations for lung volume reduction surgery and lung transplantation. Thorac Surg Clin 2005;15(1):143157. M a r s h a l l B E . A n e s t h e si a f o r o n e - l u n g v e n t i l a t i o n [ L e t t e r ] . A n e s t h e s i o l o g y 1 9 8 8 ; 6 9 : 6 3 0 6 3 1 . Raffin L, Cherqui MM, Sperandio M, et al. Anesthesia for bilateral lung transplantation without cardiopulmonary bypass: initial experience and review of intraoperative problems. J Cardiothorac Vasc Anesth 1992;6(4):409417.

C.7. At what specific points in the procedure are problems anticipated?


Anesthesia induction Lateral positioning Single-lung ventilation Clamping of the PA Graft implantation Graft reperfusion

C.8. What problems are associated with the lateral position?


Single-lung transplantation is usually performed in the lateral decubitus position, often with the upper leg and pelvis angled to allow groin exposure for potential femoral cannulation and CPB. Not surprisingly, position-related changes in venous return, coupled with compression of the dependent lung by the mediastinum and diaphragm, may promote systemic hypotension and ventilation/perfusion mismatch. Furthermore, PA pressure usually tends to rise after lateral

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positioning, probably because of gravity-induced shifts in pulmonary blood flow distribution, vascular congestion, and increased vascular resistance. Triantafillou AN, Heerdt PM, Patterson GA. Lung transplantation. In: Youngberg JA, Lake CA, Roizen MF, et al. eds. Cardiac, thoracic and vascular anesthesia. New York: Churchill Livingstone, 2000:703.

C.9. How does single-lung ventilation affect cardiopulmonary function? What are the problems of single-lung ventilation in this patient? How would you treat them?
Isolated ventilation of the dependent lung is often accompanied by a marked acute increase in peak inspiratory pressure and a subsequent gradual progressive rise in PA pressure. As noted earlier, because of the beneficial effect of gravity on redistributing blood away from the nondependent nonventilated lung, single-lung ventilation is often tolerated better from a respiratory standpoint by patients undergoing single-lung transplantation in the lateral position than those undergoing bilateral lung transplantation in the supine position. Close monitoring of right ventricular performance during conversion to single-lung ventilation is extremely important because of the increase in afterload produced by hypoxic vasoconstriction and redistribution of blood flow. Though unusual, if the right ventricle becomes hypokinetic and distended, and if the ejection fraction decreases, ventilation may have to be altered to minimize airway pressure. P.99 T r i a n t a f i l l o u A N , P a s q u e M K , H u d d l e s t o n C B , e t a l . P r e d i c t o r s , f r e q u e n cy , a n d i n d i c a t i o n s f o r cardiopulmonary bypass during lung transplantation in adults. Ann Thorac Surg 1994;57:1248 1251.

C.10. How would you deal with problems related to clamping of the PA?
To assess the cardiopulmonary response to diverting the entire cardiac output through one lung, progressive occlusion of the vessel is first performed manually (Fig. 4.2). Careful assessment of right ventricular function is performed with the TEE looking for evidence of right ventricular distension or hypokinesis. If well tolerated, the vessel is then clamped and stapled. If occlusion is poorly tolerated, the vessel is unclamped and a pulmonary vasodilator such as prostaglandin E1 or NO and/or positive inotropic infusion begun. If severe respiratory or cardiovascular derangement persists after reclamping of the vessel despite pharmacologic intervention, heparin is administered and CPB instituted to avoid profound hypoxia or right ventricular failure. However, for most patients undergoing single-lung transplantation, hypoxemia during single-lung ventilation and after PA clamping is rarely a problem and right ventricular performance can be adequately maintained. Triantafillou AN, Heerdt PM, Patterson GA. Lung transplantation. In: Youngberg JA, Lake CA, Roizen MF, et al. eds. Cardiac, thoracic and vascular anesthesia. New York: Churchill Livingstone, 2000:703.

C.11. What hemodynamic alterations would you expect during graft implantation and reperfusion? How would you correct them?
During the process of performing the vascular and bronchial anastomoses, major disturbances on cardiac filling and rhythm can be produced (Fig. 4.2). Though often transient, systemic hypotension and pulmonary hypertension can ensue. Transient hypotension may follow the introduction of the vasodilator-containing lung graft preservatives into the systemic circulation. Incomplete de-airing of the lung can lead to coronary air embolism, leading to transient

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myocardial ischemia. The latter is manifested by ST-segment elevation and regional wall P.100 motion abnormalities on TEE. This condition is typically responsive to intravenous nitroglycerin while maintaining perfusion pressures with phenylephrine. After reperfusion and subsequent ventilation of the new lung, PA pressures and arterial blood gases should be closely followed. PA pressure usually falls after reperfusion of the donor organ. If a substantial decrease is not observed, potential causes include anastomotic problems with the atrial cuff or the PA. When pulmonary anastomotic problems are suspected, the surgeon should palpate to assess whether the PA catheter is located proximal or distal to the anastomosis. If a proximal location is confirmed, direct measurement of PA pressures should be performed with a needle connected to pressure tubing handed off the operative field. Assessment of the PA and venous flow pattern by TEE can sometimes be of benefit in evaluating adequacy of the anastomoses. Early graft dysfunction can manifest shortly after reperfusion of the first lung and may be the result of various insults. Occurring in 15% to 35% of cases, early graft dysfunction ranges in severity from modest chest radiograph abnormalities to fulminant pulmonary edema with hypoxia and cardiovascular compromise. Immediate treatment includes adjustment of ventilation, addition of PEEP, and pulmonary vasodilators. Nitric oxide (NO) may be effective for improving oxygenation and reducing PA pressures, and some clinicians advocate prophylactic NO administration although benefit of this intervention has recently been questioned. Should graft dysfunction become evident after implantation of the first lung, but before completion of the second lung transplantation, consideration should be given to initiating CPB. When severe hypoxemia persists after lung transplantation despite maximal medical therapy including the use of inhaled NO, extracorporeal membrane oxygenation (ECMO) is indicated.

Figure 4.2 Tracings of femoral arterial blood pressure, along with pulmonary artery (PA) and central venous (CV) pressures, before and after occlusion of the left PA (A) and during implantation of a left lung graft (B). (All pressures are in millimeters of mercury.)

Date H, Triantafillou AN, Trulock EP, et al. Inhaled nitric oxide reduces human allograft dysfunction. J Thorac Cardiovasc Surg 1996;111:913919. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Perrin G, Roch A, Michelet P, et al. Inhaled nitric oxide does not prevent pulmonary edema after lung transplantation measured by lung water content: a randomized clinical study. Chest

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2006;129(4):10241030. Trulock EP. Lung transplantation. Am J Respir Crit Care Med 1997;155:789.

C.12. When is CPB necessary for lung transplantation?


CPB may be used electively for patients with severe PA hypertension, in whom double-lumen endobronchial tubes cannot be placed, or when visualization of hilar structures is poor. However, in the absence of intraoperative complications, CPB is not desired because it can increase bleeding and blood product usage. It has also been suggested that CPB may aggravate postoperative lung dysfunction although this has not been evident in cases where lung transplant was performed in conjunction with cardiac surgery. Nonetheless, the use of CPB has been associated with longer duration of mechanical ventilation and hospitalization, although it is difficult to differentiate whether the latter results directly from CPB or is the result of a c o m p l i c a t e d p r o c e d u r e t h a t r e s u l t e d i n t h e n e e d f o r C P B . I n d i c a t i o ns f o r C P B i n c l u d e r i g h t ventricular dysfunction not responding to medical therapy, early graft dysfunction occurring during implantation of the second lung during bilateral procedures, and surgical misadventures. Unplanned CPB is reported to occur in 17% to 41% of lung transplantation procedures, but predicting which patients may require this intervention is extremely difficult. Some report that CPB is more likely to be necessary for restrictive lung diseases than obstructive diseases. In an attempt to derive the benefits of CPB while reducing complications, some centers advocate the use of heparin-bound ECMO systems. This approach allows for pulmonary support both during and after the procedure with minimal systemic anticoagulation. P.101 Aeba R, Griffith BP, Kormos RL, et al. Effect of cardiopulmonary bypass on early graft dysfunction in clinical lung transplantation. J Thorac Cardiovasc Surg 1994;57: 715722. de Hoyos A, Demajo W, Snell G, et al. Preoperative prediction for the use of cardiopulmonary bypass in lung transplantation. J Thorac Cardiovasc Surg 1993;106:787795. Lau CL, Hoganson DM, Meyers BF, et al. Use of an apical heart suction device for exposure in lung transplantation. Ann Thorac Surg 2006;81(4):15241525. Parekh K, Meyers BF, Patterson GA, et al. Outcome of lung transplantation for patients requiring concomitant cardiac surgery. J Thorac Cardiovasc Surg 2005;130(3):859863. Triantafillou AN, Pasque MK, Huddleston CB, et al. Predictors, frequency and indications for cardiopulmonary bypass during lung transplantation in adults. Ann Thorac Surg 1994;57:1248 1251. Wang Y, Kurichi JE, Blumenthal NP, et al. Multiple variables affecting blood usage in lung transplantation. J Heart Lung Transplant 2006;25(5):533538.

C.13. Should fluid administration be restricted, and are blood products commonly required?
The amount of crystalloid that can be safely administered intraoperatively without adversely affecting the graft appears to be widely variable. Although efforts should be made to minimize fluid infusion intraoperatively, many patients undergoing lung transplantation require large amounts to maintain hemodynamic stability. Not uncommonly, central venous and pulmonary capillary wedge pressures of 3 to 5 mm Hg immediately after a transplantation are evident despite infusion of large amounts of crystalloid and colloid, as well as only moderate blood loss. Review of fluid management during 215 lung transplantations performed without CPB revealed that intraoperative crystalloid administration varied widely (4 to 32 mL/kg/hour), with a mean of 13 6 mL/kg/hour. Using the PaO2/FIO2 ratio on arrival in the intensive care unit and time to

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extubation as indices of early graft function and initial outcome, this study showed no correlation between the amount of fluids administered and either of these indices. Before the development of the bilateral lung transplantation procedure without CPB, patients with a history of surgery involving the lung or pleura or chronic infectious lung diseases were not deemed acceptable candidates for lung transplantation because of the anticipated excessive bleeding associated with dissecting a scarred lung after anticoagulation for CPB. Now, without the uniform requirement for heparinization, such patients are generally regarded as operative candidates. As with other surgical procedures in which hemorrhage is anticipated, continuous infusion of aprotinin has been proposed to reduce intraoperative bleeding in patients with cystic fibrosis or a history of previous intrathoracic surgery. Interestingly, aprotinin may also have beneficial effects on the function of the transplanted lung after reperfusion. Variables reported to increase the need for blood product usage include the use of CPB, double-lung procedures, and patients with cystic fibrosis. If blood products are to be administered, the anesthesiologist must know whether the patient has antibodies to cytomegalovirus (CMV) and must closely check blood products to confirm they coincide with the patient's status. Bigham M, Dickstein ML, Hogue CW Jr. Cardiac and lung transplantation. In: Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia. Philadelphia: Lippincott Williams & Wilkins, 2001:636. Kyriss T, Wurst H, Friedel G, et al. Reduced blood loss by aprotinin in thoracic surgical operations associated with high risk of bleeding. A placebo-controlled, randomized phase IV study. Eur J Cardiothorac Surg 2001;20(1):3841. P.102 Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Wang Y, Kurichi JE, Blumenthal NP, et al. Multiple variables affecting blood usage in lung transplantation. J Heart Lung Transplant 2006;25(5):533538.

C.14. Would you extubate the patient upon conclusion of the procedure?
Because of the cardiopulmonary insult associated with the procedure, the large postoperative volume shifts, hypothermia, and the frequent need for postoperative bronchoscopy, the trachea of lung transplant recipients is not generally extubated immediately after the procedure. Accordingly, unless intraoperative events (e.g., hyperinflation of the remaining intact lung) suggest that postoperative differential lung ventilation will be required, or unless functional issues such as profound oropharyngeal edema or difficult intubation are present, the doublelumen endotracheal tube is exchanged for a single-lumen tube. In many patients, the endotracheal tube change can be facilitated by use of an exchange catheter. However, great care should be taken to not advance the catheter too far and damage the graft. It is often beneficial to perform fiberoptic bronchoscopy to examine bronchial anastomoses and aggressively suction secretions or blood after replacement of the DLT with a single-lumen endotracheal tube. As with many procedures, careful inspection of the upper airway for edema should be performed with a laryngoscope before removal of the double-lumen endobronchial tube for placement of the single-lumen endotracheal tube.

D. Postoperative Management D.1. What are the major complications after lung transplantation?
Early graft dysfunction, episodes of rejection, infection, and airway complication are the major

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early complications of lung transplantation. Early graft dysfunction varies in severity from mild shunting and chest radiograph infiltrates to gross pulmonary edema. Management is with fluid restriction, diuretics, PEEP, NO, and ECMO for severe cases. Immunosuppression is usually initiated before surgery and the induction phase of therapy is continued for 5 to 10 days. The exact regimen varies between institutions but typically includes azathioprine, steroids, cyclosporine, and polyclonal antilymphocyte/antithymocyte globulins or interleukin-2 receptor antagonists. Acute rejection episodes are usually treated with intense steroid therapy and optimization of other immunosuppressant dosages. A challenge arises in differentiating acute rejection from infection as a source of shunting and chest radiograph infiltrates. Transbronchial biopsy is often necessary to make the distinction from histologic specimens. Bacterial pneumonia is the most frequent infection in the first 2 weeks. Though unusual in the first 2 weeks after transplantation, cytomegalovirus is the second most common source of infectious pneumonitis. This virus is treated with ganciclovir. Broad-spectrum antibiotics are given perioperatively, and the regimen is adjusted based on the results of donor and recipient cultures. Antibiotic therapy for patients with cystic fibrosis is challenging, and the drug chosen is dictated by the patient's cultures and prior history of the organisms colonizing his or her lungs. Prophylactic acyclovir appears to be effective in reducing infections caused by herpes simplex, and trimethoprim-sulfamethoxazole is given to prevent infections from Pneumocystis carinii. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Trulock EP, Edwards LB, Taylor DO, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-second official adult lung and heart-lung transplant report2005. J Heart Lung Transplant 2005;24(8):956967. P.103

D.2. How is postoperative ventilation managed, and for how long is it required?
After most procedures, the FIO2 can be rapidly reduced and weaning from the ventilator can be initiated as soon as the patient is warm and stable. An exception to this approach is the patient who has undergone single-lung transplantation for pulmonary hypertension. Because of a propensity for episodes of cardiopulmonary instability during the first 24 to 48 hours postoperatively, it is usually advantageous to keep these patients sedated, paralyzed, and ventilated during this period. Postoperatively, ventilation/perfusion mismatch and intrapulmonary shunt are often more pronounced after single-lung transplantation than bilateral lung transplantation. Not surprisingly, patients with restrictive disease usually display the best pulmonary function after single-lung transplantation, because the graft receives the majority of both ventilation and perfusion. Alternatively, after single-lung transplantation in emphysemic patients, the remaining native lung often receives a substantial portion of the tidal volume, whereas in pulmonary hypertensive patients, the native lung continues to be ventilated but receives very little blood flow. On rare occasions, differential ventilation of the transplanted and native lung is needed after single-lung transplantation for obstructive lung disease. In these situations, the double-lumen endobronchial tube is left in place and two ventilators are employed. The native lung is ventilated with low tidal v o l u m e ( 2 t o 3 m L / k g ) a n d r a t e , o r e v e n j u s t c o n n e c t e d t o C PA P w i t h o u t i n t e r m i t t e n t m a n d a t o r y ventilation. Nonetheless, the condition usually resolves rapidly with return of spontaneous ventilation. Postural changes in arterial oxygen saturation are often prominent in single-lung transplant recipients. In general, patients who received a single lung for pulmonary hypertension or emphysema display better postoperative pulmonary function with the transplant side up, whereas the opposite may be true in certain patients with restrictive lung disease. The precise

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etiology of this response is unclear but probably reflects positional variation in ventilation/perfusion matching. Bigham M, Dickstein ML, Hogue CW Jr. Cardiac and lung transplantation. In: Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia. Philadelphia: Lippincott Williams & Wilkins, 2001:636. Triantafillou AN, Heerdt PM, Patterson GA. Lung transplantation. In: Youngberg JA, Lake CA, Roizen MF, et al. eds. Cardiac, thoracic and vascular anesthesia. New York: Churchill Livingstone, 2000:703.

D.3. What special precautions should be taken when a lung transplant recipient requires general anesthesia for subsequent nonpulmonary surgery?
In general, after lung transplantation, the patient can be treated like any other ill immunocompromised patient. Recipients have subsequently undergone various surgical procedures unrelated to their pulmonary disease after lung transplantation and have few anesthetic problems. Not surprisingly, differences in the compliance and expiratory flow rates of a native and transplanted lung after single-lung transplantation for emphysema can result in alterations in intraoperative capnography. This phenomenon has been described as producing a biphasic pattern of carbon dioxide exhalation, with the first peak reflecting exhalation from the transplanted lung and the second peak exhalation from the native lung. In addition, the transplanted lung is denervated so the cough reflex is present only in the proximal native airway and mucociliary function is impaired. In contrast, hypoxic pulmonary vasoconstriction is intact after lung transplantation and central respiratory control is unaffected. However, a blunted response to carbon dioxide may persist for patients with preoperative hypercapnia. The major factor limiting long-term survival from lung transplantation is bronchiolitis obliterans. This progressive condition characterized by progressive narrowing of small airways must be considered in patients with prior lung transplantation presenting for surgery and anesthesia after the initial recovery phase. Other perioperative considerations for the patient with a prior lung P.104 transplant undergoing subsequent surgery are based on whether the patient was the recipient of one versus two lungs. In the former case, ventilation/perfusion of the remaining diseased native lung is influenced by the functional status of the transplanted lung. For patients with obstructive lung disease, overinflation of the native lung and resultant mediastinal shift with associated ventilation and hemodynamic consequences, although rare, must be considered when employing positive pressure ventilation. Bigham M, Dickstein ML, Hogue CW Jr. Cardiac and lung transplantation. In: Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia. Philadelphia: Lippincott Williams & Wilkins, 2001:636. C e r z a R A . C a r d i o p u l m o n a r y b y p a s s i n a p o s t - l u n g t r a ns p l a n t p a t i e n t . J C a r d i o t h o r a c V a s c Anesth 1996;10:384386. Myles PS. Pulmonary transplantation. In: Kaplan JA, Slinger PD, eds. Thoracic anesthesia. Philadelphia: Elsevier Science, 2003:295314. Williams EL, Jellish WS, Modica PA, et al. Capnography in a patient after single lung transplantation. Anesthesiology 1991;74:621622.

D.4. What are the long-term outcomes of lung transplantation?


Increased experience and improved techniques have made lung transplantation a realistic option for many patients. However, the procedure is not without substantial risk, and a favorable

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outcome is by no means ensured. Survival is better for patients with COPD compared with those with persistent pulmonary hypertension or idiopathic pulmonary fibrosis. However, there are data to suggest that lung transplant does not have significant survival benefit in patients with COPD. Since 1994, 1-, 3-, 5-, and 10-year survival rates after lung transplantation are 76%, 60%, 49%, and 24%, respectively. The major cause of early mortality is graft dysfunction and infection, and the major causes of late mortality are infection and rejection. Interestingly, there is a relatively high incidence of cancer in the lung transplantation population with over 11% of 5-year survivors developing lymphoma or other malignancy. Trulock EP, Edwards LB, Taylor DO, et al. Registry of the International Society for Heart and Lung Transplantation: twenty-second official adult lung and heart-lung transplant report2005. J Heart Lung Transplant 2005;24(8):956967.

D.5. Are there surgical alternatives to lung transplantation?


Some patients with severe emphysema who are not deemed transplant candidates may benefit from lung volume reduction surgery (LVRS) or reduction pneumoplasty. Performed either through a median sternotomy or through a bilateral thoracoscopy, the goal of LVRS is to remove up to 30% of the patient's most severely compromised lung tissue. Postoperatively, this allows the previously hyperexpanded chest and depressed diaphragm to resume a more normal shape, therefore improving chest wall mechanics and eventually pulmonary function. However, beneficial effects of the procedure are not immediately evident, usually requiring 1 to 2 months. Furthermore, whether the improvement in pulmonary function is sufficient to warrant the risk of the procedure remains controversial. Nonetheless, recent data indicate that for many patients, LVRS represents a viable alternative to transplantation. Tutic M, Lardinois D, Imfeld S, et al. Lung-volume reduction surgery as an alternative or bridging procedure to lung transplantation. Ann Thorac Surg 2006;82(1):208213.

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Chapter 5 Tracheoesophageal Fistula


Jacques H. Scharoun

A 12-Hour-Old Full Term Infant


weighing 2.5 kg presents with choking and cyanosis during its first feed. Neonatal intensive care unit (NICU) staff is unable to pass a feeding tube into the stomach. The baby also has copious oral secretions. Before birth polyhydramnios was seen.

P.106

A. Pathophysiology and Differential Diagnosis A.1. What is the diagnosis? What are the clinical features of this disease?
This patient has esophageal atresia with tracheoesophageal fistula. This occurs in 1 per 4,000 live births. The diagnosis is suspected prenatally by the presence of polyhydramnios caused by failure of the fetus to swallow amniotic fluid (secondary to esophageal atresia). After birth, the neonate will have copious drooling. Attempting to feed the baby will result in coughing and cyanosis. An orogastric tube (OGT) will coil up in the upper esophageal pouch rather than pass into the stomach. Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New York: McGraw-Hill, 2002:1016. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1482. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:550.

A.2. What is the pathophysiology of this disease?


In this abnormality the distal trachea is connected to the lower esophagus through a fistula. This causes three problems. First, inhaled air can bypass the lungs and distend the stomach, which will eventually impede ventilation and cause atelectasis. Second, acidic stomach contents are at continual risk of leaking back into and damaging lung t i s s u e . T h i r d , o r a l s e c r e t i o n s t e n d t o p o o l i n t h e p r o x i m a l e so p h a g e a l p o u c h r e s u l t i n g i n i n t e r m i t t e n t a s p i r a t i o n , c o u g h i n g , a n d c y a n o s i s. Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New York: McGraw-Hill, 2002:1016. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1482.

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Hammer GB. Pediatric thoracic anesthesia. Anesth Analg 2001;92:14491464.

A.3. How does this lesion occur during development?


The median ventral diverticulum of the foregut differentiates into a separate esophagus and trachea by the end of the fifth week of gestation. New insights into the embryologic o r i g i n o f T E F c o m e f r o m r a t s t u d i e s w h e r e i n f e t a l r a t s e xp o s e d t o A d r i a m y c i n r e l i a b l y produce TEF closely resembling the most common version seen in humans. In this model, the lung bud was found to trifurcate instead of normal bifurcation. Two branches become normal lung with pseudostratified columnar epithelium. The third branch grows caudally until it merges with the distal esophagus. Hence the fistula comes from respiratory tissue. Bolstering this conclusion is the finding that the fistula expresses thyroid transcription factor-1 (TTF-1), which is found only in respiratory tissue of the foregut. Human studies also corroborate this finding. Sonic Hedgehog (Shh) is a secreted signaling glycoprotein involved in directing differentiation of the foregut and lung. Defective Shh signaling is associated with VACTERL type anomalies (including T E F ) i n S h h - k n o c k o u t m i c e s t u d i e s . T i s s u e w a s s u r g i ca l l y o b t a i n e d f r o m t h e e s o p h a g e a l pouch and fistula in neonates undergoing repair of TEF. This tissue was then stained to detect Shh. The proximal pouch, but not the fistula, stained positive for Shh. This suggests that the fistula is not an esophageal structure, despite superficial resemblance. P.107 Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1481. Crisera CA, Grau JB, Maldonado TS, et al. Defective epithelial-mesenchymal interactions dictate the organogenesis of Tracheoesophageal fistula. Pediatr Surg Int 2000;16:256261. Kim JH, Kim PCW, Hui C. The VACTERL association: lesions from the Sonic hedgehog pathway. Clin Genet 2001;59:306315. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:550. Spilde T, Bhatia A, Ostlie D, et al. A role for Sonic hedgehog signaling in the pathogenesis of human Tracheoesophageal fistula. J Pediatr Surg 2003;38(3):465468.

A.4. How are different types of TEF classified?


There are five types of TEF according to the classic Gross classification Type A is pure esophageal atresia with no involvement of the respiratory tree. This occurs in 8% of cases. Gross Type B has esophageal atresia and a fistula connecting the proximal e s o p h a g e a l p o u c h t o t h e t r a c h e a . T h i s o cc u r s i n l e s s t h a n 1 % . T h e m o s t c o m m o n i s t y p e C with esophageal atresia and fistula linking the distal esophagus to the trachea. This occurs in 75% to 80% of cases. Rarely, type D occurs with two fistula connecting both proximal and distal esophagus to the trachea (2%). Type E, known as an H-type fistula has no atresia. Instead, an intact esophagus has a linkage with trachea through a fistula, and it occurs in 4%. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1481.

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M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:551.

A.5. What other problems may this child have, and when should these be investigated?
Unfortunately TEF often does not occur in isolation. Serious additional anomalies can occur in the spectrum known as VACTERL (formerly known as VATER)

V = vertebral anomalies A = anal canal defect (anal atresia) C = cardiac malformation (ventricular septal defect [VSD], atrial septal defect [ A S D ] , T e t r a l o g y o f F a l l o t , r i g h t s i d e d a r c h , p a t e n t d u ct u s a r t e r i o s u s [ P D A ] ) TE = TEF R = renal dysplasia L = limb defect (radial aplasia)

A p a t i e n t i s c o n s i d e r e d t o h a v e V A C T E R L a ss o c i a t i o n w i t h t h e p r e s e n c e o f t h r e e o r m o r e of these lesions. Nearly one-third of TEF patients will have an additional VACTERL lesion and an additional one-fifth will have two VACTERL problems. Nearly half of children with TEF will have significant cardiac disease including ASD, bilateral superior vena cava (SVC), and VSD. Other possible gastrointestinal (GI) problems include malrotation of the midgut, and duodenal atresia. Renal problems can include malposition, hydronephrosis, and ureteral abnormalities. P.108 Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1782. Diaz LK, Akpek EA, Dinavahi R, et al. Tracheoesophageal fistula and associated congenital heart disease: implications for anesthetic management and survival. Pediatr Anesth 2005;15:862869. Krosnar S, Baxter A. Thoracoscopic repair of esophageal atresia with Tracheoesophageal fistula: anesthetic and intensive care management of a series of eight neonates. Pediatr Anesth 2005;15:541546. M c M u l l e n K P , K a r n e s P S , M o i r C R , e t a l . F a m i l i a l r e c u r r e n ce o f t r a c h e o e s o p h a g e a l fistula and associated malformations. Am J Med Genet 1996;63:525528.

A.6. What should the parents be told regarding perioperative risk?


The survival of TEF babies has improved over the years because of improvements in intensive care unit (ICU) care, anesthesia, and surgical technique. Waterston developed the first classification of prognosis of TEF in 1962 as follows:

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Group A: birth weight greater than 2.5 kg, healthy, survival 95% Group B: birth weight 1.8 to 2.5 kg and healthy, or greater than 2.5 kg with moderate pneumonia, or other anomalies, survival 68% Group C: birth weight less than 1.8 kg or greater than 1.8 kg with severe pneumonia or severe congenital anomaly, survival 6%

With improvements in neonatal care, the survival in groups A and B both approach 100%, so new classification systems have been developed to provide more useful information, as birth weight greater than 1.5 kg no longer independently predicts m o r t a l i t y . O f t h e s e p e r h a p s t h e m o s t u se f u l i s t h e S p i t z c l a s s i f i c a t i o n , w h i c h i s predicated on finding that cardiac disease is leading risk factor and/or cause of mortality in the TEF group.

Spitz group I: birth weight more than 1.5 kg, no major cardiac disease. Survival 97% Spitz group II: birth weight less than 1.5 kg, or major cardiac disease. Survival 59% Spitz group III: birth weight less than 1.5 kg and major cardiac disease. Survival 22%

This date was based on a review of 372 infants from 1980 to 1992. With ongoing improvement in care, A recent review of 188 cases from 1993 to 2004 found Spitz group I survival 99%, group II 82%, and group III 50%. Choudhury SR, Ashcraft KW, Sharp RJ, et al. Survival of patients with esophageal atresia: influence of birth weight, cardiac anomaly, and late respiratory complications. J Pediatr Surg 1999;34:7074. Konkin DE, O'Hali WA, Webber EM, et al. Outcomes in esophageal atresia and Tracheoesophageal fistula. J Pediatr Surg 2003;38:17261729. Lopez PJ, Keys C, Pierro A, et al. Oesophageal atresia: improved outcome in high-risk groups? J Pediatr Surg 2006;41:331334. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:550. P.109

B. Preoperative Evaluation and Preparation B.1. What laboratory workup should be obtained before surgery?
Firstly, one must assess the presence and severity of pulmonary disease, especially looking for aspiration pneumonia, and respiratory distress associated with prematurity. Plain chest x-ray may show infiltrates. A radio-opaque orogastric tube (OGT) will be coiled in the proximal esophageal pouch, whereas an abdominal x-ray may show air in

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the bowels entering through the fistula. Because of the risk of aspiration, use of contrast dye to delineate the fistula should be used only when there is diagnostic uncertainty. Ideally, contrast would be given under fluoroscopy so that any aspiration can be immediately detected. This should only be done if the baby is stable enough to be transported to the fluoroscopy suite. Of note, an OGT that appears to enter the stomach may also reflect esophageal perforation caused by repeated traumatic insertion attempts. Second, an echocardiogram is mandatory as major cardiac defects strongly influence survival and may impact on anesthetic management. In addition, one wants to look for presence of a right-sided aortic arch, because this may affect the positioning and surgical approach. Spinal plain films should be done to exclude vertebral anomalies, especially if epidural pain management is being considered. Renal ultrasound should be done to rule out abnormalities, especially hydronephrosis. In addition, complete blood count (CBC), arterial blood gas, and electrolytes should be drawn, and at least 1 unit of packed red blood cells should be type and crossed. Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New York: McGraw-Hill, 2002:986, 1017. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1482. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:551.

B.2. What options are there if patient has severe lung disease?
In the past, most children with TEF were routinely given a gastrostomy (under local) followed by a staged repair. Beginning in the 80 s, this conservative management began to be questioned, and now primary repair is considered standard of care. However, there remains a subset of neonates with severe pneumonia or respiratory distress syndrome (RDS) who are considered a poor anesthetic and surgical risk (Waterston type C). If the child is intubated because of respiratory disease one technique to optimize ventilation while minimizing gastric distension (through the fistula) is to employ high frequency oscillator ventilation to minimize the peak inspiratory pressure. If this is insufficient, a simple gastrostomy is placed to allow drainage of gastric fluid (to minimize further aspiration) and prevent or relieve gastric distension that can occur with positive pressure ventilation (PPV) in the setting of a type C TEF. This procedure can be p e r f o r m e d u n d e r l o c a l a n d o b v i a t e s t h e n e e d f o r a t h o r a co t o m y . T h e p r o b l e m w i t h t h i s approach is that by decompressing the stomach, gas from the trachea can now bypass t h e l u n g s a n d e x i t t h r o u g h t h e s t o m a c h . T h i s i s e s p e c i a l l y a c o n ce r n i f t h e b a b y ' s l u n g s are noncompliant from pneumonia or RDS. This can make it difficult or impossible to ventilate the baby adequately. Fortunately, this can be alleviated if the gastrostomy tube is placed underneath a water seal therefore allowing gas to escape when it exceeds a predetermined threshold. More recently, Ratan SK et aldescribe another salvage technique which involves occluding the fistula retrograde through a gastrostomy: The child is given local

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anesthetic over the incision site and a styletted 10 French Foley catheter is advanced through a gastrostomy to a position P.110 just above the gastroesophageal junction using fluoroscopy. The balloon is then inflated and the catheter is either clamped or placed under water seal. In this way the baby could be ventilated with positive pressure while avoiding gastric distention or inadequate ventilation from gas bypassing lungs. This technique runs the risk of esophageal rupture and fatal pneumothorax if the catheter is not placed properly. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1483. O x f o r d J , C a s s D T , G l a s so n M J . A d v a n c e s i n t h e t r e a t m e n t o f o e s o p h a g e a l a t r e s i a o v e r three decades: the 1970s and the 1990s. Pediatr Surg Int 2004;20:402407. Ratan SK, Rattan KN, Ratan J, et al. Temporary transgastric fistula occlusion as salvage procedure in neonates with esophageal atresia with wide distal fistula and moderate to severe pneumonia. Pediatr Surg Int 2005;21:527531. Shaul DB, Schwartz MZ, Marr CC, et al. Primary repair without routine gastrostomy is t h e t r e a t m e n t o f c h o i c e f o r n e o n a t e s w i t h e so p h a g e a l a t r e s i a a n d T r a c h e o e s o p h a g e a l fistula. Arch Surg 1989;124:11881190.

B.3. Describe management in the NICU before surgery


After diagnosis of TEF is established and other coexisting anomalies investigated, the baby should be immediately made NPO (nothing by mouth). He should be kept in a warmed isolette with the head elevated at least 30 degrees to minimize reflux through the fistula. An nasogastric tube (NGT) should be placed in the proximal esophageal pouch and kept on intermittent suction to minimize aspiration of oral secretions. Antibiotics to treat aspiration pneumonia should be given when appropriate. Ampicillin and gentamicin should be given in those patients who have coexisting significant cardiac d i s e a s e a s p r o p h y l a xi s . E n s u r e t h a t b l o o d i s a v a i l a b l e f r o m t h e b l o o d b a n k . B e c a u s e t h e patient will require a thoracotomy with lung retraction and intermittent compression of the trachea and great vessels, an arterial line is mandatory for the case. This should ideally be placed in the NICU. An umbilical artery line may be conveniently placed by a qualified neonatologist. Two additional IV lines should also be placed, as the patient will be NPO. Avoid placing lines in the right arm as this arm will most likely be elevated with l i m i t e d a c c e s s d u r i n g r i g h t t h o r a co t o m y a n d a c c e s s l i m i t e d . Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New York: McGraw-Hill, 2002:986, 1017. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1483. Hammer GB. Pediatric thoracic anesthesia. Anesth Analg 2001;92:14491464. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:551.

B.4. Should these patients be routinely intubated

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preoperatively for airway protection?


Unless mandated by severe pulmonary disease, the child is not intubated routinely preoperative to minimize the possibility of gastric distension from PPV through the fistula. It is noted that intubation does not protect the child from aspiration of gastric contents through the fistula. P.111 Hammer GB. Pediatric thoracic anesthesia. Anesth Analg 2001;92:14491464.

C. Intraoperative Management C.1. What IV access and monitoring are appropriate before induction? After induction?
At least one peripheral IV should be in place before induction. A second may be placed after patient is anesthetized. If the surgeon intends to give the child total parenteral nutrition (TPN) postoperatively, a central may be placed. Arterial line placement for blood gas and hemodynamic monitoring should be placed before incision if it has not a l r e a d y b e e n i n s e r t e d i n t h e N I C U . I f a p e ri p h e r a l A - l i n e i s n o t f e a s i b l e , a n u m b i l i c a l arterial line may be placed by someone experienced in this technique. ECG, oxygen saturation, end-tidal CO2, and rectal temperature should be also be monitored. A precordial stethoscope should be placed over the left axilla to assess breath sounds in case of inadvertent movement of the endotracheal tube (ETT) during surgical retraction or positioning. A second precordial stethoscope placed over the stomach may be useful to assess if the fistula is being ventilated. If a gastrostomy tube is present, the end may be placed underneath a water seal. The presence of bubbling indicates ventilation through the fistula, which will occur if the tip of the ETT is proximal to the opening of the fistula. A capnograph inserted into the gastrostomy tube will indicate the same thing. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:552.

C.2. Discuss fluid and temperature management for this baby


As with all neonates undergoing surgery, meticulous attention to fluid management and temperature is essential. The child should be transported to the operating room (OR) (in head up position) in a warmed isolette, with a stocking cap on the head to minimize temperature shifts. The OR should be prewarmed to at least 85F. Surgical irrigation and IV crystalloid should be warmed, as well as any blood products stored on ice. Using a forced-air convective warming system is strongly recommended. An appropriate size heat-moisture exchanger placed in the airway can be useful. Keep in mind that the neonate is more prone to develop hypothermia for a number of reasons including limited s u b c u t a n e o u s f a t . O n e w a y t h e b a b y c o m p e n s a t e s i s w i t h b r o w n f a t n o n sh i v e r i n g thermogenesis. When choosing anesthetic technique, keep in mind that volatile anesthetics including halothane and isoflurane can decrease thermogenesis by up to 70%. Considering that the patient has been NPO since birth (and what ever was fed probably

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did not reach the stomach because of esophageal atresia, it is advisable to administer dextrose-containing solution at a controlled rate during the operation. D10/0.2 NS administered intravenously at maintenance rate using a controlled-infusion pump is an excellent way to avoid hypoglycemia. Insensible losses should be estimated at 3 to 4 mL/kg/hour and replaced with isotonic solution. Urine output (ideally 1 mL/kg/hour) may be difficult to assess accurately in a lowbirth weight baby. Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New York: McGraw-Hill, 2002:1003, 1012. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1483. P.112 M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:541.

C.3. What are the options regarding induction and intubation?


The goal is to intubate the baby to allow adequate gas exchange with the lowest possible inspiratory pressure needed to inflate the lungs, avoid atelectasis, and avoid distension of the abdomen. Positive pressure mask ventilation should be avoided. There are several options. First is to keep the child spontaneously ventilating until the fistula is ligated. This requires a deep inhalational technique with gentle assisting of each breath to minimize atelectasis. Intubation can performed either awake or after inhalation induction. In this way, the lowest inspiratory pressure is required, minimizing distension of the stomach. Awake intubation used to be common, but attention must be paid to the possibility of increased intracranial pressure or intraventricular hemorrhage in the premature infant, as well as the obvious discomfort to the child. Good intubating conditions can be achieved with deep volatile agent, but maintaining adequate ventilation and surgical conditions during a thoracotomy without relaxant may be challenging. Rapid sequence IV induction and intubation (to minimize face-mask ventilation) is another option provided attention is paid to minimizing inspiratory pressure. As important as the intubation is the correct positioning of the ETT. The goal is to have the tip of the ETT distal to the fistula yet proximal to the carina. If the tube is deliberately placed deep (into the right mainstem) with the bevel facing forward, then slowly pulled back just until breath sounds occur on the left equal to the right, the tube is likely to be in good position. If the patient has a preexisting gastrostomy, the ETT should be pulled back almost until gas begins to bubble from the end of the gastric tube (which has been placed under water seal), then readvanced until the bubbling stops. If the tube is in good position, then the child can be paralyzed and normal positive p r e s s u r e v e n t i l a t i o n ( P P V ) m a i n t a i n e d . T h e d i f f i c u l t y l i e s i n m a i n t ai n i n g g o o d p o s i t i o n o f the ETT during surgical manipulation and turning the patient lateral. Andropoulos DB, Rowe RW, Betts JM. Anaesthetic and surgical airway management during Tracheoesophageal fistula repair. Pediatr Anaesth 1998;8:313319. Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New

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York: McGraw-Hill, 2002:1017. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:552.

C.4. What is the role of fiberoptic bronchoscopy in this patient?


Perioperative bronchoscopy before commencing TEF repair has become common for two reasons. First, the airway can be examined directly to help guide the surgical technique. Second, if deemed appropriate, the fistula can be occluded using a Fogarty occlusion catheter, thereby allowing unimpeded PPV without distending the abdomen. Kosloske AM et al. in 1988 reported a series of 42 neonates with TEF who underwent bronchoscopy before incision. They reported 31% had crucial findings impacting on the surgical technique, especially with regard to level of fistula (a cervical level fistula does not necessarily require thoracotomy). Identifying the level of the fistula can assist in correct positioning the ETT (11% may have it below the carina in one series). Reeves, Burt, and Smith report using a rigid bronchoscope to guide placement of a 2-French Fogarty arterial embolectomy catheter into the TEF and the balloon inflated. The bronchoscope was removed and the patient was then intubated using a 3.0 ETT. Andropoulos, Rowe and Betts describe 61 cases of TEF managed with rigid bronchoscopy. Three babies (those with large fistula) electively had their fistula occluded and all three experience immediate improvement in P.113 ventilation. If the fistula was small, it was deemed unlikely to cause ventilatory problems and was left unmodified. Another seven had a catheter placed in the fistula to help the surgeon identify it. This technique of isolating the trachea and esophagus before ligation may be useful in skilled hands. However, there is a real possibility that during positioning or surgical manipulation, the Fogarty balloon may slide back into the trachea. This could precipitate immediate complete airway obstruction if not promptly recognized and treated. Andropoulos DB, Rowe RW, Betts JM. Anaesthetic and surgical airway management during Tracheoesophageal fistula repair. Pediatr Anaesth 1998;8:313319. Kosloske AM, Jewell PF, and Cartwright KC. Crucial bronchoscopic findings in esophageal atresia and Tracheoesophageal fistula. J Pediatr Surg 1988;23:46670. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:552. Reeves ST, Burt N, Smith CD. Is it time to reevaluate the airway management of Tracheoesophageal fistula? Anesth Analg 1995;81:866869. V e y c k e m a n s F , H a m o i r M , R o m b a u x P , e t a l . P re o p e r a t i v e t r a c h e o s c o p y i n n e o n a t e s w i t h esophageal atresia (letter). Anesth Analg 2002;96:18271828.

C.5. Discuss the surgical technique


First, the patient is positioned in the lateral position, usually left side down. If the patient has a right-sided aortic arch sometimes the surgeon may wish to position him with right side down. A retropleural approach is used which minimizes the danger from

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an anastomotic leak. The fistula is exposed and ligated (usually occurs within 45 minutes). The upper esophagus is mobilized, then the distal esophagus. The esophagus is joined together. Following this, a feeding tube is placed across the anastomosis to allow feeding (if the patient does not have a gastrostomy). The lung should be carefully reexpanded to eliminate atelectasis before closure. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005.

C.6. Discuss common intraoperative problems for this repair


Interference with ventilation is the most common problem and can have many causes. Lung retraction with resulting atelectasis leads to frequent desaturation. It may be difficult if not impossible to maintain normocarbia. The PCO2 may rise to 7080 mm Hg despite all attempts to optimize ventilation. If the patient has a Fogarty catheter in the fistula, it may be displaced into the trachea causing total airway obstruction. Surgical manipulation of the soft trachea makes it vulnerable to kinking or displacement of ETT distal (into right mainstem) or proximally (above the fistula). Frequent compression of vital structures in the mediastinum can lead to profound hemodynamic compromise. Blood and secretions are a constant problem, which risk obstructing the tube. The ETT should be suctioned frequently, more so if blood is seen. (It does not require much blood to clog a 3.0 ETT.) The retracted lung may need to be intermittently reexpanded to avoid severe hypoxia. Severe gastric distension before ligation of the TEF may require emergent gastric needle decompression. It is crucial to maintain close communication with the surgeon. Avoid hypothermia. Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New York: McGraw-Hill, 2002:1017. P.114 M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:552.

D. Postoperative Issues D.1. When should the baby be extubated?


Although some surgeons prefer to have the baby extubated immediately in the OR to minimize tension on the suture line, this can be risky. Tracheomalacia can precipitate airway obstruction requiring immediate reintubation. Many of the children have lung disease from prematurity or aspiration pneumonia. After receiving narcotics for pain they may be prone to hypoventilation. If early extubation is planned an epidural technique might be helpful. However, if the child is to remain intubated, care should be made to limit inspiratory pressure to protect the repair from disruption. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005:1483. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:552.

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D.2. What pain control options are available?


If the patient is going to remain intubated postoperative (most likely) then a narcotic technique is advisable. Fentanyl at 10 to 20 g per kg with muscle relaxant will give hemodynamic stability and allow analgesia to be continued in the postoperative period. F o r e x p e r i e n c e d p r a c t i t i o n e r s , e p i d u r a l c a n a l s o b e p l a ce d . A n e p i d u r a l c a t h e t e r threaded through the caudal space can be threaded up to the thoracic dermatomes. Check the placement of the catheter using fluoroscopy before using it. This technique should only be undertaken by someone highly experienced in regional anesthesia for children, with full awareness of the risks and ability to manage complications. Bissonnette B, Dalens B, eds. Pediatric anesthesia: principles and practice, 2nd ed. New York: McGraw-Hill, 2002:549, 1017.

D.3. What are early and late complications of TEF repair?


Early anastomosis leakage occurs in up to 15%. This may require immediate exploration, or managed expectantly. Esophageal dysmotility, and gastroesophageal reflux disease (GERD) are common. Stricture of the esophageal anastomosis may require repeated dilatations. Tracheomalacia may be evident postoperative and vocal cord paresis has been reported. Brunicardi FC, Anderson DK, Billiar TR, et al. eds. Schwartz's principles of surgery, 8th ed. New York: McGraw-Hill, 2005. Diaz LK, Akpek EA, Dinavahi R, et al. Tracheoesophageal fistula and associated congenital heart disease: implications for anesthetic management and survival. Pediatr Anesth 2005;15:862869. M o t o y a m a E K , D a v i s P J , e d s. S m i t h ' s a n e s t h e s i a f o r i n f a n t s a n d c h i l d r e n , 7 t h e d . Philadelphia: Mosby, Elsevier Science, 2006:552.

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Chapter 6 Congenital Diaphragmatic Hernia


Fun-Sun F. Yao David Stein John J. Savarese

A Full-Term Male Baby


w as born with r espiratory dis tress and cy ano sis . Ph ysical exa mina tio n sho wed bar rel ch est a nd sc aph oi d ab do men . Th e br eath sou nds we re a bse nt in the le ft side o f the ch est; th e he art so un ds wer e be st he ard in the r ig ht side o f the chest. L ab ored r espi ra tio n, n asal fl ari ng , an d ster nal re traction were foun d. T he b ab y weighe d 2 ,800 g. Bl oo d pr essu re wa s 60/3 0 mm Hg ; hea rt ra te, 16 0 be ats p er min ute ; r esp ira tion, 7 0 brea ths per minute; temp erature, 36 C (96.8F). Arterial blood gas anal ysis on room a ir sho wed th e fol l owi ng : pH, 7 .20; PCO 2 , 55 mm Hg; PO2, 35 mm Hg; and CO 2 co nte nt, 19 mEq p er L .

P.116

A. Medical Disease and Differential Diagnosis A.1. What differential diagnoses are compatible with these signs and symptoms?
Congenital cardiopulmonary anomalies should be considered whenever cyanosis and respiratory distress are present. A scaphoid abdomen is present due to the absence of abdominal contents. The presence of the barrel chest, bowel sounds in the chest, and the shift of heart sounds to the r i g h t d e f i n i t e l y s u g g e s t t h e d i a g n o s i s o f C D H . To c o n f i r m t h e d i a g n o s i s , a c h e s t r a d i o g r a p h should be performed to demonstrate gas-filled loops of bowel and probably the spleen or liver in the chest. The lung on the side of the hernia is compressed into the hilum, and the mediastinum is shifted to the opposite side of the chest. If in doubt, radiopaque dye may be injected through a nasogastric tube to delineate the stomach and intestine in the chest. Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:11941196. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002: 435. P.117 Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:696697.

A.2. Describe the incidence and classification of CDH


The incidence of CDH is estimated to be 1 in 2,500 to 5,000 births. The male/female ratio is 2:1, and the left diaphragm is more frequently involved than the right (5:1).

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The diaphragm is embryologically formed from the fusion of several components; therefore, a number of developmental defects may occur, resulting in herniation of abdominal contents into the chest. Embryologically, two fundamental types of defects may occur:

Complete or partial absence of the diaphragm Failure of complete muscularization

Embryologic classification is not convenient clinically. A practical classification is used based on the anatomic location of the defects in the diaphragm:

Absent diaphragm. Very rare Diaphragmatic hernia. (Fig. 6.1)


Posterolateral (Bochdalek): 80% Anterior (Morgagni): 2% Paraesophageal: 15% to 20%

Eventration. Very rare

Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:11941196. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550.

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Figure 6.1 Potential sites of congenital diaphragmatic hernia.

P.118

A.3. What are the causes of hypoxemia in patients with CDH?


The causes of hypoxemia are as follows:

Atelectasis resulting from compression of the developed lung by the herniated abdominal organs

Pulmonary hypoplasia with a decrease in the number of alveoli and bronchial generations. The hypoplastic lung will have abnormal pulmonary vasculature resulting from a disruption of normal development of the lung tissue, secondary to the crowding of the herniated abdominal organs in the thorax.

Persistent pulmonary hypertension, causing increased right-to-left shunting through a patent foramen ovale and ductus arteriosus

Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:435436. Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:696697.

A.4. How does the diaphragmatic hernia develop in the fetus? Why do varying degrees of pulmonary hypoplasia usually accompany CDH? How do they affect the prognosis?
Embryologic development of the diaphragm, gut, heart, and lungs takes place at about the same time, and abnormal development of one organ affects development of the others. Normally, the pleural and peritoneal cavities are separated by the diaphragm from the 8th to the 10th week of gestation. At about the same time, the gut physiologically herniates into the yolk stalk but then returns to the peritoneal cavity. The pleuroperitoneal canals progressively narrow and are finally closed by the 10th week. CDH may result either from the early return of the midgut to the peritoneal cavity or from delayed closure of the pleuroperitoneal canal. The lung is also undergoing development at this time. Alveolar buds begin to differentiate by the 6th week; airways develop from the 10th to the 12th week. Bronchial branching continues until the 16th week of gestation. Alveolar multiplication continues until 8 years of age. The degree of pulmonary hypoplasia is related to the timing of the herniation of abdominal organs into the pleural cavity. The earlier the herniation, the more severe the pulmonary hypoplasia. Hypoplasia of the left ventricle may also occur, resulting in cardiac insufficiency. The degree of pulmonary hypoplasia determines the prognosis of CDH. Severe bilateral hypoplasia predicts high mortality. With unilateral hypoplasia, the patient may survive with aggressive therapy. When pulmonary hypoplasia is insignificant, the prognosis is excellent. Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams &

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Wilkins, 2006:11941196. Behrman RE, Kliegman RM, Jenson HB, eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Berdon WE, Baker DH, Amoury R, et al. The role of pulmonary hypoplasia in the prognosis of newborn infants with diaphragmatic hernia and eventration. Am J Roentgenol 1968;103:413421. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002: 435. P.119 Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550.

A.5. How do you assess the severity of pulmonary hypoplasia?


The severity of pulmonary hypoplasia is assessed by the intrapulmonary shunt (QS/QT) or the alveolararterial difference in oxygen tension (PaO2PaO2). A (PaO2PaO2) of more than 500 mm Hg when breathing 100% oxygen is predictive of nonsurvival, and a (PaO2PaO2) of less than 400 mm Hg is predictive of survival. A (PaO2PaO2) between 400 and 500 mm Hg represents a zone of uncertain prognosis. The severity of pulmonary hypoplasia may also be evaluated more aggressively by cardiac catheterization and pulmonary angiogram to define the size and branching pattern of the pulmonary arteries. Patients with severe pulmonary hypoplasia typically will have a fixed rightto-left shunting at the level of the patent ductus arteriosus or patent foramen ovale caused by pulmonary hypertension. Pulmonary angiography demonstrates a small diameter of affected pulmonary artery compared with the main pulmonary artery. The postductal PaO2 never rises to more than 60 mm Hg in nonsurvivors. Harrington J, Raphaely RC, Downes JJ, et al. Relationship of alveolar-arterial oxygen tension difference in diaphragmatic hernia of the newborn. Anesthesiology 1982;56: 473. Vacanti JP, Crone RK, Murphy JD, et al. The pulmonary hemodynamic response to perioperative anesthesia in the treatment of high-risk infants with congenital diaphragmatic hernia. J Pediatr Surg 1984;19:672679.

A.6. Discuss persistent pulmonary hypertension in the patient with CDH


Pulmonary hypertension is one of the major causes of hypoxemia in CDH. There are several causes of pulmonary hypertension in these patients:

Increased pulmonary vascular resistance and pressure result from a hypoplastic lung. The pulmonary vasculature is abnormal, with a decrease in volume and marked increase in muscular mass in the arterioles.

Right-to-left shunting of oxygen depleted venous blood at the patent foremen ovale and the patent ductus arteriosus. This shunting results in varying degrees of hypoxemia, hypercarbia, and acidosis causing high pulmonary vascular resistance and pressure.

When pulmonary artery pressures are higher than systemic pressures, right-to-left shunting occurs across the ductus, resulting in higher PaO2 in the upper extremities than in the lower extremities. When right ventricular failure (precipitated by pulmonary hypertension, progressive hypoxemia, and acidosis or by closure of the ductus) increases right atrial pressure to a level

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higher than the left atrial pressure, right-to-left atrial shunting ensues, producing further hypoxemia. Left ventricular failure from hypoxemia and acidosis induces systemic hypotension, resulting in increased ductal shunting and hypoxemia. A vicious cycle is established. Unless pulmonary artery pressure is decreased, progressive hypoxia and death may ensue. Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:11941196. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. P.120 Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:424425, 435, 887. Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550.

A.7. How do you make a diagnosis of right-to-left shunting through the patent ductus arteriosus or patent foramen ovale?
If right-to-left shunting occurs through the patent ductus arteriosus, the preductal PaO2 is at l e a s t 1 5 t o 2 0 m m H g h i g h e r t h a n t h e p o s t d u c t a l v a l u e . A r i g h t - t o - l e f t s h u nt o f 2 0 % i s c o n s i d e r e d normal for a newborn infant. If shunting occurs through the patent foramen ovale, the preductal PaO2 is below the value predicted for 20% shunt. When the degree of preductal shunting is severe, detection of ductal shunting is impossible. Echocardiography with color Doppler, cardiac catheterization, and pulmonary angiography will confirm the diagnosis. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:11711173. Nelson NM, Prod'Hom LS, Cherry RB, et al. Pulmonary function in the newborn infant: the alveolar-arterial oxygen gradient. J Appl Physiol 1963;18:534. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:696697.

A.8. What other congenital anomalies are usually associated with CDH?
The incidence of other congenital anomalies in newborns with CDH is as follows:

Cardiovascular system. 13% to 23%; for example, atrial septal defect, ventricular septal defect, coarctation of aorta, and tetralogy of Fallot

Central nervous system. 28%; for example, spina bifida, hydrocephalus, and acephalus Gastrointestinal system. 20%; for example, malrotation and atresia Genitourinary system. 15%; for example, hypospadias

David TJ, Illingworth CA. Diaphragmatic hernia in the southwest of England. J Med Genet 1976;13:253. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:11711173.

B. Preoperative Evaluation and Preparation

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B.1. How would you interpret the following arterial blood gas analyses: pH, 7.20; PCO 2 , 55 mm Hg; PO2, 35 mm Hg; and CO 2 content, 19 mEq per L? How would you correct them?
The blood gas analyses showed mixed respiratory and metabolic acidosis and severe hypoxemia. Severe hypoxemia is caused by the pulmonary pathologies and persistent pulmonary hypertension (PPH). Hypoxemia stimulates respiratory chemoreceptors and causes hyperventilation, resulting P.121 in respiratory alkalosis initially. However, if hypoxemia is not corrected, the patient will become exhausted and CO2 retention ensues. Severe pulmonary hypoplasia may also cause CO2 retention. Severe hypoxemia induces anaerobic metabolism, resulting in lactic acidosis. Hypoxemia and respiratory acidosis should be treated with mechanical ventilation and oxygen therapy. Metabolic acidosis should be corrected by administration of sodium bicarbonate and improvement of circulation with fluid therapy. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:435437. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:696697.

B.2. What immediate treatment should be given to improve the newborn's respiratory status preoperatively?
Immediate intervention should include decompression of the stomach with an orogastric or nasogastric tube and administration of supplemental oxygen by mask. Positive pressure ventilation by mask should be avoided to prevent distention of the intrathoracic stomach, which will further compress the lung and compromise respiration. If cyanosis and hypoxemia persist, awake intubation should be done to facilitate mechanical ventilation. Positive airway pressure during mechanical ventilation should not exceed 30 cm H2O to reduce the risk of tension pneumothorax. Although pneumothorax can happen on either side, it occurs more frequently on the contralateral side of the hernia because the pressure needed to expand the hypoplastic lung is higher than that required to rupture the normal lung. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:435437. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:696697.

B.3. Should CDH be repaired urgently once the diagnosis is made and confirmed?
In the past, CDH was considered a surgical emergency, in the belief that the herniated contents caused lung collapse and respiratory failure. However, recognition of the role of pulmonary hypertension, in addition to pulmonary hypoplasia and the effects of surgical repair on pulmonary function, has prompted critical reevaluation of that strategy. It is now clear that lung compression by the herniated viscera is a minor factor in the cardiopulmonary compromise compared with the pulmonary hypertension and hypoplasia. The consensus today is to delay surgery and concentrate on medical stabilization. The goal of preoperative therapy is to reverse the PPH that results in right-to-left shunting across the patent foramen ovale and the ductus

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arterious. Improvement in the infant's status is apparent by improved oxygenation and ventilation. Doppler echocardiography may be used to confirm the decreased pulmonary vascular resistance. The time it takes to stabilize the condition varies from 24 to 48 hours in infants with only mild pulmonary hypertension and hypoplasia up to 7 to 10 days in neonates with severe pulmonary hypertension and hypoplasia. P.122 Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:11941196. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Charlton AJ. The management of congenital diaphragmatic hernia without ECMO. Paediatr Anaesth 1993;3:201. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:436437. Haugen SE, Linker D, Eik-Nes S, et al. Congenital diaphragmatic hernia: determination of the optimal time for operation by echocardiographic monitoring of the pulmonary arterial pressure. J Pediatr Surg 1991;26:560.

B.4. How would you treat persistent pulmonary hypertension (PPH) and improve oxygenation?
Pulmonary vascular resistance is greatly increased in the hypoplastic lung, and blood flow is minimal because of medial hyperplasia of pulmonary arterioles. When further aggravated by hypoxemia, acidosis, decreased FIO2, or sudden changes in pulmonary blood volume, pulmonary vasoconstriction increases and fetal circulation persists. The treatment of pulmonary hypertension includes the following measures in sequence:

Continue general anesthesia in the intensive care unit, using fentanyl 3 g/kg/hour, and pancuronium 0.1 mg/kg/hour to blunt the autonomically mediated cardiovascular response (pulmonary vasoconstriction) to stimulation.

Minimize endotracheal suctioning to avoid transient hypoxemia or decrease in FIO2. H y p e r v e n t i l a t e t h e n e o n a t e w i t h l o w t i d al v o l u m e a n d h i g h r e s p i r a t o r y r a t e ( 6 0 t o 1 2 0 breaths/minute) to pH of 7.55 to 7.60. Respiratory alkalosis is the most consistently effective therapeutic modality to achieve pulmonary vasodilation.

Moderately restrict fluid to 2 to 4 mL/kg/hour. Administer pharmacologic vasodilators if the aforementioned measures fail to control pulmonary hypertension. Morphine, prednisolone, chlorpromazine, phentolamine, acetylcholine, bradykinin, tolazoline, prostaglandin E1, prostaglandin D2, and inhaled NO have been tried with some success. Milrinone would be helpful if right ventricular failure is apparent.

Ligate the patent ductus arteriosus to prevent shunting. This is theoretically possible but practically has been associated with sudden right ventricular failure.

Support with ECMO if pharmacologic intervention fails. ECMO has been associated with a 50% to 65% survival rate.

Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams &

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Wilkins, 2006:11941196. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:436437. Vacanti JP, Crone RK, Murphy JD, et al. The pulmonary hemodynamic response to perioperative anesthesia in the treatment of high-risk infants with congenital diaphragmatic hernia. J Pediatr Surg 1984;19:672679.

B.5. What are the effects of nitric oxide (NO) on pulmonary and systemic circulation?
When produced in vivo, NO is endothelium-derived relaxing factor (EDRF) producing smooth muscle relaxation and vasodilation. Inhaled NO is unique, as it is a selective pulmonary vasodilator and has no effect on systemic circulation because it is inactivated immediately on exposure to P.123 hemoglobin. Clinical studies are limited but have shown some improvement in oxygenation in neonates with persistent pulmonary hypertension (PPH) exposed to 20 to 80 parts per million (ppm) of NO. NO has been reported to be ineffective before ECMO therapy in those patients with both CDH and pulmonary hypoplasia. After ECMO followed by surgery, NO was effective in improving oxygenation. However, NO has not been shown to improve survival. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Charlton AJ. The management of congenital diaphragmatic hernia without ECMO. Paediatr Anaesth 1993;3:201. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:436437. Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550. Wheeler M. Practical anesthetic management of neonatal surgical emergencies. ASA annual meeting refresher course lectures Park Ridge, IL: American Society of Anesthesiologists, 2001:116.

B.6. How is ECMO established?


Venovenous or venoarterial bypass is used. Venovenous bypass is established with a doublelumen catheter through the internal jugular vein, with blood removed from and infused into the right atrium through separate ports. Venoarterial bypass is used preferentially by some centers because it provides the cardiac support that is often needed. The right atrium is cannulated through the internal jugular vein. Blood is allowed to passively flow by gravity into the ECMO circuit, where it is pumped with an occlusive blood pump into the membrane oxygenator. From the oxygenator, blood is returned through a catheter placed through the right common carotid artery into the ascending aorta. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:436437.

B.7. What are the advantages of ECMO?


The theoretical advantages are as follows:

Diversion of as much as 80% of cardiac output from the right atrium into the extracorporeal circuit immediately reduces or eliminates right-to-left shunting through the

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foramen ovale or ductus arteriosus.

Right ventricular work is decreased because of reduced pulmonary blood flow and pressure.

Pulmonary vasoconstriction is reduced because hypoxemia and acidosis are corrected by ECMO. Improved systemic oxygenation and reduced ductal blood flow may lead to spontaneous closure of the ductus arteriosus.

The hypoplastic lung is allowed to grow rapidly and alveolar size is increased. The incidence of bronchopulmonary dysplasia is reduced because FIO2 and airway pressure are lowered by ECMO.

Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002: 437438. P.124

B.8. What are the indications and contraindications to ECMO?


Patients with severe hypoxemia, hypercarbia, and pulmonary hypertension who do not respond to maximal conventional respiratory and pharmacologic intervention are candidates for ECMO. However, due to the necessity for anticoagulation and the consumption and inactivation of platelets, ECMO is associated with serious complications of intracranial and pulmonary hemorrhage. The entry criteria include a gestational age of 34 weeks or greater, the presence of a reversible disease process, a minimal weight of 2,000 g, and a predicted mortality of greater t h a n 8 0 % . ( P r e d i c t e d m o r t a l i t y i s c o m m o n l y e s t i m a t e d b y t h e o x y g e n a t i o n i n d e x [ FI O 2 x m e a n airway pressure x 100/PaO2].) Values of oxygenation index in excess of 40 predict mortality greater than 80%. The contraindications to ECMO include the following:

Gestational age less than 34 weeks Weight less than 2,000 g Preexisting grade II or greater intracranial hemorrhage Congenital or neurologic abnormalities incompatible with good outcome More than 1 week of aggressive respiratory therapy Congenital heart disease

Dilley RE, Zwischenberger JB, Andrews AF, et al. Intracranial hemorrhage during extracorporeal membrane oxygenator in neonates. Pediatrics 1986;78:699. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:438439. Redmond CR, Goldsmith JP, Sharp MJ, et al. Extracorporeal membrane oxygenation for neonates. J La State Med Soc 1986;138:40. Stolar CJ, Snedecor SS, Bartlett RH. Extracorporeal membrane oxygenation and neonatal respiratory failure: experience from the extracorporeal life support organization. J Pediatr Surg 1991;26:563.

B.9. When is the optimal time to repair CDH?


The newborn should be maintained on ECMO until the pulmonary hypertension is reversed and

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improvement in lung function is evident. Doppler echocardiography may be used to confirm the reversal of PPH. This is usually seen within 7 to 10 days but in some infants is not apparent for up to 3 weeks. Newborns who do not demonstrate significant improvement over this time have pulmonary hypoplasia that will not benefit from further extracorporeal life support. Timing of repair of the CDH on ECMO is controversial. Some centers prefer early repair to allow a greater duration of postrepair ECMO, whereas many centers defer repair until the infant has demonstrated the ability to tolerate weaning from ECMO support. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 1994:436437. Haugen SE, Linker D, Eik-Nes S, et al. Congenital diaphragmatic hernia: determination of the optimal time for operation by echocardiographic monitoring of the pulmonary arterial pressure. J Pediatr Surg 1991;26:560. P.125

B.10. What other measures should you take to prepare the patient for surgery?
The patient should be examined carefully for the presence and severity of associated congenital anomalies as described in section A.8. Those patients with congenital heart disease in addition to CDH have significantly increased mortality. Hypothermia should be prevented and corrected. Hypothermia can aggravate the hypoxemia and acidosis. Hypothermia can also lead to coagulopathy and arrhythmia. The neonate should be maintained in a neutral thermal environment of 36.5C to 37.5C (97.7F to 99.5F). Laboratory studies should include arterial blood gases, complete blood cell count, electrolytes, blood sugar, blood type, and cross-match for blood products. Venous access should be ready before surgery. Peripheral veins in the upper extremities are preferred because reduction of the hernia often increases abdominal pressure and partially obstructs the inferior vena cava, making lower extremity veins less reliable. Neck veins are avoided in case ECMO is required. Central venous access should be attempted through the umbilical or femoral vein.

B.11. How would you premedicate this patient?


No premedication should be given to the neonate with CDH. The newborn should not have any anxiety, and sedatives will further depress the already compromised cardiopulmonary function.

C. Intraoperative Management C.1. What monitors would you use for this neonate during surgery?
Respiratory

Precordial and esophageal stethoscope Two Pulse oximeters, for preductal and postductal oxygen saturation Capnometry

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Inspiratory pressure measurement Inspiratory oxygen concentration Intraoperative arterial blood gas analysis

Cardiovascular

Five lead electrocardiogram Blood pressure cuff Precordial stethoscope Arterial line: right radial artery for preductal PaO2 Central venous pressure (CVP) line for evaluating volume status and right ventricular performance

Thermoregulatory

Esophageal or rectal temperature probe

C.2. How would you induce and maintain anesthesia?


If the neonate has not been intubated, intubation should be performed with spontaneous ventilation. Positive pressure ventilation should be avoided before intubation to prevent gastric distention and further compromise of respiration. An awake intubation can be performed after preoxygenation. However, if the neonate is too vigorous for awake intubation, he can be intubated without a muscle relaxant after breathing sevoflurane and oxygen spontaneously. P.126 The choice of maintenance anesthetics depends on the severity of cardiovascular dysfunction. Patients in shock and severe hypoxemia may tolerate only oxygen and a nondepolarizing relaxant such as rocuronium or vecuronium. If blood pressure is adequate and stable, inhalation agents and narcotics in addition to a muscle relaxant, may be titrated to maintain anesthesia. Narcotics and nondepolarizers may be continued postoperatively to control ventilation and minimize hormonal response to stress, which may increase pulmonary hypertension. Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:11941196. Dierdorf SF, Krichna G. Anesthetic management of neonatal surgical emergencies. Anesth Analg 1981;60:204214. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:437. Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550.

C.3. Would you use nitrous oxide for anesthesia? Why?


No. Nitrous oxide should not be used in patients with CDH before hernia reduction and abdominal closure. Because nitrous oxide has a higher diffusion capacity than nitrogen (35:1),

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the amount of nitrous oxide diffused from blood to the gut is much more than the amount of nitrogen diffused from the gut to the blood. Therefore, nitrous oxide may distend the intrathoracic gut and compress the functioning lung tissue, further compromising pulmonary function. Moreover, a distended gut may cause difficulty in abdominal closure and may increase abdominal pressure, compressing the inferior vena cava and resulting in hypotension. Barash PG, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:11941196. Eger El II, Saidman LJ. Hazards of nitrous oxide anesthesia in bowel obstruction and pneumothorax. Anesthesiology 1975;26:61. Fink R. Diffusion anoxia. Anesthesiology 1955;16:511519. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:437.

C.4. Would you use 100% oxygen during anesthesia?


Selection of the appropriate inspired concentration of oxygen depends on the severity of pulmonary dysfunction. Retrolental fibroplasia (retinopathy of prematurity) is a potential danger during neonatal anesthesia. Current guidelines suggest that infants are at risk of retrolental fibroplasia until 44 to 50 weeks of gestational age. However, hypoxia causes pulmonary vasoconstriction and pulmonary hypertension, which may increase right-to-left shunting of desaturated blood at preductal or ductal level. Serial arterial blood gases may be used to d e t e r m i n e t h e o p t i m a l FI O 2 . A i r i s a d d e d t o o x y g e n i f t h e P a O 2 o n 1 0 0 % o x y g e n i s m o r e t h a n 9 0 to 100 mm Hg. The PaO2 should be optimally kept at 80 to 100 mm Hg or the arterial oxygen saturation between 95% and 98%. Dierdorf SF, Krishna G. Anesthetic management of neonatal surgical emergencies. Anesth Analg 1981;60:204214. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:436437. P.127 Motoyama EK, Davis PJ, eds. Smith's anesthesia for infants and children, 7th ed. Philadelphia: Mosby, Elsevier Science, 2006:545550.

C.5. How would you ventilate the patient?


Ventilation is controlled either manually or by a respirator. Small tidal volumes should be used to keep the airway pressure below 30 cm H2O to prevent contralateral pneumothorax. High respiratory rates (60 to 120 breaths/minute) should be adjusted to achieve hyperventilation to a PaCO2 between 25 and 30 mm Hg to lower pulmonary vascular resistance and minimize right-toleft shunting through the patent ductus arteriosus. Bray RJ. Congenital diaphragmatic hernia. Anesthesia 1979;34:567. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:436437.

C.6. How would you maintain the neonate's body temperature?


The neonate is particularly susceptible to heat loss because of a large surface to volume ratio, lack of insulating fat, and a naturally flaccid and open posture. Body temperature should be monitored carefully and maintained within the normal range. The following steps are used to maintain body temperature:

Warm the operating room to 80.6F (27C).

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Use radiant warming lamps and a heating blanket. Use a Heat Moisture Exchanger on the ventilator circuit. Warm transfused blood and intravenous fluid to 37C (99.5F).

Dierdorf SF, Krishna G. Anesthetic management of neonatal surgical emergencies. Anesth Analg 1981;60:204214. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:430437.

C.7. The surgeon returned the intrathoracic stomach and intestine to the peritoneal cavity and the ipsilateral lung was found to be hypoplastic and collapsed. The resident anesthesiologist tried to expand the collapsed lung manually with positive airway pressure. Five minutes after the abdomen was closed, the blood pressure suddenly dropped from 70/40 to 30/20 mm Hg, the heart rate from 150 to 80 beats per minute, and the pulse oximeter from 95% down to 60% saturation. What would you do immediately?
Any sudden deterioration in blood pressure, heart rate, oxygen saturation, or pulmonary compliance is suggestive of tension pneumothorax. Auscultation of the chest, particularly the contralateral side, should be done immediately. If absent or diminished breath sounds confirm the diagnosis, a chest tube should be inserted immediately. A large-bore intravenous catheter with needle may be inserted to release the tension pneumothorax if a chest tube is not immediately available. The tension pneumothorax is usually on the contralateral side, because the high airway pressure required to inflate the hypoplastic lung may rupture the normal alveoli on the contralateral side, resulting in pneumothorax. Moreover, the ipsilateral chest usually already has a chest tube after surgery. If there is no pneumothorax, or if deterioration is not improved after insertion of a chest tube, inferior vena cava compression (causing decreased venous return and decreased cardiac P.128 output) should be considered. The peritoneal cavity is often underdeveloped and unable to fully accommodate the returned abdominal organs, which increases the intraabdominal pressure. In this circumstance, the abdominal wound should be opened to relieve the compression on the vena cava and diaphragm. A Silastic patch may be used to cover the abdominal defect temporarily and the defect will be closed at a later time. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:437.

C.8. Discuss fluid therapy in this patient


Fluid therapy should be aimed to correct the preoperative deficit, provide maintenance fluid, and replace intraoperative evaporative, third space, and blood losses. Kidneys are 80% to 90% mature by 1 month of age. Before that time, the infant cannot tolerate the extremes of renal stress. Neonates are obligate sodium losers; therefore, exogenous sodium should be supplied. In addition, neonates have decreased glycogen storage and are prone to hypoglycemia after brief periods of starvation. Therefore, glucose should also be provided. However, hyperglycemia may predispose the patient to intracranial hemorrhage and should be avoided. The preoperative fluid deficit may be evaluated by careful history taking, signs and symptoms of dehydration, urine output, and CVP monitoring. Maintenance fluids consisting of

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5% dextrose in one-fourth to one-half strength saline are given at 4 mL/kg/hour. Intraoperative evaporative and third space losses are replaced with Ringer's lactate or saline at approximately 6 to 8 mL/kg/hour. Each milliliter of blood loss is replaced with 3 mL of Ringer's lactate or 1 mL of 5% albumin. Blood pressure, heart rate, urine output, CVP, hematocrit, and sodium and glucose levels are monitored following the fluid therapy. Dierdorf SF, Krishna G. Anesthetic management of neonatal surgical emergencies. Anesth Analg 1981;60:204214. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. New York: Churchill Livingstone, 2002:696697.

C.9. At the conclusion of surgery, would you extubate the patient in the operating room?
No. The patient should not be extubated in the operating room because varying degrees of pulmonary dysfunction are always present postoperatively. The endotracheal tube should be left in place and the baby should be transported to the intensive care unit for further postoperative care.

D. Postoperative Management D.1. What postoperative problems would you expect in this patient? What is the mortality rate in patients with CDH?
The postoperative course is often characterized by a honeymoon period of rapid improvement, followed by sudden deterioration with profound arterial hypoxemia, hypercapnia, and acidosis. The mortality in patients with CDH varies from 30% to 60%. Factors affecting the mortality include the following:

Pulmonary hypoplasia Associated congenital defect. Cardiovascular and central nervous systems P.129

Inadequate preoperative preparation. Hypothermia, acidosis, shock, and tension pneumothorax

Ineffective postoperative management. Hemorrhage, tension pneumothorax, inferior vena cava compression, persistent fetal circulation, excessive suction on chest tube

Behrman RE, Kliegman RM, Jenson HB, eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Vacanti JP, Crone RK, Murphy JD, et al. The pulmonary hemodynamic response to perioperative anesthesia in the treatment of high-risk infants with congenital diaphragmatic hernia. J Pediatr Surg 1984;19:672679. Waldschmidt J, vonLengerke HG, Berlien P. Causes of death in operated neonates with diaphragmatic defects. Prog Pediatr Surg 1979;13:239.

D.2. The neonate's blood gas analyses improved right after surgery. However, 3 hours later, severe hypoxemia recurred in spite of ventilatory support with high inspired oxygen concentration. What are the possible causes? How should this

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patient be treated?
As discussed earlier, a tension pneumothorax should be considered and treated if it exists. In the absence of a tension pneumothorax, persistent hypoxemia suggests persistent pulmonary hypertension (PPH) with right-to-left shunting of venous blood. Recurrent pulmonary hypertension carries a high mortality. ECMO support should be continued or reestablished if already discontinued before surgery. If the infant cannot be weaned from ECMO after repair, options include discontinuing support or therapies such as NO or lung transplantation. Highfrequency jet ventilation and oscillatory ventilation have had limited success in patients with CDH. Behrman RE, Kliegman RM, Jenson HB, et al. eds. Nelson textbook of pediatrics, 17th ed. Philadelphia: WB Saunders, 2004:13531355. Gregory GA, ed. Pediatric anesthesia, 4th ed. New York: Churchill Livingstone, 2002:437438.

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Chapter 7 Ischemic Heart Disease and Coronary Artery Bypass Grafting


F u n - S u n F . Y ao N ik o l a os S k ub a s M an u e l L . F o n t e s

A 57-Year-Old Man
w it h trip le- ve sse l co ron ary art ery dise ase (C AD ) w as sch ed ule d fo r co ron ary art ery byp ass gra ft ing (C ABG). He h ad a myoc ardi al i nf arct ion 7 m on th s a go . H e wa s t aki ng n itro glyce r in, d ig oxin , me to pr o lol, is oso r bid e din itra te ( I sor d il), an d nif e dip ine . Hi s b loo d pre ssur e (BP ) w as 12 0/ 80 m m Hg a nd h is he art rat e (HR ) 6 0 pe r m inu te .

P.132 P.133 P.134

A. Medical Disease and Differential Diagnosis A.1. What is triple-vessel coronary artery disease (CAD)? Name the branches of the coronary arteries
T r i pl e- v es s e l C AD i n vo l ve s p r o gr e ss i v e a r t e r i os cl e r o si s o f t he m a j o r b r a nc h es o f t he c o r o n ar y a r t er i es w i t h e v e n tu a l l u m i n al ob st r uc ti o n an d m y o c ar di a l i nj ur y . T h e i nt i m a l di s ea se i s t y pi ca l l y s e gm en t al b u t ca n b e d i f fu s e i n s e v e r e c a s es . T he c o r o na r y ar t er i e s a r e th e f ol l o w i n g:

T h e r i g h t c o r on a r y a r t e r y ( R C A ) T h e l e ft a n te r i o r de s ce nd i ng b r an ch ( L AD ) o f t he l e ft m a i n T h e l e ft c i r c um fl e x br a nc h ( C F X) o f t he l e ft m a i n

P.135

Figure 7.1 Branches of the coronary arteries.

T he b r an c h e s of c o r o n ar y a r t er i es a r e sh o w n i n F i g . 7 .1 . T he LA D a nd C F X ar i s e f r o m t he l e ft m a i n c o r o n ar y a r t er y . T h e s i n u s no d e i s s u pp l i e d b y th e R C A i n ap p r o x i m at el y 5 0% to 6 0 % o f hu m a n b e i n gs an d b y th e l e ft C F X ar te r y i n th e r em ai n i n g 4 0% t o 5 0 %. T he at r i o v e n t r i c ul a r ( A V ) n o d e i s s u pp l i e d b y th e R C A i n 8 5% to 9 0 % of hu m a n s a nd b y t he l e ft C F X a r t er y i n th e r em a i n i n g 1 0 % to 15 %; th er e f o r e , t he R C A i s do m i n an t i n 8 5% t o 9 0 % of p a ti e nt s. T h e mo s t c om m o n a r t e r i es f o r co r on ar y b yp a ss g r af ti n g ar e L AD , o b tu se m a r g i n a l ( b r an c h of C F X) , a nd p o s t e r i or d e s c en d i n g ( br a nc h o f R C A ) ar te r i e s . B r a un w al d E , Z i p es D P , Li b by P , e ds . H ea r t di s ea se , a t e xt bo o k of c a r d i ov as c ul ar m e di c i n e , 6t h e d. P h i l ad e l p h i a : E l s ev i er S c i e nc e , W B S a un d er s , 2 00 5 :4 30 43 4 .

A.2. What are the indications for coronary artery bypass grafting (CABG)?
T he i n di c a t i o ns fo r C AB G a r e t h e ne e d fo r i m p r ov em e nt o f t he qu a l i ty o r d ur a ti on of l i fe . P at i e n ts w h os e a ng i na i s n ot c o nt r ol l e d b y m ed i c a l tr e at m e n t or w ho h a v e u n ac c ep ta b l e s i de - e f fe ct s w i t h s uc h m an a ge m e n t sh o ul d b e c on s i d er ed fo r c or on a r y r e v a s c u l a r i z at i o n . T he c a nd i d a te s f or C A BG a r e us u al l y ol de r p at i en ts w i th m o r e di ff u s e C A D an d d ec r ea s e d l e ft v en t r i c u l ar f u nc ti o n. T h e i n d i c at i o n s f or C A BG a r e:

U ns ta b l e a n gi na pe c to r i s o r ep i so d es o f p r o l on ge d m yo c ar di a l i s c he m i a P er s i s t e nt a n gi n a pe c to r i s , de s pi te op ti m al m e di ca l t he r ap y R ep ea t ed e p i s o de s o f m y o ca r d i al i sc h em i a fo l l o w i ng m y oc a r d i a l i nf a r c ti o n P r i nz m e t al ' s an g i n a ( va r i a nt a n gi n a) w i t h c o r o na r y ar te r y ob s tr uc t i o n

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H i g h- g r a de l e ft m a i n co r o n ar y a r t er y o bs tr u ct i o n , do u bl e - or t r i p l e - v e s s e l ob s tr uc t i o n, or p r o x i m al LA D a r t er y o bs t r u c t i on A c u te m y oc a r d i a l i nf a r c ti on , c ar d i o ge n i c sh oc k , i n tr a ct ab l e v e n tr i c u l a r a r r hy t hm i a s S ta bl e a ng i na pe ct o r i s th a t i n t er fe r es w i th d e si r e d l i f e s ty l e

P.136 B r a un w al d E , Z i p es D P , Li b by P , e ds . H ea r t di s ea se , a t e xt bo o k of c a r d i ov as c ul ar m e di c i n e , 6t h e d. P h i l ad e l p h i a : E l s ev i er S c i e nc e , W B S a un d er s , 2 00 5 :1 28 1 1 3 34 .

A.3. What is percutaneous transluminal coronary angioplasty (PTCA)? Discuss its indications, contraindications, and results
P T C A h as d e v e l o p ed r a pi d l y s i n c e i t s i nt r od uc t i o n b y Gr u en tz i g i n 19 7 7. I t i s no w a n a c c e pt ab l e m e t ho d o f tr e at i n g s e l e c t e d pa t i e nt s w ho ha v e an g i n a p ec to r i s . T h i s te c hn i q u e i nv ol v es t h e pa s sa ge of a sm al l ( 3 F ) c a th e te r i nt o t he i n v o l v e d c or on a r y a r t e r y a n d t hr ou g h th e s te n o s i s . W i t h t he ba l l o on po r t i o n o f th e c at h et er s t r a d dl i n g t he st en o si s, i n fl a ti on s a r e pe r f o r m ed th a t r e s u l t i n en l a r ge m e n t o f th e s te n ot i c l u m e n . T h e l um i n a l w i d en i ng i s a c h i ev ed by a c on tr o l l ed i n j u r y i n v ol vi n g, t o a v a r y i n g d eg r ee , p l a qu e c o m p r e s s i on , i nt i m a l fi s s u r e s , an d m ed i al s t r e tc h i n g. P T C A h as r e - d ef i ne d w ho i s c an d i d at e f o r el ec t i v e s ur gi c al m yo c ar d i a l r e v as c u l ar i z a ti on . T he i n di c at i o n s fo r P T C A h av e c ha n ge d d ur i ng t h e r e c en t p as t . W i t h th e c u r r en t a va i l a bl e t ec h no l o g y, P T C A i s c on s i d er e d a t he r a p eu t i c o p ti on i n a n y i n d i v i d u al w i t h d i s a bl i ng i s c h em i c s y m p t o m s d es pi t e go o d m ed i c a l t he r a p y an d f o c a l o bs tr u ct i v e c or on a r y d i se as e r eg a r d l e s s o f c a u s e . T h e i n di c a t i o ns fo r P T C A ar e a s f ol l o w s :

I s o l a t ed d i s c r e t e pr o xi m a l s i n gl e - v es s el d i se as e P r o x i m a l d o ub l e - ve ss e l di se a se P os tc o r o na r y ar t er y by p as s g r a ft i ng w i th n e w st e no t i c l es i on s o r s t e no s i s a t d i s ta l a na s to m o s i s R es te n os i s fo l l o w i ng PT C A C on tr a i n di c at i o n s to C A BG C or on a r y s te n os i s fo l l o w i ng ca r d i ac t r an sp l an t at i o n O c c l u d ed v e ss el s w i t hi n t h e l a s t 6 m o n th s a nd l e ss th an 15 m m i n l en gt h P os ts t r e pt o k i na s e th e r a py fo r r ev as c ul ar i z a ti on

P T C A i s c o nt r ai nd i ca te d i n t he fo l l o w i ng :

L ef t m ai n C AD i n w hi ch th e d i s ta l v es s el s a r e n o t pr o te ct e d b y at l e as t o ne c o m p l et el y p at e nt l a r g e c ol l a t er al v e s s e l M u l ti v e s s e l d i s ea s e w i t h se v er e d i f fu s e ar t er i o s cl er o si s A bs en c e of a di s cr et e o bs t r u ct i ng l e si on A bs en c e of a fo r m a l c ar di a c su r gi ca l p r o g r a m w i t hi n t he i n s t i t u ti on

T he r e s u l t s o f P T C A ar e a s f ol l o w s: T h e pr i m a r y s u cc es s r at e i s a pp r o x i m at e l y 9 0 %. T h e pr i m a r y w e ak ne s s of th e p r o c e d ur e i s r e s te n os i s , a t a r at e o f a pp r o x i m at e l y 3 0 %, 6 m o nt h s af t er t h e pr o ce du r e. D i l a ta t i o n c an be r e pe at e d w i t h a 9 0% s u c c e s s r at e . T h e a r t e r y t e nd s t o r e m ai n p at en t a ft e r t h e s ec o nd a ng i o p l a s ty . W i t h th e i nt r od uc t i o n o f co r on ar y s te n ts , w hi ch ac t a s a m et al s c af fo l d, t h e r e s te n os i s r a te a f te r P T C A h as b e en d e c r e as i n g , an d f e w e r pa t i e n t r eq ui r e s u b s e qu e nt r e va s cu l a r i z at i o n : 1 0% t o 1 5% af te r s te n ti ng v e r s u s 25 % t o 3 5% a f te r P T C A a l o ne . T he l a r g e s t d e c r ea s e i n l u m i n al d i am et e r fo l l o wi n g s te nt pl ac e m e nt i s e v i d en t w i t h i n t h e fi r st 6 t o 9 m o nt h s af t er s te n t p l a c e m en t a nd i s t he r e s u l t of pr ol i fe r a t i v e n eo i n t i m al t i s s ue gr ow t h i n r e s p o ns e t o t he a s s oc i at ed i n j u r y an d i nf l am m a t i o n. R e ce n tl y, ph ar m ac ol o gi c a ge n ts ( s i r ol i m us , a n i m m un o s u p pr es s a n t, an d p ac l i t ax el , a n a nt i n e o p l as ti c ) ar e c ou p l e d w i t h p ol y m e r s t h at e l ut e o r sl o w l y r e l ea se th e se i n hi bi t or s fr o m th e s te n t s u r fa c e . T he dr ug - el ut i ng s t en ts ha v e r e d uc ed th e n ee d f o r t a r g e t - l e s i o n r ev as c ul ar i z a ti o n to an e v en l o w e r r at e, 4% t o 6 %. H ow ev e r , t h e PT C A i s a di ff e r e nt th e r a pe u ti c a pp r o a ch t h an C A BG . P T C A i s ta r ge ti n g th e a r e a o f l es i o n o n l y , w h e r e a s C A BG by p as s ta r ge t s no t o nl y t he e x i s t i ng , b ut f u tu r e l e si o n ar e as . T hi s m a y b e t he r e as o n th a t, a t l ea s t i n th e i nt er m ed i a t e te r m , C A BG i s c on s i d er e d to be s u p e r i o r f o r p at i en t s w i t h m ul ti v e s s e l d i s ea s e. D i e ge l er e t a l . s h ow e d th a t, f o r i s o l a te d h i g h - g r a d e l e s i o n s of th e L AD , C AB G th r ou g h a l ef t a nt er i or t h or ac o to m y i s a s e ff e c t i v e a s PT C A w i t h s t e nt p l a c e m en t. Al th o ug h s te n ti ng pr ov i de d e xc el l en t s ho r t - te r m r e s u l t s w i t h f ew e r pe r i p r o c ed ur a l ad v er s e ev en t s , C A BG w a s s u p er i o r w i t h P.137 r eg ar d t o t he n e ed fo r r e p ea t ed i n te r v e nt i o n i n t he ta r g e t ve s se l a nd f r e e do m f r o m a ng i na a t 6 m o nt hs of f o l l ow - up . B r a un w al d E , Z i p es D P , Li b by P , e ds . H ea r t di s ea se , a t e xt bo o k of c a r d i ov as c ul ar m e di c i n e , 6t h e d. P h i l ad e l p h i a : W B Sa u nd er s , 20 0 5: 1 30 8 1 31 1 . D i e ge l er A , T hi e l e H , F al k V , et al . C om pa r i s on of s t en ti n g w i t h m i n i m al l y i n v a s i v e b y p as s s ur g er y f or s te n os i s of t h e l ef t a nt er i or d e s c en d i n g c or on a r y a r t er y . N En g l J M ed 2 0 02 ; 3 47 : 56 1 5 66 . M ol i t e r n o D J . H ea l i n g a ch i l l es s i r o l i m us v e r s us p a cl i t a xe l . N E ng l J M e d 20 0 5; 3 53 :7 2 4 7 27 .

A.4. What are the results of coronary artery bypass surgery?


K ua n e t a l . r ep o r t ed a p er i o p er at i ve m yo c ar d i a l i n f ar ct i on r a te o f 4 % t o 6 %. T he ov e r a l l o p er a ti v e m o r t al i ty r a t e o f C AB G a t m a j or m e di c a l c en t er s i s a pp r o x i m at e l y 1 % . R e o pe r a t i o n i s as s oc i a t ed w i th a hi gh e r o pe r a t i v e m o r ta l i t y , a p pr ox i m a te l y 2% to 3 % . R a h i m to o l a e t a l . s t ud i e d t h e s t a t u s o f p at i e n ts w ho u n de r w e nt C A BG f o r un s ta b l e a n gi na ov er a 10 - ye a r pe r i o d. T h e 1 - m on th m o r t a l i ty r a te w a s 1 . 8 %. T h e 5 - y ea r s ur v i v al r a t e w a s 92 % a nd t h e 1 0- y ea r s ur v i v a l r at e w as 83 %. C A BG w a s r ep ea t ed at a r a te of 1 % t o 2 % pe r y ea r ; 81 % o f p at i e n ts w e r e a n gi n a- f r e e or ha d o nl y m i l d a ng i n a . Lo o p e t al . f ou n d th a t t he 1 0 - y ea r s ur v i v al r a te a m on g t he gr ou p r ec e i v i n g t he i n te r na l m am m a r y ar t er y gr a ft , a s c o m pa r e d w i t h t he gr ou p r ec e i v i n g t h e v e i n gr a f t s ( e x c l us i ve o f h os pi t al d e at h s ) , w a s 9 3. 4 % ve r su s 8 8% f o r th o se w i th o n e- ve s s e l d i s ea s e; 9 0 .0 % v er s us 7 9 .5 % f or t h os e w i t h t w o - v e s s el d i s e a s e ; a nd 8 2 .6 % v er s u s 7 1. 0 % f or t h os e w i t h t hr ee - ve ss e l di se a se . A t th e e n d of th e f i r st 10 p o s t op e r a ti v e y e a r s , t he p a te n c y o f i nt e r n al m a m m ar y a r t e r y g r a f ts i s 8 5% to 9 5 %, w h er e as t he p a te n c y o f s ap h en ou s v ei n g r a f ts i s o nl y 3 8% to 4 5 %. A s y s te m at i c ov er v i e w o f th e s ev e n r a n do m i z ed tr i a l s th at co m p a r e d c or on a r y b y pa s s s u r g e r y w i th m e di c a l t he r ap y b et w e e n 1 97 2 a n d 1 9 84 y i el d ed 2 , 64 9 p at i e n ts . P at i e n ts u n de r go i n g C AB G h ad a si g ni fi c an tl y l ow e r m o r t a l i ty at 5 , 7 , a nd 10 y e ar s , bu t b y 10 y e ar s 4 1% of t h e pa t i e n ts i n it ia ll y r an d om i z e d to m ed i c a l th e r a py ha d u nd e r g on e C AB G . T h e r e fo r e, c o r o na r y by p as s s ur ge r y pr o l o ng s s ur v i v al i n p a ti en t s w i th s i gn i fi c a n t l e f t m a i n C A D i r r es p ec t i v e of s y m pt o m s , i n pa ti e nt s w i t h m ul ti v es se l d i s e as e a nd i m pa i r e d l e f t v e n tr i c u l a r fu n c t i on , a nd i n p at i en t s w i t h th r e e - v es s el d i s e as e t ha t i nc l ud e s th e p r o x i m al

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L AD c o r o na r y ar t er y ( i r r e sp e ct i v e o f l ef t ve n tr i c u l a r f un ct i on ) . Su r g i c a l t he r a p y al s o ha s b e en d e m o ns t r a te d t o p r o l o n g l i f e i n pa t i e nt s w i t h t w o - v e s s el d i s ea s e an d l e ft v en t r i cu l ar d y sf un c ti on , p ar t i c ul a r l y i n th o se w i th a c r i t i c a l s t e no s i s o f t he p r ox i m a l LA D c or o na r y ar te r y . A l t h ou g h no s t ud y h as d oc um e nt ed a s ur v i va l b en e fi t w i t h s ur gi c al t r ea tm e nt i n p at i en ts w i th s i ng l e- v e s s e l d i s ea s e, t h er e i s s o m e ev i d e nc e t ha t s uc h p at i en ts w h o h av e i m p a i r ed l ef t v en tr i c u l a r f un ct i on h a ve a po o r l o n g- te r m su r vi va l r at e w i t h m ed i c a l th e r a py al on e . Su c h p at i e n ts w i th a n gi na an d /o r e v i d e n c e o f i s c h em i a at a l o w o r m od er a te l e v e l o f ex e r c i s e , es p ec i a l l y t h os e w i t h o bs tr u ct i o n o f t he p r ox i m a l LA D c or on a r y a r t e r y , m ay be ne f i t f r om c o r o na r y r e v a s c u l a r i z at i on b y e i t h er a ng i o p l a s ty o r b y p a ss s ur g er y. H an na h e t a l . s t ud i e d p r os pe c ti ve l y 37 , 21 2 p at i e n ts w h o u nd er w en t C AB G a nd 2 2 ,1 0 2 pa t i e nt s w ho un d er w e n t s t e nt i n g , C A B G w a s a s s o c i at e d w i t h a s i g ni f i c an t l y h i gh er l i ke l i h oo d o f s ur vi va l ( ha z ar d r at i o s f or de at h 0 . 75 f o r tw o - an d 0 .6 4 f or th r e e - v es s el C AD , c om p ar ed w i th s t en t i n g) . T he C A BG pa ti e nt s h ad s i gn i f i c a nt l y l o w er m e di an ej ec t i o n f r a ct i on s, w e r e m o r e l i k e l y th an pa t i e nt s w ho r e c e i v e d s t e nt s t o h av e h ad a m y oc a r d i a l i nf a r c ti o n i n t h e w ee k b ef o r e t he p r oc ed u r e , h ad a si g ni fi c an tl y h i g h er p r ev al e nc e o f nu m er ou s c oe x i s ti n g c o n di ti o ns an d w er e s i g ni f i c an t l y m or e l i k e l y t o h a v e t hr e e- v e s s e l d i s ea s e. H ow ev e r , s te n t i m p l a n ta ti o n i s as so c i a te d w i t h a m u ch l o w e r i n - ho s p i ta l m or ta l i t y th a n C AB G. B r a un w al d E , Z i p es D P , Li b by P , e ds . H ea r t di s ea se , a t e xt bo o k of c a r d i ov as c ul ar m e di c i n e , 6t h e d. P h i l ad e l p h i a : W B Sa u nd er s , 20 0 1: 1 31 1 1 32 8 . P.138 H aa s e J , J u ng T , S to r ge r H , et a l . Lo n g- t er m ou t co m e af te r i m p l an ta t i o n o f b ar e m e t al s t en t s fo r t he t r ea tm e nt o f c or o na r y ar te r y di s ea s e : r at i on al e f or th e c l i ni c a l u s e of an ti p r o l i f er at i v e s te n t co a ti n gs . J I nt e r v C ar d i o l 2 00 3 ;1 6( 6 ) : 46 9 4 73 . H an na h E L , R a c z M J , W a l fo r d G, e t a l . Lo n g- te r m ou tc o m e s o f c o r on a r y - a r t e r y b y pa s s gr af t i n g v er s u s s te n t i m pl a nt a ti on . N E n gl J M e d 2 00 5; 3 52 :2 1 74 2 18 4 . K an dz a r i D E , Le o n M B , P op m a JJ , e t a l . E N D E AV O R II I I nv es t i g at o r s . C om pa r i s on of z o ta r o l i m us - e l ut i n g a n d s i r ol i m us - el ut i ng s t en ts i n p a ti e nt s w i t h na t i v e c or on a r y a r te r y d i s e a se : a r an d om i z e d co n tr ol l ed t r i a l . J Am C o l l C a r d i o l 2 00 6 ;4 8( 1 2) :2 4 40 24 4 7 L oo p F D , L y tl e B W , C os g r o ve D M , e t al . I nf l ue nc e o f t he i n te r n a l m a m m a r y ar te r y gr af t o n 1 0- y e a r s u r v i v a l a nd ot h er c a r d i a c e v e n ts . N E ng l J M ed 1 98 6 ;3 14 : 1 6. L y t l e BW , L oo p F D , C os g r o ve D M , e t al . L on g - t er m ( 5 t o 12 ye ar s ) s e r i a l s t u di es of i n te r n a l m a m m a r y a r te r y an d s ap h en ou s v ei n c o r o na r y by p as s g r a ft s. J T ho r a c C ar d i o v a s c Su r g 19 8 5; 89 : 24 8 2 58 . R ah i m t oo l a SH , N an l e y D , Gr u nc ke m ei er G, e t a l . T e n- y ea r s ur v i v a l a ft e r c o r on ar y b y p a s s s u r g er y . N E ng l J M ed 1 9 83 ; 30 8 :6 76 .

B. Preoperative Evaluation and Preparation B.1. Which preoperative tests would you order?
I n ad d i t i o n t o t he r o ut i n e s ys t em i c ex am i na ti o ns o f a l l or ga n s y s t em s , s p ec i al a t te nt i on s h ou l d be pa i d to t h e c a r di ov a s c ul a r s t a tu s .

R en al fu nc t i o n u r i na l ys i s , b l o o d ur e a ni t r o ge n ( BU N ) , c r e a ti n i n e T h e r o ut i n e e va l ua ti o n o f th e h ep a ti c f un ct i on i s n ot an y m or e t he s t an da r d, u n l e s s s p e c i fi c a l l y i n di c a t ed , t ha t i s , p r ev i o u s h i s to r y of h e pa ti t i s o r j au nd i c e o r t he pa ti e nt i s d r u g a b us er .

P ul m o n ar y f un ct i on c h es t x - r ay f i l m ( a bs ol u te l y i n di c at ed i n r e op er a te d s te r n o to m i e s to i n v e s t i ga t e t h e p r ox i m i t y o f t he s t er nu m t o t he a n te r i o r s ur fa c e of th e h ea r t ) , ba s el i n e a r t e r i al bl oo d g as e s, a n d s pi r o m e t r y i f i nd i c a te d .

H em at o l o gi c f un c ti on co m p l et e b l o od co u nt , p r o th r om bi n t i m e ( PT ) , p a r t i a l t hr o m b op l as ti n t i m e ( PT T ) , p l a t el et s ( pl a te l e t f un c ti on i f a v ai l a b l e a n d/ o r i nd i c a te d)

M e t ab o l i s m e l ec tr o l y te s a nd bl o od s u ga r C ar di o v a s c u l a r fu n ct i o n r e st i n g a nd ex er c i s e E C G ( i f a s t r es s t es t w a s p e r f or m e d p r e o pe r at i v e l y ) , c a r d i a c c at h et er i z a ti o n an d c o r o na r y an g i o gr a ph y, l oc at i on a n d se v er i t y o f c or on a r y o c cl us i on , e ch oc a r d i o g r a ph y , a nd l e ft v e nt r i c u l ar f u nc ti o n ( f r om c a t h et e r i z a t i o n a nd /o r e c h o c a r d i og r ap hy ) .

B.2. How would you evaluate the patient's left ventricular function?

M e d i c a l hi s t o r y p r es en c e o r ab s en ce of m y oc ar d i a l i n f ar c t i on a n d a ng i n a S y m pt o m s a n d cl i n i ca l s i g ns of l e ft v e nt r i c ul ar fa i l u r e ( dy s pn e a at r e s t o r e x e r c i s e , n oc t ur na l o r t h op n ea ) a nd /o r r i g h t he a r t f a i l ur e ( as c i t es , p i t ti n g e de m a , j ug u l a r v ei n d i s te n ti on )

C ar di a c c a t he te r i z at i o n , a ng i o g r a ph y , a nd e c ho ca r di og r ap h y

E j e c t i on f r ac ti o n ( n o r m al l y ~ 65 % ) L ef t v en tr i cu l a r e nd - di as t ol i c pr es su r e ( L V ED P) or p u l m on a r y a r te r y oc c l u s i on pr es s u r e ( P A OP : n or m a l 6 t o 1 5 m m H g ) L ef t v en tr i cu l a r w al l m ot i o n n o r m al ( w al l th i ck en i ng of > 3 0 %) , h y p o k i ne s i a ( w a l l th i c k en i ng 1 0 % t o 30 % ) , a k i n es i a ( w a l l t hi c k e n i n g < 10 % ) , o r d y s k i n es i a ( o ut w ar d m o t i o n d ur i ng s y st ol e ) F i g. 7. 2

C ar di a c i n d ex ( n or m a l 2 .2 to 3 L/ m i n ut e/ m 2 )

E nd - s y s t ol i c pr es s ur e v ol um e r el a ti on ( E SP V R ) f r o m m ul t i p l e pr es s ur e v ol um e l oo p s

P.139

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Figure 7.2 Echocardiographic evaluation of the left ventricle (LV). The transgastric mid-papillary short axis view of the left ventricle is shown in left. By placing a cursor line across the middle of the inferior (top of the image) and anterior (bottom of the image) segments of the left ventricular myocardium, the motion of the segments over time is shown in the image right. The percent wall thickening can be either visually estimated, or measured, between diastole and systole. Abnormal regional wall motion (RWM) most commonly is the result of coronary artery disease (CAD), which interrupts perfusion to fairly well defined territories and hence results in abnormal motion in those segments. There is a gradation of wall motion abnormality that consists progressively of hypokinesis, akinesis, and subsequently dyskinesis in which a wall moves away from the center of the ventricle. Because wall thickening and endocardial motion are intrinsically tied, virtually all RWM abnormalities are expected initially to be associated with abnormalities of thickening as well as endocardial motion.

( Se e a l s o C ha pt e r 8, qu e st i o n A .3 . ) B r a un w al d E , ed . H ea r t di s ea se , a t e xt bo o k o f ca r d i ov a sc ul a r m e d i c i n e , 6t h e d. Ph i l a de l p h i a : W B Sa u nd e r s , 2 00 5: 2 48 38 0. J oh ns o n B, Ad i A , Li c i n a M G, e t a l . C a r d i ac p h ys i o l og y. In : K ap l a n J A, R e i c h D L, La k e C L , e t al . e ds . K ap l an ' s c a r di ac an e s t he s i a . P hi l a d el ph i a: W B S au nd e r s , 2 00 6 :7 1 8 4.

B.3. What are the three major determinants of myocardial oxygen consumption? How are they measured clinically?
T he t h r e e m aj or de te r m i na n ts o f m yo ca r di a l ox yg e n c on su m pt i o n a r e m y oc a r d i a l w al l t en s i o n, c o nt r ac ti l i t y , a n d H R . P.140

Figure 7.3 Echocardiographic evaluation of the systolic function of the left ventricle. The transgastric mid-papillary short axis view of the left ventricle is shown in systole (A) and diastole (B). The endocardial border is traced (without including the endocardium of the two papillary muscles), and the end-systolic and end-diastolic areas are calculated. The percentage area change (fractional area change) is calculated as: FAC = (EDA - ESA)/EDA. The FAC correlates with, but does not substitute the percentage ejection fraction. al-PM, anterolateral papillary muscle; pm-PM, posteromedial papillary muscle.

M y o c a r di al W a l l T e ns i o n i s e st i m a te d b y th e f ol l ow i n g :

T h e L a pl ac e e q ua ti o n st a te s t ha t t he w a l l t e ns i o n ( T ) i s a n al og o us t o t he di am e te r o f th e v en t r i c l e ( R , r a di u s ) a n d th e i nt r ac a v i ta r y p r es s u r e ( P ) a nd i nv er s e l y p r o po r ti on a l to th e m yo ca r d i al w a l l t h i c kn e ss ( T h) : T = P x R 2T h

P r e l o a d LV E D V , L VE D P , l ef t a tr i al p r e s su r e , o r P AO P A ft er l o a d s ys to l i c v en t r i cu l ar p r es su r e or sy st ol i c BP i f t h er e i s no ao r t i c s t en o s i s

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C on tr a c t i l i t y i s m ea su r ed b y t he fo l l o w i ng :

I nv as i v e t e c h ni q ue s. M a xi m al v e l o ci ty of c o nt r a c ti on ( V m a x ) , d P /d t ( p r es s u r e ti m e i n d i c es of v e nt r i c l e : h ow f a s t ( dt ) t he i n tr a v e nt r i c ul a r pr e s s ur e ( dP ) d ev el o ps ) , or l e ft v e nt r i cu l ar e n d- sy s to l i c p r e s su r e / vo l u m e r a ti o

N on i n v as i v e t ec h ni qu e . Pr e ej e ct i o n p er i o d ( P EP ) / l e f t ve n tr i c u l a r e j e c t i on t i m e ( LV E T ) , a nd g l ob a l an d r eg i on a l v e n tr i c ul a r w a l l m o t i o n b y e c h oc a r d i o g r a ph y ( F i g . 7. 3 )

B r a un w al d E , ed . H ea r t di s ea se , a t e xt bo o k o f ca r d i ov a sc ul a r m e d i c i n e , 6t h e d. Ph i l a de l p h i a : W B Sa u nd e r s , 2 00 5: 1 28 4 . O 'B r i e n E R M , N a t ha n H J. C o r o na r y ph y si ol o gy a n d a th er o sc l e r os i s . I n: K a pl a n J A , R ei c h D L , L ak e C L, et a l . ed s . Ka p l a n' s c a r d i a c a ne s th es i a . P h i l ad e l p h i a : W B Sa u nd er s , 20 0 6: 9 7 10 2 .

B.4. Which factors determine myocardial oxygen supply?


M y o c a r di al ox y g e n su p pl y = co r o n ar y b l o o d fl o w x a r t er i a l o xy g en c o nt e nt T h e c o r on ar y b l o o d fl o w de p en d s on th e f ol l o w i n g :

A or ti c d i a s t o l i c p r e ss u r e ( D AP ) L VE D P P.141

P at en c y of c o r o n ar y a r t er i e s C or on a r y v a sc ul a r to n e

A nd i t c an be d e te r m i ne d b y th e f o r m ul a : C or on a r y b l oo d f l o w = co r o n ar y p er f us i o n p r e s su r e m yo ca r di al v a s c u l a r r es i s ta n c e , O r , ( D AP - LV ED P ) m y o c ar di a l v a s c u l a r r es i s t an c e A r t er i a l O 2 c o n te nt i s d e te r m i n e d b y th e f ol l ow i n g e qu a ti o n: C aO 2 = 1 . 34 x H b x O 2 s at ur a ti on + ( 0 .0 03 1 x P a O 2 ) O 'B r i e n E R M , N a t ha n H J. C o r o na r y ph y si ol o gy a n d a th er o sc l e r os i s . I n: K a pl a n J A , R ei c h D L , L ak e C L, et a l . ed s . Ka p l a n' s c a r d i a c a ne s th es i a . P h i l ad e l p h i a : E l s ev i er S c i e nc e , W B S a un d er s, 20 06 : 97 10 2.

B.5. Would you discontinue digoxin? Why? What is its half-life?


I n or d er t o p r e v en t d i g i t a l i s i nt ox i ca ti o n af t er C P B, d i gi ta l i s p r e p ar a ti on s a r e us ua l l y d i s c on t i n ue d o n e ha l f- l i fe ( 1 .5 to 1 . 7 d ay s fo r d i g o x i n , 5 to 7 d ay s f or d i g i t o x i n) be fo r e s u r ge r y . D i g i t a l i s i nt ox i ca ti o n i s qu i t e p os s i b l e , e s p e c i al l y af t er C P B w h e n ac i d- ba s e a nd e l ec tr o l y te s a r e a b no r m a l . If a d i gi ta l i s - d e pe n de nt p at i e n t i s i n C H F , d i g i ta l i s i s c on ti n ue d u nt i l th e n i g h t be f or e s ur ge r y . H o w e v e r , th e p r e d i s po s i n g f ac t o r s to di gi t al i s i n to x i c at i o n , e s p ec i al l y h y po p ot as s em i a a nd h y pe r c a l c em i a, h a ve t o b e p r e v en te d . R oy s t e r R L , B ut te r w o r t h J , G r o ba n L , e t al . C ar d i o va s cu l a r p ha r m a c o l og y . In : K ap l a n J A , R e i c h D L, La k e C L , e t a l . e d s . K a pl an ' s c ar di a c an e s t he s ia . P hi l a d el ph i a: E l s e vi e r Sc i en ce , W B S au nd e r s , 2 00 6 :2 49 .

B.6. Would you discontinue the -blocker (metoprolol)? Why? What is its half-life? What is the role of the -adrenergic blockers in treating congestive heart failure (CHF)?
T he - b l o c k e r ( m et o pr ol o l ) s h ou l d be co nt i nu ed no t o nl y u p u nt i l s u r g e r y , bu t p r o b ab l y th r ou gh o ut th e p er i o p er at i v e p e r i od . I n p at i e n ts w i th u n s t ab l e a ng i n a , s ud de n w i t h dr aw a l of - b l o c ke r m ay p r od uc e a n e xa ce r ba t i o n o f s y m p t om s a nd m a y p r e c i pi t at e a c u t e m y o c a r d i a l i nf a r c ti o n. T h e do s e o f - b l o c k e r d oe s n ot n ee d t o b e r e d uc ed be fo r e su r ge r y fo r f ea r o f br a dy ca r di a, hy po t en s i o n, or d i f f i c ul t y i n w e an i ng f r om C P B. T h e ha l f- l i fe of o r a l p r op r a n ol o l i s 3 . 4 t o 6 h ou r s a nd o f m et o pr ol o l 3 h ou r s. B o th p r op r a n ol ol an d m et op r ol o l ar e m et ab o l i z e d i n t he l i v e r . Pr op r an o l o l d i s ap p ea r s fr om t h e p l a s m a a nd at r i a w i t h i n 2 4 t o 4 8 h ou r s af te r d i s c on ti n ui ng do s es o f 3 0 t o 24 0 m g p er d a y. S h an d a nd Ke a ts h a v e s h ow n t ha t w i t h a 0 .5 - m g d o s e o f p r o p r a no l ol I V , bl o od le ve l s as hi gh as 5 0 n g pe r m L a r e o b ta i n e d, bu t r ap i d l y dr o p of f t o i m m ea su r ab l e l e v el s w i t hi n 5 t o 1 0 m i n ut e s . N o m y o c a r di al de p r e s s i o n h a s be e n s e e n w i t h th e s e s m al l i nt r a v en ou s d os e s . C u r r en t a dv a nc e d ca r di ac l i fe s u pp o r t ( AC L S) g u i d e l i ne s s ug g es t a 5 m g b ol u s of m e to p r o l o l a t 5 - m i n u te i n te r v a l s , a nd a 0. 1 m g pe r k g b ol us do s e of p r op r a n ol o l di v i d ed i n to th r e e e q ua l d os es at 2 - t o 3 - m i n u te i n te r v a l s . R ed uc t i o ns i n H R w i t h a - b l o ck e r ( p r o p r a no l ol o r m et o pr ol o l ) o c c u r a t l o w er s e r u m l e v el s t ha n d ep r es s i o n of m y oc a r d i a l c on t r a c t i l i ty . A c c or d i n gl y , as d r ug l ev el s d ec r ea s e af te r d i s c on ti n ua ti o n o f th e r a py , r ed u ct i o n s i n c h r o n ot r o p i c r e s p on s e l a s t l o n ge r t ha n r ed u c t i o n s i n i n ot r o p y . T h i s i s a n i m p or t an t c on ce p t i n t r e at i ng t a c h y c a r d i a s i n p at i e n ts w i th s i gn i f i ca nt ve nt r i c ul a r dy s f u nc ti o n P.142 a nd C H F : a s m al l d os e i s ap p r o p r i at e , an d i nd i ca te d , w h e r e a s a l a r ge do s e m a y s up pr e s s e v en f u r t he r t he i n ot r op i c s t at e . N um er o us s t ud i e s h av e c on f i r m e d i m p r o v em e nt s i n ca r d i ac f u nc ti o n, ex er c i s e c a p ac i t y , an d l o ng - t e r m s ur v i v al i n p a ti en t s w i t h he a r t f a i l ur e r es u l t i n g f r o m m y o c a r di al i n fa r c t i o n, hy p er tr op h i c c a r d i o m yo pa t hy , o r i d i op a th i c d i l a te d c a r d i o m y o pa t hy w i th - a nt ag o ni s t s . - A n t a go n i s ts m a y a l s o b e of be ne f i t i n p at i e n ts w i th d i as to l i c d y sf un c ti on , s ec o nd ar y t o h yp er t en si o n. P ot en t i a l b en e fi ts o f - ad r en e r g i c b l oc ka d e i n he a r t f a i l ur e i nc l ud e d ec r e a s e d H R an d n o r m al i z a ti on of - r ec ep t or f u nc t i o n. S l ow er H R s i m p r o v e di a s t ol i c f un c t i on , b y i n c r e as i ng t h e di a st ol i c fi l l i ng ti m e a n d m yo ca r d i al p e r f u s i on an d b y de c r e as i ng t h e m y o c a r d i al o x y g e n c o n s u m p t i o n . - A dr e ne r g i c r e c ep t o r s ar e d ow n- r eg ul a te d i n h ea r t fa i l u r e . b ut t h ei r r e s po n se i s n or m a l i z ed by l o ng - t e r m - b l o c k a de . P ar ti a l - a g on i s t s m a y p r o v i d e b as el i ne s y m p at h et i c dr i v e b ut ac t a s an t ag o ni s t s a ga i ns t e xc es s i v e sy m pa th e ti c s ti m u l at i o n . R oy s t e r R L , B ut te r w o r t h J , G r o ba n L , e t al . C ar d i o va s cu l a r p ha r m a c o l og y . In : K ap l a n J A , R e i c h D L, La k e C L , e t a l . e d s . K a pl an ' s c ar di a c an e s t he s ia . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :2 1 9 2 25 .

B.7. If the patient who is on metoprolol develops hypotension intraoperatively, how would you manage it?
T he m o r e c o m m on ca us e s of i n tr a op er a ti ve hy po t en si o n, s u ch a s h y po v o l em i a , d ee p a n es th e s i a, an d s ur gi c al m a ni pu l at i o n , s h o ul d b e c or r e c t e d f i r s t . T he r e a r e n o s pe c i f i c an ta g on i st s fo r m et o pr ol o l . I n r ar e i ns t an ce s , i t i s n ec e s s a r y t o a dm i n i s t er at r o p i n e f or b r ad y c a r d i a or e p i n ep h r i n e, i s o p r o t er en o l , g l uc ag o n, c al c i u m , o r d i g i t a l i s t o co u nt er a ct t h e n eg at i ve i n ot r o p i c s t at e a s s oc i at ed w i th - b l o c k a de . C ar d i o ge n i c h y po te n s i o n i s us ua l l y a s s o c i a te d w i t h h i g h P AO P a nd l o w BP . R oy s t e r R L , B ut te r w o r t h J , G r o ba n L , e t al . C ar d i o va s cu l a r p ha r m a c o l og y . In : K ap l a n J A , R e i c h D L, La k e C L , e t a l . e d s . K a pl an ' s c ar di a c an e s t he s ia . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :2 1 9 2 25 .

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B.8. What is nifedipine? How does it work?


N i f ed i pi ne i s a c a l c i um c ha n ne l b l o c ke r . T h e c om m o n l y u se d c a l c i u m c ha n ne l b l o c k e r s i n t he U n i t e d St a te s a r e n i fe di p i n e , v e r a p a m i l , a nd di l t i az em h y d r o c hl or i de . F i v e cl a ss e s of c o m p o un ds ha ve be e n ex a m i ne d : ph e ny l a l k y l a m i n es , d i h y dr op y r i di n es , b en z ot hi a z e pi n es , d i p he n y l p i p er a z i ne s , an d a d i a r y l am i n o pr op y l a m i n e. A t p r e s en t, ve r a p am i l ( a p h en yl a l k yl a m i ne ) ; di l t i az em ( a b e nz ot h i a z e p i n e ) ; n i c a r d i p i ne , n i f e di pi n e, i s r a di p i n e, am l o d i p i n e , f el od i pi ne , a n d ni m od i p i ne ( d i h yd r op yr i di ne s ) ; a n d be p r i di l ( a d i a r y l am i n o pr op y l a m i n e et h er ) a r e a p pr ov e d f o r c l i n i c al us e i n t h e U ni t ed S t at es . T he y i nh i bi t e x c i t a ti on c o nt r ac ti o n co u pl i n g o f m yo ca r di al an d s m o ot h m us c l e b y b l o c k i ng c a l c i um i n fl ux at c e l l ul a r m e m b r an e s . T hi s r es u l t s i n de c r e as e d m y o c a r d i al c on tr a c t i l i t y a nd v a s od i l a ti on . T he r ef or e , m y o ca r d i a l o xy g en co ns u m p ti o n i s de c r e as ed . C al c i u m c ha nn e l bl o c k er s a r e ef fe c ti v e f o r t he t r ea tm e nt o f v ar i a n t a ng i n a ( Pr i nz m e t al ' s an g i n a) , a ng i na pe ct o r i s, a n d p os si b l y a c ut e m y o c a r d i al i n fa r c t i o n. ( S ee al s o C h a pt er 1 8 , q ue s t i on A . 11 .) A l t ho u gh n i tr at e s an d - a dr en e r g i c bl oc k er s a r e e f fe ct i v e f or an g i n a, th e c al c i u m c h a nn el bl oc k er s a r e l o ng er ac ti n g an d m ay be us ed i n t h e pr e s e nc e o f c hr on i c ob s tr uc t i v e p ul m o n ar y d i s ea s e an d a st h m a . C al ci u m al s o pl a y s a k e y r o l e i n c a r d i ac e l ec t r i c a l a c t i v i ty . T h e e l e c t r i c a l ac t i v i t y o f th e s i n o at r i a l ( S A ) a nd A V n o da l c el l s a r e e sp ec i al l y d e pe n de n t on th e c al ci u m or s l o w c u r r en t , w h e r e a s th e r em a i n i n g o f t he s p ec i a l i z ed c o nd u c t i o n s y s t em i s m or e d ep e nd en t o n t he so di u m or f as t cu r r en t . Ve r ap a m i l ha s a m o r e p r of ou n d i nf l u e nc e o n th e c a l c i u m c ur r e n t of th e S A an d A V n od e s . T h i s d r ug h a s be e n m os t u s e fu l i n t he t r e a tm e nt o f s up r av en t r i cu l ar P.143 t ac hy a r r hy t hm i a s , w h i c h a r e of te n c a us ed by r e en tr y t hr o ug h t he A V n o de . I n c o n tr as t , ni f ed i p i ne h a s l e s s i n f l u en c e o n t h e S A n od e a nd no e f fe c t on A V c on du c ti on ti m e . T he r ef or e , ni f ed i p i ne m i gh t b e u se d w he n f ur th e r s u p pr es s i o n o f AV c o nd u c t i o n i s u nd e s i r a b l e . T he r e l a t i v e c a r d i ov a s c ul a r ef fe c ts o f c al c i u m c h a nn el bl oc k er s a r e s h ow n i n T a b l e 7 . 1. V e r a pa m i l w a s fo u nd t o p r o f ou n dl y d ep r e s s th e c ar d i o v a s c u l a r s y s t em d u r i ng hi g h c o nc e nt r a t i o ns of h al ot h an e , en f l u r a n e, o r i so f l u r a n e an e st h es i a . H ow e ve r , b e ca u s e o f a t e nd e nc y fo r i nc r ea s e d i nc i de n c e o f s i n u s ar r e s t an d b r ad y c a r d i a an d m or e h em od y na m i c d ep r es si o n d ur i n g e nf l ur an e a ne s th e si a, R o ge r s et al . c o n c l u de d t ha t i nt r a v en ou s v e r a pa m i l i s b et te r t ol e r a te d d u r i ng l o w- do s e is o fl ur a ne an d h al ot h an e a ne s th es i a th a n d ur i n g c om p ar ab l e co n ce n tr at i o n s o f en f l u r a n e an e s t he s i a .

Table 7.1 Relative Cardiovascular Effects of Calcium Channel Blockers. VERAPAMILDILTIAZEMNIFEDIPINE Antiarrhythmic Cardiac depression Vasodilation Tachycardia +++ ++ + ++ + ++ + +++ ++

C ur r a n M P, R o bi n s o n D M , K ea t i n g G M . I n tr av e no u s ni ca r di p i n e: i t s us e i n t he s h or t - t er m t r e at m en t o f hy p er t e n s i on an d v ar i o u s o t h er i n di c at i o n s . D r u g s 2 00 6 ;6 6( 1 3) :1 7 55 1 7 82 . G r a dm a n AH , V i v a s Y. N e w dr u gs f o r hy p er te n si on : w h at d o t he y o ff e r ? C u r r H y p e r t en s R ep 20 0 6; 8( 5 ) : 42 5 4 3 2. R oy s t e r R L , B ut te r w o r t h J , G r o ba n L , e t al . C ar d i o va s cu l a r p ha r m a c o l og y . In : K ap l a n J A , R e i c h D L, La k e C L , e t a l . e d s . K a pl an ' s c ar di a c an e s t he s ia . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :2 2 5 2 30 .

B.9. How would you premedicate the patient? Why?


T he p a ti en t s ho u l d be s e da te d w e l l , to pr ev e nt a n xi e ty , w h i ch m a y pr e c i pi t at e a ng i n a . W e us ua l l y a d m i ni s t e r a s ho r t ac t i n g b en z o d i a z ep i n e ( m i d az ol a m 1 t o 2 m g) IV a s s oo n a s b as i c m o ni t or i n g i s a pp l i e d. A l t ho u gh a t r o p i n e o r sc o po l a m i n e i s no t c on t r a i n d i c at e d, a t r o pi n e i s no t g i v en at th e N ew Y o r k P r e s by t e r i a n H os pi t al - C o r n el l M e d i c a l C en t e r b ec a us e o f th e p os s i b i l i t y o f ta c hy ca r di a , w h i c h w i l l i nc r e a se O 2 d em an d . A l l a n ti an g i n al an d a nt i hy pe r te ns i ve d r ug s a r e c o nt i n u ed up t o t he ti m e of s u r g er y .

C. Intraoperative Management C.I. Before Cardiopulmonary Bypass


C.I-1. How do you monitor the patient?

E C G s i m u l t an e ou s l ea d s V 5 a n d II , m ul ti p l e - l e ad S T - s eg m en t a na l y s i s i f a v a i l a bl e A r t er i a l l i n e f or BP a n d a r t er i a l b l o o d g as es P A c a t he te r p ul m on ar y a nd ce n tr al v e no u s pr e ss ur e s ( C VP ) , he m od y n a m i c p ar am e te r s ( c ar di a c ou t pu t , s t r o k e v o l um e, s y s t e m i c a nd p u l m on a r y v as cu l ar r es i st an c e)

C VP l i n e o n l y i f t he pa ti e nt h a s go o d l ef t ve n tr i c u l a r f un c t i on a n d n o pr o bl em s a r e ex pe c te d U r i ne o u tp u t T e m pe r at ur e e so p ha g ea l ( o r P A) an d b l a d de r ( or r ec t al o r t y m p an i c or n a s o ph a r y ng e al ) P.144

L ab or a to r y ar te r i a l b l o od ga se s , el e ct r o l yt es , h em a to cr i t, A C T , a nd ox y g e n s at ur a ti on of t h e m i x ed v e no u s bl o od ( S VO 2 ) O x y ge n a na l yz er fo r i ns pi r e d g a s m i xt u r e E nd - t i da l C O 2 a na l y z er P ul s e ox i m e te r fo r p l e t hy sm o gr ap h y ( a d eq u ac y o f pe r i p he r al p u l s e, pu l s e r at e ) an d a r te r i al ox y g e na t i o n T r a ns e s o ph a ge a l ec h oc ar d i o gr a ph y ( T E E) i f n o t co n tr ai n di c a t ed ( e s o ph a ge a l [s tr i c t ur e o r s te no s i s , v ar i c es , Z en k er ' s di v er t i c u l u m ] o r s t o m a c h [ r ec e nt h i s to r y of b l ee d i n g, ac ti v e ul c er s] p a th o l o gy )

C er eb r al o x i m et e r es pe c i a l l y f or pa ti e nt s w i t h h i g h r i s ks o f p o s t op e r a ti v e ne u r o l o g i c o u tc o m e s , s u c h a s t ho s e u nd er g oi ng hy p ot h e r m i c c i r c u l a t or y

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a r r es t.

B i s pe c tr al i n de x t o e ns ur e a de q ua t e l e v el o f u nc o ns ci o us n es s a nd e l i m i n a te t h e r i s k of i n tr ao p er a ti v e a w ar e ne s s .

C.I-2. What is Allen's test?


T he A l l e n' s t e s t i s u se d t o d et ec t t he pr es e nc e o f ad e qu a te c o l l at e r a l u l n a r c i r c u l a ti o n. T h e r a d i a l a nd u l na r a r t er i es a r e oc c l u de d b y t he ex am i n e r ' s h a nd s. T he p a ti en t i s t he n a sk ed to m a ke a ti g ht f i s t t o e m p ty th e b l o o d fr om th e h an d . T h e h an d i s h el d a bo v e th e h e ar t l e v el t o h e l p v e no us dr ai n ag e . If t h e p at i e n t i s un de r a n es th e si a, th e b l o od i n t h e h an d m ay b e d r a i ne d b y a t hi r d pe r s o n s qu ee z i n g t he h a nd . T he n t he fi s t i s o p en e d s l o w l y an d p u t do w n to th e h ea r t l e v e l . On l y th e u l n a r co m pr es s i o n i s r e l e a se d a nd th e f l u s h of t h e h an d i s w a t c h ed .

N or m a l l es s t ha n 7 s ec o nd s ( pr e se nc e o f a de q ua te co l l a te r a l c on n ec ti o ns b e tw ee n t h e s u p er fi c i a l [u l na r ] an d d ee p [ r a d i a l ] pa l m a r ar c he s ) B or de r l i ne 7 to 15 s e co nd s A bn or m al g r ea te r t ha n 1 5 s ec o nd s

A m od i fi ed Al l e n 's te st m a y be do n e w i t h a D op pl e r de t ec to r o r a p ul s e ox i m e te r . T h e r es u l t s o f Al l e n ' s te s t ar e a bn o r m al i n a p pr ox i m a te l y 3% o f y ou n g h ea l t h y i n d i v i d u al s . H o w e v er , S l o go f f et al . s tu di e d th e c o m p l i c a t i o ns fo l l o w i ng r a di a l ar t er y c an nu l at i o n i n 1 69 9 c ar d i o v a s c u l a r s ur g i c al pa ti e nt s . T h ey c on c l u de d t ha t i n th e a b se nc e o f p er i p h er a l va sc u l a r d i s ea s e, A l l e n 's t e s t i s n ot a pr e di c t o r of i s c h e m i a o f th e h an d d u r i ng or a f te r r a d i a l a r t er y c an n ul a ti on , a nd t h at r a di a l ar te r y ca n nu l a t i o n i s a l ow - r i sk , h i g h- b en ef i t m o n i t or i ng t e c h ni q ue t h at de s e r v e s w i d e c l i ni c a l u s e . H ow e v e r , i n t h e c u r r e nt l i ti g i o us s e tt i ng a nd i n t he fa c e of so m e e v i d e nc e t o th e c on t r a r y , i t i s pr ob a bl y p r u d en t t o c o n ti nu e t o p er fo r m Al l en ' s te s t an d d oc u m e n t th e r es u l t s . S o m e a u th o r i ti es st i l l c on s i d er t h e us e o f A l l en ' s t es t a s th e s ta n da r d of c a r e . A l a s t r ue y J , Pa r k e r KH , P ei r o J, et a l . C a n t he m o di f i e d A l l en ' s t es t a l w ay s d et e c t s u ff i c i e n t c o l l a t e r al f l ow i n t he ha n d? A co m p u ta ti o na l s t u dy . C om p ut M et ho d s Bi o m e c h Bi om e d En g i n 20 06 ; 9( 6) : 35 3 3 61 . B ar be a u GR , A r s e na ul t F , D ug as L, e t a l . Ev al u at i o n o f t he ul no p al m a r a r t e r i al a r c h e s w i th pu l s e o x i m et r y an d p l e th y s m og r ap h y : c om p ar i s o n w i t h th e A l l en ' s t es t i n 10 1 0 pa t i e n ts . Am H e ar t J 2 0 04 ;1 4 7( 3 ) : 48 9 4 93 . C ed er h ol m I , So r en se n J , C ar l s so n C . T hr om b os i s fo l l o w i ng pe r c u ta ne o us r a di a l ar te r y c a n nu l at i o n . Ac t a An a es th e s i ol Sc an d 1 9 86 ;3 0 :2 2 7. H i l di c k - Sm i t h D . U s e o f t he Al l e n 's t e st a n d t r a ns r a d i a l c at h et er i z a ti o n. J A m C ol l C ar d i o l 2 00 6; 4 8( 6 ) : 12 8 7. R ei c h D L , M i t tn ac h t A, Lo n do n M , et al . M on i t o r i ng of t h e he a r t a n d v a s c u l a r s y s t em . I n: K a pl an J A , R ei c h D L , L ak e C L, e t a l . e d s . Ka pl a n' s c ar d ia c a ne s t h es i a . P h i l ad e l p hi a : W B Sa un d er s, 20 06 : 38 8 . P.145 S l o go f f S, Ke at s A S, Ar l u n d C . On t h e sa f et y o f r a d i a l a r t er y c an n ul at i on . A ne s t h es i o l og y 1 98 3 ;5 9 : 4 2.

C.I-3. Why do you need multiple temperature monitoring?


I n m a n y m e d i c al c e nt e r s , m e a su r e m en t o f tw o o r m or e t em pe r at ur e s i s a c o m m o n p r a c t i c e . D u r i n g c oo l i n g a nd r e w a r m i n g , th e r e i s u n ev en di s t r i b ut i on o f b od y h ea t . Es o ph ag e al , n as o ph ar y ng ea l , bl a dd e r or ty m p an i c s i t es m e as ur e c or e t em p er at u r e ; t he r e c t al s i te r e pr e s e nt s p er i ph er a l te m pe r a t ur e. D u r i n g c oo l i n g an d r ew a r m i n g b y t he e x tr ac o r p or e al c i r c ul a ti on ( E C C ) , th e e s o p ha ge a l te m pe r a t ur e c ha n ge s r ap i d l y , w h er ea s t he r e c t a l t e m pe r a t ur e c ha ng e s s l o w l y . T h e o pp o s i te ch an g es a r e w i t ne ss e d d ur i n g s ur fa c e c oo l i n g or w a r m i n g : th e r ec t al t e m p er a tu r e c h a ng es qu i c k l y , w h e r e a s t h e e s o p ha g ea l t em pe r at ur e c ha n ge s s l o w l y . In or de r t o e st i m a te t h e ac c ur at e t em p er at u r e a n d to ac h i e v e ev en di s t r i b ut i on o f b od y h e at , i t i s n e c e s s a r y t o r ec o r d b o th e s o ph a ge a l an d r ec t al t e m p er a tu r e s . H o w ev er , b l a d de r t em pe r at ur e m on i to r i n g th r ou gh a u r i na r y bl a dd er c a th e te r i s qu i te c o nv en i en t a nd po pu l ar , a s it r ef l e c ts a b o dy te m p e r a tu r e be t w e en es o ph ag e al a n d r ec ta l t em p er at u r e . T em pe r at ur e s ar e m ea s ur ed du r i n g co o l i ng , t o e ns u r e t h at t h e or g an s m os t s us c e p ti bl e t o p ot en t i a l h y p o pe r f u s i on ac tu a l l y r ec ei v e th e p r o t ec t i v e ef f ec t o f t he d e s i r e d h y p o th e r m i a . I n th i s r e g ar d, th e b r a i n i s t h e or g an m o s t l y m o ni t or ed na s o p ha r y n ge a l , t y m p an i c m e m br an e a nd es o ph ag e al t e m p e r a tu r e s a r e th e u s u al l y ac c ep te d b e st e st i m a te s o f b r a i n te m p e r a tu r e, a l th ou g h t he y , at t i m e s , o v er e s t i m at e o r u nd e r e s t i m a te t h e a c t ua l b r a i n t e m pe r a t ur e. D u r i n g r ew ar m i n g, c e r e b r a l hy p er th e r m i a i s o f te n d et e ct ed an d s ho u l d b e a v o i de d ( by m a i n ta i ni ng a g r a di e nt o f 5 C be tw e en t h e ar t er i a l b l o o d a nd b r ai n, w i th th e b r a i n ha v i n g th e l o w e r te m pe r a t ur e) an d c or r e c te d i m m ed i at el y , be c au s e i t i n c r ea s es t h e c e r eb r a l o x y g en c o ns u m p ti o n, a n d m a y e x a c er ba t e po s to p er at i ve n eu r o p s y c h o l o g i c d ys f un c ti on . G r a v l e e GP , D av i s R F , K ar us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 6 7 56 8 . M or a- M a n ga n o C T , C ho w J L, Ka ne v sk y M . C a r d i op u l m on a r y b y p a s s a n d t he a n es th e s i o l o gi s t. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n 's ca r d i ac a ne s t h es i a . P h i l ad e l p hi a : W B Sa un d er s, 20 06 : 89 9 9 0 0.

C.I-4. How do you know that the tip of the pulmonary artery (PA) catheter is in the RV or PA?
T he r e ar e t hr ee m a i n di ff e r e nc e s i n th e p r e ss u r e t r ac i n g s, a s s ho w n i n F i g. 7. 4.

Figure 7.4 Pressure tracings of right atrium (RA), right ventricle (RV), pulmonary artery (PA), and pulmonary artery occlusion pressure (PAOP).

P.146

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D i a s t o l i c Pr e s s ur e I s H i g he r i n P A th a n i n R V , b ec au s e th e c l o s ed pu l m o na r y v a l v e m ai n ta i n s a d i as to l i c g r ad i e n t be t w e en t h e P A a nd t h e R V

P A pr e s s ur e 2 0 2 5/ 5 1 0 m m Hg R V pr e s s ur e 2 0 2 5/ 0 5 m m H g

Pressure Contour

P A pr e s s ur e t r a ci n g h as a di cr o ti c no t ch , w hi ch i s c r ea te d b y t he c l os ur e o f p ul m o n ar y v al v e , a n d th e d i a s to l i c p ar t i s de s c e n d i ng ( d ec r ea s i n g) . R V pr e s s ur e t r a ci n g h as a sh ar p d r o p a nd a p l a te a u i n ea r l y d i a s to l e , a nd th e d i a s to l i c p ar t i s as c en di n g ( i n c r ea s i n g) .

Ventricular Filling

I n th e l at e d i a s to l i c p ha s e, P A p r e s su r e i s d e cr ea s i n g, be c a u s e of d i as to l i c r un o ff i n t h e pu l m o na r y c i r c u l a ti o n, w h er e as t h e R V pr es su r e is i nc r e a s i ng , b ec a us e o f ve n tr i c u l a r f i l l i ng .

C.I-5. What is normal pulmonary artery occlusion pressure (PAOP)?


N or m a l 4 t o 1 2 m m H g B or de r l i ne 13 t o 1 7 m m H g H ea r t fa i l u r e o ve r 1 8 m m H g

B r a un w al d E , Z i p es D P , Li b by P , e ds . H ea r t di s ea se , a t e xt bo o k of c a r d i ov as c ul ar m e di c i n e , 6t h e d. P h i l ad e l p h i a : W B Sa u nd er s , 20 0 5: 4 09 4 1 1.

C.I-6. Is it necessary to monitor pulmonary artery (PA) pressure for coronary artery operations?
T he i n di c a t i o n t o m o n i t or PA p r es su r e de p en d s on th e l ef t v en tr i c u l a r f un c ti on . P at i en ts m a y b e di v i d ed i n to tw o c at eg o r i es on t h e b as i s o f l e ft v en t r i cu l ar f un c t i on . F or p a ti en t s w h o h av e g o od l e ft v e nt r i cu l ar f u nc ti o n ( e j ec ti o n fr a c t i o n s > 0 .5 a n d n or m a l v en tr i c u l a r w al l m ot i o n ) , t h e C V P c or r el at e s w e l l w i th th e P AO P; th er e fo r e , p ul m on ar y p r e s su r e m o ni t or i n g m ay n o t b e ne c es s a r y fo r t hi s g r o u p of pa ti e nt s . On t h e ot h er h a nd , f or pa t i e nt s w i t h p oo r l ef t v en tr i c u l a r f un c t i on ( e j e c t i on f r ac ti o ns < 0 .4 or v en t r i cu l ar d y ss yn e r g y) , t he C V P d oe s n ot c o r r el a te w i th t h e PA O P; t h er ef o r e , p ul m o n ar y p r e s s u r e m o ni t o r i n g i s i nd i c a te d. Ot he r i nd i ca ti o ns f o r m o n i t or i ng P A p r e s su r e i n cl u de t h e pr e s e n c e o f p ul m on ar y h y p e r t en s i o n, c o m b i ne d c or on a r y s t en o s i s an d v a l v ul a r di se a se , a nd c o m p l e x c ar d i a c l es i o n s. H ow ev e r , i n a r e c e nt ob se r va ti o na l s tu dy of c r i t i c al l y i l l p at i en ts , a ft e r ad j us tm e nt f o r tr ea t m e n t s e l e c ti on bi a s , m on i to r i n g PA pr es s ur e w as a s s o c i a te d w i t h i nc r e a s e d m or ta l i t y an d i n cr ea s ed u t i l i z a ti on of r e so ur c es . T h e c a us e o f th i s ap p ar en t l ac k o f b en e fi t i s un c l e ar . T he r e s u l t o f t h i s a n al y s i s s h o ul d b e c on fi r m e d i n ot h er s t ud i e s . T h e se f i nd i n g s j u s ti fy r e co n si de r at i o n o f a r an d om i z e d c o n tr ol l ed t r i a l o f r i g ht h e ar t c at he t er i z a t i on an d m ay g u i d e p at i en t s el ec t i o n f or s u c h a st ud y . C on no r s AF , S pe r of f T , D a w s o n N V , e t a l . T h e ef f ec ti v en es s o f r i g ht he a r t c at h et e r i z a ti o n i n i n i t i al c a r e o f c r i ti c al l y i l l p at i e n ts . J AM A 19 9 6; 2 76 : 8 8 9 8 97 . D j a i a n i G, Ka r s k i J , Y u di n M e t a l . C l i n i c a l ou t co m e s i n p at i e n ts u n de r g o i n g e l e c ti v e c o r o n ar y a r t er y b y p as s g r a f t s u r ge r y w i th a n d w i t ho u t ut i l i z a t i o n o f p ul m o n ar y a r t er y c at h et er - g e ne r at ed da ta . J C a r d i o t ho r a c V a sc A n es th 20 06 ; 20 :3 0 7 3 10 . F on te s M L, Be l l o w s W , N go L , e t a l . M c SP I R es ea r ch G r o u p. As s e s s m en t o f v e n tr i c u l a r f un c t i on i n c r i t i c al l y i l l p at i e n ts : l i m i t at i on s o f p ul m o n ar y a r t er y c at he t er i z a ti on . J C a r d i o t ho r a c V as c A ne s th 1 9 99 ; 13 :1 8 M an ga n o D T . M on i to r i n g pu l m o na r y ar t er i a l p r e s su r e i n c o r o na r y - ar te r y di s ea s e . A ne s th e s i ol o gy 1 9 80 ;5 3 :3 6 4 36 9 . P.147 V en de r J S. Ed i t o r i al : P ul m on ar y a r t e r y c at h et e r ut i l i za ti o n: T h e us e , m i s us e, or a b us e. J C a r di ot h or ac Va s c An es t h 20 0 6; 2 0: 29 5 2 9 9.

C.I-7. What are the complications of PA catheterization? From Venopuncture Sites (as for central venous pressure)
C om m o n c om p l i c a ti o ns :

I nf ec t i o n s ep si s H em at o m a Air embolism T h r om b os i s C at he t er s h ea r i n g an d e m b o l i za t i o n

S ub c l a v i an ap p r o ac h :

P ne um o th or a x H em ot h or ax H y d r o t ho r a x

I nt er n al j u gu l a r a pp r oa c h:

P ne um o th or a x

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N ec k h em at o m a f r o m p u nc tu r e of ca r o ti d a r t e r y P os s i b l e v a gu s n er ve i n j u r y an d b r a c hi al pl ex u s i n j ur y T h o r a c i c d u c t p e r f or a ti on fr om l e ft s i de a p pr oa c h

T he b a s i l a r o r c e p ha l i c v e i n a p pr oa c h h as f e w e r co m pl i c a ti on s , bu t t he fa i l u r e r a te i s h i g h er .

From Pulmonary Artery Catheter


A r r hy th m i a s 1 .5 % t o 1 1% , c om pl e te h e ar t b l o ck , t hr o m b oe m bo l i s m , p u l m on a r y i nf a r c ti o n fr o m c o n ti nu o us w e dg i ng , m a s s i v e he m o r r h ag e f r o m p e r f or at i on o f P A or r i gh t a tr i u m ( R A ) , fa i l u r e t o w ed g e, he m o p ty si s , i n tr a ca r d i ac k n ot ti n g, b a l l o on r u pt ur e , en d oc a r d i a l t hr om b i , a n d t r i c u s p i d v a l v e i n j u r y . F on te s M L. C o m p l i c at i o n s o f ce n tr al v e no u s ca n nu l a t i o n. Pr ob l em s i n an e s t h es i a . P hi l a d el p hi a: Li pp i nc o t t W i l l i a m s & W i l k i n s , 19 9 8. M ur ph y G S, Ve nd e r JS . M on i to r i n g th e a ne s th e ti ze d p at i en t. In : B ar as h P G, C u l l e n BF , S to e l t i n g R K, e d s . C l i n i c a l an e s t h es i a , 5 th ed . P hi l a d el ph i a: L i p pi n c o tt W i l l i a m s & W i l ki ns , 2 00 6 :6 7 8 6 79 . R ei c h D L , M i t tn ac h t A, Lo n do n M , et al . M on i t o r i ng of t h e he a r t a n d v a s c u l a r s y s t em . I n: K a pl an J A , R ei c h D L , L ak e C L, e t a l . e d s . Ka pl a n' s c ar d ia c a ne s t h es i a . P h i l ad e l p hi a : W B Sa un d er s, 20 06 : 40 4 4 0 6.

C.I-8. What are the hemodynamic consequences of myocardial ischemia? How can you detect myocardial ischemia? Is PAOP a sensitive indicator of myocardial ischemia?
F or f o ur d e c a de s f ol l ow i n g T en n an t a nd W i gg e r s ' c l a ss i c ob s er v a t i o n o n th e e f fe c t s o f c o r on a r y o c c l us i o n o n m y o c a r di al c o n t r ac t i o n, i t w as be l i e v e d t ha t t r a ns i en t s ev er e i s c h em i a ca us e d ei t he r i r r ev e r s i b l e ca r d i ac i n j u r y th at i s , i n f ar c t i on o r p r o m pt r e c o v e r y . H o w e v e r , i n t h e 1 97 0s i t b e c a m e c l ea r t ha t a ft e r a b r i e f ep i s o de of s e ve r e i s ch e m i a, pr ol o ng e d m y o ca r d i a l d ys f un c ti on w i th g r ad u al r e tu r n of c o nt r a c ti l e a c ti v i t y oc c ur r e d , a c o n di t i o n t er m e d m y o c ar di a l s tu nn i ng . A l t er n at i v e l y , s ev er e c hr o ni c i sc he m i a c a n r e su l t i n di m i n i s he d c on t r a c t i l e p e r f or m an c e s u c h as c h r o ni c r eg i on a l w a l l m o ti o n ( R W M ) a bn o r m al i ti es ( hi be r na ti o n) . P.148 A c u te m y oc a r d i a l i sc he m i a a f fe ct s s ys t ol i c an d d i a st o l i c p um p f un c t i on . D i a s t o l i c d y s fu n c t i o n u s u a l l y m an i f e s t s b ef or e s y s to l i c a l t e r a t i o ns i n f u nc ti o n. T h e i m m ed i a t e i m p ac t o n v en tr i c u l a r c om pl i an ce i s r e l a te d t o t he e t i o l o g y o f th e i s c h em i c e v en t . D e c r e as ed m y oc a r d i a l o x y g en s u pp l y i s i n i t i a l l y a c c o m p a ni ed b y an i n c r e as e i n c o m pl i a n ce . I n co n tr as t , i n c r e as e d m y o ca r d i al o x y g en de m a n d i s as s o c i a te d w i t h a n i m m ed i at e l os s o f v e n t r i c u l a r c om pl i an c e ( e .g . , th e v en tr i c l e b ec om e s st i f f er ) . T h er e fo r e , t he ve nt r i c l e r e qu i r e s a h i g h er f i l l i n g p r e s s u r e ( e nd di as t ol i c p r es s u r e [E D P] ) t o m a i nt ai n a g i v e n s tr ok e v ol u m e . A c as c a d e of ev en t s o cc ur s, th at m a y i nc l u d e w a l l m o t i o n a bn or m al i t i es , d y s r h y t h m i as , a nd c o n du c t i on b l oc k . An 8 0 % r e d uc t i o n o f c o r o n ar y b l o o d fl o w c a u se s a k i ne s i s , w he r e a s a 9 5% d e cr ea s e ca u se s d ys k i n es i s . I f t he i s c h em i a be c om es s e v e r e, t h e r i s e i n ED P w i l l l e a d to pu l m o na r y ed e m a ( F i g . 7. 5 ) . A l t ho u gh a nu m be r o f se n si ti ve te ch n i q u es a r e av a i l ab l e fo r d et e c t i o n o f i s c he m i a , s uc h a s m a g ne t i c r es o na n c e s p ec t r o s c op y , r a d i o - l a be l e d l ac t at e d et er m i n at i on s , or d i r e ct m e as u r e m e n t of en d- d i a st o l i c p r e ss u r e , th e s e ar e i m p r a c t i c a l . T h e m os t p op ul a r an d a c c e pt e d s i g n of i s c h e m i a i s EC G S T s eg m e n t c h a ng e s . T he EC G c r i te r i a f o r i s ch e m i a a r e h o r i zo n ta l o r do w n- s l o pi ng ST - s e gm en t d e pr es s i o n a t l e a s t 0 . 1 m V at 0 . 06 s e c o nd fr om J - po i nt , u ps l o pi n g ST - s e gm e nt d e pr es s i o n a t l e a st 0 . 2 m V at 0 . 08 se co n d fr o m J - po i nt , a nd ST - s eg m en t e l e v at i o n a t l ea s t 0. 15 m V ( 1 m V = 10 m m ) . O th e r EC G s i g n s o f i s c he m i a i nc l u d e i nv er t ed T w a ve s a nd a ne w o n se t o f ar r h y th m i a s or c o nd u c t i o n a b no r m a l i ti es .

Figure 7.5 Hemodynamic consequences of myocardial ischemia. Ischemia occurs when demand exceeds supply. CHF, congestive heart failure; EF, ejection fraction; LVEDP, left ventricular end-diastolic pressure; LVEDV, left ventricular end-diastolic volume; ST, ST-segment changes. (From Barash PG. Monitoring myocardial oxygen balance: physiologic basis and clinical application. ASA Refresher Courses in Anesthesiology 1985;13:24, with permission.)

P.149 R eg i o n al w a l l m o ti on ab no r m a l i t i e s ( R W M A ) , de te c te d w i t h t w o - d i m e ns i o n al ec ho c ar di o gr ap h y , h a v e be en s h o w n t o b e t he e a r l i e s t a n d m os t s en s i t i v e s i g n o f m y o c a r d i al i s c h em i a . R W M A a r e p r od u ce d w i t h j us t 2 5% d e c r ea s e i n c o r o n ar y b l o od fl o w i n t h e a bs en c e of EC G c ha ng e s , w h er ea s E C G s i gn s o f i s c he m i a a r e ap p ar en t w i t h a 5 0 % d ec r e a se i n c or o na r y bl oo d f l o w . D u r i n g e x e r c i s e , p at i e n ts w i t h C AD de v e l op R W M A a f te r 3 0 s e c o n ds , w he r ea s E C G c ha ng e s d o no t o c c u r un t i l a f te r 9 0 se c on ds . S m i t h et al . f ou nd th at R W M A w a s fo u r ti m es m o r e s e ns i t i v e t h an E C G ST - s e gm en t c ha n ge i n d e t e c t i ng i nt r a o pe r a t i v e i s c he m i a . M o r eo v er , ST ch an g es ca nn o t be an a l y z e d i f th e p a ti en t h as c o nd u c t i o n d i s t ur b an c e s , s u c h as bu nd l e- b r a nc h b l o c k or v e nt r i c ul ar p ac ed r h y t h m s . T he y h av e a l s o f ou n d th a t pa t i e nt s e xp e r i en c i n g p er s i s te nt R W M A w e r e m o r e l i k e l y to h a v e m y oc ar d i a l i nf ar c t i on t h an th os e h av i ng on l y

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t r a ns i en t c ha ng e s . N o p a ti en t w i t ho u t a n ew w a l l m o ti o n ab n or m a l i t y h ad m y oc ar d i a l i n f ar c t i on . A l t ho u gh T E E i s th e m os t s en s i t i v e m on i t o r fo r m y o c a r di al i s c he m i a , a r ec e nt s tu d y b y Ei se n be r g et al . c on cl u de s t ha t, r o ut i ne m o ni to r i n g f or m y oc ar d i a l i s c he m i a w i t h T EE or 1 2 - l ea d E C G du r i n g n on c a r di ac s u r g e r y a pp e ar s to ha v e l i tt l e i n c r e m e n ta l c l i ni c al v a l u e o ve r p r e op e r a ti v e c l i ni c a l d at a a nd tw o- l ea d E C G m o ni to r i n g, i n i d en ti f y i ng p a ti e nt s a t h i g h r i s k fo r p er i o p er at i v e i s c h em i c ou t co m e . M ea s u r em en t o f P AO P h as b e en su gg e st ed as a n e a r l y a nd s e ns i t i v e i n di c a t or o f i s c he m i a , t o be us e d w h e n t h e E C G i s n o t di a gn o s t i c . A l t ho u gh ac ut e i nc r e a s e s i n PA O P or de ve l op m e n t of V w a v es m a y r e f l e ct i s ch em i a, t h e ab s en c e of a c h a ng e i n P AO P d oe s n ot e n s u r e t h e a bs e nc e o f i s c he m i a . H a g gm ar k e t al . r ep o r t ed th at th e s en si t i v i t y , sp e ci fi ci t y, a n d pr e di ct i ve v a l u e ( po s i t i v e a nd n e ga t i v e) of P A O P a b no r m a l i ti e s fo r i s c he m i a r a ng ed be t w e en 40 % a nd 6 0% . I n C A B G pa t i e nt s , Li e be r m a n e t al . a l s o f ou n d a l ow p o si ti v e pr e di c t i v e v a l u e ( 2 4 %) bu t a h i g h er n e ga t i v e p r e di c ti v e v a l u e ( 85 % ) ; h o w e v e r , th e P AO P w as n o b et t er t h an C V P m e a su r e m en t, ex ce p t i n pa t i e nt s w i t h m od e r a te to s e v e r e pr eo p er at i v e v e nt r i c ul ar d y s f u nc t i o n. L e un g e t a l . f ou n d t ha t 6 1% o f T EE w al l - m o t i o n a bn o r m al i t i es i n C AB G p at i en ts oc cu r r e d w i t ho u t s i g ni fi c an t c ha n ge s ( > 20 % o f c o n tr o l ) i n H R , s y s t ol i c ar t e r i a l p r e s s u r e , o r PA p r es s u r e. O n l y 1 0% o f e pi s od e s w e r e ac co m pa n i e d b y 5 m m H g or g r e a te r c ha n ge s i n PA pr es s ur e. R o i z e n et al . f ou nd t h a t 11 ou t o f 12 pa ti e nt s d ev e l o pe d T EE w a l l m ot i o n a bn o r m al i ti es w h en th e a or ta w a s c r o ss - cl am pe d a b ov e t he s u pr a c e l i a c ar te r y , b u t th a t PA O P r e m ai ne d n o r m al ( 1 2 m m H g ) i n 10 ou t o f 12 , w it h o nl y 2 o ut of 1 2 h a v i ng tr an s i e nt i n cr e as es . T he r ef or e , th e se s t ud i e s q ue s ti on th e v al u e of PA c a th et e r i z a t i o n a nd m o ni t o r i n g f or d e te c t i on o f i n t r ao p er at i v e i s c he m i a . B ar as h P G. Se qu e nt i al m on i to r i n g o f m y oc a r d i a l i sc h em i a i n t h e pe r i o pe r at i v e p e r i od . A SA A n nu a l M e e ti ng R e fr e s h er C o ur s es L e c t ur e s , P a r k R i d g e, I L . A m e r i c a n S o c i et y o f A ne st h es i o l og i s t s. 2 0 02 ;2 3 3. E l l i s J E , R o i z e n M F , M a nt ha S, e t a l . An es t he si a f or va sc u l a r s ur ge r y . I n B ar as h P G, C u l l e n BF , S to e l t i n g R K, ed s . C l i n i c a l a ne s t h es i a , 5 th ed . P hi l a d el ph i a: L i pp i nc ot t W i l l i a m s & W i l k i n s , 20 0 6: 94 2 9 4 5. H ag gm a r k S , H oh n er P , O st m a n M , e t al . C om p ar i s o n of he m o d y n a m i c , e l ec tr o c a r d i og r a p hi c , m e c h a ni c a l , an d m et a bo l i c i n di c a t or s of i n tr a op e r a ti v e m y o c a r di al i s c h e m i a i n va sc u l a r s ur gi c al p a ti en t s w i t h co r on ar y a r t e r y d i s e as e . An e s t he s i o l o g y 19 8 9; 7 0: 19 25 . L on d on M , M i t tn a c h t A , Ka p l a n J A. A n es t he si a f or m y oc ar d i a l r ev as c ul ar i z a ti o n. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n ' s c a r d i ac a n es t he si a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :6 2 7 6 28 .

C.I-9. How would you monitor ECG? Why V 5 ? If you do not have precordial leads in your ECG machine, how can you monitor the LV?
M ul ti p l e - l ea d E C G m o n i t or i n g p r o v i d e s th e b es t c l i n i c al l y av ai l ab l e m e th o d o f de t ec ti n g pe r i o pe r at i v e i s c h em i a . B as e d p r i m a r i l y on r e s u l t s o b t a i n e d fr o m e x e r c i s e t r e a dm i l l t es t i n g, co m b i ni ng EC G l ea ds II a n d V 5 , c an d e te c t 96 % o f i s c he m i c e v e n ts , a nd t h e o pt i m a l l e a ds f o r i n tr a op e r a t i v e m y oc a r d i a l i s c h em i a . H ow ev e r , L o nd on et al . r e c en t l y f ou n d t ha t t he s t an da r d P.150 c om bi n at i o n o f l ea d s II a n d V 5 w a s on l y 80 % s en s i t i v e , w h e r e as c o m b i ni ng l e ad s V 4 an d V 5 i n c r e as e d s e n s i t i v i t y t o 90 % i n p at i e n ts w i t h k no w n o r s us pe c te d C AD u n de r g o i n g n on c ar di a c su r ge r y w i th ge ne r al a n es th e s i a . T h e s en s i t i v i t y i nc r ea s e d t o 9 6% by c o m b i n i n g l e ad s I I, V 4 , a n d V 5 . I f on l y on e l ea d c an b e d i s p l a y e d , V 5 s h ou ld be us ed be ca u s e l e ad V 5 h as t h e g r e at e s t s e ns i t i v i ty : 7 5% i n tr ao p er at i v e l y an d 8 9% du r i n g ex e r c i s e t r e a dm i l l t es ti n g. S e e a l s o C ha pt e r 18 , q u es ti o n C . 3 . L on d on M J , H o l l e nb e r g M , W on g M G, e t a l . In tr a op er a ti ve m y oc a r d i a l i s c he m i a : l oc al i z a ti o n by c o nt i nu o us 1 2 - l ea d e l e c tr oc a r d i o g r a ph y . An e s t h es i o l og y 1 98 8 ;6 9: 2 32 2 4 1.

C.I-10. Discuss the principles and clinical applications of intraoperative transesophageal two-dimensional echocardiography
T EE i s a w el l - e s t a bl i s h ed t e ch n i q ue to v i su al i ze c a r d i a c a na t om y a nd f u nc ti o n. E c ho c ar di o gr ap h y i s ba s e d o n f un d am en t al u l tr as o ni c p r i nc i pl es . U l t r a s ou n d i s de f i n ed as s o un d a bo v e th e u p pe r t hr es h ol d o f hu m an h e ar i n g ( 2 0, 00 0 H z ) . T he ul tr as o un d w av e s ( 1 t o 7 M H z ) a r e c r e at ed by a p pl y i n g a n al t er na t i n g e l e c t r i c c ur r en t o f 50 0 t o 1 ,5 0 0 pu l se s p er s e co n d on an a p pr o pr i a te pi e z o el e c t r i c c r y s t a l . A s h or t b ur s t or p u l s e o f h i g h- fr e q u e nc y , l o w - i n t en s i t y s o u nd i s t he n e m i tt e d an d d i r e ct e d th r o u gh th e h um a n bo d y to de te c t bo u nd a r i es be tw e en s t r u c t u r e s o f di f fe r e n t ac o us ti c i m p e da nc e . T h e u l t r as ou n d w a v e i s p ar ti a l l y r e f l e c t e d a t th e b ou n da r y of m e di a w i t h d i f fe r en t a co u s t i c i m pe da n c e , a p r o p er t y th a t i s p r i m ar i l y d e te r m i n e d b y th e s l i g ht d i ff er e nc e i n de n s i ty b et w e e n d i f fe r e n t ti s su es . T he tr an s m i ss i o n o f p ul s ed - r e fl ec t ed u l tr as o un d t hr ou g h t he h e ar t, w i th de t e c t i on of t h e r e t ur ni n g e c h oe s d et a i l i n g t he po s i t i o n a nd m o v e m e n t of c a r d i ac a c ou st i c i n t er fa c es , i s te r m e d ca r di ac ul tr a s o un d o r e c h o c a r d i og r a p hy . T he d i ff er e nc e b et w e e n t he M - m o de an d t w o - d i m e ns i on al t ec hn i qu e s i s t h at t h e M - m od e u l t r a s on i c be am i s a i m e d i n on e d i r e c t i o n a n d th e r e fo r e de p i c ts on l y on e d i m en s i o n o f th e t a r g et s t r u c t u r e i n a n i m a ge th a t d oe s n ot r e s e m b l e ca r di ac st r u c tu r e , w he r ea s b ea m s w e ep s i n a n ar c t o g i v e a p a no r a m i c v i e w o f t he h e ar t t ha t r es ul t s i n c r os s - s ec ti o na l i m a ge s t h at a r e a na to m i c al l y r e c og ni z ab l e . A l s o s ee C h ap t er 8 , q u es ti o n B. 6 . D op pl e r ec h oc ar d i o g r a ph y p r o v i d es an a l te r n a ti ve m e th o d fo r i m a g i n g b l o o d fl o w by a p pl y i n g D op pl e r f r e qu en c y s h i ft a n al y s i s t o ec ho e s re f l e c t e d by a m ov i n g t ar g et ( r e d b l oo d c el l s or c a r d i a c t i s su e ) . T h e D o p pl er pr i n c i p l e s t at e s th a t th e f r e q ue n c y o f t he r e fl e c t ed ul tr a s o un d i s d i f fe r en t f r o m t h e f r e q ue n cy o f th e e m i t te d u l t r a s ou nd . T he sh i f t i n f r e qu e nc y i s pr o po r t i on al to t h e s p e ed of t h e m o v i n g t ar ge t C ol o r - c o d ed D o pp l er f l o w i m a g i n g ( c o l o r D op p l e r ) s i m ul ta n eo u s l y p r e se n ts r e al - t i m e i m a g es o f i nt r ac ar d i a c f l o w a nd s t r u c t u r e i n t w o di m e n s i on s : c o n ti nu o us c o l o r m ap s o f fl o w s u p er i m p os ed on m on oc h r o m a t i c c r o s s- se c ti on a l ec h oc a r d i o g r a m s . C ol or D o pp l er g r ea tl y i m p r o v es th e e v a l u a ti on of v a l v ul a r fu n c t i o n a n d i n t r a c a r d i ac s h un t s . T he c l i n i c a l ap p l i c a t i o ns of i n tr ao p er at i ve e c ho ca r di og r ap h y ar e a s f ol l o w s :

M o n i t o r i ng l e ft v e nt r i c ul ar fi l l i n g a n d ej e ct i o n . W h e n l e f t v e n tr i c u l a r s ho r t - a x i s c r os s - s e c ti o n i s m o ni to r ed a t t h e l e v el o f t he m i dp a pi l l a r y m us c l e s, T E E p r o v i d es t h e an e st he s i o l o g i s t w i t h a d i r e ct , s em i q u an ti t at i v e m et h od t o a s s e s s l e ft v e nt r i c ul ar pr el o ad a n d e j e c t i o n i n r ea l t i m e, an d g ui d e th e a dm i n i s t r a ti o n o f fl u i d s a nd i n ot r o p es .

I s c he m i c h e ar t d i s ea s e. R W M ab no r m a l i t i e s, su ch as h y po k i n es i a , a k i n es i a , a nd dy s k i ne s i a , ar e t he ea r l i es t s i g ns of m y oc ar d i a l i s c he m i a ( F i g s . 7 . 2 a nd 7 . 3) , a s di s cu ss e d i n qu e st i o n C .I - 8 . M ea s ur em e nt s o f s y s to l i c w al l t hi c k e ni ng , a n ot he r e x c e l l en t s i g n o f m y o c a r d i al i s c h em i a, a r e no t r e p r o d uc i b l e be c au se of a di f fi cu l t y i n d el i n e at i n g t h e ep i c a r d i al b o r d er ac c u r at el y i n t w o - d i m e ns i on al ec ho c ar di o gr ap h y . T h e i m p ai r m e nt o f t he d i a s t o l i c fu n ct i o n c a n be qu a l i ta ti v el y e st i m a te d a nd t h e f i l l i ng pr es s ur es c a n b e e s t i m at e d u s i ng a c o m bi na t i o n o f s p e c t r a l D o p p l e r m ea s u r em en t s of t he b l oo d f l o w t hr ou g h t he p u l m on a r y v e i n s a nd t h e m i t r a l v al v e .

V al v u l ar h e ar t d i s ea s e A i r e m b o l i s m . I n t he l e ft a t r i um , L V, a n d a or ta , a i r em bo l i s m c a n b e d et e c t ed by T E E du r i n g o pe n - h ea r t s u r ge r y . T he r e f or e, T E E c an b e u s ed t o h el p t he s u r g eo n e va c ua t e ai r b ub b l e s f r o m t he l e ft h e ar t b ef or e t he he a r t e j e c ts b l oo d a nd ai r i nt o t he s y s t em i c c i r c u l a ti o n. P.151

V al v u l ar r e gu r g i ta ti o n. V a l v ul a r r e g ur gi t at i o n c an be d e te r m i ne d i nt r a o pe r at i v e l y b y c ol o r D o pp l er e c ho c ar di o gr ap h y be f or e a nd i m m e di a te l y af te r c on s e r v a ti v e va l ve r ep a i r ( a nn u l o pl a st y, co m m i s s ur ot o m y ) , o r v al v e r e p l a c e m en t. T h e d eg r ee o f v al v ul ar i n c o m p e te n c y c a n be ac c u r at el y m ea s ur ed u s i ng a c o m bi na t i o n o f tw o - d i m e ns i o n al a n d D op pl e r te c hn i q u es ( F i g s . 7. 6 a nd 7 . 7) a n d t he f u nc ti o n of t h e r ep a i r ed o r r ep l ac ed va l v e c a n be q ua nt i ta ti v el y e va l u a te d .

V al v u l ar s te n os i s. S p ec tr a l D o p pl er e c ho c ar di o gr ap h y ca n b e u s e d i nt r ao pe r at i v e l y t o m ea s ur e t he p r es s u r e gr a di en t a c r o s s a v a l v u l a r s te no s i s a n d

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c al c u l at e t he a r ea o f t he di se a se d v al v e.

C on ge n i t al he a r t d i s e as e . T E E t ec hn i qu e s al l ow s a m or e a gg r es s i v e ap p r o ac h t o c om pl e x c a r di ac r e c o n s t r u c ti on s b ec a us e t he s u r g e on h a s th e a b i l i t y t o v i s u a l i z e th e h ea r t an d e va l ua t e ad e qu a cy o f t he su r g i c a l r e p ai r i m m ed i at el y a ft e r th e o pe r at i v e p r o c ed u r e .

T h o r a c i c a o r t a. T E E ca n a cc u r a te l y di a gn o se t h or ac i c ao r ti c a ne ur y s m , di s s e c t i on , d i s r u p ti on , a n d at h er om a to s i s . At t h e N e w Y o r k P r e s by t e r i a n H os pi t al - C or n el l M ed i c a l C e n te r , w e r o ut i n e l y u s e T E E f or al l p at i e n ts t o s c r ee n s e v e r e at he r om at o s i s o f th e a or t i c a r c h a n d de s c e nd i ng ao r t a . E pi ao r ti c e c h oc a r d i o g r a ph y i s p er fo r m e d t o ex a m i ne th e a s c en d i n g a or t a an d a r c h , i f s e v e r e at h er om a to s i s i s f ou nd i n t h e de s c e n di ng ao rt a o r a r c h. S ev er e a th e r o m a t os i s of t h or ac i c ao r ta i s a n i nd ep e nd e nt p r ed i c t or o f p os t op er a ti v e ne u r o l o g i c o u tc om e . T h e a t h e r o m a i s g r a d ed as f o l l ow s : gr a de I , n or m a l t o m i l d i n t i m al th i c ke n i n g ; gr a de I I , se v er e i nt i m a l th i c k en i n g ; g r a de II I, at he r om a p r o tr u di ng l e s s th an 5 m m i n to th e l um en ; g r a d e IV , a th er o m a p r ot r u d i n g g r e at e r th a n 5 m m ; a n d g r a de V, a t he r o m a w i t h a m ob i l e c om p on en t ( F i g . 7. 8 ) .

C ar di a c tu m o r s. A t r i al m y xo m a ca n b e e as i l y d i a g no se d b y T EE . P r e - a nd p o s t op e r a t i v e T E E w i t h c on t r a s t c a n a s s es s t he pr es e nc e a nd s e v e r i t y o f m i t r a l r eg ur g i t at i on s e co n da r y t o v a l v e d am ag e f r o m a b a l l - v al v e ef f ec t o f th e m y x o m a .

O th er c a r d i a c l es i on s. H y pe r tr op h i c o b st r u c ti ve ca r d i om y o p at hy ( H OC M ) ( i di o pa th i c hy p er t r o ph i c s u ba o r t i c s t en o s i s [ IH SS ] ) c a n b e i de nt i f i ed by t h e c om bi n at i o n o f s ys to l i c a n te r i o r m o ti o n of th e m i t r a l v al v e ( S A M ) a nd l e ft v e nt r i c ul a r ou t fl ow ob s t r uc ti o n. C a r d i a c t am p on ad e c a us ed by a pe r i c ar di a l e ff us i on o r h em a to m a ca n b e d et ec t ed . P.152

N eu r o s ur ge r y. T EE w a s f ou n d to be t h e m o s t se n si ti v e m o n i t or t o d e te c t v e no u s ai r e m b o l i s m d u r i ng ne u r o s u r gi c a l o pe r at i o n s i n t h e s i t ti n g po s i t i o n . P at en t f or a m e n o va l e an d p ar a do xi c al a i r em b ol i s m c an b e d e te c t e d by T E E.

Figure 7.6 Color Doppler echocardiography. A: Superimposed on a two-dimensional image (here, the mid esophageal view), the relative velocities of the red blood cells from a selected area (triangle) are visualized. Timed to the ECG (on the bottom of the sector image), normal or abnormal blood flows can be viewed as they cross orifices. In this case, a small regurgitant jet originating from the mitral valve during systole is seen. The color of the jet displays velocity and direction, according to the scale, on the left side of the figure. The mitral regurgitation jet is moving upwards towards the left atrium (LA), and is colored red. B: In this mid-commissural view of the left ventricle (LV), the systolic mitral regurgitant jet, due to a prolapsing anterior leaflet (arrow), is directed anteriorly, inside the left atrium. RA, right atrium; RV, right ventricle.

Figure 7.7 Doppler mode. A: A typical pulsed-wave (PW) Doppler velocity consists of a spectral recording of varying intensity, depending on the acoustic density of the reflected interface (the mass of blood cells). The most dense (or brightest) portion of the spectral tracing represents the velocity of most blood cells. The velocity is recorded from a specific site (white circle), and the maximum velocity recorded is limited (usually <1.5 m/s). In this PW Doppler spectrum, E represents the diastolic early filling, and A the diastolic late (due to atrial contraction) velocity. During systole, there is a broad signal (question mark), representing systolic flow through the mitral valve (probably mitral regurgitation). However, neither the direction, nor the peak velocity can be visualized. B: In contrast, continuous-wave (CW) Doppler records the velocities of all the red blood cells moving along the path of the sound beam. A CW Doppler recording always consists of a full spectral envelope with the outer border corresponding to the fastest moving blood cells. The site of origin of a high-velocity jet is inferred from the particular lesion that is being examined. The maximum velocity that can be recorded can be as high as 8 m/s. Here, the direction (from bottom to top, or from the left ventricle towards the left atrium) as well as, the maximum systolic velocity (~5 m/s) can be visualized, detailing the mitral regurgitation jet.

A gr i c o l a E , O pp i z z i M , M e l i s ur go G, e t a l . T r an se s op h ag ea l e ch o c a r d i og r ap hy : a c o m p l e m en t a r y v i e w of t h e h ea r t . E x p e r t R e v C a r d i ov a s c T he r 2 00 4 ; 2

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( 1) :6 1 7 5. K ah n R A, S h er na n S K , Ko n st ad t S N . In tr a op er a ti ve ec ho c ar di o gr ap h y . In : K ap l a n J A, R e i c h D L, La k e C L , e t al . e ds . K ap l an ' s c a r di ac an es t he s i a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :4 3 7 4 88 . K uh l H P, H a nr at h P . T he i m pa ct of t r a n se s op ha g ea l e ch o ca r d i og r a p hy o n d a i l y c l i ni c a l p r a c ti c e . E ur J Ec h oc ar d i o gr 20 04 ; 5( 6) : 45 5 4 68 . S ha pi r a Y, Va tu r i M , W e i s en b er g D E, e t a l . Im pa c t of i n tr a op er a ti v e tr an s es op h ag e al e c ho c a r di o gr ap h y i n pa ti e nt s u nd e r g oi n g v a l ve r e pl ac e m e nt . A nn T h or S ur g 2 00 4 ;7 8( 2 ) : 5 7 9 58 3 . P.153 T r o i a n os C A , Ko n s t ad t S . E va l u a ti on of m i tr al r e gu r gi ta t i o n. Se m i n C ar d i o th o r a c V as c A ne s t h 2 00 6 ;1 0 ( 1 ) : 6 7 71 .

Figure 7.8 Atheromatous aortic disease. An echocardiographic picture of the short axis view of the descending thoracic aorta is shown. The anterior aortic wall is irregularly thickened, and a large atheroma (8 mm) is present at 5 o'clock (arrow). This is a grade IV atheroma.

C.I-11. How would you induce anesthesia?


M i d az o l a m 1 t o 2 m g i s gi ve n a s s oo n a s t he s t an da r d m o n i t or s a r e ap p l i ed an d t he a r te r i a l l i n e i s i n s e r t e d u nd er l o c a l a ne s th e s i a. A s m oo t h i n d uc t i o n i s e s s en t i a l t o pr e v e nt hy po t en s i o n, hy pe r te ns i on , a nd ta ch y ca r d i a. D i f f er en t t ec h ni q ue s m ay b e u s e d t o a c h i e v e a s m o o t h i n du c t i on . F or p a ti en t s w i th go o d l ef t v en tr i c u l a r f un ct i on , a ne s th es i a i s i n du c ed w i th f e nt an y l , 5 to 1 0 g p er k g , an d t hi o pe n ta l , 2 t o 4 m g pe r k g. T h e pa t i e n t i s v e nt i l a t e d b y m a s k w i th 1 00 % o x y ge n . A ft er a d m i n i s tr at i on o f s uc c i n yl c ho l i n e, 1 m g p e r k g , o r p an c u r on i u m 0 .1 m g p e r k g th e t r a c h e a i s i n tu b at e d. A l t e r n a ti v e l y , a n es th e s i a i s i nd uc e d w i t h th i op e nt al , 4 m g p er kg , a nd d e ep e ne d w i t h f en ta n y l 5 to 1 0 g p er k g a nd 2. 0 % i s of l ur an e f o r 3 to 5 m i n ut e s . W he n a d eq ua t el y a ne s th et i ze d, t he p a ti en t i s g i v en a m u s cl e r el ax a nt a n d i n t ub a te d. If t h e pa t i e n t ha s a h i s t or y o f hy p er te n s i o n or th e i ni ti a l s y s t o l i c B P is ov er 15 0 m m Hg , f en ta n y l 10 g p er k g i s u s u al l y r e q ui r e d t o b l u nt th e i nt ub a ti o n- as so c i a t ed h y pe r t e ns i o n a n d ta c hy c a r di a. F o r pa t i e n ts w i t h p o or l ef t v en t r i c u l ar f u nc ti o n, p o te n t i n h al at i on a ge n ts s uc h a s , i s of l ur an e , se v of l u r an e a nd de sf l ur an e a r e av o i d ed du r i n g i n d uc ti o n a nd m a i n te n an c e of an es t he s i a . Ad d i t i o n al m i da z o l am 2 to 5 m g a n d l es s t hi op e nt al 1 to 2 m g pe r k g w i l l be gi ve n f or i n du c ti on ; h o w e v e r , i n l i eu o f t he i n c r e as i n g i n c i de n c e o f d el i r i um i n t he e l d er l y p o s t o pe r a t i v el y , b en z o d i a z ep i n e s s h o ul d b e a vo i d e d i n pa ti e nt s o l d e r th a n 70 y e ar s . Al t er na t i v el y , et o m i da te 0. 2 m g p er k g m ay b e a d m i ni s te r e d f or i n du c ti on . P.154 S ee a l s o C h ap t er 1 2 , qu e st i o n C .6 fo r o th er m e as u r e s t o pr e ve nt ta c h y c a r d i a an d h y p e r t e ns i o n a t t he t i m e o f i nt u ba ti o n. L on d on M , M i t tn a c h t A , Ka p l a n J A. A n es t he si a f or m y oc ar d i a l r ev as c ul ar i z a ti o n. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n ' s c a r d i ac a n es t he si a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :6 0 5 6 09 .

C.I-12. How would you maintain anesthesia?


A ga i n , s m o o th a n es th e si a i s e ss en t i a l to ac h i e ve a ba l an ce be t w e en m y oc a r d i a l o x y g en d e m a nd an d s up p l y . D i f fe r en t a ge nt s a nd te c hn i q u es m a y be us ed t o ac c om pl i s h t h e sa m e go a l . A co m b i na ti o n of fe n ta ny l ( or a n ot h er s y n t he t i c o p i o i d ) a nd i s of l ur an e ( or pr op o fo l ) i s a po pu l ar c h oi c e . A ft e r th e p at i en t i s i nt ub a te d , a m i x tu r e of 6 0 % ai r a nd 40 % o xy g en i s a dm i ni st e r e d t o k e e p th e p a ti en t u nc o ns c i o us . T he d e pt h o f a ne s t h es i a m u st be t i tr at e d to m e et th e r eq ui r em en t s of th e v ar y i n g i n t en s i t i e s o f s u r gi c a l s t i m u l at i o n . Sk i n i n c i s i o n a nd s t er n al s p l i tt i ng a r e v er y p ai nf u l . B u t th e s tr o ng es t s ti m u l at i o n i s u su a l l y fr o m st e r n al r e tr a c t i o n w i t h t he s e l f - r e ta i n i ng r e tr ac t or . F e n ta n y l , 5 g ( 0 . 1 m L ) p er k g , i s gi v e n r i g h t b ef or e t he s k i n i n c i s i o n. An ot h er d o se of f e nt an y l 5 g pe r k g i s us ua l l y g i v e n b ef or e s te r no to m y . T h en f e nt a ny l , 5 g p e r k g , i s g i v en ev er y 3 0 t o 60 m i n ut e s to m a i n t ai n a ne st h es i a . V er y h i g h d o se s o f fe n ta ny l o r s uf en t an i l , h av e b e en s u c c es s fu l l y u s e d f or c a r d i a c a n es th e s i a. T h e p os s i b i l i t y o f o x y ge n t ox i c i ty f r o m t he us e o f 10 0 % o xy ge n s ho u l d a l so b e k e pt i n m i n d . L on d on M , M i t tn a c h t A , Ka p l a n J A. A n es t he si a f or m y oc ar d i a l r ev as c ul ar i z a ti o n. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n ' s c a r d i ac a n es t he si a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :6 0 5 6 19 .

C.I-13. What is the better anesthetic agent for this operationan inhalation or intravenous agent?
T he c h oi c e of a n es th e ti c a ge n ts i s s ti l l de ba t ab l e. B o th i n ha l a t i o n, i n tr a v e no u s a nd c o m b i n e d a ge nt s h av e b ee n u s ed s u c c es s fu l l y . Bo t h ha v e ad v an t ag es a nd d i s a d v a nt a ge s . U n de r st an d i n g t he ca r d i ov as c ul ar ef fe c ts o f e ac h a ne s th et i c ag e nt an d c ar ef u l ti t r a ti o n of ea c h dr ug w i l l i m pr ov e t he ba l an c e be tw e en m y o c a r di al ox y g e n de m an d a nd su pp l y. E a r l y d et ec t i o n a nd a p pr o pr i a t e c o n tr ol of t h e m a j or d e te r m i n a nt s o f m y o c a r d i al o x y g e n c o n s u m p t i o n ( BP , H R , P AO P) ar e m a n da t or y i f m y oc a r d i a l i sc h em i a i s t o b e a vo i d e d. A n ot h er c o ns i d e r a ti o n i s th e d es i r a bi l i t y of e a r l y e x t ub a ti o n. H i g h - d o s e n a r c ot i c an d l ar g e d os es of s e da ti v es a n d m u s cl e r el ax a nt s s ho u l d b e a vo i de d i f ea r l y e x tu ba t i o n i s pl a nn e d. T hr ee l a r g e - s c a l e ou t co m e st ud i es o f p at i en ts un d er go i ng C A BG s u r g er y r ep o r t ed th at an es t he t i c c ho i c e d i d n ot a f f e c t i n c i d en c e of p e r i op e r a ti v e m o r bi di t y a nd m o r t al i ty . H o w ev e r , s tu d i e s d o p oi nt to w a r ds a be ne f i c i a l e ff e c t o f v ol a ti l e ag en t s i n pr ec o nd i t i on i ng t h e m y o c a r d i um a g ai n s t a n i s c he m i c i n j u r y .

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G ua r r a c i no F , L a nd on i G , T r i ta p ep e L , et al . M yo ca r di al da m a g e pr e v e n te d b y v o l at i l e a ne s th et i c s : a m ul t i c en t er r an d om i z e d c on t r o ll ed st ud y . J C ar di o th or a c Va s c An e st h 2 00 6 ; 20 ( 4) :4 7 7 48 3 . L on d on M , M i t tn a c h t A , Ka p l a n J A. A n es t he si a f or m y oc ar d i a l r ev as c ul ar i z a ti o n. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n ' s c a r d i ac a n es t he si a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :6 0 9 6 14 . P.155 S l o go f f S, Ke at s A S, D e ar W E , e t al . S te a l - pr on e c o r o na r y an a to m y an d m y o c a r di al i s c h e m i a a s s oc i a t ed w i th f o ur pr i m ar y a ne s th e t i c ag e nt s i n h um an s . A ne s t h A na l g 1 99 1; 7 2: 2 2 27 . S m u l T M , L an g e M , R e d el A , e t a l . D es f l u r a n e- i n d uc e d pr e co nd i ti on i ng ag ai n s t m y o c ar d i a l i n f ar c t i on i s m ed i at ed by n i tr i c ox i d e . An e s t he s i o l o g y 2 00 6; 1 05 ( 4) :7 1 9 72 5 . T um an KJ , M c C ar th y R J, Sp i e s s BD , e t a l . D oe s c ho i ce o f a n es th e ti c a ge nt s i gn i fi c a n tl y a ff ec t o ut c om e a ft er c o r o n ar y a r t er y s ur ge r y ? A n es t he s i o l o gy 1 98 9 ;7 0: 1 89 1 9 8.

C.I-14. What are the cardiovascular effects of halothane, enflurane, isoflurane, desflurane, sevoflurane, morphine, and fentanyl?
I n ge n er al , h a l o th a ne , e nf l u r an e , i s of l ur an e , d es fl u r a ne , a nd se v o f l u r a n e p r o du c e a d os e- r el at e d d ep r e s s i on i n v e nt r i c u l ar f u nc ti o n a nd v a s c ul a r to n us . H al ot h an e s en s i t i z es th e h ea r t to c a te c ho l a m i n e m uc h m or e th a n e nf l u r an e, i s of l ur an e , de s fl u r a ne , a nd s e v o f l u r a n e. I s of l u r an e a nd de s f l ur an e d e pr es s c ar di a c ou t pu t t o a l es se r d eg r ee t h an do es ha l o t ha n e or en fl u r a ne s e c o n da r y to th ei r g r e a te r v a s od i l a ti n g c a p ac i t y . T h e H R c h a ng e s l e a s t w i t h h a l o th a ne a nd i n c r ea s es m o s t w i th d e sf l u r an e. Is of l ur an e m ay ca us e t ac h y c ar d i a ; t he m e c h an i s m i s u nc l ea r . M o s t s t ud i es s u gg es t t ha t h al o t h a ne , e nf l u r an e, an d i s o fl u r a ne de c r e as e c or on a r y v a sc ul a r r e s i s ta n ce . O f th e se , i so fl u r a ne i s t h e m o s t po t en t c or on a r y v a s o di l at or . A l l o f t he po te n t dr u gs d e cr ea s e a r t er i a l p r e s su r e i n a do se - r e l a t ed m a nn e r . T h e m e c h a ni s m of B P d e c r ea s e i n c l u de s v as o di l a t i o n , m y oc a r d i a l d ep r es si o n a nd d e c r ea s ed c a r d i ac o u tp ut , a nd de c r e as e d sy m p a th e ti c n er v o u s s y s te m to n e. W i th h a l o th a ne , d ec r ea s e d c a r d i a c o ut p ut i s t he pr ed o m i na n t c a u s e . H al ot h an e a l s o i nc r e a se s v en o us c o m p l i a nc e, an d i n pa t i e n ts w h o ha v e hi g h s y m pa th e ti c t on e, s u c h as t h os e w i t h h ea r t fa i l u r e , h al o th an e d e c r ea s e s s y s te m i c v as c ul ar r e si st a nc e . En f l u r a n e ca u se s b ot h v as o di l a t i o n a nd d e c r ea s ed m y oc a r d i a l c on t r a c t i l i ty . W i t h i s o fl ur a ne a n d d e s fl u ra ne a lo w p er i ph er a l r es i s ta n c e i s t h e m a j o r c au s e o f hy p ot en s i o n. Ev i d e nc e o f th e r e l a ti v e l y gr e at e r m y oc a r d i a l d ep r es s i o n w i t h ha l ot h an e a nd e n f l u r a ne i s t h e gr e at er i n cr e as e i n r i g ht a t r i al p r es su r e se e n w i t h th e se dr ug s t ha n w i t h i so f l u r a n e. N ar c o t i c s s u c h as m o r p h i n e a nd fe nt a ny l a t th e i r c l i n i c a l do s e ha v e m i n i m al c a r d i o v as c u l ar e f fe c t s . Bo t h m a y c au s e b r a dy c a r di a . Ne it h er s e ns it i z e s t he h ea r t to c a te c h o l a m i n e or de p r e ss e s m y oc a r d i a l f un c ti on . T he c a r d i ov as c ul ar ef fe c ts o f m or p hi ne de p en d o n th e d o s e u s ed . L ar ge do s es o f m or ph i ne s ul fa t e ha v e r e p or te d l y c a us e d m y oc a r d i a l l ac t at e p r o d uc ti o n an d r ed u c t i o n i n c or on a r y b l oo d f l o w i n a ni m a l s . S et h na f o un d t ha t m or p hi n e s u l fa t e , 0 .2 5 m g p er k g I V, di d n ot p r od uc e a gl ob a l m y o ca r d i al i sc h em i a i n p a ti e nt s w i t h C A D . H i g h do s es o f m or p hi ne , 1 m g p e r k g , p r o du c e a s i g n i f i c an t d e c r ea s e i n a r t er i al B P a nd s y st e m i c va s cu l a r r es i st an c e ac c om pa n i e d b y an av e r a ge 75 0 % i n c r e as e i n p l a s m a h i s t a m i n e. On t h e o th er ha nd , h i g h d o s e s o f f e n ta ny l , 50 g pe r k g, d o n o t pr o du ce an y s i g ni f i c an t c ha n ge s i n B P, v a sc ul a r r e s i s ta nc e , an d p l a s m a h i s t am i ne l e v e l s . L on d on M , M i t tn a c h t A , Ka p l a n J A. A n es t he si a f or m y oc ar d i a l r ev as c ul ar i z a ti o n. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n ' s c a r d i ac a n es t he si a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :6 0 7 6 14 . M al an T P , D i N ar do JA , I sn er R J , e t al . C ar d i o va s cu l a r e ff e ct s of s e v o f l u r a n e c o m pa r e d w i t h t h os e o f i s o fl ur a ne i n v ol u nt ee r s . A n es t h e s i ol o gy 1 9 95 ; 83 :9 1 8 9 28 . S et hn a D H , M o ff i tt E A , Gr ay R J , e t al . C ar d i o va s cu l a r e ff e ct s of m o r p h i n e i n p at i e n ts w i t h c or o na r y ar t e r y di s ea s e . A ne s t h A n al g 1 98 2 ; 6 1 : 1 09 11 4 . S k u ba s N , L i c ht m an A D , Sh a ar m a A, e t a l . An es t he si a f or ca r d i ac s u r g er y . In : B ar as h P G, C u l l e n BF , S to e l t i n g R K, ed s . C l i n i c a l a ne s t h es i a , 5 t h ed . P hi l a d el ph i a: L i pp i nc ot t W i l l i a m s & W i l k i n s , 20 0 6: 91 6 9 1 9. P.156

C.I-15. Is isoflurane dangerous for the patient with coronary artery disease (CAD)?
I n pa t i e nt s w i t h C AD , t he us e o f i s o fl ur a ne i s s ti l l co nt r ov er s i a l . R e i z e t a l . r e po r te d t ha t 1 % i s o fl u r a ne i n du c ed c o r o n ar y v a s od i l a ti on th a t w a s n ot r e l a t ed t o n or m a l a ut o r e gu l at i o n a n d th a t bo t h d ec r e a se d c or on a r y p e r f us i on p r es s u r e ( s y s t em i c hy po t en s i o n) , a nd r e di s tr i b ut i on of m y o c ar d i a l bl o od fl ow ( c or on a r y s te al ) m ay c o nt r i b ut e t o d ev el o pm en t o f r eg i o n al m y oc ar d i a l i sc he m i a . A no th e r R e i z s t u dy , u s i ng 1. 5 m i n i m u m al v e o l a r c on c e n t r a t i on ( M AC ) i s o fl u r a ne n i t r o u s ox i de a n es th e si a , co n cl ud e d th a t i s o fl ur a ne m a y ca u se c o r o na r y s t e al w i th m y oc ar d i a l i s c he m i a i n p at i e n ts w i th C A D . H o w e v e r , Sm i t h e t a l . r e po r t e d t ha t t he s u bs ti t ut i o n o f 0 .5 % t o 1 .1 2% i s of l ur an e f or 85 g p er k g o f f en t an y l di d n ot r e s u l t i n a n i nc r ea s e d i nc i de nc e o f m y o c a r di al is ch e m i a, as s e en b y S T - se g m e nt or s e gm en t al w a ll -m ot i on c h an g es i n p at i en ts wi th CA D. M o re ov e r , T a rn ow et a l . de m on st r at ed th at 0. 5 % is of l ur an e w i t h 5 0 % ni t r o us ox i d e i m p r o v e d t h e to l er an c e to pa ci n g- i n d uc e d m y o ca r d i al i sc h em i a i n p a ti e nt s w i t h s i g ni fi c an t C AD . T w o l a r g e- s c a l e p r os p ec ti v e ou t c o m e s t ud i es b y S l o g of f e t a l . a n d T u m an e t a l . co ul d f i n d n o e vi d en ce th at th e i nc i d e nc e o f i s c he m i a w as i n c r e as ed by i s of l u r an e i n p at i e n ts w i th C AD un d er go i ng c o ro na r y ar t er y b y p as s g r a f ti ng ( C AB G ) su r g e r y . F ur th e r m or e , th i s fi nd i ng he l d tr ue ev en fo r p at i e n ts w i th s t ea l - p r o ne c o r o n ar y a na to m y i n th e s t u di e s by Sl og o f f et a l ., P ul l e y e t a l . , a nd L e un g e t a l . S ev er a l an i m a l s tu di e s fu r th er co nf u se d t hi s i ss ue . P r i e be p r ov ed th at i s of l ur an e w as a m y o c a r d i al d e pr es s an t a nd a po t en t c or o n a r y v a s o d i l at o r i n t h e d og . S i l l e t al . d em o ns tr a te d t ha t h i g h c on ce n tr at i on s o f i s o fl ur a ne ( 1 .5 % a nd 2. 5% ) d i l a te d i nt r a m y o c a r di al ar te r i o l e s r at he r t ha n e p i c ar d i a l c or on a r y a r t e r i es i n t he i n ta c t do g. Bu ff i ng to n e t a l . r e po r te d t ha t i so fl u r a ne ( 1 .2 % t o 1 .5 %) pr od u c e d a d e c r ea s e i n c o l l a te r a l f l o w a nd a de c r e m e n t i n c o l l a te r a l z on e c on tr a c t i o n w hi l e en h an c i n g f l o w i n th e n or m a l l y p e r f us e d zo n e. T h ey c o nc l ud ed th a t i s of l ur an e w a s an ar te r i o l a r v as od i l a t o r a n d he n c e p r od u c e d c or on a r y s te al i n d o gs w i th c h r o ni c c or o na r y oc cl u si on . O n t he c o nt r a r y, C as o n e t al . f ou n d th a t i n th e d og , i s o f l u r a n e or ha l o t ha ne at 0. 5% M A C a nd 1 . 5 M A C h ad l i t tl e e ff e c t o n c or o na r y va sc u l a r r e s i s ta n ce , a nd i s ch e m i a w a s p r e c i p i t a te d b y ta c hy c a r di a o r hy p ot e ns i o n r at h er t h an b y c or o n a r y s t ea l . M o r eo v e r , D a v i s a nd F r an k d em on s tr at e d th a t i s o fl ur a ne de cr e as ed m y oc a r d i a l i nf a r c t s i z e af t er l e ft a n te r i o r de s c e nd i ng ( L AD ) c or on a r y a r t e r y o c c l u s i on i n d o gs . I n a dd i t i on , G i l be r t et al . r ep or t ed g r ea te r c or o na r y r e se r ve i n s w i ne an e s t he t i z ed w i th i s of l ur an e v er s us h a l o t h a ne at 0 . 5 to 2. 0 M AC . R e c en t l y , H a r tm an et a l . d em on s tr at e d th a t a de no s i n e b ut n o t i s o fl u r a ne r e di s tr i b ut e d b l o od fl ow aw ay fr om c o l l at e r a l - d ep e nd en t m y o c ar di u m i n t h e p r e s e n c e o f a c o r o n ar y s t e al p r o ne an a to m y i n t he ch r o n i c a l l y i n s tr um e nt ed do g . T h e y fu r t h er f o un d t ha t r ed u c t i o n s i n m y oc a r d i a l p er f us i o n d ur i ng i s of l u r an e a ne s th es i a de p en d o n s y s te m i c a r t e r i al pr es s ur e a nd t h at i s of l u r an e d i d n o t p r o du c e c o r on ar y s te a l i n th i s m o de l o f m u l ti v e s s e l C AD . F ur th e r m or e, C h en g e t a l . fo un d t ha t n e i t he r i s o fl u r a ne no r h al ot h an e a s t he s o l e a n es th e ti c i n cl i ni ca l c on c en tr a ti on s c au s ed s i gn i fi c a n t c o r o n ar y v as o di l a t i o n o r c o r o n ar y s te a l w h e n th e c or o na r y p er fu s i o n p r e s s u r e d e cr ea s ed f r om 5 5 t o 3 0 m m H g i n a s w i n e m od el of c h r o ni c c or o na r y oc c l u s i on w i th c o l l a t e r a l d ev e l o pm e nt . O n th e b as i s of r e ce n t an i m a l a nd r e ce n t cl i n i ca l s tu di e s, w e c an c o nc l ud e t ha t i s o fl u r a n e i n c l i n i c a l c o n c e n tr at i o n s m a y b e u s e d s af e l y i n p at i en t s w i t h CA D p r o v i d ed t h at h y po t en si o n an d t a ch yc a r d i a a r e a vo i d e d. C he ng D C H , M o y e r s JR , K nu ts o n R M , e t a l . D o se - r e sp on s e r e l at i o n s h i p of i s of l u r an e a nd ha l o t ha n e v e r s u s c o r on a r y p e r f us i o n p r e s s u r e s . Ef f ec ts on f l ow r ed i s t r i bu t i o n i n a c ol l a t er al i ze d c hr on i c sw i n e m od e l . A n es t he s i o l o gy 19 92 ; 76 : 11 3 1 22 . G i l be r t M , R o be r t s S L, Bl om b er g R W , e t a l . G r ea te r c or o na r y r e s e r v e i n s w i n e an e s t he t i z ed w i th i s of l ur an e v er s us h a l o th a ne . A ne s th es i ol og y 1 9 85 ;6 3 :A 15 . H ar tm a n J C , K am pi n e JP , S ch m el i n g W T , et a l . St e al - p r o n e c or on a r y c i r c ul at i on i n c hr o ni c a l l y i n s t r u m en te d d og s : i s o fl ur a ne v e r s us ad e no s i n e. A ne s t h es i o l og y 1 99 1 ;7 4: 74 4 7 56 .

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P.157 L eu n g J M , G oe h ne r P , O' K el l y BF , e t al . I so f l u r a n e an e st he s i a a n d m y o c a r d i al i s c h em i a: c o m p ar a ti v e r i s k v e r s us s u fe n ta n i l a n es t h e s i a i n pa t i e nt s u nd e r g oi n g c o r on ar y a r t e r y b yp a ss g r af t s ur ge r y. A n es th e si ol o gy 1 9 91 ; 74 :8 3 8 8 47 . L i l l e h au g S L, T i nk er JH . W h y d o pu r e v as o di l a t or s c au se co r o n ar y s te al w h en an e s t he t i c s d on ' t ( o r s el d om d o ) ? ( e di to r i a l ) . A ne s t h A n al g 1 99 1; 7 3: 6 81 6 82 . L on d on M , M i t tn a c h t A , Ka p l a n J A. A n es t he si a f or m y oc ar d i a l r ev as c ul ar i z a ti o n. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n ' s c a r d i ac a n es t he si a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :6 0 9 6 14 . P r i eb e H J . D i ff er e nt i a l e ff e ct s o f i s o fl ur a ne o n r eg i on a l r i g ht a n d l e f t v e n tr i c u l a r p er fo r m a nc es an d o n c or on a r y , s y s te m i c , an d p u l m on a r y h e m o dy n am i c s i n t he d o g. A n es t he s i o l o gy 19 87 ; 66 : 26 2 2 72 . P ul l e y D D , K i r v as s i l i s G V , Ke l er m e n os N , e t a l . R e gi on a l a nd g l ob al m y oc a r d i a l c i r c u l at o r y a nd m e ta b ol i c ef f ec ts o f i s o f l u r a n e a nd h a l o th a ne i n p a ti en t s w i t h s te al - p r on e c or o na r y an at o m y . A ne st h es i o l og y 1 99 1 ;7 5: 7 56 76 6. R ei z S , Ba l fo r s E , S or e ns e n M B , e t al . I so f l u r a n e: a po w er fu l c or on a r y v a s o d i l at o r i n p a ti e nt s w i t h c o r on a r y a r t e r y d i s e as e . An e s t he s i o l o g y 1 98 3; 5 9: 9 1 97 . R ei z S , Os tm a n M . R e gi o na l c or on a r y h e m o d yn am i c s d u r i ng i s of l u r an e - n i t r o u s ox i de a n es t he s i a i n p at i e n t s w i t h i s c h em i c he a r t d i s e as e . An e s t h A na l g 1 98 5 ;6 4: 5 70 5 7 6. S l o go f f S, Ke at s A S, D e ar W E , e t al . S te a l - pr on e c o r o na r y an a to m y an d m y o c a r di al i s c h e m i a a s s oc i a t ed w i th f o ur pr i m ar y a ne s th e t i c ag e nt s i n h um an s . A ne s t h A na l g 1 99 1; 7 2: 2 2 2 7 . T ar no w J , M a r k s c h i es - H o r n un g A , S ch ul t e- Sa s se u U . Is o fl ur a ne i m pr ov e s th e t ol e r a nc e t o p ac i n g - i nd u c e d m y o c ar di a l i s c h e m i a. An e s t he s i o l o g y 1 98 6 ;6 4: 1 47 1 5 6. T um an KJ , M c C ar th y R J, Sp i e s s BD , e t a l . D oe s c ho i ce o f a n es th e ti c a ge nt s i gn i fi c a n tl y a ff ec t o ut c om e a ft er c o r o n ar y a r t er y s ur ge r y ? A n es t he s i o l o gy 1 98 9 ;7 0: 1 89 1 9 8.

C.I-16. What is the cardiovascular effect of nitrous oxide?


N i t r o u s ox i d e i s a w ea k c e nt r a l n er vo u s sy s te m d ep r e s sa n t. I t h as b e en ge ne r al l y c o ns i de r e d t o h av e m i n i m a l ef f ec t s on o t he r o r g a n s y s t e m s . N i t r o u s ox i de h as s i gn i f i c a nt c a r d i ov as c ul ar ef fe c ts t h at m a y be de pr e ss an t o r s ti m u l a t or y d ep e nd i n g o n t he an es t he ti c s w i t h w h i c h i t i s c o m b i ne d . W h e n h i g h- d os e f en ta n y l i s u s e d d ur i ng c o r o n ar y su r ge r y , t he ef fe c ts o f N 2 O d ep e nd on t h e p at i e n t' s c ar d i a c fu n c t i o n . F o l l o w i n g th e a d m i ni s tr at i o n o f 5 0% N 2 O , t he r e ar e n o s i g ni f i c an t c ha n ge s i n an y o f t he he m o d yn am i c pa r am et e r s i n p at i en ts w i th no r m a l l e ft v e nt r i c ul a r fu n c t i o n ( LV E D P < 1 5 m m H g ) . On t h e c o n tr ar y , th e r e i s a s i g ni f i c an t d ec r ea s e i n c a r d i a c i nd e x an d s tr o ke v o l u m e i n de x i n p at i en ts w i th l e ft v e nt r i c ul ar dy s f u nc t i o n ( L V ED P > 1 5 m m H g ) . W h en ad de d t o o th e r i nh al a ti on an e s t he t i c s, N 2 O i n cr ea s es ar te r i a l pr e ss ur e a nd sy s t e m i c v as c u l ar r es i s t an c e, s u gg e s t i n g t ha t i t h as a v a s o c on s t r i c ti v e ac ti o n. N i t r ou s o x i d e i nc r e a s e s p ul m o n ar y v as cu l ar r e si st an c e i n pa t i e nt s w i t h m i t r a l s te n os i s an d p ul m o n ar y h y p e r t en s i o n. T he p u l m on a r y v a s c ul a r ef f ec ts of n i tr ou s o xi d e ar e a l s o v ar i a b l e . P at i en ts w i th el ev a te d P A pr e s s ur e m ay ha v e fu r t h er i n c r ea s e s w h en n i tr ou s o x i d e is a dd e d. K o ns ta d t et al . d i d n o t co r r o bo r at e t he se fi nd i ng s i n p at i e n ts w i th m i t r al v a l v ul a r di s ea s e . A s t ud y i n i n f an ts fa i l e d t o s h ow fu r t h er i n c r ea s es o f p ul m o n ar y v as c u l ar r e si st an c e w i t h th e a d di ti o n of ni tr o us o x i d e. T he c o nt r i b ut i o n o f n i t r o u s ox i de t o m yo c ar di a l i s c he m i a i s co n tr ov e r s i a l . Ph i l b i n et a l . s u g ge s t e d t ha t a dd i t i on o f n i t r ou s o x i de t o a n es t he s i a w i t h h i g h - d os e f en ta n y l ( 1 00 g /k g fo l l o w e d b y 1 g/ k g/ m i n ut e) , o r su f en t an i l ( 3 0 g / k g f o l l ow e d by 0. 3 g/ k g / m i nu t e) , c a n p r o d uc e c l i n i c al l y i m pe r c e pt i bl e r eg i o n al m y o c a r di al i s c h e m i a i n th e a r e a s su p pl i e d b y s te no t i c c o r o na r y ar t er i e s o f d og s . H o w e v er , m o n i t o r i ng w i th t w o- di m en s i o na l T EE d i d no t r ev e al m y oc ar d i a l i s c he m i a i n P.158 p at i e n ts w i th C A D , w h en n i tr ou s o xi d e w a s a dd e d to l o w - d os e f en t an y l ( 1 5 g / k g f o l l ow e d by 0. 2 g/ k g / m i nu t e) , o r hi gh - do s e s u f e n t a n i l ( 2 0 g /k g ) . C l i ni c a l l y , n i t r o u s ox i de m a y be us ed be f or e C PB i f h i g h - d os e n ar c ot i c s a r e no t u s e d a nd hy po t en s i o n do e s n ot o c c u r . H o w e v er , a f t er C P B, n i tr ou s o x i d e s ho ul d b e a v o i de d b ec au s e o f th e p os s i b i l i ty o f e xp a nd i n g a n y ai r b ub b l e s r e m ai n i n g i n th e c or o na r y an d c er eb r al c i r c ul a t i on . B al as a r a s w a th i K , Ku m ar P , R ao T L K, et a l . Le f t ve n tr i c ul a r en d - d i a s to l i c p r e s s u r e ( L VE D P) a s a n i nd ex f o r n i t r o u s ox i de u s e du r i n g c or on a r y a r t e r y s ur ge r y. A n es th e s i ol o gy 1 9 81 ; 5 5: 7 08 70 9. C ah al a n M K , P r a k as h O , R u l f EN , e t a l . A d di ti o n of ni tr o us o x i d e t o fe n ta ny l a ne s th e s i a d oe s n ot i n du c e m y oc a r d i a l i s c h em i a i n p a ti en t s w i t h i s c h e m i c h ea r t d i s ea s e. A n es th e s i o lo gy 19 87 ; 67 :9 2 5 9 29 . M es s i n a AG , Y ao F S , C a n ni n g H , et a l . T h e e ff e ct o f n i t r o u s o x i de on l e ft v e nt r i c ul ar p u m p pe r f o r m an c e an d c on t r a c t i l i t y w i t h c o r o na r y ar t er y d i s ea s e: e f fe ct o f pr e op er a ti v e ej ec t i o n f r a ct i on . A ne st h A n al g 1 99 3; 7 7: 9 54 9 6 2. P hi l b i n D M , F ox P , D r u m m o nd G, e t a l . Po st sy s to l i c s ho r te ni n g o f c a n i n e l ef t v e n tr i c l e s u p pl i e d b y a s t en ot i c c o r on ar y a r t e r y w he n n i tr ou s o x i d e i s a d de d i n t he p r es en c e o f na r c o ti cs . A ne s th e si ol o gy 1 9 85 ;6 2 :1 6 6 17 4 .

C.I-17. What kind of muscle relaxant would you use? Why?


W e us u al l y us e p an cu r on i u m . W h e n fu l l pa r al yz i ng d o se s a r e g i v e n i n a b ol u s , p a nc ur o ni um ge n er al l y pr od u c e s t ac h y c ar d i a a n d hy p er te n s i on c a u s e d b y v ag ol y ti c e ff ec t a nd no r e p i n e ph r i n e r e l ea se d f r o m c ar d i a c sy m pa th e ti c n er v e s . Pa n c u r o n i u m i s a b et t er c ho i c e i f h y p o te n s i on ( B P < 80 m m H g s y s to l i c al l y ) a nd b r ad y c a r d i a ( H R < 50 / m i nu t e) a r e pr e se nt . T he o r e ti ca l l y , p an c ur on i um m a y i nc r e a s e m y oc ar d i a l O 2 c o ns u m p ti o n c a u s e d b y ta c hy c a r di a a nd h y p er t en s i o n. N e v e r t h el es s , pa n cu r o n i u m i s th e m os t c om m on l y us ed m u s c l e r e l a x an t f or C A BG . I n pr a c t i c e , m o s t pa t i e nt s w i t h C AD r e c e i v e - ad r en e r g i c b l o c k i ng a g en t s , w hi c h ca n c o un te r ac t t he v a go l y t i c e f fe ct s o f p an c u r on i u m . Al s o, t h e br a dy c a r di a a s s oc i at ed w i t h th e p op u l a r n ar c o t i c a n es t h e ti c t ec hn i qu e s c a n a tt e nu at e t he ta ch y ca r d i a i n d uc e d by pa n cu r o n i u m . V e c u r o n i u m a nd c i s a t r a c u r i u m ha v e n o m a j or c ar d i o v a s c u l a r e ff e ct s, bu t t he i r i nt er m ed i a t e du r at i o n o f a ct i o n n e ce ss i t a te s f r e qu e nt ad m i n i s tr a ti on of t h e r e l ax an t . Pi p ec ur o ni um an d d ox a c u r i u m ar e n ew l o ng - ac ti n g, n o nd e po l a r i z i n g m us c l e r el a x a nt s . T h e y se e m to h a ve no h e m o dy n am i c si de - ef fe c ts a s s o c i a te d w i t h n eu r o m us c u l ar b l oc k a d e. T h ey c a n be us e d i n l a r g e b ol u s do s es . L on d on M , M i t tn a c h t A , Ka p l a n J A. A n es t he si a f or m y oc ar d i a l r ev as c ul ar i z a ti o n. I n : Ka p l a n J A, R e i c h D L, L a k e C L , et al . e ds . K ap l a n ' s c a r d i ac a n es t he si a . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :6 1 5 6 16 .

C.I-18. If ST-segment depression is seen during surgery, how would you treat it? What is the relation between perioperative myocardial ischemia and postoperative myocardial infarction?
S T - s e g m e nt de pr e ss i o n i nd i ca te s m yo c ar di a l i s ch e m i a , ei th e r fr o m i n c r e as e d O 2 d e m a nd or d e c r ea s ed O 2 s u p pl y . T h e t r e a tm en t i nc l u d es t h e f ol l o w i n g: I nc r e a s e O 2 su p pl y. C o r r e ct h y po te n si on an d h yp o xe m i a . D ec r e a s e O 2 de m an d . C o r r e ct h y pe r t e ns i o n , ta c hy ca r di a, an d i nc r e a s e d P AO P o r C VP b y d ee p en i ng a n es th e s i a o r by us i n g v as o di l a t or s a nd m e t op r ol ol or e s m o l o l . Al l t he m a j o r d et er m i n an t s of de cr e as ed O 2 d em a nd h a v e to b e c on s i d er e d an d c o r r ec te d t o t he i r no r m a l l e v el s .

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P.159 G er s o n e t a l . ( i n ex p er i m en t al do gs ) f ou n d th a t el e va ti o n o f ST s e gm e nt s i n d uc e d by oc c l u s i on of t h e c o r on a r y a r t e r y w a s l e s s p r om i ne n t w i th ha l o t ha n e t ha n w i t h a c om b i n at i on o f n i t r op r u s si de an d p r o p r a no l ol . T he s e c a n b e e x p l a i ne d t he e f fe c t s o f h al o th an e o n c or on a r y v a s c ul a r r e s er v e an d t he k n ow n e ff ec t s of ni tr o pr us si d e (r e du c ti on of m y o c ar di a l bl o od fl ow to i s c h em ic my oc a r d i u m ). I f th e r e a r e no ob v i o us c h an g es i n B P, H R , a nd p u l m on a r y w e dg e p r e s s u r e , n i t r o g l y c e r i n i s i nd i c a te d i f c o r on a r y s p as m i s s u s p e c t ed . N i t r og l y c er i n m a y b e g i v en by i n tr av e no u s dr i p . S ub l i n g ua l n i f ed i pi ne or i n tr av e no u s ni c a r di pi n e o r di l t i az em m a y a l s o b e gi v en t o r el i ev e c or on a r y s p as m . S l o go f f an d K e at s r e p or t ed t h at p e r i op e r a ti v e m y o ca r d i al i s ch em i a oc c ur r e d i n 3 7% o f a l l pa ti e nt s u nd er g oi n g C A B G. T he y p r o v ed t h at pe r i o pe r a t i v e m y o c a r di al i n fa r c t i o n w as a l m o st th r e e t i m e s as fr eq u en t i n pa t i e nt s w i t h i s c h em i a ( 6 .9 % ) c o m p a r e d w i t h p at i e n ts w i t h o ut i s c h em i a ( 2 .5 % ) . I n tr ao p er at i ve t ac hy c ar di a w as as so c i a te d w i t h a h i gh er i n ci d en ce of m y oc ar d i a l i s c he m i a a n d i n f ar c t i on . H ow ev e r , K n i g ht et a l . de m on s t r at ed t h a t 42 % o f C AB G p at i e n ts h ad p r eo p er at i v e e p i s od e s of m y oc a r d i a l i sc h em i a , 8 7% of w h i c h w e r e c l i ni c a l l y s i l e nt . T he y f ur th e r fo u nd th at an es t he s i a a n d s u r ge ry di d n ot w o rs en th e p r e op e r a ti v e i s c he m i c p at t er n. F u r t h er m o r e , S l o g of f a nd Ke at s i n a no th e r s t u dy p o s t u l a te d t ha t a pp r ox i m a te l y 90 % o f ne w m y o c ar d i a l i s c he m i a o bs e r v ed d ur i n g a ne s th e s i a w as t h e m a n i f es t at i o n o f s i l en t i sc h em i a o b s e r v e d i n th e p at i en t b ef o r e t h e op e r a ti o n an d o n l y 1 0 % w a s r el a te d t o an e s t he t i c m an ag e m e n t. T he r ef or e , th e r el a ti on be t w e en i n tr a op er a ti ve i s c h e m i a a nd p o s t o pe r a t i v e o ut c o m e i s s t i l l u ns ol v ed . G er s o n J I, H i c k ey R F , B ai nt o n C R . T r e a tm en t o f m y o ca r d i al i s c h em i a w i th ha l ot ha n e o r ni tr o pr us s i d e- p r o pr a no l o l . An e s t h A na l g 19 8 2; 6 1: 10 14 . H i l l AB , B ow l ey C J , N a h r w ol d M L, et a l . In t r a na s al a d m i ni s tr at i o n o f n i t r o g l y c e r i n . A ne s t h es i o l og y 1 98 1 ;5 4 :3 46 34 8 . K ni gh t A A, H o l l e nb e r g M , L on d on M J , et a l . Pe r i o p er at i v e m yo c ar di a l i s c he m i a : i m p or ta n c e o f t he pr eo p er at i v e i s c h em i a pa t t e r n . A ne s th e s i ol o gy 1 98 8 ;6 8: 6 81 6 8 8. M an ga n o D T . P er i op er a ti ve ca r d i ac m o r b i d i ty . An e st h es i o l og y 1 99 0 ;7 2: 1 53 1 8 4. S l o go f f S, Ke at s A S. D o es pe r i o pe r a t i v e m yo ca r di al i s ch e m i a l ea d t o po s to pe r at i v e m y o c ar di a l i n f ar c t i on . A ne s t h es i o l og y 1 98 5 ; 6 2: 1 07 11 4. S l o go f f S, Ke at s A S. R a nd o m i ze d t r i a l of an es t he t i c a g en ts on o u tc om e o f c or on a r y a r te r y by pa s s op e r a ti o ns . A ne s t h es i o l og y 1 98 9 ;6 9 :1 79 18 8 .

C.I-19. Would you use prophylactic nitroglycerin during coronary artery bypass grafting (CABG) to prevent intraoperative myocardial ischemia or perioperative myocardial infarction?
N o. I t h as be en r e po r te d t ha t p r o p hy l a c ti c a dm i n i st r a ti o n of ni tr o gl y c e r i n, 0. 5 o r 1. 0 g/ k g / m i nu t e, d u r i ng fe n ta ny l a ne s t h es i a i n pa t i e nt s u nd e r g oi n g C A B G d i d n o t pr e v e n t m y oc a r d i a l i sc h em i a or r e du ce th e i nc i d e nc e o f p er i o p er at i v e m y o c ar di a l i n f ar c t i on . R oy s t e r R L , B ut te r w o r t h J , G r o ba n L , e t al . C ar d i o va s cu l a r p ha r m a c o l og y . In : K ap l a n J A , R e i c h D L, La k e C L , e t a l . e d s . K a pl an ' s c ar di a c an e s t he s ia . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :2 1 3 2 19 .

C.I-20. How would you correct hypertension?


B l o od pr es s ur e = bl o od f l ow x r e si st a nc e H y p er t en s i o n i s us ua l l y d u e to i n ad e qu a te d e pt h o f a ne st h es i a . O c c a s i on a l l y i t i s d u e t o fl u i d o v er l o a di ng . T he tr ea t m e nt of h y pe r t e ns i o n i n c l ud e s th e f ol l o w i n g: P.160

D ee pe n t he an e st he s i a . I nh al a ti on ag e nt s, su ch as h a l o th a ne , e nf l ur an e , an d i s o f l u r a n e a r e m o r e e f fe c t i v e t h an n a r c ot i c s b e c a us e o f t he i r v a s o d i l at o r e ff ec t .

V as od i l a to r s . w h en i n ha l a t i o n a ge n ts a r e no t u se d .

S od i u m n i t r op r u s si de pr od u ce s m or e a r t er i ol ar d i l a ti o n t ha n v en od i l a ti o n. D o s e : 1 0 t o 10 0 g p er m i n u t e I V d r i p t i t r at i o n N i c ar d i p i n e . D o s e 0. 5 g/ kg / m i nu t e, t i tr at e d to ef fe c t. L ab et a l o l . D o se 5- m g i n cr e m e nt s , ti tr a te t o e f fe ct . N i t r o g l y ce r i n p r o d uc e s m o r e ve no d i l a ti on th an ar te r i o l a r d i l a ti on . D os e : 20 to 2 0 0 g pe r m i n ut e I V d r i p ti t r a t i o n, o r b ol u s i n 20 g i nc r e m en t s S ee a l so C h ap te r 1 4 , qu e st i o n C .1 0 .

C.I-21. How would you treat hypotension?


H y p ot e ns i o n i s u s u al l y ca u se d b y h yp ov o l e m i a , de e p an e st h es i a , b r a d y c ar d i a , o r C H F . T h e t r e at m en t s ar e a s fo l l o w s :

I nc r e a s e f l ui d i nf us i on a n d p ut t h e pa t i e nt i n h e ad - d o w n po s i t i o n w he n C VP o r P AO P i s l ow . L i g ht e n th e l e ve l o f an e st he s i a o r u se a va s oc on s tr i c t or : p he ny l ep hr i ne , 0 .1 m g I V i nc r e m en t s , t o c or r e c t v a s o d i l a ti on pr od u c e d b y an e s t h es i a . A tr op i ne , 0 .2 t o 2 .0 m g , f or b r ad yc a r d i a , o r i so pr o te r e n ol , 1 m g p er 1 0 0 m L D 5 W I V d r i p t i t r a ti o n, r a r e l y i n di c at ed T r e at C H F w h e n PA O P i s hi gh an d T EE s h ow s h yp o ki ne s i a :

L i g ht e n th e l e ve l o f an e st he s i a . R es tr i c t f l u i ds . D i u r e t i c s fu r os em i de ( L as i x ) 2 0 t o 40 m g I V I no tr o pe s

C aC l 2 ( 0. 5 t o 1 .0 g ) . E pi ne p hr i n e 2 to 8 g p er m i nu t e IV dr i p D ob ut a m i ne or d o pa m i n e 5 t o 2 0 g /k g /m i n u te I V d r i p A m r i n o ne 0 . 75 t o 1 .5 m g p e r kg , t he n 5 to 1 0 g/ k g / m i nu t e IV dr i p , o r M i l r i no n e 0 .0 5 m g pe r k g, th en 0. 5 t o 0. 7 g/ k g/ m i n ut e I V dr i p N or ep i ne ph r i n e i f pe r i p he r al v a sc ul a r r e s i s ta n c e i s l ow . I AB P

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C.I-22. What are the indications for intravenous metoprolol, labetalol, or esmolol during surgery? How much would you give? What are the relative contraindications? Indications

S T - s e g m e nt d e pr e ss i o n a ss o ci at e d w i t h ta c hy ca r di a; no r e s p on s e to de e pe ni n g t he l e v e l o f an e s t he s i a S up r a v en tr i c u l a r t ac h yc ar d i a o v er 1 2 0 pe r m i n u te R ec ur r e n t v e n tr i c u l a r a r r hy t hm i a s

Contraindications

A s t hm a , r e a ct i v e c hr on i c ob s tr uc t i v e p ul m o n ar y d i s ea s e

H ow ev e r , e s m o l o l i s ca r di os e l e ct i ve a n d a pp ea r s to ha ve l i tt l e ef f ec t o n br o nc hi a l or v a s c u l a r t on e a t do s es t h at d e c r e as e H R i n h u m a n s . I t h as be en us ed s uc c e s s f ul l y i n l o w do s es i n p a ti en t s w i th as th m a. E s m o l o l i s m e t ab o l i z e d r ap i dl y i n th e b l o o d b y an es te r as e l oc at e d i n th e e r y th r oc y t e c y t o pl as m . Es m o l ol i s a s ho r t - a c ti ng - b l o c ke r w i t h a n el i m i na t i o n h al f- l i f e o f 9 m i n ut e s an d a p h ar m a c ol o gi c h al f- l i f e of 10 t o 2 0 m i n u te s . P.161

Dosage

M e t op r ol ol , 1 - to 2- m g i n cr e m e nt s e ve r y 1 t o 2 m i n ut e s, t o ta l d os e 5 t o 1 0 m g E s m ol o l , 1 0 - m g i n c r e m e n ts u p t o 0 .5 m g p e r kg f o l l ow e d b y 50 to 3 0 0 g /k g /m i n u te I V d r i p . L ab et a l o l , 5- m g i n cr e m e nt s , ti tr a te t o e ff e ct . N ot i n di ca t ed i f B P i s de c r e as e d.

R oy s t e r R L , B ut te r w o r t h J , G r o ba n L , e t al . C ar d i o va s cu l a r p ha r m a c o l og y . In : K ap l a n J A , R e i c h D L, La k e C L , e t a l . e d s . K a pl an ' s c ar di a c an e s t he s ia . P hi l a d el ph i a: W B S au n de r s, 2 0 06 :2 1 9 2 25 .

C.I-23. How would you correct increased pulmonary artery occlusion pressure (PAOP)?
I t i s i m po r t a nt t o t r e a t th e p a ti en t a s a w ho l e. A l l m o n i t or ed pa r am et e r s s ho u l d be t a k e n i nt o a c c o un t . In c r e as ed PA OP i s u s ua l l y d ue to a l i gh t l ev e l of a ne s t h es i a or C H F . C o m b i n i ng t h e r e a di ng s o f P AO P a nd BP w i l l p r o d uc e a d i ff er e nt i a l d i a g no s i s . Oc c as i o n al l y an i n c r ea s ed P A OP w i th h y po te n s i on an d l ow c a r d i a c o ut p ut i s c au s ed b y h yp e r t r o p hi c o bs tr u ct i v e c ar d i o m y o pa th y ( H O C M ) , al s o k n o w n a s i di o pa th i c hy p er tr o ph i c s u b ao r t i c s t en o s i s ( IH SS ) . H O CM c an b e d i a g no s ed b y T EE , w hi c h de m on st r at es sy st o l i c an t er i o r m ot i on ( S AM ) o f m i tr a l v a l v e a n d l e f t v e n tr i c u l a r o ut f l o w ob s t r uc ti o n, mi tr al re gu r gi t a t io n a nd u s ua l l y g o od l e ft v e nt r i cu l ar c o nt r a c ti l i t y.

Inadequate Anesthesia: Increased PAOP with Hypertension


D ee pe n t he l e ve l o f a ne s th es i a w i t h i n h al at i on a g en t s, s u c h a s i s o f l u r a n e, h a l o th a ne , o r e nf l u r a n e, w h i c h a l s o h av e a v a s o di l at o r ef fe c t. G i v e a v as o di l a t or . N i t r o gl y ce r i n i s a b et t er v e no di l at or th an ni tr o pr us s i d e.

Congestive Heart Failure: Increased PAOP with Hypotension and Low Cardiac Output

L i g ht e n th e l e ve l o f an e st he s i a . R es tr i c t f l u i ds . U s e a r te r i al va so d i l at o r s . G i v e d i u r e t i c s. U s e i n ot r o p es .

HOCM (IHSS)

- B l oc k e r a n d vo l at i l e a ge n ts t o d ec r ea se H R a n d co n tr ac t i l i t y F l u i d l o ad i ng t o k ee p L V f ul l a nd de cr e as e l ef t v en tr i cl e o ut fl o w tr ac t ( LV O T ) o b s t r u c t i on I nc r e a s e a f te r l o ad t o k ee p L V f ul l

R ei c h D L , M i t tn ac h t A, Lo n do n M , et al . M on i t o r i ng of t h e he a r t a n d v a s c u l a r s y s t em . I n: K a pl an J A , R ei c h D L , L ak e C L, e t a l . e d s . Ka pl a n' s c ar d ia c a ne s t h es i a . P h i l ad e l p hi a : W B Sa un d er s, 20 06 : 39 9 4 0 3.

C.I-24. What should you do during sternal splitting?


S to p v en ti l at i o n a n d de f l a te th e l un g s to p r ev e nt l u ng i n j u r y fr om t h e el e c t r i c s aw .

C.I-25. Would you monitor PAOP continuously? Why?


N o, I f t he Sw an - Ga nz ca th e te r b al l o o n i s i n fl a te d c on t i n uo u sl y, pu l m o na r y i n fa r c t i o n d i s ta l t o t he oc c l u s i on m a y e ns ue . U s u a l l y p ul m o n ar y a r t er y d i a s t o l i c p r e s s u r e ( P AD P) i s m on i to r e d c on t i n uo u sl y b ec a us e t he g r ad i e n t b et w e e n PA D P an d P AO P i s s m a l l . P.162 S k u ba s N , L i c ht m an A D , Sh a ar m a A, e t a l . An es t he si a f or ca r d i ac s u r g er y . In : B ar as h P G, C u l l e n BF , S to e l t i n g R K, ed s . C l i n i c a l a ne s t h es i a , 5 t h ed .

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P hi l a d el ph i a: L i pp i nc ot t W i l l i a m s & W i l k i n s , 20 0 6: 91 6 .

C.I-26. Discuss autologous transfusion and blood conservation for cardiac surgery
A ut ol o go u s tr an s fu si o n i s th e c ol l e c ti on an d r ei n fu si o n of th e p at i e n t' s o w n bl o od o r b l o o d c o m po ne n ts . T he r e al i z a t i on th a t ho m ol og o us b l oo d i s r es po n s i bl e f or tr an s m i ss i o n o f a cq u i r ed i m m u no d ef i ci en c y sy n dr om e ( AI D S ) , he p at i t i s , t r a n s f u s i on r e ac t i o n, an d a ut o s e ns i ti z a ti o n h as l e d t o i n c r e as ed i nt er e s t i n a ut o l o go u s tr a ns fu s i o n a nd bl oo d c on s er va t i o n . T h e r e a r e s e v e r al o p ti o ns f o r au t ol og o us t r an s f u s i on : p r e o pe r at i v e a ut o l o go u s b l o od do na t i o n , p r e op e r a ti v e us e o f e r y th r op o ie ti n , in tr a op e r a ti ve no r m o vo le m i c h e m o d i l ut i o n , i n t r a op e r a t i v e p l a sm a ph er e si s, ph ar m ac ol o gi c t r e a t m e n t, an d p er i o p er at i ve b l o od s a l v a ge .

Preoperative Autologous Blood Donation


D on at i on s a r e a p pr o pr i a t e fo r p r o p er l y s e l e ct e d p at i e n ts w i t h s ta b l e C A D , s t ab l e v a l v u l a r d i s ea s e, a n d c on ge n i t al he a r t d i s e as e . T h e r i s k o f bl o od d o na t i o n m ay b e h i g h er f o r pa t i e nt s w i t h u ns t ab l e an g i n a o r se v er e a or ti c s te n os i s ; t he s e pa t i e nt s a r e us ua l l y n o t c o n s i de r ed g o od c a nd i da t es f o r au t ol og o us b l oo d d on a ti on . T he pa ti e nt s h ou l d ha v e a h em og l ob i n of g r ea t er t ha n 1 1 g p e r dL to d o na t e bl o od . T he o p ti m a l d on a ti on pe r i o d b eg i n s 4 t o 6 w e ek s b ef o r e s u r g er y , an d t he l a s t do na t i o n i s us u al l y c o l l e c t ed no l a te r t ha n 7 2 h ou r s be fo r e s u r ge r y . D es p i t e t he p o te n ti al b e ne f i t s o f th e m et h od , i t i s r a r e l y us ed cu r r e nt l y be c a u s e o f l o gi s t i c a l r e a s o ns ( m u l t i pl e p r e op e r a ti v e v i s i t s to t h e h os p i t al , c os t ) .

Preoperative Use of Erythropoietin


T hi s i s an e s ta b l i s h e d, e f fi ca c i o us bu t r el at i ve l y e x pe n si ve th er a py t o r ed u c e b l oo d t r a n s f us i on s . T o o p ti m i z e th e h em o gl ob i n r e s po ns e , or a l or i n t r a v e no u s i r o n s up pl e m e nt a ti on i s r e co m m e nd ed . T he m e th o d i s pa r t i cu l a r l y i n di c a t ed i n a ne m i c p a ti en t s .

Intraoperative Normovolemic Hemodilution


T hi s i s th e r em ov a l of bl oo d t h r o ug h a n a r t er i al o r v en o us c a th e te r i m m ed i a t el y a ft er i n du c ti on of a n es th e s i a , be f or e C PB o r t h e ad m i n i s tr a ti on of h e pa r i n . D ep en d i n g o n t he p a ti en t 's si ze an d h em a to cr i t , 5 00 to 1, 00 0 m L o f bl o od i s c ol l ec te d i nt o b l o o d b ag s c on ta i ni ng C P D A - 1 an t i c oa g ul a nt a n d is ke pt at r o om t em pe r at ur e . T hi s b l o od i s s p ar ed th e r i g or s o f C PB , i n c l u d i n g h em ol y si s, p l at e l e t d es tr u c t i o n , an d c l o t ti ng fa c t o r de g r a da t i o n . T h e a ut o l o g o u s bl o od i s t r a n s f us e d a ft er r ev er s al o f t he he pa r i n w i th p r ot am i ne . I t ha s b ee n d e m o ns t r a te d t ha t t he ef fe c t of on e u ni t o f f r e s h w h ol e b l o o d on pl a te l e t a gg r eg at i on a f t e r C PB i s a t l ea s t eq ua l , i f no t s up e r i or , t o th e e ff e ct o f 8 t o 1 0 s to r e d p l at el e t un i ts . H o w ev e r , i f t he p a ti e nt 's he m a t oc r i t i s b el ow 33 % o r th e h e m o gl o bi n i s be l ow 1 1 g p er d L , no r m o v o l em i c he m o d i l ut i on i s n ot r e co m m e nd e d be c au s e fu r th er de c r e as i n g t he ox y g e n- c a r r y i n g c ap a c i t y m a y w or s e n m y o c a r d i al i s c h e m i a. In a dd i t i on , h em od i l u t i o n d ur i n g C PB w i l l f u r t he r d ec r ea se he m a t oc r i t t o l ev el s t ha t r eq u i r e h om ol o go u s bl o od t r an s f u s i on . N or m ov o l e m i c h em od i l u ti o n s h o ul d b e pe r fo r m e d c a u ti ou s l y i n p at i en ts w i th cr i t i c a l l e f t m a i n co r on ar y s te n os i s an d a or ti c s te n os i s be c a u s e s u dd e n c a r di ac ar r e s t ha s b ee n o b s e r v e d du r i n g t he p r oc ed u r e .

Intraoperative Plasmapheresis
C oa gu l op a th y a s s oc i at ed w i th hy po t he r m i a, s h oc k, C P B, m u l t i p l e tr a ns fu s i o ns , a nd th e b l o o d s a l v a ge te c hn i q u e, w h i c h r em ov e s c l o tt i n g f ac t or s a nd p l a te l et s , of te n n e ce ss i t a te s u se o f f r e s h- fr o ze n p l a sm a a nd pl a te l e t p ac k s to c o nt r ol p o s t op e r a ti v e bl e ed i n g a n d c l o tt i n g p r o b l e m s . R ec e nt l y a pl a s m ac ol l e c ti on s y s t e m ha s b ee n d ev e l o p ed t o s al v ag e u p to 1, 0 00 m L o f p l a te l et - r i c h p l as m a be fo r e C P B . T h i s te c h n i q u e do e s no t c au s e h em od i l u ti o n; t h er ef o r e , i t c a n b e u ti l i z ed P.163 i n al l p at i en ts , i nc l ud i n g t ho s e w i t h an e m i a. T h e p l a te l et - r i ch p l as m a c a n b e s t o r e d a t r o o m te m pe r a t ur e u nt i l tr an s fu s e d , us u a l l y af te r p r o t am in e r ev e rs al of t he h e pa r i n . It i s r e co m m e nd ed th at th e c ol l e c te d p r o d uc t b e pl a c e d o n a r oc k e r u n ti l i n f us i o n a n d t h a t th e p H b e he l d c on s t a nt .

Pharmacologic Treatment
T he p r op hy l ac ti c u se of a p r o ti n i n , - a m i n oc a pr oi c a ci d ( EA C A) a n d tr a ne x a m i c a c i d r e du c e s b l o o d tr a ns f u s i o n s i n c a r d i a c s ur g er y . Ap r o t i n i n i n hi b i t s a h os t o f pr o te as e s , i n c l ud i ng t r yp si n , pl a sm i n , k al l i k r e i n an d f ac to r X II a a c t i v a ti o n o f c o m p l em en t . T h e a d ul t d os e i s 2 m i l l i on k a l l i k r ei n i nh i bi t i o n un i ts ( K IU ) fo r t he p a ti en t a n d by p as s p um p f ol l o w ed b y 5 0 0, 00 0 K IU pe r h ou r f or 4 ho ur s . T h e s y n t he ti c a nt i fi br i no l y t i c s , E A C A a n d t r a ne x am i c a c i d , b i n d t o p l a s m i n o ge n a nd p l as m i n , th e r e by i n hi b i t i n g b i n d i n g o f p l a sm i no ge n a t t he l y s i ne r e s i d ue s o f fi b r i no g en . E ff e c t i v e a nt i f i br i n o l y s i s r eq u i r e s a lo a di ng do s e of 10 0 t o 1 50 m g pe r k g f or E A C A o r 1 0 m g pe r k g fo r t r a n ex am i c ac i d an d a c o ns t an t i nf us i on f o r ea c h at on e - t en t h th e l oa d i n g d os e e ac h h ou r .

Perioperative Blood Salvage


T hi s i s th e c ol l e c ti on an d r ei n fu si o n of bl oo d l os t d u r i ng a n d i m m ed i a t el y a ft e r s u r g e r y . T he p o s t tr a ns fu s i o n s ur v i v al o f p er i o p er a ti v e l y - s a l v a ge d r ed c e l l s h as b e en s h ow n t o b e co m pa r a b l e t o t ha t o f a l l o ge ne i c r e d c el l s . A t t he c o nc l us i o n o f C PB , a l l b l oo d r em ai n i n g i n th e o x y g en a to r a nd b y pa s s c i r c u i t s sh o ul d b e s a l v a ge d a n d, i f n ee d ed , i nf u se d. Bl oo d s al v ag ed i n t r a op e r a ti v el y m a y b e t r a ns f us e d di r e c t l y ( un w a s he d ) or p r oc es s ed ( w as he d ) be f or e i nf u s i on . C om m e r c i al l y av ai l ab l e eq u i p m e n t ex i st s fo r e ac h o p ti on . B l o o d c o l l e c t e d by i n tr a op er a ti v e s a l v a ge r e pr e s e nt s a n e x c el l en t s ou r c e o f r ed - c e l l s u pp or t . H ow ev e r , s a l v ag e d bl o od i s d e fi ci en t i n c oa g ul at i on f a ct or s a nd pl at e l e ts . P os to p er at i v e b l oo d s al va g e i s an o th er te ch n i q u e of au to l og ou s b l oo d t r a ns f us i o n u ti l i z i n g b l o o d l o s t fo l l o w i n g s u r ge r y . B l o o d s a l v a ge d f o l l ow i n g c a r d i a c s ur ge r y i s g e ne r al l y c o l l ec t ed fr om m e di as t i n al an d c he s t dr a i n s a nd t r an s f u s e d w i t ho u t w a s hi ng . B ec a us e i t i s us ua l l y d e fi br i n a t e d , i t do e s no t r eq u i r e a nt i c o ag u l a ti o n be f or e t r a ns f us i o n . Al t ho ug h d i l u te , t he bl oo d i s s te r i l e an d c on t ai ns v i ab l e r e d c el l s . D r u m m on d J C , Pe tr o vi ch C T . H e m ot h er ap y a nd he m o s ta si s . In : B ar a s h P G , C u l l e n B F , S t oe l t i ng R K , ed s . C l i n i c a l a ne s th es i a , 5 t h ed . P hi l ad e l p hi a : L i p pi n c o tt W i l l i a m s & W i l ki ns , 2 00 6 :2 1 7 2 19 . G r a v l e e GP , D av i s R F , U tl ey J R . C a r di op u l m on a r y b y pa ss , p r i n c i pl e s an d p r a c ti c e . P hi l ad e l p hi a : Li p pi nc o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 36 54 2 . L i l l y K J , O' G ar a P J, T r ea n or P R , et a l . C a r di op u l m on a r y b y pa s s : i t' s n o t th e s i z e , i t ' s h ow y o u us e i t ! R e v i e w of a c o m p r eh e ns i v e b l o o d- c o n s e r v a ti on s tr at e gy . J E x t r a C o r p o r T e c hn ol 20 0 6; 36 ( 3) :2 6 3 2 68 . S ha nd e r A, M o s k o w i tz D , R i j h w a ni T S . T he s a fe ty an d e ff i c a cy o f bl o od l e s s c a r d i a c s ur g er y . S e m i n C ar di o th o r a c Va s c An e s t h 2 00 5 ;9 ( 1 ) :5 3 6 3. S pa hn D R , C as ut t M . E l i m i na t i n g b l o o d tr a ns fu s i o ns . N ew as pe c ts a n d pe r s p ec t i v es . A ne s th e s i ol o gy 2 0 00 ;9 3 :2 4 5 25 5 . V an d e r Li n de n P . P er i o p er at i ve b l oo d c on se r va ti o n st r at eg i es : a n u pd at e f or c l i n i c i an s . C a n J A n ae s t h 2 00 6 ; 5 0 ( 6 S u pp l ) : S1 S 2 .

C.II. During Cardiopulmonary Bypass


C.II-1. What anticoagulant would you give before CPB? How much would you give? What is its mechanism?
H ep ar i n ha s b ee n u s ed c o nv en t i o n al l y i n d o se s o f 30 0 ( 20 0 t o 4 00 ) u ni t s pe r k g o f bo d y w e i gh t, as s u m i n g a n i n i ti al c o nc e nt r a t i o n o f at l e as t 2 t o 4 u n i t s p er m L of w h ol e b l o o d. E m pi r i c al l y ,

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P.164 a ft er 2 ho u r s o f t he i n i t i al d o se , s ub se q ue n t do s es o f 1 m g p er k g a r e gi v en f o r ea c h a dd i t i on al ho ur of b y pa s s . B ec a us e t he r e is m a rk ed in di v i d ua l v ar i a t i o n, he pa r i n d o se s a r e b e st m o ni to r ed by t h e ce l i t e- AC T t es t . H ep ar i n ac t s i n d i r ec t l y b y m ea n s of a pl a sm a co f ac to r . T h e h e pa r i n c of a c t or , o r an t i t h r o m b i n I I I, i s a n 2 - g l o bu l i n a n d a p r o t ea s e i n hi b i t or th at ne ut r al i z e s s ev er a l ac t i v at e d c l o tt i n g f ac t or s: X I Ia , k al l i k r e i n , X Ia , I Xa , X a, II a, an d X II Ia . A nt i th r o m bi n I II f o r m s i r r e v er s i b l e c o m p l e x es w i t h t h r o m b i n ( I Ia ) a n d, a s a r es ul t , bo t h pr o te i n s a r e i n ac t i v at e d. I n hi bi t i o n o f th r om bi n a n d fa c to r Xa ac c ou nt s f or m o s t o f t he an t i c oa g ul an t e f f e c t o f h e p a r i n . H e p ar i n i n c r ea s es th e r at es of t h e th r om bi n - a nt i th r o m bi n r e a ct i o n a t l ea s t 1, 0 00 - f o l d b y s er v i n g a s a c at al y ti c t em pl a t e t o w hi c h bo t h th e i nh i bi to r a nd t h e p r o t ea s e bi nd . H ep a r i n a l s o b i n ds to c o fa c t o r II , a g l yc op r ot ei n o f 6 5, 00 0 D a t ha t i na c ti v a t es t h r o m b i n i n d ep en d en t l y o f a nt i th r o m b i n I II . T h i s r e a c t io n o c c u r s m o r e s l o w l y a n d r eq ui r es h i gh er he pa r i n c o nc e nt r a t es t h an d o es t h r o m b i n i n h i b i t i on t h r o u gh t h e he p ar i n - AT I I I c o m pl ex . S pi es s B D , H o r r ow J, K a pl an JA . T r a ns f us i o n m ed i ci ne an d c oa g ul at i on d i s o r d e r s . I n: K a pl an J A , R ei c h D S N , La k e C L , e t al . e ds . K ap l an ' s c a r di ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :9 4 8 95 1 .

C.II-2. What is the half-life of heparin? How is it eliminated?


T he b i ol og i c ha l f- l i f e of he pa r i n v a r i es w i th do sa g es a n d te m pe r at ur e . It h a s a r em ar k ab l e i n d i v i d u al v a r i at i o n . T h e a v er ag e h a l f - l i f e i s ap p r o x i m at el y 1 0 0 m i n ut e s i n no r m o th er m i c m an fo r t he i n i t i a l d os e s of 30 0 u ni t s, i nc r ea s i n g w i t h hi g he r d os e s an d d e c r ea s i n g te m pe r a t ur e . W h en 1 0 0 , 40 0 , or 80 0 u ni t s of h ep a r i n ar e g i v e n i n t r a ve n ou s l y , th e a p pr ox i m a te ha l f - l i fe i s 1 , 2 .5 , a nd 5 ho u r s r e s p ec t i v el y . H e p ar i n c o nc e nt r a t i o ns de c l i ne p r og re s s i v e l y at al l t em pe r at ur e s , b u t th e r at e o f d ec l i n e i s de l a y ed i n p r o p or t i o n t o th e h y p o th e r m i a . T he p r i m ar y m ec ha n i s m f or h e pa r i n e l i m i n at i on r e m a i n s u nc e r t ai n . H e p ar i n ap p ea r s to b e c l e a r e d a nd d e gr a de d p r i m a r i l y by t h e r e t i c u l o en d ot h el i a l s y s t em ; a s m a l l am o un t o f he p ar i n al so ap p ea r s i n t h e ur i ne . S pi es s B D , H o r r ow J, K a pl an JA . T r a ns f us i o n m ed i ci ne an d c oa g ul at i on d i s o r d e r s . I n: K a pl an J A , R ei c h D S N , La k e C L , e t al . e ds . K ap l an ' s c a r di ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :9 4 9.

C.II-3. How do you monitor heparin dosage? What is the activated coagulation time (ACT) test?
H ep ar i n th e r a py c a n b e a ss es s ed b y t he PT T , h e pa r i n a s sa y, he pa r i n - p r ot am i ne t i tr at i o n , a nd t h e AC T t es t . T h e m os t c on v en i e n t a n d p r a c ti c a l m et h od u s ed t o m o n i t or he pa r i n t h er ap y i n t he o p er a ti ng r o om i s t he ce l i t e- AC T t es t . T h e r e i s a v er y g oo d c o r r el at i on a m on g t he AC T , pl as m a he p ar i n un i t s , an d t hr om b i n t i m e . Af t er c e nt r a l v en o us i n j e ct i on o f a he pa r i n b o l u s , th e o ns e t of m a x i m a l A C T pr ol o ng at i on i n t he r a d i a l a r t er y b l o od s a m p l e o c c ur s w i t hi n 1 m i n ut e . Pr e v i ou s w or k s ug g es te d t ha t h ep a r i n a ct i o n p e ak s 1 0 to 20 m i nu te s a ft e r ad m i n i s t r a t i o n, b u t th i s fi n di ng pr ob a bl y r ep r e s en t ed a n a r t i f a c t fr om o th er fa c t o r s p r ol on g i n g t he A C T su c h as he m o d i l ut i on an d h yp ot h er m i a . T w o m i l l i l i t er s o f b l o od ar e p ut i n to a te s t t u be c o n t a i n i ng c e li te to a c ti va t e c oa gu l at i o n . T h e n t he t u be i s k ep t a t 3 7 C ( 98 .6 F ) a n d cl o t fo r m a ti on i s w a tc he d f o r AC T . T h e n or m a l c on t r o l v al ue of A C T i s 1 0 5 t o 16 7 s ec o nd s . A b as el i ne v a l u e i s de t er m i n ed b e fo r e th e a dm i ni st r a t i o n o f h ep ar i n, a n d th e t e s t i s r ep ea t ed 3 to 5 m i n ut es af te r h ep a r i n i s gi v en a n d a t i n t er v a l s of 3 0 t o 6 0 m i n ut e s th e r e af t er . W i t h th e d o se o f h ep a r i n i n m i l l i gr a m s p er k i l o g r a m o n th e v er t i c al ax i s a n d A C T i n s ec o nd s o n th e h o r i z o nt a l ax i s , a do s e - r e s p o ns e c ur v e c a n b e P.165 p l o tt e d. A C T v a l ue s a r e m a i n ta i ne d a t l e a st t w i c e t he c o nt r o l v al u e an d s h ou l d ne v e r d ec r ea s e l e s s th an 30 0 s ec o nd s d ur i n g n o r m ot h er m i a. At t h e N e w Y or k P r e s b y te r i a n H o s pi ta l - C or ne l l M e d i c al C e nt e r , w e k ee p t he AC T a bo v e 48 0 s ec o nd s . S ho r e - Le s s e r s on L. C o ag u l a ti o n m o n i t or i ng . I n: K a pl an JA , R ei c h D S N , La k e C L , e t al . e ds . K ap l an ' s c a r di ac an es t he s i a , 5t h e d . Ph i l a de l ph i a : E l s e v i er S c i en c e, W B S au n de r s , 2 00 6 :5 5 8 55 9 .

C.II-4. What is total cardiopulmonary bypass (CPB)? What is partial bypass?


T ot al by pa s s i n d i c at e s th a t al l t he ve no u s r e t ur n f r o m s up er i or a n d i n f er i o r v en a e c a v ae , a nd th e c or on a r y s i nu s i s dr a i n ed to t h e ox y ge n at or , a nd no b l oo d i s pu m pe d b y th e R V t o th e l un g s. T h e P A an d s ys t em i c p r es su r e tr a c i ng s b ec o m e n o np u l s at i l e . P ar ti a l by p as s m e a ns th at s o m e of t h e bl o od r e t u r n i s s t i l l p um pe d b y b ot h r i g h t an d L Vs . S om e v en o us b l oo d i s d r a i n e d to th e o x y ge n at o r an d p um p ed ba c k t o t h e ar t er i a l s i d e . F e m o r al f e m o r a l b y p a s s i s o ne e x a m p l e of pa r t i al C P B. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 5 2 55 3 .

C.II-5. What is the purpose of venting the LV? How can it be done?
A l t ho u gh a l l th e v e no us r e tu r n i s b y pa s se d f r o m th e R V , 2% to 5 % o f c ar di a c ou t pu t i s dr a i n i n g t o t he L V . T h i s r e p r e s e n t s t h e p h y s i ol o gi c s hu n t fr om th e b r o nc h i a l , th e b es i a n , a nd p l eu r a l v ei n s. O t he r s ou r c e s of bl oo d f l o w t o t he l e ft h e ar t d ur i n g C PB i n c l u de a o r t i c r e gu r gi t a t i o n f r o m a or ti c i ns u ff i c i e n c y a n d e x t r a c ar di a c l e f t- to - r i gh t s hu nt s s uc h a s p at e nt d u ct us ar te r i o s u s a nd Bl al o c k - T a us s i g , W a te r s t on , a nd Po t ts s hu n ts . T he l e ft v e nt r i c ul ar su mp dr ai n p r e v e n ts o v er di s te nt i on o f t he LV , w hi ch m a y c au se po s tp um p h ea r t fa i l u r e . A s u c t i o n n ee d l e i n s e r t e d pr o x i m a l t o t he a o r t i c c r o s s - c l a m p m a y s er v e t h e s am e p ur po s e. V en ti n g of th e L V c an b e a cc o m p l i s he d b y i n s er ti n g a c at he t er t o t he fo l l o w i ng s i te s :

A or ti c r oo t s uc h a s ca r di op l eg i a ca n nu l a fo r C AB G J un c t i on o f t he r i gh t s up e r i or pu l m o na r y ve i n an d t he l e ft a t r i um an d a dv a nc i n g t hr o ug h t he l e ft a t r i um an d m i t r a l v al v e i n t o t h e L V A pe x o f th e L V P A or th e l ef t a tr i u m o nl y

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :9 9 1 03 .

C.II-6. How many types of oxygenators are there? What are the advantages of each type?
T he r e ar e t w o b a s i c t yp es of o x yg en a to r s i n t e r m s o f th e i r i nt e r f ac e w i t h b l o o d.

Direct Gas Interface


Disk V er ti c a l s c r e en B ub bl e

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Without Gas Interface


M e m br an e s o l i d o r m i cr o po r o u s Fl u i d f l ui d u s i n g fl u or oc a rb on li qu i d

P.166 T he d i s k a n d s c r ee n o xy ge n at o r s a r e no t d i s p os ab l e an d h a ve p r ov en to b e s om e w h a t di ff i c u l t t o c l ea n, pr ep a r e , a nd r e s t e r i l i z e . T he b u bb l e ox y ge na t or h a s th e a d va nt a ge s o f si m pl i c i t y , di s po s a b i l i t y , an d r el a ti v e l y l o w c os t . T he d i s a dv a nt a ge s o f ga s i nt e r f ac e o xy g en at o r s i n cl ud e t h e fo l l o w i n g:

P r o te i n de n at u r a ti on I nc r e a s e d f r a gi l i t y o f ce l l s S us c e p ti bi l i t y to he m ol ys i s D en at u r a ti o n of pl at e l e t m em br a ne m a te r i a l s r e su l t i ng i n p l a t el et ag g r e ga t i o n, c l um p i n g F o r m a ti o n o f ai r e m b ol i sm L ar ge pr i m i n g v o l u m e V ar i a b l e r e s e r v o i r l ev e l r e s ul ti n g i n po te n ti a l sh i f t s of bl oo d v o l u m e b e tw e en i n tr ac o r p or e al a n d e x t r a c o r po r e a l c i r c u i t

T he m e m b r a n e ox y ge na t or h a s b ec om e m or e p op u l a r , ec on o m i c a l , an d e ff i c i en t , an d l e s s t r a u m a ti c t o b l o od . I ts ad v a n ta g es i n c l ud e t he f o l l o w i ng :

L es s t r a um a t o b l o od co m p o ne n ts N o de f oa m i n g D ec r e a s e d c om pl e m e nt ac ti v at i o n I nd ep e nd e nt c o nt r o l o f o xy ge n a n d ca r bo n d i o xi d e ex c ha n ge U s e o f a i r ox yg e n m i xt u r e w i th ou t t h e r i sk of g a se o us m i c r oe m b o l i

H ow ev e r , t h e ad v an ta g e o f a m em br a ne o x yg en a to r f or a sh or t p er f us i o n ( < 2 ho u r s ) i s un c l e ar , a l t ho u gh l o w e r p l a s m a h e m o gl o bi n l ev el s a r e pr es e nt u s i n g m em br a ne o x y g en a to r s . T he d i s a dv a nt a ge s o f m e m b r an e o xy g en at o r s i n cl ud e t he fo l l o w i ng :

E x p en s e P ot en t i a l d i f fi c ul ty i n e l i m i n at i ng a l l bu b bl e s du r i n g p r i m i n g M o d er a te l y l a r g e p r i m i n g vo l um e

T he m a j o r d i f fe r e n ce s i n ch a ng e s of cl ot t i n g f ac to r s be t w e en th e b ub b l e a n d m e m br an e o x y g en a t o r s be c o m e ap p ar e nt a f te r 4 t o 6 h ou r s of EC C. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 5 5 8. S k u ba s N , L i c ht m an A D , Sh a ar m a A, e t a l . An es t he si a f or ca r d i ac s u r g er y . In : B ar as h P G, C u l l e n BF , S to e l t i n g R K, ed s . C l i n i c a l a ne s t h es i a , 5 t h ed . P hi l a d el ph i a: L i pp i nc ot t W i l l i a m s & W i l k i n s , 20 0 6: 91 0 . W a g ne r J A. Ox y g e na to r a na t om y a nd f u nc t i o n. J Ca rd i ot h or ac V a sc A n es t h 19 9 7; 11 : 17 5 2 8 1.

C.II-7. What kind of priming solution would you use? How much priming solution would you use? When would you prime with blood? Why?
T he u s ua l p r i m i n g so l ut i o n f or ad ul t s at th e N ew Y o r k P r es by t er i a n H os p i t al - C o r n e l l M ed i c a l C en te r i nc l ud es 1, 40 0 m L o f b al an c e d s a l t s o l u ti o n ( N o r m os o l ) 1 00 m L o f 2 5% a l bu m i n a n d 20 0 m L o f 20 % m an n i t o l . T he pr i m i ng v o l u m e s v ar y w i t h t he s i z e o f t h e ox y ge na t or s u s e d a nd th e t ub i n g v ol u m e ; m os t o x y ge n at o r s f or ad ul t p a ti en t s ha v e pr i m i ng v o l u m e s o f 5 00 to 1 , 00 0 m L. I n g en e r a l , bl o od i s a dd e d to th e o x y g en at o r i f th e p at i e n t i s m a r k e dl y a ne m i c ( pr ep u m p h e m a to c r i t b el ow 30 %) or i f t he pr i m i n g v ol u m e i s l ar g e i n r e l a t i o n t o th e p a ti en t 's b l oo d v ol u m e , s uc h a s i n pe di a tr i c pa t i e nt s . In o r de r t o m ai nt a i n o x y g en c a r r y i n g c ap ac i ty , t he h e m a to c r i t i s ke p t at l e v e l s ab o v e 1 8 % to 20 %. M a nn i t o l h as l o ng be en us e d as an o s m o t i c d i u r et i c i n s i t u at i o n s w he r e he m o l y s i s or d i m i ni sh e d r e n al fu nc t i o n i s ex p ec te d . M a n ni to l h as be e n fo u nd t o d e c r ea s e th e P.167 i nc i d e nc e o f r e n al f a i l ur e d ur i ng h y po t en si o n by pr om o ti ng os m o t i c d i ur es i s an d i nc r ea s i n g r e n al b l oo d f l o w b y de c r e a s i ng r e na l v as c ul ar r e s i s t a nc e. H ep ar i n, 3 , 00 0 t o 1 0, 00 0 u ni t s, i s a dd e d to th e p r i m e de p en di n g o n th e s i z e o f t he p r i m e v o l um e . T h i s al l o w s he p ar i n to b e d i s t ri bu t ed ov er th e t hr om b og en i c s u r fa ce s o f t he C P B ci r cu i t . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :1 9 1 19 3 , 6 48 .

C.II-8. What are the advantages and disadvantages of hemodilution? Advantages of Hemodilution

A n i n c r e as e i n m i c r o ci r cu l a t i o n d ue t o a r e du c ti on of b l oo d v i s c o s i t y D ec r e a s e d m et ab o l i c a ci do s i s I nc r e a s e d u r i ne ou tp u t R ed uc e d bl o od de m a n ds

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R ed uc e d i n c i d en c e o f he p at i t i s, A I D S , o r r e ac t i o ns fr om bl oo d t r a n s f us i on s R ed uc e d po s to p er at i ve b l oo d l os s

Disadvantages of Hemodilution

D ec r e a s e d o xy ge n c ar r yi ng ca pa c i t y P os to p er at i v e e x tr ac e l l ul a r fl u i d o v er l o a d P os s i b l e p u l m on a r y e d em a H y p ot e ns i o n f r o m d ec r ea se d v i s c os i t y a nd pe r i p he r a l r es i s t an c e D ec r e a s e d c on ce n tr at i on o f c al c i u m , m a gn e si um , p ho s ph a te , a nd z i nc

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :1 8 6 19 4 .

C.II-9. What kind of pumps do you use? Are they pulsatile or not?
T he r e ar e t hr ee ty pe s o f p um ps av ai l ab l e fo r m od er n C PB m a ch i ne s : th e d ou b l e - h e ad e d no n oc c l u s i v e r o l l e r pu m p, t h e c e n tr i f u ga l b l o od pu m p , a n d th e v en tr i c u l a r - t y p e p ne u m a ti c o r h yd r a u l i c p um p. O n l y t h e fi r st t w o ty p es a r e i n c o m m on us e . T he r o l l er p u m p i s t he m o st co m m o nl y u se d p um p. It i s d r i ve n b y a n a ft er l oa d- i nd ep e nd e nt m o to r . O n c e th e p um p s pe e d i s s e t , i t w i l l c on t in ue th e f or w a r d d i s pl a c e m e n t of th e s am e b l o o d vo l um e ( o r e ve n a i r vo l u m e) e v en i f t he r e s i s ta nc e i s i nc r e a s e d b y k i n k i ng or c l am pi n g th e a r t e r i al l i ne . T hi s w i l l r e s ul t i n t he r u pt ur e o f c on n ec ti o ns b e tw ee n s ec t i o ns of t u bi ng . S o m e c e nt er s u s e pr es s u r e g au ge s o n t he ar t e r i a l i n f l o w l i n e t o av o i d t h i s t y pe o f d i s a s t er . T he c e nt r i f ug al pu m p i s a ki ne t i c p u m p t h at o p er at e s on th e c on s tr ai n ed v o r t ex pr i n c i p l e . B l o o d i s dr i v e n th r o u gh th e p um p b y c e n tr i f u ga l f or c e s g e ne r a t ed b y a v or te x i n t he p u m p . T he a d va n ta ge s o f c en tr i fu ga l p um p s ar e a s f ol l o w s :

L es s t r a um a t o b l o od co m p o ne n ts t h an t h e r o l l e r p um p. L es s r i s k of i n cr e as i n g a r t e r i al l i ne pr es s ur e b ec au s e b l o od fl ow de c r e as es w h en l i ne r e s i s ta nc e i s i nc r e a s e d. I nf l o w r es p on si v en es s i f a l ar g e qu a nt i t y o f a i r i s i nt r o d uc e d i n t o th e p um p , c o h es i v e f or c es w i l l n o l on g er e x i s t b et w e e n l a y e r s o f bl o od a n d p um pi n g w i l l s t o p.

L es s r i s k of m i cr o - a i r e m bo l i s m be c au se sm al l , l o w - d en s i t y a i r b ub b l e s a r e tr ap p ed i n t he c e n te r of th e v or te x .

V en tr i c u l a r - t y p e p um p s, a l th ou g h po t en t i a l l y m or e p ow e r f ul , a r e r a th er c u m b e r s om e a nd ha v e no t b ee n w el l a c c e pt e d. T hi s t y p e o f p um p i s m a i nl y u s e d f or p ul s a t i l e b y p as s . P.168 T he f i r s t tw o t y p e s of pu m p s a r e no n pu l s a ti l e . P ul s at i l e p um p s ar e c om m e r c i al l y av a i l ab l e no w . M e t ho ds av a i l ab l e t o ge ne r at e p u l s a t i l e f l o w i nc l u d e an i nd w e l l i ng IA BP , a n e xt r a c or po r ea l b al l o o n, ve nt r i c ul a r - ty pe pu m p s , Ke e l e p u m p , P ol y s t an pu l s a ti l e pu m p , m od i fi ed r o l l e r pu m p s , a nd m o di f i e d c e n t r i f u ga l p um ps . S om e s tu d i e s i nd i c a te t h at w i th p r ol on g ed pe r f u si on , p ul s at i l e f l o w a pp e ar s t o be m o r e ph y s i ol og i c an d s u pe r b fo r o r g an fu nc t i o n; ho w e v er , s c i en t i s ts a r e l e s s ce r ta i n th at i t i s a n i m p or ta n t f ac to r d ur i n g s h or t- te r m by p as s . T h e d i f fe r en c e s b et w ee n t he tw o m o d es an d a b e ne fi t f or p u l s a ti l e p er fu s i o n a r e m o s t c l ea r l y m an i f e st ed i n i d en t i f i a b l e h i gh - r i sk p a ti en t g r o u ps . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :3 7 4 7, 82 83 . H or ni c k P, T a y l or K. P u l s at i l e a n d no n pu l sa ti l e pe r fu si o n: t h e c o n ti nu i ng c o nt r o v er s y . J C a r d i o t ho r a c V as c A ne s th 1 9 97 ; 11 : 3 1 0 3 15 .

C.II-10. How do you monitor the patient during cardiopulmonary bypass (CPB)? Clinical Monitoring

M A P s h ou l d be k e pt b e tw e en 5 0 a nd 10 0 m m H g to m a i n ta i n ti s s u e p er fu s i o n . In h y pe r te ns i v e p a ti en t s an d i n o l d e r pa t i e nt s , a h i g he r M AP i s f r e qu e nt l y ut i l i ze d t he r e i s v e r y l i t t l e s u pp or t f or th i s i n t h e l i te r at u r e .

P A pr e s s ur e s ho u l d b e l ow or z e r o t o p r e v en t o ve r d i st en t i o n o f th e L V . C VP s h ou l d be l o w or ze r o to m a ke s u r e t h er e i s no ob st r uc ti o n to v e no u s r e t ur n f r o m t he h e ad ( w he n m on i t o r e d f r o m a s i t e p r o x i m al to t h e RA ) o r t he r e i s a d eq ua t e d r a i n a ge o f b l o o d t o th e C PB ci r c ui t ( w h e n m o n i t or e d fr o m i n s i d e t he R A ) .

P um p- f l o w r a t e sh o ul d b e a de q ua te fo r t i s su e p er f us i o n a nd ox y g e na t i o n. U r i ne o u tp u t sh o ul d b e m a i nt a i n ed ab ov e 1 m L /k g/ h ou r b y a de qu a te pe r f u s i on . ECG. E l e c t r o e nc e ph al o gr a m ( E EG ) i s u se d i n pa t i e nt s i n w ho m c er eb r al c i r c ul at i on p r ob l em s m a y o c c u r . B ot h r ec ta l a nd es op h ag e al t e m p er a tu r e s a r e r e co r de d. A ne s t h es i a s h ou l d b e m a i nt ai n ed a t t he ap p r o pr i at e l ev el . P up i l l ar y s i z e sh o ul d r em ai n n o r m al a n d e qu al . T r a ns c r a ni a l D o p pl er ( T C D ) a nd /o r T EE m a y be us e d to de te c t ao r ti c a nd c e r e br a l em b ol i s m . C er eb r al o x i m et e r to m a i n ta i n ad e qu a te b r ai n o xy ge n s a tu r a t i o n ( > 40 % ) .

Laboratory Monitoring at Least Once Every Hour


A r t er i a l b l o o d g as es ar e k ep t a t no r m a l r an ge . V en ou s P O2 sh o ul d b e 40 to 4 5 m m H g.

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H em at o c r i t m a i n ta i ne d b et w ee n 2 0% a n d 3 0% . E l e c t r o l y t es N a + , K + , i on i ze d C a 2 + . A C T m ea s ur ed ea c h ho u r an d m ai n ta i n e d a bo ve 40 0 t o 4 80 s e c o n ds . B l o od s u ga r p r o b ab l y sh o ul d b e ke p t be l ow 2 5 0 m g pe r d L.

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 5 5 56 9 . M or a- M a n ga n o C T , C ho w J L, Ka ne v sk y M . C a r d i op u l m on a r y b y p a s s a n d t he a n es th e s i o l o gi s t. I n : Ka p l a n J A, R e i c h D SN , La k e C L, e t a l . e d s . Ka pl a n' s c ar di a c an e s t he s i a , 5 th e d . P hi l a d el ph i a: E l se vi e r Sc i en ce , W B Sa u nd e r s , 2 00 6 :8 93 93 5 . Y ao F S , T s e ng C C , T r i f i l e tt i R R , e t a l . N e ur o l o gi c c om p l i ca t i o ns fo l l o w i ng c a r d i ac s u r g er y i s as s oc i a t ed w i th c e r e br a l de s at u r a ti on . A n es th An al g 2 00 0 ;9 0 ( 45 ) : 7 6. P.169

C.II-11. How much BP would you keep during CPB? Why?


C on tr o v e r s y c on t i n ue s o ve r w ha t c on s ti tu t es a d eq u at e p r e ss u r e s w h i l e th e p at i e n t i s on b y pa s s . T he M A P i s us u al l y m a i n ta i ne d a t a pp r o x i m at e l y 5 0 t o 1 00 m m H g t o e n s u r e ad eq u at e t i s su e p e r f us i o n . B P de p en d s on ca r d i ac o u tp ut ( p um p f l o w ) an d t ot a l pe r i p he r al r e s i s t a nc e ( T P R ) . W e b e l i e v e th at ad e qu at e c ar di a c ou t pu t ( pu m p fl ow ) i s m o r e i m p or ta n t fo r t i s su e p e r f us i on t h an B P . D ur i n g h y p o th er m i c c a r d i o p l e gi a , hi g he r s ys te m i c p r e s su r e s ( m e a n bl o od pr es s ur e > 7 0 m m H g ) a r e o f te n a v o i d e d b ec au s e of i n c r e as ed no n c o r o n ar y c ol l a t er al bl oo d f l o w i nt o t he he a r t t hr o ug h t he pe r i c ar di u m an d p ul m on ar y v en o us d r ai n ag e. Su c h c o l l a te r a l f l o w o f r el at i v e l y w a rm b l oo d t en d s to wa sh th e c ol de r c ar d i o pl e gi c s ol ut i on o u t of th e h ea r t an d d ec r ea se s t he hy p ot he r m i c p r o te c t i on a g ai n s t m y o c ar d i a l i s c he m i a . T he r a ng e o f c e r eb r o v as cu l ar a u to r e g ul a ti on du r i n g hy p ot h er m i a i s c o n tr ov e r s i a l . Al th o ug h p o ol ed da t a fr om c l i n i c a l s t u di es i n d i c at e a l o w e r a ut or e gu l a t or y t hr es h ol d o f 20 to 3 0 m m H g i n pa ti e nt s w i t ho u t ce r eb r o v as cu l ar d i s e as e o r p r e e x i s t i n g h y p e r t e ns i o n , ot h er s t ud i e s s ug g es t a p r e s s u r e - de pe n de n t c e r eb r a l c i r c u l a t i o n w he n M AP i s l es s t ha n 5 0 m m H g . U nt i l pr o sp ec t i v e s tu di e s c l e ar l y d e fi n e th e a ut o r e gu l at o r y t hr e s h o l d u n de r v ar i o u s c l i n i c a l c on d i t i o n s , B P o f l es s t ha n 5 0 m m H g s h ou l d be r e ga r d e d a s po t en ti a l ph y si ol o gi c t r e s p a s s , w hi c h m a y c o m pr o m i s e c e r e br a l c i r c u l a t i o n. In p a ti en t s w i t h c e r e b r o v as c u l ar d i s ea s e or hy pe r te ns i on , h i g h er p e r f us i on p r es su r e i s r e co m m e nd e d. F o r pa t i e nt s o v e r 5 0 y ea r s o f a g e, w e r ec o m m en d t o k ee p M AP e q ua l t o th e p a ti en t 's a ge . F or e x am pl e , M A P i s ke p t a t ap p r o xi m a t el y 7 0 m m H g f o r pa t i e nt s 7 0 y ea r s ol d a nd 80 m m H g fo r p at i en t s 80 y e ar s o l d . W e r e c e n tl y s tu d i e d 2 48 p a ti en t s r a n do m i z ed to e i th er l o w M A P ( 50 to 7 0 m m H g) o r h i g h M AP ( 8 0 to 10 0 m m H g ) d u r i ng C P B an d f o u n d a n a c r os s - t he b oa r d i m pr o v e m e n t i n co m b i ne d c ar di a c an d n e ur ol o gi c o ut co m e w i t h hi g he r M AP . H ow ev e r , M AP ha d n o s i g ni f i c an t e ff e c t o n n eu r ol o gi c o ut c o m e , i n t ho s e p at i e n ts a t l ow r i s k f o r ce r eb r a l e m b o l i za t i o n ( no r m a l to m i l d a o r t i c at he r os c l e r o s i s b y T EE ) . P a ti en t s at hi g h r i s k fo r a dv er s e ne u r o l o g i c o u tc o m e ( s e v er e a or ti c a th e r o s c l er os i s by T E E) h a d a s i g ni f i c an t l y l o w e r r i s k of w o r s e n eu r ol og i c ou t c o m e w h e n r a n do m i z ed t o h i g h er M A P. M o r e r e c e nt l y , w i d e ne d p ul s e p r e s s u r e w a s s h o w n t o b e a b e tt er p r ed i c t or o f c er e br al an d r en a l i s c h e m i c o ut c o m es o v er t h at o f s y s t ol i c o r d i a s t o l i c B P. Ot he r r ec e nt d a ta s u gg e s t t h at M AP d u r i ng C P B i s no t a p r i m ar y p r e di c to r o f co g ni ti v e de c l i ne or s t r o k e fo l l o w i ng c a r d i ac s u r g er y . H o w e v er , t he r e w a s a n a s s oc i a t i o n a m o n g hy p ot en s i o n ( < 5 0 m m H g ) a nd ag e , an d d ec l i n e i n sp a ti al an d f i g u r a l m e m or y . T h er e fo r e , w e r e c om m e n d m a i nt e na nc e o f h i g h M AP d u r i ng C P B i n pa t i e n ts w i t h i nc r e a s e d r i s k o f ne u r o l o g i c o u tc om e s uc h a s h i s to r y of ce r e b r o v a s c u l a r a c c i d e nt ( C VA ) o r tr a ns i e n t i s c he m i c a tt a c k ( T I A ) , h y p e r t e ns i o n , c a r ot i d s t en o si s, a dv an c ed ag e, an d s ev e r e a o r t i c a t he r o s cl er o si s d et ec t ed b y T EE . W i t h th e r ec e nt i n tr od u ct i on o f n on i nv as i ve c e r e br a l ox i m e tr y , th e f r o n ta l c o r te x o x y ge n s a tu r a t i o n c an b e m on i to r e d b y n ea r - i n f r a r ed s p ec tr o s c op y . T h e t ec hn i qu e m ea s u r es t h e o xy ge n s at u r a ti o n of th e m i x ed ar te r i a l a nd v e no u s bl o od i n t he br ai n c or t ex . B ec au s e th e v o l u m e of b l oo d i s pr e do m i n an tl y v en o us , i t r e fl e c t s t he b a l a n ce b e tw ee n o xy g en su pp l y an d d e m a nd i n t h e br a i n . O ur s t ud y s ho w e d g o od c o r r el a ti on be tw e en b r ai n o x y ge n s a tu r a t i o ns an d n eu r o l og i c an d c og n i t i v e o ut c om es . T he M A P sh o ul d b e k ep t a t l e v el s e no u gh t o m ai n ta i n ad e qu at e c er e br al ox y g e n s a t ur at i on s ( at l e as t 7 0% o f b a s e l i n e v al ue s o r > 4 0% s a tu r at i o n ) . A r o ns o n S, F o nt e s M L . H yp e r t en s i o n: a ne w l oo k a t a n o l d p r ob l e m . C u rr O p i n An es t he s i o l 2 00 6; 1 9: 59 64 . F on te s M L. N e w i n s i g h ts i n h yp e r t en s i o n. AS A R ef r e s he r C ou r s e A ne s th es i ol 2 0 06 ; 34 :4 3 5 3 . G ol d J P, C h ar l s o n M E , W i l l i a m s - R us s o P, et a l . Im p r o ve m e n t o f ou t c o m e s a ft e r c o r o n ar y a r t e r y b y p a s s : a r an d om i z e d tr i al c o m p ar i ng i n tr ao p er at i v e h i gh v er s u s l ow m e an ar te ri a l pr e s s ur e . J T ho r a c C ar d i o va s c Su r g 19 9 5; 11 0 :1 3 02 1 3 11 . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 5 7 56 1 . P.170 H ar tm a n GS , Y ao F , B r u e fa ch M , e t a l . C a r d i op ul m on a r y b yp a s s a t h i g h p r es s u r e r e d uc es s t r o k e i n c i d en c e i n pa ti e nt s w i t h T E E d i a g no s ed s e v e r e ao r t i c a th er o m a to u s di s ea se . A n es th e si ol o gy 1 9 95 ; 83 :A 1 41 . M ur k i n J M , F a r r ar J K , T w e ed A , e t a l . C e r e br a l au t or eg u l a ti o n a nd f l ow /m e ta bo l i s m c o u pl i ng d u r i ng c a r d i op ul m on a r y b y p a s s : t he i n fl ue n c e of P a C O 2 . A ne s t h A na l g 1 98 7; 66 :8 2 5. N ew m a n M F , K r am er D C , C r o ug h w e l l N D , et al . D i f fe r e n ti a l ag e e ff e c t s o f m e a n ar t er i a l p r e s s u r e an d r ew ar d i n g c og ni t i v e d y s fu n c t i o n a ft e r c a r di ac s u r g e r y . A ne s t h A na l g 1 99 5; 81 :2 3 6 2 42 . Y ao F S F , T s e n g C C , B o yd W C , et a l . C o g ni ti v e dy s fu nc t i o n f ol l o w i n g c ar di a c s u r ge r y i s a s s o c i at e d w i t h c e r eb r a l o x y g en de s a t ur at i on . A ne s t h es i o l og y 1 99 9 ;9 1( 3 A) :A 7 3. Y ao F S F , T s e n g C C , B o yd W C , et a l . F r o nt al l o be dy sf u nc ti o n fo l l o w i n g c a r di ac s u r g e r y i s a s s o c i at e d w i th c e r e b r a l o x y ge n d e s a tu r at i o n . An n T ho r ac S u r g 1 99 9 ;6 8: 1 46 4.

C.II-12. How would you treat hypotension during CPB?


M ea n a r t er i al p r es su r e ( M AP ) = ca r di a c ou t pu t ( C O ) x t ot al pe r i p he r a l r es i s t an c e ( T PR ) H y p ot e ns i o n m ay be c a us e d by l o w ca r di a c ou t pu t o r l o w p er i p h er a l r e s i s ta n c e . F i r s t , c a r di a c ou t pu t s ho ul d b e c or r e c te d b y i n c r e as i ng t h e p um p- f l o w r a t e. T he n, i f t h e c a r di ac ou tp u t i s ad eq u at e , pe r i p he r al r e si st a nc e c an b e r ai s ed b y g i v i ng v a s o p r e s s o r s . W e us e t he p r i m ar i l y - ad r en er g i c v a so pr e s s or p he n y l ep h r i ne i n i n cr em en t s o f 0. 5 m g to r a i s e t he M A P t o 50 m m H g . Ac c or di n g to Po i s e ui l l e 's l a w , l o w T P R u s u a l l y i s du e t o d e c r e a s e d v i s c o s i t y o r i nc r e a s e d v as c u l ar d i am et e r ( v a so di l at i o n ) . D ur i ng C P B us i ng b l oo d - f r e e p r i m i n g s ol ut i on s , to ta l v i s c o s i t y i s r e d uc ed by h e m o di l ut i o n a l th ou g h pl a s m a v i s c o s i t y i s i n c r e as ed by h y po th e r m i a . A s h or t p er i o d o f h yp o te ns i on w i th a M A P o f ap p r o x i m a t el y 3 0 t o 40 m m H g i s us u al l y s e en i n t h e fi r s t 5 to 1 0 m i n ut e s of by pa s s . I t i s du e t o t he fo l l o w i ng ca us e s:

I na de q ua t e pu m p fl o w at th e b eg i n n i n g o f b yp as s H y p ox i c v a s o d i l a ti on fr om i n i t i a l p er f us i o n w i t h b l o o d- fr e e pr i m e s c ar r y i n g n o o x y g en

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V as od i l a ti o n fr o m va s oa ct i ve m a te r i al s r el e as ed be c au se of t h e i n i ti al r e ac t i o n o f th e s er u m pr o te i n s , bl o od c e l l s , an d p l a te l e t s w i t h t he f o r e i g n s ur fa c es o f t he he ar t - l un g m ac h i n e

D ec r e a s e d p l a sm a l ev e l s o f c at e ch ol a m i ne s b y h em od i l u ti o n I nf us i on o f c ar d i o pl e gi c s ol ut i on , w hi ch co nt a i n s n i t r o g l y c e r i n

B al as a r a s w a th i K , Gl i ss on SN , El - Et r A A, e t a l . Ef fe c t of p r i m i n g v ol u m e o n s er u m c a t ec ho l am i n e d u r i ng c a r d i o p ul m on ar y b y p a s s . C an A n ae s t h S o c J 1 98 0 ;2 7: 1 35 1 3 9. M or a- M a n ga n o C T , C ho w J L, Ka ne v sk y M . C a r d i op u l m on a r y b y p a s s a n d t he a n es th e s i o l o gi s t. I n : Ka p l a n J A, R e i c h D SN , La k e C L, e t a l . e d s . Ka pl a n' s c ar di a c an e s t he s i a , 5 th e d . P hi l a d el ph i a: E l se vi e r Sc i en ce , W B Sa u nd e r s , 2 00 6 :8 95 89 7 .

C.II-13. How would you treat hypertension (a MAP of over 100 mm Hg)?
H y p er t en s i o n du r i n g b yp a ss i s u su al l y th e r es u l t o f i na d eq u at e d ep t h of an es t he s i a , w h i c h c a us es i n c r e as ed c a te c ho l am i n e o ut p ut a n d i n c r e a s e d v as cu l ar r es i s ta n c e . P um p - f l o w r at e s ho u l d n o t be r e du c ed t o l o w e r th e p r e s s u r e . L o w pu m p fl o w m a y c au s e ti s s u e hy p ox i a al th o ug h B P i s h i g h. T h e mo s t ef f ec ti v e t r e at m en t i nv ol v es a d m i ni s te r i ng an i n ha l at i o n a g en t s uc h a s i s o fl ur a ne t h r o ug h t h e v a p or i z e r i n t h e h ea r t l u ng m a c h i ne . I nt r a v en o us a g en ts , s uc h a s s od i u m t hi o pe nt a l , d i az e pa m , m i da zo l am , a nd l a r g e d os e s of na r c o ti c s m a y b e us e d, b u t th e y ar e f r e q ue n t l y n ot e f fe c t i v e a n d P.171 h av e t o be s u p pl em e nt ed w i th va so d i l at o r dr u gs . O ne m a y us e n i t r op r u s s i de , n i t r og l y c er i n , o r n i c ar di p i n e .

C.II-14. How do you prepare an intravenous infusion of sodium nitroprusside, nicardipine, and nitroglycerin? What are the usual doses? Which do you prefer to use?
I nt r a v en ou s s ol u ti on s m ay be p r ep a r e d b y ad d i n g t o 2 50 m L o f 5 % de x tr os e i n w at er 50 m g o f n i t r o g l y c e r i n o r s od i u m n i t r op r u s s i d e , o r 2 5m g o f ni c ar di p i n e, t o m a k e a c on c e n tr at i on o f 2 0 0 g p e r m L ( n i t r o g l y ce r i n o r n i t r op r u s s i de ) o r 1 00 g p er m L n i c a r d i p i ne . T he u s ua l d os e s ar e n i t r og l y c er i n o r n i t r op r u s si de 0 .5 t o 1 0 g/ k g / m i nu te , o r 0 .0 5 g/ kg / m i nu t e ni c ar di p i n e, de te r m i ne d b y c ar ef u l ti t r a ti o n ( T a bl e 7 .2 ) . W e p r e f er n i tr og l y c er i n or ni c a r di pi n e i n f us i o n . So d i u m n i t r o p r u s s i de d i l a te s b ot h a r t e r i al an d v en o us s m o o th m u sc l e . I t i s v e r y ef fe c ti v e i n r e du c i n g b ot h p r e l o a d an d a f t e r l o ad . I t m a y c au s e c y a ni de an d t hi oc y an at e t ox i c i ty . B ec a us e n i t r o p r u ss i de d i l a te s t he i n tr a m y oc a r d i a l a r t e r i ol e s , i nt r ac or o na r y s t ea l m ay oc c u r . T h e s ol u ti on ha s t o be co ve r ed w i t h a l u m i n um f o i l t o p r e ve n t d ec om p os i t i on f r om e x po su r e to l i gh t . N i tr o gl y c e r i n p r i m a r i l y c a u s e s v en o di l a t i o n, r e s u l ti ng i n r e du c t i on o f p r e l oa d a nd m y oc a r d i a l o x y ge n c on s um pt i on . A t l a r ge r d os e s an d b y t he i n tr av e no u s r o ut e , i t ha s m i l d a r t er i o l ar d i l a t i o n a nd r e du c e s a ft e r l oa d . It ha s n o k n o w n t o x i c i t y an d d o es n ot p r od uc e i n tr ac or o na r y st ea l b e ca us e i t d i l at e s ep i ca r d i al a r te r i es . I t m ay r e di s t r i b ut e b l o o d fl o w t o th e s ub en d oc a r d i u m a n d i n c r e as e c ol l a t er al c i r c u l a t i o n t hr o ug h t he m y oc ar d i u m . N i ca r d i pi ne i s a sy st e m i c a nd c o r o na r y ar t er i a l d i l a to r . T h e a f t er l o a d i s de c r e as e d, w h i l e t he p r el oa d i s n ot a f fe c t e d. I t m ay c a us e a s l i g ht i n cr ea s e i n H R ( r e f l e x t ac hy c ar di a ) . G er s o n J I, Al l e n F B, S e l t ze r J L, et a l . Ar t er i a l a nd ve no u s di l at i o n b y n i t r o p r u s s i de a n d n i t r o g l y c e r i n : i s th er e a d i ff er e nc e? An e s t h A na l g 19 8 2; 61 : 25 6 2 60 . L aw s o n N W , J o hn s on J O . Au t on om i c ne r vo us sy st e m : p h ys i o l og y a nd p h ar m a c ol og y . In : B a r a s h P G , C u l l e n B F , S t oe l t i ng R K , ed s . C l i ni c a l a ne s th es i a , 5 t h e d. P h i l ad e l p h i a : L i p pi n co tt W i l l i a m s & W i l ki ns , 2 00 6 :3 2 7 33 0 .

C.II-15. How much pump flow would you maintain during CPB?
T he p u m p b l oo d f l o w i s eq u i v al e nt to c a r d i a c o ut p ut a n d to su p pl y ti s s u e o x y ge n at i on . T he n o r m al av er a ge c a r d i a c o ut p ut f o r ad u l t s i s 70 m L /k g /m i n u te o r 3 .1 L / m i nu t e/ m 2 . Be c au s e of hi gh e r m e t ab ol i sm , p ed i a t r i c p at i e n ts n e ed h i gh e r fl ow r a te s f or ea c h un i t of b o dy w e i g h t. U s u a l l y 7 0% of n o r m al c a r d i a c o ut pu t i s e no u gh t o m ai n ta i n ti ss u e ox y ge na t i o n . W h en bo d y su r fa c e i s u s ed , b ot h p ed i a t r i c a nd a d ul t p at i en ts r e qu i r e a b ou t t he s a m e pu m p fl ow , 2 .2 to 3 . 1 L /m i n u te /m 2 . I n s um m ar y, a t n o r m ot he r m i a a nd n o r m al he m o g l o b i n l e v e l s , t he pu m p fl ow i s a s f ol l o w s :

Adults 50 to 70 mL/kg/min Children 100 to 150 mL/kg/min

or or

2.2 to 3.1 L/min/m2 2.2 to 3.1 L/min/m2

H ow ev e r , s o m e p e r f us i o n t e am s u se l o w fl o w ( 4 0 m L/ kg / m i nu t e) , l ow p r es s u r e ( a p pr ox i m a te l y 40 m m H g) by pa s s qu i te s u c c es s f u l l y . T h i s te c h n i q u e ha s t he a dv an t ag e s of l e s s b l ee d i n g t hr ou g h i n t r a ca r di a c co l l a te r a l s, l e s s t r a u m a to b l oo d c el l s an d p l a te l et s , an d l ow e r f l ui d r eq u i r e m e nt s , bu t i t al s o ha s t he p ot en t i a l f or i n ad e qu at e p er f us i o n . C l i ni ca l l y , l o w - f l o w a nd l o w - p r e s s u r e t e c h ni q ue s a r e u s ed i n c o nj un c ti on w i th hy po t he r m i a a n d h e m o di l ut i o n . T h e r e fo r e, p um p b l o od fl ow s h o ul d b e ad j us te d a cc o r d i n g l y t o m at c h th e o x y g en s u pp l y w i t h de m an d. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 6 0. P.172

Table 7.2 Cardiac Anesthesia Intravenous Medicationsa. DRUG Amicar (EACA) AMOUNT TO ADD 15 g TOTAL VOLUME WITH D5 W 150 mL CONCENTRATION DOSAGE RANGE 1 mL = 100 mg 10 mL = 1 g 1 mL = 1.8 mg Load: 10 g over 1/2 hr Maintenance: 1 g/hr x 5 hr Initial: 150 mg over 10 min Followed by: 1 mg/min x 6 hr (360 mg). Then: 0.5 mg/min x 18 hr

Amiodarone

450 mg

250 mL

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Amrinone

500 mg

500 mL

1 gt = 17 g 1 mL = 1 mg 1 mL = 10,000 kIU

Load: 0.75 mg/kg over 10 min Maintenance: 220 g/kg/min Test: 1 mL Load: 200 mL or 2,000,000 kIU Maintenance: 50 mL/hr or 500,000 kIU/hr Load: 1.0 g/kg over 10 min Maintenance: 0.20.7 g/kg/hr Load: 0.10.15 mg/kg Maintenance: 0.50.25 g/kg/min 520 g/kg/min

Aprotinin (regimen A, full dose)

2,000,000 kIU

200 mL (premixed)

Dexamedetomadine

1 mL = 4 g

Diltiazem

25 mg

100 mL

1 mL = 0.25 mg

Dobutamine

500 mg

250 mL

1 gt = 33.3 g 1 mL = 2 mg 1 gt = 26.6 g 1 mL = 1.6 mg

Dopamine

400 mg

250 mL (premixed)

Renal: 15 g/kg/min : 10 g/kg/min : 1015 g/kg/min 28 g/min 50300 g/kg/min

Epinephrine Esmolol

2 mg 5g

250 mL 250 mL

8 gtt = 1 g 1 gt = 333 g 1 mL = 20 mg 2 gtt = 1 g 15 gtt = 1 mg 1 mL = 4 mg 1 mL = 7.5 g 3 gtt = 1 g 1 mL = 200 g 1 gt = 1.66 g

Levophed Lidocaine

8 mg 2g

250 mL 500 mL (premixed) 250 mL 100 mL

432 g/min 14 mg/min

Metaraminol Milrinone

200 mg 20 mg

50400 g/min 0.3751 g/kg/min

Nicardipine

25 mg

250 mL

Loading dose: 5 mg/hr Maintenance: Increase by 2.5 mg/hr every 15 min Maximum amount: 15 mg/hr 110 g/kg/min

Nitroprusside

50 mg

250 mL (premixed) 250 mL (premixed) 250 mL 500 mL (premixed) 100 mL undiluted 100 mL

1 gt = 3.33 g

Nitroglycerin

50 mg

1 gt = 3.33 g

1080 g/min

Phenylephrine Procainamide

20 mg 2g

19 gtt = 25 g 15 gtt = 1 mg 1 mL = 4 mg 1 mL = 1 mEq 1 mL = 1 unit

25125 g/min Loading dose: 5001,000 mg (20 mg/min) Dosage: 14 mg/min 13 mEq/kg/hr (titrate to pH) Initial dose: 0.04 U/min, 2.4 U/hr Titrate: 0.0050.01 U/min (0.30.6 mL/hr) every 10 min to max of 0.1 U/min or 6 U/hr

Sodium bicarbonate Vasopressin

100 mEq 100 units

aThere are 60 guttae per milliliter (gtt/mL); therefore, gtt/min = mL/hr. EACA: aminocaproic acid.

P.173 K ol k k a R , H i l be r m a n M . N e ur o l o gi c al d y sf un c ti on fo l l o w i ng ca r d i ac o p er a ti on w i th l o w fl o w , l o w pr e s s ur e c ar d i o pu l m o na r y by p as s . J T h o r a c C a r di o v a s c S u r g 1 98 0 ;7 9: 4 32 4 3 7. M or a- M a n ga n o C T , C ho w J L, Ka ne v sk y M . C a r d i op u l m on a r y b y p a s s a n d t he a n es th e s i o l o gi s t. I n : Ka p l a n J A, R e i c h D SN , La k e C L, e t a l . e d s . Ka pl a n' s

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c ar di a c an e s t he s i a , 5 th e d . P hi l a d el ph i a: E l se vi e r Sc i en ce , W B Sa u nd e r s , 2 00 6 :8 98 .

C.II-16. How would you adjust the pump flow during hypothermia?
H y p ot h er m i a d ec r ea se s o xy g en c o ns u m p ti o n. T h er ef o r e , th e p u m p f l ow m a y be de c r e as ed pr op o r t i o n al l y i f t h e bl o od ox y g e n c o n te nt do e s no t c ha n ge . T he o x y ge n c on s um pt i on at d i ff er e nt b o dy t e m p er a tu r e s i s l i s te d i n th e f o l l ow i n g t e x t .

Temperature (C) O2 Consumption (%)

37 100

32 60

30 50

28 40

25 2530

20 20

10 10

B ec au s e th e O 2 c o n su m p t i o n a t 30 C ( 8 6 F ) i s ha l f of t h at a t 3 7 C ( 98 . 6 F ) , t he r e qu i r e d p um p f l o w a t 30 C ( 8 6 F ) i s 50 % o f t h e f l ow a t 3 7 C ( 98 . 6 F ) ( 5 0 t o 70 m L /k g /m i n u te ) . T h er e fo r e , a p u m p f l ow o f 2 5 t o 35 m L /k g /m i n u te i s a de q ua t e fo r a du l ts a t 3 0 C ( 86 F ) , i f th er e i s n o he m o d i l u ti on . D ur i ng p r of ou n d h y p ot h er m i a ( 10 C to 20 C [5 0 F t o 6 8 F ] ) t he p a ti e nt s u su al l y c a n t ol e r a te to ta l c i r c u l at o r y a r r e s t w i t h ou t p um p s up p or t f or a p pr ox i m a te l y 60 t o 9 0 m i n u te s. T he d e c r ea s e i n m e ta b ol i s m d ur i ng h y po th e r m i a i s n o t a l i n ea r p r o c es s . F r om 3 7 C t o 3 0 C ( 98 . 6 F t o 86 F ) , t he m e ta bo l i s m d ec r e a s e s a pp r o x i m at e l y 7 % b y ea c h de g r e e c en t i g r a d e. B e l o w 3 0 C ( 86 F ) t he r a te of m e ta bo l i s m de c r e a s e s l o w s do w n. U s ua l l y e v e r y 7 C t o 8 C ( 4 4. 4 F t o 4 6 . 4 F ) de c r e as e i n t em pe r at ur e r ed u c e s o xy ge n c o ns um p ti on by 5 0 %. C l i n i c a l l y, i t h as be e n de m on s t r at ed th at pu m p f l ow s a s l ow a s 3 0 m L/ k g / m i nu t e o r 1. 2 L /m i n u t e /m 2 w i l l n ot c o m p r o m i s e w h o l e - bo dy ox yg e n de l i v er y w he n m od e r a te sy s t e m i c h y p ot h er m i a i s e m p l o y ed .

C.II-17. How would you adjust the pump flow during hemodilution?

Oxygen delivery Arterial oxygen content

= =

cardiac output x arterial oxygen content 1.34 x Hb x O2 saturation + (0.003 x PaO2)

H em od i l u ti o n r e d uc es he m o g l o b i n c o nc en t r a ti o n an d h e nc e d ec r e a s e s o x y ge n c o nt en t . In or de r t o d el i v e r th e s am e a m o u nt o f o x y g en , t he pu m p f l ow ha s t o b e i n c r e as e d ac c or di n gl y d ur i n g h e m o di l ut i o n . F o r e xa m p l e, i f t he he m at oc r i t i s d i l ut e d fr o m 40 % t o 2 0% d u r i ng C P B, th e p um p f l o w h as to b e d ou b l e d ( i n c r ea s ed by a fa ct o r of 40 /2 0 = 2 ) . C l i n i c al l y, b o th h y po t he r m i a an d h em o di l u t i o n a r e a p pl i e d s i m u l t an e ou s l y , s o th a t th e a dj u s t m e n t ha s t o b e d on e a t th e s am e t i m e. F o r ex a m p l e , t he pu m p fl ow fo r a du l t s a t a t em p er at u r e o f 3 0 C ( 86 F ) a n d a h em at o c r i t of 2 5 % w i l l be as f o l l ow s : 5 0 to 70 m L /k g/ m i n x 50 % x 4 0/ 2 5 = 40 t o 5 6 m L/ kg / m i n

C.II-18. What are the advantages of hypothermia? Does hypothermia offer neuroprotection?
H y p ot h er m i a d ec r ea se s o xy g en c o ns u m p ti o n an d h el p s to pr es e r v e t he f u nc ti o n o f ti s s u es d u r i n g a h y p ox i c or i s c h e m i c i n s ul t. Pu m p f l ow m a y b e de c r e as e d d ur i n g C PB w i th hy po t he r m i a. H y p ot h er m i a h as be en sh o w n t o c on f er s i g n i f i ca nt pr ot e ct i o n i n t he s e tt i n g o f t r a ns i en t, bu t n ot p e r m an e nt , i s c he m i a . T he m e c h a n i s m i s u nc l ea r . T h e r ed uc t i o n i n c e r eb r a l m et a bo l i c P.174 r at e i s be l i e v e d t o b e l e s s i m p or ta n t w h e n co m pa r e d w i t h t he ef fe c t of hy po t he r m i a o n th e r el e as e o f ex c i t at o r y n e ur ot r an s m i tt e r s , c a te c ho l a m i n es , o r o th e r m ed i a t or s o f c e l l u l a r i nj ur y . It i s f o r th i s r e as o n th a t m i l d hy p ot h er m i a ( 33 C to 3 5 C [ 9 1. 4 F t o 9 5 F ] ) p r o v i d es s i gn i f i c a nt ne u r o pr o t e c t i on . T he e f fe c t of h y po th e r m i a du r i n g C P B o n p os t op er a ti ve co gn i ti v e or n e ur ol o gi c f un c t i on r e m a i n s c on t r o v e r s i al . A ni m a l m od e l s s h o w p r of o un d r ed uc t i o n i n i nf ar c t s i z e an d r el e as e o f ex c i t at o r y a m i n o a ci d w i t h m i n i m al l e v e l s of hy po t he r m i a. H o w e v e r , c l i n i c a l s tu di e s c o m pa r i n g no r m o th e r m i c an d m od er a te l y h y p ot h er m i c C PB ha ve yi el d ed c o nf l i c ti ng r e su l ts a n d di d n o t pr o du c e ev i d e nc e o f p r o te c t i on fr om c o gn i t i v e d e c l i n e . T h i s m a y r e l a te t o d i f f er en c es i n d ef i n i ng n o r m ot h er m i a . M a n y gr o up s a l l ow te m p e r a tu r e to dr i f t d ow n w a r d s d ur i ng n o r m ot h er m i c C PB , w i t h t em pe r at ur e d e c r ea s i n g t o be l ow 3 4 C ( 9 3. 2 F ) . M c l ea n i n a r ec e nt s t ud y o f th i s ty p e sh o w e d n o d i f fe r e n ce i n c o gn i t i v e o r n eu r ol og i c ou t c o m e be t w e en w a r m a n d m o d er a te l y h y po t he rm i c gr ou p s . In a c t ua l i t y , th i s i s a s t ud y o f m i l d ve r su s m o d er a te h y po th e r m i a c o nf i r m i n g t he ex pe r i m en t al a n i m al da ta t h at as l i tt l e as 2 C t o 3 C ( 3 . 6 F t o 5. 4 F ) o f h y p ot h er m i a m ar k ed l y r e du c es e x ci ta t or y a m i no a c i d r e l e a se a n d ne u r o l o g i c i n j u r y c o m p a r e d t o no r m o th e r m i a . T he s i ng l e l a r ge s t u d y c om pa r i n g t r u e n or m o t he r m i a w i th hy p ot he r m i a d ur i n g C PB sh ow e d a s i g ni f i c an t l y g r ea te r i nc i de nc e o f f oc al ne u r o l o g i c i n j u r y i n t he w a r m gr ou p , s u p po r t i ng t h e b en ef i ci al r ol e o f hy p ot he r m i a i n ne u r o pr o te ct i on . I n a dd i t i on , r ec en t d at a s ho w ed th at m i ni m u m C PB te m p e r a tu r es g r ea te r t ha n 3 5 C ( 95 F ) i n c r ea s e d t h e i n c i d en c e o f pe r i o pe r at i v e s tr o ke a p pr ox i m a te l y fo u r f ol d ( 4. 5 % vs . 1 .2 % ) . I n th i s c o n te x t , t he av oi d an ce of c e r e b r a l h yp er th e r m i a de s er ve s c om m e n t. H y pe r t h er m i a a s l i t tl e a s a 2 C ( 3 . 6 F ) i nc r e a s e i n t e m p er a t u r e s i gn i f i c a n tl y w or s e n s ne u r o l o g i c al ou tc o m e s. It h a s be e n d em on s tr at e d i n a r a t m od e l , t h at f o l l ow i ng 1 0 m i n u te s o f i s c he m i a d ur i ng w h i c h t em p e r at ur e w as i n c r e as ed f r o m 3 5 C to 39 C ( 9 5 F t o 1 02 .2 F ) , t he p e r c en t ag e o f d am ag e d n eu r o n s i n c r e as e d fr o m 15 % t o 8 0% . T hi s i s c l i n i c a l l y r el e v a nt b e c a u s e c e r e b r a l t em pe r at ur e s ab o v e 3 9 C ( 1 02 .2 F ) h a ve b e en do cu m en te d i n p at i en ts du r i n g r e w ar m i n g, a pe r i o d w h e n c e r eb r a l e m b o l i c r i s k i s gr e a t es t. T h er e fo r e , h y p er t he r m i a s h o ul d b e ca r ef ul l y m o n i t or e d an d a v oi de d . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 1 7 41 8 . M c l ea n R F , W o ng B I . N o r m o th e r m i c v e r s us hy po t he r m i c ca r di op u l m on a r y b y pa s s : c en t r a l n er v o u s s y s te m o ut c o m es . J C ar di o t h o r a c V as c A ne s t h

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1 99 6 ;1 0: 4 5 53 . M or a- M a n ga n o C T , C ho w J L, Ka ne v sk y M . C a r d i op u l m on a r y b y p a s s a n d t he a n es th e s i o l o gi s t. I n : Ka p l a n J A, R e i c h D SN , La k e C L, e t a l . e d s . Ka pl a n' s c ar di a c an e s t he s i a , 5 th e d . P hi l a d el ph i a: E l se vi e r Sc i en ce , W B Sa u nd e r s , 2 00 6 :8 99 89 0 . Y ao F S F , B a r b ut D , L e on F J , et al . C e r eb r a l h yp e r t h er m i a d ur i n g c a r d i o p ul m o n ar y b y p as s r ew a r m i n g i n p at i e n ts u n de r g o i n g c ar di a c s u r ge r y . A ne s th e si ol o gy 1 99 8 ;8 9( 3 A) :A 2 38 .

C.II-19. How does blood viscosity change during hypothermia and hemodilution?
B l o od v i s c o s i ty v a r i es i n ve r se l y w i th te m p e r a tu r e; a 2% i n cr ea s e oc c ur s fo r e v e r y 1 C ( 1. 8 F ) de c r e a s e i n t em p er at u r e . A t a h em at o c r i t o f 4 0 %, a de c r e as e i n te m pe r a t ur e f r o m 3 7 C to 27 C ( 9 8 .6 F t o 8 0 .6 F ) i nc r e a se s v i s c o s i t y by ap p r o x i m a t el y 2 5% . H em od i l u t i o n w i t h ba l an c ed s a l t s o l u ti o n w i l l de c r e as e b l o o d v i s c o s i t y . D e c r ea s i n g t he h e m a t oc r i t f r o m 4 0% t o 2 0% at 2 7 C ( 8 0. 6 F ) de c r e as e s v i s c o s i ty by a p pr o x i m a te l y 40 % . It ha s b ee n r ec o m m en d ed t h at t h e h em at o c r i t be a d j u st e d to th e s am e n um e r i ca l v al ue as t h e co r e b od y t em pe r at ur e i nC i f b l oo d v i s c o s i t y i s to b e k ep t a p pr ox i m a t e l y c o ns t an t . F o r e x a m p l e, n or m a l v i s c o s i t y a t 37 C ( 9 8 .6 F ) w i t h h em at o cr i t of 4 0 % ap p r o x i m at es th a t s e e n at 25 C ( 7 7 F ) w i th he m a t oc r i t o f 2 5% . P.175 G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 6 1.

C.II-20. What are the main causes of death associated with accidental hypothermia?
V en tr i c u l a r f i b r i l l a ti o n an d a s ys to l e ar e t he m a j o r r hy th m d i s t ur ba n c e s l ea d i n g t o c a r di ac ar r e s t du r i n g h y p ot h er m i a . In h u m a n s ex t er na l l y c o ol ed f o r c ar di a c s ur ge r y , v e nt r i c u l ar f i br i l l a t i o n g en e r a l l y o cc u r s a t 2 3 C ( 73 F ) a nd as y s t ol e a t 2 0 C ( 6 8 F ) . H o w e v er , a s y s t ol e a n d v e n tr i c u l a r fi b r i l l a ti on ha ve be e n r ep or t ed a t 2 1 C t o 2 8 C ( 69 .8 F to 82 .4 F ) . R e s pi r a t or y a r r es t u s u a l l y a c c om p an i e s c ar d i a c a r r es t d ur i n g a c c i de n ta l h y p ot h er m i a . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :7 1 7. S ou th w i c k F S, D a l g l i sh PH . R ec ov e r y a f te r p r o l o n ge d a sy st o l i c c ar di a c ar r es t i n pr o fo un d h y p o th e r m i a . J AM A 1 98 0; 2 43 : 12 50 12 5 3.

C.II-21. Would you give anesthesia during cardiopulmonary bypass (CPB)? Why?
Y es . A ne s t h es i a i s m a i n ta i ne d w i t h i nt er m i t te n t ad m i n i s tr a ti on of i n tr av e no u s ba r bi tu r at es or b e nz od i az e pi ne s a nd na r c o ti c o r i n h al at i on a g en t s th r ou gh th e p um p o x y ge n at o r to a c hi e ve u n co ns c i o us n es s a nd an al g es i a , t o c on tr o l BP , a nd to pr ev e nt s h i v er i n g . I n t r a v e n ou s a ge n t s a r e d i l ut e d by th e p r i m i ng s o l u t i o n d ur i n g C PB . M ea n w h i l e , hy p ot he r m i a i ts el f p r o d uc es an e st he s i a a n d pr o l o ng s t he ac t i o n d ur at i on o f i nt r av en o us a g en t s by de c r e as i n g h ep a t i c m et ab o l i sm a nd u r i n ar y e x c r et i o n . Ba r bi tu r at es m a y b e of pa r t i cu l a r b en e fi t f or t e m p or a r y f oc a l l e s i o ns ( g as em bo l i fr o m by p as s p um p o r op e n c h a m b e r ) i f m et ab o l i c s up pr e s s i o n i s n ot b e i n g a ch i ev ed by h y po th e r m i a . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :1 8 9, 2 9 2. N us s m e i e r N A , A r l u nd C , S l o g of f S . N e u r o ps y ch i a t r i c c om pl i c a ti on s a f te r c a r di op u l m on a r y b y pa s s : c e r e br a l pr ot e c t i o n b y a b a r b i t u r a t e . A ne s th es i ol og y 1 98 6 ;6 4: 1 65 1 7 0. N us s m e i e r N A , F i s h K J. N e ur o ps yc h ol og i ca l d ys fu n ct i o n a ft e r c a r di op u l m on a r y b y pa s s : a c o m p ar i s o n o f tw o i ns t i t ut i on s . J Ca rd i ot h or ac Va sc An es t h 1 99 1 ;5 :5 8 4 58 8 . Z ai de n J R , Kl oc h an y A , M a r ti n W M , e t a l . E f fe ct o f t h i o pe n ta l o n ne u r o l og i c ou tc o m e f o l l ow i ng c o r o na r y ar t er y b y p as s g r a f ti ng . A ne s th es i ol og y 1 99 1 ;7 4: 4 06 4 1 1.

C.II-22. Would you give muscle relaxants during CPB? How is the action of muscle relaxant affected during CPB?
Y es . M us c l e r el ax a nt s a r e g i ve n t o p r e ve n t di a ph r a g m a ti c m ov e m e nt th at i n te r fe r e s w i t h s ur g er y a nd t o p r e v en t s hi v e r i n g d ur i n g h y p o th e r m i a . S hi v e r i n g m ay i n c r ea s e ox y ge n c on su m pt i o n t o a s h i g h a s 48 6 % of no r m a l . T h e ef f ec t o f a m us c l e r el a x a nt i s a l t e r e d b y b ot h h y p ot h er m i a a n d he m od i l u ti on . T he p l a s m a c on c en tr a ti on of m u sc l e r e l a x an ts i s d i l u te d b y t he p r i m i n g s ol u ti on . T he r ef or e , m o r e r e l a x an t i s r e q ui r e d t o m ai nt a i n t h e s am e d eg r e e o f r el ax a ti on . H y p ot h er m i a w as or i g i n a l l y r ep o r t ed to d e cr ea s e th e e ff e ct o f n on d ep o l a r i z i n g r el ax a nt s , be c a u s e d e c r e as ed P.176 c ho l i n es te r as e e nz ym e a ct i vi ty d u r i n g hy p ot he r m i a r es ul t ed i n m or e a c e t y l c h o l i ne ac c u m ul at i on t o c om p et e w i t h t he n o nd e po l a r i z i n g r el a x a nt . C on t r a r y to t he e a r l i e r r ep o r t s , i t i s n ow e s ta bl i sh ed th a t l e ss d - tu b oc u r a r i ne , a t r a c u r i u m , v e c u r o n i u m , or p a nc ur o ni um i s n e ed e d to m a i n t ai n m us c l e r el ax a t i on du r i n g h y p ot h er m i a b ec a us e h yp o th er m i a r e du ce s r en a l an d b i l i ar y e x c r e t i o ns of b o th d - tu bo c ur ar i ne a n d p an c u r on i u m . H a m e t a l . r e po r t e d th a t hy p ot h er m i a i n m an d o es n o t a ff ec t d - t ub o cu r ar i n e p ha r m a co k i n et i cs o r t he s e ns i ti v i ty of t h e ne u r o m u s c u l a r j un c ti on to d - tu bo c ur a r i ne . H y p o th er m i a d o es p r ol on g t he on se t o f pa r al y s i s . M or e ov e r , h yp o th e r m i c C P B pe r s e f ac i l i ta te s n eu r om us c ul ar tr an s m i s s i o n a t t he e l ec tr o c h em i c a l l ev el , y et c o m p r o m i s es m e c h a ni c a l c on tr a c t i l i t y . M od i f i c a ti o ns o f p ar t i a l n eu r o m us cu l ar b l oc ka d e by hy po t he r m i c by p as s a r e t h e r e s ul t o f m u s c l e r e l ax a ti on en ha n c i n g or i n te r f e r i ng w i t h t h e i m p ac t o f h y p ot h er m i a o n n or m a l n eu r om us c ul ar tr an s m i ss i o n . T h e b e st w a y to m o ni to r m us c l e r e l a x a t i o n i s by us i n g a p e r i ph e r a l n er v e s t i m u l a to r . B uz el l o W , P o l l m a e ch e r T , S c hl ue r m a nn D , e t a l . T h e i nf l u e nc e o f h y p ot h er m i a c ar d i o pu l m o na r y by p as s o n ne u r o m u s c u l a r t r a n s m i s s i o n i n th e a bs e nc e o f m us c l e r el a x a nt s . An e st he s i o l o g y 19 8 6; 4 :2 79 28 1 . B uz el l o W , S c hl u er m a n n D , S c hi n dl er M , e t a l . H y pe r t h er m i c c ar di o pu l m o na r y by p as s a nd n e ur om u s c ul a r bl o c k ad e b y p an c ur on i um a n d v e c ur on i um . A ne s t h es i o l og y 1 98 5 ;6 2: 20 1 2 04 . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :2 7 9 29 3 . G r o ga n K , N y h an D , B e r k ow i tz D E. Ph a r m ac ol o gy o f a n es th e ti c d r u gs . I n: Ka pl a n J A , R ei c h D S N , La k e C L , e t a l . e d s . K a pl an ' s c ar di a c an e s t he s ia , 5 th ed . P hi l a d el ph i a: E l s e vi e r Sc i en ce , W B S au nd e r s , 2 00 6 :2 02 .

C.II-23. How do you know the patient is well perfused during CPB?
I f th e p er f us i o n p r e s su r e i s m a i n ta i ne d b et w e e n 5 0 m m H g a n d 10 0 m m H g , a n d th e p um p - f l o w r at e i s a de qu a te l y m a i n t ai ne d a c c o r d i ng t o t he de g r e e o f h y p ot h er m i a a nd he m od i l u ti on , t he r e sh o ul d b e a de qu a te ur i n e o ut p ut , g r e at e r th a n 1 m L/ k g / ho u r , n o m et a bo l i c a c i d os i s , a nd no r m a l m i x e d v e no us ox yg e n t en s i o n of 40 t o 4 5 m m H g . H ow e ve r , ce r e b r a l p er fu s i o n i s no t r ou t i n el y m on i to r e d a nd th e a ut o r e gu l at i o n r an g e o f BP m a y b e hi g he r t ha n t he n o r m al r a ng e i n th e e l d e r an d h i gh - r i s k p at i en ts . C er e br al ox i m e tr y sh o ul d b e u s e d f or p a ti en t s w i t h i n c r e as e d r i s k fo r n eu r ol og i c an d c og n i t i v e o u tc om e s . I t i s r ec om m e n de d t o k ee p c er eb r al o x yg e n sa t ur at i on o v er 4 0 %. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 5 9 56 0 . M or a- M a n ga n o C T , C ho w J L, Ka ne v sk y M . C a r d i op u l m on a r y b y p a s s a n d t he a n es th e s i o l o gi s t. I n : Ka p l a n J A, R e i c h D SN , La k e C L, e t a l . e d s . Ka pl a n' s c ar di a c an e s t he s i a , 5 th e d . P hi l a d el ph i a: E l se vi e r Sc i en ce , W B Sa u nd e r s , 2 00 6 :8 95 89 8 . Y ao F S F , T s e n g C C , B o yd W C , et a l . N e u r o l o g i c al co m p l i c at i on s f ol l o w i n g c ar di a c s u r g e r y i s a s s o c i at e d w i t h c e r eb r a l o x y g en d e s a t ur at i on . A ne s t h A na l g

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2 00 0 ;9 0: 7 6. Y ao F S , T s e ng C A , H o C A , e t al . C er eb r al o x yg e n de s at ur a ti on i s a s s o c i a te d w i t h e ar l y po s t o pe r a t i v e n eu r o p s y c h o l o g i c al dy s f u nc t i o n i n pa t i e nt s u nd e r g oi n g c ar di a c su r ge r y . C ar di o th o r a c Va s c An e st h 2 00 4 ;1 8 :5 52 55 8 . P.177

C.II-24. How much gas flow would you use for the oxygenator? What kind of gas would you use? Why?
N or m a l a l v eo l ar v e nt i l a ti on i s 4 L p er m i n u te a n d p ul m o n ar y c i r c u l a t i o n i s 5 L p e r m i nu t e. T h e V / Q r at i o i s 0. 8. T h e o x y ge n at o r i s n o t as ef fi c i e nt as h u m a n l un gs . W e u s u al l y st a r t w i t h 2 L of g a s fo r e a ch l i t e r of pu m p - fl ow r a te , a nd th en ad j us t t he g a s - fl o w r a t e ac c or di n g to bl oo d P aC O 2 an d P aO 2 . T he ga s f l o w m ay b e d ec r ea s e d i f t he P a C O 2 is l o w an d t h e Pa O 2 i s t oo hi gh . T he r a ti o m ay be i n c r ea s ed i f t he Pa C O 2 i s ov e r 40 m m H g o r th e P aO 2 i s un d er 1 0 0 m m H g. I n t he pa s t w e u s ed a m i xt u r e o f 9 9% ox yg e n a nd 1 % c ar b on d i ox i d e f o r th e b ub b l e o x y g e na t o r . Be c au s e of l o w C O 2 pr o du c t i on d u r i n g hy p ot he r m i a, h i g h C O 2 e l i m i n at i o n f r o m h i g h g as fl ow , a nd hi g h C O 2 di f fu si o n c a p ac i t y , 1% C O 2 w a s a dd e d to ox y g e n to pr ev e nt s e v e r e hy p oc ap n i a . B ec au s e th e r o ut i n e u s e o f m em b r a ne ox yg e na t or s o xy ge n - a i r m i xt ur e s, i n st ea d o f 1 00 % o x y g en h a v e b e en us ed . I n a b ub b l e ox y g e na to r b u bb l e s c on t ai ni n g ni t r o ge n m ay be s l o w l y a bs o r b ed i n to th e s ys te m i c c i r c ul at i on , i nc r e a si ng th e r i s k o f ga s eo us m i c r o em bo l i . I n a m e m b r a n e ox y ge na t or t h i s r i s k d o es n o t ex i s t . M e a nw h i l e, a i r - o x y g en m i x t ur e s al l ow b e tt er co nt r ol o f o xy g en t e ns i o n d u r i ng C P B. Be c a u s e w e u s e al p ha - s ta t r eg u l a t i o n f or a c i d - b a s e m a na g e m en t, i t i s n ot ne c e s sa r y t o ad d C O 2 t o t he ve nt i l a ti n g ga s d ur i ng h y po t he r m i a to e l ev a te P a C O 2 an d d ec r e a s e th e p H .

C.II-25. What are the disadvantages of hypocapnia during CPB?

C er eb r al b l oo d f l o w d ec r e a se s a pp r o x i m at e l y 2 % t o 4 % fo r e ac h m m H g de c r e as e i n P aC O 2 w he n P a C O 2 i s i n t he r a ng e o f 2 0 m m H g t o 6 0 m m H g , d ue t o c er e br al va so c on st r i c ti o n. C e r e br a l ox y ge n s at ur a ti on de c r e as e s ap p r o x i m a t el y 1 % fo r e a c h m m H g de c r e as e i n P aC O 2 R es pi r a t or y a l k al o si s s hi ft s t he ox yg e n di s so ci a ti on cu r v e t o t he l e ft , w hi c h i n c r e as es th e O 2 a f f i ni t y to he m o g l o b i n a n d de c r e as e s t h e r el e as e o f O 2 t o th e t i s s ue s. H y p ok a l e m i a o cc u r s b e ca us e a l k a l o si s s hi f ts t he po t as si u m i n tr a c e l l u l a r l y . A l k al o s i s d ec r e a se s i o n i z e d ca l ci um .

S m i th AL , W o l l m an H . C e r e br a l bl o od f l ow a n d m e t ab o l i sm : e ff ec t s of an es t he t i c d r u g s an d t e c h ni q ue s . An e s t he s i o l o g y 19 7 2; 36 : 37 8 4 0 0. Y ao F S F , T s e n g C C , Y u J , et al . R el at i on sh i p b et w e e n E T C O 2 an d c er eb r al o x yg en sa t ur at i o n . A ne s t h es i o l og y 2 00 0 ;9 3( 3 A) :A 3 20 .

C.II-26. The arterial blood gases and electrolytes during CPB are pH, 7.36; PaCO 2 , 42 mm Hg; PaO 2 , 449 mm Hg; CO 2 content, 24 mEq per L; Na, 128 mEq per L; K, 5.8 mEq per L; Ht, 20%. The patient's temperature is 27 C (80.6F). At what temperature are blood gases measured? How would you correct the blood gases according to patient's body temperature? Would you treat the arterial blood gases at 37C (98.6F) or at patient's body temperature?
B l o od ga s e s a r e m e a su r e d a t a c on s ta nt te m p e r a tu r e of 37 C ( 9 8. 6 F ) . T h ey m a y be c o r r e c t ed ac c o r di ng to b o dy t e m p e r a tu r e. E a c h d e gr ee c e n ti gr a de b el ow 37 C ( 9 8. 6 F ) i n c r e a se s b l o od pH b y 0 .0 1 5. I f p H i s 7. 4 0 at 37 C ( 9 8. 6 F ) i n v i tr o , i n v i v o pH w i l l b e 7 . 5 5 a t 2 7 C ( 80 . 6 F ) b o dy t e m p er a t u r e ( 7 .4 0 + 0 .0 15 x [3 7 - 2 7 ] = 7. 55 ) . T h e p H i nc r e a se s a t l o w er t e m p er a tu r e s , be c au s e of i n c r ea s ed P k a a nd d e c r ea s ed C O 2 t e ns i o n f r o m i nc r ea s e d C O 2 b l oo d s ol ub i l i ty du r i n g hy p ot he r m i a. In v i vo P a O 2 i s de c r e as e d be c au s e of i n c r e as ed ox y g e n s o l ub i l i ty d u r i ng hy p ot he r m i a. A t t he N e w Y or k P r e s b y te r i a n H o s pi ta l C or ne l l M e d i c al C e nt e r , w e m ea su r e b l o od ga se s a t 3 7 C ( 98 .6 F ) a n d i n t er pr e t at 37 C ( 9 8. 6 F ) w i t ho u t c o r r e c t i n g t he m t o b od y t em pe r at u r e . T h e n o r m al v al ue s o f b l o od ga s es a t 3 7 C ( 98 . 6 F ) a r e pH 7. 40 0 .0 5 , P aC O 2 4 0 5, P a O 2 9 5 5; D u r i ng hy po t he r m i a, t h e no r m a l v al ue s o f b l o od ga s e s a r e no t t he s am e a s th o s e a t 3 7 C ( 98 . 6 F ) . P.178 T he s a m e b l oo d s pe ci m en h a s d i f fe r e n t P O 2 v al ue s w he n m ea s ur ed at d i ff er e nt t e m p e r a tu r e s . Ye t , th e o x y g en c o nt e nt r e m a i n s u nc h an g ed . I t i s ea s i e r to c al c u l at e t he o x y g en co n te nt at 3 7 C ( 9 8. 6 F ) th a n at ot he r t em p er at u r e s w he r e ox y g e n di s s o c i a ti on c u r v e s ar e s hi f te d. O pt i m a l m a n ag em e nt o f p H a nd P a C O 2 fo r p at i en ts un de r go i n g h y po th e r m i c C P B r e m ai ns c o nt r ov er s i a l . T h e t w o s t r a te g i e s f or i nt e r p r e t i n g b l o o d ga s es a r e t he p H - s ta t ( te m p e r a tu r e- co r r e ct e d) m e th od an d t he al ph a - s ta t ( te m pe r a t ur e- u nc or r ec te d ) m e t h o d. T h e p H - s t a t s t r a t eg y a i m s a t k e e pi ng c o n s t an t a r t e r i al p H a t 7. 4 0 an d P a C O 2 at 4 0 m m H g at an y g i v en te m p e r a tu r e. A Pa C O 2 o f 60 m m H g a na l y z ed at 3 7 C ( 98 . 6 F ) w o ul d b e e qu i v a l e n t t o a Pa C O 2 o f 4 0 m m H g i f c o r r ec t ed f or a bo d y te m p e r a tu r e o f 27 C ( 8 0 .6 F ) . T h e a l p ha - s t at s t r a t eg y a i m s a t k e e pi ng a c o n s t an t r at i o of [O H - ] : [ H + ] at ap pr o x i m a t el y 1 6 : 1 . T h i s i s b as ed on th e p r e m i se th a t th e p H o f bl o od i s r eg u l a te d t o k ee p t he s t at e o f d i s s o c i a ti o n of i m i d a z o l e m o i e t y ( i .e . , th e a l p h a o f i m i d a z o l e) c o ns ta n t. H i s ti di n e, w h i c h c on t ai ns th e i m i da z ol e m o i et y , i s a n i nt e gr a l pa r t of t h e a c t i v e s i t e o f m a n y en z y m e s y s te m s . T he fu n c t i o n o f e nz y m e s y s te m s ha s b e en s ho w n to b e o p ti m a l w he n t he r a ti o o f [O H - ] : [H + ] i s ap p r o xi m at el y 1 6 : 1 . T hi s r a t i o r e pr es e nt s d i f f e r en t p H v a l ue s a t d i f f e r e n t te m pe r a t ur e s . T he d i ff er e nc es be tw e en pH - s ta t a nd al p ha - s t at s t r a te g i e s a r e l i s t ed i n T ab l e 7 .3 . W i t h th e p H - s t a t s tr at e gy , t he b l oo d g as v a l u e s ar e c or r e c te d t o t h e p at i e n t' s t em p er at u r e ; t he p a ti en t i s t r e at e d as i f h e w er e a h i be r n a ti n g an i m a l . W i th t h e a l p ha - s t at s t r a te g y , t h e b l o od ga s v al ue s a r e no t c or r e c te d r eg ar d l e s s of t h e pa t i e nt ' s a ct ua l t em p er at u r e ; t he p a ti e nt i s t r e at e d a s i f h e w e r e a po i k i l o th e r m . St u di e s i n d i c at e t ha t m y o c a r di a l fu n c t i o n i s be t te r p r e s e r v e d w he n t he a l ph a - s ta t s tr at e gy i s e m p l oy ed . M or e ov er , m ai n te na n c e of c e r e br a l bl o od f l ow a u to r e g ul at i on ap pe a r s t o r em a i n i n ta c t w i th a l ph a - s ta t m an ag e m e n t, w he r ea s f l o w b ec o m e s p r e ss ur e d e pe nd e nt w i th p H - s ta t m an a ge m e n t. T h er ef o r e , m os t m ed i c a l c e n te r s us e a l p ha - s t at m a n a g em e nt o f b l o o d g as es du r i n g hy p ot h er m i c C PB . H ow ev e r , B a sh ei n e t a l . f o un d n o d i f fe r en c e i n n e ur op s y c ho l og i c ou t c o m e be tw e en p a ti e nt s r a n do m i z ed to a l ph a- s ta t o r pH s ta t m a n ag e m e nt . H ow ev e r , m o r e r ec e nt s t ud i e s h a ve s h ow n l es s d ec l i n e i n co gn i ti v e pe r f o r m an c e w h e n a l p ha s ta t m an ag e m e nt i s u s ed , e s p e c i al l y i n c a s e s w i t h p r o l o n ge d C PB t i m e s . T h i s d a ta m a y su p po r t an e m bo l i c t hr e sh o l d a b ov e w hi c h r e c o g ni z a b l e n e ur o l o gi c i nj u r y o c c u r s . D ur i n g d ee p h y p o th e r m i c c i r c ul a to r y ( D H C A) bo th an i m a l an d c l i n i c al s t ud i es h a v e s h ow n t ha t p H - s t a t i s as s o c i a t e d w i t h b et t er n e ur o l o gi c o ut c om e p r o ba b l y b ec au s e o f i n c r e as e d ce r e b r a l b l o o d fl o w , w h i c h p r o vi d es b e tt er br ai n c oo l i n g a nd g r ea t er c e l l ul ar ox y g e n a v a i l a bi l i ty . I n s um m a r y , m os t r ec e nt o u tc om e s tu di e s s u p po r t th e u ti l i z at i o n o f a l p h a- st at fo r a du l t C P B a nd pH - s ta t f or c h i l d r e n u nd e r D H C A . B as he i n G, T o w n e s BD , N es s l y M L, et a l . A r an do m i z ed st ud y o f c ar bo n d i ox i d e m an a ge m e n t du r i n g h y p o th er m i c c ar d i o p ul m o n ar y b y p a s s . An e s t he s i o l o g y 1 99 0 ;7 2: 7 1 5. D ah l b a c k a S , H e i k k i n e n J, Ka ak i ne n T , et al . p H - st a t ve r s u s a l p ha - s t at a c i d - b a s e m a na g em en t s tr a te gy du r i n g hy p ot h er m i c c i r c u l a t or y a r r es t c om b i n ed w i th e m b ol i c br a i n i n j u r y . A nn T h or a c Su r g 20 0 5; 79 ( 4) :1 3 16 13 25 . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :1 9 9 20 4 . I gl es i as I , M ur k i n J M . C e nt r a l n e r v ou s s ys te m d ys f un ct i on a f te r c ar di o pu l m o na r y by pa s s . I n : Ka p l a n J A, R e i c h D SN , L ak e C L, e t a l. ed s. Ka p l a n' s c a r d i a c a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :1 1 16 1 1 17 . J on as R A . H y p ot h er m i a , ci r c u l a to r y ar r es t a nd t h e pa e di a tr i c b r ai n. J C a r di ot h or ac Va s c An es t h 1 99 6; 1 0: 6 7 4.

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M ur k i n J M , F a r r ar J K , T w e ed W A , et al . C e r eb r a l a u to r e g ul at i on a n d f l o w / m e t ab o l i s m c o up l i n g d ur i n g c ar d i o pu l m o na r y by p as s : th e i nf l u e nc e o f Pa C O 2 . A ne s t h A na l g 1 98 7; 6 6: 8 2 5 8 32 . P.179

Table 7.3 Different Hypothermic Acid-Base Regulatory Strategies. CEREBRAL EFFECT ON TOTAL CO2 pH AND PaCO2 INTRACELLULARIMIDAZOLEANDENZYMESTRUCTUREBLOOD FLOW ISCHEMIC AND FUNCTION CONTENT MAINTENANCESTATE BUFFERING AND COUPLING TISSUE Increases Normal corrected values Acidotic (excess H+) Excess (+) charge Buffering decreased Altered and activity decreased Flow close to normothermic ? Flow and metabolism uncoupled Flow decreases (appropriate) ? Flow and metabolism coupled ? Lessens hypothermic protection

STRATEGYAIM pH-stat Constant pH

Alphastat

Constant OH-/H+

Constant

Normal uncorrected values

Neutral (H- = OH-)

Constant net charge Buffering constant

Normal and activity maximal

? Allows full hypothermic protection

From Tinker JH, ed. Cardiopulmonary bypass: current concepts and controversies. Philadelphia: JB Lippincott Co., 1989:16, with permission.

P.180 M ur k i n J M , M a r t z k e J S, B u ch a n AM , e t a l . A r a nd o m i ze d s tu d y of th e i nf l u e nc e o f pe r fu s i o n te c hn i q u e a nd p H m an a ge m en t s tr at e gy i n 3 16 pa ti e nt s u nd e r g oi n g c o r on ar y a r t e r y b yp a ss s u r g e r y . II . N eu r ol og i c an d c og n i t i v e o u tc om e s . J T h or ac C a r d i ov as c S ur g 1 99 5 ; 1 10 : 3 4 9 3 62 . O 'D w y e r C , Pr ou g h D S , J oh n st on W E . D et er m i n an t s of ce r e b r a l p er fu s i o n d ur i n g c ar d i o pu l m o na r y by p as s . J C a r di ot h or ac Va s c An es t h 1 99 6; 1 0: 54 65 . P ok el a M , D ah l b a c k a S , Bi a nc ar i F , e t al . p H - st a t ve r su s a l p ha - s t at pe r f u s i on s t r a t eg y d ur i n g e x p e r i m e n ta l h y p o th er m i c c i r c u l at o r y a r r e s t : a m i c r o d i a l ys i s s tu dy . A nn T h or a c Su r g 20 0 3; 7 6( 4) : 12 15 12 2 6. P r o ug h D S, St um p D A, R o y R C , e t a l . R e sp on s e o f ce r e b r a l b l o o d fl o w to ph en y l e p hr i n e i nf u s i on du r i n g hy p ot h er m i c c ar di o pu l m o na r y by pa s s : i n fl ue n c e o f P aC O 2 . An e s t h es i o l og y 1 98 6; 6 4: 5 76 5 8 1. T al l m an R D . A c i d- b as e r eg u l a ti o n, a l ph a- s ta t, an d t he e m pe r o r 's ne w c l o th e s . J Ca rd i ot ho r ac V a sc A n es th 19 9 7; 11 : 28 2 2 88 .

C.II-27. If the blood level of the venous reservoir is low, what would you replace it with? Blood or balanced salt solution?
W e tr y t o m a i nt ai n a h e m a to c r i t o f at l e as t 1 8% to 2 0 % d ur i n g h em o di l u t i o n. If t h e he m at oc r i t d e c r ea s es b e l o w 1 8% to 2 0 %, b l oo d i s ad d ed to t h e C P B c i r c u i t . I f t he h e m a to c r i t i s ab o ve 2 0 %, a ba l an ce d s al t s ol u ti on ( N or m o s ol ) i s ad d ed to t h e ox y ge na t or . H ow ev e r , h e m a to c r i t v a l ue s i n t he r a ng e o f 15 % t o 1 8% a p pe a r to be w e l l t o l e r a t ed c l i n i c a l l y. W h e n ce r eb r a l o xy g en s a tu r at i o n ( r S O 2 ) i s l e s s th an 40 % , w e u s e p ac k e d r ed c e l l s t o i m p r o v e ox y g e n c ar r y i n g c ap ac i ty . W h e n r SO 2 i s o v er 4 0 %, i tm e an s t he pa ti e nt h a s ac c ep ta b l e c e r e b r a l o x y ge n at i o n a l t h ou g h he m at oc r i t i s b el o w 18 % . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 3 5 44 2 . Y ao F S F , T s e n g C C , W oo D , e t a l . M a i n t ai ni n g ce r eb r a l o xy g en s a tu r a t i o n d ur i ng c a r d i a c s ur g er y d ec r e a s e d n eu r o l og i c a l c o m pl i c a t i on s . An e s t he s i o l o g y 2 00 1 ;9 5: A 15 2.

C.II-28. How do you estimate the fluid balance during CPB?


D ur i n g C PB , a l l i n tr av e no u s l i n es a r e sh u t of f . T h e i nt a ke i n cl ud e s c a r di op l eg i c s o l u t i o n, fl ui d o r b l o od ad d ed t o t he ox y g e na t or d u r i ng C P B, an d t he d ec r e a s e d b l o o d l e v el i n t he ox yg e na to r . T h e o u tp ut i n cl u de s u r i ne an d t he i n c r ea s ed bl oo d l ev e l i n t h e o x y ge n at o r .

C.II-29. How would you preserve the myocardium during CPB?


T he m o s t p o pu l a r a nd ef fe c ti ve m e th o d o f pr o te ct i n g t h e m y o ca r d i um i s t o r e d uc e m y o c a r di al ox y g e n d em an d b y h y p ot h er m i a a nd c a r d i op l eg i a . H y p o t h er m i a i s i n d uc ed by a c o m b i na ti o n o f sy st e m i c b l o od co ol i ng b y h e at e x c h an g er s i n th e o x y g en a to r , l o c a l a pp l i c at i on o f c ol d s al i ne s o l u t i o n or i c ed s l us h t o t he e x t er n al s u r f ac e a nd ch am b er s o f th e h e ar t ( i f t he he a r t i s o pe n ) , a n d i n f us i o n o f c ol d c ar di o pl eg i c s o l ut i o n t hr o ug h t he ao r t i c r o o t, v en o us gr af t s , r et r o g r a de c o r o n ar y s i n us , o r c or on a r y o s ti um t o t he co r o n ar y a r t er i al t r ee . T he m y oc ar d i a l te m pe r a t ur e m ay b e d e c r ea s ed t o 1 0 C t o 1 5 C ( 50 F t o 5 9 F ) . I n ad d i t i o n t o i nd u ci ng hy po t he r m i a an d c ar d i o p l e gi a , on e m ay ta k e th e f ol l o w i n g m ea s u r es b e fo r e ao r t i c c r o s s - c l a m pi ng :

A v o i d ta c h y c a r d i a or i n cr e as ed co nt r ac ti l i t y by di sc o nt i n u i n g p ac i ng a t r ap i d r a t e an d d i s c on t i n ui n g i n o tr op e s i f th ey w e r e ut i l i z e d. P.181

I ni ti a ti ng r a pi d a r r e st ( as y st ol e ) U ti l i z e pr op e r ve n ti ng m e th o ds an d e ns u r e a d eq ua t e ve n ou s d r a i na ge to t h e p um p t o av o i d v e nt r i c ul ar di s t e nt i o n , w h i c h d e c r ea s es s u be n do c a r di al b l o od s u pp l y .

P r e v e n t an d t r e a t ve n tr i c u l a r f i b r i l l a ti on , w hi c h i n c r e as e s ox y ge n d em a nd i n n or m ot he r m i c m y o c a r d i um . M a i nt a i n a d eq u at e c or on a r y p e r f us i on p r es su r e of at l e as t 5 0 m m H g a n d gr e at er th an 70 m m H g i n th e p r e s en c e of s e v e r e c o r o n ar y d i s ea s e o r l e ft v en tr i c u l a r h yp e r t r o ph y .

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :2 2 8 25 0 .

C.II-30. What is the cardioplegic solution? How much would you use?
C ar di o pl eg i c s o l ut i o n c on t ai n s m a i n l y hi g h co n ce n tr at i o n s o f po t as s i u m ( 1 0 t o 3 0 m E q /L ) o r m a g ne s i u m ( 1 6 0 m E q /L ) to r e l a x t he h e a r t . F l a c c i d c a r d i op l e g i a

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i ts el f r ed u c e s m y o ca r d i al o x yg e n co n su m p t i o n a nd p r ov i d e s o pt i m al c o n di ti o ns f o r s u r g e r y . B i c ar b on at e o r t r i s ( h y d r o x y m et hy l ) - a m i n om e th an e ( T H A M ) i s u s u al l y ad d ed to r a i s e th e p H t o l e v el s b et w ee n 7 .4 0 a nd 7. 80 to i n c r ea s e th e i nt r ac el l ul ar s h i f t o f p ot as s i u m a nd t o d ec r ea s e t h e m et a bo l i c a c i d os i s f r om i s c he m i a . S te r o i d s , ca l ci um , a nd pr oc a i n e m ay b e a d de d t o st a bi l i z e l y s os om a l an d c el l m em b r a ne s . Gl u c o s e an d i ns ul i n ar e a d de d t o pr o v i de en e r g y a nd i m p r o v e th e i nt r a c el l u l ar s h i f t o f po t as si u m . N i tr og l yc er i n i s a d de d t o d i l at e c or o na r y v e s s e l s , r e s ul ti n g i n be t te r p er fu s i o n t o th e m y o c ar di u m , i nc l ud i n g i s c he m i c a r e a s . A t t he N e w Y or k P r e sb y te r i a n H o s pi ta l - C or n el l M e d i c a l C e n te r , f o r c r y s t al l o i d c a r di o pl eg i a w e ad d 2 0 m E q o f p ot a s s i u m c hl o r i de a n d 1 0 m Eq o f s od i um b i c a r b o na te to 1 , 00 0 m L o f 5% gl uc o se i n a 0 . 22 5 % s a l t s o l u t i o n , r e s u l ti ng i n a f i n al p H o f 7 . 8 3, po ta s s i um of 2 0 m Eq pe r L , an d o s m o l a r i t y o f 38 0 m Os m p er L. W h e n b l o od c a r d i op l e g i a i s u s ed , f ou r p ar ts of b y pa ss bl oo d a r e m i x e d w i t h o ne pa r t of c a r d i o p l e g i c s ol u ti on . T he c o m p o s i ti o n o f f u l l - s t r e n gt h s ol ut i on i s a s f ol l o w s : 5 0 0 m L of 5 % g l u c os e i n a 0 .2 2 5% s a l t s o l u ti o n, 7 0 m Eq of p o ta s s i um c h l o r i d e, 1 0 m Eq of s o di um bi c a r bo na t e, a n d 1 m g o f ni t r o gl y ce ri n. Bl oo d c ar di o pl eg i a s e e m s t o h av e s ev e r a l a dv a nt ag e s ov e r cr y st al l o i d c a r di o pl eg i a. T h e he a r t i s a r r es t ed w h i l e b ei n g ox y ge na t ed , s o t ha t a de no s i n e t r i ph o s p h at e ( AT P) i s n ot de p l e te d b ef o r e a s ys to l e. R e pe at e d i nf us i on s p r o v i d e a s ou r c e o f o x y ge n a n d gl u c o s e fo r c on ti n ue d m et a bo l i s m an d A TP r e pl e ti on . A l t h ou gh l i t tl e o x y g en i s r el ea s ed fr om h e m o g l o bi n d ur i ng h y po t he r m i a , e n ou gh i s p r ob ab l y di s s o l v e d i n th e p l a s m a t o s us ta i n m e t ab o l i s m w h en r e i n fu s i o n i s p er fo r m e d e v e r y 30 m i nu te s . Bu f fe r i n g ca p ac i t y i s i m p r o ve d b e c a us e o f t he p r es en c e o f th e h i s t i d i n e b uf f er i n g s y s t em p r e s en t i n r e d c e l l s . M y oc ar d i a l e de m a i s r e du c e d b e ca us e o f t he o s m o l a r i t y o f bl o od . T he r i sk o f c al c i u m pa r ad o x fo l l o w i ng i s c h e m i a i s r e d uc ed an d f un c ti on a l r e c ov er y i s i m p r o v e d b ec au s e o f th e p hy s i o l o g i c c a l c i u m c on ce n tr a ti on pr ov i de d b y bl o od . T he p r es e nc e o f r e d c el l e nz y m e c a ta l a s e m a y s c a v e n ge f r ee r a di c al s p r o du c ed b y i s c he m i a . C a p i l l a r y pe r fu si o n i s i m pr o ve d a nd m o r e h o m o g en eo u s be c au s e of th e p r e s e n c e o f r ed c e l l s . H o w ev er , r es u l t s of c l i n i c a l s t u di e s i n w h i c h b l o o d c ar di o pl eg i a w a s c om p ar ed w i th cr ys ta l l o i d ca r d i op l eg i a ei th e r de t ec te d n o s i g n i f i c a nt d i ff er e nc e o r s h o w e d t ha t b l o od c a r d i op l eg ia im pr o v e d c on tr a ct il it y l at e i n th e p os t op e r a ti ve co u r s e. M u l t i p l e- do s e ca r di op l eg i a i s r e qu i r e d fo r s at i s f ac t or y r e s ul t s , w he r ea s s i n g l e - d o s e b l oo d c a r di o pl eg i a r e s ul t s i n p o or v en tr i c u l a r f un c ti on . I nt er m i t te n t, c on t i n u ou s, or s i n g l e i n fu s i o ns of c a r d i o p l e gi c s ol u ti on ha v e be e n us e d. U s ua l l y 3 00 t o 60 0 m l of c o l d c a r d i o p l e g ic s o lu ti o n is ne ed e d to p ar al y z e t h e m y o c a r d i um a n d co o l th e m yo c ar di u m to 10 C to 2 0 C ( 5 0 F to 68 F ) . I n th e c as e o f s ev er e o bs t r u ct i ve c o r o na r y l e s i o ns , a nt e gr ad e i n fu s i o n i n t o th e a or t i c r o ot m a y c a u s e m a l d i s tr i bu ti o n of t h e c a r di o pl e gi a. T h er e fo r e , r et r o g r a de i n fu s i o n t hr ou g h t he c o r o na r y si n us i n to t h e co r on ar y v ei n s m a y b e a dd i t i on al l y em p l o y e d t o e ns u r e h o m o ge n eo u s di s tr i b u ti on of c a r d i o p l e gi a . P.182 I n th e l at e 1 98 0 s a nd e a r l y 1 99 0 s w a r m ca r d i op l e g i a w i th n e ar - s y s t em i c no r m o th e r m i a w a s po p ul a r fo r b et te r m y o c ar di a l pr o te c t i o n . H ow ev e r , o n e s t u dy i de nt i fi ed a th r ee fo l d i n c r e as e i n s tr ok e s i n th e w a r m p at i e n ts . T he t e c h n i q ue i s n o l on g er p o pu l ar . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :2 1 4 21 5 , 2 28 2 50 . M c l ea n R F , W o ng B I . N o r m o th e r m i c v e r s us hy po t he r m i c ca r di op u l m on a r y b y pa s s : c en t r a l n er v o u s s y s te m o ut c o m es . J C ar di o t h o r a c V as c A ne s t h 1 99 6 ;1 0: 4 5 53 . S ha pi r o N , Ki r s h M , Jo c hi m K , et al . C om pa r i s on of t h e ef f ec t o f bl o od c a r d i o p l e g i a t o c r y s t a l l oi d c ar d i o pl e gi a o n m y o c a r d i al c o nt r a c ti l i t y i n m a n. J T h o r a c C ar di o v a s c Su r g 19 80 ; 80 : 64 7.

C.II-31. For how long a period can the aorta be cross-clamped?


W h e n c ar di o - p r o t ec ti ve st r a t eg i e s i n cl ud i ng i n te r m i t t en t h yp o th er m i c b l o o d c ar di o pl eg i a, i n i t i a t i o n o f r a p i d a r r e s t an d l ef t v e n tr i c u l a r v en t i n g a r e e m pl oy e d, t he l i m i ts o f s a f e i s ch em i c ti m e du r i n g ao r ti c c r o ss - c l am pi n g c a n b e i nc r e a s e d f r o m a s l i t tl e a s 15 to 4 5 m i n u te s t o a s m u c h as 2 4 0 m i n ut e s i n an i m a l m od el s w i t h n or m a l v en t r i cu l ar f u nc ti o n. H o w e ve r , m a n y pa t i e nt s h av e p r e o pe r at i v e v en t r i c u l a r d y s f un c t i on a n d t he p r ot ec t i o n f r o m h y p ot h er m i c c ar di o pl eg i a m a y n ot be o p ti m a l b e ca us e o f c or on a r y a r te r y o b s t r u c ti on . C l i n i c al l y , t h e ao r ta m a y be s a fe l y c r o s s - c l a m pe d f or 6 0 t o 1 20 m i nu t es w i t h ou t p er fu s i o n. T h e s ho r t e r th e c r o s s- cl am p i n g t i m e, th e b et te r t he m y oc a r d i a l f un c ti on w i l l be . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :2 1 7. R os en k r a nz GR , B uc kb e r g C D . M y oc a r d i a l p r o t ec ti o n du r i n g s ur gi c al c o r o na r y r e p er fu s i o n. J Am C o l l C a r d i o l 1 9 83 ;1 : 12 35 4 1 1 24 6 .

C.II-32. Why does urine become pink after 2 hours of CPB? What is the renal threshold for plasma hemoglobin?
P i n k u r i ne i s a s i gn of m a ss i v e h em o l y si s. H e m o l ys i s i s m ai n l y a s s o c i a te d w i t h t he f r o t hi n g, v i ol en t t ur b ul en c e, a c c e l e r at i o n , an d s h ea r f or c e s o f n eg at i ve p r e s s u r e s g en er a te d b y th e s u ct i o n a pp a r a tu s a n d i s a s so ci a te d t o a l es s er d e gr ee w i th th e a c t i o n o f t he p u m p s o r w i t h th e g as - bl oo d i n t e r f a c e e f f e c t s i n t he o x y g en a to r . T h e r en a l th r e s ho l d fo r h em o gl ob i n i s 10 0 t o 15 0 m g p er 10 0 m L. I t i s ad v i s ab l e t o m a i n t ai n a h i gh o u tp u t of a l k a l i n e u r i ne to p r ev en t p os s i b l e t u bu l a r d a m a ge fr om a c i d h e m a ti n c r y s ta l s , w hi ch ar e c on v er te d f r o m h em o gl ob i n. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 2 , 59 , 9 9.

C.II-33. At what temperature can the patient be weaned from CPB?


A n es o ph a ge al or n a so ph a r y n ge al te m p e r a tu r e of 37 C ( 9 8. 6 F ) a nd a r e c t a l or bl ad d er t e m p er a tu r e at l e as t 3 5 C ( 95 F ) m us t b e r e a c h e d be f or e t he p at i e n t c a n c om e o ff th e p um p . Af te r d i s c on ti n ua t i o n o f th e p um p , s u r fa c e w a r m i n g s h ou l d be c o nt i n u ed i n p e di a tr i c p a ti en t s t o pr ev e nt h y po t he r m i a ow i n g t o r e d i s tr i b u ti o n of he at i n t h e bo d y. H o w e ve r , i n ad u l t s th e u s e of w a r m i n g b l a n k e t s an d w ar m ed h u m i di f i e d a i r w a y g as e s ha s n o t be e n fo u nd b e ne f i c i a l i n p r e v e n ti ng P.183 t he e x pe c t e d te m pe r a t ur e af te r dr op . U s u al l y , e so p ha g ea l o r na s op ha r y n g ea l t em pe r at ur e w i l l d ec r e a s e an d r ec ta l o r b l a dd e r te m pe r a t ur e w i l l i n c r e as e d ur i n g h ea t r ed i s t r i b ut i o n . D i N ar d o JA , S c h w a r tz M J , ed s . An e st he s i a f o r ca r di ac su r g e r y . N o r w a l k : A pp l et on & L an ge , 1 9 90 :2 3 6. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :6 1 3 61 4 .

C.II-34. Why does it take longer to rewarm than to cool the patient by the pump oxygenator?
I t us u al l y ta k e s 5 t o 1 0 m i n ut e s to co ol th e p at i e n t fr o m 37 C to 25 C ( 9 8. 6 F t o 7 7 F ) of a v er a ge b o dy t e m p er a t u r e . I t t ak es 20 t o 4 0 m i n ut e s to r e w a r m th e p at i e n t fr o m 28 C to 35 C ( 8 2. 4 F t o 9 5 F ) . T he sp ee d o f h ea t e x c h an g e by th e b l o od s tr ea m d ep e nd s o n t he t e m p e r a t u r e gr ad i en t b et w ee n v en o us b l oo d a nd w a te r i n th e h e at e x ch an g er , t he p u m p b l oo d - f l o w r at e , an d t he w a te r - f l o w r at e o f th e h e at e x c h an g er . T he i n i t i a l v en o us b l oo d t em p er at u r e i s 3 7 C ( 98 .6 F ) a n d th e w at e r te m pe r a t ur e o f th e h ea t e xc h an g er i s 0 C t o 4 C ( 3 2 F t o 3 9. 2 F ) du r i n g c oo l i n g, c r ea ti n g a t em pe r at ur e g r a d i e n t of 34 C to 3 7 C ( 93 .2 F to 98 .6 F ) . D u r i n g r ew ar m i n g, th e w at er te m p e r a tu r e i s l i m i te d t o 4 2 C ( 10 7. 6 F ) o r l e s s to p r ev e nt d e na tu r at i o n a n d de s t r uc t i o n o f bl o od p r ot e i n s. T he t e m p er a tu r e gr ad i en t i s l i m i t ed to 1 0 C ( 18 F ) o r l es s t o p r e v e n t ga s e m b o l i s m fr om a de c r e as e o f g as s o l u bi l i t y i n th e b l o o d as s oc i a t ed w i t h a s h ar p i nc r e a s e i n t em p er at u r e . T he h e at e x ch a ng er w a te r f l o w d oe s n ot di ff e r m u c h du r i n g c oo l i n g an d r ew a r m i n g . H o w ev er , t he pu m p bl o o d f l o w i s u s u al l y m ai nt a i n ed to a v e r y hi gh l e ve l d u r i ng t h e i ni ti a l co o l i ng be ca u s e o f l ow BP i n t he be g i n ni n g of c o ol i ng . D ur i n g r ew a r m i n g , th e p um p b l o o d fl o w i s fr eq u en tl y m ai nt a i n ed at a l o w l ev el be ca u se th e B P i s us ua l l y h i gh a n d th e b o dy t e m p er a tu r e i s s ti l l l o w . R e w ar m i ng m a y b e a c c el e r a te d b y a dm i n i s t er i n g i n ha l a t i o n a ne s t h et i c s , or em pl o yi ng va so d i l at o r s , t o de c r e as e v as c ul ar r e s i s ta nc e a nd th er e by i n c r ea s e p um p f l o w to m a i n t ai n t he s a m e BP . B ec au s e th e i nc r ea se d

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Page 29 of 37

v as c u l ar r e s i s t an c e i s us ua l l y d u e t o i n a de qu a te an es t he si a d u r i ng r e w a r m i ng , w e pr e fe r i nh al a ti on an e s t he t i c s to v a s od i l a to r s i n p a ti en t s w i th go o d v en tr i c u l a r f un c ti on . I n c as es of p o or v e nt r i cu l ar f u nc ti o n, i n ha l at i o n a ge n ts a r e a v o i d e d be c au s e of th e p ot en t i a l c ar di a c de p r e s s i on a f te r C PB . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :5 6 7 56 8 . S ta nl e y T H , B er m a n L , G r e e n O, e t a l . Pl as m a ca t ec ho l am i n e a n d c o r ti s o l r es po n s e s t o f en ta n y l - o x y g en an e s t he s i a f o r c o r o n ar y a rt er y o pe r at i o n s . A ne s t h es i o l og y 1 98 0 ;5 3: 25 0 2 53 .

C.II-35. How would you defibrillate the heart internally during CPB?
T he h e ar t i s de f i b r i l l a te d i nt e r n al l y by a D C d e fi b r i l l at o r , w i th 5 to 1 0 w at t - s ec o nd s ( j o ul e s ) . If th e h ea r t r e m a i ns i n v en t r i c u l ar f i br i l l a t i o n, bl o od g a s e s, e l e c t r ol y t e s , a n d te m pe r a t ur e a r e r e ch ec k ed a n d l i d oc a i n e, 1 to 2 m g / k g , i s ad m i n i s te r ed be fo r e r e p ea te d D C d ef i b r i l l a t i o n a t t e m p t s . M AP i s u s u a l l y i nc r e a s e d t o 80 m m H g . Oc ca s i o n al l y , e sm ol o l , m e to pr o l o l , an d a m i od a r o n e ar e a dd e d t o tr e at i n tr ac t a b l e v e nt r i c ul a r fi br i l l at i o n o r t ac h y c ar d i a . S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 02 4 1 02 5 . P.184

C.II-36. Why is calcium chloride usually administered right before the patient comes off the pump?
W i t h h em od i l u ti o n, t h e i o n i z ed ca l c i um f r e q ue n tl y f al l s to a p pr ox i m a te l y 1. 5 t o 1 .8 m E q/ L ( no r m a l 2. 2 t o 2 .6 m E q/ L, 1. 1 t o 1. 3 m m o l /L o r 4 .5 t o 5 . 6 m g / dL ) . C al c i u m c h l o r i d e, 0. 5 t o 1 .0 g , i s fr e qu e nt l y gi ve n t o i nc r e a se m y oc ar d i a l c o n tr a c t i l i t y a nd r e v e r s e p o ta s s i um c a r d i o p l e gi a . C a l c i um i n c r e as es th e i no t r o pi c s ta te of t h e m y o c a r d i um a n d i n d uc es an i n cr ea s e i n sy st e m i c v as c u l ar r e s i s t an c e th a t o ut l a s ts t h e i n o tr op i c ef f ec ts . H ow ev e r , s o m e b e l i ev e t ha t c a l c i u m a dm i n i s t r a t i o n i s c o n tr ai n di ca t ed a t t hi s t i m e b ec a us e o f th e c om p r o m i s e d c a l c i u m h em o s t as i s th at ac c o m pa n i e s th e i n s u l t of a o r t i c c r os s - c l a m p i n g . A dm i n i s t r a ti o n o f c a l ci um m a y ex a ce r b a te i s ch em i c an d r ep e r f us i on i n j u r y by c a us i n g a c c u m u l a t i o n o f i n t r a c e l l u l a r c al c i u m . - B l o c k e r s , o n th e o th e r h an d, i nc r e a s e i n tr ac e l l ul a r ca l c i um b u t al s o pr o m o te i t s r eu p t ak e i nt o t he s a r c op l as m i c r et i c u l u m a nd m a y b e m o r e ap p r o pr i at e i n th i s s e t ti ng . T he r ef or e , us e o f c al c i u m s a l t s a t t he c o nc l u s i o n o f b yp as s s ho u l d b e g u i d ed by d e te r m i na ti o n of i o ni z ed c a l c i u m l ev e l s . C al c i u m s a l t s s ho u l d p r o b a bl y n ot b e g i v e n to p at i e n ts w i th g o od v e nt r i c ul ar fu nc t i o n i n th e a b se nc e o f h yp oc a l c em i a or hy pe r k a l e m i a b e c a u s e o f t he po te n ti al de t r i m e nt a l ef f ec ts of i a tr og e ni c h y p er c al c e m i a ; w he th e r th i s i s t r ue i n p a ti en t s w i th ve nt r i c ul a r dy s fu nc t i o n i s un k no w n . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :3 5 6 35 8 , 6 29 . S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 02 3 1 02 4 .

C.II-37. If the HR is 40 beats per minute, what should you do?


A t em p or ar y A V b l o ck a t t h e en d o f b yp a ss , be c au s e of po ta s si um c a r d i op l e g i a a n d i s c he m i c i ns u l t d u r i ng ao r t i c c r o s s - c l a m pi ng . A l t h ou g h at r op i n e m ay be t he or e ti c a l l y a d m i ni s te r e d t o t r e at si nu s o r n od al br ad y ca r d i a, m o r e f r e q ue n tl y , a te m po r a r y ep i c a r d i al p a c e m a k er i s u s u a l l y em p l o y e d . A tr i a l p ac i n g i s p r e fe r r e d b ec au s e o f i m pr o ve d c ar di a c ou t pu t w he n t he at r i a l k i c k i s p r es er v ed . V en tr i c u l a r p ac i ng i s n ec e s s ar y i f th e r e i s c om p l e te AV b l oc k . AV s e qu e nt i a l p ac i n g i s i nd i c a te d w he n v en t r i cu l a r p a ci ng do es no t p r o vi d e ad e qu a te c a r d i a c o ut p ut . S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 02 5 .

C.II-38. How does the blood sugar level change during CPB? Why? Does hyperglycemia increase neurologic complications during CPB?
B l o od s u ga r l ev e l s a r e el e va te d d u r i ng pe r i o pe r a t i v el y i n p at i e n ts u n de r g o i n g c ar d i a c s ur ge r y w i th us e o f C P B . H y p er gl y c e m i a i s m o s t pr o fo u nd d u r i ng h y p ot h er m i c C PB w i th a p pr o xi m a te l y 10 0 % o f pa t i e nt s ( di a be ti c a nd no n di ab e ti c ) ac hi e v i ng pl as m a gl u c o s e l e v e l s gr e at e r t h an 20 0 m g/ d L. T h er e a r e s ev er a l r e a s o ns fo r t hi s: f i r s t, th e p r a ct i ce o f m ak i n g p a ti en t s N P O ( no t hi ng by m o ut h) ov er n i g ht i n du c es a s t at e o f s ta r v a ti on , m ar k ed b y p er i ph er a l r es i s ta n c e to i n s u l i n a t t he l e ve l o f m u s cl e a nd f a tt y t i s su e s; t h er ef o r e , a l l ow i n g g l uc os e u pt a k e b y t he br a i n ; s e c on d , s y m p a t h o ad r e n al a c t i v a t i o n i n r es po n s e t o s ur g i c al st r e s s, a l s o t en d s t o i n d uc e a d i a b et o ge ni c s ta t e; t h i r d, ac ti v e - c o o l i ng th e b od y d ur i n g b y p a s s c a us e s a p r o fo u nd r e du c t i on i n i n s u l i n p r o du c ti on , i nd u c e s p er i p h er a l i n s ul i n r e si st a nc e , an d i s a ss oc i a t ed w i th r e na l t ub u l a r i m p ai r m e nt i n g l u c os e r eg u l a ti o n; l a s t l y , u s e of d e x t r o s e- c o n ta i n i ng c ar di o pl eg i a, i s a m a j o r c on tr i b u to r t o i n t r a o pe r a t i v e P.185 h y p er g l y c e m i a . O f i n te r es t, po st o pe r at i v e h yp e r g l y c em i a c o nt i nu es de s p i te i n s u l i n a dm i ni s t r at i o n a nd ha s b ee n s ho w n to r e m a i n a b o v e no r m a l up to s e ve r a l w ee k s po s t o pe r a t i v el y . At th e c el l u l ar l e ve l , th e a l t er a ti on s i n i ns ul i n r e c e p to r /r es i s t an c e ar e v er y s i m i l a r to t h at o f t y p e 2 di ab e te s . It i s c on t r o v e r s i al a s t o w he th e r hy p er gl y ce mi a i nc r ea se s n eu r ol og i c co m pl i c a ti on s d ur i ng C P B. U n de r c on di t io ns of l i m i te d c er e br al ox yg e n de l i v er y , an a e r ob i c gl u c o s e ox i da ti o n b ec om e s th e p r i m ar y m e t ho d o f A T P p r od uc t i o n, r e su l ti ng i n i n tr ac e l l ul a r l a c t i c ac i do s i s . H y p er gl y c e m i a, by p r ov i d i ng m o r e g l uc o s e f o r an a er ob i c ox i da ti o n, i nc r e a s e s t he d e gr ee of i n tr ac e l l ul a r ac i do si s , w h i ch , i n nu m er ou s a ni m al s t ud i e s , c o r r e l a t es w i t h t he s e v e r i t y o f s u b s e qu e nt i n j u r y . A l t h ou g h th e d e l e te r i o us e ff ec t o f h y p er g l y c e m i a i n t he fa ce of b o th g l ob a l an d f oc a l ce r eb r a l i s c h em i a i s g e ne r a l l y a c c e pt e d, a r e c e n t hu m an s t ud y c ha l l e ng e s t h e s e c o nc l u s i o ns . M et z a nd K e at s r ep or t ed z e r o n e ur o l o gi c i nj u r y i n a g r o u p o f 54 pa ti e nt s u nd e r g oi n g C A B G m a n ag ed w i th gl u c o s e - c o nt a i n i n g f l u i ds ( g l u c o s e du r i n g b y p as s a pp r ox i m a te l y 70 0 10 0 m g/ d L) v er s us 1 st r o k e an d 1 c a s e of e n c e ph a l o p at hy i n 5 3 p at i en ts i n w h om g l uc os e w as av oi d ed d u r i n g C A B G ( g l uc os e d ur i n g b y p a s s a p pr o xi m a te l y 20 0 1 00 m g /d L) . T he au th o r s c o nt en d t ha t g l uc os e d oe s n ot af fe c t ne u r o l og i c ou tc o m e i n t he pr es e n c e o f a p er m a n en t f oc a l l es i o n . Al t ho ug h p r o v oc a ti ve , t hi s s tu dy ca n b e f au l t e d fo r ( a) i t s l a c k of s e ns i ti v e m o ni to r s of ne u r o l o g i c o u t c om e a nd ( b ) i t s s m a l l s a m pl e s i z e i n r e l a t i o n t o t he o c c u r r e nc e r at e o f th e e ve n t o f i n te r es t. M o r e r e ce n tl y, th er e a r e a nu m be r o f r e p or ts th at s h ow a s t r on g a s s oc i at i o n b e t w e e n p l a s m a g l uc os e l ev e l s a n d p os to p er at i v e m o r b i d i ty a n d m o r ta l i t y. B a se d o n th e se f i nd i n g s , t i g ht g l u c os e c on tr o l i s be i n g r ec o m m en d ed f o r al l p at i en t s u n d er go i ng C P B. A c hi ev i ng o pt i m a l gl u c o s e c o nt r ol d u r i ng hy po t he r m i c C P B i s n ea r l y i m p o s s i b l e ; h o w e v e r , w i th us e o f c o n ti nu o us i n s u l i n i n fu s i o n, p l as m a g l uc o se l e ve ls ca n b e b es t m an ag e d. R e ga r di ng th e o pt i m a l r a n ge o f g l u c os e c on t r o l , t h er e c on t i n ue s t o b e s o m e de b at e a bo u t m a i nt ai n i n g p l a s m a g l uc os e b el o w th e t hr e s h ol d o f 1 10 m g/ dL . F r o m b ot h a p r ac ti ca l p o i n t a nd s a fe ty i s su e s ( h y po gl y c e m i a ) , m os t w ou l d ac c ep t t ar ge t p l a s m a g l uc o s e o f l es s t ha n 1 40 m g p e r dL as b e i n g a de q ua te . F on te s M L, Ko v a l K J, D e sv a r i eu x T , et al . E pi de m i o l o g y of hy pe r gl y c e m i a i n no n di a be ti c p at i en ts un de r go i ng h y po th e r m i c c a r d i op u l m on ar y b y p a s s . A ne s t h es i o l og y 2 00 6 ;1 05 : A7 4 9. F on te s M L, Sk ub a s N , Gi r a r d i L , e t al . G l u c os ur i a du r i n g c ar di o pu l m o na r y by pa s s : d o es hy po t he r m i a pr o v i de pr ot e c t i o n o r a b l o w t o t he k i dn ey s ? An e st h A na l g 20 0 7; 10 4 :S CA 8 1. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 1 4. G r o c o t t H P , S ta ff o r d - S m i t h M . Or ga n p r o t ec t i o n d ur i n g c ar d i o pu l m o na r y by p as s . In : K ap l a n J A , R e i c h D SN , L ak e C L, et a l . ed s . Ka p l a n 's c a r d i a c a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :9 9 2 99 3 . H i n dm a n B. C o n: gl uc o se p r i m ar y s ol u ti on s s ho u l d n o t be us e d fo r c ar d i o pu l m o na r y by p as s . J Ca rd i ot h or ac Va sc A n es t h 19 9 5; 9 :6 05 60 6 . L an i e r W L. Gl uc o s e m a na ge m en t d ur i n g c a r d i o p ul m o n ar y b yp as s : c a r di ov a s c ul a r an d n eu r ol og i c i m p l i c a t i o ns . A ne s th A n al g 1 99 1 ;7 2: 4 23 42 7.

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M et z S . Pr o: gl uc o se pr i m i n g s ol u ti on sh o ul d b e us e d fo r c ar d i o pu l m o na r y by p as s . J C a r di ot h or ac Va s c An es t h 1 99 5; 9 :6 03 60 4 . M et z S , Ke a ts A S . Be n ef i t s o f a g l u c os e- c on ta i ni ng pr i m i ng s o l u ti o n fo r c ar d i o pu l m o na r y by p as s . An e s t h An a l g 19 91 ; 72 : 42 8 4 34 . O 'D w y e r C , Pr ou g h D S , J oh n st on W E . D et er m i n an t s of ce r e b r a l p er fu s i o n d ur i n g c ar d i o pu l m o na r y by p as s . J C a r di ot h or ac Va s c An es t h 1 99 6; 1 0: 54 65 . S ta nl e y T H , B er m a n L , G r e e n O, e t a l . Pl as m a ca t ec ho l am i n e a n d c o r ti s o l r es po n s e s t o f en ta n y l - o x y g en an e s t he s i a f o r c o r o n ar y - a r t er y o pe r at i o n s . A ne s t h es i o l og y 1 98 0 ;5 3: 25 0 2 53 . P.186 W a s s C T , L an i er W L . Gl u co se m o du l at i o n o f i sc he m i c b r ai n i nj ur y : r e v i e w an d c l i n i c al r e c o m m e nd a ti on s . M a y o C l i n Pr o c 19 9 6; 71 : 80 1 8 12 .

C.II-39. What are the effects of CPB on platelet and coagulation factors?
P l a te l et d y s f un c ti on an d t hr o m b oc yt o pe n i a a r e fo u nd on a n d af t er C P B. P l at el e t dy s fu nc t i o n i s th e m os t c om m o n c a us e o f a b l e ed i ng pr ob l em f o ll ow in g C P B a ft er he pa r i n i s r ev e r s ed an d s ur gi c al b l ee di n g i s co n tr ol l e d . T r a ns i e n t de f ec ts i n p l at e l e t p l u g f or m a ti o n a nd a g gr eg a ti o n ar e s ee n i n a l l p a ti en t s pu t o n C PB . G en er a l l y , pl at e l e t f un ct i on r e tu r n s t o n ea r n or m a l s ta t us 2 to 4 ho ur s f ol l ow i n g C PB . T he de fe c ts a r e ex a c e r b a te d a nd pr o l o ng e d by dr ug s s uc h a s a s p i r i n an d p l a t el et gl yc o pr ot e i n G P II b/ I II a i nh i b i to r s ( c l o p i d og r el , t i r of i ba n) , w hi c h i n h i b i t pl at e l e t f un c t i on . P l a te l et c o un ts fa l l m o r e w i th t h e b ub bl e - t yp e o xy g en a to r th a n w i t h t he m e m b r a n e- ty p e ox y ge na t or , b ut r a r e l y be l o w t he l e v e l s c l i ni c a l l y r eq u i r e d fo r h em os t as i s . T hr o m b oc yt o pe n i a i s m ai n l y c au s ed by h e m o di l ut i o n , ag g r e g at i o n , ad h es i o n , a nd t h e ad e no s i n e d i p ho s ph a t e ( A D P ) - r e l e as e r ea c ti on i n d uc ed b y th e f or e i g n s ur fa c es a n d th e b l oo d- g as i n te r f a ce . H ep ar i n m a y p ot e nt i a t e p l a te l et a g gr eg a ti on an d a dh e s i o ns . T he l e v e l o f c o a gu l a t i o n f ac to r s de c r e a se s a t th e b eg i nn i n g o f b y p a s s b e c a us e o f h em od i l u ti o n; s u r f ac e a b s o r p t i o n b y th e p l a s t i c , gl as s , an d m et a l ; a n d p r o te i n de n at u r a ti o n i n d uc ed by t h e b l o od - ga s i nt er f ac e. At t h e s a m e ti m e , t h e s y n th es i s of c l ot ti n g fa c to r s by t h e l i v er i n c r e a s es s o t ha t t he c o nc e nt r a t i o n o f c l o tt i n g f ac t or s r e t ur ns to n o r m al w i th i n a p er i o d o f h ou r s . M em b r a ne ox y g e na t or s c a u s e fe w c ha ng e s i n c l ot t i n g f ac to r s . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 9 7 50 0 .

C.II-40. How would you prepare for termination of CPB?


B ef or e t er m i n at i on o f C PB , c ar d i a c a nd p u l m on a r y f u nc ti o n m u s t be op t i m i z ed . T o e ns ur e t ha t a l l - i m po r ta nt s t ep s a r e no t i na dv e r t en t l y o m i t te d , t h e p at i en t a nd a l l m o n i t or s s ho u l d b e c ar e fu l l y c he c ke d. T h e m ne m o n i c L A M P S f or L a bo r a t or y d at a , An e s t he s i a m a c h i n e , M o n i t or s , Pa t i e nt ( P u m p ) , a n d Su p po r t i s o n e u s e fu l a pp r oa c h .

Laboratory Data

A r t er i a l p H , PC O 2 , PO 2 w i t h i n n o r m al l i m i ts H em at o c r i t 2 0 % to 25 % K + 4. 0 t o 5 .5 m E q p er L I on i z e d c a l c i um 1. 1 t o 1. 2 m m o l p er L P um p m i x ed ve no u s O 2 s at u r a ti o n g r e at e r th a n 70 %

Anesthesia/Machine

A de qu a te an es t he si a A ne s t h es i a m a ch i ne f u nc ti o na l

Monitors

E C G s ta b l e r a te an d r hy th m ( us e p ac i ng i f n ec e ss ar y ) S y s te m i c B P r es to r ed t o n or m ot he r m i c l e v el s P A c a t he te r f un c ti on a l Tr a ns d uc er s r ez er o ed an d c al i b r at ed T E E o u t of fr ee z e m o d e N as op h ar y n g ea l /P A ca t he t er t e m p er a tu r e 36 C to 3 7 C ( 9 6. 8 F t o 9 8. 6 F ) B l a dd e r / r e c ta l t em pe r at ur e g r e a te r t ha n 3 5 C ( 95 F )

P.187

Patient/Pump

T h e h e ar t c on tr a ct i l i t y , si z e, r h yt hm , a nd ai r r e m ov ed T h e l u ng s a te l e c ta si s r e- e xp an d ed , f l u i d i n t h or a ci c ca v i t i e s d r a i ne d, v e nt i l a ti o n r e i ns t i t ut ed

Support

I no tr o pe s / v as op r es so r s/ va s od i l a to r s I AB P i f ne e de d

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :6 1 4.

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S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 02 3 1 02 6 .

C.II-41. How would you decide the need for inotropic support?
T he n e ed f o r i n o tr op i c su p po r t af te r C PB i s u s ua l l y a ss e ss ed by t h e fo l l o w i n g ( F i g. 7 . 9) :

P r e op e r a ti v e ve n tr i c u l a r fu n ct i o n ( e j e ct i o n f r a c ti on ) E ff ec t i v en e s s o f i nt r a o pe r at i v e m yo ca r di a l pr ot e ct i o n A de qu a c y o f s ur g i c al r e pa i r D ur at i o n o f a or t i c c r o s s- cl a m p i n g a nd C P B P at i e n t' s a ge

I f LV E F i s p r ed i c t ed to b e 2 5% to 3 5 %, m i l r i n o ne i n fu si o n m a y b e a dd e d. N o r e pi n ep h r i ne i n fu s i o n i s us u al l y n e ed e d du r i n g m i l r i n on e t he r a p y . G e ne r al l y , i nt r a a or ti c b al l oo n p um p i s al s o em p l o ye d w he n L V EF i s p r e di c te d t o b e be l ow 2 5 %. T h e c h o i c e o f v a s oa c t i v e a n d c ar di o ac ti v e ag e nt s u s e d i s f r e qu en t l y c en te r a nd / or p h y s i c i an s p ec i f i c an d , i n m o st ca se s , i n i ti at e d as pr op h y l ax i s . R e c e nt da ta s u gg e s t s t ha t t hi s p r a c t i c e s h ou l d b e av oi d ed b e c a u s e i n ot r o p i c a nd v a s o p r e s s or s c an ha ve ne g at i v e e ff e ct s, w h i c h c an r e su l t i n bo th m o r b i d an d f at a l ev e nt s . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :6 1 7 61 8 . S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 02 4 1 03 4 .

C.III. After Cardiopulmonary Bypass


C.III-1. How would you reverse heparin? How much protamine would you use? What are the other drugs used to neutralize heparin?
I t ha s b ee n r ec o m m en d ed th at 1. 1 t o 1. 3 m g o f pr o ta m i n e su l fa te i s n e ed e d to r e v e r s e e a c h 1 0 0 u ni ts o f r em a i n i n g h e pa r i n c al c ul at e d by AC T d os er es po n s e c u r v e o r pr o ta m i n e ti t r a ti o n te s t. A t t he N e w Yo r k Pr e s b y t e r i an H o s p i ta l - C or ne l l M e d i c al C e nt e r , w e g i v e 1 .0 m g o f p r o t a m i n e t o r e v er s e ea c h 10 0 u ni ts or 1 m g o f h ep a r i n i ni ti a l l y a dm i n i st er ed . O n l y t he i n i t i al d o s e o f h e pa r i n i s c o u nt e d. T h e s u b s e q ue nt l y ad d ed do s e of h e pa r i n , to k e ep th e A C T l e ve l a bo v e 48 0 s ec o nd s, i s n o t co n si de r ed b e ca u se o f i ts m e ta b ol i s m a nd el i m i n a ti on . T he AC T t es t i s r e p ea te d 1 0 m i n u te s a ft er t h e a dm i n i s t r a ti o n o f p r o ta m i n e. AC T u s u al l y r e tu r ns t o i ts co nt r ol l e ve l . If t he AC T i s s t i l l p r o l on g ed , a dd i t i on a l pr o ta m i ne i s g i v e n a c c o r d i n g t o t he A C T do s e- r e s p o ns e c ur v e. H ow ev e r , P.188 t he A C T i s a f fe c t e d b y di l ut i o n a nd by h y po t he r m i a ; d o se - r es p on s e c u r v e s u ti l i z i n g da t a o bt ai n ed d u r i ng hy p ot he r m i a m a y b e m i s l e a di n g. I n a dd i ti on , s ev e r e t hr om b oc y t o pe ni a a l s o p r o l on g s th e A C T b e ca u se c l ot f o r m at i o n u s i n g t he A C T de p en d s on pl at e l e t p ho s p h ol i pi ds s u r f a c e . F u r th e r m or e, be ca u s e he pa r i n r eb ou n d i s po s s i bl e, i t m a y be op ti m al t o a dm i ni st e r pr o ta m i n e at tw o t i m es f o l l ow i ng C P B: o n c e a f te r b y p a s s a n d ag a i n 1 or 2 h o u r s l at e r to c o un t er a ct h ep a r i n r e b ou n d.

Figure 7.9 Hemodynamic management during weaning from cardiopulmonary bypass. The hemodynamic evaluation is performed by combining information from the systemic (light shade boxes) and pulmonary (black boxes) arterial pressures. A: a combination of elevated systemic arterial and low pulmonary arterial pressure suggests either a hyperdynamic cardiac function (if cardiac output is high) or a vasoconstrictive state (if the peripheral vascular resistance is high); B: if systemic hypertension is accompanied by pulmonary hypertension, then either the volume status is elevated (if cardiac output is high), or there is generalized vasoconstriction (if cardiac output is decreased). C: in case of systemic hypotension and pulmonary hypertension, the cardiac output may be high (systemic vasodilation) or low (depressed contractility, requiring immediate intervention). D: when both systemic and pulmonary pressures are decreased, there is either vasodilation (if the cardiac output is high) or hypovolemia or depressed contractility or right-sided failure are suspected (if cardiac output is decreased). The relative treatment for each hemodynamic derangement is shown in the table. CO, cardiac output; CVP, central venous pressure; IABP, intraaortic balloon pump; LVAD, left ventricular assist device; NO, nitric oxide; PGI2, prostacyclin; RV, right ventricle; SVR, systemic

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vascular resistance , increase; , marked increase; ?, questionable.

P.189 O th er dr ug s t ha t h av e b e en u s ed t o n e ut r a l i z e he p ar i n i n c l u de pl at e l e t f ac to r 4 ( P F 4 ) , h e pa r i n as e , pr o t a m i n e v a r i a nt s , po l y b r e n e, a n d to l ui d i n e b l u e. H u m a n o r r e c om bi n an t P F 4 h a s be e n u se d i n an i m a l s an d h um an s t o r ev er s e he p ar i n an d d oe s n o t c a u s e s y s t em i c ar te r i a l h y p ot e ns i o n , or pu l m o na r y hy pe r te n si on , o r c h a ng es i n w h i t e b l o o d ce l l co u nt , p l a te l et c o un t, or c o m p l e m en t l ev el s . H e p ar i n a s e n e ut r a l i z es he pa r i n b y e n z y m a t i c c l e a v a g e of - g l y c o s i d e l i n k a g es a t A T II I b i n d i n g s i t e. H e pa r i n as e i s a n ef f ec ti v e an t ag o ni st o f h e pa r i n a nd ha s m i n i m a l ef f ec ts on p l at el e ts , w he r e a s pr o ta m i n e m a r ke dl y i nh i bi ts pl at e l e ts r es po n s i v e n es s . It a p pe a r s t o b e a p ot e nt i a l a l t e r n at i ve t o p r o t am i n e . T w o p r ot am i n e v a r i an t s, s o- c al l e d de s i g n er p r o t am i n e s a r e cu r r e nt l y un d er i n v e s t i ga ti o n. T h e s i d e ef f ec ts of p r ot am i ne s u c h a s h y p o te n s i on an d l ow c ar di a c ou t pu t w er e s i g ni f i c an t l y r e du ce d b y t he p r ot a m i ne v a r i an t s . P o l y br e ne , a l s o k no w n as he x a d i m et h r i ne br om i de , a t on e t i m e w as c o m m o nl y u se d, b ut i t w as w i th d r a w n fr om c l i n i c a l us e b ec a us e o f su s pe c te d n ep hr o to x i c i t y a nd p r od u c t i o n o f p ul m o n ar y h y p er t en s i o n. T o l u i d i ne b l ue ha s a l s o b ee n u se d f or h e pa r i n r ev e r s al , b ut i t i s l es s e ff ec t i v e t ha n p r o ta m i n e a nd i s a s s o c i at e d w i t h m e t he m o g l o b i n em i a. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 7 3 47 8 . S pi es s B D , H o r r ow J, K a pl an JA . T r a ns f us i o n m ed i ci ne an d c oa g ul at i on d i s o r d e r s . I n: K a pl an J A , R ei c h D S N , La k e C L , e t al . e ds . K ap l an ' s c a r di ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :9 5 8 96 6 .

C.III-2. What is the action mechanism of protamine?


H ep ar i n i s a s t r o n g o r g an i c ac i d ( p o l y an i on ) . Pr ot a m i ne i s a st r o n g or g an i c ba s e ( p ol y c a ti o n) . T he y c om bi n e i o n i c al l y t o fo r m a s t ab l e s a l t an d l o s e t h ei r o w n a n ti c o a gu l an t a ct i v i t y . Pr o ta m i n e co n ta i n s t w o ac ti v e si t es , o ne t h at n e ut r a l i z es he p ar i n an d a no th e r t h a t e x e r t s a m i l d a n t i c o ag u l a n t ef f ec t i nd ep e nd e nt o f h ep a r i n . G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 7 1. S pi es s B D , H o r r ow J, K a pl an JA . T r a ns f us i o n m ed i ci ne an d c oa g ul at i on d i s o r d e r s . I n: K a pl an J A , R ei c h D S N , La k e C L , e t al . e ds . K ap l an ' s c a r di ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :9 5 9.

C.III-3. What are the complications of too much protamine?


P r o ta m i n e i ts el f i s an an t i c oa g ul an t . Pr o ta m i n e ad m i n i s t er ed i n tr a v e no u s l y i n th e a b s e nc e o f h ep a r i n i n t er ac t s w i t h pl a t e l e t s a n d w i t h m an y c l o t t i ng p r o te i ns . P r o ta m i n e i nd uc e s tr a ns i e n t th r om bo c yt op e ni a i n h um an s . Pl a te l e t a gg r eg a ti on i s i m p a i r ed by t h e p r o ta m i n e h ep ar i n c o m pl ex , b ut pr ot a m i ne al on e h as n o d e l e te r i o us ef fe c ts . Pr o ta m i n e m a y b i n d t o t hr om b i n a n d i nh i b i t th r om bi n 's a b i l i t y t o c on v e r t fi b r i no g en t o f i b r i n . H ow ev e r , i t h as be en sh ow n t ha t e xc e ss p r ot am i ne m i ni m a l l y i n c r ea s e s t h e Le e - W hi t e w h o l e bl o od c o ag u l a t i o n ti m e. A f te r 6 00 m g f o r e v er y 7 0 k g bo d y w ei gh t o f p r o ta m i n e, th e c l o tt i ng t i m e i n cr ea s ed f r om 6 . 7 m i nu t es to 8 . 2 m i n ut es i n u n he pa r i n i z e d v o l un t ee r s ; t he PT T w a s n ot a f fe c te d . In ad di t i o n, th e c l o tt i ng t i m e r et u r n e d to ba se l i n e w i t hi n 3 0 m i n ut e s. T h e r e s ul ts w e r e s i m i l a r i n p at i e n ts u n de r g o i n g C PB . T he r e f or e , pr o ta m i ne do e s i n h i b i t c o ag u l a ti o n i n v i t r o a n d d oe s m i n i m a l l y p r o l o n g cl o tt i n g t i m e i n vo l un t ee r s a n d i n pa t i e nt s . H o w ev er , t he do s e s n ee d ed t o a c hi ev e c l i n i c al an ti c oa g ul an t e ff e c t s a r e m o r e t ha n d ou b l e t h os e u se d r ou ti n el y a nd gr ea t er t h an t h r e e t o fo u r ti m es t h e do s e s h o w n to r es u l t i n r et u r n o f a de q ua t e c o a gu l at i o n . Be c au s e P.190 o f pr o ta m i n e' s a pp a r e nt r a pi d d i s a pp e ar an c e an d b e ca us e s m a l l do s es o f h ep a r i n d o e x e r t a n i m p o r t a nt c l i n i c al ef fe c t, i t s ee m s pr u de nt no t t o w i t hh ol d a dd i t i on a l do s es o f p r o t am i n e i n m o d er a ti on w h en e ve r a r es i du al he p ar i n ef fe c t i s s u s p e c t ed . T he da ng e r i n gi v i n g ad d i t i o n al do s e s o f p r o t a m i n e f or c on ti n ue d b l e e di ng i s t h at t h e he m os ta t i c d e fe ct m a y n ot b e d u e to r e s i d ua l h ep a r i n. T h er ef o r e , t he s e ar c h fo r a nd c o r r ec t i o n o f t h e r ea l h e m o s t a ti c de f ec t m ay b e d el a y e d o r fo r go tt e n. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 7 3. S pi es s B D , H o r r ow J, K a pl an JA . T r a ns f us i o n m ed i ci ne an d c oa g ul at i on d i s o r d e r s . I n: K a pl an J A , R ei c h D S N , La k e C L , e t al . e ds . K ap l an ' s c a r di ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :9 6 0.

C.III-4. Why did the patient develop hypotension after protamine was administered? How do you treat and prevent this condition?
T hr ee di ff e r e nt ty pe s o f c i r cu l a t or y r ea ct i on s t o pr o ta m i n e r e v er s a l o f h ep a r i n ha v e b ee n p r o po s ed by H o r r ow :

T y p e I : Sy s t e m i c H yp ot e ns i o n f r o m R ap i d In j ec ti o n: A Pr ed i c t ab l e Ph a r m ac o l o gi c R ea c ti on T y p e I I: A n ap hy l ac ti c o r An a ph y l a ct o i d R e ac ti o n

A nt i b o dy - m e di ca t ed I m m ed i a t e a na ph y l a ct o i d r e sp o ns e w i t ho u t an t i b od y i nv o l v em e nt D el ay e d an a ph y l a ct o i d r e sp on s e ( ? no nc a r d i a c p u l m on a r y e d em a)

T y p e I II : C a t as tr o ph i c Pu l m o na r y Va so c on s tr i c ti o n w i t h Sy s te m i c H y p ot e ns i o n H ow ev e r , e t i o l o g i c al l y th e r e a r e on l y tw o t yp e s of r e ac ti o n: ( a ) ph a r m ac o l o gi c s i d e e ff e c t r e ac t i o ns a n d ( b ) i di o s y nc r at i c r e ac t i o ns . T he r e f or e , an a l t er n at i v e c l a s si fi ca t i o n w as p r op o se d b y M o o r m an , Z ap l , an d L ow e ns te i n as fo l l o w s :

P ha r m a co l o g i c h i st am i n e r e l e as e T r u e a na ph y l a xi s ( Ig E - m ed i at ed ) A na ph y l a ct o i d r e ac ti o ns P ul m o n ar y v as oc o ns tr i ct i o n N on c a r di og e ni c p ul m o n ar y e de m a

M i l d to m o d er at e s ys te m i c h y po te n si o n fr om ph a r m ac ol o gi c s i d e- e ff ec t s i s al m o s t al w a y s th e r ea c ti on s e e n w h e n pr o ta m i n e i s gi v e n r ap i dl y o r i s gi v e n t o p at i e n ts w h o ar e r el a ti ve l y hy p ov ol e m i c a nd v a so co n st r i c te d. Be c a u s e i t c an be el i c i t e d i n m o s t pa ti e nt s , i t i s c l a s s i fi ed as a ph a r m ac o l o gi c s i d e - e ff e c t , n ot a n i d i os y n c r a ti c r ea c ti on . T hi s s i d e- e ff ec t i s p os si b l y m e di at e d by hi s t a m i ne an d i s c h a r a c t e r i z e d b y v en od i l a ti o n, r e du c ed c a r d i a c f i l l i n g p r e s s ur e s , a n d d ec r e a s e d v as c u l ar r e si st a nc e. M i l d c a r d i a c d e pr es s i o n b y pr o ta m i n e i s s u gg e s t ed bu t p r o b ab l y do es no t o c c ur . T hi s t y p e o f h y p o t e ns i o n c an be c o r r e ct ed b y r a p i d v o l u m e ad m i n i s tr a ti on fr om a C P B p um p a nd ph en y l e p hr i n e i n 0 .1 - m g i nc r e m en ts . T he r e ha v e b ee n m an y a t t em p ts t o m od i fy t h e hy p ot en s iv e

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r es po n s e ( e .g ., i n tr a ao r t i c or l e ft a t r i al ad m i n i s tr a ti on , p r o t am i n e p r e t r e at m en t) , w i t h l i t tl e e v i d en c e of p r ed i c t ab l e s u c c e s s . O nl y s l o w e r r at e s of i n tr av e no u s i nf us i on o v er 5 to 1 0 m i n u te s a nd si m u l t a ne o us m a i n te n an ce of a n a d eq u at e b l o od v o l u m e ha v e b ee n s ho w n to d e c r ea s e t he i n c i de n c e o f h y p o t e n s i on . A na ph y l a c t i c or an ap h yl a ct oi d r ea c ti on i s u n co m m on an d r ar e l y s e en i n i nf a nt s a nd c h i l dr e n. T h e r e a c t i o n v ar i es f r om m i l d s k i n f l u s hi ng an d u r t i c a r i a t o s ev er e v as c ul ar c o l l a ps e. Sy st e m i c hy p ot e ns i o n i s u su al l y ac co m pa n i e d b y l o w p ul m on ar y a r t e r i al pr es s u r e a nd l o w r i g ht - s i d e d a n d l e ft - s i d e d f i l l i ng p r e s s u r e s . T h i s t y pe o f h yp o te n si on m a y b e tr e at ed an d p r e v en te d w i t h r ap i d v o l um e i nf us i on a n d a dm i n i s t r a ti o n o f v a s o c on s tr i c t o r s , a n ti hi s t a m i n es , a nd s te r o i ds . D i a be t i c P.191 p at i e n ts t a k i ng N P H i ns ul i n m a y d ev e l o p a nt i b o di e s to pr ot a m i ne an d w ou l d ap p ea r t o be at i n c r ea s ed r i s k . H ow ev e r , c l i n i c al r e a c t i o ns do n o t p r e di c t a bl y o c c ur i n t h es e p at i e n ts . S us pe c te d c r o ss - se ns i ti vi ty i n c a se s o f fi s h al l er gy or a u to s e n s i ti z at i o n i n m en a f te r v as ec t om y d o no t s ee m t o p ut m o s t p a ti en t s at i nc r e a s e d r i s k . C at as t r o ph i c pu l m o na r y hy p er te n si on oc cu r s i n ap pr o xi m a t el y 0 .2 % t o 4. 0 % o f pa t i e nt s . T h e r e a r e s e v e r al - f o l d i n c r ea s es i n P A p r e s s u r e l e ad i n g t o r i g h t v en tr i c u l a r f ai l u r e, e l ev a te d C VP , l o w f l o w a cr o ss t h e pu l m o na r y c i r c u i t , a nd l o w l e f t a tr i a l p r e s s u r e . E l e v a t ed p l as m a l e v e l s of C 5 a a na p hy l a t ox i n s a nd t hr om b ox an e a r e r e sp o ns i b l e fo r p u l m on a r y v as o co n st r i ct i on a n d a c c om p an i e d b r o n c h o c o ns t r i c t i o n . T r e at m e n t w i t h i s o pr ot e r e no l , m i l r i no ne or a m ri no n e is r ea s o n ab l e ; e p i n ep h r i ne i n 0 . 1- m g i n cr e m e nt s h as be en su cc e s s fu l l y u s ed . I f s e v er e h y p ot e ns i o n p e r s i s ts , t he pa t i e nt s h ou l d be he p ar i n i z e d a ga i n an d r et ur n b ac k o n b y p as s t o m ai nt a i n c i r c ul a ti on . A r e ce nt st ud y h as s h ow n t ha t l ef t v en t r i c u l ar i n f u s i o n of pr ot a m i ne pr ov i de s n o pr o te c t i on f r om p u l m on a r y h y p er t en s i o n an d t h at h i st am i ne a n d pl a te l e t - a ct i va ti n g fa c to r s ar e n ot i n v o l v e d i n ac ut e p u l m on a r y v a s o c o n s t r i c t i on . T he r e f or e , an ti h i s ta m i n es an d s te r o i ds m ay n o t be ef fe c ti ve i n p r ev en t i n g t hi s r ea ct i on . H ow ev e r , i t h as be en s h o w n t h at t h e r a t e of i n tr a v e no u s pr o ta m i n e i n f us i o n i n s he e p i s an i m p o r t a nt f a ct or i n th e g en e r a t i o n o f su f fi ci en t m ed i at o r s r eq u i r ed to i n i t i a t e a c ha r a c te r i s ti c p hy s i o l o gi c r es p on s e , i nc l ud i n g p u l m on a r y v a s o c o n s t r i c t i on a n d t hr om b ox an e B 2 ge n er a ti on . S l o w i n g t he r a te o f p r o t am i n e i nf u si on r e su l ts i n a p r op or t i o na l a tt e nu a ti on of t h e r e s po ns e ( F i g s . 7 . 10 a n d 7 .1 1) . I n c o n c l us i on , t he t r ea tm e nt o f h yp o te n si on af te r p r o t am i n e a dm i ni s t r a t i o n d ep e nd s o n p ul m o n ar y a r t er i a l p r e s s u r e . H y p o te n s i on w i th l o w pu l m o n ar y ar t er i a l p r e s s u r e m a y be c o r r e ct ed w i th r a pi d v ol u m e i nf u si on an d v as o c o ns t r i c t o r s , a nd h y po te n s i on w i th hi gh pu l m o na r y ar te r i a l p r e s s u r e s h ou ld be tr ea t ed w i th i no tr o pe s t ha t h av e a v a so di l at i n g e ff e ct . T he o n l y e f fe ct i ve p r ev en t i o n i s a s l o w i nf us i on o f d i l u te d p r o t a m i n e s ol ut i on . P.192 R ec en t l y Y a ng d e v e l op ed a r e a ct or de vi c e co n ta i n i ng i m m o bi l i z ed pr ot a m i ne ( d ef i ne d a s a p r o t am i n e b i o r ea c t o r ) t h at c a n be pl ac e d o n t h e d i s t al e n d of th e e x t r a c or po r ea l C PB c i r c ui t. T h e p r o ta m i n e b i o r e a ct or bi nd s a n d s e l ec ti v e l y r e m ov es he p ar i n i n t he ex t r a c o r p o r e a l de v i c e b ef or e i t i s r e tu r ne d t o t he p a ti en t . T he d e v i c e s u c c e s s fu l l y p r e v en t s pr o ta m i n e- i n d uc ed co m p l i c at i on s i n do g s . I t i s h op ed th a t i n t h e n ea r f ut ur e , th e d ev i c e c a n b e us e d c l i n i c a l l y t o r em ov e h ep a r i n w i t ho ut ad m i n i s tr a ti on of p r ot am i ne t o t he pa t i e nt s .

Figure 7.10 Plasma thromboxane B2 concentrations before and after administration of protamine infused over 3 seconds, 30 seconds, 300 seconds, and 30 minutes. Heparin is injected at 5 minutes; protamine infusion is started at 0 minutes. Data points represent mean SE values; n = 6 in each group (p <0.05 from unheparinized group). (From Morel DR, Costabella PMM, Pittet JF. Adverse cardiopulmonary effects and increased plasma thromboxane concentrations following the neutralization of heparin with protamine in awake sheep are infusion rate-dependent. Anesthesiology 1990;73:415424, with permission.)

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Figure 7.11 Pulmonary hemodynamics before and after administration of protamine infused over 3 seconds, 30 seconds, 300 seconds, and 30 minutes. Heparin is injected at 5 minutes; protamine infusion is started at 0 minutes. Data points represent mean SE values; n = 6 in each group (p <0.05 from unheparinized group). (From Morel DR, Costabella PMM, Pittet JF. Adverse cardiopulmonary effects and increased plasma thromboxane concentrations following the neutralization of heparin with protamine in awake sheep are infusion ratedependent. Anesthesiology 1990;73:415424, with permission.)

C ol em a n R N . H um o r a l m e d i a to r s of ca ta s tr op h i c r e ac ti o ns a s so c i a te d w i t h p r o ta m i n e n eu t r a l i z a t i o n. An e s t he s i o l o g y 19 8 7; 6 6: 59 5 5 9 6. G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 8 0 48 8 . P.193 H ab az e tt l H , C o n z e n P F , V o l l m a r B , et al . P ul m o n ar y h yp er t en s i o n a ft er h e pa r i n - p r ot am i n e : r o l es o f l ef t - s i d e d i n f us i o n , h i s ta m i n e an d p l at el e t ac t i v at i on f ac to r . An e s t h A na l g 19 9 0; 7 1 :6 37 63 7 . K i e n N D , Q u am D D , R e i t a n JA , e t a l . M e ch an i sm o f h yp o te ns i on fo l l o w i ng r a pi d i nf u s i on of p r ot am i ne s u l f at e i n a ne s t h et i z e d d og s . J Ca rd i ot h or ac Va sc A ne s t h 1 99 2 ;6 : 14 3 1 47 . M or el D R , C o s ta be l l a P M M , P i tt et JF . Ad v er se ca r d i op ul m on a r y e ff e c t s a nd i n c r ea s ed pl as m a th r o m bo x an e c on c e n t r at i on s f ol l o w i n g t he ne ut r al i z a ti on of h ep a r i n w i t h pr o ta m i n e i n aw ak e s he e p a r e i n fu si o n r a t e- de p en d en t. An es t he s i o l o g y 19 9 0; 73 : 41 5 4 24 . S pi es s B D , H o r r ow J, K a pl an JA . T r a ns f us i o n m ed i ci ne an d c oa g ul at i on d i s o r d e r s . I n: K a pl an J A , R ei c h D S N , La k e C L , e t al . e ds . K ap l an ' s c a r di ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :9 6 0 96 5 .

C.III-5. What are the indications for intraaortic balloon pump (IABP)?
I AB P i s pr i m a r i l y us ed fo r p um p f ai l u r e an d m yo c ar di a l i s c he m i a t ha t a r e no t r es po n s i v e to m a x i m a l p ha r m a c o l og i c s u pp o r t . T h e i n di c a t i o ns i n c l u de t h e f ol l o w i n g:

I s c he m i c h e ar t d i s ea s e

C ar di o ge ni c s ho c k A c u te m y oc a r d i a l i nf a r c ti on co m p l i c at e d b y

M ec ha n i c al de fe c ts : v en tr i cu l a r o r se p ta l r up t ur e, a c ut e m i t r a l i ns u ff i c i en c y , o r v e n tr i c u l a r a ne u r y s m C on ti n ue d i sc he m i c p a i n a n d e xt en s i o n o f i n f ar c t i on R ef r a c to r y v e nt r i c ul ar ar r h y th m i a s

D ur i n g c ar d i a c ca t he t er i z a ti on U nd er g oi ng no n ca r d i ac s u r g er y F ai l e d P T C A a nd aw ai t i n g C AB G

C ar di a c s u r g e r y

B ef or e C PB an d p os to p er a ti ve l y A ft er C P B: l o w ou t pu t s yn d r o m e

P ul s a t i l e C PB . R a r e

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P ed i a t r i c c o n ge n i t al he a r t d i s e as e. R a r e N eu r o s ur ge r y. T em p or ar i l y i n cr ea s es t o ta l c er eb r al b l oo d f l o w i n s p e c i fi c c i r c u m s t an c es .

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :1 3 5 13 6 . S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 03 4 1 03 9 . S k u ba s N , L i c ht m an A D , Sh a ar m a A, e t a l . An es t he si a f or ca r d i ac s u r g er y . In : B ar as h P G, C u l l e n BF , S to e l t i n g R K, ed s . C l i n i c a l a ne s t h es i a , 5 t h ed . P hi l a d el ph i a: L i pp i nc ot t W i l l i a m s & W i l k i n s , 20 0 6: 92 3 .

C.III-6. What are the principles of IABP?


I AB P c ou nt e r p ul s at i o n i s d es i g n ed to i n cr ea s e th e m yo c ar di a l ox y ge n s up p l y d u r i ng di as t ol e a nd t o d ec r ea s e m y oc a r d i a l o x y g en de m a n d du r i n g s y s to l e ( F i g. 7 . 12 ) . T h e b al l o o n i s i n f l a te d d ur i ng d i as to l e to i n cr e as e t he d i as to l i c a o r t i c pr es s ur e, r e s u l ti ng i n i n c r ea s ed c o r o na r y bl o od f l ow . T he b a l l oo n s h ou l d b e i n f l a te d i m m e di at e l y f o l l ow i ng t h e cl o su r e of t h e ao r ti c v al ve at t h e di c r o ti c n ot c h of ar te r i a l t r a c i ng . T he ba l l o on i s d e f l at e d j u s t be f or e t he n e x t s y st ol e t o de c r e as e t he P.194 i nt r a a or ti c p r e s s u r e a n d a ft er l oa d, r e su l ti ng i n d e cr ea s ed m y oc ar d i a l o x y ge n c o ns um p ti on . T he c a r d i ac o u tp ut i s i n c r ea s ed b e c a u s e o f i nc r e a s e d c or o na r y p er fu s i o n ( di as t ol i c au gm e nt at i on ) a nd de cr e as ed r e si s ta nc e ( s y s t o l i c u nl oa d i n g ) .

Figure 7.12 The function of the intraaortic balloon pump (IABP). In this patient with an IABP in place, the velocity (vel) of the blood flow, as it exits the left ventricle (LV), is recorded. The arterial waveform is shown in the following text. The IABP is set on a 1:2 ratio, that is, it inflates every other beat, in diastole (asterisk). The velocity (and the amount) of blood exiting the LV is increased (arrow) after the diastolic inflation of the IABP, because the LV is ejecting against lower systemic resistance. This is the reason, that the systolic arterial pressure following IABP inflation is lower (down arrow).

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :1 3 5 13 6 . S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 03 4 . S k u ba s N , L i c ht m an A D , Sh a ar m a A, e t a l . An es t he si a f or ca r d i ac s u r g er y . In : B ar as h P G, C u l l e n BF , S to e l t i n g R K, ed s . C l i n i c a l a ne s t h es i a , 5 t h ed . P hi l a d el ph i a: L i pp i nc ot t W i l l i a m s & W i l k i n s , 20 0 6: 92 3 .

C.III-7. What are the complications of intraaortic balloon pump (IABP)?


I s c he m i a o f t he l e g D i s s e c t i on o f t h e ao r ta T h r om b us f o r m at i o n a n d em b ol i z a ti on R en al ar te r y oc cl u si on S pl en i c , m e s e nt e r i c, a n d s pi na l c or d i nf a r c ti o n P.195

I nt er n al m a m m ar y o cc l u s i o n T h r om b oc y t o pe ni a I nf ec t i o n G as e m bo l i z at i o n I na bi l i t y to pl a ce t h e IA B P R et r o p er i t o ne al bl ee d i n g A r t er i a l v e no us fi st u l a

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :4 3 5 44 2 .

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K ap l a n J , e d. C a r d i a c a ne s th e si a , 4t h e d. P h i l ad e l p h i a : W B Sa u nd er s , 19 9 9: 12 0 1 1 20 2 . S ha ne w i s e J S, H i ne s R L, K a pl an JA . D i s co n ti nu i ng c a r d i o p ul m o n ar y b y p a s s . In : K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s ca r di ac an es t he si a , 5 th e d . Ph i l a d el ph i a: E l se vi e r Sc i e n ce , W B Sa u nd e r s , 2 00 6: 1 03 6 1 03 8 . S k u ba s N , L i c ht m an A D , Sh a ar m a A, e t a l . An es t he si a f or ca r d i ac s u r g er y . In : B ar as h P G, C u l l e n BF , S to e l t i n g R K, ed s . C l i n i c a l a ne s t h es i a , 5 t h ed . P hi l a d el ph i a: L i pp i nc ot t W i l l i a m s & W i l k i n s , 20 0 6: 92 3 .

C.III-8. Can pulmonary artery occlusion pressure (PAOP) represent left ventricular end-diastolic volume (LVEDV) after coronary artery bypass grafting (CABG)?
I t ha s b ee n d e m o ns t r a te d t ha t i n n on su r gi ca l p at i en ts , t he r e w a s a s i gn i f i c a nt c o r r e l a ti o n be t w e e n c h a ng es i n P A OP a n d L VE D V . H ow e v e r , i n p a ti en t s d ur i n g t he fi r s t f ew h o ur s a ft e r C A BG th e r e w as a po o r co r r e l a t i o n b et w e e n c ha ng e s i n PA OP an d L VE D V. T h e po o r c o r r e l a t i o n w as n o t ex p l a i n e d b y c ha ng e s i n s y s t e m i c o r pu l m o na r y va s cu l a r r es i s t an ce . T he al te r ed v e nt r i c ul ar pr es s ur e v ol um e r el a ti on m a y r ef l e c t ac u te c h an ge s i n v en tr i c u l a r c om pl i an c e . A l t h ou gh m e a su r e m e n t o f PA O P r e m a i ns v a l u a bl e i n c l i n i c a l m an ag e m e n t to av oi d p ul m on ar y e de m a, i t c an n ot r e l i ab l y b e us e d as an i n de x o f l ef t v en tr i c u l a r p r e l o a d w hi l e at te m p t i n g t o o pt i m i ze s tr o ke v o l u m e . T EE c a n a c c ur a te l y as s e s s LV E D V a n d c a r di ac c o nt r ac ti l i t y . H ar s e n R M , V i qu e r a t C E , M at t ha y M A, e t a l . Po or co r r e l a ti o n be t w e en pu l m o na r y ar te r i a l w ed ge pr es s ur e a nd l e f t v e nt r i c ul ar en d - d i a s to l i c v ol um e a f t e r c or on a r y a r te r y b y pa s s gr a ft s ur g er y. An es t he si o l o g y 19 8 6; 64 : 76 4 7 70 . R ei c h D L , M i t tn ac h t A, Lo n do n M , et al . M on i t o r i ng of t h e he a r t a n d v a s c u l a r s y s t em . I n: K a pl an J A , R ei c h D S N , L a k e C L , e t al . e ds . K ap l an ' s c a r di ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :3 9 9 40 1 .

D. Postoperative Management D.1. What are the postoperative complications?


C ar di o v a s c u l a r . C o ng e st i v e h ea r t fa i l u r e , a r r hy t hm i a s , l o w o ut p ut s y nd r o m e, m y oc ar d i a l i s c he m i a o r i nf ar c ti on du e t o s ur gi c a l m an i pu l at i o n , pr o l o ng e d C PB a n d ao r ti c c r o ss - c l am p ( co r o n ar y i s c he m i a ) , u s e of c a r d i op l e g i c s o l u ti o n, a n d o c c l u s i o n o r k i n k i ng of g r af ts P ul m o n ar y . Pu m p l u ng or a d ul t r es pi r at or y d i s tr e ss s y nd r o m e du e t o t he fo l l o w i ng :

D ec r e a se d b l o od fl ow to t h e l u n g d ur i n g t ot a l C P B C ol l a p se d a l v eo l i du r i n g C PB , r es ul t i n g i n de c r e as e d s u r fa c t a nt a n d d ec r e a s e d d i s te n s i bi l i t y P.196

F l u i d ov er l o a di n g H y p er o xi a d ur i n g C PB L ef t v en tr i cu l a r f ai l u r e M i c r o em b ol i

R en al

P ol y u r i a f r o m h e m o di l u t i o n a nd di ur e ti cs O l i gu r i a f r o m h yp o pe r fu si o n

H em or r h a ge

T oo m u ch o r t oo l i tt l e pr ot a m i ne to r e ve r s e h e pa r i n T hr om b oc yt o pe ni a a nd de c r e as e d co a gu l a t i o n f ac t or s D i s s e m i n at e d i n t r a va s cu l a r c oa g ul op a th y P oo r s ur gi c al h e m o st a si s

E m b ol i s m . D u e t o a i r , d es tr o ye d o r ag g r e g at ed fo r m e d bl o od e l em en t s , f a t, e n do g en o us a n d ex o ge n ou s d eb r i s N eu r o l og i c . F un c ti on a l ch a ng e s i n b e ha v i o r , pe r s o na l i t y, o r o th e r br a i n f u nc ti o ns ; c e r eb r a l e m b o l i s m H y p er g l y c e m i a . D u e t o i nc r e a se d c at e ch ol a m i ne l e ve l s H y p op o ta s s e m i a. D u e t o he m od i l u ti on an d d i u r et i c s

G r a v l e e GP , D av i s R F , K ur us z M , et al . C ar di o pu l m o na r y by pa s s , p r i n c i p l e s a nd p r ac ti c e . P h i l ad e l p h i a : L i p pi n c o tt W i l l i a m s & W i l k i ns , 2 00 0 :3 8 2, 4 0 3, 5 0 6, 6 28 62 9. L ev y J H , T an a k a K, B a i l ey JM , et al . P os to p er a ti ve c a r d i o v as cu l ar m a na g em en t . In : K ap l an J A , R e i c h D S N , L a k e C L , et al . e ds . K ap l a n 's c a r d i ac a ne s t h es i a , 5 th ed . P hi l ad el p hi a: El se v i e r S ci en c e, W B S au n de r s , 2 00 6 :1 0 61 1 0 86 .

D.2. Would you reverse the muscle relaxants? Why?


N o. M u s c l e r e l a x a n ts a r e u su al l y no t r ev e r s ed . W he n e ar l y ex tu b at i on ( f as t- tr a c k ) i s pl a nn ed , p an c ur o ni um i s g i v e n 0 . 1 m g/ k g fo r i nt u ba t i o n a nd 0 . 05 t o 0 . 1 m g/ k g at t h e i n i ti at i on o f C PB . P at i en ts sh ou l d sp o nt a ne ou s l y r e c o v e r f r o m t he e f fe c t of m u s c l e r e l a x an ts 2 to 3 ho u r s a f te r s ur ge r y . W e d i s c o u r a g e t h e u se o f l a r ge d o s e s o f l o n g- ac t i n g m us cl e r el a xa nt s w hi c h m a y c au s e r e c ur ar i z a ti o n ev e n af t er r e v e r s a l w i t h ne o s t i g m i n e. M o r e ov e r , r e v e r s a l w i t h at r o p i n e a nd n eo s t i gm i n e m ay c a us e s ev e r e t a ch yc a r d i a or b r ad yc a r d i a i n c a r d i a c p at i en ts .

D.3. When will you wean the patient from the respirator?
G en er a l l y , th e p at i e n t i s w e an e d fr o m th e r es p i r at o r th e f ol l ow i n g m or n i n g a ft er s u r g e r y . I f th e o pe r at i v e c ou r s e i s s m o ot h a n d i f th e p at i e n t ha s g o od v en tr i c u l a r f un c ti on , t he pa ti e nt m a y be w e an e d f r o m th e r es p i r at o r ea r l y , u s u al l y 2 t o 6 h ou r s af te r s ur g er y . E ar l y tr ac he a l e x t ub a ti on ( f as t - t r a ck ) a ft e r C A B G su r g e r y h a s c o s t be n ef i ts a n d i m p r o v e s r es o ur c e u s e w he n c om pa r ed w i th l a te t r ac he a l ex t ub a t i on . E ar l y t r a c h e al e x tu ba t i o n 1 t o 6 h o ur s a ft er su r g e r y r ed u ce s t ot a l co s t pe r C AB G s ur ge r y by 25 % w i t ho u t i n c r e as i ng t h e r a t e o r c o s t s o f c om pl i c a ti o ns i n p at i en ts y ou ng e r th a n 7 5 y e a r s . C he ng D C , H av s k i J , Pe n i s to n C , e t al . E ar l y tr a ch ea l e xt u ba ti o n a ft er c o r o n ar y ar t er y g r a ft s u r g e r y r ed u c e s c os t s an d i m p r o v es r e s o u r c e us e .

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A ne s t h es i o l og y 1 99 6 ;8 5: 1 30 0 1 31 0 . H i g gi n s T L , Y ar e d J- P . Po s to pe r at i v e r es p i r at o r y c ar e . In : K ap l an J A , R e i c h D S N , L a k e C L , et al . e ds . K ap l a n 's c a r d i ac a n es t h e s i a , 5t h e d. Ph i l a de l p h i a : E l s ev i er S c i e nc e , W B S a un d er s, 20 06 : 10 9 7 10 9 9. P.197

D.4. What criteria would you use in deciding when to wean the patient from the respirator?

C on s c i ou s n e ss a w ak e a nd al er t S ta bl e v i t a l si g ns A c c ep t ab l e ar te r i a l b l o od ga se s p H , 7. 3 5 to 7. 45 ; P O 2 , ov e r 80 mm H g w i t h F IO 2 , 0 . 4; P C O 2 , 35 t o 4 5 m m H g A c c ep t ab l e r e sp i r a to r y m e ch a ni c s

V i t al c a pa c i t y g r e at e r th a n 10 to 1 5 m L/ k g M ax i m al i n sp i r a to r y fo r ce g r ea te r t ha n 2 0 t o 25 cm H 2 O

H em os t as i s l e ss t h an 1 0 0 m L pe r h ou r o f c he st tu be dr ai n ag e S ta bl e m et a bo l i c s ta t e no r m a l t em pe r at ur e a nd el ec t r o l y t es

W h e n t he p a ti en t c a n sa t i s fy t h e ab o ve cr i t er i a, t h e pa t i e n t i s p u t o n c o n ti nu o us p o s i ti v e ai r w a y p r e s s u r e ( C P A P) o f 5 c m H 2 O w i t h 5 0% ox y g e n. I f t he p at i e n t to l er at e s th e C PA P w el l f or 30 m i nu te s a nd ar te r i a l b l o od ga s es a r e ac c ep ta b l e , t he p a ti e nt i s e x t u ba te d . H i g gi n s T L , Y ar e d J- P . Po s to pe r at i v e r es p i r at o r y c ar e . In : K ap l an J A , R e i c h D S N , L a k e C L , et al . e ds . K ap l a n 's c a r d i ac a n es t h e s i a , 5t h e d. Ph i l a de l p h i a : E l s ev i er S c i e nc e , W B S a un d er s, 20 06 : 10 9 7 10 9 9.

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Chapter 8 Valvular Heart Disease


Gregg S. Hartman Stephen J. Thomas

A 78-Year-Old Man
w as ad mi tted with i ncre asi ng s hortn ess o f breath. He had chest pa in in the past but w as ab le to co nti nue wi th normal activities . He had passed out tw ice in the p ast ye ar. O n p hysi cal exa mi na tio n, a lo ud sys tol ic mur mur coul d be h ear d at th e l eft ste rnal b ord er r adi ati ng to the ne ck. Hi s vita l s ig ns we re: blo od p ressu re 1 50/9 0 mm Hg , hea rt rate 88 be ats per minute and ir regular. The electrocardiogra m (ECG) showed sinus r hythm wi th a tr ia l p rematu re co ntra ctio ns a nd l eft v entri cu la r hyp ertr oph y (LVH) w ith str ai n. A tra nstho raci c e choca rdi o gram sho wed a hyp ertr oph ie d left ve ntricle (L V) an d D opp le r exa mi na tio n de mo nstra ted sever e ao rtic sten osis (AS) with a g rad ient o f 64 mm Hg, mild aortic insufficiency (AI), and moderate mitral r egurgitation (MR). He was sc hed uled fo r ao rti c val ve r epl ace me nt (AVR) a nd possi bl e mi tral va lve (MV) repa i r or mi tral val ve repl a cement (MVR).

P.199

A. Medical Disease and Differential Diagnosis A.1. What are the major etiologies of AS, AI, MS, and MR?
AS occurs as a congenital lesion but more commonly as an acquired disease. Stenosis may develop on a previously normal valve following rheumatic fever (RF) or from progressive calcification. Congenitally bicuspid valves are also prone to calcification with eventual stenosis. Calcification of the leaflets can result in incomplete closure of the valve with associated insufficiency. AI is usually an acquired disease. The most common causes include bacterial endocarditis and rheumatic heart disease. Annular dilation may result from diseases such as cystic medial P.200 necrosis and collagen disorders or following aortic dissections with resultant insufficiency. When occurring as a congenital lesion, aortic insufficiency (AI) rarely occurs in the absence of other cardiac abnormalities. Mitral stenosis (MS) is almost always caused by rheumatic fever (RF), although only half of patients will have a history of an acute febrile illness. The inflammatory process of RF results in thickening of the leaflets and fusion of the commissures. Other rare causes include congenital stenosis and other systemic diseases including systemic lupus erythematosus and carcinoid. Pathophysiology similar to that seen with valvular MS can occur with obstructing left atrial (LA) tumors and cor triatriatum. MS commonly occurs in conjunction with other valvular heart disease; only 25% of patients present with isolated MS; approximately 40% have combined MS and mitral regurgitation (MR). MR can result from defects in the leaflets, the annular ring or the supporting chordae, the papillary muscles, or any combination of these. Primary leaflet dysfunction occurs with RF but can also follow bacterial endocarditis, connective tissue disorders, and congenital malformations. Annular dilation can follow ventricular dysfunction and left ventricular dilation.

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MV prolapse and/or rupture of papillary muscles results in incomplete leaflet closure or coaptation with resultant MR. Left ventricular ischemia can affect papillary muscle contraction and is the cause of postischemic or postinfarction MR. Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Schoen FJ. Cardiac valves and valvular pathology: update on function, disease, repair, and replacement. Cardiovasc Pathol 2005;14(4):189194. Thys DM, Hillel Z, Schwartz AJ, eds. Textbook of cardiothoracic anesthesiology. New York: McGraw-Hill, 2001:589629.

A.2. What are the major changes in the loading of the left ventricle (LV) that result from the four different lesions? Why do they occur? What changes result from them?
Aortic stenosis (AS) represents a chronic systolic pressure load on the LV. This elevation increases wall tension in accordance with Laplace's law.

The ventricle undergoes parallel duplication of muscle fibers in an attempt to compensate for the increase in tension. This results in increased wall thickness or concentric (common center) hypertrophy and some decrease in radius thereby normalizing wall stress. If the MV remains competent, the major pressure overload occurs in the LV and little change in the other cardiac chambers results. AI causes left ventricular diastolic volume overload resulting in eccentric (away from the center) hypertrophy and left ventricular dilation. Compliance, the relation between volume and pressure is altered only slightly because both end-systolic and end-diastolic volumes increase. Some concentric hypertrophy occurs as well secondary to the increase in wall stress resulting from an increase in left ventricular radius. The aortic diastolic pressure is lower with AI. Remember, the diastolic pressure is the pressure that must be exceeded by the work of the LV to open the aortic valve and result in ventricular ejection. Therefore, the increased volume work required to eject the additional blood (which flowed into the LV across the incompetent aortic valve during diastole) is reduced because the work can be performed against a lower outflow impedance (lower diastolic pressure). Stroke volume (SV) and ejection fraction (EF), therefore, may be preserved P.201 until late in the disease process. As with aortic stenosis (AS), the presence of a competent MV c o n f i n e s t h e c h a n g e s t o t h e L V . H ow e v e r , t h e l e f t v e n t r i c u l a r d i l a t i o n t h a t f o l l o w s c h r o n i c A I m a y result in mitral annular dilation or alteration in chordae tendineae geometry with resultant mitral

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regurgitation (MR). Left atrial (LA) enlargement secondary to MR can, therefore, occur. It may also occur because of LA pressure overload as left ventricular end-diastolic pressures (LVEDPs) rise in the course of aortic insufficiency (AI). Mitral stenosis (MS) results in a chronically underfilled left ventricle (LV) because of progressive obstruction to LA emptying. This chronic underloading condition can result in decreased left ventricular thickness and diminished contractile function (a disuse atrophy of sort). In addition, if the cause of the MS is rheumatic, myofibril damage may have occurred. Although the LV is pressure and volume underloaded, the left atrium is both pressure and volume overloaded. To maintain flow across the progressively narrowing mitral orifice, the pressure in the left atrium must be correspondingly increasing. Gorlin's equation for pressure gradient follows.

It would predict that the pressure gradient increases by the square of any increase in flow rate or decrease in valve area. The elevations in LA pressure leads to hypertrophy and eventually dilation that predisposes to premature atrial contractions and subsequently atrial fibrillation. The loss of atrial contraction further diminishes forward flow across the stenotic mitral valve (MV). The elevations in LA pressure limit pulmonary venous flow with consequent pulmonary engorgement. The pulmonary vasculature undergoes reactive changes including intimal fibroelastosis inducing irreversible elevations in pulmonary vascular resistance. Right ventricular (RV) failure may develop because this chamber is poorly equipped to deal with the elevations in afterload (e.g., pulmonary hypertension). RV dilation combined with increased RV systolic pressures leads to tricuspid regurgitation. MR results in volume overload of the LV. The outflow of the LV is divided between the highpressure/ low-compliance outflow tract of the arterial tree and the low-pressure/highcompliance outflow route across the incompetent MV into the left atrium. Although the volume work of the LV is increased, the high-compliance outflow route permits a large portion of this work to be performed at a low pressure; therefore, left ventricular wall tension is minimally increased if increased at all. As with AI, the volume overload results in marked left ventricular dilation and eccentric hypertrophy. In contrast, however, the left atrium is also volume overloaded and undergoes dilation. When the volume overload occurs slowly, the left atrium enlarges and minimal rises in pulmonary pressures result despite large regurgitant volumes. In contrast, the occurrence of acute MR, for example, an acute myocardial infarction with papillary muscle rupture, presents the left atrium with a sudden volume overload. Without the time to dilate, the LA pressure rapidly rises limiting pulmonary drainage with resultant pulmonary engorgement. Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures.

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Schoen FJ. Cardiac valves and valvular pathology: update on function, disease, repair, and replacement. Cardiovasc Pathol 2005;14(4):189194. Thys DM, Hillel Z, Schwartz AJ, eds. Textbook of cardiothoracic anesthesiology. New York: McGraw-Hill, 2001:589629. Zipes DP, Libby P, Bonow RO, et al. eds. Braunwald's heart disease: a textbook of cardiovascular medicine, 7th ed. Philadelphia: WB Saunders, 2005:15531615. P.202

A.3. What are pressurevolume (PV) loops? What do the different inflection points represent?
The PV loop analysis (Fig. 8.1) depicts the relation between left ventricular volume and left ventricular pressure during a single cardiac cycle. Opening and closing of the mitral and aortic valves are represented by the inflection points A, B, C, and D, respectively (Fig. 8.1). Moving from points A through D, AB depicts left ventricular filling, BC depicts isovolumetric contraction, CD shows left ventricular ejection, and DA shows isovolumetric relaxation. Point A coincides with opening of the mitral valve (MV) and represents left ventricular end-systolic volume and early diastolic pressure. Point B is closure of the MV and the end of diastolic pressure (LVEDP) and volume (left ventricular end-diastolic volume [LVEDV]). Point C represents the opening of the aortic valve and coincides with systemic, aortic diastolic pressure. Finally, point D is the closure of the aortic valve and represents left ventricular end-systolic pressure and volume, coinciding with the dicrotic notch in the aortic pressure tracing (Fig. 8.1). Left ventricular compliance is the relation between the change in pressure and change in volume of the chamber and is defined by the slope of the filling phase or segment AB. Preload is the PV relation before the onset of contraction (LVEDP). Contractility may be illustrated by the slope of a line called the end-systolic pressurevolume relation (ESPVR). The ESPVR slope is created by connecting multiple points (D) from multiple PV loops generated by changing the filling volume t o t h e l e f t v e n t r i c l e ( L V ) ( Fi g . 8 . 2 ) . I n c r e a s e d c o n t r a c t i l i t y r e s u l t s i n a s t e e p e r l i n e w h e r e a s diminished contractility results in a flatter relation. The PV loop analysis permits illustration of stroke volume (SV) and ejection fraction (EF). SV is defined as difference in volume from the e n d o f f i l l i n g t o t h e e n d o f e j e ct i o n ( E D V E S V ) , w h e r e a s E F i s t h e r a t i o o f s tr o k e v o l u m e ( S V ) t o total volume in the heart at peak P.203 filling (SV/EDV). Therefore, the PV loop analysis permits illustration of the volume-pressure relations and their changes with each of the four valvular lesions.

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Figure 8.1 Normal pressurevolume loop and valve positions. A, mitral valve (MV) opening; B, MV closure; C, aortic valve (AV) opening; D, AV closure; AB, left ventricular filling; BC, isovolumetric contraction; CD, ejection; DA, isovolumetric relaxation.

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Figure 8.2 Contractility. ESPVR, end-systolic pressurevolume relations.

Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Sagawa K, Maugan L, Suga H, et al. Cardiac contraction and the pressure-volume relationship. New York: Oxford University Press, 1988. Thomas SJ, Kramer JL, eds. Manual of cardiac anesthesia, 2nd ed. New York: Churchill Livingstone, 1993:81127.

A.4. What are representative pressurevolume (PV) loops for the four valvular lesions?
The hallmarks of aortic stenosis (AS) illustrated by the PV loop analysis framework are a high left ventricular systolic pressure and an upward and counterclockwise rotation in the enddiastolic PV relation (AB) indicative of decreased chamber compliance (Fig. 8.3). Stroke volume (SV) and ejection fraction (EF) are well preserved, but the ejection phase of the loop occurs at much higher pressures. This is permitted by an increase in contractility of a

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counterclockwise rotation of the end-systolic pressurevolume relation (ESPVR) line. The schematic PV loop for aortic insufficiency (AI) depicts the enlarged left ventricle (LV) of chronic AI. The minimal change in LVEDP despite the large volume overload is seen by the shift in the diastolic PV curve to the right (A'B') (Fig. 8.4). Low systemic diastolic pressures result in a brief isovolumetric phase (B'C') and early complete ejection. The isovolumetric relaxation P.204 phase is absent as the incompetent valve permits regurgitant filling of the LV from the Ao during diastole even before opening of the MV. In contrast, when acute AI occurs, the left ventricular compliance is unchanged. Rapid increases in left ventricular end-diastolic pressure (LVEDP) from volume overload along the unshifted left ventricular diastolic PV curve (AB) rapidly lead to increased left atrial (LA) pressure and pulmonary congestion.

Figure 8.3 Pressurevolume loop of aortic stenosis.

The PV loop of MS illustrates hypovolemia, the cause of which cannot be determined from the loop alone (Fig. 8.5). Because the predominant impact of MS occurs proximal to the LV, the PV analysis format is less useful.

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Figure 8.4 Pressurevolume loops of acute and chronic aortic insufficiency (AI).

P.205

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Figure 8.5 Pressurevolume loops of mitral stenosis.

In mitral regurgitation (MR), the diastolic PV relation (line AB) is shifted to the right, as it is in chronic AI, consistent with amarked increase in compliance (Fig. 8.6). The isovolumetric phase (BC) is nearly absent because the left atrium generally serves as a low-pressure/highcompliance route for ejection because of the incompetent mitral valve (MV). Decreases in contractility are depicted by a decrease in the slope of the end-systolic-PV line (line through D). Nevertheless SV and EF are maintained because of this low-pressure LA vent.

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Figure 8.6 Pressurevolume loop of acute and chronic mitral regurgitation (MR).

P.206 Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Sagawa K, Maugan L, Suga H, et al. Cardiac contraction and the pressure-volume relationship. New York: Oxford University Press, 1988. Thomas SJ, Kramer JL, eds. Manual of cardiac anesthesia, 2nd ed. New York: Churchill Livingstone, 1993:81127.

A.5. Draw the pressure/time curves for the left ventricle (LV), left atrium, pulmonary artery (PA) and aorta (Ao) for normal patient and patients with each of the four valvular lesions
Normal curves are shown in Fig. 8.7. The points A, B, C, and D correspond to the same points in the PV loops.

Aortic stenosis
The additional systolic pressure work of AS can be seen in the left ventricular pressure tracing (Fig. 8.8). Elevations in left ventricular end-diastolic pressure (LVEDP) (point B) can be seen to diminish the perfusion gradient for coronary flow to the LV. The augmentation in left ventricular filling late in diastole secondary to atrial contraction (LA kick from sinus rhythm) is highlighted in the inset. Rising left ventricular diastolic pressures secondary to decreased compliance necessitate elevations in left atrial (LA) pressures to permit complete left ventricular volume P.207 loading. Atrial systole provides this elevation in LA pressure synchronous with elevations in LVEDP while keeping LA pressures relatively low during the remaining cardiac cycle facilitating pulmonary venous drainage.

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Figure 8.7 Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in a healthy individual.

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Figure 8.8 Pressure curves for the left ventricle, left atrium (LA), pulmonary artery, and aorta in patients with aortic stenosis. LVEDP, left ventricular end-diastolic pressure.

Aortic insufficiency
The rapid upstroke and rapid decline of arterial pressure indicate absence of aortic valve closure and low end-diastolic aortic pressure (Fig. 8.9). Elevations in the left ventricular enddiastolic volume (LVEDV) and LVEDP are typical of AI. The early increase in LVEDP can result in left ventricular pressures exceeding those of the left atrium during diastole with resultant premature closure of the MV.

Mitral stenosis
Elevations in pressure are seen in both the left atrial (LA) and pulmonary artery (PA) tracing with mitral stenosis (MS) (Fig. 8.10). The large gradient between LA and left ventricular pressures is highlighted in the inset. Chronic elevation in pulmonary volume induces changes in the luminary vascular bed and leads to pulmonary hypertension.

Mitral regurgitation
The hallmark of MR is the marked elevations of LA pressure during systole and the occurrence of a giant cv wave and elevated PA pressures (Fig. 8.11). P.208

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Figure 8.9 Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in patients with aortic regurgitation. LAEDP, left atrium end-diastolic pressure; LVEDP, left ventricular end-diastolic pressure.

Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 4th ed. Philadelphia: WB Saunders, 1999:727784.

A.6. What are the basic principles of echocardiography? What are M-mode, B-mode and Doppler color modalities? How do transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) differ?
Echocardiography is the use of sound waves to image structures and blood flow within the heart and great vessels. To image tissue, sound waves are emitted from a transducer at known speeds and constant intervals. The sound packets bounce off structures in their path and the reflected sound waves are received at the point of origin, either by a separate receiving crystal or by the same emitting transducer, which spends a portion of its time in this listening mode. The time it takes for the reflected waves to return to the crystal is measured, and because the velocity of sound in tissues is relatively constant, solving for distance can be easily accomplished. Distance = (velocity x time) ( because the distance is traversed twice, once to the object and again on returning.) In this manner, the spatial orientation of cardiac structures can be determined. The strength of the returning signal can be quantified as an amplitude, therefore A or amplitude mode

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P.209 P.210 (Fig. 8.12B). The echo machine codes this amplitude on a black/white scale, thereby converting the amplitude to brightness or B-mode scanning (Fig. 8.12C). Fig. 8.12D shows this ice-pick view through the LV of the heart. Each change in tissue density results in some sound waves being reflected and hence an interface. In this example, bold lines are seen at the epicardial, the endocardial-chamber, the chamber-endocardial, and the epicardial borders. If these amplitude bars are displayed in a real time, a motion or M-mode display results (Fig. 8.12E). These images were difficult to reliably obtain and interpret because the views represent a linear slice without surrounding structural images for referencing. However, if the probe is rocked back and forth repetitively, multiple M-mode images can be obtained in a given instant and, therefore, a two-dimensional image formed. This rapid rocking back and forth of the ultrasound beam is performed electronically in a phased-array transducer. The images derived in this manner appear as a cine-x-ray display of myocardial movement. Therefore, echocardiography can provide information about the size, shape, location, and movement of myocardial structures.

Figure 8.10 Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in patients with mitral stenosis. LAP, left atrial pressure; LVP, left ventricular pressure; MV, mitral valve.

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Figure 8.11 Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in patients with mitral regurgitation. PAP, pulmonary artery pressure.

In addition to determining how long it takes for a given sound wave to return and, thereby, deriving the distance from the transducer, contact of the sound wave packet with the reflecting object (tissue, blood cells, air) will alter the wavelength of the sound packet according to the Doppler principle. When the object coming in contact with the sound wave is moving toward the source of the ultrasound, the reflected ultrasound wavelengths are compressed (shorter) or of higher pitch. The opposite occurs when the contacted object is moving away from the sound source. These shifts in frequency are proportional to the velocity of the contacted structure and, thereby, the speed and direction of the encountered object (usually of blood flow) can be calculated. This velocity information can be displayed on a color map (Doppler color flow) or on a time/velocity scale (spectral Doppler display). Doppler-derived blood flow velocity information can determine laminar and turbulent flow patterns, regurgitant or stenotic lesions, congenital anomalies and can permit quantification of pressure gradients. Using the modified Bernoulli equation (P = 4 v2), determination of a blood flow velocity permits the estimation of pressure gradients. Simply, the greater the velocity of blood flow the higher the pressure gradient. Only the component of blood flow parallel to the Doppler beam will be analyzed. The Doppler equation: V = c (FSFT)/2 FT (cos ), contains the cosine of the angle of incidence between the ultrasound beam and the moving object. Because the cosine of 90 degrees is zero, blood flow that is perpendicular to the ultrasound beam will not have any Doppler shift and, therefore, will not be represented in the color display. For this reason, it is important to choose an ultrasound window in which the expected blood flow direction is most parallel to the ultrasound. TTE uses imaging points or acoustic windows obtained with the transducer hand held on the chest wall. It is simple and importantly noninvasive. Most standard echocardiograms are

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obtained from this position. However, during cardiac surgery, the chest wall is in the sterile field and, therefore, unavailable. The esophagus lies immediately adjacent to the heart outside of the operative field and, therefore, affords an excellent imaging vantage point. In 1976, Yasu Oka from the Albert Einstein College of Medicine developed a practical method of intraoperative imaging. He mounted an ultrasound crystal on the end of a gastroscope and, thereby, obtained images of the heart during surgery. This has been refined considerably since. transesophageal echocardiography (TEE) has become the standard of care for heart surgery at many institutions. The close proximity of the probe to the heart affords excellent resolution. The probe is not in the operative field hence surgery is unhindered and sterility is not an issue. Though mildly invasive, the risk of esophageal injury in the anesthetized state is very low. Intraoperative TEE is beneficial for quantification of cardiac contractility, for determination of the severity of regurgitant and stenotic valvular disease, for the detection of intracardiac shunts and the occurrence of dissections, and as a guide for catheter placement. Perrino AC, Reeves ST, eds. A practical approach to transesophageal echocardiography. Philadelphia: Lippincott Williams & Wilkins, 2003:394. P.211

Figure 8.12 The process of producing the B-mode and M-mode images. A: A pulse of ultrasound is emitted into the object, and the backscattered echo is received by the same transducer. B: The received acoustic signal is converted to the electric signal (A-mode). C: The amplitude is modulated into brightness (B-mode). D: As subsequent pulses of ultrasound are emitted with the sequentially changing angles

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and the obtained one-dimensional B-mode images are compounded according to the direction of each ultrasound emission, the first frame of the sector-shaped image is formed. E: When the ultrasound is repeatedly transmitted in one direction, a series of one-dimensional B-mode images is obtained. As these are arranged against time, an M-mode image is obtained. (From Okay Y, Goldiner PL, eds. Transesophageal echocardiography. Philadelphia: JB Lippincott Co, 1992:12, with permission.) LV, left ventricle; END, endocardium; EPI, epicardium; US, ultrasound; T, time; L, length; M, motion.

P.212 Savage RM, Aronson S, eds. Comprehensive textbook of intraoperative transesophageal echocardiography. Philadelphia: Lippincott Williams & Wilkins, 2005:361.

A.7. What are the three TEE vantage points for the comprehensive imaging of the LV? How are pressure gradients measured by echocardiography? How do the pressure gradients derived from Doppler echocardiography differ from those obtained in the catheterization laboratory by direct pressure measurement?
The heart has two main axes, the longitudinal axis running from the base to the apex and the short axis perpendicular to that. Because the ultrasound beam can be thought of as a twodimensional structure, multiple scan planes are required to completely image a threedimensional structure. The left ventricle (LV) may be divided into 16 segments, 6 at the basal level, 6 at the midpapillary level, and 4 at the apical level (Fig. 8.13). By moving the transesophageal echocardiography (TEE) probe in the esophagus and by rotation of the crystal w i t h i n t h e t r a n s d u c e r t ip , t h e L V c a n b e i m a g e d f r o m t h r e e a c o u s t i c w i n d o w s . T h e s e a r e t h e midesophageal four-chamber, the transgastric short axis, and the transgastric two-chamber view. Normal ventricular motion requires that the wall segment move centrally with systole and similarly undergo thickening along this axis during contraction. Function is usually quantified as normal; mild, moderate, and severe hypokinesis; akinesis; and dyskinesis. In addition to function, TEE permits the determination of wall thickness and chamber size, important parameters in understanding the pathophysiology of valvular heart disease. As mentioned previously, pressure gradients are derived through analysis of the Doppler profiles of blood flow. A commonly determined echocardiography gradient is that which is present from the L V t o t h e a o r t a ( A o ) i n t h e s e t t in g o f a o r t i c s t e n o s i s ( A S ) . T o o b t a i n t h e c h a n g e i n b l o o d f l o w velocity across the aortic valve with TEE, the probe is advanced far into the stomach and sharply anteflexed and left deflected to obtain the window from the apex of the heart (deep transgastric long axis) and align the ultrasound beam most parallel to the path of blood flow. From this window, the continuous wave Doppler cursor is directed across the left ventricular outflow tract and aortic valve. An example of such a spectral Doppler display is seen in Fig. 8.14. The large increase in blood flow velocity in this display occurs at the narrowest point along i t s p a t h , w h i c h i n t h i s c as e i s t h e a o r t i c v a l v e . U s i n g t h e m o d i f i e d B e r n o u l l i e q u a t i o n m e n t i o n e d previously, a gradient is calculated (100 mm Hg in the example). This represents the maximum i n s t a n t a n e o u s p r e s s u r e d i f f e r e n c e b e t w e e n t h e L V a n d t h e A o . A S i s a l s o q ua n t i f i e d a t t h e t i m e of catheterization by measuring the pressures from within the LV and the Ao as a rapid response pressure transducer catheter is withdrawn from the LV back to the Ao across the stenotic valve. The standard reported gradient is the difference between the maximum left ventricular and Ao pressures. Fig. 8.15 illustrates that these peaks are not simultaneous events. Therefore, Doppler-derived AS gradients are usually higher than those derived at the time of left heart

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catheterization. Perrino AC, Reeves ST, eds. A practical approach to transesophageal echocardiography. Philadelphia: Lippincott Williams & Wilkins, 2003:77130. Savage RM, Aronson S, eds. Comprehensive textbook of intraoperative transesophageal echocardiography. Philadelphia: Lippincott Williams & Wilkins, 2005:65102. Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists task force for certification in perioperative transesophageal echocardiography. Anesth Analg 1999;89:870884. P.213

Figure 8.13 Sixteen-segment model of the left ventricle. A: Four-chamber views show the three septal and three lateral segments. B: Two-chamber views show the three anterior and three inferior segments. C: Long-axis views show the two anteroseptal and two posterior segments. D: Mid short-axis views show all six segments at the mid level. E: Basal short-axis views show all six segments at the basal level. (From Shanewise JS, Cheung AT, Aronson S, et al. eds. ASE/SCA

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guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography council for intraoperative echocardiography and the Society of Cardiovascular Anesthesiologists task force for certification in perioperative transesophageal echocardiography. Anesth Analg 1999,89:870884, with permission.)

P.214

Figure 8.14 Continuous wave Doppler across the aortic valve in the deep transgastric apical view from a patient with severe aortic stenosis.

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Figure 8.15 Pressure gradients in severe aortic stenosis are measured during systole as the difference between aortic and left ventricular pressures displayed using a 0- to 200-mm Hg scale. The peak instantaneous gradient is the maximum gradient noted; the peak-to-peak gradient is the difference between peak left ventricular and aortic pressures. The mean systolic gradient is the average of all systolic pressure gradients noted during systolic ejection (TS). (From Nanda NC, ed. Doppler echocardiography. Philadelphia: Lea & Febiger, 1993:130, with permission.)

P.215

A.8. What are the echocardiographic and cardiac catheterization criteria for the four valvular lesions?
The TEE severity scales of the various valvular lesions are summarized in Table 8.1.

Aortic stenosis
Echocardiographic criteria for AS include two-dimensional images demonstrating limited aortic valve opening and motion and left ventricular concentric hypertrophy. Doppler examination will reveal a turbulent, high-velocity jet across the aortic valve and color flow Doppler will demonstrate a turbulent, mosaic-appearing color map. The gradient across the aortic valve measured at cardiac catheterization is different from that measured by echocardiography as mentioned previously. Quantification of this Doppler-derived pressure gradient again relies on the modified Bernoulli equation. Pressure gradient = 4 v2 where v = velocity (m/second), pressure (mm Hg) Because flow is an important determinant of pressure gradients, both these catheterization and Doppler-derived values are interpreted along with cardiac output. Calculations permit the determination of a valve area. Severe AS is present when the gradient exceeds 75 mm Hg

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and/or the valve area is less than 0.8 cm2.

Table 8.1 The Transesophageal Echocardiography Severity Scales of Valvular Lesions. NORMAL 0 MILD 1+ SEVERITY SCALES MODERATE 2+ 3+ SEVERE 4+

MEASUREMENT MS MVA (cm2) Mean pressure gradient (mm Hg) AS AVA (cm2) Peak pressure gradient (mm Hg) MR Jet length/LA length Jet area/LA area Jet area (cm2) Pulmonary vein Doppler

4.06.0 <2

1.52.5 2.06.0

1.01.5 6.012.0

< 1.0 > 12

2.53.5 <10

1.22.0 1634

0.81.1 3575

< 0.8 > 75

< 1/3

1/32/3

> 2/3

< 1/3

1/32/3

> 2/3

0 S wave D wave

<3 Blunting S wave

3.06.0 S<D S D

>6 Systolic reversal of flow

AI Jet width/LVOT 0 < 1/4 1/4 1/2 1/2 2/3 > 2/3

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width Jet length (pressure dependent) 0 to middle of AML to tip of AML to PM beyond PM

AI, aortic insufficiency; AML, anterior mitral leaflet; AS, aortic stenosis; AVA, aortic valve area; LA, left atrial; LVOT, left ventricular outflow tract; MR, mitral regurgitation; MS, mitral stenosis; MVA, mitral valve area; PM, papillary muscle.

P.216

Aortic insufficiency
Catheterization criteria for aortic insufficiency (AI) rely on the qualitative estimation of the regurgitation volume and an estimation of left ventricular size and EF. Similar quantification can be made from Doppler color echocardiography derived data. A commonly used echocardiographic criteria compares the width of the regurgitant jet at the level of the valve to the width of the left ventricular outflow tract. A ratio of greater than 0.66 corresponds with severe AI.

Mitral stenosis
The severity of mitral stenosis (MS) can be obtained by the direct measurement of a diastolic gradient between the left atrium and ventricle at the time of cardiac catheterization.However, this requires a transatrial puncture, a procedure largely replaced by echocardiographic techniques. Echocardiographic diagnosis is based on gradient estimation by Doppler and by measuring the rate of decay in the pressure with the time spent in diastole (pressure half-time). The MV area in cm2 can be derived from an empirical formula wherein the MV area equals 220 divided by this pressure half-time (Hatle constant). Severe MS is present when the end-diastolic gradient exceeds 12 mm Hg corresponding to a valve area of less than 1.0 cm2.

Mitral regurgitation
In the presence of mitral regurgitation (MR), ventriculography will demonstrate the reflux of dye from the LV into the left atrium. Severe MR is diagnosed when dye refluxes into the pulmonary veins. Color Doppler echocardiography permits similar quantification. Estimation relies on an estimation of regurgitant jet volume as compared with the left atrium and through analysis of pulmonary venous flow profiles. In every case, color Doppler echocardiography is often useful in identifying the cause of the valvular lesion, its extent of involvement within and around the valve, and the associated hemodynamic changes. Therefore, for many valvular lesions, it may be sufficient for the diagnosis. Catheterization, however, is often performed to assess the presence of concomitant coronary artery disease, especially in patients of advanced age. Quinones M, Otto C, Stoddard M, et al. Recommendations for quantification of Doppler echocardiography: a report of from the Doppler quantification task force of the nomenclature and standard's committee of the American Society of Echocardiography. J Am Soc Echocardiogr 2002;15:167180.

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Schoen FJ. Cardiac valves and valvular pathology: update on function, disease, repair, and replacement. Cardiovasc Pathol 2005;14:189194. Weyman AE, ed. Principles and practice of echocardiography, 2nd ed. Philadelphia: Lea & Febiger, 1994:391574. Zipes DP, Libby P, Bonow RO, et al. eds. Braunwald's heart disease: a textbook of cardiovascular medicine, 7th ed. Philadelphia: WB Saunders, 2005:15531615.

B. Preoperative Evaluation and Preparation B.1. What are the presenting signs and symptoms of the four valvular lesions listed previously?
See Table 8.2. P.217

Table 8.2 The Signs and Symptoms for the Various Valvular Lesions. LESION AS AI Chronic Acute MS MR Chronic Acute DOE, PND, AFib Severe pulmonary edema, CHF Fatigability, dyspnea Severe pulmonary edema, CHF Pulmonary congestion, AFib SIGNS AND SYMPTOMS Angina, syncope, dyspnea/CHF

AFib, atrial fibrillation; AI, aortic insufficiency; AS, aortic stenosis; CHF, congestive heart failure; DOE, dyspnea on exertion; MR, mitral regurgitation; MS, mitral stenosis; PND, paroxysmal nocturnal dyspnea.

Aortic stenosis
The triad of angina, syncope, and congestive heart failure represent the progression of symptoms associated with AS. These symptoms correlate directly with mortality; the 50% survival data for these symptoms are 5, 3, and 2 years from the onset of these symptoms, respectively. Angina results from both increased demand for and a decrease in supply of

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coronary blood flow. Increased muscle mass from left ventricular hypertrophy and the high energy requirements to generate increased (high) systolic pressure combine to increase demands for coronary blood flow. In addition, insufficient supply secondary to decreased perfusion gradients and a decrease in coronary vasculature relative to the large amount of myocardium sum to diminish relative myocardial blood supply. Therefore, up to one third of patients with aortic stenosis can have angina in the absence of significant coronary artery disease.

Aortic insufficiency
Patients with AI have variable clinical presentations, primarily depending on the rapidity with which the left ventricular volume overload develops. When the volume increase occurs gradually as in chronic AI, there is usually a long asymptomatic period. The onset of the symptoms of fatigability and dyspnea signals either reduced cardiac output or increased left ventricular enddiastolic pressure (LVEDP) indicative of impairment of left ventricular contractile function. When aortic insufficiency occurs acutely, the ventricular compliance is unchanged; increased left ventricular diastolic volumes from regurgitant flow, therefore, lead to rapid rises in LVEDP and the clinical picture of congestive failure.

Mitral stenosis
Mitral stenosis (MS) is a slowly progressive obstruction to flow across the MV with gradual increase in left atrial (LA) pressure and volume. Symptoms of pulmonary congestion result from elevations in LA pressures and not from poor left ventricular systolic function. Atrial fibrillation develops secondary to atrial dilation.

Mitral regurgitation
The time course for the development of mitral regurgitation determines the severity of the symptoms. When the volume of regurgitant flow from the left ventricle to the left atrium increases gradually, the left atrium compensates by gradual dilatation. In contrast, the onset of acute mitral regurgitation can lead to rapid increases in LA pressures and severe pulmonary congestion and congestive heart failure. P.218 Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Thomas SJ, Kramer JL, eds. Manual of cardiac anesthesia, 2nd ed. New York: Churchill Livingstone, 1993:81127. Zipes DP, Libby P, Bonow RO, et al. eds. Braunwald's heart disease: a textbook of cardiovascular medicine, 7th ed. Philadelphia: WB Saunders, 2005:15531615.

B.2. What is the New York Heart Association (NYHA) classification of heart failure?
The NYHA heart failure classification is based on the amount of symptoms, specifically dyspnea and fatigue. The various classes are listed in the following:

Class I. No symptoms Class II. Symptoms with ordinary activity Class III. Symptoms with less than ordinary activity

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Class IV. Symptoms at rest

Criteria Committee of the New York Heart Association. Diseases of the heart and blood vessels (Nomenclature and criteria for diagnosis), 6th ed. Boston: Little, Brown and Company, 1964.

B.3. Discuss the role of premedication for patients with the four different valvular lesions
The role of premedication is to allay the anxiety of the impending surgical procedure thereby controlling the sympathetic outflow that may accompany the stress response. However, acute changes in heart rate, venous return, and systemic resistance can have particularly profound effects on patients with valvular heart disease. Patients with aortic stenosis (AS) may benefit from premedication by preventing unnecessary increases in heart rate. Concern however must be taken to ensure adequate venous return and preservation of sinus mechanism (see later). Patients with aortic insufficiency (AI) can similarly benefit from premedication because any increases in afterload, which may accompany sympathetic stimulation, can increase regurgitant volume. Drug doses should be adjusted based on the severity of debilitation and degree of systemic hypoperfusion. Patients with mitral stenosis (MS) should be premedicated with caution. Elevations in carbon dioxide resulting from narcotic-induced hypoventilation can dramatically elevate pulmonary pressures further compromising right ventricle output. Conversely venodilation may excessively diminish filling pressures. Patients with mitral regurgitation (MR) can respond similarly to those with MS, particularly when pulmonary hypertension is present. However, elevations in systemic pressure from stress can also compromise forward left ventricular output. Proper premedication can be delivered by careful dose selection and the provision of supplemental oxygen. Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Thomas SJ, Kramer JL, eds. Manual of cardiac anesthesia, 2nd ed. New York: Churchill Livingstone, 1993:81127. P.219

B.4. How would you premedicate the patient with severe AS and MR?
Premedication of a patient with severe AS and MR must be approached with caution. The patient should receive supplemental oxygen. A light premedication could be provided with small doses of benzodiazepines by mouth. However, I would prefer to titrate in small intravenous doses of sedation while the patient was under the closely monitored situation of the operating room or holding area and with inspired oxygen supplementation. In this setting, incremental doses of midazolam (0.5 mg intravenously) would be administered. It is important to remember that there may be significant delay in the onset of effect of intravenous medications secondary to pooling in the pulmonary and left atrial systems. Adequate waiting periods must be observed between each aliquot to avoid inadvertent overdose with ensuing respiratory depression, pulmonary hypertension, systemic hypotension, and right heart failure. In the elderly; however, use of benzodiazepines has been linked to postoperative delirium, which can be quite severe and difficult to treat as well as increase length of stay and resource utilization.

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C. Intraoperative Management C.1. Outline the hemodynamic management goals for each of the four valvular lesions. What are the anesthetic goals with respect to heart rate and rhythm, preload, afterload, and contractility?
Table 8.3 summarizes the hemodynamic goals with respect to heart rate and rhythm, preload, afterload, and contractility.

Aortic stenosis
Patients with aortic stenosis (AS) need the left ventricular filling obtained through a well-timed atrial contraction. Similarly, left ventricular hypertrophy renders the ventricle stiff and adequate preload is required. Reducing vascular tone will do little to relieve the fixed afterload increases from a stenotic valve but rather lower diastolic coronary perfusion gradients and should be avoided. Patients with AS experiencing angina may require the administration of an -agonist such as phenylephrine rather than nitroglycerin to increase coronary perfusion pressure.

Aortic insufficiency
T h e s e v e r i t y o f a o r t i c i n s u f f i c i e n c y ( A I ) i s d e t e r m i ne d b y t h e s i z e o f t h e r e g u r g i t a n t o r i f i c e , t h e pressure gradient between the aorta and left ventricle during diastole, and the time spent in that phase of the cardiac cycle. Elevated heart rates decrease the time spent in diastole and can lead to a decrease in heart size. Afterload reduction can lessen the regurgitant driving forces but therapeutic maneuvers to accomplish this may be limited by resulting systemic hypotension.

Table 8.3 The Hemodynamic Goals for the Various Valvular Lesions. HEMODYNAMIC GOALS LESIONS HR AND RHYTHM PRELOAD AFTERLOAD CONTRACTILITY AS AI 6070, sinus 8090 Full Maintain Maintain Lower May need support May need support

MS MR

6070 8090, sinus if possible

Full Maintain

Lower

HR, heart rate (beats/min); AI, aortic insufficiency; AS, aortic stenosis; MR, mitral regurgitation; MS, mitral stenosis.

P.220

Mitral stenosis
Patients with mitral stenosis (MS) can swiftly deteriorate in the setting of rapid heart rates. The decreased filling time necessitates the marked elevation of left atrial (LA) pressures and

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pulmonary edema can rapidly ensue. Whereas left ventricle (LV) contractility is generally preserve in mitral stenosis, use of -blockade does result in decreased right ventricular (RV) contractility, which in the setting of pulmonary hypertension can further compromise the cardiac output and systemic blood pressure. However, the loss in RV contractility is more than offset by the beneficial effects of the reduction of heart rate. Slower heart rates permit adequate time for transfer of blood from the left atrium to the LV across the stenotic mitral valve (MV) to occur. In addition, the pressure gradient across the MV is also reduced; thereby lowering left atrial pressure and diminishing pulmonary congestion. Because there is some variability in the individual response, the use of short-acting -blockers such as esmolol is prudent because an adverse response should be evanescent.

Mitral regurgitation
Patients with mitral regurgitation (MR) can rapidly deteriorate with marked increases in systemic blood pressure and afterload. As with other volume overload lesions such as aortic insufficiency ( A I ) , s l i g h t l y r a p i d h e a r t r a t e s ( 80 t o 9 0 b e a t s / m i n u t e ) s h o u l d r e s u l t i n s m a l l e r l e f t v e n t r i c u l a r volumes. This may lessen any component of MR secondary to annular dilation or chordal malalignment. Importantly, tachycardia should be avoided in patients with ischemic MR.

C.2. What are the hemodynamic goals for this patient with the combination of severe AS and MR?
In the patient with combined aortic stenosis (AS) and MR, the situation is more complex than when only a singular valvular lesion is present. Careful examination of the hemodynamic goals for each of the two lesions will reveal that therapy beneficial to patients with AS may exacerbate the severity of the MR. Early aggressive intervention is the key to these combined lesions. There usually exists less of a margin for error because minor hemodynamic aberrations can rapidly lead to cardiac collapse. A good rule of thumb is to prioritize the management based on the character of the present symptoms. Patients with AS and MR who present with syncope or angina are best managed for their AS, whereas patients with dyspnea and pulmonary edema are best managed for their congestive symptoms. It is prudent to maintain the patient's own usual h e m o d y n a m i c s a n d a v o i d p h y s i o l o g i c t r e s p a s s . Tr a n s e s o p h a g e a l e c h o c a r d i o g r a p h y ( T E E ) evaluation of left ventricular performance can be helpful in separating pulmonary congestion secondary to left heart failure from that secondary to poor diastolic left ventricular compliance. Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Thomas SJ, Kramer JL, eds. Manual of cardiac anesthesia, 2nd ed. New York: Churchill Livingstone, 1993:81127.

C.3. How would you monitor this patient with severe AS and MR?
In addition to the standard American Society of Anesthesiologists (ASA) recommended monitors, the patient would have a radial artery and a pulmonary artery (PA) catheter. Following induction of anesthesia and endotracheal intubation, a TEE probe would be inserted to confirm the valvular pathology and to assess ventricular function. Following valve replacement, the TEE would be used to check for adequacy of valvular function and the absence of paravalvular leaks and to assess postbypass ventricular function. P.221 Practice guidelines for perioperative transesophageal echocardiography. A report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologist Task Force on transesophageal echocardiography. Anesthesiology 1996;84: 9861006.

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C.4. Should the patient have a pulmonary artery (PA) catheter placed before induction?
Volume status may be particularly difficult to assess in patients with valvular heart disease yet of critical importance in the management of these patients. Patients with stenotic lesions depend on adequate filling pressures for diastolic filling of the ventricle. Patients with the volume overload lesions of aortic insufficiency (AI) and mitral regurgitation (MR) can benefit from the careful reductions in pulmonary pressure guided by the simultaneous assessment of cardiac performance. In these capacities, the PA catheter is useful. Patients with current hemodynamic stability, without severe respiratory distress, can be safely anesthetized before placement of the PA catheter. In all, there is no evidence that use of the PA catheter improves outcome in the setting of surgery. Practice guidelines for pulmonary artery catheterization: an updated report by the American Society of Anesthesiologists task force on pulmonary artery catheterization. Anesthesiology 2003;99:4.

C.5. Is a PA catheter with pacing capabilities indicated?


Patients with aortic stenosis (AS) can become severely compromised with the loss of atrial kick or the presence of slow junctional rhythms. Patients with AI or MR can experience left ventricular dilation in the setting of slow heart rates. In such cases, a PA catheter with atrial and ventricular pacing capacity can be useful in this setting. In patients with intact conduction systems, rate manipulation can often be achieved pharmacologically. Transesophageal atrial pacing is another option; transthoracic pacing elicits a ventricular response only and does not permit atrial stimulation. Transthoracic pacing is indicated when the ability to rapidly open the pericardium and obtain epicardial pacing is limited. This occurs in the setting of reoperations or with patients having a history of inflammatory pericardial disease. Pacing will be limited to capture of the ventricle alone. The loss of atrial contraction can lead to underfilling and hemodynamic compromise in patients dependent on the added volume from atrial systole. One of the other pacing modalities is best in this setting. Maisel WH, Epstein AE. The role of cardiac pacing: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery. Chest 2005;128(Suppl 2):36S38S. Risk SC, Brandon D, D'Ambra M, et al. Indications for the use of pacing pulmonary artery catheters in cardiac surgery. J Cardiothorac Vasc Anesth 1992;6:275279.

C.6. What anesthetic technique would you employ? Why?


For the patient undergoing cardiopulmonary bypass (CPB) and aortic valve replacement (AVR), general anesthesia with endotracheal intubation is the obvious choice. Both narcotics and inhalation anesthetics can be safely administered. When prolonged postoperative ventilation is anticipated, a high-dose narcotic anesthetic has numerous advantages. Recent anesthetic technique for cardiac surgery has focused on the use of techniques permitting earlier extubation, P.222 so-called fast-tracking. Anesthetic combinations using smaller total narcotic doses, inhalation anesthetics, and short-acting intravenous sedatives such as propofol are gaining popularity. For uncomplicated valve replacements with good ventricular function, the advantages of early extubation can be safely achieved. In complicated cases with longer bypass periods, poor ventricular function, or postbypass bleeding, the hemodynamic stability of a high-dose narcotic technique may be advantageous.

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DiNardo JA. Anesthesia for cardiac surgery, 2nd ed. Stamford: Appleton & Lange, 1998: 109 140. Howie MB, Black HA, Romanelli VA, et al. A comparison of isoflurane versus fentanyl as primary anesthetics for mitral surgery. Anesth Analg 1996;83:941948. Tuman KJ, McCarthy RJ, Spiess BD, et al. Comparison of anesthetic techniques in patients undergoing heart valve replacement. J Cardiothorac Anesth 1990;4:159167.

C.7. What muscle relaxant would you use for this patient?
Muscle relaxants can alter hemodynamics both from the effects of histamine release including vasodilatation and bronchospasm and through effects on rhythm. Although slowing of heart rates usually benefits the patient with angina, it may have severe consequences in patients with valvular heart disease. The typical high-dose narcotic anesthesia usually results in bradycardia secondary to the vagotonic actions. Pancuronium-mediated increases in heart rate usually offset these actions and result in a stable heart rate. Certainly the newly released long-duration relaxants doxacurium and pipe-curonium have the potential for minimal effects on hemodynamics. However, as outlined previously, the potential side effect of one agent may be rationally used to counter the adverse effect of another. Hemodynamically neutral relaxants such as vecuronium, rocuronium, or cis-atracurium could be used but their intermediate duration of action offers little if any advantage in this setting. Therefore, it is important to choose that combination of agents that will promote hemodynamic stability in a particular patient with his or her unique hemodynamic presentation. In this patient, I would use pancuronium in conjunction with the high-dose narcotic anesthetic. Fleming N. Con: the choice of muscle relaxants is not important in cardiac surgery. J Cardiothorac Vasc Anesth 1995;9:768771. Hudson RJ, Thomson IR. Pro: the choice of muscle relaxants is important in cardiac surgery. J Cardiothorac Vasc Anesth 1995;9:768771. Thys DM, Hillel Z, Schwartz AJ, eds. Textbook of cardiothoracic anesthesiology. New York: McGraw-Hill, 2001:589629.

C.8. What are the usual TEE findings in a patient with AS/AI/MR? How do you grade the severity of AS by TEE? How do you quantify the severity of MR? What is the impact of AS on the severity of MR?
The severity of aortic stenosis is usually stated in terms of aortic valve area (AVA). Normal AVA is 2.5 to 3.5 cm2. Moderate stenosis is when the AVA is within the range of 0.8 to 1.2 cm2 and severe stenosis when the AVA is less than 0.8 cm2. A patient with a large peak pressure gradient (usually more than 75 mm Hg) in the absence of excessively high cardiac output is usually considered to have severe AS as well. In the setting of low cardiac outputs, the pressure gradient may not be that great (20 to 30 mm Hg), and determination of AVA is required. This can be accomplished with echocardiography. P.223 Mitral regurgitation (MR) is graded by the amount of blood regurgitated backward into the left atrium during systole. Doppler color flow permits quantification of this flow. Common methods for MR quantification include the depth of MR jet extent into the left atrium (25% mild MR, 25% t o 7 5 % m o d e r a t e M R , a n d m o r e t ha n 7 5 % s e v e r e M R ) . O t h e r m e t h o d s o f q u a n t i f i c a t i o n i n c l u d e calculation of the area of the regurgitant jet by planimetry, by comparison of the MR jet area to the area of the left atrium, and by analysis of pulmonary vein flow profiles. It is important to

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remember that the amount of regurgitant blood flow in the setting of MR is determined by the amount of time spent in systole, the size of the defect in the mitral valve (MV), and the pressure gradient across the defect. Therefore, MR severity by Doppler color flow is load dependent. The lower pressure of the anesthetic state can often mask more severe degrees of MR seen when the patient is under his or her usual hemodynamic conditions. The left ventricular pressures are increased in the setting of aortic stenosis (AS). Therefore, the gradient across the MV is increased often leading to more severe MR. Following replacement of the stenotic aortic valve and elimination of the outflow tract obstruction, left ventricular pressures are markedly reduced. Moderate levels of MR without major structural defects in the MV apparatus usually revert to minimal or certainly less severe levels following reduction in the left ventricular outflow obstruction. Carabello BA, Crawford FA Jr. Valvular heart disease. N Engl JMed 1997;337:3241. Spain MG, Smith MD, Grayburn PA, et al. Quantitative assessment of mitral regurgitation by Doppler color flow imaging. Angiographic and hemodynamic correlations. J Am Coll Cardiol 1989;13:585590.

C.9. What special considerations particular to cardiopulmonary bypass (CPB) operations do you have for each of the four lesions? Focus on these concerns with respect to the induction and prebypass, bypass, and postbypass periods
Aortic stenosis
Critical to the management of a patient with AS is the avoidance of hypotension. Low blood pressure can initiate a cascade of events leading to cardiac arrest. Hypotension decreases the gradient for coronary perfusion with resultant ischemia. Ischemia leads to diminished cardiac output and decreased blood pressure further compromising coronary perfusion. The occurrence of cardiac arrest in a patient with AS is particularly catastrophic because closed chest cardiac massage will provide little gradient for blood flow across a stenotic aortic valve. Patients with AS are particularly dependent on their atrial kick for adequate ventricular filling volume and can rapidly become hypotensive and ischemic following the onset of supraventricular tachycardia (SVT) or atrial fibrillation. These rhythms are not uncommon during atrial cannulation. Therefore, it is of particular importance that every preparation for the initiation of CPB be made before atrial manipulation. Increased muscle mass of ventricular hypertrophy can be more difficult to adequately protect with cardioplegia. Careful attention to surface cooling, myocardial temperature measurement, and/or the use of retrograde cardioplegia can be helpful. Following aortic valve replacement (AVR), hypertension from left ventricular output now unopposed by any valvular lesion can result in stress on suture lines and excessive bleeding. It is important to remember that the compliance of the left ventricle is unchanged by surgery and still critically dependent on adequate preload and sinus rhythm.

Aortic insufficiency
Patients undergoing AVR for aortic insufficiency (AI) can often present difficult management decisions. The usual treatment measures for hypotension (-agonist) may have deleterious effects by increasing regurgitant volume. The use of combined - and -agonists (ephedrine, P.224 epinephrine, or infusions of dopamine or dobutamine) may be required. Although it would serve to lessen regurgitant volume, afterload reduction is beneficial in only a subset of patients with AI. Those patients with elevated left ventricular end-diastolic pressure (LVEDP), reduced ejection fractions, diminished cardiac output, and systemic hypertension usually benefit from

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afterload reduction. In contrast, those patients without the previously mentioned constellation may experience a decrease in forward cardiac output secondary to diminished preload from reduced venous return. Systemic hypotension usually limits the utility in the acute setting. The presence of aortic insufficiency (AI) makes initiation of cardiopulmonary bypass a critical period. Periods of bradycardia or ventricular fibrillation can lead to rapid volume overload of the LV through the incompetent aortic valve. Pacing, electrical defibrillation, and/or cross-clamping should be performed to prevent ventricular distention. Similarly, myocardial protection is compromised by AI. Generation of adequate root pressures is usually not obtainable; hence delivery of cardioplegia requires aortotomy and cannulation of the coronary ostia. Use of retrograde cardioplegia is advantageous. Following aortic valve replacement (AVR), the ventricle no longer has the lower pressure/impedance outflow afforded by the low aortic diastolic pressure. Inotropic support is often required. As with aortic stenosis (AS), the presence of an aortic suture line necessitates rapid response to hypertension to avoid bleeding and dissection.

Mitral stenosis
Patients undergoing mitral valve replacement (MVR) for mitral stenosis (MS) are particularly challenging. Marked elevations in pulmonary vascular resistance can be present with associated right heart failure. Stasis in the left atrium necessitates the careful echocardiographic examination for the presence of atrial thrombi. Manipulation of the heart before cross-clamping should be avoided. Following replacement, the chronically under filled, under worked LV may be unable to handle the new volume load. Inotropic support is often required for RV failure and occasionally to improve LV function. Afterload reduction and improved systemic perfusion through an IABP may be beneficial.

Mitral regurgitation
Similarly, patients with mitral regurgitation (MR) may have pulmonary hypertension and right heart failure. In contrast to aortic insufficiency (AI), almost all patients with MR can be greatly benefited by afterload reduction, both pharmacologically and/or through an intraaortic balloon pump. Diminution of left ventricular systolic pressure through afterload reduction decreases the pressure gradient from the left ventricle to the left atrium during systole with resultant decreased regurgitant volume. Prebypass assessment can be misleading. Preserved ejection fractions and elevated stroke volumes may mask marked left ventricular systolic dysfunction. It should be remembered that much of the left ventricular volume is ejected into the low-pressure/impedance outflow path of the left atrium. This route is no longer available after valve replacement. Following MVR, dysfunctional ventricles may be unable to provide adequate forward flow into the systemic circuit with its elevated vascular resistance and usually necessitate the use of inotropic support. Patients previously in atrial fibrillation without marked atrial enlargement often revert to or can be converted to sinus rhythm following valve replacement. The capacity of maintaining a person in sinus rhythm dramatically decreases when the diameter of the atrium is more than 5 cm. Hartman GS. Management of patients with valvular heart disease. Cleveland: International Anesthesia Research Society, 1994:141151. 1994 IARS Review Course Lectures. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 4th ed. Philadelphia: WB Saunders, 1999:727784. P.225 Thys DM, Hillel Z, Schwartz AJ, eds. Textbook of cardiothoracic anesthesiology. New York: McGraw-Hill, 2001:589629.

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C.10. The patient cannot be weaned from cardiopulmonary bypass (CPB) following an AVR and MVR. What are the possible causes?
The adequacy of myocardial preservation should be considered. Left ventricular hypertrophy (LVH) without or with accompanying coronary artery disease increases myocardial oxygen demands. Prolonged cross-clamp time necessitated by dual valve replacement can lead to inadequate and/or nonhomogeneous myocardial protection. In addition, there may be residual cardioplegia present within the myocardium. Therefore, some degree of postbypass left ventricular dysfunction can be anticipated. Inotropic support may be required. It is important to remember that although the obstruction to left ventricular ejection is acutely relieved by replacement of the stenotic valve, left ventricular compliance is largely unchanged. Adequate preload still depends on sinus rhythm and sufficient left ventricular filling pressures (pulmonary artery occlusion pressure [PAOP] or left ventricular end-diastolic pressure [LVEDP]). Elevations in pulmonary vascular resistance may render estimation of left atrial (LA) pressure through the pulmonary artery (PA) catheter inaccurate. In this setting, placement of an LA catheter is indicated. TEE may prove invaluable in identifying surgically correctable causes for inability to wean from CPB. Evaluation of left ventricular filling and contractility can help resolve the situation of low cardiac output and high filling pressures. A small underfilled left ventricle (LV) with hyperdynamic contractility and a dilated, overfilled, hypokinetic LV can both give the same hemodynamic parameters but obviously require different pharmacologic interventions. Abnormal valve seating may compromise flow into the coronary ostia and return to bypass with valve repositioning and/or coronary artery bypass grafting may be indicated. Similarly, perivalvular leaks or aortic dissections can be readily identified. Thomas SJ, Kramer JL, eds. Manual of cardiac anesthesia, 2nd ed. New York: Churchill Livingstone, 1993:81127. Thys DM, Hillel Z, Schwartz AJ, eds. Textbook of cardiothoracic anesthesiology. New York: McGraw-Hill, 2001:589629.

C.11. How would you diagnose right heart failure and pulmonary hypertension? How would you treat it?
Right heart failure is diagnosed by the elevations in right-sided filling pressures, specifically central venous pressure (CVP). Careful examination is required to rule out tricuspid insufficiency as the cause of the CVP elevation. A high CVP indicates the inability of the right heart to adequately propel the venous return volume into the pulmonary circulation. Elevation in the PA pressures is indicative of pulmonary hypertension. The combination of high CVP and high PA pressures indicates severe right heart failure. This scenario can be difficult to manage. Attempts to elevate systemic perfusion pressure with -agonists can worsen pulmonary hypertension. Administration of vasodilators to lower pulmonary pressures results in systemic hypotension. In this setting, it is often prudent to return to cardiopulmonary bypass, relieve ventricular distention, and improve myocardial perfusion. During this rest period, adjustments in inotropic therapy, ventilation, and cardiac rhythm can be instituted. Optimization of acid-base status and hemoglobin concentration should also be performed. Separation from bypass can then be reattempted. Typical inotropic agents effective in this setting are those with high degrees of -adrenergic potency. Commonly employed agents include dobutamine, epinephrine, and/or P.226 t h e p h o s p h o d i e s t e r a se - I I I ( P D E - I I I ) i n h i b i t o r s a m r i n o n e a n d m i l r i n o n e . I t i s n o t u n c o m m o n t o require the administration of -agonists to counteract the systemic vasodilating effects of prostaglandin E1 and the PDE-III agents. Some selective pulmonary vasodilating action and

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systemic vasoconstricting effects can often be achieved by administration of pulmonary vasodilating agents such as prostaglandin E1 through the right-sided access (CVP or PA catheter) and infusion of the -agonists through the LA line. Therefore, the vasoconstriction of the pulmonary arterial bed can be minimized. Nitric oxide (NO) is a potent, inhaled pulmonary vasodilator. Its half-life in the systemic circulation is extremely short permitting its administration to the pulmonary vasculature with minimal systemic hypotensive effects. NO can selectively and effectively dilate the pulmonary vasculature. The exact method of delivery, scavenging of waste gases, and high cost remain as obstacles to its clinical application. Body SC, Hartigan PM, Shernan SK, et al. Nitric oxide: delivery, measurement, and clinical application. J Cardiothorac Vasc Anesth 1995;9:748763. Kieler-Jensen N, Houltz E, Ricksten SE. A comparison of prostacyclin and sodium nitroprusside for the treatment of heart failure after cardiac surgery. J Cardiothorac Vasc Anesth 1995;9:641 646. Savage RM, Aronson S, eds. Assessment of the right ventricle. In: Comprehensive textbook of intraoperative transesophageal echocardiography. Philadelphia: Lippincott Williams & Wilkins, 2005:147155.

C.12. What role does an intraaortic balloon pump (IABP) have in this setting?
An IABP may be useful, because unlike any pharmacologic maneuver it is capable of increasing mean pressure during diastole critical for coronary perfusion while lowering afterload to systolic left ventricular ejection. Myocardial dysfunction secondary to inadequate protection during bypass can be reduced by decreased afterload and augmentation of diastolic pressures through IABP counterpulsation.

C.13. How does the IABP work to benefit the failing heart?
An IABP is a catheter with a large balloon (40 to 60 mL) at its tip. It is positioned in the thoracic Ao distal to the left subclavian artery origin and proximal to the take-off of the renal vessels. It is timed to inflate during diastole to increase diastolic perfusion pressure to the coronary arteries, great vessels, and major abdominal organs and to deflate just before systole to decrease afterload thereby increasing forward cardiac output. It is the uniquemodality, which can improve coronary perfusion pressures while reducing myocardial oxygen demand. Baskett RJ, Ghali WA, Maitland A, et al. The intraaortic balloon pump in cardiac surgery. Ann Thorac Surg 2002;74(4):12761287. Cheung AT, Savino JS, Weiss SJ. Beat-to-beat augmentation of left ventricular function by intraaortic counterpulsation. Anesthesiology 1996;84:545554.

C.14. What role does transesophageal echocardiography (TEE) play in the placement, timing, and demonstration of efficacy of an IABP?
The thoracic Ao and aortic arch can be clearly imaged by TEE. Imaging of the take-off of the left subclavian artery facilitates optimal positioning of the IABP. In addition, before insertion the Ao can be evaluated for dissection or the presence of severe atheromatous disease, both P.227 contraindications to IABP insertion. TEE can demonstrate the efficacy of an IABP by showing enhanced ventricular emptying during systole and filling during diastole.

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C.15. How would you properly time its cycle?


Inflation should occur just following the dicrotic notch and deflation before the upstroke in the aortic pressure curve. Augmentation in diastolic and mean pressures with a reduction in systolic pressure should follow its proper function.

C.16. What are the contraindications to the use of an IABP?


The most common contraindications are severe AI and severe aortic disease, atheromatous, aneurysmal, or a dissection. Although often listed as absolute contraindications, there are reports of the effective use of IABP in these settings. Sanfelippo PM, Baker NH, Ewy HG, et al. Experience with intraaortic balloon counterpulsation. Ann Thorac Surg 1986;41:3641.

D. Postoperative Management D.1. In the intensive care unit (ICU) 4 hours later, the patient became hypotensive with a low cardiac output. How could you distinguish between cardiac tamponade and pump failure? How would the transesophageal echocardiography (TEE) images differ?
The differentiation between cardiac tamponade and primary pump failure in the immediate postbypass-ICU setting can be difficult. Elevations in filling pressures, systemic hypotension, and low cardiac output are consistent with both diagnoses. The classic teaching of equalization of cardiac pressures seen in a fluid tamponade may not be present as areas of focal compression from clot can markedly reduce filling of only one chamber. Echocardiography can be beneficial in this setting by permitting visualization of chamber volume and function. The transesophageal approach has particular advantage over TTE in the postoperative setting in which the usual transthoracic window may be obscured by dressings and drainage tubing. Focal compression of the cardiac chambers from a clot or pericardial effusion can readily be distinguished from a volume-overloaded, failing heart with poor myocardial contractility. When the diagnosis is not clear, however, surgical reexploration may be indicated. Bommer WJ, Follette D, Pollock M, et al. Tamponade in patients undergoing cardiac surgery: a clinical-echocardiographic diagnosis. Am Heart J 1995;130:12161223.

D.2. Would you extubate this patient early in the ICU? Why?
No. This patient has undergone a double valve replacement. In this more complex procedure, coagulopathy and postoperative bleeding, hypothermia from incomplete and nonuniform rewarming, and pulmonary hypertension are not uncommon occurrences in the immediate postoperative period. Sedation, paralysis, and mechanical ventilation can reduce the oxygen requirements during this early phase of recovery, minimize pulmonary hypertension secondary to hypercarbia, and permit reestablishment of core temperatures. Cheng DCH. Pro: early extubation after cardiac surgery decreases intensive care unit stay and cost. J Cardiothorac Vasc Anesth 1995;9:460464. P.228 Guenther CR. Con: early extubation after cardiac surgery decreases intensive care unit stay and cost. J Cardiothorac Vasc Anesth 1995;9:465467.

D.3. What are the advantages and disadvantages of early

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extubation?
The advantages of early extubation are both medical and financial. Early extubation can lessen the adverse sequelae from prolonged endotracheal intubation including epithelial damage, decreased ciliary motility, and diminished mobilization of secretions. Positive pressure ventilation can have adverse effects on venous return. However, the overwhelming drive toward early extubation is cost and patient comfort. Early extubation can decrease cost by decreasing ICU staff requirements, decreasing the cost of sedatives, lessening the duration of ICU stays, and improving operating room use by lessening cancellation of cases secondary to blocked ICU beds. The potential advantages of early extubation, both financial and physiologic, must be weighed against the potential disadvantages of early extubation. The potential for respiratory compromise leading to hypoxemia, hypercarbia, ischemia, and the potential for infarction and neurologic injury is real. Any savings realized from early extubation can be rapidly lost by one adverse event. Success relies on careful integration of all players in the care of the cardiac surgery patient, from the management of intraoperative anesthetic techniques to the organization of the ICU and staff and the provision of postoperative analgesia. Equally important to the success of an early extubation program is appropriate patient selection. Cheng DCH. Pro: early extubation after cardiac surgery decreases intensive care unit stay and cost. J Cardiothorac Vasc Anesth 1995;9:460464. Guenther CR. Con: early extubation after cardiac surgery decreases intensive care unit stay and cost. J Cardiothorac Vasc Anesth 1995;9:465467.

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Chapter 9 Pacemakers and Implantable Cardioverter-Defibrillators


Alan Cheng Fun-Sun F. Yao

A 70-Year-Old Man
was s cheduled for urgent open cholecys tectomy. He underwent a permanent pac emaker (PPM) implantation 5 y ears ago for sic k s inus syndrome. The pacemak er was upgraded to an implantable cardioverter-defibrillator (ICD ) with dual-chamber pac ing function 6 months ago due to epis odes of ventric ular tachy cardia (VT). His blood press ure was 120/80 mm Hg, heart rate w as regular at 70 beats per minute.

P.230 P.231

A. Medical Disease and Differential Diagnosis A.1. What are the indications for permanent pacemakers (PPMs)?
Artificial pacing is generally indicated for the treatment of symptomatic bradycardia of any origin. The t wo m a j o r i n d i c a t i o n s f o r p e r m a n e n t p a c i n g a r e f a i l u r e o f i m p u l s e f o r m a t i o n a n d f a i l u r e o f c a r d i a c conduction. Clinically, sick sinus syndrome and complete heart block are the most common indications for pacemakers. The following types of arrhythmias are common indications for pacemakers:

Sinoatrial (SA) nodesick sinus syndrome, tachy-brady arrhythmia, symptomatic sinus bradycardia, hypersensitive carotid sinus syndrome, or vasovagal syncope

Atrioventricular (AV) nodesecond-degree block or third-degree AV block Trifascicular block or bifascicular block with prolonged infranodal conduction Right bundle branch block (RBBB) and left anterior hemiblock with hemodynamic symptoms RBBB and left posterior hemiblock with hemodynamic symptoms Alternating left bundle branch block (LBBB) and RBBB High-risk patients with congenital long Q-T syndrome or those with documented sustained pausedependent ventricular tachycardia

Syncope without an electrocardiogram (ECG) diagnosis Cardiomyopathypatients with medically refractory hypertrophic obstructive cardiomyopathy or decompensated heart failure in patients with dilated cardiomyopathy despite optimal medical therapy (e.g., biventricular pacing)

Atlee JL, Bernstein AD. Cardiac rhythm management devices (part I). Anesthesiology 2001; 95:1265 1280. Kusumoto FM, Goldschlager N. Cardiac pacing. N Engl J Med 1996;334:8998. Salukhe TV, Dob D. Pacemakers and defibrillators: anesthetic implications. Br J Anesth 2004; 93:95 104. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

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A.2. What is sick sinus syndrome?


Sick sinus syndrome describes an array of clinical disorders due to irreversible sinus node dysfunction. This may be manifested by episodes of sinus arrest, sinus pause or bradycardia secondary to inadequate sinus node automaticity. As a result, episodes of tachyarrhythmias from ectopic atrial foci can occur as well. Twenty-fourhour Holter monitoring is necessary to make a diagnosis. When episodes of tachycardia and bradycardia coexist, it is often referred to as tachy-brady syndrome. This is one of the most common indications for pacemakers and is characterized by the following:

Unexpected persistent severe sinus bradycardia Episodes of sinus arrest or exit block Paroxysmal or chronic atrial fibrillation or atrial flutter Alteration of paroxysms of rapid regular or irregular atrial tachyarrhythmias and periods of slow atrial and ventricular rates (tachy-brady syndrome)

Slow return to sinus rhythm following cardioversion Lack of increase in sinus rate above 90 per minute following intravenous administration of 1.5 to 2.0 mg atropine

P.232 Ferrer MI. The sick sinus syndrome. Circulation 1973;47:635641. Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med 2000;342:703 709. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.3. How would you diagnose first-, second-, and third-degree atrioventricular (AV) block, right bundle branch block (RBBB) with left anterior fascicular hemiblock, and left posterior fascicular hemiblock?
First-degree AV block is characterized by a PR interval of greater than 0.20 seconds. Second-degree AV block is subdivided into two types. Mobitz type I, or Wenckebach block, is characterized by a progressively lengthening PR interval, which occurs until a P-wave is not conducted down the AV node and a QRS complex is dropped. The site of block is typically in the AV node. Mobitz type II block is characterized by a loss of AV conduction with no progressive lengthening of the PR interval prior to the sudden dropping of the QRS complex. The site of block is typically below the AV node and within the His-Purkinje system. Third-degree AV block, also called complete heart block, occurs when all electrical activity from the atrium fails to progress into the Purkinje system. The site of block can lie either in the A V n o d e o r t h e H i s - P u r k i n j e s y s t e m . T h e a t r i a l a n d v e n t r i c u l a r c o n t r a c t i o n s h a v e n o r e l a t i o n wi t h e a c h other. The QRS complex is normal in complete AV nodal block. The QRS complex with complete i n f r a n o d a l b l o c k i s f r e q u e n t l y w i d e , a n d t h e v e n t r i c u l a r r a t e i s s l o w, a v e r a g i n g 4 0 b e a t s p e r m i n u t e . RBBB with left anterior hemiblock is indicated when the electrocardiogram shows RBBB and left axis deviation in the absence of an inferior myocardial infarction (MI). Complete RBBB with right axis deviation is indicative of RBBB and left posteroinferior hemiblock in the absence of a lateral MI or evidence of right heart failure. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.4. Is it necessary to insert a temporary pacemaker before general anesthesia for an asymptomatic patient with bifascicular block?
Only a small minority of patients with bifascicular block develops transient or established complete heart

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block and require implantation of a permanent pacemaker (PPM). The risk of progression to complete heart block in asymptomatic patients is very small and such patients do not require a PPM; therefore, it is not necessary to insert a temporary pacemaker before general anesthesia. However, it is advisable to have an external pacemaker available in the operating room. Berg GR, Kotler MN. The significance of bilateral bundle branch block in the preoperative patient. Chest 1971;59:6267. Gauss A, Hubner C, Radermaker P, et al. Perioperative risk of bradyarrhythmias with asymptomatic chronic bifascicular block or left bundle block. does an additional first degree atrioventricular block make any difference? Anesthesiology 1998;88:679687. T r o h m a n R G , K i m M H , P i n s k i S L . Ca r d i a c p a c i n g : t h e s t a t e o f t h e a r t . L a n c e t 2 0 0 4 ; 3 6 4 : 1 7 0 1 1 7 1 9 . Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787. P.233

Table 9.1 The NASPE/BPEG Generic (NBG) Pacemaker Identification Code. LETTER V LETTER I LETTER II LETTER III LETTER IV PROGRAMMABILITY ANTITACHYARRHYTHMIA CHAMBER CHAMBER MODE OF (S) PACED (S) SENSED RESPONSE RATE MODULATION FUNCTION(S) O= None A= Atrium V= Ventricle D= Dual(A + V) O= None A= Atrium V= Ventricle D= Dual(A + V) O= None T= Triggered I= Inhibited D = Dual (T + I) O = None O = None

P = Single programmable M = Multiprogrammable C= Communicating R = Rate modulation

P = Pacing

S = Shock

D = Dual(P + S)

BPEG. British Pacing and Electrophysiology Group; NASPE, North American Society of Pacing and Electrophysiology; NBG, North American and British Generic.

A.5. What are the three-letter and five-letter identification codes of the North American Society of Pacing and Electrophysiology (NASPE) and British Pacing and Electrophysiology Group (BPEG) generic (NBG) code for pacemaker classification?
With the growing complexity of pacing modes and location and function of cardiac pacing leads, difficulties with terminology became apparent. In the 1970s, the Intersociety Commission for Heart Disease Resources (ICHD) suggested a classification code, which is now widely accepted. The original nomenclature involved a three-letter identification code, as shown in the first three columns of Table 9.1. In 1980, this code was extended to five letters; the last two letters can be deleted when not applicable. In 1987, the NASPE (now known as the Heart Rhythm Society) and BPEG adopted a new five-letter code to describe the operation of implantable pacemakers (Table 9.1). The five-letter code is also called the NBG pacemaker code. The first letter describes the chamber(s) that the pacemaker can pace, the second letter describes the chamber(s) that it senses, and the third letter describes the

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response of the pacemaker to sensed intrinsic activity. The last two letters describe additional features such as rate responsiveness that are commonly omitted when not used. For example, a VVI pacing mode paces in the ventricle, can sense intrinsic activity in the ventricle and inhibits pacing when it senses intrinsic activity. A VOO pacing mode paces in the ventricle but does not sense intrinsic activity nor does it inhibit pacingit simply paces regardless of the heart's electrical activity. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.6. How many modes of pacing are available in modern day permanent pacemakers (PPMs)? How do they work?
Modern day pacemakers are programmable into one of three modes of pacing: asynchronous pacing, single-chamber demand pacing, and dual-chamber atrioventricular (AV) sequential demand pacing. P.234 Asynchronous or fixed-rate (e.g., AOO, VOO, DOO [see question A.5 for details]) modes pace at a preset rate that is independent of the inherent heart rate. They can be atrial, ventricular, or dual chamber. Competition and ventricular fibrillation (VF) are the potential complications when normal heart rate reappears. VF can theoretically occur because the pacing spike can potentially be delivered during ventricular repolarization, resulting in an R on T phenomenon. This, however, is very rare. S i n g l e - c h a m b e r d e m a n d p a c i n g ( e . g . , A A I , V V I ) p a c e s a t a p r e s e t r a t e o n l y wh e n t h e s p o n t a n e o u s h e a r t rate drops below the preset rate. The ventricular-inhibited pacer is the most popular type and is suppressed by normal electrical activity of the QRS complex. For example, if this patient's device was programmed to VVI 70 beats per minute, the device would pace in the ventricle only when the native ventricular rate fell below 70 beats per minute. Once the native ventricular rate resumed above 70 beats per minute, the device would sense this activity and inhibit further pacing. Single-chamber demand pacing in the atrium functions in a similar way but is rarely used alone in the United States. Dual-chamber AV sequential pacing requires two pacemaker leads, one in the right atrium and one in the right ventricle. The atrium is stimulated to contract first; then, after an adjustable PR interval, the v e n t r i c l e i s s t i m u l a t e d t o c o n t r ac t . F o r e x a m p l e , i f t h i s p a t i e n t ' s d e v i c e w a s p r o g r a m m e d t o D D D 7 0 beats per minute with a PR interval (AKA: AV delay) of 200 ms, the device would begin pacing the atrium first if the intrinsic sinus rate fell below 70 beats per minute. After the atrium has been paced, t h e d e v i c e w i l l wa i t f o r 2 0 0 m s t o s e n s e i n t r i n s i c v e n t r i c u l a r a c t i v i t y . I f i t d o e s n o t s e e i n t r i n s i c a c t i v i t y w i t h i n 2 0 0 m s , i t w i l l t h e n p a c e i n t h e v e n t r i c l e a s we l l . D D D p a c e m a k er s c a n a l s o p a c e i n t h e v e n t r i c l e in response to intrinsic atrial activity. For example, if the intrinsic atrial rate was 80 beats per minute, the device would inhibit pacing in the atrium because the base rate was set to 70 beats per minute. But because it is a dual-chamber device capable of sensing and pacing in both chambers, it will wait 200 ms from the time of the intrinsic atrial activity and watch for intrinsic ventricular activity as well. If it does not see intrinsic ventricular activity occurring within 200 ms from the intrinsic atrial activity, it will then pace in the ventricle. Programmable pacemakers have been widely used since 1980. Pacing rate, pulse duration, voltage output, and R-wave sensitivity are the most common programmable functions. Refractory periods, PR intervals, mode of pacing, hysteresis, and atrial tracking rate can be programmed in modern pacemakers. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.7. The patient was mechanically hyperventilated during surgery and his pacemaker gradually increased his heart rate. What feature of the

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permanent pacemaker (PPM) is accounting for this?


All modern day pacemakers have the ability to adjust the pacing rate according to the patient's level of activity in an effort to obtain a more physiologic response to exercise. This is known as rate-response (adaptive) pacing and is denoted by an R in the fourth position of the NBG coding schema. Various activity-detecting systems have been developed in years past to create a reliable rate-responsive pacemaker. They included muscle movement, respiratory rate, minute ventilation, central venous temperature, QT interval, myocardial contractility (dp/dt), oxygen saturation and pH in mixed venous blood, and ventricular depolarization gradient. Nowadays, PPMs used in the United States rely on sensors of motion (Medtronic, St. Jude Medical, Guidant-Boston Scientific) or sensors of changes in minute ventilation (Medtronic, Guidant-Boston Scientific). Because of the latter phenomenon, patients undergoing general anesthesia who are subjected to mechanical P.235 hyperventilation (e.g., neurosurgery) can experience an increase in the rate of pacing. As a result, most device manufacturers recommend disabling the rate-responsive features before surgery. If reprogramming the device is not readily available, a magnet may be placed over the pacemaker site to temporarily convert it to asynchronous pacing. Most properly functioning pacemakers within the United States respond to magnets in this way. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.8. What are the advantages and disadvantages of atrial pacing only?
Atrial pacing only increases cardiac output by 26% over the cardiac output of ventricular pacing only because atrial contraction contributes to approximately 15% to 25% of the diastolic filling of the ventricle. It has been shown that coronary blood flow increases and coronary resistance decreases during atrial pacing only. Atrial pacing has also been shown to reduce the incidence of atrial fibrillation. Atrial pacing only is seldomly used in the United States and often is implanted with the addition of a ventricular pacing lead in the event of atrioventricular (AV) block. Healey JS, Toff WD, Lamas GA, et al. Cardiovascular outcomes with atrial-based pacing compared with ventricular pacing: meta-analysis of randomized trials, using individual patient data. Circulation 2006;114:1117. Yoshida S, Ganz W, Donoso R, et al. Coronary hemodynamics during successive elevation of heart rate by pacing in subjects with angina pectoris. Circulation 1971;44:10621071.

A.9. What are the indications for and complications associated with atrioventricular (AV) sequential permanent pacemakers (PPMs)?
When ventricular pacing alone cannot maintain adequate cardiac output and atrial pacing alone is not justified, as in complete AV block, AV sequential pacing is indicated. Because of the success of atrial transvenous leads, bioengineering advances such as thinner polyurethane insulation and improved device programmability, the indications for dual-chamber pacing have broadened. It can be used for sick sinus syndrome and all degrees of heart block. PPMs programmed to DDD pacing are the ultimate form of physiologic pacing. Programmable features include the mode of pacing, the AV delay, the maximum atrial rate that the ventricle will follow (atrial tracking), and the minimum atrial rate for sensing at which atrial pacing commences. The major advantage of such pacing is the ability to increase the cardiac output by 200% to 300% under extreme stress and a reduced incidence of atrial fibrillation development. Historically, the major disadvantage of DDD pacing has been the possibility of pacemaker-mediated tachycardia. More recently, another disadvantage recognized has been the development of ventricular dyssynchrony (see question A.13) due to ventricular pacing. Long-term follow-up of patients with dualchamber pacemakers demonstrated reductions in left ventricular ejection fractions when compared to atrial pacing alone, especially in the setting of preexisting left ventricular dysfunction. Nielsen JC Bottcher M, Nielsen TT, et al. Regional myocardial blood flow in patients with sick sinus syndrome randomized to long-term single chamber atrial or dual chamber pacingeffect of pacing mode

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and rate. J Am Coll Cardiol 2000;35:14531461. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787. P.236

A.10. How would you know if the patient's permanent pacemaker (PPM) was atrially, ventricularly, or atrioventricular (AV) sequentially pacing?
In atrial pacing, an electrical spike appears before the P wave and the QRS complex is usually normal. In ventricular pacing, the electrical spike is followed immediately by a widened QRS complex. In AV sequential pacing, there are two spikes, one before the P wave and another preceding the QRS complex. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.11. What is the maximum amount of energy that a modern day permanent pacemaker can provide in terms of pulse amplitude and pulse width?
In order to successfully pace the heart, PPM must provide enough energy to allow for cardiac depolarization. Energy is a direct function of the amount of voltage produced (pulse amplitude) and the duration of time the voltage is delivered (pulse width). Although small variations exist among all modern day PPMs, the maximum pulse amplitude or output of stimulation usually is 7.5 volts (V). The maximum pulse width or the duration of stimulation is usually 1.5 msec. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.12. During a new permanent pacemaker implantation, what are the acceptable values for modern day pacemaker leads in terms of pacing thresholds, amplitude of sensed R waves, and resistance?
Because current PPMs have a maximal pacing output of 7.5 V at 1.5 msec, the pacing threshold cannot exceed the previously mentioned values. In fact, fluctuations in the pacing threshold can occur during the first few weeks after a pacing lead has been implanted. There is an initial sharp rise in the pacing threshold during the first 2 weeks because of tissue reaction around the tip of the electrode despite the presence of steroid embedded at the tip. Then it falls to two to three times the acute level from the scar formation. As a result, all device manufacturers recommend that the pacing output be at least two times the voltage of the threshold value or three times the pulse width of the threshold value. In the chronic state, pacing thresholds remain essentially at the same level in 80% of patients. For Ventricular lead, the intrinsic R waves should be at least 5 to 6 mV in amplitude to allow for proper sensing by the PPM because most modern day PPM have preset sensitivity settings approximately 2.0 to 3.0 mV. Impedance should be between 250 and 1,300 ohms. In atrial lead implantation, the acceptable sensing P wave values are at least 1.5 to 2.0 mV, and pacing threshold is 0.6 to 2.0 V. B o n o w R O , Z i p e s D P , L i b b y P , e t a l . e d s . B r a u n wa l d ' s H e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

A.13. What is a biventricular permanent pacemaker (PPM) or cardiac resynchronization therapy (CRT) device? What are the indications for such a device?
It has long been recognized that individuals with interventricular conduction abnormalities, specifically left bundle branch block (LBBB) conduction patterns, have a predilection toward P.237 impaired left ventricular systolic function. In fact, the most common ventricular conduction delay seen in patients with congestive heart failure is LBBB. On a mechanistic level, individuals with LBBB

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demonstrate ventricular dyssynchrony, a phenomenon whereby the left ventricle contracts in a stepwise p r o c e s s . U n l i k e n o r m a l i n d i v i d u a l s wh e r e t h e l e f t v e n t r i c u l a r s e p t u m a n d t h e l e f t v e n t r i c u l a r l a t e r a l f r e e wall contract nearly simultaneously, patients with LBBB have a delay in the activation of the left lateral free wall. As a result, there is marked impairment in left ventricular systolic function and increased m y o c a r d i a l wo r k a n d o x y g e n c o n s u m p t i o n . O n e a p p r o a c h t o c o r r e c t t h i s d y s s y n c h r o n y i s t o resynchronize the heart through the use of a biventricular pacemaker/implantable cardioverterdefibrillator. These devices are capable of pacing both the left ventricular septum (through a pacemaker lead in the right ventricle) and the left ventricular lateral free wall simultaneously (through a pacemaker lead in the coronary sinus), therefore allowing for activation of the entire left ventricle at the same time. Candidates for implantation of a biventricular device include individuals with severe cardiomyopathy (EF < = 3 5 % ) , a n d L B B B w i t h N e w Y o r k H e a r t A s s o c i a t i o n ( N Y HA ) c l a s s I I I o r c l a s s I V s y m p t o m s d e s p i t e optimal medical therapy. N e s s e r HJ , B r e i t h a r d t O - A , K h a n d h e r i a B K , e t a l . E s t a b l i s h e d a n d e v o l v i n g i n d i c a t i o n s f o r c a r d i a c resynchronization. Heart 2004;90:vi5vi9.

A.14. What are the usual life spans of permanent pacemakers (PPMs) and implantable cardioverter-defibrillators (ICDs)?
The lithium-powered pacemakers can last 5 to 10 years for dual-chamber pacing and 7 to 12 years for single-chamber pacing. The silver-vanadium oxide batteries used in ICDs typically last for 5 to 8 years. Atlee JL, Bernstein AD. Cardiac rhythm management devices (part I). Anesthesiology 2001; 95:1265 1280. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767802.

A.15. What is an implantable cardioverter-defibrillator (ICD)? How does it work?


An ICD system consists of a pulse generator and leads for tachyarrhythmia detection and therapy. ICDs provide antitachycardia and antibradycardia pacing; synchronized (cardioversion) or nonsynchronized (defibrillation) shocks; telemetry; and diagnostics, including stored event electrograms and history logs. Essentially, the pulse generator is a self-powered computer within a hermetically sealed titanium casing ( c a n ) . O n e o r t wo ( i n s e r i e s ) 3 . 2 V l i t h i u m s i l v e r v a n a d i u m o x i d e b a t t e r i e s w i t h h i g h p o w e r d e n s i t y a r e used to power the pulse generator, circuitry, and aluminum electrolytic storage capacitors. Most ICD designs use two capacitors in series to achieve a maximum voltage for defibrillation. A major challenge in ICD design is the large range of voltages that must be controlled in a very small package. Therapeutic defibrillatory shocks approach 850 V in modern day devices. Modern ICDs use transvenous lead systems for sensing, pacing, and shocks. Epicardial leads are still used in infants and small children. Ventricular demand pacing for bradycardia is a standard feature of all single-chamber ICDs. Dual-chamber ICDs have all the capabilities of dual-chamber pacemakers, including rate-adaptive pacing and automatic mode switching. However the response to magnet differs. See section C.8. Current ICDs have many programmable features, but essentially they measure each cardiac R-R interval and categorize the rate as normal, too fast (short R-R interval) or too slow. When the device P.238 detects a sufficient number of short R-R intervals within a period of time (all programmable), it will declare a tachycardia episode. The internal computer will decide between antitachycardia pacing (less energy use, better tolerated by patient) and shock based on its programmed algorithm. If shock is chosen, an internal capacitor is charged which take approximately 5 to 13 seconds. Most devices are programmed to reconfirm ventricular tachycardia (VT) or ventricular fibrillation (VF) after charging to prevent inappropriate shock therapy. Typically, ICDs deliver no more than six shocks per episode. Once a shock is delivered, the ICD will redetect to determine whether or not the shock successfully terminated the arrhythmia. A tachycardia episode is considered terminated when sinus rhythm has been restored

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for a certain period of time (varies with manufacturer). Atlee JL, Bernstein AD. Cardiac rhythm management devices (part I). Anesthesiology 2001; 95:1265 1280. F u s t e r V , A l e x a n d e r R W , O ' R o o k e RA , e d s . H u r s t ' s t h e h e a r t , 1 1 t h e d . N e w Y o r k : M c G r a w - H i l l , 2004:9891000. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:787802.

A.16. What are the indications for implantable cardioverterdefibrillators (ICDs)?


Initially ICDs were indicated for hemodynamically significant ventricular tachycardia (VT) or ventricular fibrillation (VF). Newer indications include the following and continue to evolve:

Cardiac arrest resulting from VT/VF not resulting from a transient or reversible cause Spontaneous sustained VT with structural heart disease Syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiology study (EPS)

Ischemic cardiomyopathy (EF 30%) without a recent myocardial infarction (within the last 4 weeks) or revascularization in the past 3 months.

I s c h e m i c o r n o n i s c h e m i c d i l a t e d c a r d i o m y o p a t h y ( E F 3 5 % ) w i t h Ne w Y o r k H e a r t A s s o c i a t i o n ( NY H A ) c l a s s I I o r I I I h e a r t f a i l u r e s y m p t o m s s t a b l e f o r t h e p a s t 9 m o n t h s .

Brugada syndromeright bundle branch block (RBBB) and ST segment elevation leads V1 to V3 Arrhythmogenic right ventricular dysplasia Long and short Q-T syndrome Hypertrophic obstructive cardiomyopathy

Goldberger Z, Lampert R. Implantable cardioverter-defibrillators: expanding indications and technologies. JAMA 2006;295:809818. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:787802.

A.17. What is the North American Society of Pacing and Electrophysiology (NASPE)/British
Pacing and Electrophysiology Group (BPEG) generic defibrillator (NBD) code? Like pacemakers, implantable cardioverter-defibrillators (ICDs) have a generic code to indicate lead placement and f u n c t i o n . T h e N B D c o d e i s s h o wn i n T a b l e 9 . 2 . H o w e v e r , t h e m o s t r o b u s t f o r m o f i d e n t i f i c a t i o n , c a l l e d the label form, replaces the fourth letter of the NBD with the appropriate generic pacemaker code. P.239

Table 9.2 NASPE/BPEG Generic Defibrillator (NBD) Code. LETTER I LETTER II SHOCK ANTITACHYCARDIA CHAMBER(S) PACING CHAMBER(S) O = None O = None LETTER III TACHYCARDIA DETECTION E = Electrogram LETTER IV ANTIBRADYCARDIA PACING CHAMBER(S) O = None

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A = Atrium

A = Atrium

H= Hemodynamic (not yet available)

A = Atrium

V= Ventricle D = Dual(A + V)

V = Ventricle

V = Ventricle

D = Dual(A + V)

D = Dual(A + V)

BPEG, British Pacing and Electrophysiology Group; NASPE, North American Society of Pacing and Electrophysiology; NBG, North American and British Generic.

American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

B. Preoperative Evaluation and Preparation B.1. How would you preoperatively evaluate the patient described earlier?
Preoperative evaluation should include the routine systemic workup, paying particular attention to cardiovascular disorders. The systemic routine includes complete blood count, urinalysis, coagulation screening with prothrombin time and partial thromboplastin time, serum electrolytes, blood urea nitrogen (BUN), blood sugar, chest x-ray film, and electrocardiogram. Special attention should be paid to the history, symptoms, and signs of myocardial infarction (MI), congestive heart failure, and arrhythmia. Serum electrolytes, especially potassium level, must be in the normal range. For the patient with a cardiac rhythm management device (CRMD), preoperative evaluation should include the following:

E s t a b l i s h wh e t h e r a p a t i e n t h a s a C R M D Define the type of CRMD D e t e r m i n e d e p e n d e n c y o n p a c i n g f u n c t i o n o f t h e CR M D Determine CRMD function

American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198. Salukhe TV, Dob D. Pacemakers and defibrillators: anesthetic implications. Br J Anesth 2004; 93:95 104. P.240

B.2. How do you determine whether the patient has a cardiac rhythm

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management device (CRMD) and define what type of CRMD?


Determining whether a patient has a CRMD should be based on (a) a focused history including but not limited to the patient interview, medical records review, review of available chest x-ray films, electrocardiogram, or any available monitor or rhythm strip information and (b) a focused physical examination (checking for scars, palpating for device). Defining the type of device is accomplished by (a) obtaining the manufacturer's identification card from the patient or other source, (b) ordering chest x-ray studies if no other data are available, or (c) referring to supplemental resources (e.g., manufacturers' databases, pacemaker clinic records, consultation with a cardiologist). American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

B.3. How do you determine whether the patient is dependent on pacing function of the cardiac rhythm management device (CRMD)?
CRMD dependency for pacemaking function may be determined by one or more of the following: (a) a verbal history or an indication in the medical record that the patient has experienced a bradyarrhythmia that has caused syncope or other symptoms requiring CRMD implantation, (b) a history of successful atrioventricular nodal ablation that resulted in CRMD placement, or (c) a CRMD evaluation that shows no evidence of spontaneous ventricular activity when the pacemaking function of the CRMD is programmed to VVI pacing mode at the lowest programmable rate. The electrocardiogram will show pacing spikes if the patient is dependent on the pacing function. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

B.4. How do you know if the implanted permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD) is working?
The cardiac rhythm management device (CRMD) function is ideally assessed by interrogating the device. If interrogating the device is not an option, one can slow the intrinsic heart rate to a rate below that of the pacemaker by carotid massage or a Valsalva maneuver. Carotid massage to slow the heart rate should be used cautiously because it could result in an arteriosclerotic plaque embolizing to the cerebral circulation. If the rate does not slow down enough for the pacemaker to take over the ventricle, device can be tested by placing a magnet over it to convert it to a fixed-rate pacing mode. In this mode, one will see pacing spikes march through the rhythm strip with no regard for the intrinsic electrical activity of the heart. The rate at which the pacemaker will pace in the presence of a magnet varies among device manufacturers and is dependent on the battery life. P.241 American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

B.5. What information would you like to obtain from interrogating his device?
Device interrogations provide information on the status and current programmed settings of a permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD). The important primary information for

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anesthesiologists include (a) battery life, (b) programmed pacing mode such as VVIR, DDDR, (c) pacemaker dependency, (d) intrinsic rhythm, (e) magnet rate and rhythm (f) prior recorded arrhythmic events, and (g) pacemaker lead parameters (including pacing threshold, ability to sense intrinsic activity, and lead impedance). Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

B.6. How do you preoperatively prepare the patient for surgery and anesthesia?
Preparation for patient safety and proper maintenance of the device during a procedure includes the following:

Determining whether electromagnetic interference (EMI) is likely to occur during the planned procedure;

D e t e r m i n i n g w h e t h e r r e p r o g r a m m i n g t h e c a r d i a c r h y t h m m a n a g e m e n t d e v i c e ( CR M D ) p a c e m a k i n g function to an asynchronous pacing mode or disabling any special algorithms, including rateadaptive functions, is needed;

Suspending antitachyarrhythmia functions if present; Advising the surgeon performing the procedure to consider use of a bipolar electrocautery system or ultrasonic (harmonic) scalpel to minimize potential adverse effects of EMI on the pulse generator or leads;

Assuring the availability of temporary pacing and defibrillation equipment; and E v a l u a t i n g t h e p o s s i b l e e f f e c t s o f a n e s t h e t i c t e c h n i q u e s o n C RM D f u n c t i o n a n d p a t i e n t - C R M D interactions.

American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

B.7. Would you recommend reprogramming this device to asynchronously pace before surgery?
The patient has an implantable cardioverter-defibrillator (ICD) with dual-chamber pacing because of sick sinus syndrome and ventricular tachycardia. I would recommend P.242 reprogramming the device to asynchronous pacing mode before surgery for the following reasons:

Electrocautery during surgery may inhibit pacing function The patient may become pacemaker dependent during abdominal surgery A magnet cannot convert the pacemaker in an ICD system to asynchronous mode pacing. A magnet placed over an ICD only disables tachycardia detection and therapy of the ICD. This is true of all devices used in the United States. One notable exception are ICDs manufactured by ELA Medical (Cedex, France) which, in the presence of a magnet, will not only disable tachycardia detection therapy but also convert pacing to a fixed rate at 96 beats per minute.

American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A

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report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

B.8. Would you reprogram the implantable cardioverter-defibrillator (ICD) preoperatively?


T h e I CD c a n b e r e p r o g r a m m e d t o d i s a b l e t h e a n t i t a c h y c a r d i a f u n c t i o n b e f o r e s u r g e r y i n t h e o p e r a t i n g room where a defibrillator is readily available. Alternatively, amagnet can be placed over the ICD to disable the antitachycardia function in the operating room. The advantage of placing a magnet on an I CD i s t h a t t h e m a g n e t c a n b e e a s i l y r e m o v e d a n d t h e a n t i t a c h y c a r d i a f u n c t i o n i s q u i c k l y e n a b l e d i n case of ventricular tachycardia (VT)/ventricular fibrillation (VF) during surgery. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:787802.

C. Intraoperative Management C.1. How would you monitor this patient?


Intraoperative monitoring should include both continuous electrocardiogram (ECG) and continuous peripheral pulse monitorings. Peripheral pulse can be monitored by palpation of the pulse, auscultation of heart sounds, pulse plethysmography or oximetry, a tracing of arterial wave form, or ultrasound peripheral pulse monitoring. Arterial line and central venous pressure or pulmonary artery pressure monitoring may be used only if the patient has poor ventricular function. The artifact filter on the ECG monitor should be disabled in o r d e r t o d e t e c t t h e p a c i n g s p i k e s . T h e E CG m o n i t o r s h o u l d b e s e t i n d i a g n o s t i c m o d e i n s t e a d o f monitoring mode. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198. P.243

C.2. What drugs and equipment would you like to have on hand in the operating room?
A complete array of drugs and equipment must be immediately available for cardiopulmonary resuscitation. The minimal requirements include, electrocardiograph (ECG) monitor, a transcutaneous external pacing and DC defibrillator, and the usual drugs for resuscitation. Atlee JL, Bernstein AD. Cardiac rhythm management devices (part I). Anesthesiology 2001; 95:1265 1280. Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

C.3. How would you set up the transcutaneous external pacer and defibrillator?
We prefer using defibrillating electrodes such as Zoll Pads to paddles because the electrodes can be placed before surgery at the desirable positions and connected to a defibrillator/pacemaker readily available for pacing and defibrillation. The electrodes should be placed as far (more than 6 in. or 15 cm) f r o m a c a r d i a c r h y t h m m a n a g e m e n t d e v i c e ( C RM D) a s p o s s i b l e . T h e e l e c t r o d e s a r e p o s i t i o n e d perpendicular to the CRMD system. There are three recommended electrode placements:

Anteroposterior placement. The right arm (RA) electrode placed under the left scapula and the left

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l e g ( L L ) e l e c t r o d e a t a p e x o f t h e h e a r t ( a s s h o wn i n F i g . 9 . 1 ) .

Apex-anterior placement. The RA electrode placed under the right clavicle and the LL electrode at the apex of the heart (Fig. 9.2A).

Apex-posterior placement. The RA electrode placed over the right scapula and the LL electrode at the apex of the heart (Fig. 9.2B).

It is important to remember that the presence of a CRMD should not deter standard resuscitation efforts. Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillator. Crit Care Med 2004;32(Suppl):S155S165.

C.4. Had this patient's implantable cardioverter-defibrillator (ICD) been implanted the day before surgery, would you consider avoiding certain inhalational gases for anesthesia?
It has been reported that nitrous oxide could cause pacemaker malfunction by increasing gas in the prepectoral pacemaker pocket. Despite air evacuation with antibiotic solution before closure of the prepectoral pocket, a small amount of air remains entrapped in the pocket. In general, this small amount of air should have no clinical significance. However, nitrous oxide is 35 times more soluble in blood than nitrogen. When nitrous oxide is used for anesthesia, the amount of nitrous oxide diffused from blood to the air pocket is much more than the amount of nitrogen diffused from the air pocket to blood. Therefore, this causes an expansion of the gas in the pocket, which leads to loss of anodal contact and pacing system malfunction. It is advisable not to use nitrous oxide in a patient with a newly implanted pacemaker. Lamas GA, Rebecca GS, Braunwald NS, et al. Pacemaker malfunction after nitrous oxide anesthesia. Am J Cardiol 1985;56:995. P.244

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Figure 9.1 Anteriorposterior placement of defibrillating electrodes.

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Figure 9.2 Placement of defibrillating electrodes. A: Apexanterior placement with both pads placed anteriorly. B and C: Apexposterior placement are shown with the device in the left prepectoral region (B) and the right pectoral region (C). (Reprinted with permission from Ellenbogen KA, Kay GN, Wilkoff BL, eds. Clinical cardiac pacing and defibrillation. 2nd ed, Philadelphia: Saunders, 2000;944.)

P.245

C.5. Electromagnetic interference (EMI) from electro cautery during the case results in significant noise on your cardiac monitor. You recall that EMI can also inhibit pacing function from the permanent pacemaker (PPM). In this pacemaker-dependent patient, how can you determine whether inappropriate inhibition of the PPM is occurring?
During electrocautery, the electrocardiogram is frequently useless because of interference. The best monitor available to determine if inhibition is taking place is a hand on the pulse. The precordial or esophageal stethoscope, pulse oximeter, or blood pressure is also acceptable. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

C.6. What are the potential responses of pacemakers and implantable cardioverter-defibrillators (ICDs) to electrocautery?
The responses of pacemakers to electrocautery or other electromagnetic interference include the following:

Inhibition of pacing Asynchronous pacing Reset to Backup mode Myocardial burns, rare Ventricular fibrillation (VF), rare

T h e r e s p o n s e s o f I CD s i n c l u d e t h e f o l l o w i n g :

Inhibition of pacing

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Asynchronous pacing Inappropriate tachy therapy Inhibition of tachy therapy

Salukhe TV, Dob D. Pacemakers and defibrillators: anesthetic implications. Br J Anesth 2004;93:95 104. Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillator. Crit Care Med 2004;32(suppl):S155S165.

C.7. How would you prevent the effects of electromagnetic interference (EMI) on the pacemaker or implantable cardioverterdefibrillator (ICD) from the electrocautery?
The safest way to prevent intraoperative EMI response is appropriate reprogramming. The following precautions should be taken to minimize the effects of electrocautery:

Place the cautery grounding plate as close to the operative site and as far from the cardiac r h y t h m m a n a g e m e n t d e v i c e ( CR M D ) a s p o s s i b l e t o m a k e s u r e t h a t t h e c u r r e n t p a t h w a y d o e s n o t p a s s t h r o u g h o r n e a r t h e C RM D s y s t e m . F o r s o m e c a s e s , t h e g r o u n d i n g p l a t e m i g h t n e e d t o b e placed on a site different from the thigh (e.g., the superior posterior aspect of the shoulder contralateral to the CRMD generator position for a head and neck case). P.246

Do not use cautery within 15 cm of the pacemaker as it may interfere with the battery circuitry. If in contact with a break in the insulation of the electrode, it may cauterize the myocardium at the electrode tip rendering it insensitive to pacing impulses.

Limit cautery use to 1-second bursts every 10 seconds to prevent repetitive asystolic periods. If the pacemaker is inhibited by the cautery, place a high-powered magnet over the demand nonprogrammable pacemaker to convert it to fixed-rate mode.

Using bipolar electrocautery forceps or ultrasonic (harmonic) scalpel reduces electromagnetic interference.

American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198. Salukhe TV, Dob D. Pacemakers and defibrillators: anesthetic implications. Br J Anesth 2004;93:95 104. Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillator. Crit Care Med 2004;32(suppl):S155S165.

C.8. What are the effects of a magnet over pacemakers and implantable cardioverter-defibrillators (ICDs)?
The effect of placing a magnet over a pacemaker or ICD can vary quite considerably depending on the device manufacturer, model and individual programmed modes. This information may be obtained by consulting the device manufacturer's representative. Most pacemakers will switch to a fixed-rate pacing m o d e w h e n a m a g n e t i s p l a c e d . H o we v e r , t h e r e s p o n s e o f a p a c e m a k e r t o a m a g n e t p l a c e m e n t m a y a l s o include the following:

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Asynchronous pacing without rate responsiveness No response Brief (10 to 100 beats) asynchronous pacing Continuous or transient loss of pacing

The response of an ICD to a magnet placement is different from the response of a pacemaker. Magnets will disable tachyarrhythmia detection and therapy which, except in some Guidant-Boston Scientific devices, are reenabled when the magnet is removed. Magnets generally will, with a few exceptions, not a f f e c t t h e p a c i n g m o d e o r r a t e o f I CD s . T h e r e f o r e t h e p a c e m a k e r i n a n I C D c a n b e i n a p p r o p r i a t e l y inhibited by electrocautery even when a magnet is placed. It is important to remember that some Guidant-Boston Scientific ICDs are permanently disabled when a magnet is placed for more than 30 seconds. The ICD will not be reactivated when the magnet is removed. To reactivate the Guidant-Boston Scientific ICDs, the magnet has to be reapplied over the ICD for more than 30 seconds and then removed. If a magnet is to be used during surgery, the magnet effects should be tested in the operating room before surgery to ensure that the desired effects will occur during surgery. Salukhe TV, Dob D. Pacemakers and defibrillators: anesthetic implications. Br J Anesth 2004;93:95 104. Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillator. Crit Care Med 2004;32(suppl):S155S165. P.247

C.9. In the middle of surgery, the patient developed ventricular tachycardia. What would you do?
For a patient with an implantable cardioverter-defibrillator (ICD) and magnet-disabled therapies:

Advise the surgeon performing the procedure to terminate all sources of electromagnetic interference (EMI).

Remove the magnet to reenable antitachycardia therapies. Observe the patient and the monitors for appropriate cardiac rhythm management device (CRMD) t h e r a p y . T h i s c a n b e d e l a y e d f o r a s l o n g a s 1 0 t o 1 2 s e c o n d s a s t h e I CD i s c h a r g i n g u p .

If the activities mentioned in the preceding text do not restore ICD function, proceed with emergency external defibrillation or cardioversion.

For a patient with an ICD and programming-disabled therapies:

Advise individual performing the procedure to terminate all sources of EMI while magnet is removed.

Reenable therapies through programming if the programmer is immediately available and ready to be used.

Observe the patient and the monitors for appropriate CRMD therapy. If the activities mentioned in the preceding text do not restore ICD function, proceed with emergency external defibrillation or cardioversion.

F o r e x t e r n a l d e f i b r i l l a t i o n ( s e e a l s o q u e s t i o n C. 3 ) :

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Position defibrillation/cardioversion pads or paddles as far as possible from the CRMD generator. Position defibrillation/cardioversion pads or paddles perpendicular to the major axis of the CRMD to the extent possible by placing them in an anteroposterior location.

If it is technically impossible to place the pads or paddles in locations that help to protect the CRMD, defibrillate/cardiovert the patient in the quickest possible way and be prepared to provide pacing through other routes.

Use a clinically appropriate energy output.

American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

C.10. What precautions should be taken when a patient with a cardiac rhythm management device (CRMD) is undergoing extracorporeal shock wave lithotripsy (ESWL)?
ESWL is no longer contraindicated for patients with pacemakers. The only exception to this general statement is the abdominally placed pacemaker generators. Because these generators are in the blast path of the shock wave, such patients should not be treated with ESWL. However, most transvenous pacemaker generators are placed in a pectoral location that is at a safe distance from the blast path. Consider preoperative disabling of atrial pacing if the lithotripsy system triggers on the R wave. Although most pacemakers are not affected by ESWL, sometimes it may cause pacemaker malfunctions t h a t i n c l u d e t h e f o l l o wi n g :

Switching to magnet mode Reaching upper rate limit P.248

Pacing irregularity Oversensing of asynchronous shocks Damage to rate-sensing piezoelectric crystal Intermittent inhibition of ventricular output in dual-chamber pacemaker Electromagnetic interference

There may be a rate increase in a rate-response (adaptive) pacemaker after ESWL shocks. Therefore, special precautions should be taken preoperatively. The type of pacemaker, indications for its placement, degree of patient dependence, and pacemaker programmability must be determined before lithotripsy. A dedicated pacemaker programmer should be available in the lithotripsy suite should pacemaker malfunction be caused by the shock waves. In addition, an alternative means of pacing, such as transcutaneous pacing, should also be available in case the pacemaker becomes permanently damaged. Low-energy shock waves (< 16 kV) should be used initially; then the energy level is gradually increased while pacemaker function is monitored carefully. It is best to disable tachycardia detection of an ICD during ESWL and to thoroughly test the ICD following the procedure. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients

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with cardiac rhythm management devices. Anesthesiology 2005;103:186198. Atlee JL, Bernstein AD. Cardiac rhythm management devices (part I). Anesthesiology 2001; 95:1265 1280.

C.11. Is electroconvulsive therapy (ECT) contraindicated in patients with pacemakers or implantable cardioverter-defibrillators (ICDs)?
It is advisable to consult with the ordering physician, the patient's cardiologist, a cardiac rhythm management device (CRMD) service or the device manufacturer. ECT appears safe for patients with p a c e m a k e r s b e c a u s e l i t t l e c u r r e n t f l o w s wi t h i n t h e h e a r t d u e t o t h e h i g h i m p e d a n c e o f b o d y t i s s u e s . However, the seizure and succinylcholine fasciculations may generate sufficient myopotentials for pacemaker inhibition (unipolar devices) or ventricular tracking (adaptiverate devices). Therefore, it is advisable to program the pacemaker to nonsensing (asynchronous) mode for pacemaker-dependent patients. An external pacemaker should also be available. All ICDs should be programmed so that tachycardia detection is disabled before ECT and reprogrammed to its original programmed parameters afterwards. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198. Atlee JL, Bernstein AD. Cardiac rhythm management devices (part I). Anesthesiology 2001; 95:1265 1280. Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillator. Crit Care Med 2004;32(suppl):S155S165. P.249

C.12. Is magnetic resonance imaging (MRI) contraindicated in patients with a cardiac rhythm management device (CRMD)?
MRI is generally contraindicated in patients with a CRMD. If MRI must be performed, consult with the ordering physician, the patient's cardiologist, the diagnostic radiologist and the CRMD manufacturer. M R I c a n c a u s e r a p i d p a c i n g , i n h i b i t i o n , r e s e t t i n g o f D D D p a c e m a k e r s , a n d t r a n s i e n t r e e d s wi t c h malfunction with asynchronous pacing. Serious malfunction with no output or rapid pacing may occur b e c a u s e p u l s e d e n e r g y f r o m M RI c a n e n t e r t h e l e a d b y c a p a c i t i v e c o u p l i n g a n d c a u s e r a p i d v e n t r i c u l a r pacing. Recent studies suggest that MRI may be safe, at least with some models of pacemakers or i m p l a n t a b l e c a r d i o v e r t e r - d e f i b r i l l a t o r s ( I C D s ) , p r o v i d e d t h e CR M D g e n e r a t o r a n d l e a d s a r e n o t i n s i d e t h e magnet bore. When an MRI is considered absolutely essential, it is reasonable to program the p a c e m a k e r t o i t s l o w e s t v o l t a g e a n d p u l s e wi d t h o r t o O O O m o d e , p r o v i d e d t h e p a t i e n t h a s a n a d e q u a t e u n d e r l y i n g r h y t h m . T h e p u l s e wa v e f o r m s h o u l d b e c l o s e l y m o n i t o r e d i n p a c e m a k e r - d e p e n d e n t p a t i e n t s and an external pacemaker and defibrillator should be available. Device function must be checked after MRI. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198. Atlee JL, Berstein AD. Cardiac rhythm management devices (part I). Anesthesiology 2001; 95:1265 1280. Salukhe TV, Dob D. Pacemakers and Defibrillators: anesthetic implications. Br J Anesth 2004;93:95 104.

C.13. What are the precautions during radiofrequency ablation for a

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patient with a cardiac rhythm management device (CRMD)?


Avoid contact of radiofrequency catheter with the CRMD generator and leads R a d i o f r e q u e n c y c u r r e n t p a t h f a r a w a y f r o m t h e CR M D g e n e r a t o r a n d l e a d s Discuss these concerns with the operator

American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

D. Postoperative Management D.1. How would you monitor this patient in the postanesthesia care unit?
Cardiac rate and rhythm should be continuously monitored throughout the immediate postoperative period. Backup pacing capability and cardioversion-defibrillation equipment should be immediately available at all times. P.250 American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

D.2. How would you confirm that the cardiac rhythm management device (CRMD) is functioning properly after surgery?
Postoperative interrogation and restoration of CRMD function are basic elements of postoperative management. The CRMD first should be interrogated to assess postoperative device functions. If interrogation determines that CRMD settings are inappropriate, the device should be reprogrammed to appropriate settings. For an implantable cardioverter-defibrillator (ICD), all antitachyarrhythmic therapies should be restored. Consultation with an electrophysiologist or pacemakerICD service may be necessary. American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverterdefibrillators. A report by the American Society of Anesthesiologists task force on perioperative management of patients with cardiac rhythm management devices. Anesthesiology 2005;103:186198.

D.3. What types of environmental electromagnetic interferences (EMIs) may temporarily affect the function of a permanent pacemaker (PPM)?

Microwave oventhe patient with the older generation of pacemaker should not approach within 3 f e e t o f a n o p e r a t i n g m i c r o w a v e o v e n . H o we v e r , a m o d e r n p a c e m a k e r s y s t e m c a n e a s i l y r e j e c t t h e interference.

Diathermycontraindicated Electrocauterydo not use within 15 cm of the implanted pulse generator.

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Electric razordo not use on the skin area over the implant site. Amateur radio transmitting equipmentlinear power amplifiers are contraindicated. Power transmission lineshigh-voltage electric fields produced by 765 kV power lines should be avoided.

Arc weldingcontraindicated Telephone transformercontraindicated. Cellular phonesanalog cellular phones are safe; however, digital cellular phones should not be placed over the pacemaker.

Radiofrequency catheter ablation of arrhythmias potentially can produce similar disturbances of pacemaker behavior caused by electrocautery and can produce upper rate pacing in a minute ventilation-driven DDDR pacemaker.

Magnetic resonance imaging (MRI)generally contraindicated. Radiation therapythis can damage pacemaker electronics and can cause unpredictable transient or permanent malfunction including runaway behavior. The effect is cumulative and similar whether the dose is given at one time or spread over several treatments. Given a sufficiently high cumulative absorbed dose, all pulse generators will fail catastrophically. Appropriate shielding of the pulse generator during radiation therapy is mandatory. P.251 In some cases, the pacemaker may need to be repositioned before initiating radiation therapy.

Z i p e s D P , L i b b y P , B o n o w R O , e t a l . e d s . B r a u n wa l d ' s h e a r t d i s e a s e , a t e x t b o o k o f c a r d i o v a s c u l a r medicine, 6th ed. Philadelphia: WB Saunders, 2005:767787.

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Chapter 10 Thoracoabdominal Aortic Aneurysms


Manu Sethi Charles D. Collard M a n u e l L. F o n t e s

A 67-Year-Old Woman
p rese nts fo r eva lu ati on and surg ica l treatmen t of a th ora coa bdo mi na l a orti c an eu rysm ( TAAA). The patient's past medical history is significant for a type III aortic diss ection 8 yea rs ag o, hyp erte nsi on , chro ni c ob structive pulmonary disease (COPD), smoking ( one pac k/day) , and chro ni c re nal insufficien cy. Th e pa tient cu rre ntly complains o f i nte rmitte nt ba ck pa in . Compute d to mog rap hy (C T) re vea ls a 9-cm T AAA o rig i nati ng jus t distal to the left subclavian arter y that extends to the iliac bifurcation. Chest x-r ay sh ows th ora ci c aor tic a neu rysmal di l ati on, wi th di spl ace men t of th e l eft br onch ia l mai nste m. Ech oca rdi og ram show s conc entri c l eft ve ntri cu la r hyp ertro ph y and a no rmal e je cti on fr acti on. T he la bo rator y fin ding s sho w hemog lo bin 9 .3 g p er d L, he ma tocrit 3 7%, bloo d u rea ni trog en (BUN ) 22 mg p er d L, an d cre ati ni ne 1.9 mg p er d L.

P.253

A. Medical Disease and Differential Diagnosis A.1. What are the causes of aortic aneurysms?
A true aneurysm is defined as a localized dilation of the aorta, 50% over the normal diameter, which includes all three-vessel layers (i.e., the intima, media, and adventitia). Causes of aortic aneurysms include the following:

Atherosclerosis. Atherosclerosis is the predominant etiology of descending thoracic aortic aneurysms, affecting the medial wall diffusely, thereby diminishing the cushioning property of the aorta. With medial necrosis and subsequent remodeling, which is nonhomogeneous, segments of the aortic wall become weakened and prone to dilation as well as rupture.

Aortic dissection. Chronic aortic dissections often dilate over time and are at high risk for aneurysm formation. Aortic dissections and aneurysms often coexist, in particular, in older patients suffering from hypertension and atherosclerosis.

Collagen vascular diseases a. Marfan syndrome. Marfan syndrome is an autosomal dominant disorder classically associated with cystic medial degeneration in young patients. Both the amount and organization of elastin are decreased in patients with Marfan syndrome. b. Ehlers-Danlos syndrome. Ehlers-Danlos syndrome is a heterogeneous group of heritable connective tissue disorders, characterized by articular hypermobility, skin extensibility, and tissue fragility.

Familial thoracic aortic aneurysm syndrome. Cystic medial degeneration is also seen in patients with ascending thoracic aortic aneurysms who do not have overt connective tissue disorders. When familial, they are now referred to as the familial thoracic aortic aneurysm

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syndrome.

Trauma Bicuspid aortic valve. Many ascending thoracic aortic aneurysms are associated with a bicuspid aortic valve. Cystic medial degeneration is often seen in these cases. Cardiologists should routinely image the ascending aorta in patients with a bicuspid aortic valve, as 50% will develop aortic dilatation.

Turner's syndrome. Turner's syndrome is associated with multiple cardiovascular anomalies, including a bicuspid aortic valve (30%) and aortic coarctation. Thoracic aortic aneurysms are not uncommon, and typically involve the ascending aorta. It has been recommended that all P.254 women with Turner's syndrome undergo a complete cardiac evaluation at least every 5 years to detect potential aneurysm formation.

Inflammation a. b. Takayasu arteritis Polyarteritis

Infection a. b. c. d. Bacterial Viral Spirochete Fungal

Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation 2005;111:816. Johnston KW, Rutherford RB, Tilson MD, et al. Suggested standards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg 1991;13: 452. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 5th ed. Philadelphia: WB Saunders, 2006. Kouchoukos NT, Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997;336: 18761889.

A.2. How are dissecting aortic aneurysms classified?


The term dissecting aneurysm is a misnomer, because the condition is not an aneurysm but an aortic dissection (i.e., a dissection of the aortic wall). Aortic dissections result from cystic medial necrosis (i.e., mucoid and cystic degeneration of elastin fibers within the aortic media). Currently, there are several aortic dissection classification systems. The DeBakey classification system classifies aortic dissections by their site of origin and distal extension (Fig. 10.1).

Type I dissection begins in the ascending aorta near the aortic valve and extends throughout the aorta down to the common iliac arteries. Type I aortic dissections are common.

Type II dissection is limited to the ascending aorta. Type II dissections are common in

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patients with Marfan syndrome; however, the rarest form of dissection.

Type IIIa dissection begins distal to the left subclavian artery and ends in the descending thoracic aorta. Its localized nature makes it accessible to surgical excision if needed.

Type IIIb dissection begins distal the left subclavian artery and extends into the abdominal a o r t a . T y p e I I I b d i s s e ct i o n s r a r e l y r e q u i r e s u r g i c a l i n t e r v e n t i o n .

In contrast, the Stanford classification system classifies aortic dissections into two types based on their clinical course and surgical significance:

A type A dissection originates in the ascending aorta and includes DeBakey's type I and type II dissections.

A type B dissection originates in the descending aorta and is equivalent to DeBakey's type III dissection. Type B dissections may dissect retrograde into the aortic arch or ascending aorta.

Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990;264: 25372541. Daily PO, Trueblood H, Stinson E, et al. Management of acute aortic dissections. Ann Thorac Surg 1990;10:237247. P.255 DeBakey ME, Cooley DA, Crawford ES, et al. Aneurysms of the thoracic aorta. J Thorac Surg 1958;36:393420. O'Connor CJ, Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: Part I. J Cardiothorac Vasc Anesth 1995;9:581588. Schwartz SI, ed. Principles of surgery, 6th ed. New York: McGraw-Hill, 1994:915916.

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Figure 10.1 The DeBakey classification system.

A.3. How are thoracoabdominal aortic aneurysms (TAAAs) classified?


Crawford described four TAAA types (Fig. 10.2):

Type I TAAA originates below the left subclavian artery and extends to the celiac axis and mesenteric arteries.

Type II TAAA involves the same areas as type I, but extends caudally to include the infrarenal aorta. This type is associated with prolonged surgical times and worse overall outcomes.

Type III TAAA begins in the lower descending thoracic aorta (T6) and involves the remainder of the aorta.

Type IV TAAA begins at the diaphragm and involves the entire abdominal aorta.

Crawford ES, Crawford JL, Safi HJ, et al. Thoracoabdominal aneurysms: preoperative and intraoperative factors determining immediate and long-term results in 605 patients. J Vasc Surg 1986;3:389404.

A.4. Describe the natural history, medical management and timing of surgical intervention for thoracoabdominal aortic aneurysms (TAAAs)
Both the etiology and location of an aneurysm may affect its growth rate and propensity for dissection or rupture. Surgical intervention is performed when the aneurysm is large enough to be considered at significant risk for rupture. The mean rate of growth for all thoracic aneurysms is 0.1 cm per year. The rate of growth is greater for descending versus ascending aorta aneurysms,

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P.256 for dissected versus nondissected aneurysms, and for in patients with Marfan syndrome. The initial size is an important predictor of the rate of thoracic aneurysm growth. With regards to aneurysm size and the risk of rupture or dissection, the annual rate is 2% for aneurysms less than 5 cm, 3% for aneurysms 5 to 5.9 cm, and 7% for aneurysms 6 cm or more in diameter.

Figure 10.2 The Crawford thoracoabdominal aortic aneurysm (TAAA) classification system.

Medical therapy to slow aneurysm growth or to reduce the risk of dissection or rupture has met w i t h l i m i t e d s u c ce s s . L o n g - t e r m - b l o c k e r t h e r a p y h a s b e e n s h o w n t o s i g n i f i c a n t l y s l o w t h e r a t e of aortic dilatation and to lower mortality. The goal of antihypertensive therapy is to maintain systolic blood pressure (BP) between 105 and 120 mm Hg. Patients should be followed with serial imaging studies for surveillance. A second imaging study should be obtained 6 months after initial diagnosis. If the aneurysm is unchanged in size, it is then reasonable to obtain an imaging study annually in most cases, excepting patients with Marfan syndrome or acute aortitis. Should there be a significant increase in aneurysm size between studies, the study interval should be decreased to 3 or 6 months. The optimal timing of surgical repair of thoracic aortic aneurysms depends both on the aneurysm size and the patient's associated comorbidities. For most ascending thoracic aortic aneurysms, surgery is indicated at a diameter of 5.5 cm or more. The threshold for surgery is raised to 6 cm or more for patients with an increased operative risk (e.g., the elderly or those with comorbidities). Conversely, among patients who are at increased risk of aortic dissection or rupture (e.g., Marfan syndrome or bicuspid aortic valve), aortic repair is recommended earlier (5 cm or smaller). Indeed, when patients with a bicuspid aortic valve require valve replacement

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surgery, the recommendation is for prophylactic replacement of the ascending aorta if its diameter is 4 cm or more. In general, for most descending thoracic aortic aneurysms, surgery is recommended at an aortic diameter 6 cm or more. P.257 Davies RR, Goldstein LJ, Coady MA, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg 2002;73: 1728. Devereux RB, Roman MJ. Aortic disease in Marfan's syndrome. N Engl J Med 1999;340: 1358 1359. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation 2005;111:816.

B. Preoperative Evaluation and Preparation B.1. How should thoracoabdominal aortic aneurysms (TAAAs) be surgically evaluated?
Preoperative assessment of the patient for elective TAAA repair requires a fine balance between the risks of aneurysm rupture vs. surgical morbidity. Most surgeons agree that a TAAA measuring 6 cm or more with a growth rate greater than 1 cm per year warrants surgical correction as a result of increased risk of rupture. The mortality of TAAA repair ranges from 3% to 23%. The incidence of spinal cord injury is 3% to 18%, with long-term survival being shorter in patients who suffer postoperative paraplegia or paraparesis. In one report, the 5-year survival rate for patients with spinal cord injury was 44%, whereas it was 62% for those without spinal cord injury. Spinal cord injury is caused by inadequate blood flow to the spinal cord during or after surgery. The period of cross clamping is most vulnerable as well as immediate period following declamping, whereby reperfusion injury can occur. Once the decision has been made to proceed with surgical repair, a comprehensive radiographic evaluation of the aorta is necessary for operative planning. Studies may include helical computed tomography (CT), contrast arteriography, and magnetic resonance (MR) angiography. All iodinated contrast studies should be performed well in advance of the planned procedure to avoid contrast-related renal dysfunction. Patients with baseline renal insufficiency may receive N-acetylcysteine to reduce the risk of contrast-related nephropathy and progressive renal failure. Preoperative assessment of the aneurysm anatomy and of the major branches is critical to surgical planning. Surgeons must decide to use a clamp-and-sew technique versus a distal aortic perfusion technique. Factors determining this decision include the expected difficulty of aortic exposure and completing the proximal aortic anastomosis. Unfortunately, the studies used to assess the aneurysm vasculature are imperfect with respect to delineating the spinal cord blood supply. CT angiography and MR angiography detect the artery of Adamkiewicz in only 50% to 80% of patients. This is significant as the risk of postoperative paraplegia is 5% if the artery of Adamkiewicz is identified preoperatively and reimplanted, whereas it is as high as 50%if the artery is not identified and reattached. Kieffer E, Ricard T, Chiras J, et al. Preoperative spinal cord arteriography in aneurysmal disease of the descending thoracic and thoracoabdominal aorta: preliminary results in 45 patients. Ann Vasc Surg 1987;3:3446. Levine WC, Lee JJ, Black JH, et al. Thoracoabdominal aneurysm repair: anesthetic management. Int Anesth Clin 2005;43:3960. Svensson LG, Crawford ES, Hess KR, et al. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17:357370. Tabayashi K. Spinal cord protection during thoracoabdominal aneurysm repair. Surg Today

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2005;35:16. P.258

B.2. Describe the anesthetic evaluation of the patient scheduled for thoracoabdominal aortic aneurysm (TAAA) repair
The preoperative assessment of a patient undergoing TAAA repair requires a thorough multisystem evaluation. Over 50% of patients are symptomatic at presentation. These include back pain, epigastric pain, hoarseness related to left recurrent laryngeal nerve palsy, shortness of breath, cough, and hemoptysis. Hypertension (70% to 90%) and coronary artery disease (CAD) (50%) are common in this patient population. Hemodynamic stress placed on the heart by proximal aortic cross-clamping mandates a thorough preoperative cardiac evaluation. Adequate knowledge of preoperative ventricular function, valvular function, and coronary anatomy can guide hemodynamic management and surgical decision making. The elective patient with clinical symptoms or electrocardiogram (ECG) signs of myocardial ischemia should undergo stress testing and, if necessary, coronary angiography. Angioplasty or coronary artery bypass graft surgery should be performed in patients with clinically significant CAD. The risk of perioperative cardiac morbidity and mortality is approximately 12% to 15%. Recent studies have shown that perioperative blockade may minimize this risk. Therefore, -blocker therapy should be initiated early and continued throughout the perioperative period. Postoperative respiratory failure is the leading cause of mortality in patients undergoing TAAA repair. Pulmonary function must be carefully evaluated as one-lung ventilation is essential for surgical repair of type I, II, and III aneurysms. As a large aneurysm can distort the left mainstem bronchus, the chest x-ray and computed tomography scan may give vital information regarding double lumen endotracheal tube placement. Patients actively smoking should be advised to quit smoking at least 2 weeks before surgery. Those showing good response to bronchodilators should be started on the same preoperatively to optimize pulmonary function. Patients with poor diffusing capacity or severe chronic obstructive pulmonary disease may require the use of cardiopulmonary bypass for TAAA repair as they may not be able to tolerate one-lung ventilation. Among patients presenting for surgical correction of TAAA, 13% to 24% have baseline renal i n s u f f i c i e n c y ( s e r u m c r e a t i n i n e > 1 . 5 m g / d L ) , p r i ma r i l y r e l a t e d t o h y p e r t e n s i o n , d i a b e t e s , a n d atherosclerotic disease. As type II, III, and IV thoracoabdominal aneurysms involve the visceral and juxtarenal aorta, renovascular disease is often encountered. Preoperative renal insufficiency is associated with an increased risk of postoperative renal failure, which in turn, is associated with increased mortality. Therefore, baseline renal function should be assessed. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 5th ed. Philadelphia: WB Saunders, 2006. Kouchoukos NT, Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997;336: 18761889. Levine WC, Lee JJ, Black JH, et al. Thoracoabdominal aneurysm repair: anesthetic management. Int Anesth Clin 2005;43:3960.

B.3. Describe the spinal cord blood supply


The spinal cord has a system of longitudinal and transverse arteries. Anatomic studies have shown that the most important longitudinal arteries are a single anterior spinal artery supplying 75% of the cord and a pair of posterior spinal arteries supplying 25% of the cord. The territory supplied by the anterior spinal artery is divided into three functionally distinct levels: cervicodorsal, midthoracic, and thoracolumbar. The cervicodorsal region receives its blood

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supply from the vertebral, subclavian, thyrocervical, and costocervical arteries. Themidthoracic region is supplied by a meager left or right intercostal artery arising between the fourth and the ninth thoracic P.259 vertebrae. The thoracolumbar region of the anterior spinal artery receives its blood supplymainly from one of the intercostal arteries called the arteria radicularis magna (ARM) or the artery of Adamkiewicz. It arises at the level of T5-8 in 15%, T9-12 in 60%, L1 in 14%, and L2 in 10% of patients. The ARM is often involved in the surgical repair. The anterior spinal artery is smaller above than below the entry of the ARM. Resistance to blood flow is 51 times greater going up the anterior spinal artery. Therefore, distal aortic perfusion during thoracic aortic cross-clamping protects the spinal cord below the ARM, but has minimal impact above it. This is why paraplegia still occurs in approximately 2% to 15% of patients having thoracic aortic surgery with distal aortic perfusion. However, reimplantation of intercostal arteries during surgery reduces the incidence of neurologic injury. Bromage PR. Epidural anesthesia. Philadelphia: WB Saunders, 1978:5054. DiChiro G, Fried LC, Doppman JL. Experimental spinal angiography. Br J Radiol 1970;43: 1930. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 5th ed. Philadelphia: WB Saunders, 2006. Miller RD, ed. Anesthesia, 6th ed. Philadelphia: Churchill Livingstone, 2005. Piccone W, DeLaria GA, Najafi H. Descending thoracic aneurysms. In: Bergan JJ, Yao JST, eds. Aortic surgery. Philadelphia: WB Saunders, 1989:249. Svensson LG, Richards E, Coull A, et al. Relationship of spinal cord blood flow to vascular anatomy during thoracic aortic cross-clamping and shunting. J Thorac Cardiovasc Surg 1986;91:7178.

B.4. What coexisting diseases commonly accompany thoracic aortic aneurysms?


The preoperative assessment of a patient undergoing thoracoabdominal aortic aneurysm (TAAA) repair requires a thorough multisystem evaluation. Because TAAAs are more common in the elderly, the frequency of comorbid disease is high. Hypertension, coronary artery disease, chronic obstructive pulmonary disease (COPD), diabetes and renal insufficiency are common in this patient population. Cambria RP, Clouse WD, Davison JK, et al. Thoracoabdominal aneurysm repair: results with 337 operations performed over a 15-year interval. Ann Surg 2002;236:471479. Svensson LG, Crawford ES, Hess KR, et al. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17:357368, discussion 368370. Svensson LG, Hess KR, Coselli JS, et al. A prospective study of respiratory failure after highrisk surgery on the thoracoabdominal aorta. J Vasc Surg 1991;14:271282.

B.5. What factors are associated with an increased risk of thoracoabdominal aortic aneurysm rupture?
Both aneurysm size and rate of expansion are predictors of rupture. The annual rupture rate is 2% for aneurysms less than 5 cm, 3% for aneurysms 5 to 5.9 cm, and 7% for aneurysms 6 cm or more in diameter. Therefore, the risk of rupture rises significantly when thoracic aneurysms reach a 6 cm size. Certain concomitant diseases also predict an increased risk of rupture, such as smoking, chronic obstructive pulmonary disease (COPD), advancing age, pain, and renal

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failure. Hypertension, although correlating with aneurysm development, has not been conclusively shown to increase the risk of rupture. P.260 Dapunt OE, Galla JD, Sadeghi AM, et al. The natural history of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 1994;107:13231333. Davies RR, Goldstein LJ, Coady MA, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg 2002;73:1728. Griepp RB, Ergin MA, Galla JD, et al. Natural history of descending thoracic and thoracoabdominal aneurysms. Ann Thorac Surg 1999;67:19271930. Juvonen T, Ergin MA, Galla JD, et al. Prospective study of the natural history of thoracic aortic aneurysms. Ann Thorac Surg 1997;63:15331544.

C. Intraoperative Management C.1. What hemodynamic monitors should be used for the patient undergoing thoracoabdominal aortic aneurysm (TAAA) repair?
Although the anesthetic management for TAAA repair varies amongst institutions, invasive hemodynamic monitoring, a double lumen endotracheal tube for one-lung ventilation, and rapid volume infusers are standard. Large bore peripheral IV's and central venous access are essential, as the potential for rapid intraoperative blood loss is significant. A rapid infusing system capable of heating and delivering fluids up to 500 mL per minute should be immediately available. An arterial line is usually placed in the upper extremity. During type I and II aneurysm repairs, the arterial line should be placed in the right radial artery as the proximal aortic crossclamp may disrupt left subclavian arterial blood flow. If left-heart bypass or a shunt is planned, a femoral arterial line may also be inserted to monitor distal aortic perfusion pressure. Transesophageal echocardiography (TEE) is also often used tomonitor heart function and volume status. Similarly, a pulmonary arterial catheter may be useful for monitoring intraoperative hemodynamics and for postoperative management. Levine WC, Lee JJ, Black JH, et al. Thoracoabdominal aneurysm repair: anesthetic management. Int Anesth Clin 2005;43:3960.

C.2. What blood bank support is necessary?


Thoracoabdominal aortic aneurysm repair is associated with the potential for massive blood loss. As such, early and timely communication with the blood bank is necessary to ensure that adequate quantities of packed red blood cells (pRBCs), fresh frozen plasma, and platelets are available. Five to ten units of pRBCs should be immediately available in the operating room, with a similar number of units available in the blood bank. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 5th ed. Philadelphia: WB Saunders, 2006.

C.3. What type of anticoagulation is used for thoracoabdominal aortic aneurysm (TAAA) repair? What can be done to minimize blood transfusion?
Heparin (100 U/kg) is typically administered 5 minutes before aortic cross-clamp placement. Unlike full cardiopulmonary bbypass (CPB), a reduced dose of heparin may be used for leftheart bypass. Autologous blood can be collected from the patient before or during (i.e., hemodilution)

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P.261 surgery. Use of blood salvaging techniques, such as the cell saver, can also limit homologous red cell transfusion. However, cell saving techniques may wash out valuable plasma clotting factors and platelets, resulting in a dilutional coagulopathy and thrombocytopenia. Additionally, if heparin is used as an anticoagulant in the cell saver, additional protamine sulfate may need to be administered. Although antifibrinolytic therapy may be used to minimize blood loss, several studies have suggested that antifibrinolytic therapy is of limited efficacy in the setting of TAAA repair. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 5th ed. Philadelphia: WB Saunders, 2006. Shore-Lesserson L, Bodian C, Vela-Cantos F, et al. Antifibrinolytic use and bleeding during surgery on the descending thoracic aorta: a multivariate analysis. J Cardiothorac Vasc Anesth 2005;19:453458.

C.4. Describe the surgical approach to thoracoabdominal aortic aneurysm repair

Position. The surgical approach is typically through the left chest, with the patient in a partial right lateral decubitus position and the hips almost supine to allow femoral cannulation.

Incision. The incision is tailored to complement the aneurysm extent. For types II, III, or IV, a thoracoabdominal incision is made from the symphysis pubis, extending midline to the umbilicus, curving straight into the costal cartilage and into a posterolateral thoracotomy incision. For types I and V, a modified thoracoabdominal incision is used, where the incision extends from the umbilicus to the chest and exposes the upper abdominal aorta. In this manner, an aortic cross can be applied either above or below the renal arteries.

Cannulation for left heart bypass. Left atrial to femoral artery bypass is often used in patients with significant myocardial dysfunction or other systemic disease, and in patients with extensive aneurysms that would require prolonged aortic cross clamping. Typically, an outflow cannula is placed in the left atrium, and blood is shunted through a centrifugal pump to an inflow cannula in the right femoral artery. Unlike cardiopulmonary bypass (CPB), left heart bypass requires reduced heparinization, that is, 100 U per kg of heparin approximately 5 minutes before cannulation. Potential advantage of left heart bypass include improved perfusion of the lower extremities and possibly of the anterior spinal artery through collateral vessels, while the proximal aorta is cross-clamped. Left heart bypass therefore minimizes the development of acidosis in the lower extremities, which in turn improves hemodynamic stability upon release of the aortic cross clamp. Left-heart bypass is typically initiated at a rate of 500 mL per minute, and once the proximal aortic clamp is placed, the flows are adjusted to maintain the proximal aortic pressure above 90 mm Hg or distal mean pressure of approximately 70 mm Hg.

Proximal aortic anastomosis. In type I and II repairs, the proximal thoracic aorta distal to the left subclavian is dissected away from the esophagus in order to prevent esophageal aortic fistula. Following placement of the proximal aortic clamp, a second clamp is placed at the sixth or eighth intercostal space of the mid-descending aorta. An appropriately sized Dacron graft is then sutured proximally to the descending thoracic aorta and checked for hemostasis. Once the proximal anastomosis is completed, the mid-descending thoracic clamp is moved to the infrarenal abdominal aorta. In type II aneurysms, left heart bypass is stopped and the aneurysm is opened. The celiac axis, superior mesenteric

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artery (SMA), and renal arteries are then identified and perfused with special catheters in order to protect the mesentery. The catheters perfusing the kidneys are typically passed through an ice-bath, maintaining the renal artery temperature below 15C (59F). Where feasible, reattachment of patent segmental intercostal and lumbar arteries in the T8 to L1 region is then performed. Intercostal arteries P.262 in the T4-8 region are usually ligated if they exhibit excessive retrograde bleeding, indicating good collateral circulation. If the intercostal arteries between T8 and L1 are occluded by intimal atherosclerosis, patent intercostal arteries in the T4-8 region may be reattached to preserve circulation.

Visceral aortic anastomoses. The visceral aortic anastomoses are evaluated intraoperatively. If the celiac axis, SMA, and renal arteries are close together, a single patch may be used to anastomose the viscera to the graft. Frequently, the left renal artery is pushed more caudad and is reattached with a bypass graft. Once the anastomoses are complete, visceral perfusion is stopped and the cannulas removed. The patient is then placed in a head down position, the aortic graft flushed proximally, and then the aortic cross clamp slowly released. The clamp is then moved to the abdominal aortic graft distal to visceral anastomoses.

D i s t a l a o r t i c a n a s t o m o s i s . T h e g r a f t i s n o w c u t t o t h e a p p r o p r i a t e l e n gt h a n d i s s u t u r e d t o the infrarenal aorta. Before the completion of the distal anastomosis, the graft is flushed proximally and the aorta distally. The lower clamp is slowly released to restore the pulsatile flow to the viscera. Any patent lumbar arteries are usually ligated.

Other techniques. Other techniques include the clamp and sew technique and use of CPB with deep hypothermic circulatory arrest (DHCA). The clamp and sew technique involves clamping the proximal descending thoracic aorta and replacing the aneurysm with a g r a f t . T h e d i s t a l a n a st o m o s i s t o t h e l o w e r a b d o m i n a l a o r t a i s t h e n p e r f o r m e d w i t h o u t a clamp, allowing the distal aorta to decompress. Although this technique avoids the need for full heparinization, it imposes a time limit on the surgeon as there is no pump to support distal or collateral perfusion. CPB with DHCA is used when the proximal aorta cannot be clamped without disrupting cerebral blood flow. Advantages of this technique include lack of hemodynamic changes with aortic clamping and unclamping, a bloodless surgical field, and organ protection because of low temperatures. Disadvantages include the need for full heparinization and the potential neurological risks of DHCA.

Coselli JS, LeMaire SA. Left heart bypass reduces paraplegia rates after thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 1999;67:19311934. Coselli JS, LeMaire SA, Figueiredo LP, et al. Paraplegia after thoracoabdominal aortic aneurysm repair: Is dissection a risk factor? Ann Thorac Surg 1997;63:2836. Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia, 5th ed. Philadelphia: WB Saunders, 2006. O'Conner CJ, Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: Part II. J Cardiothorac Vasc Anesth 1995;9:734747. Safi HJ. How I do it: thoracoabdominal aortic aneurysm graft replacement. Cardiovas Surg 1999;7:607613.

C.5. How would you induce the patient for thoracoabdominal aortic aneurysm repair?
The goal of anesthetic induction is to avoid anything that will increase the risk of aneurysm

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rupture, whereas at the same time, maintaining adequate end-organ perfusion. In general, the systolic blood pressure (BP) should be kept between 105 to 115 mm Hg, the heart rate between 60 to 80 bpm, and the cardiac index between 2 to 2.5 L/minute/m2. Short acting agents such as nitroglycerin, nicardipine or esmolol are ideal for hemodynamic control. Use of nitroprusside is discouraged because it has been associated with a higher risk of neurological complications. If motor evoked potentials (MEPs) are being monitored, either succinylcholine or a short acting nondepolarizing agent such as cis-atracurium may be used to facilitate tracheal intubation. P.263 Anesthetic maintenance may be achieved using a low concentration of an inhalation agent, combined with an infusion of propofol or short acting narcotic (e.g., sufentanil, remifentanil). If MEPs are not being monitored, the patient may be fully paralyzed, and inhalation agents with intermittent narcotics used. Hensley FA, Martin DE, Gravlee GP, eds. A practical approach to cardiac anesthesia, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2003:617647.

C.6. What major organ systems are threatened during thoracoabdominal aortic aneurysm repair?
The most significant threat to organ function and survival is the aortic cross clamp duration. The aortic cross clamp time is in turn related to the surgeon, surgical technique, and aneurysm type.

Spinal cord. Prolonged spinal cord ischemia can result in paraplegia or paraparesis. Factors contributing to spinal cord ischemia include the duration of the aortic cross-clamp, preexisting cord ischemia, and variability in the spinal arterial supply.

Kidneys and visceral mesentery. Ischemia of the kidneys can result in renal dysfunction or failure. Bowel ischemia can lead to an increase in intestinal permeability and sepsis.

Lungs. The lung parenchyma is subjected to manipulation, compression, and retraction throughout the surgery. Much of this manipulation occurs after the patient is anticoagulated. Tracheobronchial bleeding can significantly complicate perioperative ventilation.

Heart. Alterations in preload, afterload, and oxygen carrying capacity subject the heart to profound alterations inmyocardial oxygen delivery and consumption. These factors, along with intraoperative acidosis, hypocalcemia, and hypokalemia, can all negatively affect myocardial contractility and conduction. It is critical to assess these patients preoperatively for coronary disease given the many concomitant risk factors shared in patients with aortic disease and ischemic heart disease. In the setting of severe multivessel disease, it is common to perform coronary revascularization first, followed by thoracoabdominal surgery a few months later.

O'Conner CJ, Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: Part I. J Cardiothorac Vasc Anesth 1995;9:581588. O'Conner CJ, Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: Part II. J Cardiothorac Vasc Anesth 1995;9:734747.

C.7. What strategies are used for spinal cord protection?


Although type I and II thoracoabdominal aortic aneurysms (TAAAs) carry the greatest risk of injury, neurologic deficits can be seen with all types. Further, the risk of spinal cord injury increases with the duration of aortic clamping, with cross clamp times exceeding 60minutes being associated with substantial risk; however, as little as 30 minutes of ischemia can increase

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the risk of paralysis. In general, there are two strategies to decrease the incidence and severity of spinal cord injury: (a) maintenance of spinal cord blood flow and (b) use of neuroprotective a d j u n c t s t o a t t e n u a t e t h e e x c i t at o r y a n d i n f l a m m a t o r y m e c h a n i s m s t h a t c o n t r i b u t e t o i s c h e m i c injury.

Preoperative identification of the arteria radicularis magna (ARM). The risk of paraplegia is 5% if the ARM is identified preoperatively and reimplanted, whereas it is reported to be as high as 50% if it is not identified and reattached. However, postoperative paraplegia cannot always be prevented even if the ARM is identified and reimplanted.

Distal aortic perfusion/left heart bypass. Left heart bypass has the advantage of allowing mesenteric perfusion during the proximal clamp phase, minimizing myocardial hemodynamic P.264 stress by reducing preload and reducing time pressure on the surgeon to complete the proximal anastomosis. To minimize spinal cord injury, the distal aortic perfusion pressure should be 60 mm Hg or more. The risks of paraplegia are 2.2%, 2.3%, and 5.8% with left heart bypass, passive shunts (e.g., Gott shunt) and the clamp and sew technique, respectively; nevertheless, there can be significant differences in outcomes amongst centers and amongst surgeons.

Reattachment of the intercostal arteries. Reattachment of patent segmental intercostal and lumbar arteries in the T8 to L1 region is performed whenever feasible. This may require local end-arterectomy of the artery's origin. Intercostals in the T48 zone are typically oversewn, unless situated so as to be easily preserved in a beveled proximal aortic anastomosis in type I, II, or III TAAAs.

Hypothermia. Passive cooling (34C to 35C [93.2F to 95F]) is used to limit ischemic damage by reducing the tissue metabolic rate, which decreases the loss of intracellular adenosine 5-triphosphate (ATP) stores and lactic acid production. The precise temperature, however, to maximize this protective effect while minimizing related complications such as cardiac dysrhythmias and coagulopathy, is not well defined. After completing all anastomosis, effort is made to warm-up the patient so as to limit shivering and coagulopathy.

Placement of a cerebrospinal fluid (CSF) drain. Spinal cord perfusion pressure (SCPP) = MAP - CSF pressure. Although mean arterial pressure (MAP) minimally changes from central aorta to the periphery, there is concern over utilizing this modified estimation of SCPP. This is particularly worrisome in patients with systolic hypertension, which comprise most patients with aortic aneurysms, whereby the MAP may be overestimated. Nevertheless, evidence derived from animal models suggests that decreasing the CSF pressure to 10 mm Hg or more during aortic clamping enhances spinal cord perfusion and decreases the risk of injury. Therefore, a passive CSF drain is often used in the immediate perioperative period to keep the CSF pressure between 10 mm Hg and 12 mm Hg in patients at high risk for paraplegia (type I, II, and III TAAAs). Critically important is the rate and amount of volume removed. Excessive CSF drainage could cause cerebral hemorrhage consequent to massive intracranial fluid shifts or, more plausibly, from tearing of cerebral bridging. Recently, Darlik et al., reported a 3.5% incidence of subdural hematoma associated with TAAA surgery utilizing CSF drain. Of 230 patients, 8 were diagnosed with this complication that resulted in 50% surgical mortality. The result of a multivariate analysis identified CSF drain in excess of 690 79 mL to be an independent predictor of a subdural hemorrhage. Similarly, Settepani et al., reported on two rare cases of intracerebellar hematoma that was related to CSF drainage following thoracoabdominal aortic repair. Other reported side effects of CSF drainage include meningitis and

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iatrogenic paraplegia.

Neuroprotective agen