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The

5-Minute
Anesthesia
Consult
CHIEF EDITORIAL ASSISTANT

Matthew C. Gertsch, MD
Resident Physician
Department of Anesthesia, Critical Care and Pain Medicine
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts

EDITORIAL ASSISTANTS

J. Scott Bluth
Medical Student
University of Texas Medical School at Houston
Houston, Texas

Mark R. Bombulie
Medical Student
University of Texas Medical School at Houston
Houston, Texas

Kelly A. Bruno
Medical Student
The University of North Carolina, School of Medicine
Chapel Hill, North Carolina

N. Matthew Decker, BS
Medical Student
Loyola University Chicago Stritch School of Medicine
Maywood, Illinois

David Frey, DO
Resident Physician
Department of Anesthesiology and Pain Medicine
University of Washington Medical School
University of Washington Medical Center
Seattle, Washington

Megan Dale Henley


Medical Student
The University of North Carolina, School of Medicine
Chapel Hill, North Carolina

Thomas J. Hopkins, MD, MMCi


Resident Physician
Department of Anesthesiology
Duke University School of Medicine
Duke University Medical Center
Durham, North Carolina

Rachel M. Little, MPH


Medical Student
The University of North Carolina, School of Medicine
Chapel Hill, North Carolina

Carolyn Mohr, MD
Resident Physician
Department of Anesthesiology
University of Colorado School of Medicine
Anschutz Medical Campus
Denver, Colorado

Olutoyosi Ogunkua, MD
Resident Physician
Department of Anesthesiology and Pain Management
University of Texas Southwestern School of Medicine
University of Texas Southwestern Medical Center at Dallas
Dallas, Texas

Michael J. Oleyar, DO
Resident Physician
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Blake W. Perkins
Medical Student
University of Illinois College of Medicine
Peoria, Illinois

Matthew M. Peterson
Medical Student
Tulane University School of Medicine
New Orleans, Louisiana

Lauren Mai Pieczynski, MD


Resident Physician
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvaniaz

Adam M. Stuart
Medical Student
Virginia Commonwealth University School of Medicine
Richmond, Virginia

Lindsay Veit, MD
Resident Physician
Department of Anesthesiology
Rush Medical College
Rush University Medical Center
Chicago, Illinois

CONSULTANT EDITOR

Anita Gupta
The 5-Minute
Anesthesia
Consult
Editor

Nina Singh-Radcliff, MD
Section Editor

Alan J. Kover, MD, PharmD


Clinical Assistant Professor
Department of Anesthesiology
The Ohio State University College of Medicine
The Ohio State University Wexner Medical Center
Columbus, Ohio

Associate Editors

Kris E. Radcliff, MD
Assistant Professor of Orthopedic Surgery and Neurological Surgery
Thomas Jefferson University
The Rothman Institute
Philadelphia, Pennsylvania

Emily J. Baird, MD, PhD


Assistant Clinical Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Julie Scott Taylor, MD, MSc


Clinical Assistant Professor
Department of Anesthesiology
Stanford University
Palo Alto, California
Acquisitions Editor: Brian Brown
Product Manager: Nicole Dernoski
Production Manager: Bridgett Dougherty
Senior Manufacturing Manager: Benjamin Rivera
Marketing Manager: Lisa Lawrence
Design Coordinator: Teresa Mallon
Production Service: Aptara, Inc.

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Library of Congress Cataloging-in-Publication Data

Singh-Radcliff, Nina.
The 5-minute anesthesia consult / [edited by] Nina Singh-Radcliff.
p.; cm. - (5-minute consult)
Includes bibliographical references and index.
ISBN 978-1-4511-1894-0 (alk. paper)
I. Title. II. Series: 5-minute consult.
[DNLM: 1. Anesthesia-Handbooks. 2. Perioperative Period-Handbooks. 3. Surgical Procedures, Operative-Handbooks. WO
231]
617.9’6-dc23 2012023881

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However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from
application of the information in this book and make no warranty, expressed or implied, with respect to the currency,
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10 9 8 7 6 5 4 3 2 1
To my parents, Dilip and Madhulika Singh, for their unconditional love and support throughout my life and career and
teaching me by example about kindness, honesty, and dedication. Children cannot choose their parents, but if I had been
given the opportunity, I would choose them. I also need to give a special thanks to Carmen, my first child, who helped me
edit the book while in utero. And finally to my husband, Dr. Kris Radcliff, who served as an Associate Editor to this book.
Words cannot convey my gratitude for his contribution to, and support, with this text. I have known Kris for almost one-third
of my life and he remains the most intelligent, kind, patient, humble, and wonderful person I know. He still makes my heart
flutter when I see him. He is the best thing that has ever happened to me and I am truly blessed to be able to call him my
husband and share my life with him.
CONTRIBUTORS

Ali R. Abdullah, MBChB


Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Erik E. Abel, PharmD, BCPS


Clinical Assistant Professor
Department of Anesthesiology
The Ohio State University College of Medicine
The Ohio State University Wexner Medical Center
Columbus, Ohio

Benjamin Abraham, MD
Department of Anesthesiology
The Cleveland Clinic
Cleveland, Ohio

Andaleeb Abrar Ahmed, MBBS, MD, MPH


Resident Physician
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Moustafa Ahmed, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Interim Chief, Philadelphia VA Medical Center
Philadelphia, Pennsylvania

Jane C. Ahn, MD
Assistant Professor
Department of Anesthesiology and Perioperative Care
University of California, Irvine School of Medicine
University of California, Irvine Douglas Hospital
Irvine, California

Arun Alagappan, MD
Resident Physician
Department of Anesthesiology
Mount Sinai School of Medicine
St. Joseph’s Hospital and Regional Medical Center
Paterson, New Jersey

Brooke Albright, MD, MAJ, MC


Assistant Professor of Anesthesiology
Critical Care Air Transport Team Physician
United States Air Force
Landstuhl, Germany

Tayab R. Andrabi
Associate Professor
Department of Anesthesiology & Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Jonathan Anson, MD
Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

John L. Ard Jr., MD


Assistant Professor
Department of Anesthesiology
New York University School of Medicine
NYU Langone Medical Center
New York, New York

Radha Arunkumar, MD
Associate Clinical Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Alan Ashworth, MBChB, FRCA, FFICM


Consultant in Cardiothoracic Anaesthesia and Intensive Care
University Hospital of South Manchester
Manchester, UK

Kalliopi Athanassiadi, MD, PhD


Senior Thoracic Surgeon
Department of Surgery
University of Athens Medical School
Athens, Greece

Joshua A. Atkins, MD, PhD


Assistant Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Ahmed Fikry Attaallah, MD, PhD


Assistant Professor
Department of Anesthesiology
West Virginia University School of Medicine
Robert C. Byrd Health Sciences Center
Morgantown, West Virginia

John G. T. Augoustides, MD, FASE, FAHA


Associate Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Naola Austin, MD
Resident Physician
Department of Anesthesiology and Pain Medicine
University of Washington Medical School
University of Washington Medical Center
Seattle, Washington

Stephen O. Bader, MD
Assistant Professor
Department of Anesthesiology
West Virginia University School of Medicine
Robert C. Byrd Health Sciences Center
Morgantown, West Virginia
Sean M. Bagshaw, MD, MSc, FRCPC
Assistant Professor
Division of Critical Care
University of Alberta
Edmonton, AB Canada

Timothy R. Ball, MD
Assistant Clinical Professor
Department of Anesthesiology
Texas A&M College of Medicine
Scott & White Memorial Hospital
Temple, Texas

Andrew L. Barker, MD
Resident Physician
Department of Anesthesiology
Texas A&M College of Medicine
Scott and White Hospital
Temple, Texas

Viachaslau Barodka, MD
Assistant Professor
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Amy Barulic, BS, MHS


Research Assistant
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Colin Bauer, MD
Chief Resident
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Shawn T. Beaman, MD
Assistant Professor
Associate Residency Program Director
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

John F. Bebawy, MD
Assistant Professor of Anesthesiology and Neurological Surgery
Feinberg School of Medicine, Northwestern University
Northwestern Memorial Hospital
Chicago, Illinois

A. Katharina Beckmann, MD
Fellow, Cardiac Anesthesia
Department of Anesthesiology
Feinberg School of Medicine, Northwestern University
Northwestern Memorial Hospital
Chicago, Illinois

Sascha Beutler, MD, PhD


Assistant Professor
Assistant Program Director
Department of Anesthesiology, Perioperative and Pain Medicine
Harvard Medical School
Brigham and Women’s Hospital
Boston, Massachusetts

Dmitri Bezinover, MD, PhD


Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Amar M. Bhatt, MD
Resident Physician
Department of Anesthesiology
The Ohio State University College of Medicine
The Ohio State University Wexner Medical Center
Columbus, Ohio

Shreyas Bhavsar, DO
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Jeanna Blitz, MD
Assistant Professor
Department of Anesthesiology
New York University School of Medicine
NYU Langone Medical Center
New York, New York

J. Scott Bluth, BS
Medical Student
University of Texas Medical School at Houston
Houston, Texas

Michael L. Boisen, MD
Fellow, Cardiothoracic Anesthesiology
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Eric Bolin, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Mark R. Bombulie, BS
Medical Student
University of Texas School of Medicine at Houston
Houston, Texas

James D. Boone, MD
Instructor
Feinberg School of Medicine, Northwestern University
Northwestern Memorial Hospital
Chicago, Illinois

Mary Brady, MD, FASE


Assistant Professor
Medical Director, Post-Anesthesia Care Unit
Director, Intraoperative Transesophageal Echocardiography Program
Department of Anesthesiology and Critical Care Medicine
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Michelle Braunfeld, MD
Clinical Professor
Department of Anesthesiology and Critical Care Medicine
David Geffen School of Medicine at UCLA
Chief, Department of Anesthesiology
Greater Los Angeles Veterans Affairs Hospital
Los Angeles, California

Tod A. Brown, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Charles H. Brown IV, MD


Assistant Professor
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Kelly Bruno, BS, MD


Medical Student
University of North Carolina School of Medicine
Chapel Hill, North Carolina

Ethan O. Bryson, MD
Associate Professor
Department of Anesthesiology and Psychiatry
Mount Sinai School of Medicine
The Mount Sinai Hospital
New York, New York

Arne O. Budde, MD, DEAA


Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania
James Cain, MD
Department of Anesthesiology and Pediatrics
University of Pittsburgh School of Medicine
Children’s Hospital of Pittsburgh of UPMC
Pittsburgh, Pennsylvania

James M. Callas, MD
Chief, Department of Radiology
King’s Daughters Clinic
Temple, Texas

Neal Campbell, MD
Assistant Professor
Department of Anesthesiology & Pediatrics
University of Pittsburgh School of Medicine
Children’s Hospital of Pittsburgh of UPMC
Pittsburgh, Pennsylvania

Elena C. Capello, MD
Universita di Torino
Dipartimento di Discipline Medico-Chirurgiche
Sezione di Anestesiologia e Rianimazione
Ospedale S. Giovanni Battista

John B. Carter, MD
Associate Professor
Department of Anesthesiology
Oklahoma University College of Medicine
Oklahoma University Health Sciences Center
Oklahoma City, Oklahoma

Michael Carter, MD, PhD


Resident Physician
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Daniel Castillo, MD
Assistant Professor
Department of Anesthesiology
University of Florida College of Medicine
Shands Jacksonville Medical Center
Jacksonville, Florida
Davide Cattano, MD, PhD
Associate Professor
Department of Anesthesiology
University of Texas Medical School at Houston
Memorial Hermann Hospital
Houston, Texas

Laura F. Cavallone, MD
Assistant Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

John T. Chalabi, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Vinay Chandrasekhara, MD
Instructor
Division of Gastroenterology, Department of Medicine
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Jean Charchaflieh, MD, DrPH, FCCM, FCCP


Associate Professor
Department of Anesthesiology
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut

Verghese T. Cherian, MBBS, MD, FFARCSI


Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Jason Choi, MD
Resident Physician
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Christopher G. Choukalas, MD, MS


Assistant Professor
Department of Anesthesia and Perioperative Care
University of California, San Francisco
San Francisco VA Medical Center
San Francisco, California

Jason Han Chua, MD


Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Theodore J. Cios, MD, MPH


Resident Physician
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Carlee Clark, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Matthew D. Cohen, DO
Assistant Professor
Chief, Division of Acute Pain and Regional Anesthesia
Department of Anesthesiology
University of Oklahoma
The University of Oklahoma Health Sciences Center
Oklahoma City, Oklahoma

Seth R. Cohen, DO
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

John F. Coleman, MD
Clinical Fellow
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Lydia A. Conlay, MD, PhD


Russell D and Mary B Sheldon Professor
Vice Chairwoman for Academic Affairs
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Craig R. Cook, MD, PhD


Resident Physician
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Daniel Cormican, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Charles E. Cowles Jr., MD


Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Ryan Crowley, MD
Staff Physician
Department of Anesthesiology
Legacy Good Samaritan Hospital
Portland, Oregon
William C. Culp Jr., MD, FASE
Associate Professor
Department of Anesthesiology
Texas A&M University College of Medicine
Scott and White Hospital
Temple, Texas

Cristina Cunanan, MD
Resident Physician
Department of Anesthesiology and Critical Care Medicine
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Priti G. Dalal, MD, FRCA


Associate Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Patricia Dalby, MD
Associate Professor
Department of Anesthesiology
University of Pittsburgh School of Medicine
Magee-Women’s Hospital of UPMC
Pittsburgh, Pennsylvania

Lori Dangler, MD, MBA


Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Nisha Dave, DO, PharmD


Resident Physician
Mount Sinai School of Medicine
St. Joseph’s Regional Medical Center
Paterson, New Jersey

Alberto J. de Armendi, MD, AM, MBA


Professor
Chief, Pediatric Anesthesia
Department of Anesthesiology
Oklahoma University College of Medicine
Children’s Hospital of Oklahoma
Oklahoma City, Oklahoma

Stephen Dechter, DO

N. Matthew Decker, BS
Medical Student
Loyola University Chicago Stritch School of Medicine
Maywood, Illinois

Matthew Delph, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Jagan Devarajan, MD, FRCA


Associate Staff
Department of Anesthesiology
The Cleveland Clinic
Cleveland, Ohio

Anahat Dhillon, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care Medicine
David Geffen School of Medicine at UCLA
Ronald Reagan Medial Center
Los Angeles, California

Bradley T. Dollar, MD
Assistant Professor
Residency Program Director
Department of Radiology
Texas A&M College of Medicine
Scott and White Hospital
Temple, Texas

Kathleen S. Donahue, DO, FAAP


Associate Professor
Associate Vice Chair, OR Management
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Shawna Dorman, MD
Instructor
Department of Anesthesiology
New York University School of Medicine
NYU Langone Medical Center
New York, New York

Corey C. Downs, MD
Staff Anesthesiologist
Surgical and Perioperative Careline
VA Greater Los Angeles Healthcare System
Los Angeles, California

Emily L. Drennan, MD
Assistant Professor
Department of Anesthesiology
University of Texas Medical School at Houston
Memorial Hermann Hospital
Houston, Texas

Rebecca A. Drinkaus, MD
Assistant Professor
Department of Anesthesiology
Oklahoma University College of Medicine
Oklahoma University Health Sciences Center
Oklahoma City, Oklahoma

Peter Drocton, MD
Department of Anesthesiology
Cedars-Sinai Medical Center
Los Angeles, California
Department of Anesthesiology
Olive View - UCLA Medical Center
Sylmar, California

Mirsad Dupanovic, MD
Assistant Professor
Department of Anesthesiology
Kansas University School of Medicine
Kansas University Medical Center
Kansas City, Kansas
Victor Duval, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Ramana V. Duvvuri, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

J. Andrew Dziewit, MD
Attending Physician
Department of Anesthesia
Crozer Chester Medical Center
Upland, Pennsylvania

Jill Eckert, DO
Assistant Professor
Residency Program Director
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Nabil Elkassabany, MD
Assistant Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Matthew Ellison, MD
Assistant Professor
Department of Anesthesiology
West Virginia University School of Medicine
Robert C. Byrd Health Sciences Center
Morgantown, West Virginia

Trent Emerick, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Thomas I. Epperson III, MD


Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Zhuang-Ting Fang, MD, MSPH


Associate Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Jared Feinman, MD
Fellow, Cardiothoracic Anesthesia
Department of Anesthesia, Critical Care and Pain Medicine
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts

Larry C. Field, MD
Assistant Professor
Medical Director, Medical/Surgical ICU
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Robert S. Fitzgerald, LittB, STB, MA, STM, PhD


Professor
Environmental Health Sciences, Physiology, Medicine
The Johns Hopkins University
Baltimore, Maryland

Linzy Fitzsimons, MD
Resident Physician
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Melissa Flanigan, DO
Assistant Professor
Department of Anesthesiology
West Virginia University School of Medicine
Robert C. Byrd Health Sciences Center
Morgantown, West Virginia

Andrew Fond, MD
Assistant Clinical Professor
Department of Anesthesiology and Pain Management
University of Southern California
Los Angeles, California

Siyavash Fooladian, MD, MPH


Fellow, Cardiothoracic Anesthesiology
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Caroline Fosnot, DO, MS


Clinical Instructor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

John J. Freely Jr., MD


Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Megan M. Freestone-Bernd, MD
Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania
Katy E. French-Bloom, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

John C. Frenzel, MD
Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

David Frey, BA
Medical Student
Ohio University College of Osteopathic Medicine
Athens, Ohio

David P. Frey, DO
Resident Physician
Department of Anesthesiology and Pain Medicine
University of Washington Medical School
University of Washington Medical Center
Seattle, Washington

Elizabeth A.M. Frost, MD


Professor of Anesthesiology
Mount Sinai School of Medicine
The Mount Sinai Hospital
New York, New York

Kamilia S. Funder, MD
Physician
Department of Anesthesia
Copenhagen University Hospital, Rigshospitalet
Copenhagen, Denmark

Jorge A. Galvez, MD
Fellow, Pediatric Anesthesiology
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Children’s Hospital of Philadelphia
Philadelphia, Pennsylvania

Wei Dong Gao, MD, PhD


Associate Professor
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Stephanie Gargani, MD
Resident Physician
Department of Anesthesiology
Mount Sinai School of Medicine
St. Joseph’s Regional Medical Center
Paterson, New Jersey

Andrew Geller, MD
Resident Physician
Department of Anesthesiology
Charles Drew University of Medicine and Science
Cedars-Sinai Medical Center
Los Angeles, California

Matthew C. Gertsch, MD
Resident Physician
Department of Anesthesia, Critical Care and Pain Medicine
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts

Ileana Gheorghiu, MD
Assistant Professor
Department of Anesthesiology
University of Maryland School of Medicine
University of Maryland Medical Center
Baltimore, Maryland

Brian Gierl, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Lori Gilbert, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Philadelphia VA Medical Center
Philadelphia, Pennsylvania

Ronnie J. Glavin, MB, ChB, MPhil, FRCA, FRCP (Glas)


Consultant Anesthetist
Victoria Infirmary
Glasgow, United Kingdom

Christine E. Goepfert, MD, PhD, DESA


Instructor and Visiting Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Emily Gordon, MD
Instructor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Shannon M. Gossett-Popovich, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Amitabh Goswami, DO, MPH


Fellow, Pain Management
Department of Anesthesiology and Pain Medicine
University of California, Davis School of Medicine
UC Davis Medical Center
Sacramento, California

Ori Gottlieb, MD
Assistant Professor
Department of Anesthesia and Critical Care
Pritzker School of Medicine, University of Chicago
The University of Chicago Medicine
Chicago, Illinois

Vijaya Gottumukkala, MB, BS, MD, FRCA


Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Basavana G. Goudra, MD, FRCA, FCARCSI


Assistant Clinical Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Andreas Grabinsky, MD
Assistant Professor
Department of Anesthesiology
University of Washington School of Medicine
Harborview Medical Center
Seattle, Washington

Ashley Greene, DO
Resident Physician
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Michael S. Green, DO
Assistant Professor
Interim Chair
Department of Anesthesiology and Perioperative Medicine
Drexel University College of Medicine
Hahnemann University Hospital
Philadelphia, Pennsylvania

Alina M. Grigoire, MD, MHS, FASE


Associate Professor
Director, Division of Cardiothoracic Anesthesiology
Department of Anesthesiology
University of Maryland School of Medicine
University of Maryland Medical Center
Baltimore, Maryland

Michael Grover, MD
Resident Physician
Department of Anesthesiology
University of Texas School of Medicine, San Antonio
University of Texas Health Science Center at San Antonio
San Antonio, Texas

Anthony H. Guarino, MD
Director, Pain Management
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Vadim Gudzenko, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Maged N. Guirguis, MD
Department of Anesthesiology and Pain Management
The Cleveland Clinic
Cleveland, Ohio

Gregory MT Hare, MD, PhD


Associate Professor
Department of Anesthesia
St. Michael’s Hospital
Toronto, Canada

Jagtar Singh Heir, DO


Clinical Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Rachel Helle, DO
Resident Physician
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Laura B. Hemmer, MD
Assistant Professor
Feinberg School of Medicine, Northwestern University
Northwestern Memorial Hospital
Chicago, Illinois

John Henao, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Andrew Herlich, DMD, MD, FAAP


Professor
Department of Anesthesiology
University of Pittsburgh School of Medicine
Chief, UPMC Mercy
Pittsburgh, Pennsylvania

Ibetsam Hilmi, MBChB, FRCA


Associate Professor
Department of Anesthesiology
Institute of Clinical and Translational Sciences
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Jonathan K. Ho, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

John W. Hoffman, Jr., DO, MS


Clinical Instructor
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Michael P. Hofkamp, MD
Assistant Professor
Department of Anesthesiology
Texas A&M, -College of Medicine
Scott and White Hospital
Temple, Texas

Allen Alexander Holmes, MD, MS


Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Joe C. Hong, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Kimberly Howard-Quijano, MD
Clinical Instructor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Tyken C. Hsieh, MD
Staff Cardiac Anesthesiologist
Department of Anesthesiology
Mills-Peninsula Health Services
Burlingame, California

Angela T. Hsu, MD
Attending Physician
Department of Anesthesiology
Kaiser Permanente
Downey, California

Eric S. Hsu, MD
Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Allen Hu, MD
T. Kate Huncke, MD
Clinical Associate Professor
Department of Anesthesiology
New York University School of Medicine
NYU Langone Medical Center
New York, New York

Catherine Ifune, MD, PhD


Associate Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Mohamad Iravani, MD
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Selma Ishag, MB, BS, MD


Assistant Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri
%

Jonathan S. Jahr, MD
Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Ranu Jain, MD
Assistant Professor
Assistant Director, Pediatric Anesthesia
Department of Anesthesiology
The University of Texas School of Medicine at Houston
Children’s Memorial Hermann Hospital-Texas Medical Center
Houston, Texas

Piotr K. Janicki, MD, PhD


Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Richard C. Jensen, MD
Resident Physician
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Rongjie Jiang, MB, MS


Resident Physician
Department of Anesthesiology
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut

Quinn L. Johnson, MD
Assistant Clinical Professor
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Praveen Kalra, MBBS, MD, FCCP


Assistant Professor
Department of Anesthesiology
Oklahoma University College of Medicine
Oklahoma University Health Sciences Center
Oklahoma City, Oklahoma

Mandip S. Kalsi, MD
Fellow, Regional Anesthesia
Hospital for Special Surgery
New York, New York

Valbona Kanarek, MD
Chief Resident
Department of Anesthesiology
Mt. Sinai School of Medicine
St. Joseph’s Hospital and Regional Medical Center
Paterson, New Jersey

Revati Kanekar, MD
Resident Physician
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Ivan M. Kangrga, MD, PhD


Associate Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Susan Kaplan, MD
Clinical Associate
Department of Anesthesiology and Critical Care
University of Pennsylvania
Philadelphia, Pennsylvania

Menelaos Karanikolas, MD, MPH


Assistant Professor
Department of Anesthesiology
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Keyvan Karkouti, MD, FRCPC, MSc


Associate Professor
Department of Anesthesia
University of Toronto
Toronto, Ontario

Jeffrey Katz, MD
Chief Resident
Department of Anesthesia and Critical Care
Pritzker School of Medicine, University of Chicago
The University of Chicago Medicine
Chicago, Illinois

Paul Kerby, MB, BS


Chief Resident
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Patrick Kim, MD
Resident Physician
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Peter H. Kim, MD

Andrew A. Klein, MD
Consultant
Anaesthesia and Intensive Care
Papworth Hospital
Cambridge, United Kingdom

Antoun Koht, MD
Professor of Anesthesiology, Neurological Surgery & Neurology
Feinberg School of Medicine, Northwestern University
Northwestern Memorial Hospital
Chicago, Illinois

Iosifina Kolliantzaki, MD
Department of Anesthesiology
Aghia Sophia Children’s Hospital
Athens, Greece

James J. Konvicka, MD
Assistant Professor
Department of Anesthesiology
Texas A&M College of Medicine
Scott and White Healthcare
Temple, Texas

Edward Kosik, DO

John D. Kot, MD
Resident Physician
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Joseph Koveleskie, MD
Assistant Professor
Department of Anesthesiology
Tulane University School of Medicine
Tulane Medical Center
New Orleans, Louisiana

Alan J. Kover, MD, PharmD


Clinical Assistant Professor
Department of Anesthesiology
The Ohio State University College of Medicine
The Ohio State University Wexner Medical Center
Columbus, Ohio

Kenneth F. Kuchta, MD
Associate Clinical Professor
Chief, Vascular Anesthesiology
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Anand Lakshminarasimhachar, MBBS, FRCA


Assistant Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Daniel A. Lazar, MD
Attending Anesthesiologist
North Shore Manhasset Hospital
Manhasset, New York

Stephane Ledot, MD
Hadassah Hebrew University School of Medicine
Jerusalem, Israel

Thomas Ledowski, MD, PD, DEAA, FANZCA


Professor of Anesthesiology
University of Western Australia
School of Medicine and Pharmacology
Perth, Australia

Annie D. Lee, MD
Resident Physician
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Jonathan D. Leff, MD
Assistant Professor
Chief, Cardiothoracic Anesthesiology
Department of Anesthesiology
Albert Einstein College of Medicine
Montefiore Medical Center
Bronx, New York

Philip Levin, MD
Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Jinlei Li, MD, PhD


Assistant Professor
Department of Anesthesiology
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut

Yun Rose Li, BS


Medical Student
Perelman School of Medicine at the University of Pennsylvania
Philadelphia, Pennsylvania

Jeffrey W. Lim, MD, PhD


Assistant Professor
Department of Anesthesiology
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut
Sharon L. Lin, MD
Attending Physician
Department of Anesthesiology
Swedish Medical Center
Seattle, Washington

Keith E. Littlewood, MD
Associate Professor
Vice Chair for Education
Department of Anesthesiology
Assistant Dean for Clinical Skills Education
University of Virginia School of Medicine
University of Virginia Health System
Charlottesville, Virginia

Marc A. Logarta, MD, DABA, FANZCA


Consultant Anesthetist
Campbelltown Hospital
Canterbury Hospital
Sydney, Australia

David W. Lui, DMD, MD


Assistant Professor
Department of Oral and Maxillofacial Surgery
Virginia Commonwealth University School of Dentistry and School of Medicine
VCU Medical Center
Richmond, Virginia

Calvin Lyons, MD
Resident Physician
Department of Surgery
The Methodist Hospital
Houston, Texas

Edna Ma, MD
Attending Physician
Department of Anesthesiology
Olive View - UCLA Medical Center
Sylmar, California

Aman Mahajan, MD, PhD


Professor
Chief, Cardiothoracic Anesthesiology
Vice Chair of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Victor L. Mandoff, MD
Associate Professor
Department of Anesthesiology and Critical Care Medicine
The University of Arkansas College of Medicine
The University of Arkansas for Medical Sciences
Little Rock, Arkansas

Gerard R. Manecke, Jr., MD


Professor and Chair
Department of Anesthesiology
University of California, San Diego School of Medicine
University of California, San Diego Medical Center
San Diego, California

Federica Manfroi, MD

Michael Mangione, MD
Associate Professor
Department of Anesthesiology
University of Pittsburgh School of Medicine
Chief of Anesthesiology
VA Pittsburgh Healthcare System
Pittsburgh, Pennsylvania

Natesan Manimekalai, MD
Assistant Professor
Department of Anesthesiology
University of Florida College of Medicine
Shands Jacksonville Medical Center
Jacksonville, Florida

Ana Maria Manrique-Espinel, MD


Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Brian L. Marasigan, MD
Assistant Professor
Residency Program Director
Department of Anesthesiology
University of Texas Medical School at Houston
Memorial Hermann Hospital
Houston, Texas

Julie Marshall, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Jayson T. Maynes, MD, PhD


Assistant Professor
Hospital for Sick Children/SickKids Research Institute
University of Toronto
Toronto, Canada

Richard McAffee, MD
Assistant Professor
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Mary E. McAlevy, MD
Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Russell K. McAllister, MD
Associate Professor
Residency Program Director
Department of Anesthesiology
Assistant Dean of Quality and Patient Safety
Texas A&M College of Medicine
Scott & White Memorial Hospital
Temple, Texas

Dwayne E. McClerkin, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Stephen M. McHugh, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Julie McSwain, MD, MPH


Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Li Meng, MD, MPH


Associate Professor
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Spyros D. Mentzelopoulos, MD, PhD


Assistant Professor
Department of Critical Care
University of Athens Medical School
Athens, Greece

David G. Metro, MD
Associate Professor
Residency Program Director
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Berend Mets, MB, ChB, PhD, FRCA, FFASA


Eric A. Walker Professor and Chair
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Tricia A. Meyer, PharmD, MS, FASHP


Associate Professor
Department of Anesthesiology
Director, Department of Pharmacy
Texas A&M College of Medicine
Scott and White Hospital
Temple, Texas

Agnes Miller, MD
Director, Resident Education
Department of Anesthesiology
Maimonides Medical Center
New York, New York

Sara Miller, MD
Resident Physician
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Brian Milne, MD, MSc, FRCPC


Professor
Department of Anesthesiology and Perioperative Medicine
Queen’s University
Kingston General Hospital
Kingston, Ontario

Beth H. Minzter, MD, MS, FIPP


Department of Pain Management
Anesthesiology Institute
The Cleveland Clinic
Cleveland, Ohio

Nanhi Mitter, MD
Assistant Professor
Director, Adult Cardiothoracic Anesthesiology Fellowship
Department of Anesthesiology and Critical Care Medicine
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland
Kanishka Monis, MD
Fellow, Pain Management
Department of Anesthesiology
University of Texas School of Medicine, San Antonio
University of Texas Health Science Center at San Antonio
San Antonio, Texas

Richard C. Month, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Teresa L. Moon, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Kenneth R. Moran, MD
Assistant Clinical Professor
Department of Anesthesiology
The Ohio State University College of Medicine
The Ohio State University Wexner Medical Center
Columbus, Ohio

Allyson J.A. Morman, MD


Resident Physician
Department of Anesthesiology
University of Virginia School of Medicine
University of Virginia Health System
Charlottesville, Virginia

Juan Moya-Amor’s, PhD


Professor of Surgery
Chief, Department of Thoracic Surgery
Hospital Universitari de Bellvitge
L’Hospitalet de Llobregat
Barcelona, Spain

Daniel Mulcrone, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Eman Nada, MD, PhD


Fellow, Neuroanesthesia
The Cleveland Clinic
Cleveland, Ohio

Carsten Nadjat-Haiem, MD
Associate Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Sharanya Nama, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Gundappa Neelakanta, MD
Clinical Professor of Anesthesiology
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Jacques Prince Neelankavil, MD


Assistant Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Eric W. Nelson, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina
Sara C. Nelson, MD
Attending Physician
Department of Anesthesiology
Naval Medical Center San Diego
San Diego, California

Edward C. Nemergut, MD
Associate Professor of Anesthesiology and Neurosurgery
University of Virginia School of Medicine
University of Virginia Health System
Charlottesville, Virginia

Anh-Thuy Nguyen, MD
Associate Clinical Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Linh Trang Nguyen, MD


Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Teodora Orhideea Nicolescu, MD


Associate Professor
Chief, Division of Cardiothoracic Anesthesiology
Department of Anesthesiology
Oklahoma University College of Medicine
Oklahoma University Health Sciences Center
Oklahoma City, Oklahoma

Daniel R.C. Nieva, MD


Assistant Professor
Department of Anesthesiology
Washington University School of Medicine
St. Louis Children’s Hospital
St. Louis, Missouri

Dave Nisha Davendra, PharmD, DO


Assistant Clinical Professor
Department of Anesthesiology
Mount Sinai School of Medicine
St. Joseph’s Hospital and Regional Medical Center
Paterson, New Jersey

Mark E. Nunnally, MD, FCCM


Associate Professor
Department of Anesthesia and Critical Care
Pritzker School of Medicine, University of Chicago
The University of Chicago Medicine
Chicago, Illinois

Satoru Ogawa, MD
Department of Anesthesiology
Emory University School of Medicine
Emory University Hospital
Atlanta, Georgia

Olutoyosi Ogunkua, MD
Resident Physician
Department of Anesthesiology and Pain Management
University of Texas Southwestern School of Medicine
University of Texas Southwestern Medical Center at Dallas
Dallas, Texas

Erik Olness, MD
Assistant Professor
Department of Anesthesiology
West Virginia University School of Medicine
Robert C. Byrd Health Sciences Center
Morgantown, West Virginia

Onyi Onuoha, MD, MPH


Assistant Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Todd M. Oravitz, MD
Associate Professor
Chief, Liver Transplantation Anesthesiology
Department of Anesthesiology
The University o Pittsburgh School of Medicine
VA Pittsburgh Healthcare System
Pittsburgh, Pennsylvania
Pascal O. Owusu-Agyemang, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Nirvik Pal, MD
Clinical Instructor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Edward Park, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Dorothea Rosenberger Parravano, MD, PhD


Associate Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Andrea Parsons, MD
Assistant Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Parisa Partownavid, MD
Associate Clinical Professor
Associate Director, Ambulatory Surgery Center
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Mitesh Patel, MD
Chief Resident
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Neesa Patel, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Shetal H. Patel, MD
Fellow, Obstetric Anesthesiology
Department of Anesthesiology
Charles Drew University of Medicine and Science
Cedars-Sinai Medical Center
Los Angeles, California

Swati Patel, MD
Clinical Professor of Anesthesiology
Chief, Division of Pediatric Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Tara L. Paulose, MD
Department of Anesthesiology
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut

Katerina Pavenski, MD, FRCPC


Department of Laboratory Medicine
St. Michael’s Hospital, Toronto, Canada
Department of Laboratory Medicine and Pathobiology, University of Toronto Toronto, Canada

Alison R. Perate, MD
Assistant Professor
Department of Anesthesiology
Perelman School of Medicine at the University of Pennsylvania
Children’s Hospital of Philadelphia
Philadelphia, Pennsylvania
Lauren Mai Pieczynski, MD
Resident Physician
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Raymond M. Planisic, MD
Professor of Anesthesiology
Director, Transplantation Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Keyuri Popat, MD
Associate Professor
Department of Anesthesiology and Pain Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Wanda M. Popescu, MD
Associate Professor of Anesthesiology
Yale-New Haven Hospital
New Haven, Connecticut

Marek Postula, MD, PhD


Assistant Professor at the Department of Experimental and Clinical Pharmacology
Medical University of Warsaw
Senior Assistant at the Department of Noninvasive Cardiology and Hypertension
Central Clinical Hospital
The Ministry of the Interior
Warsaw, Poland

Debra Domino Pulley, MD


Associate Professor
Department of Anesthesiology and Pain Medicine
Washington University of School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Carlos A. Puyo, MD
Assistant Clinical Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Farooq A. Qureshi, MD
Fellow, Pain Management
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Henry Ra, MD
Resident Physician
Department of Anesthesiology and Critical Care Medicine
David Geffen School of Medicine at UCLA
Ronald Reagan Hospital Center
Los Angeles, California-

Fabrizio Racca, MD
S.C. Anestesia e Rianimazione Pediatrica Azienda Ospedaliera
SS Antonio Biagio e Cesare Arrigo
Alessandria, Italy

Siamak Rahman, MD
Associate Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Niraja Rajan, MB, BS, FAAP


Assistant Professor
Medical Director, Hershey Outpatient Surgery Center
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Sivam Ramanathan, MD
Associate Professor of Anesthesiology
Charles Drew University of Medicine and Science
Cedars-Sinai Medical Center
Los Angeles, California

Chitra Ramasubbu, MD
Fellow, Pain Management
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

George J. Ranier, MD
Assistant Professor
Department of Anesthesiology
West Virginia University School of Medicine
Robert C. Byrd Health Sciences Center
Morgantown, West Virginia

V. Marco Ranieri, MD
Universita di Torino
Dipartimento di Discipline Medico-Chirurgiche
Sezione di Anesthesiologia e Rianimazione
Ospedale S. Giovanni Battista
Torino, Italy

Srikantha L. Rao, MBBS, MS


Associate Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Rashmi R. Rathor, MD
Fellow, Abdominal Organ Tranplant
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Elizabeth Rebello, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Venugopal S. Reddy, MD, EDIC, FFARCS


Associate Professor
Department of Anesthesiology
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Rebecca L. Reeves, DO
Resident Physician
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Wendy HP Ren, MD, FAAP


Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan UCLA Medical Center
Los Angeles, California

Joseph Resti, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Cameron J. Ricks, MD
Assistant Professor
Department of Anesthesiology and Perioperative Care
University of California, Irvine School of Medicine
University of California, Irvine Douglas Hospital
Irvine, California

Horst Rieke, MD, PhD


Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Francisco Rivas-Doyague, MD
Medical Doctor
Department of Thoracic Surgery
Hospital Universitari de Bellvitge
L’Hospitalet de Llobregat
Barcelona, Spain
Laura L. Roberts, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Adam Romanovsky, MD
Assistant Clinical Professor
Divisions of Critical Care and Nephrology
University of Alberta
Edmonton, AB Canada

Harvey K. Rosenbaum, MD
Clinical Professor of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan UCLA Medical Center
Los Angeles, California

Jay A. Roskoph, MD, MBA


Clinical Assistant Professor
Department of Anesthesiology
University of Pittsburgh School of Medicine
Chief Department of Anesthesiology
UPMC-St. Margaret Hospital
Pittsburgh, Pennsylvania

Marc A. Rozner, PhD, MD


Professor of Anesthesiology and Perioperative Medicine
Professor of Cardiology
University of Texas MD Anderson Cancer Center
Houston, Texas

Daniel M. Rusu, MD
Assistant Professor
Department of Anesthesia and Critical Care
University of Kentucky College of Medicine
University of Kentucky Healthcare
Lexington, Kentucky

Ali Salehi, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Alain A. Salvacion, MD
Fellow, Cardiothoracic Anesthesia
Department of Anesthesiology
Feinberg School of Medicine, Northwestern University
Northwestern Memorial Hospital
Chicago, Illinois

Samuel Samuel, MD
Associate Fellowship Director of Pain Management
The Cleveland Clinic
Cleveland, Ohio

Mona G. Sarkiss, MD, PhD


Associate Professor
Department of Anesthesiology and Perioperative Medicine
Department of Pulmonary Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Poovendran Saththasivam, MD
Resident Physician
Department of Anesthesiology
Drexel University College of Medicine
Hahnemann University Hospital
Philadelphia, Pennsylvania

Matthew V. Satterly, MD
Fellow, Pain Management
Department of Anesthesia and Critical Care
Pritzker School of Medicine, University of Chicago
The University of Chicago Medicine
Chicago, Illinois

Shashank Saxena, MD
Clinical Assistant Professor
Department of Anesthesiology
University of Pittsburgh School of Medicine
Staff Anesthesiologist
VA Pittsburgh Health Care System
Pittsburgh, Pennsylvania
R. Alexander Schlichter, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Peter M. Schulman, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
Oregon School of Medicine
Oregon Health and Science University
Portland, Oregon

Jeffrey J. Schwartz, MD
Associate Professor
Department of Anesthesiology
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut

Johanna C. Schwarzenberger, MD
Clinical Professor
Director, Pediatric Cardiac Anesthesiology
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Korrin Scott, MD
Resident Physician
Department of Anesthesiology
University of Virginia School of Medicine
University of Virginia Health System
Charlottesville, Virginia

Jennifer Scovotti, MA
Research Associate
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Los Angeles, California

Khaled Sedeek, MD
Associate Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

E. Gail Shaffer, MD, MPH


Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Kirk H. Shelley, MD, PhD


Professor
Department of Anesthesiology
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut

Justin C. Shields, MD
Resident Physician
Department of Anesthesiology
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Shawn T. Simmons, MD
Associate Clinical Professor
Medical Director, Hyperbaric Medicine Service
Department of Anesthesia
University of Iowa Carver College of Medicine
University of Iowa Hospitals
Iowa City, Iowa

Amrik Singh, MD
Associate Professor
Residency Program Director
Department of Anesthesiology and Pain Medicine
University of California, Davis School of Medicine
UC Davis Medical Center
Sacramento, California

Davinder Singh, MD
Assistant Professor
Department of Anesthesiology and Perioperative Care
University of California, Irvine School of Medicine
University of California, Irvine Douglas Hospital
Irvine, California

Sukhdip Singh, MD
Resident Physician
Department of Anesthesiology
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Sumit Singh, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Nina Singh-Radcliff, MD
Assistant Clinical Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Christopher A. Skorke
Assistant Professor
Medical Director, Medical/Surgical ICU
Department of Anesthesiology and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Jose M. Soliz, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Dmitri Souzdalnitski, MD, PhD


Pain Management Department
The Cleveland Clinic
Cleveland, Ohio
Martin M. Stechert, MD
Associate Clinical Professor
Department of Anesthesiology and Perioperative Care
University of California, San Francisco School of Medicine
UCSF Medical Center
San Francisco, California

Chris A. Steel, MD
Attending Physician
Director of Anesthesia Services
White River Health System
Batesville, Arizona

Jacob Steinmetz, MD, PhD


Consultant
Department of Anesthesia
Copenhagen University Hospital
Rigshospitalet, Copenhagen

Jochen Steppan, MD
Fellow, Cardiothoracic Anesthesia
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Joel Stockman, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

William David Stoll, MD


Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Bradley A. Stone, MD
Attending Anesthesiologist
Mission Hospital
Asheville, North Carolina
Suzanne Strom, MD
Assistant Clinical Professor
Residency Program Director
Department of Anesthesiology and Perioperative Care
University of California, Irvine School of Medicine
University of California, Irvine Douglas Hospital
Irvine, California

Adam M. Stuart, MD
Medical Student
Virginia Commonwealth University School of Medicine
Richmond, Virginia

Mariya Svilik, MD
Staff Physician
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Rajeshwary Swamidurai, MD
Attending Physician
Department of Anesthesiology
Lodi Memorial Hospital
Lodi, California

Kenichi A. Tanaka, MD, MSc


Associate Professor
Department of Anesthesiology
Emory University School of Medicine
Atlanta, Georgia

Rob C. Tanzola, MD, FRCPC


Assistant Professor
Department of Anesthesiology and Perioperative Care
Queen’s University
Kingston General Hospital
Kingston, Ontario

Vijay Tarnal, MBBS, FRCA


Clinical Assistant Professor
Department of Anesthesiology
The University of Texas Medical Branch School of Medicine at Galveston
The University of Texas Medical Branch at Galveston
Galveston, Texas

Adam Thaler, DO
Resident Physician
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Ilka Theruvath, MD, PhD


Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Svjetlana Tisma-Dupanovic, MD
Assistant Professor
Department of Cardiology
Kansas University School of Medicine
Kansas University Medical Center
Kansas City, Kansas

Catherine Dawson Tobin, MD


Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Lan Chi Tran, MD


Resident Physician
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Timothy T. Tran, MD
Resident Physician
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri
Ravi S. Tripathi, MD
Assistant Clinical Professor
Department of Anesthesiology
The Ohio State University College of Medicine
The Ohio State University Wexner Medical Center
Columbus, Ohio

Angela Truong, MD
Associate Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Dam-Thuy Truong, MD
Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

January Y. Tsai, MD
Assistant Clinical Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Judith A. Turner, MD, PhD


Assistant Clinical Professor
Residency Program Director
Department of Anesthesiology and Critical Care
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Kalpana Tyagaraj, MD
Residency Program Director
Director, Obstetric Anesthesiology
Department of Anesthesiology
Maimonides Medical Center
New York, New York

Shital Vachhani, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas

Dierk A. Vagts, MSc, DEAA, EDIC


Professor
Department of Anesthesiology and Intensive Care Medicine, Emergency Medicine, Pain
Therapy and Palliative Care
Academic Teaching Hospital of Johannes Gutenberg University
Mainz, Neustadt Weinstrasse, Germay

Sonia Vaida, MD
Professor of Anesthesiology, Obstetrics and Gynecology
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Elizabeth Valentine, MD
Assistant Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Andrea Vanucci, MD, DEAA


Assistant Professor
Department of Anesthesiology
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Swarup S. Varaday, MBBS, FRCA, FCARSI


Assistant Professor
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Malina M. Varner, MD
Instructor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania
Aditya Venkataraman, MD
Chief Resident
Department of Anesthesiology and Pain Medicine
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri

Thomas Verbeek, MBChB


Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Bruce Vrooman, MD
Department of Pain Management
Cleveland Clinic
Cleveland, Ohio

Samuel H. Wald, MD
Clinical Professor
Department of Anesthesiology and Critical Care
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Cynthia Wang, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Ellen Y. Wang, MD
Clinical Assistant Professor
Department of Anesthesiology
Stanford University
Lucile Packard Children’s Hospital
Palo Alto, California

Steve Wang, MD
Assistant Professor
Department of Anesthesiology and Pain Medicine
University of Texas MD Anderson Cancer Center
Houston, Texas

Izabela M. Wasiluk, MD
Assistant Professor
Department of Anesthesiology
University of Florida College of Medicine
Shands Jacksonville Medical Center
Jacksonville, Florida

Huafeng Wei, MD, PhD


Assistant Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Jiadong Wei, MD

Yoram G. Weiss, MD, MBA, FCCM


Associate Professor in Anesthesiology and Critical Care Medicine
Hadassah Hebrew University School of Medicine
Jerusalem, Israel
Adjunct Associate Professor
Department of Anesthesiology and Critical Care
University of Pennsylvania
Philadelphia, Pennsylvania

Gregory E. R. Weller, MD, PhD


Assistant Professor
Department of Anesthesiology
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania

Joseph R. Whiteley, DO
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

J. Aaron Williams, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Sylvia H. Wilson, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina

Stephen P. Winikoff, MD
Professor
Department of Anesthesiology
Mount Sinai School of Medicine
St. Joseph’s Hospital and Regional Medical Center
Paterson, New Jersey

Jeremy Wong, MD
Assistant Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Christopher Wray, MD
Assistant Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Jennifer Wu, MD, MBA


Assistant Professor
Department of Anesthesiology
University of Texas Medical School at Houston
Memorial Hermann Hospital
Houston, Texas

Sulin G. Yao, MD
Attending Physician
Department of Anesthesiology
Atlanticare Regional Medical Center
Pomona, New Jersey
Peter K. Yi, MD
Assistant Professor
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

Dirk Younker, MD
Russell D and Mary B Sheldon Professor of Anesthesiology
Vice Chairman for Clinical Affairs
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Zdravka Zafirova, MD
Assistant Professor
Department of Anesthesia and Critical Care
Pritzker School of Medicine, University of Chicago
The University of Chicago Medicine
Chicago, Illinois

Alan P. Zaggy, MD
Assistant Professor
Department of Anesthesiology and Perioperative Medicine
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri

Mark Zakowski, MD
Associate Professor of Anesthesiology, Adjunct
Charles Drew University of Medicine and Science
Chief, Obstetric Anesthesiology
Cedars-Sinai Medical Center
Los Angeles, California

Sherif Zaky, MD, PhD


Assistant Professor of Anesthesiology
The Cleveland Clinic
Cleveland, Ohio

Sessunu M. Zemo, MD
Resident Physician
Department of Anesthesiology
Baylor College of Medicine
Ben Taub Hospital
Houston, Texas

Fei Zheng, MD, MPH, MS


Resident Physician
Department of Anesthesiology
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland

Dayna Zimmerman, BS
Research Assistant
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Los Angeles, California

Keren Ziv, MD
Associate Clinical Professor
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California

Zachary M. Zumbar, MD, MPH


Attending Physician
Midwest Pain Physicians
Uniontown, Ohio
FOREWORD

I t is a pleasure to introduce the 5 Minute Anesthesia Consult to readers around the globe.
This concise compendium of topics pertinent to modern anesthesiology practice will be
useful as a rapid reference for busy anesthesiology clinical practitioners, anesthesiology
residents, medical students and others in training, nurse anesthetists, anesthesiology
assistants, perioperative nurses, post-operative intensive care personnel, and other allied
health professionals caring for patients before and after anesthetic administration. The
contents are offered in both text format as well as applications for smart devices, to be readily
at hand in any clinical situation in any clinical location.
The editor has drawn from a wide spectrum of expert authors from multiple institutions to
compile approximately 480 two-page chapters, in template formats for easy-to-retrieve
information. The content is organized into sections on important topics in physiology,
pertinent issues for major co-existing diseases/co-existing conditions, key information for
important surgical procedures, and guidance for managing a variety of complications
encountered in anesthetic practice. In addition, the 5 Minute Anesthesia Consult contains a
drug section in a condensed, easily accessible format with current information about
anesthetic drugs and adjuvants, chronic medications that patients may be taking in the
perioperative period, and medications used to treat complications encountered in the peri-
anesthetic period.
As anesthesiology care is extending to encompass the spectrum from early evaluation and
optimization/management of pre-procedural risk factors, through post-procedural care to
minimize subsequent complications and/or re-admission, every practitioner can benefit from
timely access to a “one-stop” content source to support evidence-based anesthesiology care, a
source that concisely presents the most important concepts on a topic in an accessible
manner.
I look forward with enthusiasm to the broad distribution and availability of the 5 Minute
Anesthesia Consult to support high quality patient outcomes on an international basis.
PATRICIA A. KAPUR, MD
Professor and Chairwoman
Department of Anesthesiology
David Geffen School of Medicine at UCLA
Los Angeles, California, USA
April 2012
PREFACE

T he 5 Minute Medicine Consult was amongst the medical texts and references that
lined my mother’s bookshelf when I was in high school. I was drawn to the unique style
that made it “easy to read,” even at my level. The topic-specific and highly templated
format was the first of its kind amongst medical references. Years later, I have been given the
amazing opportunity to add to The 5 Minute Consult Series.
The goal of The 5 Minute Anesthesia Consult is to emulate that style by creating an
evidence-based, focused, and practical textbook that will be relevant to students, trainees,
nurse anesthetists, and physicians. The 480 topics are presented alphabetically, but are
presented in a second table of contents organized in four sections: Physiology, Co-Existing
Disease, Surgical Procedure, and Management. Each topic follows a two-page outline format
that is consistent with the section and easy to read. Additionally, we have provided a focused
Drug section.
The chapters in the Physiology section were specifically written to simplify complex topics
and then extrapolate them to pathophysiologic processes and apply them to relevant
perioperative matter.
The Surgical Procedures section describes key surgical steps, followed by anesthetic
considerations for preoperative preparation, intraoperative care, and postoperative concerns.
The goal of this section is to “involve” the anesthesia practitioner in the surgical procedure by
providing an understanding of, and appreciation for, our surgical colleagues’ work.
The chapters in the Co-Existing Disease Section describe basic pathophysiology concepts,
followed by key considerations to optimizing and managing patients throughout the
perioperative period.
The Management Section covers a comprehensive list of perioperative complications that
can arise in anesthetic practice. For example, the author of the Anaphylaxis chapter had a
patient who “crumped” after being exposed to medication. Despite appropriately treating the
patient with epinephrine and following ACLS protocol, the patient remained unresponsive to
therapy. The author saved her patient’s life by administering glucagon, which she describes in
her chapter as the treatment for refractory anaphylaxis that may be seen in patients who are
beta-blocked.
Each chapter provides a list of additional complementary topics that are available within
the book to allow readers the opportunity to supplement their knowledge of a given topic.
I sincerely hope that the practical nature and quality of this text will contribute to your
learning and benefit our patients in the ever-growing field of anesthesia. I welcome feedback
and suggestions at fiveminuteanesthesia@aol.com.
ACKNOWLEDGEMENTS

T he completion of this text would not have been possible without a number of special
people. The authors have given their time and expertise to prepare, revise, and re-revise
their chapters to attain the overarching vision for this textbook. I enjoyed the
opportunity to meet (and learn from) so many talented and enthusiastic practitioners and
teachers, as well as work with so many of my close friends, colleagues, former attendings, and
mentors. I would like to express my utmost gratitude for their quality contributions; their
work has resulted in what I believe is one of the best anesthesia texts out there.
My Publisher, Brian Brown, Senior Product Manager, Nicole Dernoski, and Lippincott
Williams & Wilkins/Wolters Kluwer Health provided me with mentorship, a team of high-
level professionals, and invaluable resources. I would like to thank them for providing me
with this tremendous opportunity to expand the highly successful 5 Minute Consult Series.
Thank you Drs. Patricia A. Kapur, Randy Steadman, Sam Wald, Rima Matevosian, Susan
Chan, Jordan Miller, Aman Mahajan, Barbara Van de Wiele, Phil Levin, Victor Duval, Nir
Hoffman, Carsten Nadjat-Haiem, Keren Ziv, Eric Hsu, Kenneth Kuchta, Michael Ferrante,
Michelle Braunfeld, Zhuang Fang, Swati Patel, Mitchell Lin, Michael Sopher, Ali Salehi,
Siamak Rahman, Parisa Partownavid and the UCLA Department of Anesthesiology for
teaching me to think critically, being patient, and serving as role-models. Your efforts,
dedication, and love for teaching and your patients have had far-reaching influences on me.
12 LEAD EKG
Elizabeth Valentine, MD
Nina Singh-Radcliff, MD

BASICS
DESCRIPTION
• The 12-lead EKG is a noninvasive test that provides information on the electrical function of
the heart and aids in the diagnosis of pathophysiologic processes.
• Serves as a baseline for perioperative changes and as a screening tool to identify cardiac
abnormalities.
• Continuous 3- or 5-lead EKG is an American Society of Anesthesiologists (ASA) standard
monitor used for general anesthesia and monitored anesthesia care.
PHYSIOLOGY PRINCIPLES
• P wave (80 ms): Denotes atrial depolarization. Myocardial depolarization is normally
initiated by spontaneous sinoatrial (SA) node depolarization. The signal is quickly and
efficiently conducted along a specialized conduction pathway. In the atria, this pathway is
via interatrial tracts (anterior, middle, and posterior); they begin by depolarizing the right,
followed by the left, atria. The conduction cells depolarize adjacent myocardial cells, which
have a different histology.
• QRS (80–120 ms): Denotes the varying stages of ventricular depolarization. The Q wave is
the initial negative deflection and results from septal depolarization. The R wave follows
and is the first positive deflection. It results from depolarization of the larger, more
muscular left ventricle; right ventricular depolarization is normally obscured. The S wave is
the final negative deflection caused by lateral wall depolarization.
• T wave: Denotes ventricular repolarization. The beginning of the wave represents a period
of absolute refractoriness, where a subsequent depolarization (no matter how strong) cannot
initiate a aberrant rhythm. The latter portion of the wave is a time of relative refractoriness,
where a strong enough depolarization can result in a runaway rhythm.
• PR interval (120–200 ms): Time from the start of atrial depolarization to atrioventricular
(AV) nodal conduction to conduction through the His-Purkinje system.
• QRS width: Represents the time for ventricular depolarization
• J point: Describes the intersection between the QRS complex and ST segment. When the
heart rate is increased, atrial repolarization may be observed at the very end of the QRS
complex as J point depression.
• ST segment: Denotes the end of depolarization to the beginning of repolarization and is
usually isoelectric
• QT interval (QTc <440 ms): Beginning of ventricular depolarization to the end of
ventricular repolarization. Time for ventricular repolarization is heart rate dependent; thus,
the QT is usually corrected for heart rate (QTc).
• Rate: Typically measured between sequential R waves; the RR interval (0.6–1.2 s) is useful
due to its prominent wave that allows for easy detection. A rate <60 bpm is bradycardia; a
rate >100 bpm is tachycardia.
• Rhythm: The location of regular P waves preceding each QRS suggests an atrial rhythm. The
relationship between the P wave and QRS complex provides information about underlying
conduction defects or dissociation.
• Axis: The average direction of the various complexes determines the axis. The normal QRS
axis is between 0 and 100° in the frontal plane. Left or right axis deviation can suggest
underlying pathophysiology.
ANATOMY
• A total of 12 leads allows for “visualizing” the electrical function from different angles
through the heart. Considering the leads in different combinations can aid in clinical
diagnosis.
• Standard limb leads (I, II, III): Form the points of Einthoven’s triangle, an equilateral
triangle whose vertices lie at the left and right shoulders and the pubic region and whose
center corresponds to the vector sum of all electric activity occurring in the heart at any
given moment. This allows for the determination of the electrical axis.
• Augmented limb leads (aVR, aVL, aVF): Together with the standard limb leads, record the
electrical activity along the frontal plane.
• Precordial leads (V1, V2, V3, V4, V5, V6): Record the electrical activity along the horizontal
plane.
• Anterior leads (V3 and V4): Allow evaluation and assessment of the electrical function of the
anterior wall of the heart. Usually supplied by the left anterior descending artery.
• Inferior leads (II, III, and aVF): Allow evaluation and assessment of the electrical function of
the inferior heart muscle. The inferior wall is usually supplied by the right coronary artery.
DISEASE/PATHOPHYSIOLOGY
• ST segments: Ischemia or infarct may present as either elevation or depression of the ST
segment. A routine preoperative EKG may appear normal if a patient is not experiencing
active ischemic symptoms. Thus, a high index of suspicion must be maintained for patients
at risk for coronary ischemia.
• Axis deviation: Common conditions associated with left axis deviation include left bundle
branch block or left anterior hemiblock, inferior MI, or left ventricular hypertrophy.
Common causes of a right axis deviation include right ventricular hypertrophy, chronic lung
disease, right bundle branch block, or lead reversal.
• Bundle branch blocks: A prolonged QRS suggests either a right (RBBB) or a left bundle
branch block (LBBB). They are described as either partial (QRS <120 ms) or complete (QRS
>120 ms). Although a RBBB can represent pulmonary or right heart disease, it is more
commonly benign. Alternatively, a LBBB is more likely to indicate underlying cardiac
pathology (CAD, CMO, valvular disease). A new onset LBBB should prompt a thorough
cardiac workup. The anterior or posterior fascicle of the left bundle may be blocked in
isolation (termed hemiblock). A nonspecific intraventricular conduction delay describes a
nonpathologic widening of the QRS complex that does not meet the criteria for either LBBB
or RBBB.
• AV blocks: Impaired conduction between the atria and ventricles of the heart are described
as first, second, and third degree. First-degree AV block is defined as a PR interval >0.2 s.
Second-degree AV block may be Type 1 (Mobitz 1, Wenckebach), defined as progressive
prolongation of the PR interval with eventual dropped QRS; or Type II (Mobitz 2), where
the PR remains unchanged prior to the sudden failure of conduction of a P wave and a
dropped ventricular beat. In third-degree AV block, there is no association between P waves
and QRS complexes. While first-degree and Mobitz I AV block are generally benign
conditions, Mobitz II (can progress to complete heart block) and third-degree AV blocks are
indications for cardiac pacing.
• P waves: Abnormal P wave morphology may indicate an ectopic atrial rhythm, whereas a
changing P wave morphology may suggest either a wandering atrial pacemaker or
multifocal atrial tachycardia. An irregular rhythm with no clear P waves suggests atrial
fibrillation. A regular “saw tooth” pattern may suggest atrial flutter.
• Arrhythmias: A narrow QRS suggests a supraventricular (above the ventricles) rhythm while
a wide QRS suggests either a ventricular source or aberrant conduction of a supraventricular
rhythm.
• QT prolongation: Prolonged QTc is a risk factor for developing ventricular arrhythmias
(Torsades de Pointes) and is an independent risk factor for sudden cardiac death. QTc may
be prolonged due to genetic causes (long QT syndrome), drugs (haloperidol, methadone), or
diseases (hypothyroidism).
• Delta waves: Describes a slurred upstroke of the QRS complex and is found in patients with
Wolff–Parkinson–White (WPW) syndrome. WPW is caused by the bypass of the AV node via
an accessory pathway called the bundle of Kent. This accessory pathway does not have the
rate-slowing property of the AV node, thus allowing for extremely fast heart rates and
potential hemodynamic instability. The combination of cardiac arrhythmias and an
accessory pathway may degenerate into ventricular fibrillation.
• R on T phenomenon: The beginning of the T wave is a time of absolute refractoriness; the
latter portion of the wave is a time of relative refractoriness. An abnormal depolarization
signal (aberrant pacemaker, PAC, PVC, cardioversion) cannot depolarize the entire ventricle
during the absolute refractory period; however, it may potentially do so during the relative
refractory period. This can result in degeneration into ventricular tachycardia or fibrillation.
• Artificial pacemaker: May be identified by tell-tale “pacer spikes” on EKG or telemetry. May
be atrial, ventricular, or sequentially paced. QRS will appear widened if ventricularly paced.
• Medication toxicities:
– Digoxin: Characteristic downward sloping of the ST segment. May also see an increased
PR and decreased QTc interval.
– Tricyclic antidepressants (TCAs): Characteristic rightward change in the frontal plane QRS
vector. A large R wave in aVR is quite sensitive for TCA toxicity; may also see an
increased QRS and QTc interval.
• Electrolyte abnormalities:
– Hypokalemia: EKG changes result from delayed ventricular repolarization. May include T
wave flattening and/or inversion, ST segment depression, prominent U wave, increased P
wave amplitude, and prolonged PR interval. Increased myocardial cell automaticity may
predispose to atrial or ventricular arrhythmias.
– Hyperkalemia: EKG changes are due to delayed depolarization and hastened
repolarization. Changes commonly progress in order from symmetrically peaked T waves
→ widened QRS → prolonged PR interval → loss of P wave → loss of R wave → ST
depression → EKG that resembles sine wave → ventricular fibrillation → asystole.
– Hypocalcemia: QTc prolongation and cardiac irritability leading to arrhythmias
– Hypercalcemia: Shortened ST segment and QTc interval
– Hypomagnesemia: PR and QT interval prolongation, cardiac irritability
– Hypermagnesemia: May see PR prolongation and QRS widening
PERIOPERATIVE RELEVANCE
• Intraoperative bovie, electrical interference, patient shivering, tremors, or movement may
closely resemble an intraoperative arrhythmia. Close inspection may reveal the QRS
“marching through” the interference; other times, it may be indistinguishable from a true
arrhythmia. Close evaluation of other monitors (blood pressure, pulse oximetry or arterial
plethysmograph, verification of palpable peripheral pulses) may provide clues in this
circumstance.
• Malpositioning of leads may result in the appearance of ST changes. Thus, it is good practice
to place leads in proper position if it does not interfere with the surgical field and to note
baseline abnormalities in the EKG tracing.
• Body habitus: Large breasts or obesity may result in low-voltage EKG.
• Pulmonary artery catheters and central lines: For patients with LBBB, there is a risk of
complete heart block with insertion. In this circumstance, it is prudent to have pacing
capabilities readily available. Similarly, in patients with WPW, the pulmonary artery
catheter or a wire for central line placement can induce a hemodynamically intolerable
tachyarrhythmia.
• Extracorporeal shock wave lithotripsy: Older machines time shocks to be delivered during
the R wave to prevent R on T phenomenon.
• Cardioversion: Machines synchronize the delivery of electrical discharge to the R wave to
prevent R on T phenomenon.
GRAPHS/FIGURES

FIGURE 1. EKG waves, segments, and intervals


FIGURE 2. The 12 leads allow for assessment of the electrical function of the three-dimensional heart.

REFERENCES
1. Correll DJ, Hepner DL, Chang C, et al. Preoperative electrocardiograms: Patient factors
predictive of abnormalities. Anesthesiology. 2009;110(6):1217–1222.
2. Eagle KA, Berger PB, Calkins H, et al. Practice advisory for preanesthesia evaluation: An
updated report by the American Society of Anesthesiologists Task Force on Preanesthesia
Evaluation. Anesthesiology. 2012;116:522–538.

ADDITIONAL READING
• ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac
surgery. Circulation. 2002;105:1257–1267.
• Guidelines for electrocardiography: A report of the American College of
Cardiology/American Heart Association Task Force on assessment of diagnostic and
therapeutic cardiovascular procedures. J Am Coll Cardiol. 1992;19:473–481.
See Also (Topic, Algorithm, Electronic Media Element)
• Myocardial ischemia
• QT prolongation
• Wolff–Parkinson–White (WPW) syndrome
• Cardiac action potentia
• Coronary arteries

CLINICAL PEARLS
• The axis of lead II is parallel to that of atrial depolarization; thus, it has the largest P wave
and helps to determine rhythm. Lead II also represents the inferior wall of the left ventricle,
which is typically supplied by the right coronary artery. EKG abnormalities in this area may
suggest ischemia or disease in this distribution.
• Lead V5 is most sensitive for detecting ST segment changes when a single lead is monitored
(detects abnormalities in 75% of cases). The combination of monitoring leads V5 and II
increases sensitivity to 80% and leads V4 and V5 increases sensitivity to 90% for detecting
intraoperative ST changes (1).
• Preoperative guidelines: The ASA Task Force on Preanesthesia Evaluation does not support
the ordering of any routine preoperative testing; instead, preoperative tests should be
ordered on a selective basis based on patient history, exam, and surgical risk factors (2).
– Important clinical factors that may make preoperative EKG evaluation useful include
cardiovascular diseases (CAD, CHF, significant valvular disease), respiratory diseases
(COPD, OSA, lung cancer), or highly invasive procedures.
– While age >65 years old is an independent predictor for significant preoperative EKG
abnormalities, there was no consensus minimum age for asymptomatic patients
undergoing low-risk procedures, or in low-risk patients.
• Preoperative EKG may be useful in risk-stratification in intermediate-risk and high-risk
surgical patients for predicting cardiovascular death. An abnormal EKG in patients with
documented CAD or at high risk for CAD and undergoing major noncardiac surgery was
shown to predict long-term outcome.
ABDOMINAL AORTIC ANEURYSM
Adam M. Thaler, DO
Nina Singh-Radcliff, MD

BASICS
DESCRIPTION
• The normal aortic diameter is approximately 20 mm (2 cm). The aorta is considered
widened, dilated, or aneurismal when it increases to 1.5 times the normal diameter.
• Patients may present perioperatively for aneurismal repair as well as for nonvascular
surgeries with a known (or unknown) diagnosis of an abdominal aortic aneurysm.
EPIDEMIOLOGY
Incidence
• 12–19% of patients with an AAA have a first-degree relative with a history of AAA.
• Total incidence in the adult population: 2–4%
Prevalence
• Approximately 90% of AAAs that are found incidentally on screening are <3.5 cm.
• Most common age 65–75 years
• Male:female 7:1
• Infrarenal aneurysms comprise ∼90% of AAAs.
Mortality
• Mortality: Ruptured AAA is the 13th leading cause of death in the US, causing an estimated
15,000 deaths per year.
• AAA rupture is usually fatal (70–80%) and only 50% present to the hospital alive.
ETIOLOGY/RISK FACTORS
• Chronic smokers (4 times more likely than nonsmokers) (1)
• Male gender
• Atherosclerosis
• Hypertension
• Marfan syndrome, Ehlers–Danlos syndrome, syphilis, trauma, mycotic infection (rare causes)
PATHOPHYSIOLOGY
• The extracellular matrix is comprised of elastin and collagen, which provides tensile
strength. Tensile strength is defined as the maximum stress that a material can withstand
while being stretched or pulled before being deformed or broken. Thus, they provide a
necessary function to the aorta—to endure the pulsatile, high pressures of blood being
ejected from the left ventricle.
• The pathogenesis of aneurysms involves alterations in the connective tissue of the aortic
wall. It has been proposed that adventitia elastin degradation is a primary, and hallmark,
event that leads to AAA formation; collagen disruption is the ultimate cause of rupture.
• Inflammation is believed to play a role with macrophages and T lymphocytes capable of:
– Producing proteolytic enzymes that can cause protein degradation
– Causing smooth muscle apoptosis
– Releasing pro-inflammatory cytokines
• Degradation that results in weakening of the aortic wall and aneurysmal development can
result from a number of different causes:
– Arteriosclerosis most commonly affects the abdominal aorta (compared to the thoracic). It
is also more likely to result in aneurysm (compared to stenosis in the infrarenals).
– Infection
• Laplace’s law states that T = (R × ΔP)/H, where T is tension, R is radius, ΔP is change in
pressure, and H is wall thickness. Thus, vessel diameter widening, increased arterial
pressures, and decreased wall thickness result in increased tension; the increased tension
can serve to further exacerbate the size of the aneurysm.
• Morphology: A fusiform aneurysm has a fairly uniform shape, with symmetrical dilation that
involves the full circumference of the aortic wall. Saccular aneurysms have a localized
dilation that appears as an outpouching of only a portion of the aortic wall. A
pseudoaneurysm is not an aneurysm, but instead, is a well-defined collection of blood and
connective tissue outside the vessel wall.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Patients with a diagnosis of AAA often have comorbid cardiovascular conditions such as
cerebrovascular, coronary, or renal disease.
• Both the size and rate of growth of aneurysm are important when determining the need for
intervention.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Usually asymptomatic
• Expanding AAA may present with abdominal or back pain (due to pressure on surrounding
tissues) or pain in the legs (due to disturbed blood flow).
• Ruptured AAA: Classic triad (hypotension, back pain, pulsatile abdominal mass) presents in
only 1/2 of patients.
History
• How and when the AAA diagnosed; any change in size, current plan of treatment
• Risk factors
• Comorbid conditions; patients are considered “vasculopaths” and disease in other vessels
should be considered until proven otherwise.
Signs/Physical Exam
Presence of an abdominal bruit or lateral propagation of the aortic pulse wave offers subtle
clues and may be more frequently found than a pulsatile mass.
MEDICATIONS
• No medical therapy has been found to be effective at decreasing the growth rate or rupture
rate of asymptomatic AAAs. There may be some protective effects with ACE inhibitors, beta-
blockers, and statins.
– Beta-blockers can reduce cardiac morbidity and mortality and should be continued
perioperatively. HR control and decreased contractility result in less systolic pressure
generated against the aneurysm wall.
– Statins’ pleiotropic effects have been shown to decrease postoperative cardiac, cerebral,
and renal morbidity in patients undergoing major vascular surgery; should be continued
perioperatively.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Electrolytes, CBC, BUN/CR, PT/PTT
• 12-lead EKG
• Echocardiography, stress testing, and coronary angiography may be indicated to evaluate
the myocardium.
• Carotid ultrasound if bruits are present, especially if history of stroke or TIA.
• Ultrasound report should be reviewed even in patients presenting for nonvascular surgery.
• CT scan with contrast or MRA is typically performed when patients present for repair;
provides information on the position, diameter, and involvement of the mesenteric vessels.
• Type and crossed units for open AAA repair
CONCOMITANT ORGAN DYSFUNCTION
• Aortic disease is indicative of other atherosclerotic diseases including coronary, cerebral,
peripheral vascular, and renal diseases.
• Chronic obstructive pulmonary disease
• Diabetes mellitus
CIRCUMSTANCES TO DELAY/ CONDITIONS
• In patients presenting for nonvascular surgery, symptomatic and large aneurysms (i.e., >5.5
cm in diameter) as well as growth >1 cm/year should be considered for endovascular or
surgical repair.
• Acute coronary or cerebral event
CLASSIFICATIONS
• There are many classification systems in determining the risk of AAA rupture which take
into account the rate of increase, size, comorbid factors, etc (2).
• Biggest predictors of risk of rupture (annually) are diameter of the aneurysm and rate of
expansion.
– <4.0 cm in diameter = <0.5%
– 4.0–4.9 cm in diameter = 0.5–5%
– 5.0–5.9 cm in diameter = 3–15%
– 6.0–6.9 cm in diameter = 10–20%
– 7.0–7.9 cm in diameter = 20–40%
– >8.0 cm in diameter = 30–50%

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Anxiolytics as needed; anxiety may increase BP and the risk of AAA rupture.
• Beta-blockers may be titrated to heart rate goals, particularly if taking chronically.
• Perioperative statin therapy initiation may be indicated for their pleiotropic effects.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Non vascular procedures: Based on the type of surgery, patient comorbidities, and physical
exam
• Open AAA repair: Neuraxial techniques may be appropriate; however, traumatic placement
may necessitate the delay of surgery (patients are heparizined intraoperatively).
Monitors
• Standard ASA monitors
• Non vascular procedures: Additional monitoring depends on the surgery and patient
comorbidities.
• Open AAA repair:
– 2 large-bore peripheral IVs or a central introducer sheath for possible rapid fluid and
blood administration
– Arterial line to assess rapid hemodynamic changes and the potential for hypotension and
MI; may be placed pre-induction.
– Pulmonary artery catheter may be indicated when pulmonary vascular resistance, cardiac
output, and mixed venous oxygen saturation can help guide therapy.
– TEE may be indicated to evaluate myocardial function and detect regional wall motion
abnormalities.
Induction/Airway Management
• A slow, controlled induction is necessary to ensure an adequate depth of anesthesia and
minimize hemodynamic changes. Hypotension can impair perfusion, while hypertension can
result in aneurysmal rupture (transluminal pressures, coughing, bucking, etc.).
• Short-acting agents, such as esmolol and nitroglycerin, may be necessary to blunt the
patient’s response to tracheal intubation and the subsequent increased tension against the
aneurysmal wall that could result in rupture.
Maintenance
• Maintenance agents (non vascular and AAA repairs): Balanced volatile or intravenous
techniques may be utilized.
• Hemodynamics (non vascular and AAA repairs): Close titration of intravenous and
inhalation agents with an emphasis on reducing tension against the aneurysmal wall.
Maintaining HR and MAP within 20% of baseline is generally appropriate (3).
– Short-acting drugs permit a rapid termination of effect, if desired, and allow for enhanced
titration.
– Opioids, beta-blockers, and vasodilating drugs can be used to control pain and BP. Esmolol
has ultra-short action and organ-independent elimination making it particularly useful.
• Aggressive fluid replacement may cause dilutional and hypothermic coagulopathy. This can
result in secondary clot disruption from increased blood flow, increased perfusion pressure,
and decreased blood viscosity thereby exacerbating bleeding.
Extubation/Emergence
• Standard extubation criteria; special attention to blood loss, hemodynamics, and
normothermia. Consider postoperative intubation in complicated AAA repairs or with
significant comorbidities.
• Smooth extubation (avoid coughing and bucking)
• Control of hypertension and tachycardia is important; consider beta-blockers and/or
vasodilators.

POSTOPERATIVE CARE
BED ACUITY
• Non vascular repair: Depends on surgery, comorbidities, intraoperative course
• AAA repair: ICU or monitored setting, given the high risk of cardiac complications. (MI
occurs more frequently postoperatively than intraoperatively). The postoperative period is
marked by increased myocardial oxygen demand, increased catecholamine levels, hypoxia,
hypercoagulability, and large fluid shifts. Consider supplemental oxygen (nasal cannula,
face mask), incentive spirometry and deep breathing, and early mobilization.
COMPLICATIONS
In AAA procedures, cardiac complications, such as myocardial ischemia or infarction are most
commonly seen. Additionally, hemorrhage or coagulopathy, peripheral embolization, and
aortocaval or aortoduodenal fistula can occur.

REFERENCES
1. Hatch C. Abdominal aortic aneurysm repair. In: Manual of anesthesia practice.
Charlottesville, VA: Unbound Medicine, 2011.
2. Leonard A, Thompson J. Anaesthesia for ruptured abdominal aortic aneurysm. Contin Educ
Anaesth Crit Care Pain. 2008;8(1):11–15.
3. CDC Aortic Aneurysm Factsheet. Available at:
http://www.cdc.gov/dhdsp/data_statistics/fact_sheets/docs/fs_aortic_aneurysm.pdf

ADDITIONAL READING
• Abdominal aortic aneurysm on UpToDate
• http://emedicine.medscape.com/article/463354-overview
See Also (Topic, Algorithm, Electronic Media Element)
• Thoracic aneurysm
• Endovascular aneurysm repair
• Abdominal aortic aneurysm, infrarenal
• Abdominal aortic aneurysm, supraceliac

CODES

ICD9
441.4 Abdominal aneurysm without mention of rupture

ICD10
I71.4 Abdominal aortic aneurysm, without rupture

CLINICAL PEARLS
• Preoperative preparation should involve a careful assessment of the disease and
comorbidities.
• The US Preventive Services Task Force recommends screening for AAA using ultrasound
imaging one-time for men aged 65–75 years who have ever smoked, even if they have no
symptoms. Men aged ≥60 years with a family history of AAA may also be tested.
ABDOMINAL AORTIC ANEURYSM RUPTURE
John W. Hoffman, Jr., DO, MS
Shawn T. Beaman, MD

BASICS
DESCRIPTION
• The abdomen is the most common site for an aortic aneurysm.
– Abdominal aortic aneurysms (AAA) are most commonly located between the inferior
mesenteric and renal arteries.
– Approximately two-thirds of all AAAs extend into the iliac arteries
• Ruptured AAA (rAAA) is a surgical emergency.
EPIDEMIOLOGY
Incidence
• AAA is present in 5–10% of patients >65 years old (1)[C].
• Estimated to occur in 7.7 to 26.8 per 100,000 person-years in recent large European study
(remarkable variation was noted across countries).
Morbidity
• Respiratory insufficiency (5–10%)
• Myocardial infarction (10–15%)
• Renal insufficiency (2–5%)
• GI complications (3–4%)
• Lower extremity ischemia (2–5%)
Mortality
• rAAA is the 13th leading cause of death in the US, with up to 15,000 deaths annually.
• 30–50% of patients with a rAAA do not survive transport to a hospital.
• Operative mortality after rupture ∼ 50%
ETIOLOGY/RISK FACTORS
• Risk factors associated with AAA rupture (6)[C]:
– Anteroposterior aneurysm diameter >5 cm
– Elevated diastolic pressure
– Obstructive pulmonary disease
• Causes of AAA:
– Atherosclerosis (most common) (2–5)[C]
– Connective tissue diseases (e.g., Marfan syndrome, Ehlers–Danlos syndrome, and cystic
medial necrosis) (2)[C]
– Infectious etiologies are uncommon (e.g., syphilis, salmonellosis, brucellosis, tuberculosis)
(2)[C].
• Risk factors associated with presence of AAA:
– Smoking: Duration (years) of tobacco exposure is more important than absolute number of
cigarettes (2)[C].
– Age >65 years old
– Male gender: Incidence is 4 times higher in men; women have delayed development of
AAA by ∼10 years compared with men.
– Hypertension
– Presence of peripheral arterial aneurysms (e.g., popliteal or femoral arterial aneurysm)
– Family history of AAA (first-degree relative)
– Decreased serum high-density lipoprotein
– Caucasian ethnicity
PATHOPHYSIOLOGY
• Collagen and elastin fibers provide most of the tensile strength of the aortic wall. An
imbalance between aortic wall matrix metalloproteinases and their inhibitors, chronic
inflammatory infiltrates, smooth muscle apoptosis, and increased production of pro-
inflammatory cytokines contribute to aneurysm formation.
• The average rate of growth of a AAA is 0.4 cm/year
• Risk of rupture is proportional to wall stress/tension, which increases as the AAA expands
(Laplace’s law).
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Intravascular volume replacement
• Inotropic support of cardiac output
• Maintenance of adequate tissue oxygenation
• Immediate surgical control of rupture

PREOPERATIVE ASSESSMENT
SYMPTOMS
Back, chest, or abdominal pain
History
• Comorbidities are common.
– Atherosclerosis associated with coronary artery disease, stroke, peripheral vascular
disease, and renal insufficiency
– Smoking associated with obstructive pulmonary disease
• Presence of connective tissue disease
• Medical optimization is not feasible due to the emergent nature of the surgery.
Signs/Physical Exam
• Pulsatile abdominal mass
• Hypotension
TREATMENT HISTORY
Pre-existing vascular grafts or repairs
MEDICATIONS
• Vasodilators (nitroglycerin and/or nitroprusside)
• Short acting beta blockers (e.g. esmolol) are utilized to decrease the heart rate.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Baseline and serial cardiac biomarkers, BUN/Cr, CBC with platelets, coagulation profile, and
TEG if available
• ECG may be normal or show nonspecific ST segment or T wave changes, left ventricular
hypertrophy, ischemia, or infarction.
• Chest radiograph may suggest concomitant pulmonary disease.
• CT angiography is quick, highly sensitive, and specific; 64-slice multidetector CT with
cardiac gating may allow for simultaneous evaluation of pulmonary and coronary arteries.
• TEE allows rapid evaluation of cardiac function, volume status, and valvular integrity.
• MRI/MRA has high sensitivity and specificity, avoids radiation, and iodinated contrast; but
is more time-consuming and contraindicated with metallic implants.
CONCOMITANT ORGAN DYSFUNCTION
• Cardiovascular: Coronary artery disease (30–40%), hypertension, peripheral vascular disease
• Neurologic: Cerebrovascular disease
• Pulmonary: Chronic obstructive pulmonary disease (COPD), smoking history
• Renal: Chronic renal insufficiency
• Endocrine: Diabetes mellitus
CIRCUMSTANCES TO DELAY/ CONDITIONS
None; rAAA has a mortality that exceeds 80% if not repaired.
CLASSIFICATIONS
• Anterior intraperitoneal rupture (20%): Rapid bleeding into the peritoneal cavity usually
results in exsanguination and death before the patient arrives at the hospital (1)[C].
• Retroperitoneal rupture (80%): Tamponade effect limits internal hemorrhage. Associated
with a lower mortality rate (1)[C].

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Analgesia: Small incremental doses of opioids
• Sedation: Avoid in hemodynamically unstable patients
• Bronchodilators: Symptomatic patients with COPD
• Antihypertensive/anti-anginal: Continued until time of surgery if hemodynamically stable
• Blood products: pRBCs, platelets, FFP, cryoprecipitate
Special Concerns for Informed Consent
• May not be possible in emergency
• Blood consent
INTRAOPERATIVE CARE
Choice of Anesthesia
• General endotracheal anesthesia
• Continuous epidural anesthesia may be considered if rupture is contained and coagulation
status is normal. However, placement should not occur in hemodynamically unstable
patients or if it will delay surgery.
Monitors
• ECG with ST-segment analysis
• Arterial line: Pre-induction placement in radial artery is commonly performed. Femoral
artery insertion may permit monitoring of distal perfusion pressures.
• Central venous access is appropriate for monitoring pressures and administration of
vasoactive medications.
• TEE facilitates continuous evaluation of intravascular volume, valvular integrity, and
ventricular function.
• Pulmonary artery catheterization provides SvO2, SVR, CO, PAP.
• Temperature (central and peripheral sites if bypass is to be used)
• Foley catheter
• Cell salvage, rapid infuser
Induction/Airway Management
• Slow, controlled titration of induction medications: In patients at risk for pulmonary
aspiration, the decision to proceed with an RSI should be balanced against the potential for
hypertension.
– Control of hypertensive response to laryngoscopy and intubation can be accomplished
with moderate-dose narcotics.
– Avoid hypotension which may contribute to cardiac ischemia and further deterioration of
peripheral perfusion.
• Single-lumen endotracheal tube is sufficient for surgery contained to the abdominal cavity.
Lung isolation with a double-lumen tube or bronchial blocker is preferred for procedures
extending into the thorax.
• Positive pressure ventilation may decrease venous return and further decrease cardiac
output and peripheral perfusion.
Maintenance
• Position: Supine with transperitoneal approach; the lateral decubitus position and
retroperitoneal approach may be preferred in certain situations.
• Thermoregulation: Forced air and fluid warming systems are necessary due to significant
heat loss with open procedures.
• Fluid management: Maintenance of intravascular volume may be challenging due to
significant hemorrhage and evaporative losses; no specific colloid or crystalloid strategy has
emerged as superior.
• Coagulation: Consumption and dilution of coagulation factors and platelets may be
significant; replacement is guided by conventional coagulation studies as well as TEG, if
available.
• Renal protection: Maintenance of renal blood flow and urine output is essential. IV sodium
bicarbonate, mannitol, and fenoldapam may decrease the risk of kidney injury (mannitol
and fenoldapam should not be used in hemodynamically unstable patients).
• Placement of aortic cross-clamp
– Increase in left ventricle (LV) afterload and potential for cardiac collapse. Acute increases
in systemic vascular resistance (SVR) can be mitigated with vasodilators (nitroprusside,
nitroglycerin, calcium channel blockers, propofol).
– Decrease in venous return: Gentle administration of IV fluids may augment preload.
– Suprarenal clamping decreases renal perfusion. Consider administration of mannitol
(0.25–0.5 g/kg) prior to clamping.
• Removal of aortic cross-clamp
– Release of vasoactive metabolites into the central circulation can lead to hypotension and
cardiac arrhythmias.
– Decreases in the SVR are mitigated with IV fluids and vasopressors (phenylephrine or
epinephrine). Profound, unresponsive hypotension can be temporarily treated with re-
instigation of the aortic clamp.
Extubation/Emergence
• Ongoing cardiac or pulmonary instability, bleeding, hypothermia, or neurologic injury may
necessitate continued mechanical ventilation; otherwise patients may be extubated at the
conclusion of the procedure.
• Pain, hypertension, and tachycardia should be anticipated and addressed.

POSTOPERATIVE CARE
BED ACUITY
• Intensive care unit
• Monitoring of BP, HR, and LV function
• Analgesia with intravascular or neuraxial opioids
• Continued assessment of graft patency and peripheral perfusion
COMPLICATIONS
• Hemorrhage
• Coagulopathy
• Myocardial ischemia/infarction
• Renal failure
• Incision and/or graft infection
• Spinal cord ischemia, paralysis
• Impotence
• Bowel ischemia
• Embolism
• Lower extremity ischemia
• Pneumonia, respiratory insufficiency
• Hypothermia

REFERENCES
1. Assar A, Zairians C. Ruptured abdominal aortic aneurysm: A surgical emergency with many
clinical presentations. Postgrad Med J. 2009;85:268–273.
2. rattheim BJ, Elkemo TA, Altreuther M, et al. Regional disparities in incidence, handling
and outcome of patients with symptomatic ruptured abdominal aortic aneurysms in
Norway. Eur J Endovasc Surg. 2012.
3. ozniak F, LaMuraglia GM, Musch G, et al. Anesthesia for open abdominal surgery. Int
Anesth Clin. 2005;43(1):61–78.
4. Thompson R, Geaghty P, Lee J. Abdominal aortic aneurysms: Basic mechanisms and
clinical implications. Curr Probl Surg. 2002;39:110–130.
5. Adam van der Vliet J, Boll A. Abdominal aortic aneurysms. Lancet. 1997;349:863–866.
6. Bernstein E, Chan E. Abdominal aortic aneurysm in high risk patients: Outcome of selective
management based on size and expansion rate. Ann Surg. 1984;200(3):255–263.
7. Falk J, Rackow EC, Blumenberg R, et al. Hemodynamic and metabolic effects of abdominal
aortic cross-clamping. Am J Surg. 1981;142:174–177.
8. Subramaniam B, Singh N, Roscher C, et al. Innovations in treating aortic diseases: The
abdominal aorta. J Cardiothorac Vasc Anesth. 2011 (article in press).
9. Gelman S. The pathophysiology of aortic cross clamping and unclamping. Anesthesiology.
1995;82(4):1026–1060.
See Also (Topic, Algorithm, Electronic Media Element)
• Abdominal aortic aneurysm
• Abdominal aortic aneurysm dissection

CODES

ICD9
441.3 Abdominal aneurysm, ruptured

ICD10
I71.3 Abdominal aortic aneurysm, ruptured

CLINICAL PEARLS
• rAAA is a surgical emergency. Mortality exceeds 80% without intervention; with repair it
can decrease to ~50%.
• Patients often present with significant cardiac, cerebral, and/or renal vascular disease.
• Application of the aortic cross-clamp leads to an abrupt increase in afterload and may
precipitate cardiac collapse.
• Removal of the aortic cross-clamp causes a decrease in SVR and release of vasoactive
metabolites into the central circulation.
ABDOMINOPERINEAL RESECTION (APR)
Vijaya Gottumukkala, MB, BS, MD, FRCA

BASICS
DESCRIPTION
General
• Ernest Miles (1869–1947) devised the approach in the 1930s as a curative procedure for all
rectal cancers. It involves resection of the anus, rectum, and a portion of the sigmoid colon,
as well as a wide perineal and lymph node dissection.
• Abdominoperineal resection (APR) is now reserved for conditions where the rectum needs to
be removed and there is involvement of the primary sphincter complex or tumors in the
lower third of the rectum that do not have adequate clearance for sphincter preservation. It
requires a permanent colostomy.
• Laparoscopy-assisted APR and low anterior resection (LAR) are more commonly performed
today. LAR is a modified technique that allows for sphincter preservation.
Position
• Modified lithotomy
• Trendelenburg, as needed
Incision
Midline abdominal and perineal
Approximate Time
5–10 hours
EBL Expected
500–1,500 mL
Hospital Stay
7–10 days
Special Equipment for Surgery
• 2 table set-up (abdominal and pelvic sets)
• Long pelvic instruments, stapling devices
• Cystoscopy set with ureteric stents
EPIDEMIOLOGY
Incidence
• Colorectal cancer is the 4th most common cancer and the second leading cause (10%) of all
cancer-related deaths.
• From 2003 to 2007, the median age at diagnosis for colorectal cancer was 70 years of age.
At diagnosis, about 20% had distant metastasis.
• 5–10% of all colorectal cancers are associated with a familial colorectal cancer syndrome,
and an additional 15–20% are associated with a familial disposition.
• Risk for colorectal cancer increases with age (90% of cases occur in patients >50 years),
and with a diet rich in red meat and animal fat.
• Aspirin, NSAIDs, and COX-2 inhibitors have been reported to have protective effects against
colorectal cancer.
Prevalence
• As of January 1, 2007, in the US there were approximately 1,112,493 men and women alive
with a history of colon and/or rectal cancer.
• Based on rates from 2005 to 2007, 5.12% of men and women born today will be diagnosed
with cancer of the colon and/or rectum during their lifetime.
• High incidence of local recurrence despite margin-free resection
Mortality
• The overall 5-year relative survival in the US for 1999–2006 was 65.0%; for high-risk
patients it is 20%.
• Hormone replacement therapy has been shown to significantly reduce mortality in women
with colorectal cancer.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Patient population with sequelae related to the primary pathology and significant medical
comorbidities (age, smoking, diabetes, hypertension, atherosclerosis, coronary artery
disease, malnutrition). Optimize preoperative comorbid burden for optimal postoperative
recovery.
• Maintenance of tissue oxygenation, perfusion, and euvolemia. Patients are often placed on a
clear liquid diet 1–3 days prior to surgery, combined with bowel prep (laxative, enemas,
whole gut irrigation with saline via a nasogastric tube, polyethylene glycol electrolyte
lavage, or mannitol solution).
• Effective analgesia (epidural preferred for open procedures)
• Extubation at the end of surgery
• Postoperative monitoring in a high-dependency unit for 48 hours

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Symptomatic, depending on the size and location of the tumor
• Change in bowel habits and pencil stools
• Rectal or lower abdominal pain, spotting of blood in stool, lower GI bleeding, hematochezia,
and tenesmus
• May be acutely or chronically ill depending on the primary pathology (Crohns disease,
ulcerative colitis)
History
• Inflammatory bowel diseases (Crohns disease, ulcerative colitis), inherited colon cancers
(familial adenomatous polyposis, Gardner syndrome, Peutz–Jeghers syndrome, juvenile
polyposis, and hereditary non-polyposis colon cancer)
• Careful assessment of the sequelae and complications of the primary colonic/rectal
pathology, medical comorbidities, nutritional and functional status
Signs/Physical Exam
• Systemic signs of inflammatory bowel disease (IBD)
• Anemia, weight loss, fever of unknown origin
• Abdominal wall and/or internal colonic fistulae
• Palpable mass in the recto-sigmoid on examination
MEDICATIONS
• Therapy for IBD: Antidiarrheals, aminosalicylates (5-ASA), corticosteroids,
immunomodulators (azathioprine and 6-mercaptopurine, cyclosporine), antibiotics, and
pain medications
• Patient may have recently completed adjuvant chemoradiation prior to surgery and/or
planned for after surgery.
• Chemotherapy for colorectal cancer is 5-FU and leucovorin based. Irinotecan or oxaliplatin
is added in metastatic disease.
• Medications for the comorbidities (antihyperglycemics, antihypertensives, anticholesterol
medications, aspirin, etc.)
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• CBC, PT/PTT, creatinine, prealbumin, and LFTs
• Electrolytes if on diuretics, ACE I, renal insufficiency
• Colonoscopic evaluation (location, size, and number of masses)
• CT scan (tumor location, size, perirectal and vascular involvement, peritoneal and liver
metastasis)
• Other tests (TEG, ECG, CXR, cardiac echocardiogram, exercise stress test, PFTs) as indicated
CONCOMITANT ORGAN DYSFUNCTION
• Anemia from bleeding or occult blood loss
• Metastasis: Abdominal pain (hepatomegaly) and liver dysfunction from hepatic metastasis;
skeletal pain from bony metastasis; ascites from peritoneal dissemination; bladder
dysfunction, sacral or sciatic neuropathy, and vaginal discharge and bleeding from pelvic
metastasis
• Obesity/malnutrition
• Inflammatory bowel disease and its associated sequelae
• Age-related morbidities: Diabetes, hypertension, coronary artery disease

TREATMENT
PREOPERATIVE PREPARATION
Premedications
• Anxiolytic and analgesic medications, as needed
• Gastric volume reducing and acid-neutralizing medications, if indicated
• Continue appropriate medications (antibiotics, anti-inflammatory/immunomodulators,
antihypertensives, antiarrhythmics, and others) as needed
• There is an increasing trend to use alvimopan to hasten recovery of bowel function.
Special Concerns for Informed Consent
• Blood consent for possible transfusion
• Consent for epidural catheter for postoperative analgesia
• Potential for postoperative intubation and intensive care
Antibiotics/Common Organisms
• Prophylactic cefotetan or cefoxitin; metronidazole plus an aminoglycoside may be used for
cephalosporin allergy.
• Gram-negative aerobes and anaerobic bacteria
• Mechanical bowel preparation decreases fecal bulk, but does not decrease the concentration
of bacteria in the stool.
INTRAOPERATIVE CARE
Choice of Anesthesia
• General anesthesia with ETT
• Epidural catheter for postoperative analgesia: Need to rule out contraindications, review
medication list (herbals, clopidogrel, low-molecular-weight heparin, or other drugs that
alter coagulation), consider preoperative PT/PTT/INR or other advanced coagulation tests
as needed (TEG, PFA). Not contraindicated with usual thromboprophylaxis for postoperative
DVT (heparin 5,000 U SQ BID).
Monitors
• ASA standard monitors
• Arterial line (beat-to-beat blood pressure monitoring, systolic pressure variation [SPV] to
evaluate intravascular volume status, blood draws for lab work); consider placing the
arterial line pre-induction for high-risk patients.
• 2 large-bore IVs for volume resuscitation if needed. Central line access is not usually
necessary unless there is poor IV access or a need for postoperative TPN.
• Foley catheter: Ureteric stents are placed preoperatively to identify ureters during the
resection.
Induction/Airway Management
Standard induction technique and strategies to maintain hemodynamic stability and full
stomach precautions if indicated
Maintenance
• Avoid nitrous oxide. Air–oxygen mixture with an FiO2 of 0.5 will help identify oxygenation
issues early.
• Continuous epidural infusion of local anesthetic/narcotic mixture may be used for analgesia
throughout the procedure.
• Nasogastric tube placement may be requested.
• Volume: APR is a major procedure with complex bowel resection; bleeding may be
encountered from the presacral venous plexus. Additionally, insensible fluid losses can
result. Intravascular volume status and maintenance of organ perfusion should be closely
monitored.
• Surgeon may request intraoperative indigo carmine to rule out injury to the ureters; it may
temporarily result in a decrease in the pulse oximeter reading.
• Blood glucose, serum electrolytes, ABG, ACT and other coagulation parameters as may be
checked needed.
Extubation/Emergence
• Standard extubation criteria
• Post-extubation sensory–motor exam and evaluation of epidural puncture site for
effectiveness and complications

POSTOPERATIVE CARE
BED ACUITY
• High-dependency unit or ICU for 48 hours
• May need monitoring of invasive hemodynamic parameters to guide fluid volume/blood
product transfusion
ANALGESIA
• Epidural: Follow ASRA guidelines for maintenance and removal of epidural catheters
• Multimodal approach involving IV PCA if epidural contraindicated or laparoscopic
procedure
COMPLICATIONS
• Intra-abdominal abscess, wound infections (10%), anastomotic leaks (15%)
• Postoperative ileus
• Injury to the ureters, hypogastric or parasacral nerve plexus
• Postoperative fever and leukocytosis are not uncommon.
• Adverse cardiac events (hypotension, hypertension, arrhythmias, ischemia, infarct, and CHF)
• Postoperative delirium in elderly
• Postoperative neuropathies from positioning
• Epidural site infection or hematoma (very rare)
PROGNOSIS
• Overall local recurrence is 30% after a margin-free resection.
• The best prognosis in patients with locally advanced rectal cancer appears to be after
preoperative chemoradiation, maximal surgical resection (margin free), and localized
intraoperative radiation therapy (IORT) in selected cases.

REFERENCES
1. Ferg BW, Berger DH, Fuhrman GM. Cancer of the colon, rectum and anus. In: Chang G,
Feig BW. The M.D. Anderson surgical oncology handbook, 4th ed. Philadelphia, PA:
Lippincott Williams & Wilkins, 2006:261.
2. Lindholm ML, Träff S, Granath F, et al. Mortality within 2 years after surgery in relation to
low intraoperative bispectral index values and preexisting malignant disease. Anesthes
Analges. 2009;108(2):508–512.
3. Green D, Paklet L. Latest developments in the peri-operative monitoring of the high risk
surgical patient. Int J Surg. 2010;8(2):90–99.
4. Kimberger O, Arnberger M, Brandt S, et al. Goal-directed colloid administration improves
the microcirculation of healthy and perianastomotic colon. Anesthesiology.
2009;110(3):496–504.

ADDITIONAL READING
• Cancer Facts and Figures 2010. Atlanta, GA: American Cancer Society, 2010.
• Surveillance, Epidemiology and End Results (SEER) Program of the National Cancer Institute
See Also (Topic, Algorithm, Electronic Media Element)
• Insensible fluid losses
• International normalized ratio
• Partial thromboplastin time
• Prothrombin time

CLINICAL PEARLS
• Major bowel resection surgery can require significant blood products and fluid resuscitation
in the perioperative period.
• There exists a risk for positioning and surgery-related neuropathies.
• Patients are prone to the occurrence of late DVTs.
ACE INHIBITORS AND HYPOTENSION
John B. Carter, MD

BASICS
DESCRIPTION
• Significant hypotension has been reported after the induction of general anesthesia in
patients on angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor
blockers (ARBs).
• At this time, guidelines have not been established regarding preoperative management
(withdrawal or continuation) of ACEI or ARBs. Large randomized controlled studies are
lacking and most information stems from retrospective studies:
– Elective, noncardiac surgical patients who have taken ACEI or ARBs on the morning of
surgery appear to have an increased risk of moderate hypotension (systolic blood pressure
[SBP] <85 mm Hg) (1) and vasopressor requirement (2).
– Vascular surgical patients who have taken ACEI or ARBs on the morning of surgery appear
to have an increased incidence of hypotension and level of severity (3).
– Cardiac surgical patients who withhold ACE inhibitors before surgery appear to maintain a
greater MAP and require less vasopressors while on bypass. Additionally, they may
require more vasodilator therapy post-bypass and do not incur hypotension at the time of
anesthesia induction (4).
EPIDEMIOLOGY
Incidence
• ACEI/ARBs are frequently prescribed for antihypertensive therapy with particular
advantages in:
– Renal protection in diabetes mellitus (DM) and hypertension (HTN)
– Prevention of cardiac remodeling after myocardial infarction (MI)
• Lower risk of cerebrovascular accident (CVA) and MI (4)
Prevalence
Approximately 50 million individuals in the US (and 1 billion worldwide) have HTN.
Morbidity
In addition to causing hypotension, ACEI/ARBs can also cause renal impairment and
hyperkalemia. They are contraindicated in renal artery stenosis and should be used with
caution in hypovolemia.
ETIOLOGY/RISK FACTORS
Concurrent use of diuretics with ACEI/ARBs has been associated with a higher risk of
hypotension during anesthesia (2).
PHYSIOLOGY/PATHOPHYSIOLOGY
• The physiology of the renin-angiotensin-aldosterone system (RAAS) plays an essential role in
the short-term regulation of blood pressure and long-term regulation of intravascular
volume.
– Angiotensinogen is an inactive glycoprotein produced in the liver.
– Renin is secreted by the kidneys into the bloodstream when pressure receptors sense low
blood volume. Renin is highly specific in cleaving angiotensinogen to angiotensin I.
– Angiotensin converting enzyme (ACE) is a nonspecific enzyme in the vascular
endothelium which converts angiotensin I to angiotensin II. ACE also inactivates
bradykinin, a potent vasodilator.
– Angiotensin II can cause immediate vasoconstriction of arterial and venous vessels, with a
resultant increase in the systemic vascular resistance (SVR) and venous return. It
constricts renal efferent arterioles during moderate decreases in perfusion pressure in
order to preserve the glomerular filtration rate (GFR). Small amounts are also produced
independently of ACE.
– Aldosterone is produced by the adrenal glands in response to angiotensin II and
hyperkalemia. It plays a role in sodium retention and increasing the blood volume; it has
a slower response and longer duration (5).
• Blood pressure regulation is also maintained by other systems.
– The sympathetic nervous system maintains vascular tone, heart rate, and contractility;
however, induction of anesthesia results in a reduction of sympathetic tone in both the
arterial and venous vessels. This results in a lower SVR as well as decreases in effective
blood volume and preload.
– Vasopressin (antidiuretic hormone) is an important compensatory mechanism in
hypovolemia.
• Refractory hypotension: ACEI and ARBs impair the RAAS; general anesthesia impairs the
sympathetic nervous system. Thus, the combination leaves the vasopressin system as the
main mechanism of maintaining blood pressure.
• Other:
– Genetics may influence which patients are susceptible to hypotension following induction.
– Neuraxial blocks: Whether ACEI or ARBs cause refractory hypotension in patients
receiving an epidural or spinal is unclear.
PREVENTATIVE MEASURES
• Patients may be asked to withhold their ACEI/ARB on the day of surgery.
• If they are not withheld, cancellation of surgery is not necessarily warranted. Consider
volume administration, the use of an induction agent other than propofol (or lower doses),
and having vasopressors including vasopressin available.

DIAGNOSIS
Despite intraoperative hypotension being an independent predictor of mortality in the first
year after surgery (12), no standard definition exists.
• A common practical approach is to establish the patient’s baseline from several readings and
attempt to stay within 20% (6).
• However, the lowest “safe” blood pressure will vary with an individual’s comorbidities such
as aortic stenosis or cerebrovascular insufficiency.
• Adequate cerebral perfusion has been cited as a MAP >70 mm Hg (7), with higher MAPs
often necessary in chronic HTN. MAPs <70 mm Hg may be tolerated for a short time in
hypertensive patients. Cerebral ischemia resulting in stroke was not noted in these studies.
DIFFERENTIAL DIAGNOSIS
Hypotension, in general, may be seen in ∼9% of patients in the first 10 minutes following the
induction of anesthesia (8). The following predictors were found:
• ASA III-V
• Age >50
• Baseline MAP <70 mm Hg
• Use of propofol for induction
• Increased doses of fentanyl
• Chronic HTN
• Hypovolemia

TREATMENT

• Volume infusion
• Sympathomimetics such as ephedrine or phenylephrine as first-line treatment. One study
showed that doses of ephedrine and phenylephrine did not usually exceed 20–25 mg and
200 mcg, respectively (3).
• Vasopressin may be helpful in refractory cases. It is usually administered as an infusion for
vasodilatory shock; bolus therapy is off label. It may have a more sustained effect than other
pressors.
• Terlipressin, an AVP analog, may also be useful (9).
• Methylene blue has been reported in the treatment of refractory hypotension. The
mechanism of action is an in inhibition of cGMP in the endothelium.

REFERENCES
1. Comfere T, Spring J, Kumar M, et al. Angiotensin system inhibitors in a general surgical
population. Anesth Analg. 2005;100:636–644.
2. Pigott DW, Nagle C, Allman K, et al. Effect of omitting regular ACE inhibitor medication
before cardiac surgery on haemodynamic variables and vasoactive drug requirement. Br J
Anesth. 1999;83:715–720.
3. Bertrand M, Gilles G, Meersschaert K, et al. Should the angiotensin II antagonists be
discontinued before surgery. Anesth Analg. 2001;92:26–30.
4. White W. Angiotensin-converting enzyme inhibitors in the treatment of hypertension: An
update. J Clin Hypertens. 2007;9:876–882.
5. Colson P, Ryckwaert F, Coriat P. Renin angiotensin system antagonists and anesthesia.
Anesth Analg. 1999;89:1143–1155.
6. Howell SJ, Sear JW, Foex P. Hypertension, hypertensive heart disease, and perioperative
cardiac risk. Br J Anaesth. 2004;92:570–583.
7. Drummond JC. The lower limit of autoregulation: Time to revise our thinking?
Anesthesiology. 1997;86:1431–1433.
8. Reich D, Hossain S, Baez B, et al. Predictors of hypotension after induction of general
anesthesia. Anesth Analg. 2005;101:622–628.
9. Meersschaert K, Brun L, Gourdin M, et al. Terlipressin-ephedrine versus ephedrine to treat
hypotension at the induction of anesthesia in patients chronically treated with angiotensin
converting-enzyme inhibitors: A prospective, randomized, double-blinded, crossover study.
Anesth Analg. 2002;94:835–840.
10. Hohne C, Meier L, Boemke W, et al. ACE inhibition does not exaggerate the blood
pressure decrease in the early phase of spinal anaesthesia. Acta Anaesthesiol Scand.
2003;47:891–896.
11. heterpal S, Khodaparast O, Shanks A, et al. Chronic angiotensin-converting enzyme
inhibitor or angiotension receptor blocker therapy combined with diuretic therapy as
associated with increased episodes of hypotension in noncardiac surgery. J Cardiothoracic
Vasc Anesth. 2008;22:180–186.
12. Monk TG, Saini V, Weldon BC. Anesthetic management and one-year mortality after
noncardiac surgery. Anes Analg. 2005;100:4–10.

ADDITIONAL READING
• Augoustides J. Angiotensin blockade and general anesthesia: So little known, so far to go. J
Cardiothoracic Vasc Anesth. 2008;22:177–179.
• Smith I, Jackson I. Beta-blockers, calcium channel blockers, angiotensin receptor blockers:
Should they be stopped or not before ambulatory anaesthesia. Curr Opin Anesth.
2010;23:687–690.
See Also (Topic, Algorithm, Electronic Media Element)
• Angiotensin
• Hypotension
• Renin

CODES

ICD9
458.8 Other specified hypotension

ICD10
I95.2 Hypotension due to drugs

CLINICAL PEARLS
• Hypertensive patients often demonstrate very labile blood pressures. Excessive drops in MAP
cause concern for a possible increase in morbidity and possibly mortality.
• Following induction of anesthesia in association with use of ACEI/ARBs, there appears to be
an increased incidence of hypotension due to a reduction in vascular tone, especially on the
venous return. The angiotensin II system is unable to compensate for the hypotension;
therefore, these patients are more volume sensitive to maintain preload.
• Arguments against discontinuing ARBs and ACEI include: Neuroprotection, as well as
improved hemodynamic stability, decreased ischemia–reperfusion injury, and renal
protection.
ACLS ANESTHETIC MANAGEMENT
Mark E. Nunnally, MD, FCCM

BASICS
DESCRIPTION
• The American Heart Association’s Advanced Cardiac Life Support (ACLS) course is evidence-
based consensus products to assist practitioners with emergency scenarios, in particular
cardiac arrest. They are intentionally broad in scope (1).
• Algorithms treat distinguishable syndromes to specify care. These are often cardiac rhythm
based (e.g., asystole vs. ventricular tachycardia).
• ACLS guidelines, however, may not fit the most common arrest scenarios seen in the
operating room (OR).
– ACLS treats probabilities; these are not specific to the surgical setting.
– There is no provision in ACLS for a previously ventilated patient.
– Arrest in the OR is witnessed, usually evolves over minutes, and can be treated with a
broad range of resources.
EPIDEMIOLOGY
Incidence
• Data for arrest or near arrest in the OR are difficult to assess. Best estimates are 4.3–19.7
cardiac arrests per 10,000 anesthetics for adults (approximately 10% of these are directly
attributed to anesthesia) and 2.6–11 per 10,000 for children (much higher in infants) (2,4).
• Arrest during neuraxial anesthesia is estimated at 1.8 per 10,000 anesthetics and is more
common with spinal anesthesia than epidural anesthesia (4).
• Most available data on intraoperative cardiac arrest come from registries or closed-claims
databases. These are useful tools for studying rare events but cannot be trusted for accurate
incidence data.
Prevalence
• Arrest is an incident phenomenon, but there are many prevalent factors in the OR that
influence the risk and type of arrest.
– Intraoperative hypovolemia is common and an important cause of shock.
– Patient comorbidities contributing to arrest include cardiac and thromboembolic disease.
– Anesthetic agents are potent and their overdose accounts for the majority of arrests
attributable to anesthesia. Induction drugs and volatile anesthetic agents are potent
vasodilators and negative inotropes.
– Arrest at induction has declined while arrest during maintenance or emergence has
remained the same. Esophageal intubation and airway loss are less common since the use
of capnography and pulse oximetry became routine (8).
– Complications of intravascular access (e.g., hemorrhage, pneumothorax, tamponade) are
rare but serious causes.
• The frequency of arrhythmias under anesthesia is different. The most common arrhythmias
include (7):
– Bradycardia followed by asystole (45%)
– Unknown (33%)
– Ventricular tachycardia/ventricular fibrillation (14%)
– Pulse-less electrical activity (7%)
Morbidity
• Hypoxic neurologic injury is the salient morbidity of cardiac arrest. It is a prominent factor
in closed-claims data, associated with some of the highest payments.
• Pancreatitis, hepatic dysfunction, renal failure, and the multiple organ dysfunction
syndrome (MODS) can follow prolonged shock after cardiac arrest.
Mortality
• Estimated mortality from an intraoperative arrest ranges from 20% to 50%, compared with
84–97% for out-of-hospital cardiac arrest (US data) (5).
• In one large series from the Mayo Clinic, in-hospital mortality was 21% from arrests directly
attributable to anesthesia, versus 71% in those that were not. Other smaller series suggest
higher mortality in anesthesia-attributable arrest (up to 80%) (6).
• Factors associated with mortality include: ASA patient status, emergency surgery, diabetes
mellitus, end-stage organ failure, protracted hypotension or use of vasopressors prior to
arrest, invasive monitoring, and type of surgery (cardiac surgery worst).
• Unlike other patient populations, asystole is associated with good survival (80% in one
series), suggesting it is mediated by autonomic or drug effects, and is therefore reversible in
many cases.
• Mortality differences suggest that the combination of different etiologies, witnessed arrest,
and timely availability of advanced resuscitation techniques make intraoperative arrest
different from community arrest.
ETIOLOGY/RISK FACTORS
• Arrest in the OR is multifactorial.
• Ischemic heart disease and conduction abnormalities share etiologies with causes of arrest
outside the OR.
• Patient comorbidities are the most likely contributors to cardiac arrest, followed by surgical
and anesthetic factors.
• Anaesthetists cannot prepare for every emergency the same way. Training in arrest
management should target 4 specific cause groups:
– Events specific to anesthetic intervention (e.g., pneumothorax, high spinal)
– Reactions to specific agents (e.g., local anesthetic systemic toxicity, malignant
hyperthermia)
– Factors that occur more frequently, even though they do not always cause arrest, such as
hypovolemic shock and hypoxemia
– Relatively “common” rare causes (somewhere between 0.1 and 1 in 10,000 anesthetics)
• Some causes of arrest in the OR that result from direct intervention include:
– Hypoxemia
– Hemorrhage
– Vagal stimulation
– Emboli (e.g., venous air embolism)
– Over-ventilation/auto-PEEP
– Drug reactions (anaphylaxis, malignant hyperpyrexia)
PHYSIOLOGY/PATHOPHYSIOLOGY
• Since arrest data come from retrospective sources, only correlation can be ascertained.
Causation must be speculative.
– Preload (hemorrhage, capillary leak, hypovolemia)
– Afterload (vasoplegia, drug effect)
– Pump function (right heart, left heart, contractility, dysrhythmia)
– Impaired filling (tamponade, auto-PEEP, abdominal compartment syndrome)
• Retrospective evaluation of arrests suggests a correlation with preclinical signs.
– Hypotension
– Tachycardia
– Abrupt drops in end-tidal CO2 are particularly ominous.

PREVENTATIVE MEASURES
• MOST of what anaesthetists do involves avoiding arrest scenarios. Skilled anaesthetists
proactively avoid disaster before signs of deterioration become apparent.
• The time between a problem becoming detectable and arrest can be short as problems
escalate.
• Rapid treatment is most likely to improve outcomes.

DIAGNOSIS
• Disaster evolves quickly; thus, diagnosis and rescue treatment should occur simultaneously.
• Monitor failures are far more common than arrest, but must be addressed quickly and arrest
scenarios should always be ruled out first.
• Factors associated with arrest include:
– Change in ECG to pulse-less rhythm
– Loss of palpable pulse or arterial waveform pulsatility
– Loss of end-tidal CO2 (very specific, values <10 mm Hg are associated with severe loss of
cardiac output and the need for chest compressions).
– Loss of plethysmograph waveform
• Do not spend more than 10 seconds seeking a pulse before beginning chest compressions.
Return of spontaneous circulation (ROSC) is associated with preserved myocardial oxygen
tension, which depletes rapidly without CPR.
• Screening for specific risks helps identify sources of arrest (e.g., history of allergy/adverse
drug reactions, obstructive airway disease, aortic stenosis, prolonged QT syndrome).
• Pulse pressure variation >15%, with a tidal volume of 8–10 mL/kg, predicts fluid
responsiveness. In a population at high risk for hypovolemia, this can be very useful.
• If available, a focused, rescue transesophageal echocardiography can aid with diagnosis
(comparative chamber size, wall motion abnormalities, and signs of embolic phenomena).
• Chest radiography may aid with ruling out probable complications of central venous
cannulation (e.g., hemorrhage, pneumothorax).
DIFFERENTIAL DIAGNOSIS
• Pathophysiologic mechanisms are a useful way to organize etiologies and treatments.
• Anesthetic causes: Drug overdose, high neuraxial block, local anesthetic systemic toxicity,
malignant hyperthermia, drug swap, anaphylactic reaction
• Respiratory causes: Hypoxemia, auto-PEEP, hypoxemia, bronchospasm, tension
pneumothorax
• Cardiovascular causes: Hemorrhage, hypovolemia, acute coronary syndrome, pulmonary
hypertension, right heart failure, pulmonary embolism (thrombus, air, fat, etc.), long QT
syndrome (Torsades de Pointes), pacemaker failure, oculocardiac syndrome, tamponade,
increased intra-abdominal pressure, inferior vena cava (IVC) compression (e.g., flex
position, gravid uterus)
• Metabolic causes: Electrolyte imbalance (hyperkalemia), transfusion reaction

TREATMENT

• CPR should be initiated quickly (allow no more than 10 seconds to find a pulse in suspected
arrest) [C].
• Compression rate should be 100/minute and each compression should be at last 51 mm in
depth (1).
• Respiratory rate should be no more than 10 breaths/minute (1).
• Local anesthetic systemic toxicity: Intralipid™ rescue is associate with ROSC (1) and good
outcomes have been reported even after 60 minutes of CPR (7).
• Fluid responsiveness should be immediately assessed. Fluids are beneficial in most cases (7).
• Amiodarone is a first-line agent in ventricular tachycardia and ventricular fibrillation (1).
• Consider pacing for hemodynamically significant bradycardia (1).
• In right heart failure, physiologic considerations include adequate filling, perfusion pressure
(both systolic and diastolic systemic pressures), and inotropic support (7).
• Embolic arrests, including venous air embolism, should be treated as right heart failure (7).
• Wide-complex bradycardia and asystole are consistent with hyperkalemia. Early treatment
with an IV calcium chloride bolus is indicated (7).
• Emergency pacing is indicated for:
– Bradycardia unresponsive to chronotropes (7)
– Escape rhythms, drug overdose, acidosis, electrolyte abnormalities (7)
– Significant sinus node dysfunction, Mobitz type II 2nd degree, 3rd degree heart block,
alternating bundle branch block, or bifascicular block (1).
– Overdrive pacing of tachycardias (supraventricular tachycardia or ventricular tachycardia)
(7).

FOLLOW-UP
• During post-arrest care, one should consider: Targeted temperature management
(therapeutic cooling) (1) and avoidance of hyperoxia (PaO2 >100 mm Hg) (7).
• Patients surviving anaphylaxis or malignant hyperthermia, or those with a difficult airway,
should be given documentation they can bring for future operative encounters (7).
CLOSED CLAIMS DATA
• Death or brain damage was associated with induction of anesthesia in 62% of cases during
1985–1992, versus 35% of cases from 1993 to 1999 (8).
• Caplan et al. describe 14 cases of high spinal, suggesting that bradycardia is an important
early warning sign and that epinephrine is associated with ROSC (3).
Pregnancy Considerations
• The gravid uterus can compress the aorta and IVC after the 20th week of gestation.
• Resuscitation of the mother may not be possible until the fetus is delivered by emergency
hysterotomy.
• During arrest, hysterotomy should be performed at the bedside since there is insufficient
time to transport the patient to the OR.
Pediatric Considerations
• CPR recommendations in pediatric patients vary by the patient’s age.
• Resuscitation drugs should be dosed according to the patient’s weight.
• Intravenous access can be uniquely difficult in pediatric patients. Intraosseous lines are a
method to get quick reliable access to the circulation.
• Cardiac output in children frequently depends on heart rate (rather than on contractility),
making the treatment of bradycardia an important part of pediatric resuscitation.

REFERENCES
1. American Heart Association. ACLS Provider Manual, 2010.
2. Newland MC, Ellis SJ, Lydiatt CA, et al. Anesthetic-related cardiac arrest and its mortality:
A report covering 72,959 anesthetics over 10 years from a US teaching hospital.
Anesthesiology. 2002;97:108–115.
3. Zuercher M, Ummenhofer W. Cardiac arrest during anesthesia. Curr Opin Crit Care.
2008;14:269–274.
4. Peterson GN, Domino KB, Caplan RA, et al. Management of the difficult airway: A closed
claims analysis. Anesthesiology. 2005;103:33–39.
5. Gabrielli A, O’Connor MF, Maccioli GA. Anesthesia-centric ACLS. Available at:
http://www.asahq.org/For-Members/Publications-and-Research/
∼/media/For%2520Members/Publications/Other/Anesthesiology-CentricACLS.ashx.
6. Nichol G, Thomas E, Callaway CW, et al. Regional variation in out-of-hospital cardiac
arrest incidence and outcome. JAMA. 2008;300:1423–1431.
7. Sprung J, Warner ME, Contreras MG, et al. Predictors of survival following cardiac arrest in
patients undergoing noncardiac surgery: A study of 518,294 patients at a tertiary referral
center. Anesthesiology. 2003;99:259–269.
8. Caplan RA, Ward RJ, Posner K, et al. Unexpected cardiac arrest during spinal anesthesia: A
closed claims analysis of predisposing factors. Anesthesiology. 1988;68:5–11.

ADDITIONAL READING
• Cheney FW. The American Society of Anesthesiologist closed claims project: What have we
learned, how has it affected practice, and how will it affect practice in the future?
Anesthesiology. 1999;91:552–556.
• Cheney FW, Posner KL, Lee LA, et al. Trends in anesthesia-related death and brain damage:
A closed claims analysis. Anesthesiology. 2006;105:1081–1086.

CODES

ICD9
427.5 Cardiac arrest

ICD10
I46.9 Cardiac arrest, cause unspecified

CLINICAL PEARLS
• Cardiac arrest associated with anesthesia is different; good recovery is frequent with timely
intervention.
• Hypovolemia is a common cause of arrest and vigilance is important. Pulse pressure
variation >15% can be an important clue to volume responsiveness.
• Take no more than 10 seconds to find a pulse before starting compressions.
• Bradycardia and asystole are often related to reversible factors.
ACROMEGALY
Adam Thaler, DO

BASICS
DESCRIPTION
• The term acromegaly comes from the Greek words for “extremities” and “enlargement.”
• Acromegaly is a condition caused by an abnormal overproduction of growth hormone (GH)
from the anterior pituitary, usually by a pituitary tumor. The result is an overgrowth of
skeletal, soft, and connective tissues. Enlargement is seen in:
– Major organs including the heart, lungs, liver, and kidney
– Hands, feet, jaw, and tongue
– Airway anatomy including the tongue, epiglottis, mandible, and generalized soft tissue
(making airway management potentially difficult)
EPIDEMIOLOGY
Incidence
• Annual new patient incidence: 3–4 per million per year
• In the US: 1:20,000 persons
Prevalence
• Most common age at diagnosis is 40–45 years.
• All ethnic groups and gender are affected equally.
Morbidity
• Increased prevalence of cardiovascular risk factors
• Difficult airways are seen in 10–43% of patients (compared to 3.6% in the general
population). Mallampati Class I and II may present with airway difficulty in up to 20% of
patients.
Mortality
• Premature death can occur twice as frequently when GH concentration is >10 ng/mL.
• Cardiovascular causes are the most frequent cause of death in untreated acromegaly; the
majority of patients die before the age of 50 years.
• Survival in patients with uncontrolled disease is reduced by an average of 10 years
compared with age-matched controls.
ETIOLOGY/RISK FACTORS
• No major risk factors
• Weak risk factors include:
– MEN type I syndrome
– McCune–Albright syndrome
– Isolated familial acromegaly
– Carney complex
– Family history of aryl hydrocarbon-receptor interacting protein (AIP) mutation
PATHOPHYSIOLOGY
• Hypothalamus: Growth hormone-releasing hormone (GHRH) is produced and secreted by
the hypothalamus via the hypophyseal tract to the anterior pituitary gland (as is
somatostatin).
• Pituitary gland: GHRH stimulates the anterior pituitary gland to produce and secrete GH
into the bloodstream, whereas somatostatin inhibits GH production and secretion.
• Tissues: GH travels to and stimulates the liver to produce another hormone called insulin-
like growth factor 1 (IGF-1). IGF-1, in turn, promotes growth of bone and other tissues.
• “Feedback loop”: Normally, levels of GHRH, GH, somatostatin, and IGF-1 are tightly
controlled by each other. Levels are affected by: Sleep, exercise, stress, food intake, and
blood sugar levels.
• Excessive GH results from pituitary adenomas in >95% of cases. Secretion of GH by a
pituitary tumor is not controlled by the feedback loop resulting in excessive IGF-1 with
subsequent abnormal tissue growth.
– Carbohydrate and fat processing is affected causing diabetes and high levels of fats in the
blood. This, in turn, can lead to atherosclerosis and heart disease.
– Myocardial growth can result in conduction disturbances.
– Hepatomegaly
– Kidneys: Positive fluid balance may be due to chronic hypertension, causing
vasoconstriction, preoperative hypovolemia, lower cardiac output, fluid volume
dysautoregulation, and/or renal dysfunction.
– Lungs: Lower arterial pH
– Tumors can also grow to considerable size and cause problems by pressing on and
invading surrounding tissues.
• Gigantism is the term used when acromegaly occurs in children.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Patients with acromegaly may have glottic or subglottic stenosis, nasal turbinate
enlargement, vocal cord thickening, or recurrent laryngeal nerve involvement. Be aware of
the potential for a difficult airway, perform a careful exam, and consider having backup
airway devices available.
• Address comorbid conditions including diabetes, hypertension, and cardiac disease.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• May be divided into 2 groups: Tumor compression of surrounding tissues or those caused by
excess GH and IGF-1 in the blood. Compression of surrounding tissues can present as
headaches or partial loss of vision in one or both eyes. Bitemporal hemianopsia is due to
pressure on the optic chiasm.
• Pituitary tumors also can damage the pituitary gland itself, disrupting hormone production.
Hormone imbalances are responsible for symptoms such as impotence, low sex drive, and
changes in the menstrual cycle.
• Symptoms due to excess GH or IGF-1 include increase in ring size or tightness of rings
(“sausage-like” fingers), shoe size, sweating, jaw prominence, as well as coarseness or
thickening of facial features (especially the nose), macroglossia, or skin tags.
History
• Onset: The average time from onset to symptoms to diagnosis is 12 years.
• Snoring may suggest obstructive sleep apnea; present in 75% of patients. If on CPAP,
establish settings.
• If the patient has diabetes mellitus, assess blood sugar control; present in 25% of patients.
Signs/Physical Exam
• Musculoskeletal:
– Prognathism
– Osteoarthritis
– Osteoporosis
– Kyphosis
– Skeletal muscle weakness
• Airway:
– Macroglossia
– Vocal cord thickening with hoarseness
– Thickening of the laryngeal and pharyngeal soft tissues: Leading to subglottic narrowing
– Enlarged epiglottis
– Hypertrophy of the periepiglottic folds
– Calcinosis of the larynx
– Recurrent laryngeal nerve injury
• Endocrine:
– Peripheral neuropathy
– Thyroid nodule; goiter (25%): May compress trachea
• Cardiovascular:
– Increased prevalence of valvular heart disease
Significant AI (30%)
Significant MR (5%)
– Hypertension (46%)—volume overload
Cardiomegaly
Dysrhythmias (40%)
LV dysfunction: EF ∼ 42%
CHF (3–10%)
MEDICATIONS
• Octreotide is a somatostatin analog that inhibits GH secretion. It is capable of causing GI
side effects such as nausea, bloating, and gas in up to 30% of patients.
• Dopamine agonists, bromocriptine and cabergoline, work at the level of the pituitary to
reduce GH and subsequent IGF-1 secretion.
• Pegvisomant is a GH receptor blocker and a new category of drugs. Studies have shown that
it normalized IGF-1 levels in >90% of people treated. Side effects include reaction at the
injection site, sweating, headache, and fatigue.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• GH and IGF-1 levels
• GH suppression test is a confirmatory test measured before and after drinking 75 g of
glucose. The inability to sufficiently suppress serum GH confirms the diagnosis.
• ECG changes, such as ST-segment depression, T-wave abnormalities, and conduction defects,
are noted in >50% patients.
• Chest radiography can show bone thickening.
• CT or MRI of the head to confirm that an adenoma is in the pituitary gland.
• CT scans of the abdomen/pelvis and chest look for tumors of the pancreas, adrenal glands,
ovaries, or lung that might secrete GH or GHRH.
CONCOMITANT ORGAN DYSFUNCTION
• Hypertension
• Diabetes mellitus
• Arthritis
• Colonic polyps
• Coronary artery disease
• Conduction disturbances
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Severe symptoms such as CHF or critical aortic stenosis
• Returning GH levels to normal can reduce the incidence of upper respiratory tract
complications. Regression of the mucosal hyperplasia and thickening could be achieved
preoperatively.
CLASSIFICATIONS
• Biochemical criteria:
– Elevated age- and sex-matched plasma IGF-1, random plasma GH >0.4 mcg/L, and lack of
GH suppression below 1 mcg/L following an oral glucose load
– Severity is judged according to GH levels, which correlate with the tumor mass.
• Imaging criteria: Severity of pituitary adenoma judged according to:
– Pituitary tumor volume
– Suprasellar extension and compression of neural structures
– Invasion of sphenoid bone and cavernous sinuses
• Pathology criteria: Positive GH immunostaining confirms the diagnosis of a pituitary GH-
secreting adenoma. On the basis of the number of cytoplasmic granules, somatotroph
adenomas are divided into 2 types:
– Densely granulated
– Sparsely granulated (more aggressive)
TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Antihypertensive medications, as needed
• Insulin, as needed
INTRAOPERATIVE CARE
Choice of Anesthesia
Regional blocks may be considered to avoid airway instrumentation; however, in the event of
a complication, or failed block, it would require airway instrumentation in less than ideal
conditions or emergently.
Monitors
• Standard ASA monitors
• Arterial line may be considered in patients with poorly controlled hypertension or diabetes,
or with coronary artery disease.
• Foley catheters may be placed to carefully monitor fluid management; patients may be
1,200–1,500 mL overloaded.
Induction/Airway Management
• Preparations should be made for a potential difficult airway.
– Larger face mask may be required because of prognathism.
– Smaller ETT may be needed because of subglottic narrowing and distortion.
– If direct laryngoscopy is difficult, fiberoptic intubation can also be challenging.
Maintenance
• Balanced anesthetics with volatiles and intravenous agents have been utilized.
• Hypertension may be seen intraoperatively, especially after the nasal septum is prepped
with cocaine, epinephrine, or phenylephrine.
• In patients with aortic regurgitation, “fast and loose” describes providing afterload reduction
and higher heart rates. Bradycardia and increases in SVR increase the regurgitant volume in
patients with aortic regurgitation.
• Glucose monitoring may be necessary in long cases or in poorly controlled diabetics.
• Fluid regulation may be altered: Urine output is significantly lower in acromegalic patients
resulting in greater positive fluid balance.
Extubation/Emergence
Patients are at increased risk for airway obstruction and may have difficult airways; ensure
that the patient is fully awake and following commands before extubating.

POSTOPERATIVE CARE
BED ACUITY
• Consider supplemental oxygen (nasal cannula, face mask)
• Prepare for the potential backward displacement of the already large tongue post-extubation
that may cause respiratory compromise.
COMPLICATIONS
• Airway difficulties
• Mild perioperative metabolic problems occur with respect to blood glucose and fluid
balance.

REFERENCES
1. Nemerget EC, Dumont AS, Barry UT, et al. Perioperative management of patients
undergoing transsphenoidal pituitary surgery. Anesth Analg. 2005;101:1170–1181.
2. Seidman PA, Kofke WA, Policare R, et al. Anaesthetic complications of acromegaly. Br J
Anaesth. 2000;84(2):179–182.
3. Hakala P, Randell T, Valli H. Laryngoscopy and fiberoptic intubation in acromegalic
patients. Br J Anaesth. 1998;80(3):345–347.
4. Scacchi M, Cavagnini F. Acromegaly. Pituitary. 2006;9(4):297–303.
5. Nabarro JD. Acromegaly. Clin Endocrinol (Oxf). 1987;26(4):481–512.

ADDITIONAL READING
• Katznelson L, Atkinson JL, Cook DM, et al. American Association of Clinical
Endocrinologists medical guidelines for clinical practice for the diagnosis and treatment of
acromegaly-2011 update: Executive summary. Endocr Pract. 2011;17(4):636–646.
See Also (Topic, Algorithm, Electronic Media Element)
• Cushing syndrome
• Diabetes mellitus
• Difficult airway

CODES

ICD9
253.0 Acromegaly and gigantism

ICD10
E22.0 Acromegaly and pituitary gigantism

CLINICAL PEARLS
• Greater than 50% of patients develop cardiac complications: Cardiomyopathy with
arrhythmias, left ventricular hypertrophy, decreased diastolic function, hypertension
• Greater than 60% of patients develop respiratory complications: Upper-airway obstruction
with sleep apnea, associated with soft-tissue laryngeal airway obstruction and central sleep
dysfunction
ACUTE ADRENAL INSUFFICIENCY
Cristina Cunanan, MD
Anahat Dhillon, MD

BASICS
DESCRIPTION
• Also called adrenal crisis, acute adrenal insufficiency is a life-threatening condition
secondary to inadequate adrenal steroid production not matching increased demands during
stress (e.g., infection, surgery) (1).
• Manifestations result from mineralocorticoid deficiency, in association with prostaglandin
excess, and decreased responsiveness to norepinephrine and angiotensin II (2):
– Severe hypotension
– Circulatory collapse
– Hypothermia
– Altered mental status
– Hypoglycemia
• Primary adrenal insufficiency (PAI) (3):
– All 3 layers of the adrenal cortex are affected.
– Involves glucocorticoid, mineralocorticoid, and adrenal androgen deficiencies
– Seen with autoimmune adrenalitis, adrenal hemorrhage, adrenalectomy, AIDS, and
tuberculosis
• Secondary adrenal insufficiency (SAI) (2):
– Results from disorders of the hypothalamic–pituitary–adrenal (HPA) axis that may involve
tumors, irradiation, trauma, surgery, exogenous glucocorticoid therapy (most common),
enzyme inducers that enhance the clearance of synthetic glucocorticoids (rifampin and
carbamazepine), or drugs that inhibit cortisol synthesis (ketoconazole, etomidate) (3)
– These conditions can cause a deficiency in adrenocorticotropic hormone (ACTH) or
corticotropin-releasing hormone (CRH), leading to atrophy of the adrenal zona fasciculata
where glucocorticoids are synthesized.
– Mineralocorticoid function is better maintained, and hence, less likely to cause an adrenal
crisis.
• Initiation of thyroxine replacement in patients with hypothyroidism may induce adrenal
crisis due to increased cortisol metabolism (4).
EPIDEMIOLOGY
Incidence
3.3–6.3 adrenal crisis per 100 patient years (4,5)
Prevalence
• Of PAI, 93–140 per million; age of diagnosis peaks in the 4th decade of life; women more
frequently than men (5).
• Of SAI, 150–280 per million; age of diagnosis peaks in the 6th decade of life; women more
frequently than men (5).
Morbidity/Mortality
• Data regarding morbidity and mortality in patients with adrenal insufficiency are scarce (6).
• The risk ratio for death is more than 2-fold higher in patients with PAI; it is attributed to
malignancy and cardiovascular and infectious diseases (7).
• In patients with PAI, mean age at death for females is 75.7 years, and for males mean age is
64.8 (this is 3.2 and 11.2 years less than the estimated life expectancy, respectively) (8).
• In children with PAI, there is a 3- to 4-fold increase in mortality compared with the general
population (8).
ETIOLOGY/RISK FACTORS
• Risk of adrenal crisis is higher in:
– PAI compared to SAI (3.3–6.6 per 100 vs. 2.5–5.8 per 100)
– Women compared to men (4.4 per 100 vs. 1.6 per 100 years) (4,5)
• In SAI patients, there is a higher risk of adrenal crisis in female patients and with the
presence of diabetes insipidus.
• Precipitating factors for adrenal crisis include (5):
– Infectious disease (particularly GI infections)
– Surgery
– Strenuous physical activity
– Cessation of glucocorticoid replacement
– Psychic distress
– Heat
– Pregnancy
PHYSIOLOGY/PATHOPHYSIOLOGY
• HPA axis is vital to the body’s ability to cope with severe stress, such as that induced by
natural or iatrogenic trauma or infection.
• Adrenal cortex produces glucocorticoids (mainly cortisol) and mineralocorticoids (mainly
aldosterone); these hormones are required for the maintenance of metabolic control, blood
volume, and normal cardiovascular function.
• Surgery, anesthesia, trauma, and severe illness result in elevated ACTH and cortisol levels,
from a normal cortisol secretion rate of 10 mg/d to 75–150 mg/d during stress; and this
response is absent in patients with adrenal insufficiency.
• Mineralocorticoids are produced by the zona glomerulosa under the control of the renin–
angiotensin system:
– Facilitates sodium and potassium homeostasis and the maintenance of intravascular
volume
– Primary target is the kidney, where it stimulates reabsorption of sodium and secretion of
potassium and hydrogen ions.
– Deficiency results in salt wasting and volume depletion.
• Glucocorticoids have multiple effects on body tissues including:
– Increased gluconeogenesis
– Increased angiotensin synthesis by the liver
– Increased vascular reactivity to vasoconstrictors
– Decreased capillary permeability
– Decreased production and activity of nitric oxide
– Alteration of kinin and prostaglandin systems
– Facilitate conversion of norepinephrine to epinephrine in the adrenal medulla
• Glucocorticoid deficiency, therefore, results in decreased vascular responsiveness to
angiotensin II and norepinephrine, decreased synthesis of renin substrate, and increased
prostacyclin production which can aggravate the circulatory collapse seen in
mineralocorticoid deficiency.
• Chronic use of exogenous corticosteroids given in supraphysiologic doses leads to the
development of SAI, and the amount of adrenal suppression depends on the dose, duration,
frequency, time and route of administration and can occur as early as 1 week after
commencing therapy (3).
PREVENTATIVE MEASURES
• Anesthetic plan should avoid the use of drugs that inhibit cortisol synthesis (e.g., etomidate)
in patients at risk.
• Controversy remains over whether supplemental perioperative steroids are required for
patients on maintenance doses of corticosteroids who undergo surgery (9). A 2009 Cochrane
review of randomized controlled trials of supplemental perioperative steroids concluded
that there is inadequate evidence to support or refute the use of supplemental perioperative
steroids, but it is likely that the administration of daily maintenance steroid dose may be
sufficient and supplemental doses are not required.
• While this topic is controversial and the optimal dose and duration of perioperative
glucocorticoid coverage have also not been established, the following recommendations are
based on a review of expert opinion and clinical experience (3):
– For minimal stress procedures (<1 hour under local anesthesia), continue usual
replacement corticosteroid dose.
– For minor stress procedures (colonoscopy, inguinal hernia repair), administer IV
hydrocortisone 25 mg or equivalent at the start of the procedure, followed by usual
replacement doses after the procedure.
– For moderate stress procedures (open cholecystectomy, joint replacement, lower limb
revascularization, abdominal hysterectomy), administer IV hydrocortisone 75 mg/d on the
day of the procedure (25 mg q8h), then taper over the next 1–2 days to usual replacement
doses.
– For severe stress procedures (cardiothoracic, Whipple, liver resection), administer IV
hydrocortisone 150 mg/d (50 mg q8h), then taper over the next 2–3 days to the usual
replacement dose.

DIAGNOSIS
• History/physical exam
– If PAI is undiagnosed and suspected, elicit symptoms such as chronic fatigue, weakness,
lethargy, anorexia, weight loss, postural hypotension, recurring abdominal pain, loss of
libido, loss of axillary and pubic hair, and hyperpigmentation (2).
– All of the above may be present in SAI, except for hyperpigmentation, and hypotension
may be less prominent (2).
– Any patient who has received the equivalent of 20 mg/d of prednisone for >5 days is at
risk for suppression of the HPA axis; if on therapy for 1 month, HPA axis suppression can
last up to 6–12 months after cessation of therapy (10).
– Other modes of steroid administration should be noted, such as topical, inhaled, and
regional (10).
• Maintain a high level of suspicion for adrenal crisis in cases of unexplained hypotension
refractory to catecholamines, especially in patients with increased risk (e.g., prior
glucocorticoid therapy, autoimmune disease, AIDS) (2).
• ACTH stimulation test involves the administration of cosyntropin 250 mcg IV (synthetic
ACTH hormone), followed by serum cortisol measurements at 30 minutes and 60 minutes.
Plasma cortisol values:
– <3 mcg/dL (80 nmol/L) is highly suggestive of adrenal insufficiency.
– <10 mcg/dL (275 nmol/L) requires further adrenal evaluation.
– >20 mcg/dL (550 nmol/L) makes adrenal insufficiency highly unlikely (2).
• Morning plasma cortisol levels
– 10–20 mcg/dL is normal.
– <3 mcg/dL is highly suggestive of adrenal insufficiency (2).
• Other tests:
– Elevated plasma corticotropin levels in PAI
– Decreased aldosterone levels
– Hyperreninemia
– Hyponatremia
– Hyperkalemia
– Hypoglycemia
– Eosinophilia
– TSH
DIFFERENTIAL DIAGNOSIS
• Cardiogenic shock
• Anaphylactic shock
• Hypovolemic shock

TREATMENT

• Immediate administration of hydrocortisone 100 mg IV followed by 100–200 mg IV per 24


hours
• IV fluids
• Electrolyte replacement
• Improvement in response to glucocorticoids is usually seen within 12 hours (2).
• If diagnostic screening demonstrates basal or post-ACTH cortisol levels >20 mcg/dL, stop
further hydrocortisone therapy unless the patient is still critically ill.
FOLLOW-UP

• If hemodynamic stability is recovered after administration of glucocorticoid, may consider


continuing with surgical procedure.
• Final confirmation of adrenal insufficiency and evaluation of its etiology, if unknown, may
be appropriate after resolution of the acute crisis.

REFERENCES
1. Hahner S, Allolio B. Therapeutic management of adrenal insufficiency. Best Pract Res Clin
Endocrinol Metab. 2009;23(2):167–179.
2. Bouillon R. Acute adrenal insufficiency. Endocrinol Metab Clin North Am. 2006;35(4):767–
775.
3. Jung C, Inder WJ. Management of adrenal insufficiency during the stress of medical illness
and surgery. Med J Aust. 2008;188(7):409–413.
4. Hahner S, Loeffler M, Bleicken B, et al. Epidemiology of adrenal crisis in chronic adrenal
insufficiency: The need for new prevention strategies. Eur J Endocrinol. 2010;162(3):597–
602.
5. Arlt W, Allolio B. Adrenal insufficiency. Lancet. 2003;361:1881–1893.
6. Schulman D, Palmert MR, Kemp SF, et al. Adrenal insufficiency: Still a cause of morbidity
in childhood. Pediatrics. 2007;119:e484–e494.
7. Bergthorsdottir R, Leonsson-Zachrisson, M, Oden A, et al. Premature mortality in patients
with Addison’s disease: A population-based study. J Clin Endocrin Metab. 2006;91:4849–
4853.
8. Erichsen M, Løvås K, Fougner KJ, et al. Normal overall mortality rate in Addison’s disease,
but young patients are at risk of premature death. Eur J Endocrinol. 2009;160:233–237.
9. Yong SL, Marik P, Esposito M, et al. Supplemental perioperative steroids for surgical
patients with adrenal insufficiency. Cochrane Database Syst Rev. 2009;7(4).
10. Kohl B, Schwartz S. Surgery in the patient with endocrine dysfunction. Anesthesiol Clin.
2009;27:687–703.
See Also (Topic, Algorithm, Electronic Media Element)
• Cortisol
• Ulcerative colitis
• Rheumatoid arthritis

CODES

ICD9
255.41 Glucocorticoid deficiency

ICD10
• E27.2 Addisonian crisis
• E27.40 Unspecified adrenocortical insufficiency

CLINICAL PEARLS
• Risk of adrenal crisis is significantly higher in PAI than in SAI.
• The body makes approximately 10 mg/d of cortisol. During extreme stress 75–150 mg/d can
be made.
• Any patient who receives >20 mg/d of prednisone equivalent for >5 days is at risk for SAI.
• There is inadequate evidence to support empiric use of supplemental corticosteroids in
patients with risk factors for SAI.
ACUTE NORMOVOLEMIC HEMODILUTION
Teresa L. Moon, MD

BASICS
DESCRIPTION
• Acute normovolemic hemodilution (ANH) is a strategy that may be implemented to decrease
the need for blood transfusions and their associated risks; it is a form of autologous blood
transfusion. Other commonly utilized techniques include preoperative autologous donation
and cell salvage.
• The process of ANH entails the controlled removal of whole blood from the patient prior to
incision and blood loss and simultaneous replacement with an appropriate volume of
crystalloid or colloid (non-red cell containing), in order to maintain normovolemia and
avoid hypotension.
• The goal is to decrease the loss of red cell mass (as well as other blood cells and proteins)
during surgical bleeding. ANH has the following advantages:
– No risk of transfusion error
– No risk of disease transmission
– Simple
– Inexpensive
– Minimal use of collective resources
– Stored in the operating room
– Whole blood with all components is returned to the patient; minimal loss of coagulation
factors and platelets secondary to limited storage time.
– Does not require significant coordination with the patient and blood bank (unlike
autologous blood donation)
PHYSIOLOGY PRINCIPLES
• Transient intraoperative anemia is achieved by removing whole blood to a target hematocrit
while concurrently administering crystalloid or colloid to maintain normovolemia. By
decreasing the hematocrit, there is a reduced loss of erythrocyte mass during surgical
bloodshed.
• Hemodynamics during dilutional anemia
– Combination of decreased blood viscosity and local vasoregulatory factors. The
endothelium senses changes in intraluminal blood flow, shear stress, and the chemical
environment that result from hemodilution and changes in cardiac output; it appears to
respond by releasing NO and causing vasodilation. Additionally, studies have suggested
that hemodilution may decrease the blood’s ability to scavenge and inactivate NO (results
in increased levels). Autonomic nervous system-mediated vasodilation does not appear to
play a significant role.
– Cardiac output is increased (stroke volume) secondary to decreased viscosity (decreased
afterload/tension of the left ventricle); the myocardium is capable of ejecting more
volume.
– Mean arterial pressure is usually maintained within the limits of normal, secondary to the
compensatory increase in cardiac output.
– Heart rate may increase with profound anemia.
• Critical red cell mass: A concept that describes the lower limit of hemoglobin that is capable
of maintaining effective oxygen delivery. Below this threshold, ischemia and anaerobic
metabolism/lactate production can result.
• Unlike techniques such as deliberate hypotension, ANH does not directly decrease surgical
blood volume loss.
ANATOMY
• Phlebotomy may be performed via a:
– Large vein in the periphery; newly placed or pre-existing large-bore IV catheter or one-
time stick
– Central line
– Arterial line
DISEASE/PATHOPHYSIOLOGY
• Decreased blood oxygen carrying capacity occurs secondary to hemodilution. Studies have
demonstrated that tissue oxygenation is usually not sacrificed if normovolemia is
maintained.
• Cardiac ischemia: Usually presents with tachycardia and ECG changes as a result of
decreased oxygen delivery
• Edema may be present postoperatively if large volumes of crystalloid and/or colloids are
used to maintain normovolemia.
PERIOPERATIVE RELEVANCE
• Indications:
– Spinal surgery
– Prostatectomy
– Hysterectomy
– Hip arthroplasty
– Major liver resections: The reported rate of blood transfusion is rarely <30% and patients
normally require 1–2 units. One study demonstrated that the use of ANH did not result in
adverse cardiac, renal, or neurologic outcomes. Benefit were particularly pronounced in
patients who had significant blood loss that exceeded 800 mL.
• Contraindications:
– Pre-existing anemia
– Unstable angina
– Coronary artery disease with significant stenosis or recent myocardial infarction in the last
6 months
– High-grade aortic stenosis or carotid stenosis
– Renal impairment
– Bacteremia
• Invasive monitors may be needed to closely monitor the effects of anemia, including volume
status and frequent blood draws in order to monitor oxygen delivery, confirm EBL, and
electrolytes. The extent of monitoring should factor in comorbidities, the extent of
hemodilution, and expected blood loss.
• Collection:
– Phlebotomy: Whole blood is collected immediately prior to, or during, the initial stages of
surgery (ideally prior to any blood loss).
– Fluid replacement: May be done with either crystalloid or colloid to maintain
normovolemia
– Storage: Whole blood is collected into blood-collection bags with a predetermined
anticoagulant (usually CPD) and kept in the operating room. Agitation of the bags
throughout the case can decrease clotting.
• Considerations:
– Patient becomes unstable during hemodilution: May be evidenced by unexplained
tachycardia or ECG changes despite normal intravascular volume. Phlebotomy should be
halted and blood returned to the patient in order to avoid any acute cardiac events.
– Patient becomes unstable intraoperatively: The removed blood may need to be transfused
to treat severe anemia. Should be administered prior to donated blood.
– May be utilized with cell salvage techniques; however, should not be combined with
deliberate hypotension.
• Determining the amount of blood to be collected:
– Safe hematocrit: A standard, agreed-upon post-hemodilution value does not exist. Target
levels usually range from 20% to 28% and are dependent upon myocardial oxygenation
needs, as well as comorbidities (in particular cardiac and cerebral disease).
– Red cell mass: Dependent on starting hematocrit and total blood volume. Healthy patients
with normal and high hematocrits and men have a greater amount of red cells that can be
collected (compared to those who are chronically ill, anemic, or women).
– Anticipated surgical blood loss
• Efficacy of ANH is dependent upon:
– Volume removed: Patients that can tolerate a large volume of blood removal will likely
have a higher final hematocrit once surgical bleeding has stopped and the blood is
returned. Whereas patients who are unable to donate as much blood will clearly not
receive as much red blood cell mass when blood is returned.
– Effectiveness of hemodilution: Inadequate volume repletion, initially or intraoperatively,
can result in hemoconcentration and increased red blood cell mass.
– Timing of autologous blood replacement: If the collected blood is returned after surgical
bleeding is complete, the patient will have less absolute red cell losses.
EQUATIONS
• Estimated blood volume (EBV)
– Male: 70 mL/kg
– Female: 60 mL/kg
• Blood volume to be withdrawn = EBV × (Hctinitial – Hcttarget)/Hctaverage
• For a 70 kg man with a starting Hct of 40%

• ?> and target Hct 28%: [(70 mL/kg × 70 kg) × (40 − 28)]/[(40 + 28)/2] = 1,729 mL
• For a 70 kg man with starting Hct of 35%: [(70 mL/kg × 70 kg) × (35 − 28)]/[(35 +
28)/2] = 1,089 mL
• Volume replacement with appropriate amounts of crystalloid (3 × volume withdrawn) or
colloid (1 × volume withdrawn)

REFERENCES
1. Doss DN, Estafanous FG, Ferrario CM, et al. Mechanism of systemic vasodilation during
normovolemic hemodilution. Anesth Analg. 1995;81:30–34.
2. Epstein NE. Bloodless spinal surgery: A review of the normovolemic hemodilution
technique. Surg Neurol. 2008;70:614–618.
3. Matot I, Scheinin O, Jurim O, et al. Effectiveness of acute normovolemic hemodilution to
minimize allogenic blood transfusion in major liver resections. Anesthesiology.
2002;97:794–800.
4. Monk TG. Acute normovolemic hemodilution. Surg Infect. 2005;6(Suppl 1):S9–S15.
5. Murray D. Acute normovolemic hemodilution. Eur Spine J. 2004;13(Suppl 1):S72–S75.
6. Pape A, Habler O. Alternatives to allogenic blood transfusions. Best Pract Res Clin
Anesthesiol. 2007;21(2):221–239.
See Also (Topic, Algorithm, Electronic Media Element)
• Cell salvage
• Autologous blood transfusion
• Anemia
• Myocardial oxygen supply
• Blood oxygen carrying capacity

CLINICAL PEARLS
• Normovolemic hemodilution is a technique that can help prevent or decrease the need for
allogenic blood transfusion in patients who can sustain moderate anemia intraoperatively.
• In comparison to autologous or homologous blood transfusions, normovolemic hemodilution
eliminates the need for blood bank storage or testing. Since the collected blood remains in
the operating room with the patient, transfusion errors and disease transmission are
eliminated.
• The amount of whole blood collection is directly related to the preoperative hematocrit. Safe
post-hemodilution hematocrits depend upon surgical blood loss and comorbidities.
• The efficacy of ANH has produced conflicting results, which have been attributed to the
heterogeneity of the surgeries it is used for, differences in study protocol, as well as the
definition of outcome variables.
• During cardiopulmonary bypass grafting, when ANH was implemented in lieu of
homologous blood transfusion, significantly lower bilirubin levels were observed. However,
it may be associated with increased postoperative bleeding.
ACUTE RESPIRATORY DISTRESS SYNDROME
Carlos A. Puyo, MD

BASICS
DESCRIPTION
• Acute respiratory distress syndrome (ARDS) is a form of noncardiogenic pulmonary edema.
It results from lung inflammation and presents as acute hypoxemia and bilateral pulmonary
infiltrates.
– Acute lung injury (ALI) is a milder form of ARDS.
– Hyaline membrane disease is a pediatric form of ARDS (caused by a decrease in
surfactant).
• Causes stem from either pulmonary or extrapulmonary sources.
• Histologically, affected alveolar units are filled with protein-rich edematous fluid and
cellular debris; this occurs in a heterogenous manner.
• Diagnosis is based on the history, ABG, and chest radiography.
• Treatment consists of supportive measures (supplemental oxygen, mechanical ventilation)
while the lungs heal.
EPIDEMIOLOGY
Incidence
In the US, approximately 200,000 cases per year
Morbidity
• Can lead to multiorgan failure syndrome, GI ulcers, cardiac dysfunction, acute renal failure,
malnutrition, and chronic issues such as myopathy and psychiatric problems
• Lung function recovers significantly 6–12 months after initial injury.
Mortality
Estimated 25–40%, but is influenced by a variety of coexisting conditions such multisystem
organ failure
ETIOLOGY/RISK FACTORS
• Lung dysfunction due to direct lung injury:
– Pneumonia (frequent cause, high mortality)
– Aspiration
– Mechanical ventilation
– Lung contusion
– Inhalational injury
– Near drowning
• Extrapulmonary sources:
– Sepsis (frequent cause, high mortality; elderly patients are more susceptible)
– Trauma
– Pancreatitis
– Polysubstance abuse: Cocaine, opioid
– Massive blood transfusions
– Ischemia-reperfusion injury
– CNS injury
– Air/fat embolism
– Cardiopulmonary bypass
PHYSIOLOGY/PATHOPHYSIOLOGY
• Early: “Exudative phase” translates into ventilation/perfusion mismatch (shunting) and
hypoxia, decreased lung compliance, and increased work of breathing. It is associated with
the following:
– Diffuse alveolar and capillary endothelial injury
– Influx of protein-rich fluid into alveoli
– Release of tumor necrosis factor, interleukin-1, and interleukin-8
– Procoagulant activity as protein C and S levels fall and levels of tissue factor and
plasminogen activator inhibitor-1 increase
– Pneumocyte type 1 apoptosis with resultant accumulation of necrotic cellular debris in the
alveolar lumen. Pneumocyte type 2 dysfunction reduces surfactant production.
• Late: Fibroproliferative changes occur later and are characterized by:
– Chronic inflammation resulting from the proliferation of pneumocyte type 2 and
macrophages, and neutrophils filling the alveolar space.
– Fibrosis (associated with increase mortality).
– Neovascularization
PREVENTATIVE MEASURES
• Pneumonia should be diagnosed and treated aggressively.
• Identify patients at risk for pulmonary aspiration (e.g., full stomach, reflux disease, active
vomiting, recent oral contrast for radiological study, altered mental status) and implement
appropriate maneuvers to reduce risk (gastric tube suctioning, prokinetic agents, reverse
Trendelenburg, rapid sequence induction).
• Mechanical ventilation should be weaned as tolerated.
• Prevention of multiorgan dysfunction:
– Diagnose and treat sources of infection aggressively (e.g., urinary tract infection in the
elderly) to avoid sepsis.
– Limit blood transfusions, as appropriate. Consider blood salvaging techniques, blood
filters, and collection from donors without multiple HLA exposures.

DIAGNOSIS
• The diagnosis of ARDS can coexist with other (extrapulmonary) diagnoses.
– History: Acute dyspnea or hypoxemia related to trauma, sepsis, drug overdose, massive
transfusion, aspiration, or acute pancreatitis
– Physical examination: Tachypnea and tachycardia are nonspecific. Auscultation may
reveal bilateral rales. Cyanosis, fever, hypothermia.
– ABG: PaO2/FiO2 ratio <200; a ratio <300 suggests ALI. Initially a respiratory alkalosis is
seen. If ARDS is secondary to sepsis, the ABG may reveal a respiratory acidosis with or
without respiratory compensation.
– CXR is initially patchy and located peripherally; it progresses rapidly to diffuse bilateral
involvement with a ground-glass appearance.
– PCWP ≤18 mm Hg with no clinical evidence of cardiac failure.
– TEE may be helpful to determine pulmonary artery pressures and intravascular volume
status.
– CT scan: Heterogeneous alveolar involvement
DIFFERENTIAL DIAGNOSIS
• Interstitial/idiopathic pulmonary fibrosis
• Lymphangitic carcinoma
• Veno-occlusive pulmonary disease
• Intravascular fluid overload
• Pneumonia and respiratory failure: Ventilator-associated pneumonia, viral, bacterial
• Pulmonary hemorrhage
• Near drowning
• Drug reaction toxicity: Heroin, salicylate
• Cardiac disease: Left ventricle failure, mitral stenosis
• Toxic shock syndrome
• Tumor lysis syndrome

TREATMENT

• Nonpharmacologic interventions are supportive and consist of intubation and mechanical


ventilation:
– Tidal volume (6 mL/kg) using predicted body weight and plateau pressures of ≤30 cm
H2O (Level I evidence per the ARDS Network trial)
– Positive end-expiratory pressure (PEEP); higher PEEP levels do not negatively impact low-
VT strategy.
– Prone positioning can improve oxygenation and mortality (Level I evidence).
– Permissive hypercarbia allows for decreased minute ventilation with consequent decreases
in shear injury that is imposed on the alveoli with positive pressure ventilation. The pH
should be maintained at ≥7.20.
– Extracorporeal membrane oxygenation and extracorporeal carbon dioxide removal; no
outcome improvement has been demonstrated with these techniques.
– Recruitment maneuvers expand atelectatic areas and improve ventilation/perfusion
matching. However, they are ineffective in providing sustained oxygen concentration.
– Pressure–volume curve to set VT and PEEP; has uncertain clinical value.
– Open-lung strategy applying high-pressure ventilation (55 cm H2O) for 5–10 minutes and
PEEP of 16 cm H2O has uncertain value.
– High-frequency oscillatory ventilation and bilevel ventilation improve oxygenation
transiently with no benefit in mortality.
• Pharmacologic interventions:
– Fluid management: A conservative or restrictive strategy can improve oxygenation. It has
been associated with decreased morbidity and mortality.
– Inhaled nitric oxide (INO): Provides short-term reduction of pulmonary artery pressures
and oxygen improvement (Level I evidence)
– N-acetylcysteine and procysteine have some benefit in improving lung injury score.
– Corticosteroids and methylprednisolone have been used with benefit in ALI/ARDS patients
diagnosed with Pneumocystis carinii pneumonia or at high risk for fat emboli. High doses
may benefit patients with unresolved ARDS of more than 7 days duration.
– Nutritional support: Diets with high-fat content and antioxidant nutrition. The use of
eicosapentaenoic acid (EPA) and gamma-linoleic acid (GLA) appears to decrease
inflammation mediated by arachidonic acid metabolites. Evidence exists to support the
use of EPA and GLA in ARDS.
– Surfactant: Evidence demonstrates that there is a lack of improvement in oxygenation,
ventilator- free days, or mortality.
– Partial liquid ventilation appears to reduce inflammation and disease progression, but has
no obvious benefit in ventilator dependency and mortality.
– Ibuprofen and NSAIDs do not control inflammation mediated by sepsis and are likely of no
benefit in ARDS.
– Ketoconazole, pentoxifylline, lisofylline: Studies have not demonstrated a benefit.
• Diagnose and provide supportive therapy for extrapulmonary manifestations:
– Renal: Monitor for acute tubular necrosis
– Hepatic: Monitor liver function test for abnormalities such as cholestasis and
hepatocellular injury
– Hematologic: Monitor for thrombocytopenia, disseminated intravascular coagulation, and
changes in Von Willebrand factor

FOLLOW-UP

After resolution of the acute phase, mechanical ventilation and respiratory therapy should be
administered to regain muscle strength.

REFERENCES
1. Bernard GR. Acute respiratory distress syndrome. Am J Respir Crit Care Med.
2005;172:798–806.
2. Briel M, Meade M, Mercat A, et al. Higher versus lower positive end-expiratory pressure in
patients with acute lung injury and acute respiratory distress syndrome: Systematic review
and meta-analysis. JAMA. 2010;303(9):865–873.
3. Kallet RH. Evidence-based management of acute lung injury and acute respiratory distress
syndrome. Resp Care. 2004;49(7):793–809.
4. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as
compared with traditional tidal volumes for acute lung injury and the acute respiratory
distress syndrome. N Engl J Med. 2000;342(18):1301–1308.
See Also (Topic, Algorithm, Electronic Media Element)
• Aspiration
• Noncardiogenic pulmonary edema
• Burns
• Pressure volume loops
• Respiratory system compliance
• Positive end expiratory pressure (PEEP)

CODES

ICD9
518.82 Other pulmonary insufficiency, not elsewhere classified

ICD10
J80 Acute respiratory distress syndrome

CLINICAL PEARLS
• Frequent evaluation of respiratory and hemodynamic status
• Since sepsis is the most common risk factor for ARDS, infectious sources must be sought
aggressively.
• If transportation is required, consider maintaining respiratory ventilation with an ICU
ventilator.
ADRENALECTOMY
Joe C. Hong, MD

BASICS
DESCRIPTION
General
• Adrenalectomy is indicated for any malignant lesion, suspicious lesion, or hormone-
secreting lesion of the adrenal gland.
• The laparoscopic approach is considered when the lesion is nonmalignant and has the
benefit of reduced pain, faster recovery, and fewer complications.
• Open adrenalectomy is indicated for large or malignant tumors where en bloc resection and
local dissection may be necessary. It can be performed via an anterior, posterior, or
thoracoabdominal approach.
– The anterior approach allows access to the entire peritoneal cavity and the ability to treat
bilateral adrenal disease or other intra-abdominal pathology. However, it is a major
laparotomy with the potential for prolonged ileus, pulmonary dysfunction, and pain.
– The posterior approach allows avoidance of the thoracic and peritoneal cavities; this
reduces bowel injury or pulmonary problems. However, it is limited to tumors <5 cm and
precludes exploration of metastases or other intra-abdominal pathologies.
– The thoracoabdominal approach allows wide direct exposure for larger tumors and en bloc
resection of a single adrenal gland. However, it limits intraperitoneal exploration, and if
the other gland needs to be removed, it requires repositioning and a second incision.
Position
• Laparoscopic: Lateral decubitus position with the operative side up. The table is flexed at
the waist with the patient in a slight reverse Trendelenburg position to facilitate placement
of the laparoscopic ports.
• Open adrenalectomy: Supine position
Incision
• Laparoscopic: 4 laparoscopic ports, 2 cm below the respective costal margin and spaced no
less than 5 cm apart
• Open: Either a unilateral subcostal, bilateral subcostal, or midline incision is used.
Approximate Time
• Laparoscopic: Typically 2.5–3.5 hours
• Open: Typically 2–3 hours with additional time when local invasion of nearby structures is
present
EBL Expected
• Laparoscopic: 50 mL
• Open: 100–200 mL
Hospital Stay
• Laparoscopic: Routine cases in relatively healthy patients can be discharged within 24
hours. Longer in-hospital stay is dependent on patient comorbidities, need for blood
pressure monitoring, or adjustment of steroid replacement therapy.
• Open: Postoperative in-hospital stays of 4–5 days are typical.
Special Equipment for Surgery
• Laparoscopic instruments and ultrasonic or bipolar coagulator
• Invasive monitoring and possibly a transesophageal echocardiogram for management of
patients with pheochromocytoma
EPIDEMIOLOGY
Incidence
• Incidental finding on abdominal CT scan ranges from 0.6% to 1.3% (1).
• Autopsy finding in patients who had no evidence of adrenal disease: 1.4–9%
Prevalence
• Nonfunctional adrenocortical adenomas: 70% (2)
• Adrenal metastasis: 21%
• Pheochromocytomas: 11%
• Cortisol-producing adenomas: 2–15%
• Aldosteronomas: 2%
• Adrenocortical carcinomas: 1.2%
Morbidity
• Depends on the nature of the adrenal mass
• Aldosteronomas may have marked hypertension, hypokalemia, and metabolic alkalosis.
• Cortisol-producing adenomas may have labile diabetes in addition to marked hypertension,
hypokalemia, and metabolic alkalosis.
• Pheochromocytoma may have significant cardiac morbidity induced by long-standing
catecholamine excess, hypertension, arrhythmias, dilated and hypertrophic cardiomyopathy,
and congestive heart failure.
Mortality
Dependent on the nature of the adrenal mass
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Understanding the physiologic implications of the hormonally active adrenal mass is vital to
appropriate anesthetic management.
• Patients with aldosteronoma should have their antihypertensive medication (most
commonly spironolactone) maintained up to the time of surgery. Careful cardiac assessment
is necessary since these patients have increased cardiac comorbidity. Serum sodium and
especially serum potassium should be checked prior to surgery. Severely hypokalemic
patients should have their potassium replaced preoperatively.
• Patients with Cushing syndrome must have their diabetes, blood pressure, intravascular
volume status, and electrolytes optimized prior to surgery. Their Cushingoid habitus
(central obesity, moon facies, buffalo hump) may present an airway challenge.
Hydrocortisone supplementation at the time of surgery is needed since they are at increased
risk of developing acute glucocorticoid deficiency postoperatively.
• Patients with pheochromocytoma must be adequately alpha-blocked, volume resuscitated,
and concomitant organ dysfunctions identified and optimized prior to surgery.
Phenoxybenzamine is the alpha-blocker of choice. Intraoperatively, hypertension is
expected during tumor manipulation whereas hypotension is expected after ligation of the
tumor’s venous drainage (3).
• Nonfunctional masses are relatively straightforward with anesthetic goals geared toward
each patient’s comorbidities.

PREOPERATIVE ASSESSMENT
SYMPTOMS
Due to mass effect and/or physiologic effects of excess hormone production
History
Based on the nature of the adrenal mass. In patients with hormone-producing adrenal lesions,
a careful history of the medical management of the endocrinopathy is necessary. This
includes the type and dosage of medication, clinical response to therapy, and relevant
comorbidities.
Signs/Physical Exam
• Cortisol-producing adenoma: Steroid encephalopathy, central obesity, moon facies, thick
neck, muscle wasting, osteoporosis, virilization and infertility, glucose intolerance,
hypertension, hypokalemia, alkalosis, easy bruising, poor wound healing (2)
• Aldosteronoma: Hypertension, hypokalemia, alkalosis, hypernatremia, left ventricular
hypertrophy (4)
• Pheochromocytoma: Hypertension, arrhythmias, cardiomyopathy, congestive heart failure,
glucose intolerance (3)
MEDICATIONS
• Cortisol-producing adenoma: Hypoglycemic agents, potassium supplements,
antihypertensives
• Aldosteronoma: Spironolactone, potassium supplements, antihypertensives
• Pheochromocytoma: Alpha-adrenergic antagonists
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Evaluation of hormonal function is based on concomitant signs and symptoms.
• Cortisol-producing adenoma: Dexamethasone suppression test, plasma ACTH, urine-free
cortisol
• Aldosteronoma: Potassium level, aldosterone:renin ratio
• Pheochromocytoma: 24-hour urine catecholamine and metanephrines
CONCOMITANT ORGAN DYSFUNCTION
Cardiac dysfunction in the form of left ventricular hypertrophy is common in patients with
aldosteronoma and pheochromocytoma. In addition, cardiac comorbidity induced by long-
standing catecholamine excess is prominent in patients with pheochromocytoma. These
include hypertension, arrhythmias, dilated and hypertrophic cardiomyopathy, and congestive
heart failure.

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Standard anxiolytic titrated to comfort
• In patients undergoing adrenalectomy for pheochromocytoma, benzodiazepines and opioid
premedication are helpful for awake arterial line placement.
• Patients with cortisol-producing tumors and those undergoing bilateral adrenalectomy must
receive perioperative intravenous hydrocortisone.
Special Concerns for Informed Consent
If planned, risks specific to central venous and epidural catheter placement should be
discussed.
Antibiotics/Common Organisms
• First-generation cephalosporin, such as cefazolin, is recommended prior to surgical skin
incision.
• Clindamycin is an alternative for a cephalosporin allergy.
INTRAOPERATIVE CARE
Choice of Anesthesia
• General endotracheal anesthesia is the technique of choice.
• Epidural analgesia for postoperative pain may be helpful for patients undergoing open
adrenalectomy.
Monitors
• Standard ASA monitors
• Invasive monitoring is dictated by patient comorbidities.
• Pheochromocytoma: Arterial line for hemodynamic monitoring and a central line for
infusion management and vasoactive medications. Pulmonary artery catheter or TEE may be
needed if significant catecholamine-induced cardiomyopathy is present (3).
Induction/Airway Management
• Induction and airway management is dictated by preoperative airway assessment.
• Pheochromocytoma: A deep plane of general anesthesia is needed prior to attempted
laryngoscopy and intubation.
• Cortisol-producing adenomas: Cushingoid habitus (central obesity, moon facies, buffalo
hump) may complicate airway management.
Maintenance
• Inhalational anesthesia with opioid supplementation is suitable.
• Nitrous oxide should be avoided because bowel distension may limit the visibility of the
surgical field in both laparoscopic and open adrenalectomy. The increased incidence of
pneumothorax after open adrenalectomy also makes nitrous oxide relatively
contraindicated.
Extubation/Emergence
General extubation criterion can be used.

POSTOPERATIVE CARE
BED ACUITY
• For routine uncomplicated procedures, a standard floor bed is usually adequate.
• Patients with pheochromocytoma with persistent labile blood pressure requiring
postoperative infusion of vasoactive medications should be monitored in the ICU.
ANALGESIA
• Laparoscopic adrenalectomy is well tolerated. Patients are typically able to convert from
intravenous to oral analgesics on postoperative day 1.
• Epidural analgesia provides excellent pain relief for open adrenalectomy.
• Patient-controlled analgesia (PCA) may be used for patients undergoing open adrenalectomy
without epidural analgesia.
COMPLICATIONS
• Intraoperative complications include massive bleeding due to the proximity of the renal
artery, renal vein, vena cava, and aorta.
• Hypertensive, as well as hypotensive crises, can occur during adrenalectomy for
pheochromocytoma. Postoperatively, these patients may be at risk for hypotension and
hypoglycemia.
• Acute adrenal insufficiency can occur after resection of a cortisol-producing adrenal mass or
after bilateral adrenalectomy. Perioperative hydrocortisone 100 mg IV q8h is recommended.
• Injury to pancreas resulting in pancreatitis
• Injury to diaphragm and pneumothorax
• Conversion from laparoscopic approach to open adrenalectomy
• Peritoneal carcinomatosis
PROGNOSIS
Dependent on the type, malignant nature, and degree of local and distant invasion
REFERENCES
1. Brunt LM, Moley JF. Adrenal incidentaloma. World J Surg. 2001;25(7):905–913.
2. Cook DM. Adrenal mass. Endocrinol Metab Clin North Am. 1997;26(4):829–852.
3. Kinney MA, Narr BJ, Warner MA. Perioperative management of pheochromocytoma. J
Cardiothorac Vasc Anesth. 2002;16(3):359–369.
4. Young WF Jr. Adrenal causes of hypertension: Pheochromocytoma and primary
aldosteronism. Rev Endocr Metab Disord. 2007;8(4):309–320.

ADDITIONAL READING
• Graham GW, Unger BP, Coursin DB. Perioperative management of selected endocrine
disorders. Int Anesthesiol Clin. 2000;38(4):31–67.
• Lampe GH, Roizen MF. Anesthesia for patients with abnormal function of the adrenal cortex.
Anesthesiol Clin North Am. 1987;5:245–268.
See Also (Topic, Algorithm, Electronic Media Element)
• Pheochromocytoma
• Aldosterone
• Cortisol

CODES

ICD9

CLINICAL PEARLS
• Understanding the physiologic implications of the hormonally active adrenal mass is vital to
appropriate anesthetic management.
• Patients undergoing bilateral adrenalectomy will need perioperative stress dose steroids.
Postoperatively, they will need glucocorticoid and mineralocorticoid replacement.
• Patients with cortisol-producing adrenal lesions also need perioperative stress dose steroids.
The quiescent contralateral adrenal gland will be unable to produce enough cortisol in the
immediate postoperative period.
• Patients with pheochromocytoma must be adequately alpha-blocked prior to adrenalectomy.
• Pneumothorax should be considered if the patient develops postoperative respiratory
distress.
AFTERLOAD
Viachaslau Barodka, MD

BASICS
DESCRIPTION
• Left ventricular (LV) afterload is the force against which the heart must work to generate
pump work (eject blood out of the heart into the aorta).
• In the purest form, afterload is defined as wall stress, which are the forces opposed to
ventricular fiber shortening. Afterload or wall stress provides the most accurate indication
of cardiac energy expenditure. However, clinically true afterload or wall stress cannot be
measured.
PHYSIOLOGY PRINCIPLES
• Ventricular afterload is comprised of a static and dynamic component; elevation in either
component may result in increased afterload.
– Static component of the LV is comprised of the systemic vascular resistance (SVR) or
outflow of blood into resistance arterioles. Under normal physiologic circumstances and in
healthy (compliant) vasculature, the SVR is the main determinant of LV afterload.
Small arteries and arterioles are referred to as resistance vessels since they are the
principal site of SVR. The autonomic nervous system provides constant regulation on a
short time scale (seconds to minutes).
SVR; Normal 800–1400 dyne-s/cm5. SVR can be calculated from MAP, CVP, CO; SVR =
[(MAP – CVP) × 80]/CO. The pressures are measured from the “beginning” of the
circuit to the “end” of the circuit. For example, if the CO is 5 L/min, the BP is 120/80
mm Hg (MAP is 93.3 mm Hg), and the CVP is 12 mm Hg, then SVR = [(93.3–12) ×
80]/5 = 1396 dyne-s/cm5.
The static component of the right ventricle (RV) is composed of the pulmonary vascular
resistance (PVR); normal 80–120 dyne-s/cm5. The blood flow (CO) through the left and
right sides of the heart are equal; however, the afterload for the RV is significantly less.
The main component of RV afterload is PVR, which is around 10 times lower than SVR.
The formula to calculate is: PVR = [(Mean PAP – wedge pressure) × 80]/CO. The
pressures are measured from the “beginning” of the circuit to the “end” of the circuit.
For example, if the PA pressures is 25/10 mm Hg (Mean PAP is 15 mm Hg), the wedge
pressure is 8 mm Hg, and CO is 5 L/min, then PVR = [(15–8) × 80]/5 = 112 dyne-
s/cm5.
– Dynamic pulsatile component: Consists of 2 phasic elements; one is the compliance-related
forward pulse wave and the second is the reflected pulse wave. The pulsatile component
contributes significantly to total LV afterload in stiff vessels. Central arterial vessels are
the principal site of the pulsatile component.
• Despite the clinical use of SVR to determine LV afterload, it is best measured as systolic wall
stress. Stress (or tension) is defined as the force, or load, per unit cross-sectional area. Wall
stress/tension is the product of transmural pressure and chamber radius divided by the wall
thickness. For the LV: S = PR/2h; where S is the LV wall stress, P is the LV cavity pressure,
R is the radius of the LV, and h is the myocardial thickness (also known as LaPlace’s Law).
– LV cavity pressure
During systole, the LV generates pressure. That pressure should be higher than pressure
seen by the LV in the ascending aorta at each point in time during ejection to promote
forward blood flow. Pressure in the ascending aorta will depend on the peripheral
resistance, compliance of the arterial tree, and contributions of wave reflections.
Aortic valve: Any obstruction to flow from the LV cavity to the ascending aorta will
cause additional resistance and a necessary increase in the LV cavity pressure to
overcome it. Clinically, the most common causes are aortic stenosis and hypertrophic
obstructive cardiomyopathy which can cause up to 100 mm Hg extra LV pressure over
what is needed to pump blood into aorta.
Blood viscosity contributes to the resistance to blood flow, such that increased viscosity
leads to increased resistance. The blood viscosity depends, for the most part, on the
hematocrit.
– Radius: Wall stress (afterload) is dependent on the geometry of the LV itself. During
systole, the ventricular wall thickens and the radius decreases as the ventricle pumps
blood out (and reduces LV wall stress). Preload or LV end diastolic volume affects the
initial radius and, hence, wall stress during isovolemic contraction.
– Myocardial thickness: In cases of pressure overload, and resultant increases in wall stress,
the heart muscles compensate by becoming hypertrophic (wall stress is inversely related
to wall thickness, thus myocardial hypertrophy decreases wall stress). Increased muscle
mass requires less force per unit area.
– Wall stress or afterload varies over time since the LV pressure, radius, and wall thickness
are continuously changing throughout the cardiac cycle. As a result, afterload can be
calculated at the instant of aortic valve opening, at the end of ejection, or at any instant
throughout systole. Clinical investigators use peak systolic stress, end-systolic stress, or
mean systolic wall stress as indices of afterload.
• Determinants/regulation of vascular resistance (and hence afterload)
– Neurohumoral responses (long-term regulation, over days and weeks)
Renin–angiotensin axis: Juxtaglomerular cells in the kidneys secrete renin directly into
the blood. The secreted renin then converts angiotensinogen (released by the liver) to
angiotensin I. Angiotensin I is subsequently converted to angiotensin II by the enzyme
angiotensin-converting enzyme (produced by the lungs). Angiotensin II is a potent
vasoactive peptide that causes blood vessels to constrict, resulting in increased SVR.
Vasopressin (antidiuretic hormone) is secreted into the blood by the neurohypophysis. It
activates specific vasopressin receptors on the VSMC and causes vasoconstriction.
– Nitric oxide (NO) is produced by endothelial cells, diffuses into the media, and relaxes the
VSMC by activating cyclic guanylate cyclase. Hence, NO is called endothelium-derived
relaxation factor. Smoking, hypercholesterolemia, oxidative stress, or limited physical
exercise can result in endothelial dysfunction; consequently, there is a decrease in NO
production (increase in SVR).
– Hydrogen sulfide has been recently recognized as endothelium-derived hyperpolarizing
factor. Similar to nitric oxide, hydrogen sulfide causes relaxation of resistance arterioles,
vasodilation, and decreases the SVR.
ANATOMY
• The mean pressure decreases by only 1–2 mm Hg between the ascending aorta and
peripheral arteries in compliant and healthy vasculature, indicating low resistance at this
portion of the vascular tree.
• A major drop of pressure occurs over small arterioles and they constitute the major site of
resistance.
DISEASE/PATHOPHYSIOLOGY
• Increased afterload:
– Aortic stenosis: The LV needs to generate increased force to overcome the resistance of the
stenosed aortic valve and eject blood into the aorta. This results in increased LV wall
tension and stress (increased afterload). The LV usually compensates with a hypertrophic
response to return the wall stress to normal. The thickened LV, in conjunction with
increased force, however, increases the myocardial oxygen demand (increased muscle
mass working harder) and decreases the myocardial oxygen supply, especially to the
endocardium. Blood flows from the epicardium into the endocardium; additionally, it
takes more time for blood to flow across a thickened LV wall to reach the endocardium.
– Chronic hypertension: Essential hypertension in the young and middle-aged population is
frequently characterized by increases in DBP. This is the result of vasoconstrictory
responses predominating over vasodilatory responses at the level of the arterioles in the
periphery. In the elderly, the predominant form of hypertension is systolic hypertension,
while DBP is low to normal (the SVR in isolated systolic hypertension is usually normal or
even decreased). However, there is a marked increase in vascular sclerosis, stiffness, and
arterial impedance. The increased resistance is to the pulsatile (dynamic) component of
blood flow. In either case, untreated or poorly controlled hypertension requires the heart
to work harder, increases afterload, and often elicits a compensatory hypertrophic
response in the LV to return wall stress to normal.
– Hemoconcentration: Analogous to the reservoir bag on the anesthesia machine; if the bag
was filled with water or jelly as opposed to air, it would require more energy to compress
or squeeze the bag.
– Increased LV radius: A dilated LV, as with cardiomyopathy or heart failure, causes
increases in wall tension due to decreased myocardial thickness as well as increased radius
( = increase in afterload). This is analogous to the reservoir bag overfilled; more energy
would be required to empty the bag, compared to a partially or normally filled bag.
– Cor pulmonale: Elevated PVR requires the RV to squeeze harder to generate more force to
eject blood ( = increased afterload for the RV). Elevations in the PVR over prolonged time
lead to compensatory RV hypertrophy to decrease wall tension and normalize the
afterload.
• Decreased afterload
– Sepsis: Mostly due to loss of SVR
– Anaphylaxis: Mostly due to loss of SVR
– High-output cardiac failure: Due to arteriovenous shunts
– Anemia: Due to both a decrease in viscosity and lowered SVR (decreased BP)
– Hypovolemia: There is less blood to stretch the LV and, hence, less force is needed to eject
blood. To counteract for reductions in the stroke volume (and maintain BP), the
sympathetic tone is increased (increase in SVR and heart rate).
PERIOPERATIVE RELEVANCE
• Increased afterload
– Sympathetic stimulation with intubation and surgery
– Vasopressors:
Preferential alpha-1 agonists have the most profound effect on increasing the afterload
(phenylephrine and norepinephrine).
Vasopressin
Ephedrine and epinephrine will increase afterload in addition to increasing contractility.
• Decreased afterload
– An increasing depth of anesthesia with either volatile agents or IV anesthetics (e.g.,
propofol) causes a decrease in sympathetic tone (vasorelaxation) with resultant decreases
in the SVR and BP. Increased depth should be avoided in hypovolemia or hypotensive
patients.
– Neuraxial techniques: Both spinal and epidural blocks interrupt conduction of nerve
impulses through sympathetic fibers at the level of their spread. This leads to a decrease
in sympathetic tone, SVR, and preload (pooling of blood in veins). To counteract this
response, volume resuscitation and pressors may be administered as needed. In
hypovolemic or hemorrhaging patients, neuraxial techniques should not be used; they
block compensatory increases in SVR and heart rate.
– NO donors (nitroglycerin, nitroprusside) cause relaxation of both resistance arterioles and
veins and, hence, a decrease in SVR and preload. They are used for tight BP control in
procedures such as AAA and CEA.
– Inhaled NO is used to alleviate increased pulmonary artery pressures. It has minimal
systemic effects.
– Calcium channel blockers cause arterial smooth muscle relaxation and decrease
myocardial contractility.
– Phosphodiesterase inhibitors increase cardiac contractility while relaxing resistance
arterioles, decreasing SVR, and causing hypotension. They are mostly used in heart
failure, but may also require simultaneous administration of alpha-agonists to counteract
pronounced hypotension.
– Positive end expiratory pressure (PEEP). LV dysfunction with pulmonary edema results in
decreased pulmonary volume and compliance. Greater negative inspiratory pressures (and
hence transmural pressures) are required to expand the lungs. PEEP can partially offset
this.
EQUATIONS
• SVR = [(MAP – CVP) × 80]/CO; MAP = mean arterial pressure (mm Hg), CVP = central
venous pressure (mm Hg), CO = cardiac output (liters/minute)
• PVR = [(mPAP – wedge pressure) × 80]/CO; mPAP = mean pulmonary artery pressure
(mm Hg), CO = cardiac output (liters/minute)
• Tension = (ΔP × R)/H × 2; ΔP = change in pressure, R = radius, H = wall thickness
O’Rourke M, Nichols W. McDonald’s blood flow in arteries. Hodder Arnold, 2006.

REFERENCES
1. Thiele RH, Nemergut EC, Lynch C. The physiologic implications of isolated alpha1
adrenergic stimulation. Anesth Analg. 2011;113(2):284–296.
2. Thiele RH, Nemergut EC, Lynch C. The clinical implications of isolated alpha1 adrenergic
stimulation. Anesth Analg. 2011;113(2):297–304.
See Also (Topic, Algorithm, Electronic Media Element)
• Pulmonary artery catheter waveforms
• Anaphylaxis
• Hypertension
• Aortic stenosis
• Positive end expiratory pressure (PEEP)

CLINICAL PEARLS
• The SVR is considered by most professionals as equivalent to afterload and is substituted for
it; SVR is calculated from MAP and CO (SVR = MAP/CO). SVR is an oversimplified
quantification of the true resistance force against which the heart works. It has an
underlying assumption that flow is constant.
AIRWAY FIRE
Charles E. Cowles, Jr., MD

BASICS
DESCRIPTION
• Surgical fires can occur either on the patient or in the patient’s airway (1). They are most
commonly observed during procedures that involve the open delivery of oxygen near an
ignition source, like electrocautery or laser.
• Airway fires are defined as either within the airway or within the breathing circuit. Many
fires occur during relatively minor procedures of the head and neck which involve the use
of a cautery device and a simple facemask or nasal cannula.
• As with operating room (OR) fires, airway fire prevention depends on:
– An understanding of how triad elements (ignition, fuel, oxidizers) interact to create a fire
– Recognizing how standard OR equipment, materials, and supplemental oxygen can
become one of those elements
– Vigilance for circumstances that bring fire triad elements into close proximity (2)
EPIDEMIOLOGY
Prevalence
• Occurs in about 650 cases per year (1:87,646) (3,4)
• Actual incidence is likely higher, but surgical fires are under-reported.
Morbidity
20–30 serious injury cases per year (3)
Mortality
2–3 deaths per year (3)
ETIOLOGY/RISK FACTORS
• High-risk procedure: Use of an ignition source in close proximity to an oxidizer (oxygen and
nitrous oxide) (1). Fires have been reported during head and neck procedures including
tracheostomies, adenotonsillectomies, endoscopic airway surgeries, and cutaneous surgeries
of the head and neck.
• Monitored anesthesia care (MAC)/sedation cases, especially when there is/are:
– Open delivery of oxygen at a FiO2 >30%
– Drapes and towels configured in a manner to “trap” oxygen underneath drapes and allow
for significant accumulation.
– Patients with obstructive sleep apnea or other diseases (decreased functional residual
capacity) that cannot tolerate sedation without oxygen supplementation
– Surgeries that involve the head and neck or are above the xiphoid process
• Laser use in or near the airway
• Prep solution and drapes:
– Adequate drying time is not observed when using alcohol-based preps or if pooling of prep
has occurred.
– Flammable prep solutions are used in hairy locations or crevasses of the body or if large-
sized sponge containers (26 mL) are used for head and neck cases.
PHYSIOLOGY/PATHOPHYSIOLOGY
• Fire occurs when elements of the fire triangle are combined (3):
– Ignition source
Electrosurgical units (ESU), cautery, lasers, and light sources
Usually controlled by the surgeon
– Fuel
Alcohol-based preps, towels, and drapes
Usually controlled by the OR nurse
– Oxidizers
Oxygen and nitrous oxide
Usually controlled by the anesthesia provider
• Fires which occur in oxygen-enriched environments may result in a sudden flash fire where
the burn injuries occur in a matter of seconds (too quickly for extinguishment).
PREVENTATIVE MEASURES
• Often, fires are the result of a lack of communication among surgical team members.
• Injury and damages commonly occur when the response to the fire is uncoordinated and
haphazard.
• Assess the fire risk prior to every surgical procedure; this is especially important for cases
involving the head and neck or cases performed under MAC.
– Perform fire risk assessment during surgical “time out”
– Assign specific tasks for each OR team member to perform in case of a fire
• MAC/sedation cases with increased fire risk
– Do not use supplemental oxygen unless clinically necessary
– Allow sufficient time for oxidizer levels to drop before using an ignition source. This may
take several minutes.
– If an FiO2 >30% is required:
Communicate with the surgical team.
Titration of the FiO2 can be accomplished with the use of an oxygen blender or by using
the common gas outlet found on some anesthesia machines.
Consider using an ETT or supraglottic device such as the laryngeal mask airway (LMA) to
eliminate the open flow of oxygen, especially in cases above the xiphoid
Configure drapes to prevent accumulation of oxygen and to facilitate open ventilation.
• Prep solution and drapes
– Allow flammable surgical preps such as alcohol-based solutions to dry fully before the
application of surgical drapes or barriers
– Assess for pooling as a routine part of the time-out process
– Avoid 26 mL applicators in head and neck cases
• General anesthetics, particularly for procedures above the xiphoid
– Use cuffed tracheal tubes when possible
– FIO2 <30% may reduce the risk of fire, particularly for intraoral cautery.
– Decreasing the electrocautery wattage may reduce the incidence of airway fires (5).
• Laser procedures
– Use an appropriate laser tube for the type and frequency of the laser
– Use an indicator dye such as methylene blue in the distal cuff of laser tubes to detect
inadvertent rupture
– Moisten gauze or sponges if used to pack the airway
– Participate in OR-specific fire drills which include the practice of patient evacuation
methods and involvement of all team members, including surgeons and anaesthetists
• Know the location of fire extinguishers and gas cut-off valves before the case begins
• Consider assembling a cart for high-risk procedures which includes saline or water bottles,
fire extinguishers, and placards to guide response

PREOPERATIVE ASSESSMENT
• By index of suspicion and investigation of any smell of smoke, hearing loud “pop,” or seeing
smoke or flames
• Excessive movement of the patient during MAC
• Alcohol burns with a nearly invisible flame which becomes increasingly difficult to see
under bright surgical lights.

TREATMENT

The following steps should be carried out as soon as possible. The specific order or sequence
is not as important as rapidly completing the task (1):
• Stop the procedure to evaluate situation
• Stop the flow of gases
• Remove endotracheal tube (ETT)
• Remove drapes
• Pour saline or water in airway

FOLLOW-UP

• In the non-intubated patients, assess for smoke inhalation injury.


• In intubated patients:
– Examine the removed ETT for fragments that could still be present in the airway
– Re-establish ventilation but avoid the use of oxidizers to avoid re-kindling of embers
which may be present in the airway
– Perform rigid bronchoscopy if lower airway injury is suspected (1)
• Use fire extinguisher if initial attempts to extinguish the fire are not successful. Plan to
evacuate the OR if necessary.
• If fire or smoke is present, activate the facility fire alarm system, notify the local fire
department, and file a report with the fire marshal’s office according to local protocols
• Transfer to appropriate burn facility
CLOSED CLAIMS DATA
• Claims approaching $1.5 million per case have been paid for MAC cases resulting in fatal or
disfiguring burn injuries.
• Most cases involve head and neck surgeries.
• 74% of burn cases involve oxygen supplementation.

REFERENCES
1. merican Society of Anesthesiologists (ASA) Task Force on Operating Room Fires, Caplan
RA, Barker SJ, et al. Practice advisory for the prevention and management of operating
room fires. Anesthesiology. 2008;108(5):786–801.
2. Rinder CS. Fire safety in the operating room. Curr Opin Anaesthesiol. 2008;21(6):790–795.
3. ECRI New Clinical Guide to Surgical Fire Prevention [guidance article]. Health Dev.
2009;38(10):319.
4. ennsylvania Patient Safety Authority. Three “never complications of surgery” are hardly
that. Pa Patient Saf Advis. 2007;4(3):82.
5. oy S, Smith LP. What does it take to start an oropharyngeal fire? Oxygen requirements to
start fires in the operating room. Int J Pediatr Otorhinolaryngol. 2001;75(2):227–230.

ADDITIONAL READING
• Anesthesia Patient Safety Foundation (APSF). Prevention and management of surgical fires
[video]. APSF, 2009.
• Barker SJ, Polson JS. Fire in the operating room: A case report and laboratory study. Anesth
Analg. 2001;93:960–965.
• Department of the Army. Headquarters, United States Army Medical Command. Fires
associated with the performance of surgical procedures [online]. MEDCOM Regulation No.
40-48, August 2003.
See Also (Topic, Algorithm, Electronic Media Element)
• Smoke inhalation injury
• Burns
• Operating room fires

CLINICAL PEARLS
• Open delivery of oxygen should only be used as clinically necessary; oxygen concentrations
>30% pose a fire risk.
• Special precautions should be observed for high-risk procedures where use of an ignition
source is in close proximity to an oxidizer.
• Nitrous oxide supports combustion to the same extent as oxygen.
• Investigate sounds, smells, and noises that could be associated with OR fires.
• In MAC/sedation cases, replace supplemental oxygen with an ETT or supraglottic device if
the patient condition requires >30% oxygen when an ignition source is used.
ALCOHOL ABUSE
Zhuang-Ting Fang, MD, MSPH

BASICS
DESCRIPTION
• Alcohol abuse is a chronic disease with profound societal implications. More than 19% of
cases resulting in deaths of young automobile drivers were related to alcohol. Additionally,
the annual total cost of alcohol-related problems reaches a staggering $180 billion.
• Both acute alcohol intoxication and chronic alcohol abuse can increase anesthetic
complications.
EPIDEMIOLOGY
Prevalence
In the US, the rate of alcohol use disorders, including abuse and dependence, is ~8.26%; this
correlates to ~15 million people.
Morbidity
• In the perioperative period, patients with alcohol abuse have been shown to have an
increased risk of infections, bleeding disorders, need for ventilator support, and cognitive
dysfunction.
• Maternal alcohol consumption during pregnancy can lead to fetal alcohol disorders; 1%
incidence.
Mortality
• Alcohol withdrawal during surgery may be associated with a mortality rate as high as 50%.
• Alcohol use is the third leading cause of preventable death in the US, and accounts for
∼85,000 deaths annually.
ETIOLOGY/RISK FACTORS
• Gender: Men are 5 times more likely than women to develop alcohol abuse.
• Family history: The rate of alcohol abuse is about 30% in men with one alcoholic parent.
• Genetic factors: May affect the process and response to alcohol in the human body
• Cultural factors: The high rate of alcohol abuse in the US and Europe may relate to the
common use and social acceptance of alcohol use.
• Psychiatric disorders: Higher in persons with depression, anxiety, antisocial behaviors, post-
traumatic stress disorder, high self-expectations, or low frustration tolerance
PATHOPHYSIOLOGY
• Alcohol has been shown to affect the following receptors in the human brain:
– GABA: Alcohol binds to the GABA receptor and increases chloride ion movement into the
cell with resultant hyperpolarization (decreases neural activity, by making the cell
membrane potential more negative). Responsible for the sedative and anxiolytic effects
(similar to hypnotic drugs and benzodiazepines).
– Glycine: Alcohol binds to the glycine receptor and potentiates its role as the major
inhibitory neurotransmitter in the spinal cord and brain stem.
– Serotonin: Alcohol increases levels either via increased release and/or decreased
breakdown, as well as potentiates its effects on receptor function. Serotonin may enhance
the release of other neurotransmitters that play a key role in tolerance and contribute to
alcohol withdrawal syndrome (AWS).
– Glutamate: Alcohol decreases glutamate’s excitatory effect on NMDA receptors. Chronic
consumption, however, makes NMDA receptors hypersensitive to glutamate while
desensitizing the GABAergic receptors; believed to play a role in AWS.
– Opiates: Alcohol induces the release of endogenous opioid peptides (can cause euphoria
and blunt the sensation of pain). The body’s endogenous opioid system (enkephalins,
endorphins) is linked with the brain’s reward pathway; may play a role in addiction.
– Dopamine: The increased levels/effects that are seen with alcohol abuse is a poorly
understood mechanism. It has been postulated to result from disinhibition of
dopaminergic neurons, decreased breakdown, and increased release. Dopamine pathways
play a role in reward and reinforcement and may play a role in addiction.
• Alcohol is absorbed directly through the stomach wall (∼20%) and small intestines
(∼80%). The liver functions to break down alcohol.
• Effects on other organs may result from direct inflammation or possibly from “blood
sludging.” Blood sludging describes the clumping of red blood cells with resultant plugging
of small vessels, ischemia, and cell/tissue death distally. The increased pressure can result in
capillaries breaking (red eyes, blotchy skin, “drinker’s nose”).
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Preoperative evaluation should determine concomitant organ dysfunction. A high index of
suspicion for alcohol cardiomyopathy should be present, as this is often underdiagnosed.
• Prevent aspiration in patients with cirrhosis and ascites
• Anticipate prophylaxis and treatment of alcohol withdrawal and delirium tremens

PREOPERATIVE ASSESSMENT
SYMPTOMS
• A high index of suspicion is required to diagnose alcohol abuse.
• Nonspecific, but suggestive, symptoms include gastritis, tremor, and history of falling.
History
• Despite the brief preoperative encounter, a social history including alcohol use should be
elicited. If suspected, consider further focused questioning.
• Alcohol Use Disorders Identification Test (AUDIT) is 92% effective in detecting hazardous or
harmful drinking. A total score of ≥8 indicates harmful drinking behavior. It is also helpful
in identifying those at greatest risk for postoperative complications.
• Inquire about other substances of abuse
Signs/Physical Exam
• Usually nonspecific; abnormalities are usually related to the systemic diseases associated
with chronic use.
• “Drinker’s nose”: A purple nose that results from tiny broken capillaries
MEDICATIONS
No specific medications, unless being treated for abuse.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Glucose: May be low, particularly in diabetics
• CBC with platelets: Anemia
• Liver function tests, PT and aPTT: May be abnormal due to alcoholic hepatitis or cirrhosis.
• EKG: May show left ventricular hypertrophy and arrhythmias.
• CXR: May show aspiration, pleural effusions and cardiomegaly.
CONCOMITANT ORGAN DYSFUNCTION
• Nervous system: Cerebellar degeneration, tremors, delirium tremens, dementia, depression,
memory loss, Wernicke–Korsakoff syndrome, peripheral neuropathy (burning, numbness,
weakness)
• Cardiovascular: Alcoholic cardiomyopathy, hypertension
• Pulmonary: Aspiration, pleural effusion, and pulmonary hypertension (may occur in end
stage liver disease).
• Hepatic: Alcoholic hepatitis, cirrhosis
• Gastrointestinal: Absorption of B vitamins and other nutrients may be impaired. Gastritis,
ulcers, and increased risk of stomach cancer. Acute and chronic pancreatitis; may eventually
result in diabetes.
• Metabolic: Impairs fat and glucose metabolism in the liver and pancreas. Acute alcohol
ingestion can result in a steep rise in blood sugar that is met by an increased release of
insulin, with resultant hypoglycemia.
• Hematologic: Anemia can result from malnutrition or direct suppression of bone marrow.
• Malnutrition is very common and can lead to anemia (folic acid, vitamin B12 deficiency), or
hypoalbuminemia (low protein intake) and Wernicke–Korsakoff syndrome (vitamin B1
deficiency).
• Other: Sexual dysfunction (decreased testosterone), birth defects, osteoporosis
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Elective surgery should be postponed in patients with acute alcohol toxicity, alcoholic
hepatitis, or decompensated systemic diseases.
• Treatment of alcohol abuse or dependence should be considered before elective surgery in
order to decrease perioperative morbidity and mortality.
• Severe dehydration or electrolyte imbalance should be corrected prior to surgery.
CLASSIFICATIONS
• Alcohol abuse is defined by the following characteristics: Drinking even when it is
dangerous; excessive drinking; legal problems related to drinking; and interpersonal
problems with family, coworkers, and friends because of alcohol use.
• Alcohol dependence (alcoholism) is characterized by: Drinking excessive amount frequently;
the inability to stop drinking despite social, psychiatric, or medical complications; increased
tolerance of alcohol; and the occurrence of alcohol withdrawal symptoms when drinking is
discontinued.

TREATMENT

PREOPERATIVE PREPARATION
Premedications
Benzodiazepines are helpful in reducing anxiety and preventing withdrawal.
INTRAOPERATIVE CARE
Choice of Anesthesia
Regional anesthesia (spinal, epidural, or peripheral nerve blocks) may decrease systemic
effects and CNS disturbance with general anesthesia. It is also easier to monitor mental status
changes in awake patients, especially in those at risk of alcohol withdrawal. In patients with
liver disease, however, coagulopathy may preclude neuraxial techniques.
Monitors
• Standard ASA monitors
• Invasive monitoring may be considered when alcoholic cardiomyopathy is suspected or
present, and depending upon the surgical procedure.
Induction/Airway Management
• Acute alcohol intoxication may reduce anesthetic dose requirement.
• Chronic alcohol abuse may require higher anesthetic doses due to cross-tolerance (e.g.,
increased propofol induction doses). Cirrhotics have an increased volume of distribution
which may necessitate increased doses (but may have increased sensitivity to drugs and
decreased clearance). In alcoholic cardiomyopathy, intravenous induction should be
accomplished by careful titration to avoid hypotension.
• Rapid-sequence induction with cricoid pressure should be considered in patients with
delayed gastric emptying due to ascites. Intoxicated trauma patients are at an increased risk
for aspiration.
Maintenance
• In cirrhotic patients, maintenance doses may need to be decreased due to impaired liver
metabolic function.
• Non-depolarizing muscle relaxants should be cautiously titrated due to impaired hepatic
function.
• “Banana bag” infusion may be considered.
Extubation/Emergence
Normal extubation criteria apply; however, alcoholics may have impaired clearance of muscle
relaxants and gastric motility. Ensure full recovery from NMBDs and a protective gag reflex.

FOLLOW-UP

BED ACUITY
• ICU admission may be required if alcohol withdrawal or delirium tremens is suspected.
• Supplemental oxygen should be provided, especially when the patient is receiving narcotics.
COMPLICATIONS
• AWS may be seen in patients who abuse or are dependent on alcohol when they stop
drinking abruptly because of injury, surgery, or acute illness. Typically develops 6–24 hours
after their last drink. Symptoms are related to autonomic hyperactivity and include
sweating, nausea, vomiting, anxiety, agitation, tachycardia, and hand tremor. Neuronal
excitation, including grand mal seizures, usually occurs within 24–48 hours of abstinence.
Delirium tremens is the most intense and serious form of AWS. It is characterized by visual
or auditory hallucinations, confusion, clouding of consciousness, impaired attention, and
pronounced autonomic hyperactivity. It usually appears 2–4 days after the patient’s last use
of alcohol. Death from cardiovascular and respiratory collapse may occur, if untreated.
Prophylaxis is with benzodiazepines. Treatment of AWS involves establishing the diagnosis
and severity with the CIWA-Ar Score and transferring to the ICU. Medical treatment
involves a combination of benzodiazepines, haloperidol, clonidine, and beta-blockers; in
some instances, a drink with meals may be ordered. Supportive care includes the treatment
of nutritional deficiency, hypoglycemia, arrhythmias, congestive heart failure, alcoholic
hepatitis, alcoholic pancreatitis, GI bleeding, and nervous system impairment.
• Postoperative cognitive dysfunction is increased in patients aged 55 years and older after
noncardiac surgery with general anesthesia.
• Increased risk of infections may be due to alteration of T-cell mediated immunity as well as
altered immune response to surgical stress.

REFERENCES
1. Lian J, Cagetti E, Richard W, et al. Altered pharmacology of synaptic and extrasynaptic
GABAA receptors on CA1 hippocampal neurons is consistent with subunit changes in a
model of alcohol withdrawal and dependence. J Pham and Exp Therap. 2004;310(3):1234–
1245.
2. Lovinger DM. Serotonin’s role in alcohol’s effects on the brain. Alcohol Health Res World.
1997;21(2):114–120.
3. Publications from the Institute on Alcohol Abuse and Alcoholism, NIH. www.niaaa.nih.gov.
4. Spies CD, Rommelspacher H. Anesthestic alcohol withdraw in the surgical patients:
Prevention and treatment. Anesth Analg. 1999;88:946–954.
See Also (Topic, Algorithm, Electronic Media Element)
• Alcohol cardiomyopathy
• Pregnancy substance abuse
• Cirrhosis
• Alcohol withdrawal syndrome

CODES

ICD9
• 303.90 Other and unspecified alcohol dependence, unspecified
• 305.00 Alcohol abuse, unspecified
• 305.01 Alcohol abuse, continuous

ICD10
• F10.10 Alcohol abuse, uncomplicated
• F10.129 Alcohol abuse with intoxication, unspecified
• F10.20 Alcohol dependence, uncomplicated

CLINICAL PEARLS
AUDIT (Alcohol Use Disorders Identification Test) utilizes 10 questions; scoring is on a scale
of 0–4 per question. A total score of ≥8 indicates alcohol abuse or dependence. (Note: A unit
is equal to one small glass of wine, a single purchased measure of spirits or half a pint of
beer.) The questions include:
• How often do you have a drink containing alcohol?
• How many units of alcohol do you drink on a typical day when you are drinking?
• How often do you have 6 or more units of alcohol on one occasion?
• How often during the last year have you found that you were not able to stop drinking once
you had started?
• How often during the last year have you failed to do what was normally expected from you
because of drinking?
• How often during the last year have you needed a first drink in the morning to get yourself
going after a heavy drinking session?
• How often during the last year have you had a feeling of guilt or remorse after drinking?
• How often during the last year have you been unable to remember what happened the night
before because you had been drinking?
• Have you or someone else been injured as a result of your drinking?
• Has a relative or friend or doctor or another health worker been concerned about your
drinking or suggested you should cut down?
ALCOHOL WITHDRAWAL SYNDROME
Martin M. Stechert, MD
Christopher G. Choukalas, MD, MS

BASICS
DESCRIPTION
• Alcohol withdrawal syndrome (AWS) develops after the cessation of chronic alcohol
use/abuse, generally within 6–48 hours. Alcohol abuse is characterized by impaired control
over drinking, preoccupation with alcohol, use of alcohol despite adverse consequences, and
denial.
• AWS exists as a spectrum of presentations:
– Mild: Cravings and psychomotor agitation
– Severe: Hallucinations, autonomic instability (sweating, tachycardia, hypertension), fever,
and disorientation. This constellation of symptoms is known as delirium tremens (DT).
• If withdrawal symptoms are not present within a week after the last alcohol consumption,
future development is unlikely.
EPIDEMIOLOGY
Prevalence
In general, outpatient estimates are between 4% and 15%, whereas 15–40% of all inpatients
are thought to have abuse or withdrawal. Of those who experience withdrawal symptoms, 5%
have severe symptoms characterized as DT.
Morbidity
• AWS: Dysrhythmias, myocardial ischemia, delirium, and seizures
• Chronic alcohol abuse: Immunosuppression, wound infections, malnutrition, and the
complications of cirrhosis and liver failure
Mortality
• Has decreased over time; historical estimates from severe AWS or DT reached levels as high
as 40%, but the current rate is probably under 5%.
• Results from dysrhythmia, aspiration pneumonia, or underlying illness that may have been
the cause of alcohol cessation in the first place (e.g., infection, pancreatitis, etc.).
ETIOLOGY/RISK FACTORS
• Alcohol use and abuse are obvious risk factors for developing AWS. Use and abuse are
associated with a number of demographic characteristics, including:
– Male sex
– Lower socioeconomic status
– White or Native American ethnicity
– Certain psychiatric conditions (e.g., depression, anxiety disorders)
• Risk factors for the development of DT include:
– Previous history of DT
– Presence of AWS despite elevated level of blood alcohol
– History of sustained drinking
PHYSIOLOGY/PATHOPHYSIOLOGY
• The pathophysiology of AWS is probably related to the neurophysiologic changes thought to
be caused by chronic alcohol use. Although the functional consequence of receptor-
mediated effects of alcohol remain to be elucidated, ingested ethanol has a number of
receptor targets:
– NMDA-related transmission is reduced.
– GABA function is enhanced.
– Glycine transmission (complex and location specific) are enhanced
– Cholinergic and serotonergic activities are enhanced.
• In order to maintain a normal arousal state, an adaptive response to chronic alcohol
exposure yields decreased GABAA sensitivity and increased NMDA sensitivity. When ethanol
is acutely withdrawn, reduced central inhibition (via GABAA) and aberrant activation of
excitatory NMDA receptors appear to be responsible for the acute withdrawal symptoms,
including altered mental state and noradrenergic overdrive during AWS.
PREVENTATIVE MEASURES
• Prevention of AWS is a crucial aspect of treatment in the clinical arena, whereas public
health efforts to curb alcohol abuse are necessary to prevent AWS on a societal level.
• Perioperatively, prevention of AWS starts with an early identification of patients at risk for
this condition.
– The duration of potential abstinence from alcohol should be discussed with the primary
care physician and the patient, and possible management solutions must be negotiated
with the patient.
– Nutrition including multivitamin administration should be optimized preoperatively.
– Optimal medical management can be organized according to the degree of risk going into
withdrawal, including additional invasive monitoring intraoperatively and appropriate
designation (ICU, TCU) postoperatively.
– Long-acting benzodiazepines (e.g., chlordiazepoxide) administered preoperatively may
reduce the severity of AWS.

PREOPERATIVE ASSESSMENT
• AWS is a clinical diagnosis and requires a detailed history and physical examination.
– Key elements of the history include chronic alcohol use, recent cessation, and determining
whether cessation was caused by some other illness.
– Screening tools like the PAT (Paddington Alcohol Test) and AUDIT (Alcohol Use Disorders
Identification Test) questionnaires can identify patients at risk for AWS.
• Clinical manifestations of alcohol withdrawal often follow a timely schedule after the last
consumption of alcohol:
– Early symptoms, including anxiety, tremulousness, palpitations, nausea, anorexia,
typically begin after 6–8 hours.
– Generalized seizures typically occur after 6–48 hours.
– Alcoholic hallucinations after 12–48 hours
– Delirium tremens after 48–96 hours
• The latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR)
provides more precise diagnostic criteria that can be summarized as 2 or more of the
following signs and symptoms occurring (1) in the context of cessation or reduction of
previously heavy alcohol use and (2) not due to some other medical or mental disorder:
– Sweating or tachycardia
– Hand tremor
– Insomnia
– Nausea or vomiting
– Hallucinations
– Agitation
– Anxiety
– Generalized tonic–clonic seizure
• It is important to note that in an anesthetized patient, symptoms may be obscured and
limited to sympathetic surge (i.e., tachycardia, hypertension).
DIFFERENTIAL DIAGNOSIS
• Other causes of agitation and tremor, including caffeine overdose, cocaine and other
stimulant use, as well as withdrawal from nicotine, illicit drugs, and medications (e.g.,
clonidine)
• Other causes of hallucinations such as psychotic disorders, acute intoxication, sleep
withdrawal, and drug side effects
• Other causes of seizures such as metabolic or electrolyte derangements, intracranial
pathology, meningitis, or underlying seizure disorder
• Other hyper-metabolic syndromes that can mimic DT, such as malignant hyperthermia,
thyroid storm, neuroleptic malignant syndrome, and serotonin syndrome

TREATMENT

• Essential elements of therapy include:


– Excluding alternate diagnoses (see above)
– Seizure prophylaxis
– Correcting metabolic and hemodynamic derangements
– Treating symptoms such as anxiety and hallucinations
– Managing complications (e.g., aspiration pneumonia and malnutrition)
– Appropriate monitoring
• Benzodiazepines bind to GABA receptors and are cross-tolerant with alcohol; they remain
the cornerstone of treatment for AWS. They are effective at reducing anxiety, agitation, and
the incidence of seizures; and they often reduce tachycardia and hypertension. They can
also be dosed prophylactically, in a scheduled fashion, or in response to symptom severity.
The latter has been associated with decreased complications and lower doses of
administered drug.
• Propofol in intubated, mechanically ventilated patients produces results similar to those of
benzodiazepines (e.g., anxiolysis, seizure prophylaxis, etc.). Patients receiving propofol
rarely need additional benzodiazepines to treat agitation or seizures associated with AWS.
• Other agents have been used, but none have completely replaced benzodiazepines:
– Antipsychotics, such as haloperidol or quetiapine, may reduce agitation and hallucinations
but may also reduce the seizure threshold.
– Antiepileptics, such as carbamazepine, may decrease the development of seizures but have
little effect on the other manifestations of AWS.
– Intravenous infusion of ethanol can precipitate a metabolic acidosis.
– Alternative sedatives, such as clonidine and dexmedetomidine, almost certainly reduce
benzodiazepine requirements but provide no seizure prophylaxis. Dexmedetomidine
reduces ICU delirium and may reduce delirium associated with AWS.
• The Clinical Institute for Withdrawal Assessment (CIWA) provides a symptom-driven dosing
scheme that calculates a score based upon signs and symptoms of withdrawal (e.g., tremor,
sweats, delirium). Higher scores signify more severe withdrawal and would trigger
administration of benzodiazepine.
• Bed acuity: The appropriate level of monitoring for patients with AWS has never been
defined. The frequent assessments required suggest that general ward care may be
inadequate. Additionally, managing hemodynamic abnormalities requires active monitoring
of hemodynamics, such as in a telemetry, step-down, or ICU unit. The presence of the
following may necessitate ICU care:
– Coexisting cardiac, pulmonary, or renal disease
– Having a history of or being at high risk for DTs
– Requiring propofol or a continuous infusion of sedatives to control symptoms during past
admissions
• Thiamine deficiency: Common in patients who abuse alcohol. Thiamine is critical in order to
avoid Wernicke’s encephalopathy, and must be administered prior to initiating glucose or
nutritional therapy. Further treatment should target specific nutritional deficiencies
identified by serology.

REFERENCES
1. Tetrault JM, O’Connor PG. Substance abuse and withdrawal in the critical care setting. Crit
Care Clin. 2008;24:767–788.
2. De Wit M, Jones DG, Sessler CN, et al. Alcohol-use disorders in the critically ill patient.
Chest. 2010;138(4):994–1003.
3. Kosten TR, O’Connor PG. Management of drug and alcohol withdrawal. N Engl J Med.
2003;348:1786–1795.

ADDITIONAL READING
• Spanagel R. Alcoholism: A systems approach from molecular physiology to addictive
behavior. Physiol Rev. 2009;89:649–705.
• Sullivan JT, Sykora K, Schneiderman J, et al. Assessment of alcohol withdrawal: The revised
clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Brit J Addict.
1989;84:1353–1357.
See Also (Topic, Algorithm, Electronic Media Element)
• Alcohol abuse

CODES

ICD9
291.81 Alcohol withdrawal

ICD10
F10.239 Alcohol dependence with withdrawal, unspecified

CLINICAL PEARLS
• Cessation of receptor-mediated activity during alcohol abstinence is likely at the root of
AWS. It may be that chronic exposure to ethanol decreases sensitivity of GABA receptors,
and that cessation reduces GABA output, leading to a state of generalized CNS arousal.
• Seizure may be an early symptom of AWS (“rum-fit”) which can occur as early as 2 hours
after the last consumption of ethanol.
• Alcohol-dependent, ambulatory patients may never exhibit AWS syndromes during the
hospital stay.
• Whenever AWS is suspected, thiamine should be given intravenously. The administration of
glucose in thiamine deficiency can precipitate Wernicke’s encephalopathy.
ALCOHOLIC CARDIOMYOPATHY
Christopher Wray, MD

BASICS
DESCRIPTION
• Alcoholic cardiomyopathy (ACM) is classified as a non-ischemic, dilated cardiomyopathy
(CM) that results from exposure to a myocardial toxin.
• ACM shares common characteristics with all dilated CMs (depending on the clinical stage of
the disease progression):
– Dilated chambers
– Diastolic dysfunction (asymptomatic stage)
– Left ventricular dysfunction (symptomatic stage)
– Left ventricular hypertrophy (asymptomatic stage; followed by wall thinning in
symptomatic stage)
• Diagnosis is clinically based upon a history of significant chronic alcohol exposure in
conjunction with the exclusion of other causes of dilated CM.
PHYSIOLOGY PRINCIPLES
• Epidemiology of ACM:
– Second most common cause of dilated CM (4% of all CMs)
– Prevalence in Western countries is variable, but ranges from 20% to 40% of all non-
ischemic dilated CMs.
– Significantly more prevalent in men (approximately 15% prevalence in women)
– The incidence of dilated CM is much higher in chronic alcoholics than in the total
population.
– The 5-year incidence ranges from 20% to 26% in chronic alcoholics.
• Amount and duration of alcohol exposure:
– Studies have demonstrated variability and a lack of a specific linear relationship between
the amount and duration of alcohol exposure and the development of asymptomatic and
symptomatic ACM (1,2,3).
– Studies have shown changes in cardiac structure and function consistent with ACM in
patients with a history of consuming >90 g/day of alcohol for >5 years (one drink
contains approximately 12 g of alcohol). Studies in patients with symptomatic ACM have
shown a history of longer durations of drinking (>10 years) (4,5).
– Despite the correlation between chronic heavy drinking and the development of ACM, not
all heavy drinkers will progress to ACM.
– Although there may be other variables responsible for the occurrence of heart failure in
alcoholics, the duration of heavy daily alcohol use is the most reliable predictor for the
development of ACM.
PHYSIOLOGY
• Myocardial wall tension is closely related to myocardial oxygen consumption.
– Left ventricle wall tension (T) is a function of the change in pressure (ΔP), left ventricle
radius (R), and left ventricle wall thickness (h). It can be described by the law of Laplace:
T = (ΔP × R)/2h.
– ΔP reflects the afterload that the left ventricle must pump against (directly related)
– Radius is a function of preload (left ventricular end-diastolic volume) (directly related).
– Wall thickness is a function of the number of myoctes (inversely related)
– Although not intrinsically contained within the equation, heart rate also is a determinant
of myocardial oxygen; it determines the number of times that tension needs to be
generated.
• The left ventricle is ellipsoid and facilitates low wall tension
DISEASE/PATHOPHYSIOLOGY
• The pathophysiology is not completely understood, despite a large number of studies.
Animal studies have demonstrated characteristic histologic and cellular changes associated
with chronic alcohol exposure, including (1):
– Myocyte death
– Intracellular organelle dysfunction
– Interference of contractile protein function
– Abnormalities of calcium homeostasis
– Generation of reactive oxygen species (ROS)
– Changes in neurohormonal systems (sympathetic, renin-angiotensin, natriuretic peptide)
– Individual variations in the development of myocardial toxicity from alcohol suggest that
other variables including genetic or environmental factors may play a role.
• Clinical presentation: ACM presents in stages and can progress from asymptomatic to
symptomatic.
– Asymptomatic stage: Studies have demonstrated that in the early preclinical stage of ACM,
LV remodeling occurs in the form of LV dilation (increased end-diastolic and systolic
dimensions), increased LV mass, and LV hypertrophy (increased septal thickening).
Echocardiographic studies have demonstrated that diastolic dysfunction (impaired early
diastolic filling of the LV) appears to be an early feature of asymptomatic ACM, regardless
of LV mass and the presence of hypertension. Early ACM is often associated with a normal
LV ejection fraction (EF) (3,4,5,6).
– Symptomatic stage: Characterized by progressive increases in LV dilation and LV mass, as
well as the occurrence of systolic dysfunction with a decreased EF. Studies have
demonstrated significantly greater LV end-diastolic and systolic dimensions in
symptomatic ACM patients when compared to asymptomatic ACM patients (2,7).
• Tension: Dilated cardiomyopathy results in a more spherical left ventricle with subsequent
increases in wall stress (radius is increased). In the asymptomatic stage, the myocardial wall
hypertrophies and can decrease wall tension. However, in symptomatic stages, wall
thickness decreases with resultant increases in wall tension (and myocardial oxygen
demand).
• Diagnosis is clinically based upon having a history of significant alcohol consumption after
ruling out other causes of dilated CM.
– History: After excluding other causes of dilated CM, the most important factor for
diagnosis is a chronic history of heavy alcohol use.
– Symptoms/physical exam: Signs and symptoms of heart failure may be noted in patients
with symptomatic disease.
– EKG abnormalities are common and include nonspecific ST and T wave changes, QT
prolongation, and atrial arrhythmias including atrial fibrillation.
– Echocardiography allows for a noninvasive delineation of the LV chamber size, diastolic
function, and systolic function.
– There are no specific pathologic or immunologic tests for the diagnosis of ACM.
• Natural history and treatment
– Although the amount of alcohol required to cause progression of asymptomatic ACM to
overt heart failure appears variable, studies clearly show that decreases in systolic
function are significantly related to the amount and duration of alcohol consumption (1).
– Partial to complete regression of the pathologic cardiac changes associated with ACM may
occur in some patients with abstinence alone.
– LV function in ACM patients may improve with standard medical therapy for dilated CM
(diuretics, cardiac glycosides, ACE inhibitors, and beta blockade), although no therapies
specific for ACM have been studied or described. Despite improvements in the LV
function, survival is not improved in patients who continue to drink. The most important
factor impacting survival in symptomatic patients receiving medical therapy is abstinence
from further drinking.
PERIOPERATIVE RELEVANCE
• Chronic alcoholism results in a significantly higher incidence of postoperative cardiac
complications, hypoxemia, and infections.
• The anesthesia provider should maintain an appropriate index of suspicion for the presence
of ACM in patients with a history of chronic alcohol use. The presence of ACM can have
worsened and even deleterious effects during the perioperative period. Even asymptomatic
patients can have a limited cardiac reserve when exposed to severe perioperative stress that
occurs with major surgery, trauma, or shock. Preoperative cardiac evaluation, including
echocardiography, should be considered for risk-stratification and determination of the need
for medical therapy for prospective surgical patients with a history of chronic alcohol use.
• Alcoholics presenting for emergency surgery may be acutely intoxicated or at risk for
alcohol withdrawal syndrome, both of which can adversely affect a patient with ACM (8).

REFERENCES
1. Piano MR. Alcoholic cardiomyopathy: Incidence, clinical characteristics, and
pathophysiology. Chest. 2002;121:1638–1650.
2. Fernandez-Sola J. Diastolic function impairment in alcoholics. Alcohol Clin Exp Med.
2000;24:1830–1835.
3. Fauchier L. Comparison of long-term outcome of alcoholic and idiopathic dilated
cardiomyopathy. Eur Heart J. 2000;21:306–314.
4. Kupari M. Left ventricular filling impairment in asymptomatic chronic alcoholics. Am J
Cardiol. 1990;66:1473–1477.
5. Lazarevic AM. Early changes in left ventricular function in chronic asymptomatic
alcoholics: Relation to the duration of heavy drinking. J Am Coll Cardiol. 2000;35:1599–
1606.
6. McKenna CJ. Alcohol consumption idiopathic dilated cardiomyopathy: A case control
study. Am Heart J. 1998;135:833–837.
7. Mathews EC. Echocardiogrphic abnormalities in chronic alcoholics with and without overt
congestive heart failure. Am J Cardio. 1981;47:570–578.
8. Spies C. Perioperative morbidity and mortality in chronic alcoholic patients. Alcohol Clin
Exp Res. 2001;25:164S–170S.

ADDITIONAL READING
• Laonigro I. Alcohol abuse and heart failure. Eur J Heart Failure. 2009;11:453–462.
• Spies CD. Effects of alcohol on the heart. Curr Opin Crit Care. 2001;7:337–343.
See Also (Topic, Algorithm, Electronic Media Element)
• Congestive heart failure
• Alcohol abuse

CODES

ICD9
425.5 Alcoholic cardiomyopathy

ICD10
I42.6 Alcoholic cardiomyopathy

CLINICAL PEARLS
• ACM is a type of dilated CM that is diagnosed clinically, based on a history of significant
chronic alcohol exposure in conjunction with the exclusion of other causes of dilated CM.
• The duration of heavy daily alcohol use is the most reliable predictor for the development of
ACM.
• The most important factor impacting survival in ACM patients is abstinence from further
drinking; medical therapy does not improve survival in patients who continue to drink
alcohol.
• The presence of ACM in the surgical patient can have deleterious effects; the anesthesia
provider should maintain an appropriate index of suspicion for the presence of ACM in
patients with a history of chronic alcohol use.
ALDOSTERONE
Joe C. Hong, MD

BASICS
DESCRIPTION
• Aldosterone is a steroid hormone in the mineralocorticoid family that plays a vital role in
the maintenance of intravascular volume status and sodium balance.
• Aldosterone is synthesized and secreted by the zona glomerulosa of the adrenal cortex in
response to low intravascular volume, decreased renal perfusion, hyperkalemia, and
acidosis.
• Disease states include Addison disease (hypoaldosteronism) and Conn syndrome
(hyperaldosteronism).
PHYSIOLOGY PRINCIPLES
• Aldosterone is synthesized from cholesterol within the adrenal cortex by a series of
steroidogenic reactions catalyzed by enzymes of the cytochrome p450 family. It is a steroid
hormone that exerts its action by binding to an intracellular cytoplasmic receptor. This
bound complex enters the cell nucleus and stimulates DNA transcription, resulting in
protein production that mediates the ultimate effects of aldosterone.
• Renin–angiotensin system (RAS) regulation: Aldosterone secretion is regulated primarily by
RAS via the following mechanism:
– Intravascular volume depletion triggers a decrease in renal perfusion pressure.
– Renin is secreted by the juxtaglomerular cells of the afferent arteriole in response to this
decrease in renal perfusion pressure.
– Renin catalyzes the conversion of angiotensinogen to angiotensin I in plasma.
– Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to
angiotensin II, primarily in the lungs.
– Angiotensin II stimulates the synthesis and secretion of aldosterone.
• Adrenocorticotropic hormone (ACTH): Aldosterone is also under tonic control by ACTH
(secreted by the anterior pituitary gland).
• Aldosterone hormone regulates volume and blood pressure via:
– Binding to mineralocorticoid receptors located in the principal cells of nephrons. This
upregulates sodium/potassium pumps with resultant sodium and water reabsorption and
potassium sercetion by the distal tubules and collecting ducts. The net effect is the
restoration of intravascular volume and blood pressure.
– Acting on alpha-intercalated cells of the late distal tubule and collecting duct, resulting in
increased renal hydrogen ion secretion.
ANATOMY
• Aldosterone is produced by cells within the zona glomerulosa of the adrenal cortex.
• The adrenal gland is composed of the inner medulla which produces catecholamines and the
outer cortex which is divided into 3 histologic zones. Going from outside and moving
inwards:
– The outermost zona glomerulosa is the source of aldosterone production.
– Just beneath is the zona fasciculata, the source of glucocorticoid production.
– The inner-most layer of the cortex is the zona reticularis, responsible for the production of
androgens.
DISEASE/PATHOPHYSIOLOGY
• Primary adrenocortical insufficiency (Addison disease)—a hypoaldosterone state:
– Most common cause is autoimmune destruction of the adrenal cortex, resulting in acute
adrenal crisis (1). Other causes of adrenocortical insufficiency include metastatic disease
to the adrenal cortex, adrenal hemorrhage, infection of the adrenal gland (tuberculosis,
opportunistic infections with HIV, fungemia), and amyloid infiltration.
– Characterized by elevated ACTH levels but decreased levels of glucocorticoids and
mineralocorticoids
– Clinical features are related to the adrenocortical hormone deficiency. Hypoglycemia is
caused by cortisol deficiency. Hypotension, hyperkalemia, metabolic acidosis, and volume
contraction are caused by aldosterone deficiency. Hyperpigmentation is caused by
elevated ACTH secretion. Other signs and symptoms include weakness, fatigue, lethargy,
anorexia, nausea, abdominal pain, prerenal azotemia, hypercalcemia, convulsions, fever,
and syncope.
– Treatment: Replacement of glucocorticoids (hydrocortisone, prednisone,
methylprednisolone) and mineralocorticoids (fludrocortisone)
• Secondary adrenocortical insufficiency is caused by decreased ACTH secretion, resulting
primarily in a glucocorticoid deficiency. Mineralocorticoid deficiency is also seen but to a
lesser degree.
– Most common cause of secondary adrenocortical insufficiency is sudden withdrawal of
long-term corticosteroid therapy (2). Other causes include pituitary tumor, pituitary
surgery or radiation, postpartum hypopituitarism (Sheehan syndrome), and sarcoid
infiltration of the pituitary gland.
– Chronic corticosteroid therapy suppresses the hypothalamus and anterior pituitary,
resulting in decreased production of corticotropin-releasing hormone (CRH) and ACTH,
respectively. Decreased levels of CRH and ACTH cause atrophy of the zona fasciculata,
resulting in glucocorticoid deficiency. During times of physiologic stress, the patient is
unable to acutely increase cortisol production, resulting in acute secondary adrenocortical
deficiency.
• Primary hyperaldosteronism is caused by aldosterone-secreting tumors.
– Conn syndrome (aldosterone-secreting adrenocortical adenoma) is the most common
cause. Bilateral adrenal hyperplasia occurs less commonly.
– Characterized by hypertension, hypokalemia, metabolic alkalosis, and a low renin state.
Other signs and symptoms include tetany, polyuria, and an inability to concentrate urine.
– Primary hyperaldosteronism may be present in 0.5–1% of patients with hypertension (3).
– Treatment: Medically by spironolactone (aldosterone receptor antagonist), surgically with
adrenalectomy
PERIOPERATIVE RELEVANCE
• Hypoaldosterone states:
– Patients with adrenocortical insufficiency should continue their mineralocorticoid and
glucocorticoid replacement therapy up until their time of surgery. Clinical features of
overt hypoaldosteronism include hyperkalemia, hyponatremia, acidosis, and myocardial
conduction defects. Administration of mineralocorticoids (fludrocortisone 0.05–0.1 mg/d)
should occur preoperatively (1). Doses must be carefully titrated to avoid hypertension.
– Additional perioperative stress dose of glucocorticoids may be necessary since these
patients may not be able to mount an adequate stress response. The traditional
recommendation is 200 mg hydrocortisone per 70 kg body weight per day. However,
smaller doses of 100 mg per 70 kg body weight per day have been used with success (2).
– The amount of perioperative hydrocortisone is based on the anticipated stress of the
procedure. The relative degree of trauma and depth of anesthesia should be considered.
• Hyperaldosterone states:
– Patients presenting for elective surgery should be medically optimized in terms of their
adrenocortical disorder. Preoperative EKG, glucose, and serum electrolytes (particularly
sodium and potassium) should be checked. Volume status and blood pressure should be
optimized.
– Primary aldosteronism (Conn syndrome) should be suspected in patients who present with
concurrent hypertension and hypokalemia, severe refractory hypertension, adrenal
incidentaloma and hypertension, or onset of hypertension at a young age.
– Antihypertensive medications (e.g., spironolactone) should be maintained up to the time
of surgery. Careful cardiac assessment is necessary because these patients have increased
cardiac comorbidity. Serum sodium and especially serum potassium should be checked
prior to surgery. Hypokalemia is common. Severely hypokalemic patients should have
their potassium replaced preoperatively.

REFERENCES
1. Dorin RI, Qualis CR, Crapo LM. Diagnosis of adrenal insufficiency. Ann Intern Med.
2003;139:194–204.
2. Symreng T, Karlberg BE, Kagedal B, et al. Physiological cortisol substitution of long-term
steroid-treated patients undergoing major surgery. Br J Anaesth. 1981;53:949–954.
3. Young WF Jr. Adrenal causes of hypertension: Pheochromocytoma and primary
aldosteronism. Rev Endocr Metab Disord. 2007;8:309–320.

ADDITIONAL READING
• Graham GW, Unger BP, Coursin DB. Perioperative management of selected endocrine
disorders. Int Anesthesiol Clin. 2000;38:31–67.
• Lampe GH, Roizen MF. Anesthesia for patients with abnormal function of the adrenal cortex.
Anesthesiol Clin North Am. 1987;5:245–268.
• Udelsman R, Ramp J, Gallucci WT, et al. Adaptation during surgical stress: A reevaluation of
the role of glucocorticoids. J Clin Invest. 1986;77:1377–1381.
See Also (Topic, Algorithm, Electronic Media Element)
• Cortisol
• Acute adrenal insufficiency

CLINICAL PEARLS
• Patients with adrenocortical insufficiency have deficiencies in both mineralocorticoids and
glucocorticoids. Hydrocortisone has both glucocorticoid and mineralocorticoid activity.
Therefore, it is an ideal agent to use for the management of adrenocortical insufficiency.
• Patients with aldosterone deficiency should continue their fludrocortisone up until the time
of surgery. Hypokalemic acidosis or hypovolemia must be treated preoperatively.
Supplementation of mineralocorticoids (fludrocortisone 0.05–0.1 mg/d) should occur
preoperatively. Doses must be carefully titrated to avoid hypertension.
• Primary hyperaldosteronism (Conn syndrome) should be suspected in patients who present
with concurrent hypertension and hypokalemia, severe refractory hypertension, adrenal
incidentaloma and hypertension, or onset of hypertension at a young age.
ALVEOLAR ARTERIAL GRADIENT AND RATIO
Sharanya Nama, MD
Michael Mangione, MD

BASICS
DESCRIPTION
• The alveolar–arterial gradient and ratio provide a useful, objective means to determine how
effectively oxygen from the alveolus moves into the pulmonary circulation. It aids with:
– Identifying increases in venous admixtures, even in the presence of increased inspired
oxygen concentrations
– Monitoring improvement or worsening of the venous admixture
– Assessing effectiveness of treatment and interventions
– Differentiating between causes of hypoxia (impaired uptake vs. decreased alveolar oxygen
availability)
PHYSIOLOGY PRINCIPLES
• Definitions:
– PAO2 = alveolar PO2. It is determined by the alveolar gas equation and is calculated as
follows: PAO2 = [FiO2 × (Patm – PH2O) – (PaCO2/0.8)]; measured in units of mm Hg.
– PaO2 = arterial PO2. It is determined by direct arterial blood gas values and is measured
in units of mm Hg. Small amounts of oxygen are dissolved in the plasma, which are in
equilibrium with the oxygen bound to hemoglobin. Thus, a decrease in arterial oxygen
content would reflect a decrease in hemoglobin binding and decreased oxygen saturation.
• A-a gradient: The difference between the alveolar and arterial partial pressure of oxygen
– Normal adult values in nonsmokers are <15 mm Hg on room air (FiO2 = 0.21) (1). For
example, a patient with a PAO2 = 100 mm Hg and a PaO2 = 93 mm Hg has an A-a
gradient of 7.
– Higher FIO2 values result in an increased A-a gradient. For every 10% increase in FiO2,
the A-a gradient increases by 5–7 mm Hg. This effect is caused by the loss of regional
hypoxic vasoconstriction in the lungs (2).
• Advancing age: Results in a steady rise in the A-a gradient (3); PaO2 predicted = 109 – (0.4
× age in years). For example, a 60-year-old breathing room air would have an average A-a
gradient of 14 mm Hg. In comparison, someone below the age of 40 would have a gradient
of 7 mm Hg (3).
• A-a gradient: The arterial oxygen concentration divided by the alveolar oxygen
concentration. This value is useful in predicting the change in PaO2 when the FIO2 also
changes since it is relatively unaffected by varying oxygen levels (4).
– The normal a/A PO2 ratio is 0.74–0.77 when breathing room air (FIO2 = 0.21). It only
increases to 0.80–0.82 when breathing 100% oxygen (5).
• Physiologic shunting and normal venous admixture
– The thebesian veins drain venous blood from all 4 walls of the myocardium (mostly right
atrium) and empty into the left atrium.
– Deep bronchial veins drain venous blood from the bronchi and roots of the lungs and
empty into the pulmonary veins (deoxygenated blood that returns to the left atrium).
– Venous blood from these areas does not enter the pulmonary circulation; instead, it
returns to the systemic circulation without becoming oxygenated. This accounts for a total
of 2–5% of cardiac output, and the mixing of oxygenated and deoxygenated blood is
known as venous admixture.
– This normal venous admixture accounts for the 10–15 mm Hg A-a gradient and the 0.74–
0.77 a/A ratio that is considered normal.
• Hypoxic pulmonary vasoconstriction describes a physiologic phenomenon in which the
pulmonary arterioles constrict in the presence of low oxygen tension in the alveoli (e.g.,
atelectasis).
– This vessel constriction results in re-directing blood flow to well-oxygenated lung units
and away from poorly oxygenated lung units to ultimately improve ventilation-perfusion
(V/Q) matching.
– When a patient is given supplemental oxygen, more alveoli become well-oxygenated;
however, it also, in turn, decreases hypoxic vasoconstriction.
– This increase in V/Q mismatch leads to more deoxygenated blood entering the systemic
circulatory system and in turn increases the A-a gradient.
ANATOMY
• Alveolus
– Air sac that is lined with a thin membrane consisting of epithelium with collagen and
elastin
– Gas exchange occurs across this membrane where gases move down a concentration
gradient between alveolus and pulmonary capillary.
• Pulmonary circulation
– Consists of blood vessels that carry deoxygenated blood to the site of gas exchange
• Pulmonary capillaries
– Consists of a single layer of squamous epithelium surrounded by a basement membrane
– Gases must diffuse across these layers to enter circulation.
DISEASE/PATHOPHYSIOLOGY
• Hypoxia with increased A-a gradient and a/A ratio: Results from an increase in the venous
admixture secondary to blood passing through the lung without being properly oxygenated
(in addition to the physiologic admixture). Examples of this include:
– V/Q mismatch: Discrepancy between the alveolar ventilation and capillary perfusion
– Pulmonary shunt: Perfusion of the alveolar unit without ventilation, due to pathologic
processes. Atelectasis describes alveolar deflation or fluid collection of the alveolar unit.
Deflation can result from airway obstruction, mucus or blood plugging, inadequate tidal
volumes due to pain, or positioning changes; other causes include endobronchial
intubation, pneumothorax, collapse of emphysematous blebs, and one lung ventilation (6).
Fluid collection can result from pulmonary edema, pneumonia, or adult respiratory
distress syndrome (ARDS).
– Intracardiac shunt: Venous blood is diverted from the pulmonary circulation directly into
the systemic circulation. Examples include atrial or septal defects, pulmonary
atrioventricular (AV) malformations, and cyanotic congenital heart disease.
– Diffusion defects: Observed when the alveolar oxygen and carbon dioxide tensions are
normal, but oxygen uptake by the alveolar capillaries is abnormal or impaired. Examples
include pulmonary fibrosis, interstitial lung inflammation, and interstitial edema.
• Hypoxia with normal A-a gradient or a/A ratio: Can be seen in situations where the alveolar
oxygen (or carbon dioxide) is affected, but oxygen uptake by the capillaries is not impaired.
The decreased arterial oxygen concentration reflects the decreased alveolar concentration.
– Hypoxic delivery: Anesthesia machine or ventilator malfunction, or high altitude
– Hypoventilation: Respiratory depression from drugs, stroke in the pontine area,
respiratory muscle fatigue (such as myasthenia gravis), or obesity–hypoventilation
syndrome. The increase in carbon dioxide decreases the oxygen partial pressure
(concentration) within the alveoli.
PERIOPERATIVE RELEVANCE
• Assessing the A-a gradient or ratio can:
– Differentiate between hypoxia secondary to low alveolar oxygen tension or due to increase
in venous admixture from underlying pathology
– Provide an objective means to trend venous admixtures and, hence, assess pulmonary
processes
– Assess the effectiveness of treatment and interventions such as positive end expiratory
pressures (PEEP)
– The A-a gradient is directly proportional to shunt while being inversely proportional to the
mixed venous oxygen tension.
– Pulse oximetry only provides an assessment of hemoglobin binding. As oxygen saturation
reaches the high 90’s, it can no longer be a reliable marker for arterial oxygen content.
Therefore, pulse oximetry cannot aid with assessing the severity of the A-a gradient in a
given disease state. For example, patients A and B both have ARDS. Patient A is on 50%
FiO2; his PAO2 is 350 mm Hg and his PaO2 is 120 mm Hg resulting in an A-a gradient of
230 mm Hg and SpO2 of 99%. Patient B also has ARDS and is on 50% FiO2; his PAO2 is
350 mm Hg and his PaO2 is 320 mm Hg resulting in an A-a gradient of 30 and SpO2 of
99%. Therefore, it is not possible to assess the status of the underlying pathology with
higher supplemental oxygen based on oxygen saturation alone; one must obtain a blood
gas and calculate the A-a gradient.
– Assessing a/A ratio: In patients receiving higher or changing FiO2, the ratio can provide a
more consistent value that allows for comparison. Additionally, it has been shown to be
more reliable than the A-a gradient in hemodynamically stable patients (7).
– Perioperative conditions: The functional residual capacity (FRC) is decreased by several
factors that ultimately increase the venous admixture, A-a gradient, and a/A ratio.
General anesthesia
Positioning (supine, prone or steep Trendelenburg position)
Surgical procedure (laparoscopy, abdominal retractors)
Patient (obesity, pregnancy, ascites) (8)
• Maneuvers and techniques to improve lung oxygenation can be assessed objectively by
calculating the A-a gradient or a/A ratio.
– Pulmonary edema may be treated by optimizing preload (diuresis, venodilators) and
afterload (vasodilators) to increase inotropy.
– Ventilator adjustments such as PEEP, adjusting rate, volume, I:E ratios, and lung
recruitment maneuvers
– Surgical maneuvers such as decreasing the insufflation pressures during laparoscopy or
retractor tension
– Positioning changes: Elevating the head of the bed can shift the abdominal contents away
from the diaphragm and allow for increased lung expansion.
EQUATIONS
• A-a gradient = PAO2 – PaO2
• a/A ratio = PaO2/PAO2
• PAO2 = [FiO2 × (Patm – PH2O) – (PaCO2/0.8)]
• On room air (21%) at sea level, a simplified version: A-a gradient = [(150 – 5)/4(PCO2)] –
PaO2
• Normal A-a gradient ∼ (age +10)/4

REFERENCES
1. Mellemgaard K. The alveolar–arterial oxygen difference: Its size and components in normal
man. Acta Physiol Scand. 1966;67(1):10–20.
2. Williams AJ. ABC of oxygen: Assessing and interpreting arterial blood gases and acid-base
balance. BMJ. 1998;317(7167):1213–1216.
3. Kanber GJ, King FW, Eshchar YR, et al. The alveolar–arterial oxygen gradient in young and
elderly men during air and oxygen breathing. Am Rev Respir Dis. 1968;97(3):376–381.
4. Peris LV, Boix JH, Salom JV, et al. Clinical use of the arterial/alveolar oxygen tension
ratio. Crit Care Med. 1983;11(11):888–891.
5. Gilbert R, Kreighley JF. The arterial/alveolar oxygen tension ratio: An index of gas
exchange applicable to varying inspired oxygen concentrations. Am Rev Respir Dis.
1974;109:142–145.
6. Thurlbeck WM, Müller NL. Emphysema: Definition, imaging, and quantification. Am J
Roentgenol. 1994;163:1017–1025.
7. Gilbert R, Auchincloss JH Jr, Kuppinger M, et al. Stability of the arterial/alveolar oxygen
partial pressure ratio: Effects of low ventilation/perfusion regions. Crit Care Med.
1979;7(6):267–272.
8. Woodring JH, Reed JC. Types and mechanisms of pulmonary atelectasis. J Thorac Imaging.
1996;11:92–108.
ADDITIONAL READING
• Rodríguez-Roisin R, Roca J. Mechanisms of hypoxemia. Intensive Care Med.
2005;31(8):1017–1019.
See Also (Topic, Algorithm, Electronic Media Element)
• Functional residual capacity
• Mixed venous oxygen saturation
• Oxygen carrying capacity
• Pulmonary ventilation perfusion matching
• One lung ventilation
• Hypoxia, intraoperatively
• PaO2

CLINICAL PEARLS
• Pulse oximetry in the presence of a high FIO2 may not be an adequate marker of pulmonary
pathology as reflected by the A-a gradient.
• Hypoxemia caused by physiologic shunt may not be responsive to increased FiO2.
ALVEOLI
Megan Freestone-Bernd, MD
Mary E. McAlevy, MD

BASICS
DESCRIPTION
Alveoli are the thin-walled, sac-like, terminal dilations of the respiratory bronchioles, alveolar
ducts, and alveolar sacs. They serve as the functional unit for gas exchange with pulmonary
capillaries.
• The adult lung contains approximately 300 million alveoli.
• The combined maximal volume is approximately 5–6 L.
• Each alveoli is surrounded by capillaries.
• The combined surface area ranges from 50 to 100 m2.
PHYSIOLOGY PRINCIPLES
• Alveolar walls: Comprised of a thin epithelial layer that consists of alveolar type I and
alveolar type II cells.
– Alveolar type I cells are squamous epithelial cells and cover approximately 80% of the
alveolar surface. They are highly differentiated and very susceptible to injury. If the type I
cell is damaged, the type II cells replicate and modify to form new type I cells.
– Alveolar type II cells are cuboidal epithelial cells that synthesize and secrete the fluid
layer (surfactant) that lines the alveoli. The type II alveolar cells also control local
electrolyte balance and lymphatic cell functions.
– Alveolar type III cells are alveolar macrophages and are an important element of lung
defense. They are part of the lung inflammatory response and ingest foreign materials
within the alveoli.
• Alveoli size:
– Individual alveoli range from about 75 to 300 μm.
– Surface tension: Describes the force exhibited by water molecules in the alveoli towards
one another. Water has a greater attraction to each other than to air, causing the alveoli
to tend towards collapse. For example, as alveoli become smaller, water molecules come
closer together, and surface tension is increased. As alveoli increase in size, water
molecules are further apart, and surface tension is decreased.
– Law of Laplace: The pressure required to keep an alveolus open is directly proportional to
the surface tension within the alveolus and indirectly proportional to the alveolar radius.
P = 2T/r, where P = pressure, T = surface tension, and r = radius.
– Surfactant: A phospholipoprotein that contains both a hydrophilic and hydrophobic region
that lines the alveoli. It adsorbs to the alveolar air–water interface and decreases surface
tension by decreasing the interaction between water molecules. Thus, surfactants function
to stabilize the alveoli; the tendency for small alveoli to collapse would result in emptying
into larger alveoli.
– Pleural pressure: Varies throughout the lung. At the apices, the pleural pressure is the
most negative; therefore, the alveoli are more expanded than at the bases of the lungs.
• Gas exchange across the alveoli is determined by the partial pressure difference across the
membrane and the solubility of the gas. The alveoli epithelium and basement membrane
provide minimal hindrance and are optimal for this function. Carbon dioxide diffuses 20
times as rapidly as oxygen; oxygen diffuses twice as rapidly as nitrogen.
ANATOMY
• Alveoli are the terminal branches in the pulmonary tree.
• The pulmonary tree begins with the trachea which then branches into the right and left
mainstem bronchi. These bronchi then further divide into bronchioles, alveolar ducts, and
alveolar sacs.
• The lungs receive blood from the pulmonary and bronchial circulation.
– Pulmonary circulation: Deoxygenated blood flows from the right ventricles into the
pulmonary arteries which branch along with the bronchial tree until they reach the
respiratory bronchioles. At this point, they form a dense capillary network that provides a
very large area for gas exchange. Oxygenated blood returns to the left atrium via the
pulmonary veins.
– Bronchial circulation: The blood is supplied from the aortic arch, the thoracic aorta, and
the intercostals arteries. It feeds the trachea, bronchi, and bronchioles as well as the
intrapulmonary nerves, ganglia, and interstitial lung tissue. It drains into the right atrium
as deoxygenated blood.
• Zones: Blood flow through the lungs is dependent upon gravity as well as the relative
pressures in each area. These pressures include the pulmonary artery pressure (Ppa), the
pulmonary venous pressure (Ppv), and the alveolar pressure (PA). Three zones have been
described:
– Zone 1: Located at the lung apex, the perfusion pressure is about equal to the alveolar
pressure so blood flow is low (PA > Ppa > Ppv). Zone 1 therefore has ventilation without
perfusion and is essentially dead space.
– Zone 2: The middle zone where the perfusion pressure is greater than the alveolar
pressure so blood flows easily (Ppa > PA > Ppv). Zone 2 is the area of “best matched”
ventilation and perfusion; it also contains the most number of alveoli.
– Zone 3: Located at the lung base, where the perfusion pressure is much greater than the
alveolar pressure so blood flow is high (Ppa > Ppv > PA). Zone 3 has very good
perfusion, but less ventilation which results in shunting.
DISEASE/PATHOPHYSIOLOGY
• Atelectasis is the term used to describe “collapsed” alveoli; the term can be applied to a
single unit, lobe, or the entire right or left lung. Blood that perfuses the collapsed cannot
pick up oxygen or offload carbon dioxide, resulting in pulmonary shunting. As the number
of atelectatic units increases, it is less likely that the blood will be oxygenated by a proximal
or distal unit before returning to the left atrium.
• Neonatal respiratory distress syndrome (RDS) can be present in premature infants due to a
lack of surfactant. The increase in surface tension results in alveolar collapse (atelectasis),
with resultant hypoxemia, decreased compliance, and problems re-inflating the lungs.
Surfactant may be present by week 24 and is almost always present by gestational week 35.
If there are mature levels of surfactant, the amniotic fluid will have a
lecithin:sphingomyelin ratio >2:1. Corticosteroids may be given to encourage formation of
surfactant in cases of pre-term labor.
• Emphysema is a disease where alveoli undergo destruction and elastic recoil is decreased;
this results in increased alveolar size. It is most commonly caused by smoking, but can also
result from alpha-1 antitrypsin deficiency. Bronchoalveolar lavage will demonstrate the
presence of neutrophils; these cells cause damage to the lung parenchyma by secretion of
proteolytic enzymes. Alveolar damage decreases gas exchange area, leading to hypoxemia,
hypercarbia, and chronic dyspnea.
• Pulmonary fibrosis describes thickening of the alveolar wall; this impairs the diffusing
capacity of gas through the alveoli.
• Cystic fibrosis is a genetic disease of the epithelial chloride channel to open normally in
response to cyclic AMP. This defect decreases water passage across the epithelial membrane,
leading to abnormally thick mucous in the airways. Mucus can obstruct small airways
(plugs) and result in frequent pulmonary infections.
• Aspiration pneumonitis of acidic solutions may lead to destruction of surfactant-producing
type II pneumocytes and the capillary endothelium. Damage to these cells may lead to
atelectasis and leakage of fluid into the lungs. Arterial hypoxia may ensue, which leads to
pulmonary vasoconstriction with associated pulmonary hypertension, as well as tachypnea
and bronchospasm.
• Congestive heart failure describes cardiac dysfunction with “back-up” into the pulmonary
vasculature (increased capillary pressure). This initially causes dilation and recruitment of
pulmonary capillaries making it more difficult for alveoli to expand (results in decreased
lung compliance, and increased work of breathing). As capillary pressures increase, fluid
will eventually extravasate into the interstitial space around the alveoli. With further
increases in pressure, fluid will eventually enter into the alveoli.
• Acute respiratory distress syndrome (ARDS) is defined as severe hypoxemia, diffuse shadows
on CXR, low pulmonary compliance, and pulmonary edema not from left-sided heart failure.
The lung parenchyma is severely damaged due to chemical mediators and fibroblasts. There
is an inflow of protein-rich fluid into the alveoli due to increased permeability of the
alveolar capillary membranes. Diseases that may precipitate ARDS include: septic shock,
aspiration of gastric contents, pneumonia, pulmonary contusions, near drowning, severe
trauma with associated shock, and inhalation of toxic gases or smoke.
PERIOPERATIVE RELEVANCE
Positive end-expiratory pressure (PEEP) is effective in improving arterial oxygenation and
should be used when indicated. PEEP helps prevent alveolar collapse at the end of expiration
and in doing so may decrease the shear stress associated with the opening and closing of
alveoli with mechanical ventilation. PEEP also helps ventilation-to-perfusion matching as well
as decreasing right-to-left intrapulmonary shunt. Because PEEP recruits alveoli that were
previously collapsed, it helps to increase lung volumes and functional residual capacity (FRC).
However, by increasing the intrathoracic pressure, it can decrease preload to the right atrium
and decrease cardiac output.
EQUATIONS
Law of Laplace: P = 2T/r, where P = pressure, T = surface tension, and r = radius

REFERENCES
1. Daniels CB, Orgeig S. Pulmonary surfactant: The key to the evolution of air breathing.
News Physiol Sci. 2003;18:151–157.
2. Smetana GW. Preoperative pulmonary evaluation. N Engl J Med. 1999;340:937–944.
3. Staton GW, Ingram RH. Pulmonary edema. Sci Am Med. 1997:1–10.
4. Tobin MJ. Culmination of an era in research on the acute respiratory distress syndrome. N
Engl J Med. 2000;342:1360–1361.
See Also (Topic, Algorithm, Electronic Media Element)
• Atelectasis
• Surfactant
• Pulmonary ventilation and perfusion matching
• Acute respiratory distress syndrome
• Cardiogenic pulmonary edema
• Noncardiogenic pulmonary edema

CLINICAL PEARLS
• During normal spontaneous ventilation, the alveolar-to-dead space ventilation ratio is 1:1.
During mechanical ventilation under anesthesia, dependent lung regions will have alveolar
collapse, and ventilation is preferably distributed to the nondependent areas (ratio changes
to 1:2). These alveoli may become over-aerated if high levels of PEEP are used.
AMNIOTIC FLUID EMBOLISM
Kanishka Monis, MD
Poovendran Saththasivam, MD

BASICS
DESCRIPTION
• Amniotic fluid embolism (AFE) is a rare, but often fatal, obstetric emergency. It was first
described by Dr. Meyer in 1926.
• Entry of amniotic fluid into the maternal circulation via the placenta can occur during
pregnancy or in the immediate postpartum period.
• Amniotic fluid contains:
– Epithelial squamous cells from the fetal skin
– Mucin which originates from meconium
– Lanugo
– Fat from vernix caseosa
EPIDEMIOLOGY
Prevalence
Hard to assess due to a lack of sensitive and specific diagnostic studies; however, estimated to
be 7.7 in 100,000 births in the US.
Morbidity
Neurologic impairment is seen in 61% of women and 50% of infants who survive AFE
Mortality
• AFE is the fifth most common cause of maternal mortality in the world.
• Maternal mortality approaches 60%.
• Fetal mortality rate is around 21%.
ETIOLOGY/RISK FACTORS
• Advanced maternal age
• Tumultuous labor
• Placental abnormalities (placenta previa, abruptio placentae)
• Operative deliveries (Cesarean section, assisted vacuum deliveries, forceps-assisted
deliveries)
• Eclampsia
• Polyhydramnios
• Cervical lacerations
• Uterine rupture
• Medical induction of labor
PHYSIOLOGY/PATHOPHYSIOLOGY
• 4 main physiologic alterations in AFE:
– Maternal cardiovascular collapse
– Coagulopathy
– Respiratory distress
– Altered mental status
• Amniotic fluid entry. It is hypothesized that the combination of breaches to the maternal
circulation along with increased intrauterine pressures can facilitate entry of amniotic fluid
into the circulation.
– Breaches in the physical barrier can occur at the level of endocervical veins, the placental
attachement site, or at uterine trauma sites.
– Increased intrauterine pressure (and incidence of AFE) is seen in conditions such as
polyhydramnios, placenta previa, placenta abruption, operative deliveries, uterine
rupture, and cervical lacerations.
• Maternal cardio-respiratory collapse may result from the following mechanisms
– Mechanical obstruction of the pulmonary arteries (dead space; ventilation, but no
perfusion)
Amniotic debris obstructs the pulmonary artery leading to pulmonary hypertension and
acute right ventricular failure. The increased right ventricular afterload results in a
dilated right ventricle and deviation of the inter-ventricular septum. This can impair left
ventricular filling with resultant left ventricular failure. Transesophageal
echocardiography supports these findings.
– Immunologic responses. Generalized constriction of the pulmonary vasculature results in
relative shifting of blood flow to areas of lower ventilation from higher ventilation (shunt;
perfusion, but inadequate ventilation).
The complement cascade is activated and the subsequent immunologic reactions can
result in pulmonary vasoconstriction. Of note, low levels of complement (C3 and C4)
have been observed in some parturients with AFE
Endothelin has also been found in amniotic fluid and can lead to pulmonary
vasoconstriction
Other humoral mediators, such as histamine, serotonin, prostaglandins, and leukotrienes
have been linked to the onset of shock, myocardial depression, and disseminated
intravascular coagulopathy
• Coagulopathy associated with AFE is mainly related to consumption.
– Amniotic fluid contains tissue factors that activate the extrinsic pathway by binding to
factor VII.
– Amniotic fluid is also found to have a thromboplastin-like effect and factor X activating
property.
PREVENTATIVE MEASURES
• Avoid trauma to the uterus during insertion of a pressure catheter or during artificial
rupture of the membrane.
• During a Cesarean section, incision on the placenta should be avoided.
• Excessively strong and frequent uterine contractions, as may be seen with oxytocin
administration, should be minimized.
PREOPERATIVE ASSESSMENT
• A diagnosis of exclusion, based on clinical presentation, or postmortem findings
• AFE usually occurs during the intrapartum period or immediately postpartum.
• Symptoms:
– Sudden breathlessness
– Nausea/vomiting
– Dizziness
– Chest pain
– Panic attack
– Pin and needle sensation in fingers
– Bleeding
• Signs:
– Hypotension
– Respiratory distress
– Cyanosis
– Fetal distress
• Diagnostic tests and imaging:
– Nonspecific tests include CBC, coagulation profile, ABG, BUN, and cardiac enzymes.
– EKG may shown an acute right ventricular strain pattern.
– Chest radiograph may indicate a dilated right heart, prominent pulmonary arteries, and
pulmonary edema.
– Transesophageal echocardiography may reveal pulmonary hypertension, acute right
ventricular failure with leftward deviation of the inter-ventricular and inter-atrial septum
and severe tricuspid regurgitation.
– Serum markers for AFE:
Specific markers include zinc coproporphyrin (a component of meconium) and sialyl Tn
antigen (a component of meconium and amniotic fluid).
Nonspecific serum markers include serum tryptase (marker of mast cell degranulation)
and complement factors.
The presence of fetal squamous cells in the maternal circulation is suggestive but not
diagnostic of AFE.
DIFFERENTIAL DIAGNOSIS
• Pulmonary thromboembolism
• Air embolism
• Myocardial infarction/cardiac arrhythmia
• Aortic dissection
• Anesthetic-related complication (total or high spinal block)
• Allergic anaphylaxis
• Abruptio placentae
• Uterine rupture
• Sepsis
TREATMENT

• Treatment is mainly supportive care aimed at the:


– Correction of hypoxia and maintenance of oxygenation:
Administer oxygen immediately with a goal of SpO2 >90%
Ventilate by face mask, Ambu bag, or endotracheal intubation
– Correction of hypotension and maintenance of cardiac output:
Initiate cardiopulmonary resuscitation (CPR) immediately
Rapid restoration of preload using crystalloid solution
Inotropic support in cases where hypotension is refractory to fluid therapy
Maintain a systolic blood pressure >90 mm Hg
– Correction of coagulopathy:
Transfuse packed red blood cells to maintain adequate blood oxygen-carrying capacity
and oxygen delivery to tissues.
Fresh frozen plasma, platelet, and cryoprecipitate can be transfused to correct specific
laboratory coagulation derangements.
Recombinant activated factor VIIa has been used to manage severe DIC not responding to
blood products transfusion
• Pulmonary hypertension may be treated with inhaled nitric oxide, prostacyclin, and
sildenafil.

FOLLOW-UP

• Risk of recurrence in the subsequent pregnancy is unknown.


• Neurologic disability in the mother and infant remains a common complication following
AFE.

REFERENCES
1. Abenhaim HA, Azoulay L, Kramer MS, et al. Incidence and risk factors of amniotic fluid
embolisms: A population-based study on 3 million births in the United States. Am J Obstet
Gynecol. 2008;199(1):49.e1–49.e8. Conde-Agudelo A, Romero R. Amniotic fluid embolism:
An evidence-based review. Am J Obstet Gynecol. 2009;201(5):445.e1–445.e13. Erratum in:
Am J Obstet Gynecol. 2010;202(1):92.
2. Harboe T, Benson MD, Oi H, et al. Cardiopulmonary distress during obstetrical anaesthesia:
Attempts to diagnose amniotic fluid embolism in a case series of suspected allergic
anaphylaxis. Acta Anaesthesiol Scand. 2006;50(3):324–330.
3. Kane SK. Historical perspective of amniotic fluid embolism. Int Anesthesiol Clin.
2005;43(4):99–108.
4. Moore J, Baldisseri MR. Amniotic fluid embolism. Crit Care Med. 2005;33(Suppl 10):S279–
S285.
See Also (Topic, Algorithm, Electronic Media Element)
• Venous air embolism
• Dead space

CODES

ICD9
• 673.10 Amniotic fluid embolism, unspecified as to episode of care or not applicable
• 673.11 Amniotic fluid embolism, delivered, with or without mention of antepartum
condition
• 673.12 Amniotic fluid embolism, delivered, with mention of postpartum complication

ICD10
• O88.111 Amniotic fluid embolism in pregnancy, first trimester
• O88.112 Amniotic fluid embolism in pregnancy, second trimester
• O88.119 Amniotic fluid embolism in pregnancy, unspecified trimester

CLINICAL PEARLS
• Due to significant morbidity and mortality, a high index of suspicion is warranted.
• Suspect AFE when the laboring patient complains of sudden breathlessness, or incurs
hypotension or cardiac arrest.
• Rule out pulmonary thromboembolism and anesthetic complications (e.g., high spinal) in
the parturient suspected of AFE.
• The mainstay of therapy is to support oxygenation and circulation to prevent end-organ
damage with severe debilitating neurologic sequelae.
• Parturients have improved prognosis when AFE is diagnosed early and aggressive treatment
is administered.
AMYLOIDOSIS
Ahmed Fikry Attaallah, MD, PhD

BASICS
DESCRIPTION
• Amyloidosis is a progressive connective tissue disease caused by the deposition of amyloid
proteins.
• It can involve various body systems but sometimes only one organ may be affected. Factors
leading to the specific pattern of organ involvement are not understood.
EPIDEMIOLOGY
Incidence
New cases: 8 persons per million annually
Prevalence
• 95% of cases are seen in people >40 years of age.
• 66% of cases are men.
• 15–20% of primary amyloidosis patients have associated multiple myeloma.
Morbidity
Varies between patients reflecting the extent of spread and the degree of organ dysfunction
Mortality
• The average survival with primary amyloidosis is 12 months.
• Amyloidosis associated with multiple myeloma is rapidly progressive and the life expectancy
is usually <6 months.
• In secondary amyloidosis, medical or surgical treatment of the underlying cause may slow or
stop the disease progression.
• In familial amyloidosis, survival is 7–15 years.
ETIOLOGY/RISK FACTORS
• Family history of amyloidosis
• Advanced age
• Chronic infectious or inflammatory diseases
• Kidney disease requiring hemodialysis
PATHOPHYSIOLOGY
• The term “amyloid” describes an alteration in the secondary structure of a protein that
results in an aggregated and insoluble form. Amyloidosis can result from inherited
mutations in precursor genes or from plasma cell dyscrasia; amyloid deposits in the
extracellular spaces lead to organ failure and eventually death.
• Plasma cells are located in the bone marrow and function as part of the immune system by
producing antibodies. Monoclonal plasma cells produce small lambda (λ) or kappa (κ)
fragments that are processed in an abnormal manner by macrophage enzymes producing the
insoluble amyloid fibrils.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Assess for multiorgan involvement and the severity of disease progression in each system.
• The anesthetic plan should focus on monitoring and preventing hemodynamic instability.
• Maintain a high index of suspicion for a possible difficult intubation in order to prevent
perioperative airway compromise.
• Calcium channel blockers are contraindicated in cardiac amyloidosis and may produce or
worsen bradyarrhythmias. Atropine may be useless or even worsen bradycardia in patients
with familial amyloidosis.
• Consider stress dose steroids for patients on chronic therapy.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Nervous system: Hand and foot numbness, visual changes, dementia
• Cardiac: Decreased exercise tolerance, irregular heartbeat, syncope (strong predictor of
sudden death)
• Respiratory: Hoarseness of voice, shortness of breath, hemoptysis
• Renal: Turbid urine, polyuria (early), or oliguria (late)
• Digestive: Dysphagia, swollen tongue, dry mouth, constipation or diarrhea, hematemesis,
melena, fresh bleeding, acid reflux
History
• Family history of amyloidosis
• Onset of initial diagnosis
• Coexisting chronic illness
• Kidney failure/hemodialysis
Signs/Physical Exam
• Nervous system: Peripheral neuropathy, autonomic neuropathy (postural hypotension),
visual field defects
• Cardiac: Signs of restrictive cardiomyopathy and congestive heart failure, cardiomegaly,
arrhythmias
• Respiratory: Stridor, wheezing
• Renal: Nephrotic syndrome, signs of renal failure
• Digestive: Macroglossia, hemorrhage, hepatic enlargement and splenomegaly, signs of
intestinal obstruction, malnutrition, and dehydration
• Skin: Raised waxy papules or plaques
TREATMENT HISTORY
• Localized radiation therapy aimed at destroying the local collection of plasma cells
• Stem cell transplant
• Surgical care:
– Organ transplant surgery (liver, kidney, heart, or lung)
– Carpal tunnel release
– Percutaneous cementoplasty of bone lesions
– Resection of bleeding friable amyloidomas in the respiratory, GI, or urinary tracts
• Supportive care:
– Renal: Hemodialysis and peritoneal dialysis
– Cardiac: Pacemaker
MEDICATIONS
• Melphalan and prednisone regimen is considered standard therapy.
• An anthracycline analogue of doxorubicin, 4’-iodo-4’-deoxydoxorubicin, has been shown to
solubilize amyloid fibrils.
• Lenalidomide, a derivative of thalidomide, is an immunomodulator that has shown some
success in patients.
• In patients with coexisting multiple myeloma, vincristine, carmustine, dexamethasone, and
cyclophosphamide can be used.
• Proteasome inhibitor: Bortezomib may be used with relapsed/refractory myeloma.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Blood and urine tests are not diagnostic of amyloidosis, but can aid with monitoring organ
dysfunction and disease progression:
– Serum and urine protein analysis and immunoelectrophoresis
– Impaired renal function tests
– Impaired liver function tests
• Hematologic indices and coagulation profile: Anemia, increased fibrinolysis, and clotting
factors deficiency
• Pathologic diagnosis:
– Subcutaneous fat aspiration: Usually sufficient for diagnosis by immunostaining or fibril
amino acid sequence analysis
– Organ-specific biopsies: A needle biopsy of an involved organ ensures a cause-and-effect
relationship between the organ dysfunction and amyloid deposition.
– Bone marrow examination
• Extent of disease spread:
– Chest radiography
– Bone imaging (skeletal survey) of the skull, pelvis, and entire spine
– CT scan
– MRI
– Radioimmunodetection of amyloid deposits (SAP component scintigraphy or iodine-
labeled pentagonal component scanning): A noninvasive method of quantitative imaging
by iodine I123-labeled protein localizer that binds to amyloid deposits
– Cardiac involvement: EKG can show a low-voltage QRS complex, conduction arrhythmias,
and bradycardia. Echocardiography can demonstrate concentric biventricular wall
thickening, increased myocardial echodensity, restrictive filling pattern and diastolic
dysfunction, thickened valves, and decreased myocardial contractility.
CONCOMITANT ORGAN DYSFUNCTION
• Varies depending on the nature of the chronic infectious or inflammatory diseases in
secondary amyloidosis
• Amyloid deposition can commonly affect the:
– Cardiovascular system: myocardium, conduction system, and cardiac valves
– Respiratory system: Upper and lower airways (the larynx is most common site) and the
lungs (diffuse infiltration or tumorous masses)
– Renal system: Kidneys, bladder
– Digestive system: GI tract, liver, and spleen
– Central and peripheral nervous systems
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Correction of electrolyte abnormalities
• Correction of anemia and coagulopathy
• Management of cardiac arrhythmias, including temporary or permanent pacemaker
placement
CLASSIFICATIONS
• Primary amyloidosis (AL type): Most common, without pre-existing or coexisting disease
• Secondary amyloidosis (AA type): Associated with a chronic infectious or inflammatory
process
• Amyloidosis with multiple myeloma (AL type)
• Familial amyloidosis (AF type)
• Local amyloidosis (AE type): Limited to a single organ
• Senile (AS type): Aging—Alzheimer’s disease
• Hemodialysis-related amyloidosis (AH type)

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Titrate sedation very cautiously; patients are prone to airway obstruction, particularly when
macroglossia is present.
• Appropriate pacemaker management
Special Concerns for Informed Consent
Advanced amyloidosis with severe organ dysfunction poses a high risk, and code status
during the perioperative period should be clarified.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Consider regional or neuraxial blocks to avoid airway instrumentation in patients with
tongue, larynx, and tracheal involvement that may lead to obstruction, hemorrhage, or
difficult intubation.
• On the other hand, in patients with peripheral neuropathy or coagulopathy, regional
anesthesia is relatively contraindicated.
Monitors
• DC defibrillator and emergency medications should be readily available to treat cardiac
arrhythmias and possible hemodynamic instability.
• Invasive monitoring (arterial line, central venous access, and pulmonary artery catheter)
and transesophageal echocardiography (TEE) should be determined on a case-by-case basis.
Induction/Airway Management
• Dose adjustment of induction drugs to avoid significant hypotension due to potential
myocardial disease and reduced protein binding.
• Patients may have undiagnosed supraglottic amyloid deposits (tongue, pharynx, and larynx),
and blind placement of the endotracheal tube, nasal, or oral airways is not recommended
since it may result in massive airway hemorrhage.
• Perform a fiberoptic exam (before or after induction), or a careful direct laryngoscopy, to
assess the feasibility of intubation. If extensive lesions are noted, an awake tracheostomy
tube placement may be warranted.
• If excision of the supraglottic lesions is planned, a small reinforced or laser cuffed
endotracheal tube should be utilized.
• Rapid-sequence induction is recommended if GI obstruction or delayed gastric emptying is
present due to autonomic neuropathy.
• In patients without aspiration or airway bleeding risks, a laryngeal mask airway (LMA)
maybe used to avoid airway instrumentation.
Maintenance
• Impaired hepatic and renal functions may influence drug metabolism and clearance.
• Ensure proper hydration but avoid intravenous overloading (limited cardiac and renal
reserve).
• Careful positioning to prevent nerve damage and fragile skin breakdown
Extubation/Emergence
• Patients who underwent upper airway or tracheobronchial lesion excisions need to be
assessed for possible edema or bleeding and may be kept sedated and intubated
postoperatively.
• Avoid excessive coughing and straining to prevent skin eruptions and ecchymosis.

POSTOPERATIVE CARE
BED ACUITY
• Patients with airway risk or with advanced amyloidosis who underwent major surgical
procedures may require an ICU bed and remain intubated with postoperative ventilation.
• If an implantable defibrillator was programmed off, ensure that it is turned back on.
COMPLICATIONS
• Difficult, or impossible, ventilation due to subglottic amyloid deposits that may lead to
tracheobronchial tree stenosis or hemorrhage. Treatment can be attempted with helium–
oxygen mixture, jet ventilation, and emergency cardiopulmonary bypass through femoral
access (guide-wires may be placed preoperatively).
• Hypotension may be treated by inotropic agents and vasopressors.
• Excessive bleeding can be treated by blood transfusion and correction of coagulopathies.
• Bradycardia and conduction abnormalities can be treated by isoproterenol and cardiac
pacing.

REFERENCES
1. Noguchi T, Minami K, Iwagaki T, et al. Anesthetic management of a patient with laryngeal
amyloidosis. J Clin Anesth. 1999;11:339–341.
2. Minogue SC, Morrisson M, Ansermino M. Laryngo-tracheo-bronchial stenosis in a patient
with primary pulmonary amyloidosis. Can J Anaesth. 2004;51(8):842–845.
3. Hirabayashi Y, Yokosuka S, Miyashita K, et al. Anesthetic management for a patient with
amyloidosis. J Anesth. 1992;6(2):218–221.

ADDITIONAL READING
• Holmes RO, Baethge BA, Edison JD. Amyloidosis. July 2009. Available at:
http://emedicine.medscape.com/article/335414-overview
See Also (Topic, Algorithm, Electronic Media Element)
• Difficult airway

CODES

ICD9
• 277.30 Amyloidosis, unspecified
• 277.39 Other amyloidosis

ICD10
• E85.3 Secondary systemic amyloidosis
• E85.9 Amyloidosis, unspecified

CLINICAL PEARLS
• Anesthesia providers must be aware of the multisystem involvement of amyloidosis and
disease severity which varies between patients. The anesthetic plan must be tailored on a
case-by-case basis with regard to complications that can arise.
• Life-threatening events include unanticipated loss of the airway and hemodynamic
instability resistant to therapy.
AMYOTROPHIC LATERAL SCLEROSIS (ALS)/LOU GEHRIG’S
DISEASE
Christine E. Goepfert, MD, PhD, DESA

BASICS
DESCRIPTION
• Amyotrophic lateral sclerosis (ALS) is a motor neuron disease that involves select upper
motor neurons (UMN) and lower motor neurons (LMN), often with involvement of the
frontotemporal cortex, sensory cortex, and autonomic nervous system.
• ALS manifests as a progressive loss of speech, swallowing, and motor function of the
extremities as well as respiratory muscles.
EPIDEMIOLOGY
Incidence
• In the US: 1.89–2.16 per 100,000/year
• Men > women 1.5:1 in sporadic ALS
• Men = women in familial ALS
• Rapid decrease after 80 years of age
Prevalence
• In the US: 2–5.2 per 100,000
• Peak age at onset: Overall 60 years. This value is usually lower in familial disease.
Morbidity
High risk of postoperative pulmonary complications (PPCs) secondary to the inability to clear
secretions and carbon dioxide retention. The risk increases even further with a vital capacity
that is 50% of predicted levels.
Mortality
• Respiratory failure is the most common cause of death in over 84% of patients.
• Average lifespan after diagnosis: 3–5 years. However, multidisciplinary care can increase
survival.
• Poorer prognosis is associated with bulbar palsy, advanced age.
ETIOLOGY/RISK FACTORS
Multifactorial with complex interaction between genetic and molecular pathways
• Genetic susceptibility: To date, 13 genes and loci have been identified (SOD1, TARDBP, FUS,
ANG, OPTN). Familial ALS has a Mendelian pattern (5–10%).
• Sporadic (SALS): Overlap with neurodegenerative disorders
• Environmental factors: Extensive physical exertion (footballer), active service in US armed
forces, cigarette smoking, neurotoxins (beta-methyl-amino-L-alanine), statins (under
discussion)
PATHOPHYSIOLOGY
The disease process involves glutamate-induced excitotoxicity, oxidative stress, mitochondrial
dysfunction, impaired axonal transport, neurofilament aggregation, intra-cytoplasmic protein
aggregates, inflammatory dysfunction, deficits in neurotrophic factors, and dysfunction of
signaling pathways.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• There is an increased risk of PPCs, and perioperative efforts should aim at maintaining
respiratory muscle strength and avoiding pulmonary aspiration.
• Succinylcholine is absolutely contraindicated; the proliferation of extrajunctional receptors
can result in life-threatening hyperkalemia.

PREOPERATIVE ASSESSMENT
SYMPTOMS
Clinical hallmark is the presence of UMN and LMN features, involving brainstem and spinal
cord regions:
• Spinal onset in 75% (limbs, most common)
• Bulbar onset in 25%
• Initial trunk or respiratory involvement in 5%
• Atypical onset: Weight loss, cramps without muscle weakness, cognitive dysfunction
History
Duration and progression: The median time to diagnosis is ∼14 months due to the insidious
onset.
Signs/Physical Exam
• Pulmonary: Observation of breathing, respiratory rate; auscultation; swallowing; coughing;
salivation
• Neurologic exam
TREATMENT HISTORY
• Supportive, palliative, and multidisciplinary management has been demonstrated to
decrease the risk of death by 45% at 5 years. Symptomatic treatment is the cornerstone and
involves:
– Noninvasive ventilation: Prolongs survival and improves quality of life
– Diaphragmatic pacing (DPS)
– Invasive ventilation via tracheostomy (avoided in most patients)
– Gastrostomy tube
– Nutrition (50–60% of patients are hypermetabolic)
MEDICATIONS
• Riluzole (glutamate antagonist): Only drug shown to extend survival by ~2–3 months
– Most common side effects: Fatigue, nausea
– ALT/SGPT levels rise in about 50% of patients.
– Decreased lung function
– Less common: Neutropenia, pain, dizziness, anorexia
– Overdose: Encephalopathy with stupor/coma, methemoglobinemia
• Common medications for symptomatic care:
– Glycopyrronium, atropine, hyoscyamine
– N-acetylcysteine
– Benzodiazepines such as lorazepam
– Dextromethorphan and quinidine
– Baclofen and tizanidine
– Anticonvulsants, e.g., carbamazepine
– Opioids, e.g., morphine, in late state
– Antidepressants, e.g., amitriptyline or SSRI
– Modafinil
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• CBC to assess for neutropenia from riluzole
• Liver enzymes, especially ALT (affected by riluzole)
• ABG to assess for hypercarbia
• Pulmonary function tests
– Spirometry: FVC
– Maximum inspiratory pressure, sniff nasal inspiratory pressure of <40 cm H2O
• Polysomnography/nocturnal pulse oximetry: Desaturation, increased partial pressure of
carbon dioxide
• Electrophysiology: Nerve conduction, EMG, TMS, SEP
• Muscle ultrasound
• PET, MRI to exclude ALS mimics
CONCOMITANT ORGAN DYSFUNCTION
• Motor system:
– Respiratory muscles:
Caudal cranial nerve (bulbar) palsy: Dysphagia, loss of tongue mobility, impaired cough,
swallow, gag reflex, dysarthria, or slurred/nasal speech
Weakness of respiratory muscles: Dyspnea, orthopnea, desaturation, or cyanosis
– Limbs:
Muscle weakness (“lateral sclerosis”, refers to anterior and lateral corticospinal tracts
replaced by gliosis) and atrophy (“amyotrophy") that starts distally and occurs more
frequently in the upper extremities
Fasciculations and cramps
Hyperreflexia and spasticity
• Sensory system, often subclinical:
– Dysesthesia, pain and temperature, vibration and position
– Autonomic impairment (in 20%), often sympathetic hyperactivity
• Neuropsychiatric symptoms:
– Executive dysfunctions (frontal lobe) in 30–50%: Attention, disinhibition, decision making
– Frontotemporal dementia in 5–15% with profound personality changes
– Pseudobulbar affect: Emotional lability, pathologic laughter, and crying
– Memory disturbance (temporal lobe)
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Critically reassess indication for surgery
• Contemplate exclusion from surgery if the FVC is below 45% predicted; predicts the
possibility of failure to extubate
CLASSIFICATIONS
• El Escorial Diagnostic Criteria: Physical examination, electromyography; neuroimaging to
exclude other diseases
• Awaji Criteria: More sensitive for early diagnosis
• ALS Functional Rating Scale (ALSFRS): Activities of daily living

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Review concomitant medication and potential interactions with anesthetics
• Caution with benzodiazepines is warranted (additive effect on respiratory depression).
Alternatively, consider use of alpha 2-agonists such as clonidine, dexmedetomidine.
• Consider starting NPPV if the FVC is <50% to accustom the patient prior to surgery.
Special Concerns for Informed Consent
• Executive function may be impaired in up to 50% of patients; consent may be necessary
from a power of attorney/family member.
• Discuss potential postoperative respiratory failure: ICU stay, weaning failure, and/or
tracheostomy. There is a considerable increase in respiratory complications with repeated
general anesthesia/surgery.
• Patient autonomy and the right of the patient to refuse or withdraw any treatment,
including mechanical ventilation, should be respected.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Regional techniques, including epidural anesthesia, may be considered in individual cases
after careful assessment of risks and benefits (“double-crush” phenomenon vs. respiratory
problems).
• General anesthesia
– May exacerbate respiratory insufficiency significantly
– Choose short-acting drugs, if possible
Monitors
• Standard ASA monitors
• Advanced monitoring should be guided by concomitant diseases and surgery.
Induction/Airway Management
• Opioids and sedatives of choice; avoid excessive sedation
• Succinylcholine is absolutely contraindicated due to denervated muscles and the
proliferation of extrajunctional receptors. Can cause hyperkalemia.
• Risk of arterial hypotension due to suppression of sympathetic stimulation; have
vasopressors available.
Maintenance
• Any hypnotic agent may be utilized.
• Opioids: Any opioid may be administered; however, remifentanil is specifically
advantageous:
– Metabolism is independent of liver function (riluzole).
– Very short half-life
– High dosages can provide deep levels of anesthesia that preclude the need for muscle
relaxants.
• Muscle relaxants:
– Caution with all non-depolarizing muscle relaxants since they may cause prolonged and
pronounced neuromuscular blockade; consider low-dose cisatracurium.
– Contemplate alternatives, if feasible, such as use of topical lidocaine, deep intubation, or
use of an LMA
– If used, neuromuscular monitoring is mandatory.
– Anticholinesterases should be used and properly dosed to ensure adequate reversal.
• Adequate hydration
Extubation/Emergence
• Patient may not meet extubation criteria.
• Laryngospasm

POSTOPERATIVE CARE
BED ACUITY
• Routinely monitored overnight due to the risk of apnea; the outpatient setting is not
recommended even for minor procedures.
• ICU bed if necessary; patient may require prolonged postoperative ventilation.
MEDICATIONS/LAB STUDIES/CONSULTS
• Respirometer, vital capacity
• ABG to assess for hypercarbia (may present as confusion or sedation)
• The routine use of oxygen is not recommended due to the instability of the respiratory drive.
• Continue NPPV if the patient was on NPPV before
• Communication is often difficult (dysarthria, dementia): Organize a primary caregiver who
is often better able to communicate.
• Pulmonology consult recommended
COMPLICATIONS
• Arterial hypotension
• No risk for malignant hyperthermia with common triggering agents
• Respiratory complications:
– Hypercarbia
– Increased risk for pneumonia due to aspiration and immobility

REFERENCES
1. Onders RP, Carlin AM, Elmo M, et al. Amyotrophic lateral sclerosis: The Midwestern
surgical experience with the diaphragm pacing stimulation system shows that general
anesthesia can be safely performed. Am J Surg. 2009;197(3):386–390.
2. Paek CM, Yi JW, Lee BJ, et al. No supplemental muscle relaxants are required during
propofol and remifentanil total intravenous anesthesia for laparoscopic pelvic surgery. J
Laparoendosc Adv Surg Tech A. 2009;19(1):33–37.
3. Bedlack RS. Amyotrohic lateral sclerosis: Current practice and future treatment. Curr Opin
Neurol. 2010;23:524–529.
4. Cavallucci V, D’Amelio M. Matter of life and death: The pharmacological approaches
targeting apoptosis in brain diseases. Curr Pharm Des. 2011;17(3):215–229.
5. Kieman MC, Vucic S, Cheah BC, et al. Amyotrophic lateral sclerosis. Lancet. 2011;377:942–
955.
6. Wijesekera LC, Leigh PN. Amyotrophic lateral sclerosis. Orphanet J Rare Dis. 2009;4:3.
See Also (Topic, Algorithm, Electronic Media Element)
• Postoperative pulmonary complications
• Tracheostomy

CODES

ICD9
335.20 Amyotrophic lateral sclerosis

ICD10
G12.21 Amyotrophic lateral sclerosis

CLINICAL PEARLS
• Despite significant recent advances in knowledge about ALS, treatment is still focused on
improvement of quality of life.
• Respiratory failure is by far the most common cause for death in ALS patients and is
exacerbated by surgery and anesthesia.
• General anesthesia is usually preferred.
• Succinylcholine is absolutely contraindicated, and nondepolarizing neuromuscular blockade
needs to be monitored very closely.
ANAEROBIC METABOLISM
Amar M. Bhatt, MD
Ravi S. Tripathi, MD

BASICS
DESCRIPTION
• Anaerobic metabolism is the body’s mechanism of continually responding to stress and
sustaining life-preserving measures during malperfusion, until favorable conditions are
resumed.
• The human body’s major source of energy comes from the consumption of glucose via
aerobic methods:
– Aerobic metabolism: Occurs when there is an adequate delivery of oxygen. The O2
molecule functions as an electron acceptor to produce a maximal amount of energy in the
form of ATP (adenosine triphosphate).
– Anaerobic metabolism: Occurs during times of malperfusion and oxygen supply–demand
mismatch. The body generates ATP via a rapid, oxygen-free variation of glycolysis with
lactate as a byproduct (the Pasteur Effect).
PHYSIOLOGY PRINCIPLES
• ATP is a nucleotide that provides chemical energy for all cells in the body; it is produced via
carbohydrate (primarily) and non-carbohydrate metabolism.
• Aerobic metabolism (oxygen-dependent) occurs via metabolism of glucose within the
cytoplasm and mitochondria; each molecule of glucose is capable of producing 36 ATP.
– Glycolysis: Glucose is a 6-carbon structure that is first broken down into pyruvate, a 3-
carbon structure. This process takes place in the cytoplasm and results in the net
production of 2 ATP.
– Citric acid cycle (Krebs’ cycle): Using the pyruvate molecules and available oxygen, the
citric acid cycle generates 2 additional ATP per original glucose molecule via an 8-step
process and 18 different enzymes. In addition, this also generates NADH, FADH2, and
other byproducts (e.g., GTP) that can be converted to ATP.
– Oxidative phosphorylation: NADH and FADH2 are metabolized in the mitochondria to
create an additional 24 molecules of ATP per original glucose molecule. This occurs via
oxidative phosphorylation (the electron transport chain), driven by a proton gradient.
• Gluconeogenesis: In the absence of readily available supplies of glucose, the body is able to
use non-carbohydrates (e.g., lactate, glycerol, and certain amino acids or fatty acids) to
generate glucose. Gluconeogenesis takes places via enzymes found in the cytoplasm and
mitochondria of hepatic cells; liver dysfunction or failure can, thus, result in hypoglycemia
and require supplemental dextrose solutions.
• Glycogenolysis: The body can also convert complex carbohydrates, such as glycogen, to
glucose. This pathway occurs in the liver and muscle; it also requires a functioning liver.
• Anaerobic metabolism (oxygen-independent) occurs when the demand for oxygen is greater
than its supply. For each glucose molecule, only 2 ATP are produced.
– In states where oxygen is reduced/absent, pyruvate is metabolized to lactate via lactate
dehydrogenase as an end-product of anaerobic metabolism (pyruvate lactate
dehydrogenase)
– Physiologic states (exercise): The anaerobic threshold is a theoretical point during
dynamic exercise when muscle tissue switches over to anaerobic metabolism as an
additional energy source.
– Pathologic states: Stress, hypoxia, or hypotension/shock
• Central nervous system: The CNS consumes large amounts of energy to maintain normal
electrical function and cellular metabolism.
– Because it cannot store ATP, it requires a constant supply of both glucose and oxygen
(∼3–3.5 mLO2/100 g/min).
– Anaerobic metabolism can result in a 95% decrease in energy production per available
glucose. This can further worsen ischemic damage.
– It is not capable of utilizing amino acids or fatty acids as alternative sources of energy.
Thus, hypoxia, hypoglycemia, or impaired perfusion can rapidly lead to inadequate energy
levels.
• Myocardium: Due to its demand for a constant source of energy, cardiac muscle is highly
dependent on the aerobic metabolism of fats, carbohydrates, and amino acids. Under
ischemic or hypoxic conditions, the energy liberated by lactate production or anaerobic
metabolism (as compared to aerobic metabolism) is not sufficient for myocardial function
and ventricular contraction.
• Pulmonary: Lactic acidosis stimulates peripheral and central chemoreceptors to augment the
medullary respiratory center. This leads to a compensatory increase in oxygen intake and
excretion of carbon dioxide. As with any change in acid–base homeostasis, the ventilatory
response to acidosis is driven primarily by central chemoreceptors; whereas peripheral
chemoreceptors are primarily affected by hypoxemia.
• Hemoglobin: Acidosis decreases the affinity of hemoglobin for oxygen; it improves oxygen
uploading/delivery to acidotic tissue. This is expressed as a right shift in the oxygen–
hemoglobin dissociation curve.
ANATOMY
Erythrocytes do not possess mitochondria.
DISEASE/PATHOPHYSIOLOGY
• Lactate accumulation occurs during anaerobic metabolism and results in an anion gap
metabolic acidosis.
– An anion gap is a term used to describe "unmeasured anions” (e.g., lactate, ethanol,
uremia, certain toxins, ketones) during states of metabolic acidosis.
– Normal lactate concentrations range from 0.5 to 1.0 mmol/L in healthy individuals and up
to 2.0 mmol/L in the critically ill.
– Base excess is more commonly measured in the perioperative period.
• Perioperative lactic acidosis indicates tissue hypoxia from any combination of the following:
– Hypovolemia (e.g., hemorrhagic shock in a trauma patient)
– Hypoperfusion (e.g., cardiogenic shock following cardiac surgery or myocardial ischemic
events)
– Hypotension (e.g., vasodilatory shock in a septic patient)
– Multifactorial from a combination of the above. For example, a trauma patient suffering
myocardial contusions and a perforated viscus could have a combination of hypovolemia,
hypoperfusion, and hypotension.
• Lactic acidosis leads to several cellular and microvascular changes in tissues (1).
– May aggravate structural damage of neurons and glia in the cerebral cortex
– In an attempt to maintain a normal acid–base environment, cells utilize protein
transporters and enzymes via an active process to maintain a homeostatic concentration of
carbon dioxide, bicarbonate, and protons.
PERIOPERATIVE RELEVANCE
• Hyperlactatemia can result from:
– Increased lactate production (Type A): Due to anaerobic metabolism
– Decreased lactate clearance (Type B): Due to liver disease, hypermetabolic states, and
inhibition of pyruvate dehydrogenase
– Some patients may develop lactic acidosis from both mechanisms (e.g., liver failure and
shock).
– Measuring pyruvate can assist in the differentiation of Type A and Type B lactic acidosis.
A lactate-to-pyruvate ratio >25:1 supports the underlying mechanism of tissue hypoxia
or Type A lactic acidosis.
A normal lactate-to-pyruvate ratio (10:1) supports Type B lactic acidosis.
• Anaerobic metabolism is not an uncommon physiologic derangement seen in the
perioperative arena; it can result when there is a mismatch of oxygen delivery and demand:
– Hypoxia/hypoxemia: Esophageal or mainstem intubation, hypoxic mixture,
hypoventilation, V/Q mismatch, shunt
– Hypoperfusion: Hypotension, hypovolemia, hemorrhage, myocardial impairment, shock
– Vasodilation: Anesthetic medications, neuraxial blocks; anaphylactic or septic shock
• Cardiopulmonary bypass: Lactate is associated with malperfusion (2). It not only allows for
prognostication, but also serves as an indicator of the efficacy of therapies used to restore
tissue perfusion.
– Hyperlactatemia is associated with longer intensive care stays and increased postoperative
ventilatory support, renal dysfunction, infectious complications, and circulatory disorders.
– Titrating therapies to traditional endpoints may not ensure that the microvascular bed is
perfused. For example, a normal or high blood pressure may be a vasoconstrictive
response to a low cardiac output state.
• Septic shock: Hyperlactatemia is typically present in patients with sepsis or septic shock and
the etiology is multifactorial (3).
– Hypovolemia: Septic shock is associated with fluid-responsive physiology. Thus, an
elevated lactate level could indicate a “dry” patient.
– Hypoperfusion: Sepsis is also accompanied by a hypermetabolic state with enhanced
glycolysis. Patients with “normal” filling pressures (e.g., central venous pressure) and
cardiac indices (e.g., cardiac index) may not have adequate oxygen delivery.
– Cytopathic hypoxia: Despite adequate volume status and perfusion, tissue dysfunction at
the cellular level may persist in sepsis and represents impaired cellular function.
– Lactate is a well-established prognostic indicator in sepsis and septic shock. Obtaining
serial serum lactate levels aids in identifying tissue hypoperfusion in patients who are not
hypotensive but are at risk for septic shock; an elevated lactate (>4 mmol/L or 36
mg/dL) likely indicates inadequate oxygen delivery. Early goal-directed therapy should be
considered in patients with sepsis and/or an elevated lactate level.
– As part of the Surviving Sepsis Guidelines, a resuscitation bundle for patients with sepsis
includes, but it is not limited to:
A minimal initial crystalloid bolus of 20 mL/kg or equivalent
Vasopressor therapy to maintain a mean arterial pressure >65 mm Hg
Obtaining blood cultures and administering appropriate antibiotic therapy
Maintaining adequate central venous pressure and central venous oxygen saturation
EQUATIONS
• Glucose + 2 ADP + 2 Pi → 2 Lactate + 2 ATP + 2 H2O
• Pyruvate + NADH + H+ ←→Lactate + NAD+

REFERENCES
1. Cassavaugh J, Lounsbury KM. Hypoxia mediated biological control. J Cellular Biochem.
2010;112(3):735–744.
2. Javidi L. Pathophysiology of lactic acidosis and its clinical importance after cardiac
surgery. Iran J Cardiac Surg. 2008;2:18–24.
3. Dellinger RP, Levy MM, Carlet JM, et al. Surviving sepsis campaign: International
guidelines for management of severe sepsis and septic shock. Crit Care Med.
2008;36:1394–1396.

ADDITIONAL READING
• Chaitman BR. Exercise stress testing. In: Bonow RO, Mann DL, Zipes DP, et al, eds.
Braunwald’s heart disease—a textbook of cardiovascular medicine, 9th ed. Philadelphia, PA:
Saunders/Elsevier, 2011, chap. 14.
• Levy B. Lactate and shock state: The metabolic view. Curr Opin Crit Care. 2006;12(4):315–
321.
• Surviving Sepsis Campaign. www.survivingsepsis.org
See Also (Topic, Algorithm, Electronic Media Element)
• Base excess
• Metabolic acidosis
• Septic shock
• Cardiopulmonary bypass (CPB)

CLINICAL PEARLS
• Lactate production can serve as a marker of anaerobic metabolism and tissue hypoxia.
• When there is concern for adequate oxygen delivery, lactate and base deficit measurements
can serve as markers of adequate tissue perfusion.
ANAPHYLAXIS
Lori Gilbert, MD

BASICS
DESCRIPTION
• An acute, life-threatening reaction with an onset of minutes to hours. It is usually, but not
always, the result of an immunologic mechanism that involves IgE-mast cell or basophil
mediator release; such mediators can include histamine, leukotrienes, and prostaglandins.
• The newest definition of anaphylaxis encompasses 1 of 3 scenarios:
– Acute onset (minutes to hours) of skin and mucosal manifestations, as well as respiratory
compromise, hypotension, or shock
– Signs as above, after exposure to a likely antigen, in addition to GI symptoms
– Hypotension after exposure to a known antigen
EPIDEMIOLOGY
Prevalence
• During anesthesia: Ranges from 1:4,000 to 1:25,000 anesthetics
• Hospital inpatients in the US: 1:3,000; in Europe, the incidence is reported to be much
lower.
• In the US, it is estimated that between 1.25% and 16% of the general population is at risk
for possibly experiencing an episode of anaphylaxis.
Prevalence
• Lifetime prevalence from all triggers: 0.05–2%
• Food triggers: 90% of anaphylaxis cases are caused by milk, soy, eggs, wheat, peanuts, tree
nuts, fish, and shellfish.
Morbidity
• Food allergies account for 30,000 ER visits a year; it is more common among children than
adults.
• Latex anaphylaxis is responsible for >200 cases/year.
Mortality
• In the US: ∼2 in 100,000 anaphylaxis cases
• In the UK: 0.65–2% of anaphylaxis cases
• Risk factors age 10–35 years old: Active asthma, peanut allergy, and delayed administration
of epinephrine
• Risk factors age 55–85 years old: Cardiovascular or respiratory illness, use of antibiotics or
anesthetic agents.
ETIOLOGY/RISK FACTORS
• History of a prior anaphylactic episode remains the most important factor in establishing
cause and risk factors.
• Outpatient setting:
– Drug-induced: Penicillin and other antibiotics, aspirin, and NSAIDs
– IV contrast dye
– Food: Peanuts, tree nuts, fish, shellfish, soy, egg, cow’s milk
– Other: Exercise-induced, idiopathic, insect stings, seminal fluid
• Perioperative setting:
– Neuromuscular blockers (most common)
– Natural rubber latex
– Antibiotics
– Hypnotics (propofol, thiopental)
– Aprotinin
– Bupivacaine
– Radiographic contrast material
– Opioids
– Protamine
– Blood transfusions
– Methylmethacrylate (bone cement; associated with hypotension but no IgE mechanism has
been found)
– Rare causes include etomidate, ketamine, midazolam, and amide local anesthetics.
PHYSIOLOGY/PATHOPHYSIOLOGY
• Anaphylactic and anaphylactoid reactions stem from the systemic release of mediators from
mast cells and basophils. The pathogenesis of anaphylactic reactions involves an
immunologic mechanism in which IgE is created in response to allergen exposure. Receptors
on the surface of mast cells and basophils bind with IgE.
• Re-exposure of the allergen results in activation of IgE-bound mast cells and basophils with
the resultant release of pre-formed mediators that are stored in cellular granules (histamine,
tryptase, heparin, chymase, cytokines). In addition, arachidonic acid is metabolized to
prostaglandins and leukotrienes and also released.
• Anaphylaxis often produces signs and symptoms within minutes of exposure but there are
also biphasic reactions that can occur 1–72 hours after the initial attack.
• Increased vascular permeability is a hallmark of anaphylaxis that allows the transfer of large
amounts of intravascular fluid into the extravascular space within 10 minutes. As a result,
cardiovascular collapse may be the first sign of anaphylaxis with little or no cutaneous or
respiratory signs.
PREVENTATIVE MEASURES
• Primary prevention is based on allergen desensitization through immunotherapy.
• Venom immunotherapy is highly successful in preventing anaphylaxis.
• Pharmacologic prophylaxis (steroids, antihistamines) can be used to help prevent
occurrences to radiographic contrast material, fluorescein, and other dyes.
• For idiopathic anaphylaxis, prophylaxis with daily oral prednisone, combined with H1
antagonists, has resulted in decreased incidence.
• Most importantly, patient education and avoidance of known triggering substances is key in
prevention.
• A “TIME OUT" should be performed prior to any procedure and identify the presence of any
known drug allergies.

PREOPERATIVE ASSESSMENT
• Acute onset of reaction (minutes to hours)
• Cutaneous: Skin, mucosa, or both can present with hives, urticaria, angioedema, pruritus,
flushing, swollen lips and tongue.
• Respiratory: Bronchospasm, wheezing, dyspnea, stridor, reduced peak expiratory flow,
hypoxemia, respiratory arrest
• Cardiovascular: Hypotension or symptoms of end-organ dysfunction (cardiovascular
collapse), tachycardia
• Gastrointestinal: Persistent vomiting, diarrhea
• RAST testing (radioallergosorbent test) detects specific IgE antibodies to suspected or known
allergens. The suspected antigen is bound to an insoluble material and the patient’s serum is
added. If the serum contains antibodies to the allergen, those antibodies bind to the
allergen. Radiolabeled anti-human IgE antibody is added where it binds to those IgE
antibodies already bound to the insoluble material.
• Skin manifestations may be masked by surgical drapes and are not as common in the setting
of general anesthesia as in other settings.
• Bradycardia is, surprisingly, more common with anaphylaxis in the setting of general
anesthesia (not tachycardia).
• Cardiovascular collapse may be the only sign of anaphylaxis.
DIFFERENTIAL DIAGNOSIS
• Acute asthma exacerbation
• Syncope
• Panic attack/anxiety disorders
• Acute generalized hives
• Vocal cord/paradoxical vocal cord dysfunction
• Vasovagal reactions
• Nonimmunologic reactions that involve mechanisms outside of IgE mediation (transfusion
reactions, IgG or IgM antibody-mediated, antigen–antibody complexes and complement)
• Anaphylactoid reactions: The World Allergy Organization has suggested that the term be
eliminated in favor of calling all similar reactions “anaphylaxis.” Generally, the term is used
to describe non-IgE-mediated reactions; the initial treatment is the same, regardless of the
mechanism.
• Cardiovascular disorders: Pulmonary embolism, cardiogenic shock, etc.
• Flushing disorders: Carcinoid, “red-man” syndrome from vancomycin, medullary carcinoma
of the thyroid
• Other: Mastocytosis (systemic mast cell disease [SCMD]) is a clonal disorder characterized
by overproduction of mast cells in different tissues.
• Postprandial syndromes
• Diagnostic tests and interpretation:
– Serum tryptase peaks 60–90 minutes after the onset of anaphylaxis and persists for 6
hours; obtain between 1 and 2 hours after the first symptoms appear.
– Plasma histamine levels begin to rise within 5–10 minutes and remain elevated for 30–60
minutes.
– 24-hour urinary histamine metabolite
– Urinary vanillylmandelic acid to rule out pheochromocytoma and carcinoid syndrome
– Skin tests (or in vitro tests) determine the presence of specific IgE antibodies to foods,
medications (e.g., penicillin).

TREATMENT

• Discontinuation of the inciting factor (e.g., anesthetic agent or drug)


• Place the patient in the recumbent position (pertinent if antibiotics or medication is being
given on the floor or preoperative holding area)
• ABC’s: Manage airway, delivery 100% oxygen, and intubate (if appropriate)
• Rapid IV fluid replacement
• Epinephrine is the most important aspect of treatment for anaphylaxis and should be
administered immediately:
– IV: 5–10 mcg boluses
– IV drip: 1 mcg/min
– SQ: 200–500 mcg q5 minutes (aqueous 1:1,000 dilution which is equivalent to 1 mg/mL
or 0.2–0.5 mL)
– IM: 200–500 mcg into the vastus lateralis, or lateral aspect of the thigh (aqueous 1:1,000
dilution which is equivalent to 1 mg/mL or 0.2–0.5 mL)
– Cardiopulmonary arrest during anaphylaxis: 1–3 mg IV over 3 minutes, followed by 4–10
mcg/min infusion
– Severe or refractory anaphylaxis that is unresponsive to epinephrine has been reported
with patients on beta-blockers; it has been characterized by bradycardia, profound
hypotension, and severe bronchospasm; consider treating with glucagon 1–5 mg IV over 4
minutes, followed by an infusion of 5–15 mcg/min.
• Histamine 1 blocker. Diphenhydramine 1–2 mg/kg or 25–50 mg IV dose.
• Histamine 2 blockers. Ranitidine 50 mg IV diluted in 5% dextrose (total volume of 20 mL)
can be administered over 5 minutes. Alternatively, cimetidine 4 mg/kg IV may be given.
• Inhaled beta-2 agonists if bronchospasm is present
• Glucocorticoids are not helpful acutely but potentially can help prevent recurrences and
shorten the duration of attack.
• Monitors: Large-bore IV access, if not already in place, should be placed. Arterial line
placement can aid with monitoring blood pressure (particularly if chest compressions);
however, it should not interfere with immediate resuscitation with IV fluids and
epinephrine.

FOLLOW-UP
• Biphasic anaphylaxis can occur in up to one-fourth of episodes, and symptoms may recur
within hours after apparent resolution of initial presentation.
• Following resolution of the initial episode, patients should be provided with an epinephrine
pen and instructions for administration as well as instructions to go to the nearest
emergency room at the first hint of recurrence of symptoms.
• Patients should also be referred to an allergist/immunologist for further workup, possibly
including skin testing and desensitization, if appropriate.

REFERENCES
1. ieberman P, Nicklas R, Oppenheimer J, et al. The diagnosis and management of
anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol. 2010;126:477–480.
2. Hepner D, Castells M. Anaphylaxis during the perioperative period. Anesth Analg.
2003;97:1381–1395.
3. Estelle F, Simons R. Anaphylaxis. J Clin Immunol. 2010;S161–S180.
4. Kemp S, Lockey R. Anaphylaxis: A review of causes and mechanisms. J Allergy Clin
Immunol. 2002;110(3):341–348.
5. Leiberman P. Anaphylactic reactions during surgical and medical procedures. J Allergy
Clin Immunol. 2002;110(2):s64–s69.
6. Matasar M, Neugut A. Epidemiology of anaphylaxis in the United States. Curr Allergy
Asthma Rep. 2003;3:30–35.

ADDITIONAL READING
• www.aaaai.org
• www.acaai.org
• www.aafa.org
See Also (Topic, Algorithm, Electronic Media Element)
• Latex allergy

CODES

ICD9
• 995.0 Other anaphylactic reaction
• 995.60 Anaphylactic reaction due to unspecified food

ICD10
• T78.00XA Anaphylactic reaction due to unspecified food, init encntr
• T78.2XXA Anaphylactic shock, unspecified, initial encounter
• T78.2XXD Anaphylactic shock, unspecified, subsequent encounter

CLINICAL PEARLS
• Epinephrine, patient position, and oxygen are the most important therapeutic modalities in
treating anaphylaxis. Treatment (in order of importance) includes:
– Epinephrine
– Patient position (recumbent)
– Oxygen
– IV fluids
– Nebulized beta-2 agonists
– Vasopressors
– Antihistamines
– Corticosteroids
• Propofol and egg allergy: This topic has been a source of some controversy among
anesthesia providers. Propofol is formulated in a lipid emulsion containing soybean oil,
glycerol, egg lecithin, and disodium edetate with sodium hydroxide to adjust for pH.
– The egg lecithin component is a highly purified egg yolk component. The principal protein
of eggs is ovalbumin which is present in the egg white. Most egg allergies are related to
the egg white (albumin) and not the egg yolk (lecithin).
– Most allergic-type reactions to propofol are nonimmunologic because propofol can cause
direct stimulation of histamine release.
– Skin testing of egg-allergic patients is not consistent with allergies to propofol.
– However, there are case reports in the literature of anaphylaxis associated with propofol
in egg-allergic individuals.
– Furthermore, the propofol package insert monograph clearly states under
contraindications: “Propofol Injectable Emulsion is contraindicated in patients with
allergies to eggs, egg products, soybeans or soy products.”
• It is the author’s opinion that if propofol can be avoided in egg-allergic individuals, then an
appropriate substitute should be used. If propofol cannot be avoided, epinephrine, large-
bore IV access, and resuscitation equipment should be readily available.
ANEMIA
Gregory M. T. Hare, MD, PhD
Katerina Pavenski, MD, FRCPC

BASICS
DESCRIPTION
• Anemia is defined as a hemoglobin concentration <12 g/dL in females and <13 g/dL in
males.
• Red blood cells (RBCs) with normal functioning hemoglobin (Hg) are essential for delivering
oxygen to tissues. They also contribute to blood viscosity and may aid in hemostasis.
EPIDEMIOLOGY
Prevalence
• Highly variable and dependent on the etiology and patient demographics (1)
• 11–76% of patients may present with preoperative anemia. Postoperative anemia may be
present in up to 90% of patients undergoing major surgery (2,3).
Prevalence
An estimated 25% of the world’s population is anemic from nutritional, infectious,
malignancy, and genetic causes. Iron deficiency is the most common type of anemia
worldwide, and accounts for ∼50% of all cases (4).
Morbidity
Acute and chronic anemia is associated with an increased risk of stroke, myocardial
infarction, and renal injury in specific patient populations (2,5). Anemia is associated with
increased perioperative morbidity and higher likelihood of requiring an allogeneic transfusion
which is in turn associated with prolonged hospital stay and postoperative infections (6), and
increased risk of mortality (2).
Mortality
Preoperative anemia is an independent risk factor for mortality and is associated with a
greater likelihood of requiring allogeneic blood transfusion which has also been linked to
increased mortality in surgical and critical care patients (2).
ETIOLOGY/RISK FACTORS
• Decreased or impaired production
– Nutritional deficiencies (iron, folate, vitamin B12)
– Reduced erythropoietin (EPO) production due to renal failure
– Bone marrow causes: Aplastic anemia, dysplasia/cancer, or fibrosis
– Chronic inflammation (also known as anemia of chronic disease [ACD])
• Increased destruction (hemolysis)
– Intrinsic to RBCs
Membrane disorders
Hemoglobinopathies: Sickle cell disease, thalassemia
Enzyme deficiencies
– Extrinsic to RBCs
Immune (allo or autoantibody mediated)
Microangiopathy (disseminated intravascular coagulation, thrombotic thrombocytopenic
purpura)
Macroangiopathy (leaky valve)
– Infections (malaria)
Other (burns)
• RBC loss
– Bleeding (GI bleeding, menorrhagia, surgery, etc.)
– Blood donation
• RBC sequestration (related to splenomegaly)
• Dilution
– Iatrogenic (e.g., resuscitation with crystalloid)
– Pregnancy
PHYSIOLOGY/PATHOPHYSIOLOGY
• The mechanisms of anemia-induced morbidity and mortality have not been clearly
established. However, inadequate blood oxygen content and tissue oxygen delivery likely
contribute (2,7).
• Iron deficiency can result from poor nutritional intake, increased requirements (childhood,
pregnancy, breastfeeding), chronic blood loss, and impaired absorption (1).
• Vitamin deficiency can result from poor oral intake, impaired absorption or increased
requirements (e.g., folate deficiency in hemolysis).
• Renal failure leads to impaired EPO production which in turn results in anemia.
• ACD is a result of chronic inflammation. Pro-inflammatory mediators and RES cells induce
changes in iron homeostasis, proliferation of erythroid progenitor cells, production of EPO,
as well as affect the life span of red cells leading to anemia.
• Hemolytic anemia is a result of impaired red cell survival due to a variety of factors, and
can be either hereditary or acquired.
• Malignancy, both hematological and solid, may lead to anemia due to tumor occupying the
bone marrow, or bone marrow suppression resulting from the treatment of malignancy
(irradiation, chemotherapy) or from ACD.
• In addition to iron deficiency, pregnancy leads to increased plasma volume and dilutional
anemia. Dilutional anemia may also result from aggressive crystalloid resuscitation of
patients who present with bleeding.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Each unit of transfused RBCs increases the Hg level by ∼1 g/dL and Hct by 3%.
• The decision to transfuse should not be based solely on Hg level; the clinical situation must
be taken into account. Most guidelines recommend transfusion for a euvolemic Hg <6.5
g/dL. Transfusion is almost never indicated for a euvolemic Hg level >10 g/dL. The area
between 6.5 and 10 dg/L is a gray zone, and the decision to transfuse should depend upon
clinical circumstances including ongoing blood loss, presence of relevant comorbidities,
symptoms of anemia, and signs indicative of inadequate oxygen delivery or hemodynamic
instability.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Fatigue, lightheadedness, syncope, impaired mentation
• Palpitations
• Shortness of breath and/or chest pain on exertion
• Jaundice, dark urine, gallstones (suggestive of hemolytic anemia)
History
• History of anemia, investigations, and treatments to date
• History of chronic inflammatory conditions (lupus, arthritis)
• History of major organ dysfunction: Kidney, heart, liver, lungs
• Illicit drugs and alcohol intake
• History of cancer and its treatment
• History of chronic blood loss
• History of GI disorders and surgery
• Known diagnosis of hereditary RBC disorder
Signs/Physical Exam
• Pale conjunctivae
• Tachypnea, tachycardia, systolic murmur, signs of CHF
• Masses, lymphadenopathy, organomegaly
TREATMENT HISTORY
Iron, erythropoiesis-stimulating agents (ESA), Vitamin B12, folate, transfusions
MEDICATIONS
Medications with myelotoxic potential: Immunosuppressive agents (e.g., Imuran),
chemotherapy (e.g., cyclophosphamide), anticonvulsants, etc.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Hg, RDW, MCV (mean corpuscular volume). A low MCV (microcytic anemia) may indicate
iron deficiency anemia (IDA) or thalassemia. A high MCV may be suggestive of vitamin B12
or folate deficiency, liver disease, and excessive alcohol intake.
• Reticulocyte count reflects the adequacy of bone marrow compensation for anemia. A low
reticulocyte count in the face of significant anemia suggests either a lack of hematinics or a
bone marrow problem.
• Blood film
• Ferritin, serum iron, TIBC, iron saturation. A low ferritin and iron saturation point to iron
deficiency anemia (IDA). Note: Ferritin is an acute phase reactant, and may not be an
accurate marker of iron stores in a patient with chronic inflammation.
• Soluble transferrin receptor may help differentiate between IDA and ACD. A low-soluble
transferrin receptor is indicative of ACD.
• Folate, vitamin B12
• CRP is a marker of inflammation, and may be helpful in assessing patients with suspected
ACD.
• Standard biochemistry tests, such as creatinine, transaminases, and bilirubin, are useful to
determine the presence or extent of either renal or liver disease.
CONCOMITANT ORGAN DYSFUNCTION
Concomitant lung or heart disease may lower the body’s ability to compensate for anemia.
These patients may have symptoms of anemia at higher Hg levels than their healthy peers.
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Symptoms of impaired oxygen delivery to the cerebral or myocardial system
• If significant anemia (Hg <10 g/L) is present and surgery could be safely postponed, a
patient should undergo evaluation by an internist or hematologist and treated for anemia
prior to surgery. This is especially true for patients who will be undergoing high blood loss
procedures, have a rare blood type, or significant alloimmunization against RBC antigens, or
those who object to blood transfusion for religious reasons.
CLASSIFICATIONS
• Morphological: Microcytic, macrocytic, normocytic
• Kinetic: Decreased RBC production, increased RBC destruction, increased RBC loss,
sequestration and dilution

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Attempt to correct anemia with hematinics (vitamins or minerals) and ESA as necessary (8)
• If there is significant anemia and surgery is urgent (e.g., there is no time to institute blood
conservation measures or see their benefit), an allogeneic RBC transfusion may be
necessary.
• Consider administration of antifibrinolytic agents (e.g., tranexamic acid) and topical
hemostatic agents to reduce blood loss
Special Concerns for Informed Consent
• Discuss the possibility of blood product transfusion and describe associated risks
• Describe risks and benefits of the proposed blood conservation measures (e.g.,
thromboembolic risk with ESA)
INTRAOPERATIVE CARE
Choice of Anesthesia
Depends on the surgical procedure. The sympatholysis from neuraxial techniques may be
profound.
Monitors
Standard ASA monitors
Induction/Airway Management
Prepare for hypotension
Maintenance
• Blood loss intraoperatively is whole blood loss. Laboratory values may not reflect this
initially until volume replacement has occurred.
• Assess blood loss on laps, sponges, drapes, floor, as well as the suction canister
• Consider cell salvage
• Avoid hypothermia
• Use point of care testing (if available and appropriate) to guide hemotherapy
Extubation/Emergence
Postoperative intubation and ventilator support may be considered when large volume shifts
and transfusion have taken place.

FOLLOW-UP

BED ACUITY
Not applicable
MEDICATIONS/LAB STUDIES/CONSULTS
• Follow Hg levels closely, as well as symptoms and bleeding; consider transfusion as
appropriate. Over-transfusion should be avoided; in stable patients, transfuse 1 unit at a
time followed by reassessment.
• Eliminate unnecessary blood draws; collect samples into pediatric tubes.
• Consider consulting hematology or the blood conservation service to assist with iron
supplementation and other medical therapy for optimization of Hg.
• Do not forget about appropriate thromboprophylaxis especially for those patients who have
received ESA and tranexamic acid (TXA) perioperatively.

REFERENCES
1. de Benoist B, McLean E, Egli I, et al., eds. Worldwide prevalence of anaemia 1993–2005.
2. Geneva, Switzerland: World Health Organization, 2008.
3. Shander A, Javidroozi M, Ozawa S, et al. What is really dangerous—anemia or transfusion.
Br J Anaesth. 2011;107(Suppl 1):i41–i59.
4. Beris P, Munoz M, Garcia-Erce JA, et al. Perioperative anaemia management: Consensus
statement on the role of intravenous Iron. Br J Anaesth. 2008;100:599–604.
5. Stoltzfus RJ. Iron deficiency: Global prevalence and consequences. Food Nutr Bull.
2003;24:S99–S103.
6. Hare GMT, Baker JE, Pavenski K. Assessment and treatment of preoperative anemia. Can J
Anaesth. 2011;58:569–581.
7. Freedman J, Luke K, Escobar M, et al. Experience of a network of transfusion coordinators
for blood conservation (ONTraC). Transfusion. 2008;48:237–250.
8. Tsui AK, Dattani ND, Marsden PA, et al. Reassessing the risk of hemodilutional anemia:
Some new pieces to an old puzzle. Can J Anaesth. 2010;57:779–791.
9. Pasricha SR, Flecknoe-Brown SC, Allen KJ, et al. Diagnosis and management of iron
deficiency anaemia: A clinical update. Med J Aust. 2010;193:525–532.
See Also (Topic, Algorithm, Electronic Media Element)
• Blood oxygen carrying capacity
• Mixed venous oxygen saturation
• Transfusion related lung injury (TRALI)
• Transfusion infections

CODES

ICD9
• 280.9 Iron deficiency anemia, unspecified
• 284.9 Aplastic anemia, unspecified
• 285.9 Anemia, unspecified

ICD10
• D50.9 Iron deficiency anemia, unspecified
• D61.9 Aplastic anemia, unspecified
• D64.9 Anemia, unspecified

CLINICAL PEARLS
• Transfuse actively bleeding patients more aggressively than non-bleeding patients
• Use all aspects of clinical analysis to support your decision to transfuse
• Treat and diagnose anemia prior to elective surgery to avoid risk of anemia and transfusion
ANEMIA OF PREMATURITY
Alberto J. De Armendi, MD, AM, MBA
Nina Singh-Radcliff, MD

BASICS
DESCRIPTION
• The physiologic nadir of hemoglobin in newborns occurs at 8–12 weeks. It is the result of a
decrease in erythropoietin in response to the transition from a relatively hypoxic state in
utero to a hyperoxic state in room air. It is usually asymptomatic and gradually increases to
adult values within the first 2 years of birth.
• Anemia of prematurity (AOP), however, is a pathologic and exaggerated response to
decreased erythropoietin seen in premature infants (<37 weeks).
– Reduced hemoglobin, with lowest hemoglobin levels 6–7 g/dL in extremely low birth
weight (ELBW) infants
– Signs and symptoms of anemia manifest
– Independent risk factor related to apnea
– Spontaneous resolution by 6 months of age
– Starts earlier and lasts longer than in normal newborns
– Normocytic and normochromic red blood cells (RBCs)
• This patient population is at-risk for several other causes of anemia, including shortened
RBC life span and enhanced blood loss. Thus, the premature infant’s impaired ability to
increase erythropoietin levels further compounds the levels of anemia.
EPIDEMIOLOGY
Incidence
• Inversely proportional to:
– Gestational age
– Birth weight
• Advancements in technology have resulted in a new group of preterm infants that previously
could not survive; thus increasing the incidence of AOP.
Prevalence
• No sex prevalence
• No race prevalence
Morbidity
• Secondary to transfusions: Immune-related and infectious
• Apnea
• Poor feeding/decreased weight gain
Mortality
In general, mortality is increased in premature infants 42 per 1,000 (compared to term infants
1.8 per 1,000)
ETIOLOGY/RISK FACTORS
• Decreased RBC production that can be associated with prematurity (1,3,4).
– Inadequate synthesis of erythropoietin in response to hypoxia that results in suboptimal
erythropoiesis.
– Nutritional deficiencies: Iron, folate, protein, B12
• Decreased RBC life span that can be associated with prematurity (increased destruction):
– Immune hemolytic anemia: Rh or ABO incompatibility, maternal autoimmune disorders,
drug-induced
– Enzyme abnormalities: Glucose-6-phosphate dehydrogenase deficiency, pyruvate kinase
deficiency
– RBC membrane defects: Spherocytosis, stomatocytosis
– Hemoglobinopathies: Thalassemia
• Increased blood loss that can be associated with prematurity
– Frequent laboratory testing in critically ill infants (iatrogenic) can exacerbate AOP and
increase the need for transfusions.
– Fetomaternal or fetoplacental hemorrhage
– Placenta previa, placental abruption
– Internal bleeding: Intracranial, intra-abdominal, pulmonary
PATHOPHYSIOLOGY
• The fetal environment has several adaptations to accommodate the degree of hypoxia and
maximize oxygen delivery to the brain and heart (3,5).
– Hypoxic pulmonary vasoconstriction is maintained through decreased production of nitric
oxide (minimal pulmonary blood flow with oxygenation and ventilation occurring at the
placenta).
– High pulmonary artery pressures lead to high right heart pressures. This maintains the
right-to-left shunt through the foramen ovale (FO).
– Increased circulating prostaglandins that maintain the patency of the ductus arteriosus
(DA) and the ductus venosus (DV).
– Fetal hemoglobin has a strong affinity for oxygen to facilitate efficient extraction across
the placenta. The P50 is ∼19 mm Hg, compared to adult hemoglobin (∼27 mm Hg).
• Transition to the extrauterine environment involves decreased shunting secondary to
increased oxygen tensions and rapid right and left heart pressure changes. With the
neonate’s first several breaths, circulating oxygen tensions rise rapidly with resultant
increases in bradykinin and nitric oxide and decreased pulmonary vascular resistance; blood
flow increases through the pulmonary vasculature. Additionally, circulating prostaglandins
decrease rapidly and result in closure of the ductus arteriosus. The relatively hyperoxic
environment suppresses erythropoietin production (3).
• Erythropoietin: In utero, it is produced by the liver and kidneys in response to transcription
factor hypoxia inducible factor-1 (HIF-1). In the premature infant, it is believed that there is
a relative insensitivity by the hepatic oxygen sensor to hypoxia and anemia, resulting in
inadequate synthesis of HIF-1.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Delay surgery, if possible. When surgery must proceed, consider blood transfusion prior to
arrival to the operating room or during the case. Type and cross matched, leukocyte-
reduced, and CMV-negative blood should be administered.
• Minimize laboratory blood draws to those absolutely needed; additionally, decrease the
volume drawn
• Maintain a thermoneutral environment. The combination of cold and hypoxia can result in
patent ductus arteriosus (PDA) shunting.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Apnea
• Poor weight gain
• Difficulty feeding
• Decreased activity
History
• Apnea history
• Feeding history
• Weight gain history
• Retinopathy of prematurity (ROP)
Signs/Physical Exam
• Tachypnea
• Tachycardia
• Pallor
• Decreased activity
• Flow murmurs
• Distended abdomen
TREATMENT HISTORY
• Transfusions: Indications and guidelines are nonspecific, including hemoglobin levels,
apnea, bradycardia, poor weight gain, ventilator needs. Packed RBCs should be CMV-
negative and leukocyte-reduced.
• Placental RBC transfusion: Umbilical cord blood may decrease the need for non-autologous
blood transfusion. However, studies cite limitations to this method, such as insufficient
volumes collected, clotting, hemolysis, contamination, and cost.
• Reduced RBC drawing and utilization of tubes with fill-lines (allow close approximation of
the volumes needed for testing)
• Observation
MEDICATIONS
• Supplemental vitamins
– Iron
– Vitamin E
– Vitamin B12
– Folic acid
• Recombinant erythropoietin: The primary pathophysiology of AOP is an impaired ability to
increase erythropoietin production; thus, exogenous administration can be an effective
therapeutic modality. Studies have suggested that when administered early, it can reduce
the use of RBC transfusion. However, concerns have been raised that there is an increased
incidence of ROP.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
Hemoglobin/hematocrit levels
CONCOMITANT ORGAN DYSFUNCTION
Issues with prematurity, including
• Neurologic: Intraventricular hemorrhage, hydrocephalus
• Retinopathy of prematurity
• Cardiac: PDA
• Respiratory: Bronchopulmonary dysplasia, respiratory distress requiring ventilatory support,
apnea of prematurity
• Gastrointestinal: Necrotizing enterocolitis, perforation, inguinal hernia (incarceration),
history of re-anastomosis or fundoplication
• Sepsis
CIRCUMSTANCES TO DELAY/ CONDITIONS
Need optimization of hemoglobin/hematocrit prior to arrival in the operating room.
CLASSIFICATIONS
Gestational age and birth weight are indirectly related to occurrence of AOP.
• Low birth weight (LBW): <2,500 g, 36–37 weeks gestational age
• Very low birth weight (VLBW): <1,500 g, 31–36 weeks gestational age
• ELBW: <1,000 g, 24–30 weeks gestational age

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Blood transfusion, as appropriate
• May give atropine (20 mcg/kg) to prophylax against bradycardia
Special Concerns for Informed Consent
• Parental consultation for postoperative ventilatory support
• Risk of hypothermia, ROP, blood transfusions
INTRAOPERATIVE CARE
Choice of Anesthesia
Dependent on surgical procedure
Monitors
• Standard ASA monitors, with 2 pulse oximeters for preductal and postductal measurements
• Precordial stethoscope
• Urinary Foley catheter may be considered when blood transfusion is expected.
Induction/Airway Management
Majority of cases will arrive intubated to the OR.
Maintenance
• Avoid hypoxia, hypothermia, and increased airway pressures that can increase pulmonary
vascular pressures and favor right-to-left shunting.
• Avoid administering high FIO2 (retinopathy of prematurity)

Extubation/Emergence
Patients who were intubated on arrival will usually return to the neonatal intensive care unit
(NICU) intubated.

POSTOPERATIVE CARE
BED ACUITY
NICU
MEDICATIONS/LAB STUDIES/CONSULTS
• Iron
• Caffeine 10 mg/kg (2)
• Minimal laboratory requirements except monitoring of hemoglobin levels
COMPLICATIONS
• Transfusion related:
– Fluid overload
– Electrolyte imbalance
– Hypothermia
– Infectious
– Immune-related

REFERENCES
1. Peiris K, Fell D. The prematurely born infant and anesthesia: Continuing education in
anaesthesia. Crit Care Pain. 2009;9(3):73–77.
2. Welborn LG, Greenspan JC. Anesthesia and apnea: Perioperative considerations in the
former preterm infant. Pediatr Clin North Am. 1994;41(1):181–198.
3. Aher S, Malwatkar K, Kadam S. Neonatal anemia. Semin Fetal Neonatal Med.
2008;13(4):239–247.
4. Salsbury DC. Anemia of prematurity. Neonatal Netw. 2001;20(5):13–20.
5. Widness JA. Pathophysiology of anemia during the neonatal period, including anemia of
prematurity. Neoreviews. 2008;9(11):e520.

ADDITIONAL READING
• Ohisson A, Aher SM. Early erythropoietin for preventing red blood cell transfusion in
preterm and/or low birth weight infants. Cochrane Database Syst Rev. 2006;3:CD004863.
See Also (Topic, Algorithm, Electronic Media Element)
• Retinopathy of prematurity
• Hemoglobin

CODES

ICD9
776.6 Anemia of prematurity

ICD10
P61.2 Anemia of prematurity

CLINICAL PEARLS
• Anemia of prematurity is the result of impaired erythropoietin production in response to
anemia and tissue hypoxia. Additionally, in premature infants, the concomitant increase in
RBC destruction and shortened lifespan can further exacerbate the anemia.
ANESTHESIA FOR NEURORADIOLOGY
Eman Nada, MD, PhD

BASICS
DESCRIPTION
General
• Advancement in imaging technology and the growing field of interventional neuroradiology
have increased the need for anesthesia services in the “out-of-OR” setting. However, several
challenges exist:
– Radiation exposure hazards: Early effects of ionizing radiation are dose-dependent and
risk increases with increased radiation dose (may occur many years after exposure).
– Special OR setup: Suites are often crowded by large radiology equipments that are difficult
to move; the anesthesia space is usually small; large radiation protective shields and heavy
aprons can make movement and access to the patient difficult; the airway can be distant
from the machine and anaesthetist; the room is dark; and paramedical personnel are not
familiar with anesthesia support (experienced help is often remote).
– MRI hazards: Ferrometallic materials can be projectile and may cause accidents; electric
noise can distort monitored waveforms; acoustic noise may present a distraction;
electromagnetic waves can cause patient burns in areas of contact with monitor cords or
in the presence of metallic implants; and in an emergency situation it takes 90 seconds to
retract the magnet tube and have a crash cart in the room (patient may need to be
removed from the room).
• Angiographic interventions can be broadly classified as those that:
– Obliterate the lumen. Embolization of cerebral and dural arteriovenous malformation
(AVM), vessel-feeding tumors, cerebral aneurysms, and fistulae.
– Open the lumen and revascularize. Angioplasty of atherosclerotic lesions and thrombolysis
or thrombectomy of acute thromboembolic stroke.
• Intraoperative magnetic resonance imaging system (IMRIS) is used for the:
– Resection of brain tumors
– Implantation of deep brain stimulators (DBS) and electroencephalographic (EEG)
electrodes
• Anesthesia is usually requested for diagnostic procedures in:
– Pediatric patients
– Uncooperative or claustrophobic patients
– Patients with complex medical problems when strict hemodynamic monitoring is needed
Position
• Diagnostic and interventional angiographic procedures: Supine with arms tucked
• Intraoperative MRI: Supine, prone, lateral, and semi-sitting position have been reported.
Incision
• Diagnostic and interventional procedures: Typically via femoral catheterization; however,
carotid or brachial arteries may be utilized.
• Intraoperative MRI: Craniotomy incision
Approximate Time
• Diagnostic: ∼30–60 minutes
• Angiographic interventional procedures: ∼4–6 hours
• Intraoperative MRI: ∼4–6 hours
EBL Expected
• Diagnostic and interventional angiographic procedures: None to minimal
• Intraoperative MRI: ∼50–500 mL, depending on the location and size of the lesion, and
complexity of the procedure
Hospital Stay
Diagnostic procedures: Out-patient or in-patient
Special Equipment for Surgery
• Contrast material
• Endovascular catheters to deliver coils, detachable balloons, and embolizing agents
• MRI suite specially equipped to provide surgery with compatible anesthesia machines,
monitors, and other equipments
EPIDEMIOLOGY
Incidence
• In 2009, an estimated 40,663 cerebral angiograms, 109,000 angioplastic carotid
endarterectomies, and 700,000 endovascular aneurysmal repairs were performed.
• In 2010, ∼1,047 neuro interventional MRI procedures were performed; this is a 300%
increase over 5 years since its start.
Morbidity
See “Complications”
Mortality
IV contrast: 1 out of 170,000 reactions
ANESTHETIC GOALS/GUIDING PRINCIPLES
• A full preoperative evaluation should be performed even in patients receiving deep
sedation/analgesia for diagnostic procedures.
• Out-of-OR standards are necessary for the safe delivery of anesthesia. They include:
– A reliable source of oxygen with a back-up
– Airway equipment (e.g., Ambu bag)
– Standard ASA monitors
– Suction
– Waste gas scavenger if volatile agents are administered
– Anesthetic drugs and emergency drugs
– Sufficient space
– Means to provide cardiopulmonary resuscitation
– Sufficient safe electrical outlets
– Adequate illumination with battery-powered backup
• Maintain a still field as well as a patent airway and hemodynamic stability

PREOPERATIVE ASSESSMENT
SYMPTOMS
Depends on diagnosis or indication
History
• NPO status
• Shellfish, iodine, IV contrast, or protamine reactions
• Ability to lie flat, snoring, sleep apnea
• Acquired or implanted metallic devices, extensive tattoos, permanent eye make-up
Signs/Physical Exam
• Depends on diagnosis or indication and can include a baseline-focused neurologic exam,
Glasgow Coma Scale, disease-specific scoring system (Hunt Hess for subarachnoid
hemorrhage and NIHSS for stroke)
• General medical and airway exam
MEDICATIONS
• Interventional procedures: Antiplatelets, anticoagulants; calcium channel blockers for
cerebral protection or reducing vasospasm; triple H therapy for prophylaxis or treatment of
vasospasm (induced hypertension, hemodilution, hypervolemia)
• Intraoperative MRI: Steroids, diuretics, anticonvulsants
• Pain medications: For headache, surgical pain in iMRI procedures
• Medications specific to the patient’s co-morbidities
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• BUN/Cr is often attained prior to IV contrast.
• Depends on comorbidities
CONCOMITANT ORGAN DYSFUNCTION
Depends on procedure indication

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Anxiolysis as needed; caution or avoidance in elderly or altered patients as well as epileptic
patients for EEG electrode implantation
• Stroked patients may present with a full stomach; gastric acid and volume-reducing
medications should be considered.
• Parkinsonian patients scheduled for DBS should have their morning dopaminergic and
anticholinergic medications held.
• Tumor patients may require re-dosing of steroids or antiepileptics.
• Corticosteroids and possibly an antihistamine may decrease the incidence of contrast
reactions in “at-risk” patients.
• Radiation safety: Lead aprons, thyroid shields, and protective eye goggles should be
considered, as appropriate, for the patient (as well as the anesthesia provider!)
• Setup should be meticulous due to the difficulties encountered with patient manipulation
once the procedure has begun.
Special Concerns for Informed Consent
• Pediatric patients require parent consent.
• Uncooperative or altered patients require a family member or power of attorney consent.
Antibiotics/Common Organisms
• Diagnostic and interventional angiographic procedures: Usually considered clean
procedures; antibiotics are given only in high-risk procedures.
• Intraoperative MRI: Skin organisms, third-generation cephalosporins are usually given.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Diagnostic procedures may need minimal or conscious sedation and can be performed by
non-anaesthetists certified in administering sedation. Anesthesia care providers are often
called upon to provide deep sedation/analgesia or general anesthesia; the choice is based
upon the procedure, positioning, comorbidities, access/nearness to the patient, and ease of
ventilation or intubation in the event that the patient obstructs or becomes apneic.
• Interventional: Typically general anesthesia; deep sedation/analgesia is used in some
revascularization procedures.
• Intraoperative MRI: GA. Awake craniotomy is sometimes needed to resect a tumor under
MRI near eloquent area.
Monitors
• Standard ASA monitors
• Intra-arterial pressure monitoring for interventional procedures and intraoperative MRIs
• Neurophysiologic-evoked potential monitoring in some spinal cord pathology embolization
procedures
• Intracranial pressure (ICP) monitoring
• Activated clotting time (ACT)
• Neuromuscular twitch monitor
• Neurologic exam in patients under MAC
• Foley catheter to measure urine output
• Oropharyngeal temperature probes will interfere with the angiography pictures; axillary or
skin probes are better options. In IMRIS a fiberoptic probe can be used in the groin.
Induction/Airway Management
• Be prepared to induce anesthesia and manage the airway in a less than optimal position.
• Extra-long breathing tubes and infusion lines are needed because anesthetic equipments are
often relocated after induction to allow for imaging equipment to move freely or to move to
safer magnetic fields in MRI scanners.
• Some iMRI suites have an induction room outside the scanner. This provides free access to
all anesthesia equipments at induction; the patient is then transported with
assisted/controlled ventilation (Ambu bag, Bain circuit) to the scanner.
• An ETT with muscle relaxation can provide a more secure and controllable airway, along
with extreme immobilization compared to an LMA.
Maintenance
• Pressure points are secured meticulously since the patient is going to be covered and arms
tucked with limited access.
• Renal protection for contrast: No proven strategy is agreed upon; preoperative hydration for
impaired renal function is usually used. Approximately 2/3rd of the severe and fatal contrast
reactions occur within the first several minutes.
• Heparinization is required whenever catheters are introduced into blood vessels. ACT
monitoring is utilized to guide therapy. Protamine should be standby whenever heparin is
used.
• Antiplatelets are used by the neurointerventionalist after the procedure.
Extubation/Emergence
• Avoid patient coughing, bucking, or straining which can cause hypertension and increased
ICP.
• Patient should be awake enough to have a neurologic exam.

POSTOPERATIVE CARE
• May require transport over long distances to the postanesthesia care unit (PACU); monitors,
supplemental oxygenation, airway equipment, and emergency drugs should be considered
as appropriate.
• Standard PACU evaluation, care, and discharge criteria
• No flexion at the groin for a few hours after femoral groin access is removed; consider
reverse Trendelenburg positioning if “head up" is needed.
BED ACUITY
Variable
ANALGESIA
• Interventional radiologic procedures are usually not painful, and local anesthetics are
injected at the access site.
• Short-acting narcotics are often preferable to longer-acting narcotics.
COMPLICATIONS
• Vascular perforation of the access site
• Obliteration of the wrong vessel
• Contrast dye reactions can range from mild symptoms such as scattered urticaria and
pruritus to laryngeal edema, life-threatening arrhythmias, hypotension, bronchospasm,
pulmonary edema, seizures, syncope, and even death. Nonionic contrast media has been
shown to decrease the incidence significantly.
• Contrast nephropathy: Usually occurs at 1–3 days after contrast injection. Patients at
increased risk include pre-existing renal disease, volume depletion, high or repeat doses of
contrast, and administration of other nephrotoxic drugs. Use of oral or IV theophylline,
acetylcysteine, fenoldapam, statins, or bosentan (an endothelin antagonist) have not shown
consistent efficacy against renal insult.
PROGNOSIS
Variable depending on the preoperative morbidity, the underlying pathology, site and extent
of procedure

REFERENCES
1. Bergese SD, Puente EG. Anesthesia in the intraoperative MRI environment. Neurosurg Clin
N Am. 2009;20:155–162.
2. Cloft HJ, Rubenstein A, Lanzino G, et al. Intra-arterial stroke therapy: An assessment of
demand and available work force. AJNR Am J Neuroradiol. 2009;30:453–458.
3. Gasser T, Senft C, Rathert J, et al. The combination of semi-sitting position and
intraoperative MRI—first report on feasibility. Acta Neurochir (Wien). 2010;152:947–951.
4. Qureshi AI. Ten years of advances in neuroendovascular procedures. J Endovasc Ther.
2004;11(Suppl 2):II1–II4.
5. Siddiqi N. Contrast medium reactions. Available at:
http://emedicine.medscape.com/article/422855-overview
6. US Department of Health and Human Services. Agency of Human Health care and Quality.
http://hcupnet.ahrq.gov/
See Also (Topic, Algorithm, Electronic Media Element)
• Cerebral embolization
• Craniotomy, awake
• Radiation safety
• Perioperative statins

CLINICAL PEARLS
• The anesthesia provider should not forget to wear radiation protective lead before they
engage in work with challenging cases.
• Anticipate potential complications and ensure appropriate anesthetic equipment setup.
• Continuous infusion of muscle relaxant under GA will help provide a motionless patient for
embolization or revascularization.
• For resection of tumors near eloquent areas, sedation or an “asleep-awake-asleep" technique
may be utilized.
ANGIOTENSIN
Zhuang-Ting Fang, MD, MSPH

BASICS
DESCRIPTION
• Angiotensin is:
– A natural hormone that is part of the renin-angiotensin-aldosterone system (RAAS)
– Stimulated in response to acute, sustained decreases in arterial pressure and enhanced
sympathetic outflow
– A direct, potent arteriolar vasoconstrictor (angiotensin II)
– Responsible for stimulating the adrenal cortex to release aldosterone
• Medications targeting either angiotensin receptors or angiotensin-converting enzymes (ACE)
have been developed for the treatment of hypertension (HTN) and have major implications
for anesthetic management.
PHYSIOLOGY PRINCIPLES
• The body has 3 control systems to regulate arterial blood pressure:
– “Immediate control:” The autonomic nervous system reflexes are capable of minute-to-
minute control of blood pressure.
– “Intermediate control:” Renin and angiotensin
– “Long-term control:” Occurs hours after the decrease in blood pressure by altering the
sodium and water balance. This process is mediated by aldosterone with the aim of
restoring blood pressure to a normal level.
• Renin
– Synthesized and stored in the juxtaglomerular cells in the wall of the renal afferent
arterioles
– Stimulated by a decrease in renal perfusion pressure associated with dehydration, acute
hemorrhage, renal artery stenosis, or chronic hyponatremia
– Converts circulating angiotensinogen to form angiotensin I
• Angiotensinogen is synthesized in the liver and released into the plasma.
• Angiotensin I
– Decapeptide prohormone
– Not all angiotensin I comes from conversion of angiotensinogen by renin; it is also
generated by the vascular endothelium.
• Angiotensin II
– Octapeptide
– Not all angiotensin II comes from conversion of angiotensin I by ACE; it is also generated
by the vascular endothelium.
– Plasma half-life is about 50 seconds and is cleared rapidly by a variety of enzymes, namely
angiotensinases, in the circulation.
– Has significant physiological activity on the:
Cardiovascular system: Angiotensin II binds to angiotensin AT1 receptor (a G protein-
coupled receptor) on the vascular smooth muscle, leading to vasoconstriction of the
precapillary arterioles and postcapillary venules. It is 40 times more potent than
norepinephrine, which makes angiotensin II the most powerful endogenous
vasoconstrictor. This effect is most profound in the skin, splanchnic vasculature, and
kidneys, and can lead to significant decreases in blood flow to these organs. Coronary
artery and cerebral artery (to a lesser extent) are also decreased. These pressor responses
do not lead to a reflex bradycardia since angiotensin II acts centrally to reset the
baroreceptor reflex to a higher pressure. The direct mitogenic effect of angiotensin II on
cardiac cells affects cardiac remodeling, and may increase myocardial contractility and
lead to hypertrophy from chronic stimulation.
Central nervous system: Angiotensin II acts on the medullary vasomotor center leading to
sustained HTN. It can also enhance the release of vasopressin and adrenocorticotropic
hormone (ACTH) as well as regulate prolactin release in the pituitary gland.
Peripheral autonomic nervous system: Angiotensin can stimulate the chromaffin cells in
the adrenal medulla to release catecholamines, which is the underlying mechanism for
marked HTN associated with pheochromocytoma.
Adrenal cortex: Angiotensin can stimulate the synthesis and secretion of aldosterone
from the adrenal cortex, leading to the retention of sodium and excretion of potassium
and hydrogen in the kidneys.
– It regulates ovulation and hormone production in the ovary and hormone production in
the testes. It may be partially responsible for preeclamptic symptoms.
ANATOMY
• Kidneys: Produce renin
• Liver: Produces angiotensinogen.
• Vascular endothelium: Produces angiotensin (90% of angiotensin I and 64% of angiotensin
II are generated within endothelium).
• Lungs: Contain the highest concentration of ACE (peptidyl dipeptidase)
DISEASE/PATHOPHYSIOLOGY
• Hypertension: Elevated levels of renin and angiotensin lead to increased vascular resistance;
this is considered as one of the mechanisms responsible for idiopathic HTN.
• Coronary artery disease: In patients with HTN, the incidence of myocardial infarction was
independently associated with the plasma renin activity. The growth effects of angiotensin
II may play an important role in the development of coronary artery atherosclerosis and
peripheral vascular disease.
• Cardiac hypertrophy: Is caused not only by the increased cardiac workload from HTN, but
also the mitogenic effect of angiotensin II on the cardiac muscle cells (plays a role in
myocardial remodeling).
• Renin-secreting tumors
• Angiotensinogen-secreting tumors
PERIOPERATIVE RELEVANCE
• ACE inhibitors (ACE-I) or angiotensin receptor antagonists/blockers (ARBs) are commonly
used drugs in the treatment of HTN, chronic heart failure, or diabetic nephropathy.
– Heart rate: Minimal effect
– Contractility: Reflexive increase
– Cardiac output: Indirect increase
– Blood pressure: Decrease
– Systemic and pulmonary vascular resistance: Direct decrease
– Preload: Decrease
– Renovascular resistance: Decrease
– Natriuresis: Increase
• Side effects and adverse events:
– Profound and prolonged hypotension: The RAAS is responsible for restoring normotension
during surgery, especially in a state of hypovolemia and decreased vascular resistance.
Patients taking ACE inhibitors or angiotensin receptor antagonists preoperatively may
develop profound and prolonged hypotension from the blockage of this physiologic
response during surgery. Whether patients on ACE inhibitors or angiotensin receptor
antagonists should discontinue the medication preoperatively remains controversial.
– Persistent, dry cough and angioedema from increased kinins; it appears that there is a
decreased incidence with ARBs.
– Hyperkalemia from decreased aldosterone
– Exacerbates renal failure in renal artery stenosis, and vasoconstricts the efferent arterioles
of the glomeruli resulting in an increased glomerular filtration rate (GFR)
– Angiotensin “escape:” Not all angiotensin arises from the RAAS system. ACE is contained
the heart and blood vessels where it can exert harmful local effects.
– Pregnancy: May cause congenital malformations and fetal abnormalities
• Benefits: May decrease the degree of vasoconstriction from increased sympathetic tone
caused by intraoperative surgical stress; therefore, it may potentially improve perfusion of
the vital organs and maintain their normal function.

REFERENCES
1. Colson P, Ryckwaert F, Coriat P. Review article: Renin angiotensin system antagonists and
anesthesia. Anesth Analg. 1999;89:1143–1155.
2. Sarkar P, Nicholson G, Hall G. Brief review: Angiotensin converting enzyme inhibitors and
angioedema—anesthetic implications. Can J Anesth. 2006;53(10):994–1003.
See Also (Topic, Algorithm, Electronic Media Element)
• Hypertension
• ACE inhibitors and hypotension
• Hypotension
• Chronic angina

CLINICAL PEARLS
• Angiotensin is an endogenous hormone that is part of the renin–angiotensin–aldosterone
system. Its role has been exploited pharmacologically for the treatment of hypertension.
• Patients on ACE-I and ARBs may have an increased risk of refractory hypotension
perioperatively. However, this has been challenged, and there are currently no guidelines
based upon strong evidence for the preoperative management of these long-term
medications.
ANION GAP
J. Andrew Dziewit, MD
Nina Singh-Radcliff, MD

BASICS
DESCRIPTION
• Anion gap (AG) = [(Na+ + K+) – (Cl− + HCO3−)]; normal 7–14 mEq/L
• In metabolic acidosis, the concept of the AG is utilized to assist with the differential
diagnosis. It functions to distinguish acidosis as either an:
– Increase in total body acids (HCO3− anion is titrated by H+); or a
– Decrease in total body HCO3− (abnormal loss from the body).
– In both scenarios, HCO3− is reduced; a calculation of the AG aids in determining which of
these 2 mechanisms is responsible.
• The term “gap” does not imply that anions are missing, but only that they are not directly
measured. By applying the concept that the serum is electrically neutral, measurable values
for major cations and anions allow for unmeasured anions to be calculated.
• Unmeasured anions include phosphates (PO4−) and sulfates (SO4−) as well as lactates,
ketoacids, and toxins. Their corresponding cation (H+) dissociates and is titrated by HCO3−
or other buffering systems, or it increases the acid:base ratio (causing a metabolic acidosis).
PHYSIOLOGY PRINCIPLES
• The anions of organic and inorganic acids are not easily or routinely measured. However, it
is possible to measure serum Na+ and K+ (cations) and Cl− and HCO3− (anions) and
“calculate” the AG: [(Na+ + K+) – (Cl− + HCO3−)]. Or, AG = measured cations –
measured anions; potassium may be excluded.
• Normally, the serum AG is determined by negative charges on serum proteins, particularly
albumin.
• Metabolism results in the production of volatile, organic, and inorganic acids.
– Volatile acids: Carbon dioxide (CO2) is a byproduct of sugar, fat, and amino acid
metabolism. Basal CO2 production is approximately 12,000 mmols/d and is
exhaled/excreted by the lungs, as well as buffered by the bicarbonate system.
– Inorganic acids: Sulfate and phosphates are byproducts of amino acid metabolism; basal
production is approximately 50–100 mEq/d. Excretion occurs renally.
– Organic acids: Lactate and ketones. Lactate is produced via anaerobic metabolism. Ketones
result from fatty acid breakdown when insulin is not present via a beta-oxidizing process.
Both are excreted by the liver and kidneys.
• HCO3− is ubiquitous in the body and exists in equilibrium between the intravascular and
extracellular compartments. It is present in the stool and carefully regulated by the renal
tubules.
DISEASE/PATHOPHYSIOLOGY
• High AG metabolic acidosis:
– Results from an increase in an acid molecule’s corresponding anion; thus represents
increased total body acid.
– Acids are composed of a cation (H+) and an anion (A−).
– In solution, the acid compound (HA) dissociates into a H+ and its corresponding anion
(HA ←→ H+ + A−).
– The H+ is buffered by one of the body’s buffering systems, including bicarbonate (H+ +
HCO3− ←→ H2CO3 ←→ H2O + CO2) in order to “cushion” or decrease adverse effects of
the acid load.
– However, this “titration” results in a reduction in HCO3− values; when the acid load
exceeds the buffering capacity, acidosis manifests.
– Electroneutrality is maintained during this titration process (H+ cation plus a HCO3−
anion). There is no increase or decrease in positive- or negative-charged molecules.
– Increased acid production can result from anaerobic metabolism (lactic acidosis), ketone
production (diabetic ketoacidosis), toxins (methylene, ethanol, salicylates), and
hyperosmolar hyperglycemia.
– Reduced acid excretion can result from impaired renal function (uremia).
• Normal AG metabolic acidosis:
– Loss of HCO3− (or bicarbonate precursors) from the body results in an increase in the
acid:base ratio.
– There is no increase in total body acid, and hence no increase in anions.
– In order to maintain electroneutrality, a loss in HCO3− is balanced by a “gain” in Cl−; this
results in a hyperchloremic state.
– HCO3− can be lost by diarrhea, renal tubular acidosis, carbonic anhydrase inhibitors,
ureteral diversion, and intestinal losses; additionally, hyperchloremic crystalloid solutions
(normal saline, [Cl−] 154 mEq/L) serve to dilute the bicarbonate concentration as well as
increase the chloride concentration (resulting in renal excretion of bicarbonate).
• Low AG is a less commonly utilized term that describes low albumin states. Albumin is a
negatively charged protein and its loss from the serum results in the retention of other
negatively charged ions such as chloride and bicarbonate. Because they are utilized in the
calculations, there is a decrease in the gap. AG falls by 2.3–2.5 mEq/L for every 1 g/dL
reduction in serum albumin concentration.
PERIOPERATIVE RELEVANCE
• Base excess is more frequently utilized than the AG in the perioperative period. This is
because metabolic acidosis is often the result of lactic acidosis secondary to anaerobic
metabolism.
– Lactic acidosis indicates that there is tissue hypoxia either from hypovolemia,
hypoperfusion, hypovolemia, or hypotension.
– Perioperatively, this can result from surgical blood loss; evaporative/insensible losses;
episodes of hypoxia at induction, intraoperatively, or at emergence; anemia; or
hypotension.
– Base excess is useful in determining the extent of the increased acid load, as opposed to
aiding in the differential diagnosis.
• The AG can be implemented perioperatively to determine if the metabolic acidosis is
secondary to a hyperchloremic non-AG acidosis. This can manifest from as little as 2 L of
normal saline solution. Na+ 154 mEq/L is balanced by Cl− 154 mEq/L. The chloride
concentration is not physiologic and initially results in the dilution of HCO3−. Ultimately,
however, HCO3− anion is eliminated by the kidneys in order to maintain electroneutrality
(increased chloride anion load). Clinical consequences of the metabolic acidosis are unclear.
However, attempts at correcting the abnormality may actually cause more issues (iatrogenic
causes such as administering additional hyperchloremic crystalloids).
• In the ICU and at the bedside, the AG can provide a clinically useful tool to identify one of
the many causes of metabolic acidosis in the critically ill, especially when hypoalbuminemia
and lactate are considered. Additionally, it can be utilized to monitor, assess, and guide
therapy during sepsis.
• Ketoacidosis: The measured AG disturbance is often less than expected from the fall in
serum bicarbonate. This results from the renal loss of ketoacid anions (beta hydroxyl
butyrate) that accompany sodium and potassium salt excretion.
• Multiple myeloma results in a pathologic increase in cations that are not measured; IgG
paraproteinemia causes a reduced AG.
• Postcardiac surgery metabolic acidosis is typically the result of an increase in unmeasured
acids, and less commonly from lactic acidosis.
– Cardiopulmonary bypass (CPB) circuits are usually primed with 1.4–2 L of hyperchloremic
crystalloid.
– ABG taken immediately after “going on pump” demonstrates a non-AG metabolic acidosis.
– More frequent in children due to the ratio of CPB priming fluid to smaller blood volumes
(even with low-volume priming)
– This acidosis is transient and lasts <24 hours.
EQUATIONS
• AG = [(Na+ + K+) – (Cl− + HCO3−)]
• AG corrected (for albumin) = calculated AG + 2.5 (normal albumin g/dL – observed
albumin g/dL)

REFERENCES
1. Chawla LS, Shih S, Davidson D, et al. Anion gap, anion gap corrected for albumin, base
deficit and unmeasured anions in critically ill patients: Implications on the assessment of
metabolic acidosis and the diagnosis of hyperlactatemia. BMC Emerg Med. 2008;8(18).
2. ernon C, Letourneau JL. Lactic acidosis: Recognition, kinetics, and associated prognosis.
Crit Care Clin. 2010;26(2):255–282.
3. Liamis G, Milionis HJ, Elisaf M. Pharmacologically-induced metabolic acidosis: A review.
Drug Saf. 2010;33(5):371–391.
4. Filipescu D, Raileanu I, Luchian M, et al. Hyperchloremic metabolic acidosis after cardiac
surgery. Crit Care. 2006;10(Suppl1):P200.
5. Murray DM, Olhsson V, Fraser JI. Defining acidosis in postoperative cardiac patients using
Stewart’s method of strong ion difference. Pediatr Crit Care Med. 2004;5(3):240–245.
6. Liskaser FJ, Bellomo R, Hayhoe M, et al. Role of pump prime in etiology and pathogenesis
of cardiopulmonary bypass-associated acidosis. Anesthesiology. 2000;93(5):1170–1173.

ADDITIONAL READING
• Ishihara K, Szerlip HM. Anion gap acidosis. Semin Nephrol. 1998;18(1):83–97.
• Lim S. Metabolic acidosis. Acta Med Indonesia. 2007;39(3):145–150.
See Also (Topic, Algorithm, Electronic Media Element)
• Metabolic acidosis
• Diabetic ketoacidosis
• Carbon dioxide transport
• Lactic acidosis

CLINICAL PEARLS
• Anion gap represents the difference in charge between measured cations and measured
anions.
• “Missing” negative charge is composed of weak acids (A−) like albumin and phosphate and
strong unmeasured anions such as lactate.
• Frequent causes of an elevated anion gap metabolic acidosis are represented by the
mnemonic MUDPILES:
– Methanol
– Uremia
– Diabetic ketoacidosis
– Paraldehyde
– Iron, isoniazid (INH)
– Lactic acid
– Ethanol, ethylene glycol
– Salicylates
• Frequent causes of a normal anion gap metabolic acidosis are represented by the mnemonic
USEDCARP:
– Ureterostomy
– Small bowel fistula
– Extra chloride
– Diarrhea
– Carbonic anhydrase inhibitors (acetazolamide)
– Adrenal insufficiency
– RTA
– Pancreatic fistula
ANTERIOR CERVICAL DISCECTOMY AND FUSION (ACDF)
Nina Singh-Radcliff, MD
Chris A. Steel, MD

BASICS
DESCRIPTION
General
• Removal of a herniated or degenerative disc that is compressing on the cervical spine
– A herniated disk refers to the gel-like material either bulging or rupturing through a weak
area in the surrounding wall (annulus). Irritation and swelling occurs when this material
squeezes out and presses on a nerve.
– Degenerative disc disease refers to the drying out of the disc, resulting in shrinkage and
loss of flexibility and cushioning properties (increases with age). Osteophytes (bone spurs)
result from wear, damage, and inflammation. These changes can result in spinal cord
compression, or myelopathy.
• After induction and intubation, the neck is prepped; the anterior approach allows access to
the disc without disturbing the spinal cord, spinal nerves, and strong neck muscles of the
back. If an autograft will be utilized for fusion, the hip area is also prepped.
• Surgical exposure involves creating an avascular dissection place or tunnel to the disc via
moving aside muscles in the neck, retracting the trachea, esophagus, and arteries.
• Preparation to remove the disc involves localizing the affected level and utilizing spreaders
above and below to facilitate removal of the damaged disc.
• Nerve decompression consists of removal of disc fragments and osteophytes (bone spurs).
The annulus (outer wall of the disc) is incised, followed by removal of the disc; bone spurs
are removed with a Burr (a small rotary cutting tool). A microscope is utilized to remove
disc material and bone spurs near the spinal cord. The posterior longitudinal ligament
(courses behind the vertebrae) is removed to reach the spinal canal and any material
pressing on the nerves is removed.
• A foraminotomy is then performed (the foramen through which the spinal nerve exits, is
enlarged with a drill) to allow more room to exit the spinal canal.
• Fusion: After the disc is removed, the space between the vertebrae is empty and a bone graft
may be inserted to prevent the vertebrae from collapsing and rubbing together; serves as a
bridge. To prepare the graft for fusion, the outer cortical layer of bone is roughened up until
punctuate bleeding is seen. This will allow blood vessels to grow into the grafted bone. The
bone graft is shaped to fit snugly into the space and is typically further immobilized and
held together with a metal plate and screws (reduced incidence of bone graft migration,
improved fusion).
Position
Supine; shoulder roll may be utilized to enhance neck extension and exposure; arms are
typically tucked to allow the surgical team to stand on both sides of the neck.
Incision
• 2–3 inches, depending upon the number of levels
• Left-sided approach is preferred by some in order to reduce injury to the recurrent laryngeal
nerve (RLN); the right side has a 2–3% anomalous course.
Approximate Time
1–1.5 hours per level
EBL Expected
Less than 50 mL
Hospital Stay
• Advocates for same-day discharge cite that the short operative time, minimal blood loss, and
low risk of postoperative hematoma make it ideal in patients without significant
comorbidities and good home help. May significantly reduce procedure costs.
• Advocates for hospital admission cite that the need for a drain and the catastrophic risk of a
postoperative neck hematoma preclude discharge home on POD 0.
Special Equipment for Surgery
• Fluoroscopy or portable x-ray
• Bone graft (autologous or cadaveric)
• Neuromonitoring: Computer and personnel for monitoring EMG, SSEPs, and MEPs
EPIDEMIOLOGY
Incidence
150,000 per year in the US
Prevalence
Increases with age, osteoporosis
Morbidity
• Isolated postoperative dysphagia: 60% initially, 5% at 1 year (1)
• Symptomatic RLN palsy: 3.1%
• Postoperative hematoma: 1–2%
• Bone graft migration: 1–2%
• Dural penetration/tear, worsening or pre-existing myelopathy, Horner’s syndrome,
instrumentation backout, superficial wound infection: Each less than 1%
Mortality
Rare. Esophageal perforation, retropharyngeal edema or hematoma, quadriplegia
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Patients have often failed a course of conservative treatment (epidural steroid injections,
physical therapy, acupuncture, oral pain medications).
• Airway management may be affected by a limited range of neck motion due to pain,
elicitation of myelopathy, or potential for injury. The sniffing position, or even
flexion/extension, to align the oropharynx, hypopharynx, and larynx may not be possible.
• Neuromonitoring. EMG, SSEPs, and MEPs require modification of anesthetic technique to
optimize quality of results.
• Controlled hypotension may be requested to reduce bone bleeding.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Weakness, pain, paresthesias, numbness in C2–7 distribution (neck, shoulder, arms, hand)
• Arm pain often worse than neck pain
History
• No improvement with conservative therapy
• Chronic pain medications: Patients may or may not have taken their scheduled doses on day
before or day of surgery.
• Comorbidities increase with age.
Signs/Physical Exam
• Sensory and motor deficits should be clarified and noted, including the ability to swallow
and if any baseline hoarseness.
• Ability to extend the neck without experiencing symptomatic spinal cord compression
(Lhermitte’s phenomenon)
MEDICATIONS
Pain patches, pain medications
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Laboratory exam depends upon comorbidities.
• PT/PTT/INR, if clinical history of bruising, bleeding, or drugs
• MRI, CT, and myelogram are often performed prior to surgery.
CONCOMITANT ORGAN DYSFUNCTION
• Osteoporosis
• Chronic pain syndrome

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Anxiolysis and analgesia as needed; chronic pain patients may require increased dosing.
• Dexamethasone 10 mg IV may be requested by some surgeons.
Special Concerns for Informed Consent
• Smoking cessation: Nicotine reduces successful fusion.
• Hoarseness, swallowing difficulties postoperatively
• Postoperative hematoma
INTRAOPERATIVE CARE
Choice of Anesthesia
• General anesthesia with ETT
• Partial or total intravenous anesthesia (TIVA) to optimize neuromonitoring
Monitors
• EMG: Supplements visual identification to avoid RLN injury. An ETT with special electrodes
that connect to a computer can measure the muscle electrical potential of the vocal cords.
Because RLN stimulation causes movement of the cords, it allows the surgeon to identify
and avoid inadvertent nerve injury. Must avoid NMBDs (2).
• SSEPs: Assess the integrity of the posterior spinal cord. Volatile agents at a MAC >0.5
decrease the amplitude and increase the latency of the waveforms (false positive).
• MEPs: Assess the integrity of the anterior spinal cord; must avoid NMBDs.
• Arterial line based on comorbidities
Induction/Airway Management
• A limited range of motion (pain, myelopathy, prior fusion, stiffness) may preclude sniffing
position or even flexion. Consider having a video laryngoscope, fiberoptic bronchoscopy
(awake or asleep depending on ability or ease of bag mask ventilation), or other special
management devices available in the event of difficulty (alternatively, may consider
utilizing for initial attempts).
• Consider having the patient self-position their neck while on the OR table and maintaining
this position after induction; document if this is performed.
• ETT cuff may increase pressure exerted on the tracheal wall and the submucosal portion of
the RLN; when this is combined with surgical tissue retractors transmitting pressure through
the soft tissues of the neck to the trachea, it can result in ischemic injury. Maintaining a cuff
pressure <25 cm H2O to ensure adequate blood flow to the capillary beds may prevent this.
Other studies have suggested the utilization of the “just seal” pressure (air is withdrawn
from the ETT cuff until a leak around the cuff is detected, and subsequently reinjected
slowly until an air seal is barely obtained).
• Secure the ETT to the contralateral side of the incision; tape should not be attached to
maxilla or mandible on the operative side.
• Neuromuscular blockade cannot be utilized if EMG or MEP is performed. Succinylcholine or
small intubating dose of nondepolarizing muscle relaxants may be utilized to optimize
intubating conditions (opening of mouth, vocal cord aperture to pass ETT), and will wear
off quickly.
Maintenance
• Confirm that the head is supported and not levitating.
• Fluoroscopy or single shots require appropriate radiation protection.
• EMG, MEPs, and SSEPs, may have improved conduction with the use of partial or total
intravenous drug administration. Propofol is often utilized as either the sole agent, or in
conjunction with volatile, nitrous, narcotic (remifentanil, sufentanil, fentanyl), or other
sedative/analgesic (dexmedetomidine, ketamine). Choice is based upon the preference or
experience of the anaesthetist, surgeon, neuromonitoring team, institution’s availability,
cost considerations, and patient factors. The goal is to maintain a steady state, particularly
during the period where injury may occur (dissection, discectomy), and avoid bolusing
(may create false positives) (3).
• Critical to maintain an adequate level of anesthesia since sudden movements can result in
danger to the patient (coughing, bucking, sitting up), especially since NMBDs cannot
provide a layer of safety against this.
Extubation/Emergence
• Avoid coughing and bucking
• Consider 30° reverse Trendelenburg position to avoid passive aspiration
• Neurologic exam soon after emergence
• RLN injury may increase risk of aspiration and stridor.

POSTOPERATIVE CARE
BED ACUITY
• Same-day discharge is practiced at some centers; however, the potential for postoperative
hematoma with resultant airway compromise makes it controversial. Proponents argue that
it can significantly reduce healthcare costs and there is only a minimal risk of postoperative
hematoma.
• Admission: Typically 1–2 days allowing for drain removal, neurologic assessment,
monitoring of swallowing/hoarseness, and hematoma. On POD 0, the patient should sit up
in a chair and begin supervised ambulation.
• Telemetry or ICU if significant comorbidities or frequent neurologic testing needs to be done
(new neurologic deficit, stridor)
• Cervical collar often utilized to allow time for the bone graft to fuse
ANALGESIA
• Typically mild at the incision site. Significant pain can occur at the bone grafting site.
• Persistent pain is often the result of permanent damage to the nerve making it unresponsive
to decompressive surgery; spinal cord stimulators may provide relief.
COMPLICATIONS
• Airway compromise: Hematoma formation may impinge on the trachea; RLN damage can
cause unopposed adduction of the cricothyroid muscle resulting in stridor; a traumatic
intubation or surgical trauma can cause airway edema.
• Anesthesia awareness
• Tongue laceration from MEPs
• Hoarseness and swallowing difficulties often resolve in a few months; they persist in
~1/250 cases and require an ENT consult.
• Failure to fuse: Increased in smokers (nicotine inhibits bone-growing cells), osteoporosis,
obesity, and malnutrition
• Hardware fracture: The metals, rods, and plates used to stabilize the spine may move or
break before the vertebrae are completely fused. Requires surgery to remediate.
• Bone graft migration: Movement from the correct position. Occurs soon after surgery and
more likely if hardware is not utilized to secure the graft or if multiple levels are fused.
Requires surgery to remediate.
• Transitional syndrome, also known as adjacent-segment disease: Occurs when the vertebrae
above or below a fusion take on extra stress. The added stress can eventually degenerate the
adjacent vertebrae and cause pain.
• Nerve damage: Numbness or paralysis is possible from direct injury during the procedure.
• Major vascular injury (rare): Internal and external jugular veins, vertebral, carotid and
thyroid arteries
• Dural tear, venous air embolism, and pneumothorax are rare but possible.
• Vocal cord paresis, epiglottis paralysis, and aphasia require feeding tube placement.
PROGNOSIS
• Relief of arm pain: 92–100% (3)
• Relief of neck pain: 73–83%
• Weakness and numbness may persist for weeks to months.

REFERENCES
1. Daniels AH, Riew KD. Adverse events associated with anterior cervical spine surgery. J Am
Acad Orthop Surg. 2008;16:729–738.
2. Padberg AM, Thuet ED. Intraoperative electrophysiologic monitoring: Consideration for
complex spinal surgery. Neurosurg Clin N Am. 2006;17:205–226.
3. Bohlman HH, Emery SE. Robinson anterior cervical diskectomy and arthrodesis for cervical
radiculopathy: A long-term follow-up of 122 pts. J Bone Joint Surg. 1993;75(9):1298–
1307.
See Also (Topic, Algorithm, Electronic Media Element)
• Somatosensory and motor evoked potentials
• Electromyelogram

CLINICAL PEARLS
• Careful airway evaluation and management (video laryngoscopy, awake or asleep FOB may
be considered)
• Keep neutral position of the neck and minimize airway manipulation during intubation.
• Neurophysiologic monitoring may be improved with TIVA.
• Postoperative airway compromise can result secondary to hematoma formation, RLN injury,
or soft-tissue swelling.
ANTERIOR MEDIASTINAL MASS
Shital Vachhani, MD

BASICS
DESCRIPTION
• Anterior mediastinal masses include teratomas, thyroid tumors, lymphomas, and thymomas.
They can result in dangerous and fatal cardiovascular or pulmonary structure compression
at the time of anesthesia induction, muscle relaxation, and positive pressure ventilation.
• Patients present to the operating room for biopsy or excision of the mass via a sternotomy,
thoracotomy, cervical mediastinoscopy, anterior parasternal mediastinoscopy, video-assisted
thoracoscopic biopsy, or awake CT-guided percutaneous biopsy.
• There are also case reports of patients with undiagnosed anterior mediastinal masses (AMM)
presenting emergently to the operating room for ascending aortic aneurysm and Cesarean
sections (1).
EPIDEMIOLOGY
Prevalence
• Half of all mediastinal masses are anterior (2).
• 60% of surgically resected lesions are neurogenic tumors, thymomas, and benign cysts (2).
Prevalence
In children, lymphoma is the most common AMM, followed by germ-cell tumors and thymic
masses.
Morbidity
• Masses in the anterior mediastinum are more likely to be malignant than those found in
other mediastinal compartments.
• Perioperative morbidity results from mass compression on vascular or pulmonary structures.
Mortality
Not available
ETIOLOGY/RISK FACTORS
• Depends on tissue diagnosis of mass, usually secondary to a mutation
• Often an incidental finding
PHYSIOLOGY/PATHOPHYSIOLOGY
• During spontaneous ventilation (SV), airways are held open by baseline negative
intrathoracic pressures and adherence of the pleura to the chest wall.
• Intrathoracic versus extrathoracic masses:
– Intrathoracic masses are found within the chest cavity. During SV, inspiration expands the
rib cage upward and outward and “lifts” the mass off vascular and respiratory structures.
In the standing position, exhalation does not typically result in symptoms. However, in the
recumbent and supine positions, exhalation can result in compression of structures.
– Extrathoracic masses are located outside the chest cavity and are further divided into
variable and fixed lesions.
Variable lesions: Redundant airway tissue (snoring), tracheomalacia, etc. During SV,
obstruction occurs during inspiration. The negative pressure that is generated in the
chest, distal to the mass, results in collapse of the airway. During exhalation, the
position pressure that is generated by the abdominal muscles, distal to the mass, stent
the airway open.
Fixed lesions: Goiter. Obstruction to airflow occurs during inspiration and exhalation.
• AMMs (intrathoracic masses) can result in extrinsic compression of structures:
– Respiratory: Trachea, major bronchus. The mass may prevent adequate ventilation by
compressing the trachea/bronchus while perfusion remains unchanged. This can result in
a V/Q mismatch called a pulmonary shunt.
– Cardiovascular: Great vessels, right ventricular outflow tract (posterior mediastinal masses
are more likely to affect the left atrium or ventricle). Encroachment does not produce
hemodynamic effects, whereas compression results in clinical manifestations similar to
pericardial tamponade. Right ventricular failure may be responsible for hypotension with
resultant dead space lung physiology (blood flow to the alveoli is decreased; hypoxemia
can result even in the absence of tracheal obstruction).
• Infants and children have more compressible airways and may be more susceptible than
adults to extrinsic airway obstruction (1).
• Superior vena cava (SVC) syndrome: The thin-walled venous system is easily compressible
by a large mediastinal mass. Thus, if there is obstruction to venous drainage from the upper
body, this can cause interstitial edema. Therefore, collateral veins with low resistance
become dilated.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Management depends on the anatomy and pathology of the mass, as well as the surgical
procedure.
• Look for compression of the heart, great vessels, and airway structures during induction and
throughout the surgical procedure.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Respiratory symptoms: Nonproductive cough, stridor, wheezing, dyspnea, orthopnea that
worsens with recumbency or lying flat
• Syncope
• Patient may be asymptomatic and the mass incidentally found on CXR.
History
Shortness of breath or cough when lying flat (1)
Signs/Physical Exam
• Use of accessory muscles
• Plethora of the face (SVC syndrome)
TREATMENT HISTORY
If lymphoma, find out if pretreated with steroids or radiation to shrink the tumor. The
disadvantage of pretreatment is that it might affect tissue pathology (diagnosis).
MEDICATIONS
• Bronchodilators
• Steroids, if part of a chemotherapeutic regimen
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Flow volume loops to look for extrinsic or intrinsic compression in the supine and upright
positions (may see decrease in FEV1 and peak expiratory flow in supine position) (3). Their
predictive value has been questioned, particularly with the advent of newer and
sophisticated imaging modalities.
• CXR often incidentally identifies the mass; further imaging should be ordered.
• Arterial blood gas
• CT/MRI of the chest to display the location and extent of airway or cardiovascular
compromise; patients who are unable to lie flat may be done in the 30° angle, lateral, or
prone position.
• Echocardiogram to assess for cardiovascular effects (mass effect, cardiac compression, or
pericardial effusion). Anterior masses tend to compress the right heart.
• If thymoma, rule out myasthenia gravis by testing for acetylcholine receptor antibodies.
• Fine needle aspiration for biopsy
CONCOMITANT ORGAN DYSFUNCTION
• Signs of SVC syndrome from compression
• Dynamic cardiac or airway compression with positional changes
• Parathyroid masses may be associated with hyperparathyroidism.
• Thymomas may have concurrent myasthenia gravis or immune deficiency.
CIRCUMSTANCES TO DELAY/ CONDITIONS
• If the patient is a candidate to receive radiation or steroids to decrease the mass size
• If there is a potential for severe airway compromise, but a cardiopulmonary bypass (CPB)
machine and perfusionist are not available
CLASSIFICATIONS
• Mediastinal masses are described based on their location relative to the heart:
– Anterior: Teratomas, thyroid tumors, “terrible” lymphomas, thymomas (4Ts)
– Middle: Lymph nodes, vascular masses
– Posterior: Esophageal and neurogenic tumors, aneurysms
TREATMENT

PREOPERATIVE PREPARATION
Premedications
• If the patient is symptomatic, no benzodiazepines or opioids should be administered; they
can compound respiratory effects.
• If an awake, semi-sitting fiberoptic is planned (due to tracheal compression), glycopyrrolate
can be administered as an antisialagogue, and lidocaine to topicalize the airway.
Special Concerns for Informed Consent
• Thoracic epidural placement for tumor resection via a thoracotomy or sternotomy
• Postoperative intubation and ventilation may be necessary.
• CPB is a possibility.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Intubate while maintaining SV if possible
• A rigid bronchoscope and surgeon should be available for immediate assistance if airway
collapse occurs. The rigid bronchoscope can be inserted distal to the compression, and
“stent” the area open allowing adequate oxygenation/ventilation.
• Awake fiberoptic bronchoscopy may be appropriate if the mass appears to compress the
trachea. The endotracheal tube acts similar to the rigid bronchoscope to “stent” the area
open.
Monitors
• In patients with SVC syndrome, intravenous access should be placed in the lower extremity.
• Arterial line for blood pressure assessment and management; also if placed in the right
radial position, can serve as an indicator of mediastinal compression of the innominate
artery.
Induction/Airway Management
• Femoral cannulation under local anesthesia with CPB readily available, if there is a potential
for severe obstruction. If asymptomatic and there is no reason to believe that the mass will
compress the respiratory or cardiovascular structures, slow controlled induction may be
pursued.
• If unsure, try to maintain SV with inhalational agents, ketamine, or dexmedetomidine and
secure the airway.
• A surgeon should be available in the room during induction in the event that the mass
compresses the airway and SV is lost; or if a smaller endotracheal tube cannot be passed. A
rigid bronchoscope can be passed distal to the site of compression and stent the airway
open.
Maintenance
• While SV is ideal for large masses, positive pressure ventilation with a volatile agent is
usually used to optimize surgical conditions.
• Use of short-acting anesthetics is ideal.
• Avoid muscle relaxants, if possible. If they are necessary for the procedure, assisted manual
ventilation should be first attempted to assure that positive-pressure ventilation is possible
(1).
• Compression and cardiopulmonary collapse:
– Mainstem the endotracheal tube or insert a rigid bronchoscope
– Awaken the patient and return to SV
– Lateral position or prone position; positional changes can displace the mass and alleviate
compression. The history and physical is important to determine if the patient’s symptoms
are alleviated with certain positional changes.
– Chest compressions in the supine position
– Sternotomy and surgical elevation of the mass off the great vessels
– CPB
Extubation /Emergence
• Extubation should be performed only in a fully awake patient, with the rigid bronchoscope
in the room for backup in the event of airway collapse.
• Look for underlying tracheomalacia from tumor compression

FOLLOW-UP

BED ACUITY
• Floor bed may be appropriate.
• ICU care may be needed depending on the intraoperative course.
MEDICATIONS/LAB STUDIES/CONSULTS
• CBC to check for anemia
• For thoracic epidurals, the acute pain service should be contacted.
COMPLICATIONS
• Damage to the surrounding structures from procedure (e.g., phrenic and recurrent laryngeal
nerve)
• Pneumothorax

REFERENCES
1. Slinger P, Karsli C. Management of the patient with a large anterior mediastinal mass:
Recurring myths. Curr Opin Anaesthesiol. 2007;20(1):1–3.
2. Strollo DC, Rosado de Christenson ML, Jett JR. Primary mediastinal tumors. Part 1: Tumors
of the anterior mediastinum. Chest. 1997;112(2):511–512.
3. Neuman GG, Weingarten AE, Abramowitz RM, et al. The anesthetic management of an
anterior mediastinal mass. Anesthesiology. 1984;60:144–147.
See Also (Topic, Algorithm, Electronic Media Element)
• Mediastinoscopy
• Flow-volume loops
• Superior vena cava syndrome
• Recurrent laryngeal nerve

CODES

ICD9
519.3 Other diseases of mediastinum, not elsewhere classified

ICD10
J98.5 Diseases of mediastinum, not elsewhere classified

CLINICAL PEARLS
• History, physical, and review of imaging studies are critical in determining the extent of
mediastinal mass involvement.
• Major airway complications are more commonly seen in the postoperative period, rather
than in the operating room.
ANTI-DIURETIC HORMONE (ADH)
Daniel R.C. Nieva, MD

BASICS
DESCRIPTION
Antidiuretic hormone (ADH), also known as vasopressin, regulates urinary volume and
osmolality by decreasing diuresis; it also functions as a potent vasoconstrictor at higher doses.
PHYSIOLOGY PRINCIPLES
• ADH is a nonapeptide (consists of nine amino acids) with an arginine vasopressin attached
to the 8th amino acid location; thus also referred to as arginine vasopressin (AVP).
• AVP (V1) serves as an important backup system for blood pressure control and
cardiovascular sympathetic modulation in the hypotensive and hypovolemic states.
– Hypotension is sensed by baroreceptors in the left heart, aortic arch, and carotid sinus and
is a very potent trigger for AVP release. It can increase levels by 10–1000-fold.
– At these elevated concentrations, AVP acts as a vasoconstrictor of the mesentery, skin, and
skeletal tissues by stimulating the V1 receptor on vascular smooth muscle.
• ADH (V2) increases tubular conservation of water and urine osmolality, while decreasing
plasma osmolality in response to decreased (5–10%) plasma volume, increased plasma
osmolality, or pain, stress, hypoxia.
– When extracellular fluid osmolality increases, osmoreceptors in the hypothalamus shrink,
which stimulates ADH release from the posterior pituitary.
– In the thick ascending loop of Henle, it increases solute (NaCl) reabsorption; however,
water is impermeable, resulting in decreased osmolarity within the tubules.
– In the collecting ducts, it acts on V2 receptors to increase water permeability and hence
water movement along the osmotic gradient (increases water reabsorption/conservation,
no effect on solute).
• V3 receptor agonist stimulates ACTH and cortisol secretion by activating corticotropin-
releasing hormone.
• Signaling cascades:
– V1 and V3 activation stimulates phospholipase C, ultimately mobilizing intracellular
calcium stored in the endoplasmic reticulum.
– The V2 receptor responds to ADH through the activation of a G protein-coupled adenylyl
cyclase. ATP is converted to cAMP, which activates protein kinase. Protein kinase causes
water channels to fuse with the apical cell membrane and increases its permeability to
water.
• AVP promotes platelet aggregation and coagulation by increasing endothelial release of
factor VIII and von Willebrand factor (vWF).
ANATOMY
• Produced in the paraventricular and supraoptic nuclei of the hypothalamus and then
transported by way of neuronal axons to the posterior pituitary, where it is stored in
granules.
– When extracellular fluid osmolality increases, these nuclei shrink and release ADH from
the posterior pituitary. Conversely, a decrease in osmolality causes osmoreceptors to swell
and suppress ADH release.
• ADH is metabolized in the liver and kidneys and the half-life is between 5 and 20 minutes.
DISEASE/PATHOPHYSIOLOGY
• Diabetes insipidus (DI) is characterized by impairment in renal concentrating ability due to
either decreased ADH secretion (central DI) or failure of the renal tubules to respond
normally to circulating ADH (nephrogenic DI).
– Central DI causes: Trauma and postsurgical state (neurosurgical), anatomic (tumors and
infiltrative diseases, e.g., histiocytosis X), infectious (meningitis and encephalitis),
hereditary, and vascular (pituitary apoplexy)
– Nephrogenic DI causes: Chronic renal disease, electrolyte disorders (hypokalemia and
hypercalcemia), sickle cell disease, hyperproteinemias, and drugs (most notably lithium).
Nephrogenic DI is due to either a decreased response to circulating ADH or interference
with the renal countercurrent mechanism.
– Signs and symptoms of DI are polyuria and polydipsia.
– Laboratory findings are increased plasma osmolarity and decreased urine osmolarity.
– In the water deprivation test, water is withheld from the patient to induce dehydration
and to assess urinary water retention. In DI, the plasma osmolarity increases without a
urinary response to retain water. In central DI (hypothalamic), treatment with ADH
concentrates the urine. In nephrogenic DI, the kidneys fail to produce hypertonic urine
following the administration of exogenous ADH.
– Treatment of central DI involves the administration of intranasal DDAVP (1-deamino-8-D-
arginine vasopressin). Nephrogenic DI therapy is directed toward the underlying disorder
and ensuring adequate fluid intake. Thiazides induce diuresis causing an ablation of the
medullary gradient, thus decreasing urine volume output.
• Syndrome of inappropriate antidiuretic hormone (SIADH) is characterized by fluid retention,
hypoosmolality, and hyponatremia due to excessive release of ADH.
– Causes include CNS disorders including skull fracture; subdural or subarachnoid
hemorrhage; acute encephalitis; TB meningitis; Guillain–Barré syndrome; malignant
neoplasm; drugs including antineoplastics, oxytocin, narcotics, phenothiazines, tricyclic
antidepressants, carbamazepine; positive pressure ventilation; and postoperative pain.
– Signs and symptoms: Confusion, seizures, and coma due to osmotic water shifts causing
brain edema
– Laboratory findings include a decreased [Na+] (<130 mEq/L), decreased plasma
osmolarity (<270 mOsm/kg), and hypertonic urine.
– Treatment includes correction of the underlying cause, water restriction to 800–1,000
mL/d, demeclocycline which interferes with renal action of ADH, and 3% saline given
over several hours. Central pontine myelinolysis may occur if serum Na+ is corrected too
quickly.
PERIOPERATIVE RELEVANCE
• Hyponatremia (plasma [Na+] <130 mEq/L) due to SIADH should be corrected prior to all
elective procedures, even in the absence of symptoms. Lower concentrations may result in
significant cerebral edema that can be manifested intraoperatively as a decrease in the MAC
for volatile agents, or postoperatively as agitation, confusion, or somnolence.
• Anesthetic agents have little direct effect on ADH secretion. Indirectly, the surgical stress
response increases ADH secretion and may last 2–3 days postoperatively.
• Vasopressin and synthetic agonists may be used to treat intraoperative hypotension,
vasodilatory shock including anaphylaxis and sepsis, and during CPR.
– Septic shock: Endogenous AVP depletion contributes to vasodilation. AVP, when combined
with norepinephrine, increases peripheral vascular resistance and arterial blood pressure
(1)[A]. Some markers of renal function are improved with short-term AVP infusion, and
mortality is reduced at 28 days when AVP is combined with corticosteroids. Alone, AVP
permits sparing of conventional vasopressors in septic patients with relative AVP
deficiency (2)[B]. Therefore, AVP (0.01–0.04 U/min) is commonly used in the
management of septic patients and is endorsed by international sepsis treatment
guidelines (3)[A].
– Refractory hypotension in patients taking ACE inhibitors or ARBs. The administration of
vasopressin 1–2 units may be helpful in refractory cases.
– Cardiac arrest: 40 U of vasopressin via either the intravenous or intraosseous route can
replace the first or second 1 mg dose of epinephrine in patients with pulseless arrest
(pulseless electrical activity, ventricular fibrillation, or tachycardia) according to the 2010
American Heart Association guidelines on CPR (4)[B].
• DDAVP: In perioperative patients with mild hemophilia A and type 1 von Willebrand
disease, desmopressin increases endothelial release of factor VIII and vWF.
Orally administered ADH is essentially biologically inactive due to rapid hydrolysis by trypsin
and therefore must be administered parenterally. DDAVP is the only clinically available ADH
agonist and is bio-available via the intravenous, intranasal, and subcutaneous routes.
EQUATIONS
The sodium deficit, or amount of NaCl necessary to raise plasma [Na+] to the desired level,
can be estimated by the following formula:
[Na+] deficit = TBW × (desired [Na+] – measured [Na+]), where TBW = total body
weight in kilograms
FIGURE 1. In the thick ascending loop of Henle, ADH increases NaCl reabsorption thereby decreasing osmolarity within
the tubules. In the collecting ductules, ADH induces water reabsorption along the osmotic gradient resulting in more
concentrated urine.

REFERENCES
1. Treschan TA, Peters J. The vasopressin system: Physiology and clinical strategies.
Anesthesiology. 2006;105:599–612.
2. Patel BM, Chittock DR, Russell JA, et al. Beneficial effect of short-term vasopressin infusion
during severe septic shock. Anesthesiology. 2002;96:576–582.
3. Holt NF, Haspel KL. Vasopressin: A review of therapeutic applications. J Cardiothorac Vasc
Anesth. 2010;24:330–347.
4. Neumar RW, Otto CW, Link MS, et al. Part 8. Adult advanced cardiovascular life support:
2010 American Heart Association guidelines for cardiopulmonary resuscitation and
emergency cardiovascular care. Circulation. 2010;122:S729–S767.
See Also (Topic, Algorithm, Electronic Media Element)
• Diabetes insipidus
• Carotid sinus
• Syndrome of inappropriate diuretic hormone (SIADH)
• Von Willebrand disease
• Hyponatremia
• Urine osmolarity

CLINICAL PEARLS
• Antidiuretic hormone (ADH) increases NaCl reabsorption in the loop of Henle and water
permeability in the collecting duct resulting in increased water conservation, increased
urine osmolality, and decreased plasma osmolality.
• The management of nephrogenic DI is directed toward the underlying cause and also
includes fluids and thiazides. Central DI is treated with intranasal DDAVP.
• Treatment of SIADH includes correction of the underlying cause, water restriction,
demeclocycline and possibly 3% saline given over several hours. Central pontine
myelinolysis may occur if serum Na+ is corrected too quickly.
• Elevated AVP concentrations, triggered by hypotension, result in vasoconstriction.
• Vasopressin and synthetic agonists may be used to treat intraoperative hypotension,
anaphylactic and septic shock, and during CPR.
ANTIFIBRINOLYTICS
Christopher Wray, MD

BASICS
DESCRIPTION
• The 2 antifibrinolytic agents in current clinical use – epsilon-aminocaproic acid (EACA) and
tranexamic acid (TA) – are synthetic lysine analogs that are similar in mechanism of action,
molecular weight, metabolism, and clinical effects.
• Clinical uses include prophylaxis and/or adjunctive therapy for the prevention of
perioperative bleeding in a variety of patients and surgeries:
– Cardiac surgery requiring cardiopulmonary bypass (CPB)
– Liver transplantation or resection
– Orthopedic procedures (e.g., revision joints, spinal surgery)
PHYSIOLOGY PRINCIPLES
• Mechanism and regulation of fibrinolysis: The normal fibrinolytic response is a complex
physiologic reaction that prevents excessive intravascular hemostasis at the site of a
vascular injury.
– Vascular injury results in the activation of pro-coagulant pathways that culminate in the
formation of fibrin clot at the site of vascular injury.
– Intravascular fibrin and thrombin initiate the normal fibrinolytic response.
• Tissue plasminogen activator (tPA) and plasminogen are serine proteases in endothelial cells
that are released at the site of vascular injury. They bind to positively charged lysine
residues on the fibrin molecule.
– tPA and plasminogen bind to fibrin which then converts plasminogen to plasmin.
– Plasmin directly cleaves fibrin clot, resulting in fibrin degradation and clot breakdown.
– Regulation of fibrinolysis occurs via multiple local and systemic mechanisms. A delicate
balance between competing pro-coagulant and anti-coagulant systems occurs during
normal intravascular homeostasis.
• Mechanism of action of lysine analogs:
– EACA and TA share a common mechanism of action by reversibly inhibiting the binding of
plasminogen to charged lysine sites on the surface of fibrin molecules, thus preventing the
conversion of plasminogen to plasmin.
– Unlike the serine protease inhibitor aprotinin, lysine analogs do not directly inhibit the
actions of plasmin.
– The potency of TA is approximately 10 times higher than EACA.
– Plasma half-life of both drugs is approximately 2 hours, and excretion is primarily via
renal mechanisms. 95% of the drug is excreted unchanged in the urine.
DISEASE/PATHOPHYSIOLOGY
• Excessive systemic fibrinolysis may be stimulated by:
– Disease states: Sepsis, massive trauma
– Major surgery: Cardiac surgery with CPB, liver transplantation, and major orthopedic
surgery
• Consumptive coagulopathy is defined by the presence of the simultaneous generation of
both thrombin and plasmin, which results in the potential for severe diffuse bleeding.
• Systemic fibrinolysis may be detected clinically by the observation of excessive bleeding at
sites of tissue injury:
– Surgical wounds
– Intravascular catheters
– Invasive devices such as Foley catheters
• Laboratory abnormalities reflecting the degradation of fibrin clot may assist in the diagnosis
of fibrinolysis. They include:
– Increased levels of fibrin split products
– Increased D-dimer
– Decreased levels of fibrinogen
– Increased levels and activity of tPA
– Characteristic abnormalities on thromboelastogram
• Side effects of antifibrinolytics:
– Renal:
EACA has been shown to exhibit a range of nephrotoxicity (acute tubular necrosis,
myoglobin-induced renal failure, glomerular capillary thrombosis) in patients following
prolonged use and/or receiving high doses. Cardiac surgical patients with normal renal
function who receive moderate dosing protocols do not demonstrate significant renal
effects.
Both drugs should be avoided in patients with severe renal dysfunction.
– Central nervous system:
Lysine analogs cross the blood–brain barrier and have the potential to cause neuronal
hyperexcitability.
TA has been associated with a higher level of seizure activity in cardiac surgical patients
compared to aprotinin.
– Immunologic:
Lysine analogs have low molecular weights, making them less antigenic than larger
molecules associated with anaphylaxis, such as aprotinin.
– Prothrombosis:
In non-heparinized surgical patients, co-administration of antifibrinolytics poses a
potential concern for prothrombotic complications.
Studies in cardiac and liver transplant surgery patients have not shown an increase in the
rate of thrombotic complications in patients receiving antifibrinolytics (myocardial
infarction, stroke, deep vein thrombosis, pulmonary embolism, or liver graft vascular
thrombosis) (1,2).
PERIOPERATIVE RELEVANCE
• Antifibrinolytic therapy has been mainly used to control the consumptive coagulopathy that
can occur during cardiac surgery with CPB, liver transplantation, and major orthopedic
surgery.
• Cardiac surgery with CPB: Application of all extracorporeal circulation devices, including
CPB, results in the continuous systemic generation of thrombin. Despite the use of heparin
to prevent massive intravascular coagulation, thrombin generation continues throughout
CPB. TPA release, stimulated by circulating thrombin, increases throughout the duration of
CPP and remains elevated for many hours after (accompanied by accelerated fibrinolysis).
Prophylactic antifibrinolytic therapy is regularly used to decrease CPB-associated
fibrinolysis.
– Multiple studies have demonstrated decreased postoperative transfusion, decreased risk of
re-exploration, and reduced plasma markers of fibrinolysis compared to placebo.
Additionally, no increase in acute coronary artery thrombosis has been shown to occur.
TA has been studied more intensively than EACA in cardiac surgery (1,3,4).
– TA may be administered in low- or high-dose regimens. Low-dose TA: 10 mg/kg loading
dose, 1 mg/kg/hr infusion. High-dose TA: 50–150 mg/kg loading dose, 1 mg/kg/hr
infusion.
– EACA dosages: 5–10 g loading dose prior to incision, 1 g/hr infusion. The maximum safe
total dosages of EACA have been described between 30 and 90 g.
– Abnormal renal function requires lower doses.
– Some experts recommend the continuation of antifibrinolytic therapy for up to 12 hours
following CPB, although common practice is to discontinue treatment upon completion of
surgery (5).
– Topical TA administered in the wound at surgical closure has been shown to reduce
postoperative blood drainage (5).
• Orthotopic liver transplantation (OLT): Enhanced fibrinolysis is common with OLT,
especially during the anhepatic and early post-anhepatic phases of the procedure. Increased
tPA activity and decreased fibrinolytic inhibitor activity regularly occur during OLT.
Fibrinolysis contributes to blood loss and transfusion requirements during OLT. Serial
laboratory coagulation testing (thromboelastography, fibrinogen, D-dimer, fibrin
degradation products) is routinely employed to assist in the diagnosis of excessive
fibrinolysis during OLT.
– Clinical use of antifibrinolytics in OLT varies by practice: Prophylactic infusion and
selective bolus rescue dosing have been described.
– Both TA and EACA have been used clinically in OLT for many years, although TA has been
studied more extensively (2).
– TA has not been shown to increase the incidence of postoperative deep vein thrombosis or
pulmonary embolism (3,6).
– EACA: A single 1 g dose has been shown to be effective in normalizing fibrinolytic
abnormalities on thromboelastography. However, it has not definitively been shown to
impact transfusion requirements during OLT (2).
– TA has been shown to decrease blood loss and reduce transfusion requirements in
prospective studies during OLT (2,3).
– Significant preoperative renal dysfunction poses an increased risk for the exacerbation of
acute kidney injury by antifibrinolytics.
– Thromboembolic complications are a rare but devastating intraoperative complication
during OLT; there are concerns regarding the pro-thrombotic potential of antifibrinolytics
in this setting. However, antifibrinolytic therapy has never been determined as a definitive
cause of thromboembolic complications in this patient population. Antifibrinolytic therapy
should be withheld in OLT patients with a known pre-existing hypercoagulable state (2).
• Orthopedic surgery: Antifibrinolytic therapy has been employed in a variety of major
orthopedic procedures with a risk of significant blood loss, including adult and pediatric
scoliosis spine surgery and revision joints. Major prolonged orthopedic surgery may result in
significant bone and tissue trauma that can stimulate fibrinolysis. The use of a lower
extremity tourniquet, as in total knee arthroplasty, may be associated with enhanced
fibrinolysis.
– Total knee arthroplasty: Studies have demonstrated that TA use decreases blood loss and
transfusion requirements (3,6).
– Pediatric scoliosis: TA has also been shown to decrease intraoperative blood loss.
– A variety of regimens, including preoperative and postoperative oral and IV dosing, have
been described.
• Future directions in antifibrinolytic therapy:
– Fibrinogen levels: Effective antifibrinolytic therapy requires maintenance of adequate
levels of fibrinogen. Low fibrinogen levels are associated with significant post-CPB
bleeding in cardiac surgery. Cryoprecipitate transfusion has been the standard treatment
for increasing fibrinogen levels. Newly developed factor concentrates, including virus-
inactivated purified fibrinogen, may be an alternative to cryoprecipitate and fresh frozen
plasma for the treatment of hypofibrinogenemia (7).
– Aprotinin: Following the withdrawal of aprotinin in 2007, antifibrinolytic therapy has
been limited to the use of the lysine analogs.
– CU-2010—a synthetic protease inhibitor with properties similar to aprotinin—has recently
been described as a new antifibrinolytic agent; however, further clinical studies are
required (8).

REFERENCES
1. evi M. Pharmacological strategies to decrease excessive blood loss in cardiac surgery: A
meta-analysis of clinically relevant endpoints. Lancet. 1999;354:1940–1947.
2. Xia VW, Steadman RH. Antifibrinolytics in orthotopic liver transplantation: Current status
and controversies. Liver Transplant. 2005;11(1):10–18.
3. Levi M. Pharmacologic methods to reduce perioperative bleeding. Transfusion.
2008;48:S31–S38. Laupacis A. Drugs to minimize perioperative blood loss in cardiac
surgery: Meta-analysis using perioperative blood transfusion as the outcome. The
International Study of Peri-operative Transfusion (ISPOT) Investigators. Anesth Analg.
1997;85:1258–1267.
4. Edmunds HL. Managing fibrinolysis without aprotinin. Ann Thorac Surg. 2010;89:324–331.
5. Eubanks JD. Antifibrinolytics in Major Orthopaedic Surgery. J Am Acad Orthop Surg
March 2010;18: 132–138.
6. evy JH. Prohemostatic Treatment in Cardiac Surgery. Seminars in Thrombosis and
Hemostasis 2012;38:237–243.
7. ietrich W. Anesthesiology. 2009;110(1):123–130.

ADDITIONAL READING
• Dalmau A. Hemostasis and coagulation monitoring and management during liver
transplantation. Curr Opin Organ Transplant. 2009;14;286–290.
• Ide M. Lessons from the aprotinin saga: Current perspective on antifibrinolytic therapy in
cardiac surgery. J Anesth. 2010;24:96–106.
See Also (Topic, Algorithm, Electronic Media Element)
• Pulmonary embolism
• Cardiopulmonary bypass
• D-dimer
• Fibrinogen

CLINICAL PEARLS
• Excessive intravascular activity of the fibrinolytic system that results in clinically significant
bleeding may be stimulated by disease states or major surgery.
• Following the withdrawal of aprotinin, current antifibrinolytic therapy is limited to the
lysine analogs—EACA and TA.
• TA has been better studied than EACA for perioperative antifibrinolytic therapy.
• TA has been shown to improve perioperative bleeding in cardiac surgery with CPB, OLT,
and major orthopedic surgery.
ANTITHROMBIN III
Fei Zheng, MD, MPH, MS
Nanhi Mitter, MD

BASICS
DESCRIPTION
• Antithrombin III (ATIII) is one of the most important coagulation inhibitors; it stops the
progression of clot formation by inhibiting serine proteases. It is also known as
antithrombin or heparin cofactor 1.
• ATIII is the fundamental enzyme for the therapeutic action of heparin.
PHYSIOLOGY PRINCIPLES
• ATIII is a single-chain glycoprotein weighing 58 kD. It is produced by the liver and vascular
endothelial cells and is composed of 432 amino acids. ATIII circulates in the plasma with a
half-life of 2–3 days.
• ATIII inhibits serine proteases (IXa, XIa, XIIa and plasmin to a lesser degree); by blocking
their action, it prevents thrombin and factor Xa activity and ultimately clot formation.
• There are 2 functional sites on antithrombin:
– Site that binds serine proteases
– Site that binds glycosaminoglycans (i.e., heparin)
• ATIII concentrates have been developed. Currently, there are 2 types available for
intravenous administration:
– Human plasma-derived concentrate (i.e., Thrombate III®).
Prior to usage, it needs to be reconstituted with sterile water and used within 3 hours.
Must be administered intravenously; other medications should not be given through the
same line.
Classified as a pregnancy category B; safety has not been established in the pediatric
population.
Possible adverse reactions: Dizziness, chest tightness, nausea, unpleasant taste in the
mouth, chills, or cramps. Additionally, because it is derived from plasma, it has the
potential for infectious agent transmission (i.e., Creutzfeldt–Jakob, hepatitis).
– Recombinant human concentrate (i.e., ATryn®) is produced in transgenic goats with a
copy of the human antithrombin gene.
Prior to usage, it needs to be reconstituted with sterile water and should be used within
3 hours.
It is available for intravenous use only.
Classified as a pregnancy category C; safety has not been established in the pediatric
population.
Contraindications to use include a hypersensitivity to goat or goat milk.
The most common adverse reactions include hemorrhage and infusion site reaction.
ANATOMY
Produced by the liver and vascular endothelial cells
DISEASE/PATHOPHYSIOLOGY
• ATIII can have decreased levels or impaired function from either acquired or familial causes.
• Acquired causes:
– Impaired function
Heparinized patients; can decrease to 1/3rd normal values
Estrogen-based contraceptives
– Decreased levels
Neonates/infants <6 months old possibly secondary to severe malnutrition
Pregnancy: Third trimester, preeclampsia, eclampsia, disseminated intravascular
coagulation (DIC)
Cirrhosis, nephrotic syndrome, estrogen, chemotherapy, malnutrition, inflammatory
bowel disease, small bowel resection, etc.
• Familial antithrombin deficiency is mostly an autosomal dominant trait and has a 1:2,000–
5,000 prevalence in the general population. Up to 5% of individuals can present with
thrombotic disease.
– Type I (quantitative): Various DNA mutations that reduce the quantity of antithrombin.
Diagnosed with immunoassays.
– Type II (qualitative): 1 amino acid change that reduces the quality of antithrombin at
either the heparin or the thrombin binding site. Diagnosed with functional assays.
– Type III: Insufficient heparin receptors (normal quantity and quality of antithrombin)
– Clinical presentations:
Recurrent thromboembolic events
Peak incidence between 15 and 40 years of age
Most common site of thrombosis is the legs.
Thrombosis or fetal loss during pregnancy
Resistance to heparin
Family history
PERIOPERATIVE RELEVANCE
• Management of patients with ATIII deficiency (qualitative or quantitative) is controversial.
Some potential treatment options that are currently available include:
– Asymptomatic patients: No prophylaxis is needed but patients should be informed of the
increased risk of thromboembolic events under prothrombotic conditions (i.e., prolonged
bed rest, major surgeries or trauma, pregnancy, carcinoma, oral contraceptives).
– Heparin is generally the first-line treatment but it may deplete the low concentration of
normal antithrombin already present. Heparin binds to and causes a conformational
change that results in a 4,000-fold increase in ATIII activity.
– Coumadin may be added as an oral maintenance after initiation of heparin.
– Fresh frozen plasma transfusion can provide a source of antithrombin. Drawbacks include
transfusion-related acute lung injury (TRALI) and the transmission of infections.
– Antithrombin concentrates may be considered for:
Thromboembolic prophylaxis or treatment of ATIII deficiency, predominately for surgical
and peripartum women
Homozygous antithrombin deficiency not responding to heparin. Shown to be as
effective as 2 units of FFP in heparin-resistant patients undergoing elective cardiac
surgery
Acute situations (i.e., ongoing thrombosis, DIC)
Critically ill individuals
Patients in whom anticoagulation is contraindicated
– Steroids may stimulate antithrombin synthesis; however, more research is needed.
EQUATIONS
• Human plasma-derived concentrate:
– Initial dose = [(desired – current antithrombin level expressed in% of normal level) ×
weight in kg] /1.4
– For example: 70 kg patient with baseline antithrombin level of 50% and desired level of
150%. Initial dose = [(150 – 50) × 70] / 1.4 = 5,000 IU
– Maintenance dose: 60% of initial dose, given once every 24 hours
• Recombinant human concentrate:
– Initial dose = [(100 – current antithrombin activity expressed in% of normal level) ×
weight in kg] / 2.3 (1.3 in parturients)
– For example: 70 kg patient with a baseline antithrombin level of 50%. Initial dose =
[(100 – 50) × 70] / 2.3 = 1,522 IU
– Maintenance dose = [(100 – current antithrombin activity expressed in% of normal level)
× weight in kg] / 10.2 (5.4 in parturients)

REFERENCES
1. Ambruso D, Jacobson LJ, Hathaway WE. Inherited antithrombin III deficiency and cerebral
thrombosis in a child. Pediatrics. 1980;65: 125–131.
2. Avidan MS. Recombinant human antithrombin III restores heparin responsiveness and
decreases activation of coagulation in heparin-resistant patients during cardiopulmonary
bypass. J Thorac Cardiovasc Surg. 2005;130(1):107–113.
3. Beresford CH. Antithrombin III deficiency. Blood Rev. 1988;2:239–250.
4. http://en.wikipedia.org/wiki/Alexander_Schmidt_%28physiologist%29
5.
http://www.fda.gov/downloads/BiologicsBloodVaccines/BloodBloodProducts/ApprovedProd
6. http://www.talecris-pi.info/inserts/thrombate.pdf
7. Patnaik MM. Inherited antithrombin deficiency: A review. Haemophilia. 2008;14:1229–
1239.
8. Perry DJ. Antithrombin and its inherited deficiencies. Blood Rev. 1994;8:37–55.
9. Sawamura A, Gando S, Hayakawa M. Effects of antithrombin III in patients with
disseminated intravascular coagulation diagnosed by newly developed diagnostic criteria
for critical illness. Clin Appl Thromb Hemost. 2009;15(5):561–566.
10. The Medical Letter Online. Recombinant human antithrombin (ATryn). Med Lett Drug
Therap. 2009;51(1323):83–84.
See Also (Topic, Algorithm, Electronic Media Element)
• End-stage liver disease
• Cardiopulmonary bypass
• Fresh frozen plasma

CLINICAL PEARLS
• If ACT levels remain unchanged following heparin administration:
– Flush the line through which heparin was given
– Verify that the heparin is entering the bloodstream (e.g., the intravenous line is within a
vessel)
– Verify that the correct heparin dose was administered
– Check the expiration date on the heparin vial
– Administer additional heparin (up to 600 U/kg)
– Consider administering ATIII concentrate
– Consider administering FFP (2–4 units in adults)
AORTIC DISSECTION
Michael L. Boisen, MD
David G. Metro, MD

BASICS
DESCRIPTION
• Aortic dissection is characterized by the development of a tear in the aortic intima that
allows blood to enter a false lumen and cause a separation in the layers of the vessel wall.
• It is the most common aortic catastrophe, occurring with a frequency exceeding that of
abdominal aortic aneurysm rupture.
• Most acute dissections (80%) develop in the absence of a pre-existing aneurysm; thus,
distinction should be made between the terms “dissection” and “aneurysm.”
• The diagnosis of aortic dissection is missed in up to 40% of patients at initial presentation as
physical findings may be absent or nonspecific or mimic conditions for which the
therapeutic strategy is dissimilar (e.g., myocardial ischemia).
EPIDEMIOLOGY
Incidence
• Peak incidence in the 6th and 7th decades with the mean age of diagnosis at 63 years
• Males account for 65% of cases
• Circadian and seasonal patterns have been described with peak frequency between 8:00 AM
and 9:00 AM and during winter months.
• 3.5 per 100,000 persons per year (US data)
Prevalence
Actual prevalence unknown since many patients (∼20%) die prior to hospital presentation.
Autopsy series report 1 acute aortic dissection for every 128 to 745 autopsies.
Morbidity
Neurologic complications are the main cause of disability among survivors.
Mortality
• Acute dissection of the ascending aorta has a 30-day mortality rate of 20% with surgical
repair and 50% with medical therapy alone.
• Death most often results from aortic rupture, cardiac tamponade, stroke, and visceral
ischemia.
ETIOLOGY/RISK FACTORS
• Hypertension (72%)
• Atherosclerosis (31%)
• Smoking
• Bicuspid aortic valve
• Coarctation
• Deceleration trauma
• Cocaine/crack
• Pregnancy
• Iatrogenic (percutaneous cardiac and aortic or valvular surgical procedures)
• Hereditary fibrillinopathies (Marfan, Ehlers–Danlos, annuloaortic ectasia, and familial aortic
dissection)
• Vascular inflammation (Behet’s disease, syphilitic aortitis, Takayasu arteritis, and giant cell
arteritis)
PATHOPHYSIOLOGY
• The development of a tear in the intimal layer of the aorta exposes the medial layer to the
force of intraluminal blood flow. Entry of blood cleaves the intima and media longitudinally
in an anterograde and/or retrograde direction; this serves to create a second or “false”
lumen, separated from the true lumen by an intimal flap.
• Propagation of aortic dissection is linked to mean, peak, and diastolic recoil arterial pressure
as well as the rate of rise of aortic pressure (aortic dP/dt).
• Malperfusion of branch vessels can occur due to occlusion by the intimal flap or by
compression of the true lumen by expansion of the false lumen.
• Most originate in the ascending aorta (65%), followed by the descending aorta (20%), aortic
arch (10%), and abdominal aorta (5%).
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Hemodynamic stabilization, pain control, and blood pressure optimization are priorities of
initial management. In general, systolic blood pressure should be maintained at 100–120
mm Hg or the lowest level that maintains effective end-organ perfusion.
• In the past, uncomplicated distal aortic dissection (Stanford B, DeBakey III) was managed
medically; however, endovascular techniques are increasingly being applied.
• Uncomplicated distal aortic dissection (Stanford B, DeBakey III) was historically managed
medically; however, endovascular techniques are increasingly being applied.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Sudden, severe chest, back, and abdominal pain are the most common symptoms (>90%).
• Syncope (up to 20%) with or without a history of pain
• Neurologic symptoms (stroke, spinal cord ischemia, peripheral nerve ischemia)
• Acute heart failure (7%) due to myocardial ischemia or acute aortic insufficiency
• Limb ischemia
• Hoarseness (due to recurrent laryngeal nerve compression)
History
• 96% of acute aortic dissections are identified with the following prediction model:
– Aortic pain with immediate onset, a tearing or ripping character, or both
– Mediastinal widening, aortic widening, or both on chest radiography
– Pulse differentials (absence of a proximal extremity or carotid pulse), blood pressure
differentials (systolic pressure difference >20 mm Hg between arms), or both
Signs/Physical Exam
• Hypertension (69% of distal and 36% of proximal dissections)
• Hypotension, shock, or tamponade (27% of proximal dissections)
• Pulse or blood pressure differentials (20%)
• Focal neurologic deficits (12%)
• Murmur of aortic insufficiency (32%)
• Pleural effusion (left > right)
• Horner syndrome
• Superior vena cava syndrome
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Baseline and serial cardiac biomarkers, BUN/Cr, CBC with platelets, coagulation profile and
TEG, if available
• ECG may be normal (∼30%) or show nonspecific ST-T changes (40%), left ventricular
hypertrophy (26%), ischemia (15%), or infarction (10%).
• Chest radiograph findings include mediastinal widening (61%), abnormal aortic contour
(49%), pleural effusion (19%), displacement/calcification of aorta (14%). Normal findings
are present in 12% of patients.
• CT angiography is quick, highly sensitive, and specific; 64-slice multidetector CT with
cardiac gating may allow for simultaneous evaluation of pulmonary and coronary arteries.
• TEE is highly sensitive for ascending aortic dissection and allows rapid evaluation of
hemodynamic instability (tamponade, coronary dissection, valvular regurgitation, tension
hemothorax, etc.).
• MRI/MRA has high sensitivity and specificity, avoids radiation, and iodinated contrast; but
is more time-consuming and contraindicated with metallic implants.
• Aortography: Previously the reference standard, this is performed less often and rarely as
the initial study.
CONCOMITANT ORGAN DYSFUNCTION
• Compromise of aortic branches and subsequent malperfusion can affect several systems:
– Cardiovascular: Acute aortic valvular insufficiency due to aortic root dilation or leaflet
disruption; ischemia/infarction (dissections often arise from right sinus of Valsalva
causing inferior wall myocardial infarction); limb ischemia from subclavian or iliac
arteries
– Neurologic: Syncope, stroke (innominate or common carotid arteries), spinal cord
ischemia (radicular arteries), peripheral ischemic neuropathy
– Pulmonary: Left pleural effusion/hemothorax
– Renal: Ischemia, infarction, acute renal failure
• Gastrointestinal: Abdominal organ ischemia (celiac, mesenteric arteries)
CIRCUMSTANCES TO DELAY/CONDITIONS
• Delays are associated with increased mortality; thus, evaluation should be limited to the
acquisition of appropriate diagnostic studies and evaluation of conditions that will alter
surgical candidacy or affect perioperative management.
• Pericardiocentesis as a temporizing measure for tamponade has been associated with
increased risk of PEA arrest and death compared to immediate sternotomy and surgical
control of the aorta.
CLASSIFICATIONS
• Acute (<2 weeks) or chronic (>2 weeks)
• Stanford:
– Type A: Ascending aorta involved
– Type B: Ascending aorta not involved (distal to takeoff of left subclavian artery)
• DeBakey:
– Type I: Ascending aorta, arch, descending aorta
– Type II: Ascending aorta only
– Type IIIa: Descending aorta only
– Type IIIb: Descending and abdominal aorta

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Short-acting drugs permit rapid termination of effect, if desired, and should be considered.
• Morphine, beta-blockers, and vasodilating drugs can be used to control pain and blood
pressure. Esmolol is ultra-short-acting and has organ-independent elimination (metabolized
within red blood cells).
• Sodium nitroprusside may cause an increase in aortic dP/dt; it is generally added only after
a negative inotrope is administered.
• Nicardipine may be preferred in patients intolerant of beta-antagonists and does not cause a
reflex tachycardia.
• Enalaprilat may be useful in refractory hypertension due to renal artery compromise.
• Phenylephrine and norepinephrine are preferred pressors due to a relative lack of associated
increase in aortic dP/dt.
INTRAOPERATIVE CARE
Choice of Anesthesia
• No superiority has been demonstrated with any given anesthetic technique.
• For open repair, GETA is typically employed, alone or in combination with epidural
anesthesia; epidural placement may be precluded by hemodynamic instability.
• Evoked-potentials monitoring may influence technique (i.e., volatile anesthetic
concentration, use of muscle relaxant).
• For endovascular repair, local, regional, and general techniques may be used.
Monitors
• ECG with ST-segment analysis
• Temperature (central and peripheral sites if bypass is to be used)
• Foley catheter
• Arterial line: Right radial artery may be preferred if blood flow to the left subclavian artery
is disrupted due to dissection or cross-clamp placement. Femoral artery insertion may
permit monitoring of distal perfusion pressures.
• Central venous access may be appropriate for IV access and administration of vasoactive
medications.
• Pulmonary artery catheterization can provide SvO2, SVR, CO, PAP.
• TEE aids in diagnosis, anatomic localization, identification of complications, and
characterization of valvular and ventricular function in real time.
• Lumbar drains and evoked-potentials may be placed for patients at risk for spinal cord
ischemia.
• The potential for catastrophic hemorrhage necessitates appropriate vascular access,
availability of blood products, rapid infuser system, and autologous red cell salvage.
Induction/Airway Management
• Slow, controlled titration of medications to the desired effect can help maintain
hemodynamic stability. Hypertension and tachycardia increase shear stress and risk of
rupture.
• Single-lumen ETT may be typically placed for a median sternotomy approach.
• Lung isolation with a double lumen tube or bronchial blocker aids in the exposure of the
descending aorta and is preferred for procedures using the lateral thoracotomy approach.
Maintenance
• Thermoregulation: Forced air and fluid warming systems are necessary due to significant
heat loss with open procedures.
• Fluid management: Maintenance of intravascular volume may be challenging due to
significant hemorrhage and evaporative losses; no specific colloid or crystalloid strategy has
emerged as superior.
• Coagulation: Consumption and dilution of coagulation factors and platelets may be
significant; replacement is guided by conventional coagulation studies as well as TEG, if
available.
• Renal protection: Maintenance of renal blood flow and urine output is essential; IV mannitol
and fenoldopam can be employed to reduce the risk of kidney injury.
Extubation/Emergence
• Ongoing cardiac or pulmonary instability, bleeding, hypothermia, or neurologic injury may
necessitate continued mechanical ventilation; otherwise patients may be extubated at the
conclusion of the procedure.
• Pain, hypertension, and tachycardia should be anticipated and addressed.

POSTOPERATIVE CARE
BED ACUITY
Intensive care unit
COMPLICATIONS
• Aortic rupture
• Cardiac failure (ischemia, aortic insufficiency, tamponade)
• Postoperative pulmonary failure
• Neurologic deficits (stroke, paraplegia)
• Renal insufficiency

REFERENCES
1. Clouse WD, Hallett Jr JW, Schaff HV, et al. Acute aortic dissection: Population-based
incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc.
2004;79:176–180.
2. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic
Dissection (IRAD): New insights into an old disease. JAMA. 2000;283:897–903.
3. Golledge J, Eagle KA. Acute aortic dissection. Lancet. 2008;372:55–66.
4. Penco M, Paparoni S, Dagianti A, et al. Usefulness of transesophageal echocardiography in
the assessment of aortic dissection. Am J Cardiol. 2000;86:53G–56G.
5. von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection.
Arch Intern Med. 2000;160:2977–2982.
6. Isselbacher EM, Cigarroa JE, Eagle KA. Cardiac tamponade complicating proximal aortic
dissection: Is pericardiocentesis harmful? Circulation. 1994;90:2375–2379.

ADDITIONAL READING
• Nienaber CA, Eagle KA. Aortic dissection: New frontiers in diagnosis and management. Part
I: From etiology to diagnostic strategies. Circulation. 2003;108:628–635.
• Nienaber CA, Eagle KA. Aortic dissection: New frontiers in diagnosis and management. Part
II: Therapeutic management and follow-up. Circulation. 2003;108:772–778.
See Also (Topic, Algorithm, Electronic Media Element)
• Intubation/extubation criteria
• Aortic rupture

CODES

ICD9
• 441.00 Dissection of aorta, unspecified site
• 441.01 Dissection of aorta, thoracic
• 441.02 Dissection of aorta, abdominal

ICD10
• I71.00 Dissection of unspecified site of aorta
• I71.01 Dissection of thoracic aorta
• I71.02 Dissection of abdominal aorta

CLINICAL PEARLS
• Acute dissection of the proximal aorta is a surgical emergency, and preoperative evaluation
should be expedited.
• Preoperative management is directed at the reduction of arterial pressure and aortic dP/dt.
• Monitoring is essential to anesthetic management and should be individualized to the
specifics of the patient, nature of dissection, and surgical procedure.
AORTIC PRESSURE CURVE
Ryan Crowley, MD

BASICS
DESCRIPTION
• The aortic pressure curve is measured directly with an indwelling needle or catheter that is
inserted while the chest is open. The pressure in the aorta can also be directly measured by
percutaneous catheters advanced centrally from peripheral arteries.
• A transducer is then attached to the catheter to provide an arterial pressure tracing on a
physiologic monitor.
• Commonly, a more accessible central artery (femoral) or peripheral artery (radial) is
accessed using various techniques to place a catheter into the artery.
PHYSIOLOGY PRINCIPLES
• Direct monitoring of the arterial pressure curve allows for beat-to-beat measurement of
blood pressure.
• Simultaneously measuring both the left ventricular and aortic pressures demonstrates that
pressure rapidly rises in the left ventricle (LV) during early systole (see Figure 1).
• Isovolumetric contraction is the period between mitral valve closure and aortic valve
opening. When the pressure in the LV exceeds the aortic diastolic pressure, the aortic valve
opens and the upslope of the aortic pressure tracing begins.
• The peak of the aortic pressure tracing is the systolic blood pressure and in the absence of
significant aortic valve disease, also represents the LV end-systolic pressure.
• As the ventricle stops contracting and begins to relax, the pressure falls in the aorta and the
LV. When the pressure in the aortic root exceeds the LV pressure, the aortic valve closes.
This represents the second heart sound (S2).
• The dicrotic notch on the downslope of the aortic pressure tracing represents the closure of
the aortic valve. The sudden closure of the valve briefly increases the pressure in the aortic
root.
• The pressure continues to fall after the dicrotic notch as blood “runs off” to the peripheral
circulation. The lowest pressure prior to the next ejection is the diastolic blood pressure.
• Mean arterial pressure (MAP) can be estimated by the calculation: MAP = (2DBP + SBP)/3;
where DBP is diastolic blood pressure and SBP is systolic blood pressure.
ANATOMY
• The aorta is an artery composed of 3 layers. From the lumen outward it is composed of the
intima, the media, and the adventitia.
• All arteries share a similar anatomical structure, but as arteries course to more peripheral
locations, the compliant media decreases in thickness. Consequently, peripheral arteries are
less compliant than central arteries. As measurements are made in progressively more distal
arteries, there is an increase in pulse pressure (increased systolic and decreased diastolic
pressure) with only a very slight decrease in MAP.
• Due to transmission of the pressure wave from a central to peripheral location, the onset of
the pressure curve is slightly delayed in peripheral locations as compared to the aorta.
DISEASE/PATHOPHYSIOLOGY
• The aortic pressure curve can be suggestive of several pathologic states.
• A slow upstroke of the pressure tracing (decreased dP/dT) can be observed with:
– Poor LV contractility
– Aortic stenosis or arterial stenosis (e.g., coarctation of the aorta) if measured distal to the
obstruction
– Overdampening, however, can also present in this manner and should be ruled out.
• An extra wave may be seen in the aortic pressure curve, known as an anacrotic notch, which
occurs prior to peak systolic pressure. This phenomenon is most often observed in aortic
valve disease and is representative of high velocity flow.
• “Run off" describes the slope of the aortic pressure curve after the dicrotic notch and
corresponds to the afterload that the heart must contract against.
– Slow “run off" may be seen in high systemic vascular resistance (SVR) states such as
vasoconstrictor administration or a distal obstruction such as aortic coarctation
– Rapid “run off" may be seen with poor arterial compliance, aortic insufficiency, or a low
SVR state (e.g., sepsis, anaphylaxis)
• A wide pulse pressure can be indicative of very low arterial compliance (e.g., atherosclerotic
disease) or aortic insufficiency (good LV function with significant diastolic run-off due to an
incompetent aortic valve).
• Significant fluctuations in the aortic and arterial pressure tracings with respiration (>15%)
indicate decreased ventricular filling and may resolve with volume administration.
• The area under the curve (AUC) of the aortic pressure curve is proportional to stroke
volume.
• Given the same pressure, narrow curves with a small AUC represent smaller stroke volumes
than wide or “full” pressure tracings. This principle is the basis for various cardiac output
measurement devices that analyze the arterial waveform to estimate cardiac output.
• In aortic stenosis, the LV pressure tracing peak is significantly higher than the aortic
pressure peak.
– The area between the 2 tracings is the mean gradient.
– The difference between the 2 systolic peaks is the peak-to-peak gradient. The peak-to-peak
gradient is lower than the peak instantaneous gradient (PIG) derived from
echocardiography.
PERIOPERATIVE RELEVANCE
• Direct arterial blood pressure monitoring (typically peripherally) is indicated whenever
significant or rapid changes in blood pressure are anticipated.
• When displayed on a monitor with a static scale, the clinician can detect changes in systemic
blood pressure immediately by observing changes in the arterial pressure tracing.
• The blood pressure value displayed on physiologic monitors is averaged over many
preceding seconds while changes in the waveform are displayed without any delay.
• Continuous MAP determination can be utilized to ensure appropriate end-organ perfusion
pressures to the brain, kidneys, etc. in patients with limited reserve.
• Continuous diastolic blood pressure measurements can be used to ensure adequate LV
perfusion in patients at risk for ischemia (especially in conjunction with monitoring of
pulmonary capillary wedge pressure [PCWP], left atrial pressure [LAP], or pulmonary artery
diastolic pressure [PADP]).
• Continuous systolic blood pressure measurement can be used to minimize aortic wall tension
in patients with significant aortic disease (e.g., aneurysm or dissection).
EQUATIONS
• MAP = 2/3 DBP + 1/3 SBP; where MAP is mean arterial pressure, DBP is diastolic blood
pressure, and SBP is systolic blood pressure
• MAP = (2 [DBP + SBP])/3
• CO = (MAP – CVP) × SVR; where CO is cardiac output, MAP is mean arterial pressure, CVP
is central venous pressure, and SVR is systemic vascular resistance
GRAPHS/FIGURES

FIGURE 1. Aortic pressure curve (solid line) with the left ventricular pressure curve (dashed lines) superimposed.

REFERENCES
1. Marik PE, Cavallazzi R, Vasu T, et al. Dynamic changes in arterial waveform derived
variables and fluid responsiveness in mechanically ventilated patients: A systematic review
of the literature. Crit Care Med. 2009;37(9):2642–2647.
2. Morgan P, Al-Subaie N, Rhodes A. Minimally invasive cardiac output monitoring. Curr
Opin Crit Care. 2008;14(3):322–326.
See Also (Topic, Algorithm, Electronic Media Element)
• Cardiac output
• Aortic stenosis

CLINICAL PEARLS
• Blood is ejected from the left ventricle to the aorta during the period where the upstroke of
the aortic pressure curve meets the left ventricular pressure curve and until the dicrotic
notch.
• Respiratory variation in the aortic pressure tracing predicts for volume responsiveness.
• Direct measurement of arterial pressure allows for the continuous determination of
perfusion pressures to end-organs.
• As one measures arterial pressure from proximal to distal locations, the
– Systolic pressure increases
– Diastolic pressure decreases
– Pulse pressure increases
– MAP slightly decreases
AORTIC REGURGITATION
Brian L. Marasigan, MD

BASICS
DESCRIPTION
• The aortic valve, normally consisting of 3 leaflets, opens during ventricular systole and
closes during diastole. Valve closure prevents backflow of blood from the aorta to the left
ventricle (LV) and helps maintain aortic diastolic pressure and coronary perfusion pressure.
• Aortic regurgitation (AR) is the presence of a backflow leak through the valvular apparatus
during diastole.
– Ranges in severity from trace, mild, moderate, or severe; it is classified by the amount of
regurgitant volume, regurgitant orifice area size, and pressure equalization half-time by
echocardiography.
– Regurgitation may be associated with any condition that alters aortic valve closure. Aortic
dilation, aneurysm, dissection, and abscess are external causes of aortic valve dysfunction
and account for about half of all AR cases. Rheumatic valve disease, collagen vascular
diseases, connective tissue diseases (especially Marfan syndrome (1)[C]), congenital
malformations, senile degeneration, and infective endocarditis are direct valvular
conditions that commonly produce AR in the remainder of cases.
– Acute AR is the sudden onset of backflow leak usually due to an acute event such as aortic
dissection or valvular trauma.
– Chronic AR has a gradual onset and may be sustained for many years.
– May also accompany aortic stenosis—a narrowing of the open valvular area
EPIDEMIOLOGY
Prevalence
• Worldwide, rheumatic heart disease is the most common cause of AR.
• In the US, congenital and degenerative valvular and aortic disease is most common.
• Congenital bicuspid aortic valves occur in 1–2% of the US population and may contribute to
AR.
Prevalence
• 13% in men, 8.5% in women in a Framingham study (2)
• In the US population, severe AR is <1% (3).
• Chronic AR is more prevalent than acute AR.
Morbidity
• Acute AR has a higher rate of morbidity and mortality due to the underlying
pathophysiology. This can result in diastolic and systolic dysfunction and eventually
decompensation (CHF).
• Chronic AR mortality is related to the eventual decompensation of the LV; it is more
common in severe AR. Decreased ejection fraction and LV function have a poor prognosis
for recovery, even after repair.
• Surgical management becomes the common end point to both types of AR.
Mortality
• Acute AR has a high mortality due to sudden uncompensated cardiovascular changes usually
requiring immediate surgical management.
• Chronic AR mortality relates to eventual decompensation of the LV and may occur at any
age usually with severe AR. Decreased ejection fraction and LV function has a poor
prognosis for recovery even after repair.
• Yearly mortality risk relates to NYHA classification for chronic severe AR:
– Asymptomatic: 2.8%
– NYHA Class I: 3.0%
– NYHA Class II: 6.3%
– NYHA Class III–IV: 24.6% (4)
ETIOLOGY/RISK FACTORS
• Male gender has a greater risk for AR with a related increased risk of hypertension,
connective tissue and congenital valvular diseases, which may result in presentation at a
younger age.
• Severe AR is most commonly diagnosed at age 60 and above.
PHYSIOLOGY/PATHOPHYSIOLOGY
• Acute AR results in an acute increase in LV diastolic volume, decreased aortic diastolic
pressure (forward flow), decreased coronary perfusion pressure, volume overload, and
decreased diastolic function of the LV. This leads to an increase in myocardial demand,
acute fulminant CHF, and cardiogenic shock. Common causes of acute AR, including aortic
dissection, warrant emergent surgical repair.
• Chronic AR has a more insidious onset and may take years to become symptomatic. As
regurgitant volume and AR worsen over time, the LV has time to remodel with eccentric
hypertrophy and dilation. The increase in diastolic volume is compensated by the enlarged
LV, increased heart rate, and decreased systemic vascular resistance (SVR). Ejection fraction
is maintained and may prevent symptoms without exertion or positional changes. As time
passes, the ventricle becomes “too enlarged” with resultant increases in wall stress and
decreases in myocardial perfusion (leads to diminished EF, CHF, and end-organ
hypoperfusion). Recall Laplace’s law where Tension = (Pressure × Radius)/Wall Thickness;
as the radius increases, tension also increases (increases myocardial oxygen consumption).
Sympathetic stimulation increases SVR to maintain pressure but worsens AR; hinders
forward flow. Without timely surgical repair the heart may not be able to significantly
recover.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Maintenance of cardiac output, coronary perfusion, and prevention of cardiac
decompensation are the primary goals.
• Normal sinus rhythm and avoidance of bradycardia to minimize regurgitant time
• SVR may be mildly decreased, but should be balanced between facilitating forward flow
(decreasing regurgitation) and maintaining adequate coronary and systemic perfusion
pressure.
• Careful fluid management and inotropic support to prevent cardiovascular overload or
collapse

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Chronic AR may be asymptomatic for decades.
• Palpitations and tachycardia
• Fatigue
• Dyspnea on exertion
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Angina
History
• Family history of cardiac valvular disease, collagen or connective tissue disease, or
congenital malformations
• History of rheumatic disease or risk factors for endocarditis
• Commonly diagnosed after symptomatic exercise or during workup for diastolic or systolic
CHF
• May be discovered early after detailed physical exam and auscultation of heart murmur
• Usually classified by echocardiographic measurement of color Doppler flow across the valve
Signs/Physical Exam
• Syncope
• Cyanosis
• Decrescendo diastolic murmur
• Watson’s hammer pulse (bounding pulse)
• Corrigan’s carotid pulse
• Wide pulse pressure
• Signs of CHF
TREATMENT HISTORY
• Medical management of angina, CHF, diabetes, hypertension, and hyperlipidemia, if
associated
• Previous history of balloon aortic valvuloplasty or valve replacement
• Previous treatment of infective endocarditis
• Transesophageal echocardiography for diagnosis and risk stratification
MEDICATIONS
• Antihypertensives including calcium channel blockers; beta-blockers are usually not
prescribed since they may cause bradycardia.
• Anti-anginals including nitrovasodilators
• Heart failure treatments including digoxin, ACEI/ARB, and diuretics
• Statin therapy if indicated
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Basic metabolic profile: Monitoring electrolytes and kidney function
• CBC: Monitoring for preoperative infection and hematocrit and platelet counts adequate for
surgery
• CXR: Cardiopulmonary status
• CT scan for evaluation of aorta
• Echocardiogram: Diagnosis and classification of disease severity and ventricular function
• Basic coagulation studies: Adequate levels for surgery and evaluation of liver function
CONCOMITANT ORGAN DYSFUNCTION
• Dilated cardiomyopathy and diastolic dysfunction
• Concomitant mitral stenosis or regurgitation in rheumatic heart disease
• Pulmonary hypertension, congestion, and pleural effusion
• Renal insufficiency
• Hypertension
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Unrelated end-organ failure
• Recent myocardial infarction or stroke
CLASSIFICATIONS
Severe AR criteria:
• >60 mL regurgitant volume
• >50% regurgitant volume
• Effective regurgitant orifice area >0.3 cm2
• Color Doppler Vena Contracta >0.6 cm
• Regurgitant jet >60% of LVOT diameter
• Aortic valve pressure half-time <250 ms
• Early closure of mitral valve and LV dilation

TREATMENT

PREOPERATIVE PREPARATION
Premedications
Midazolam to prevent anxiety and increased sympathetic tone, as appropriate
Special Concerns for Informed Consent
Risk for intraoperative stroke, myocardial infarction, and death should be discussed.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Depends on the procedure; sedation, general (endotracheal tube or laryngeal mask airway)
and regional anesthesia may be utilized.
• Neuraxial techniques can result in a sympathectomy and facilitate forward flow (reduce
regurgitation), but may reduce coronary perfusion pressure.
Monitors
• Standard ASA monitors
• Invasive monitors may be chosen based upon the severity of AR and the surgical procedure.
Induction/Airway Management
• Smooth, controlled induction to maintain vital signs within normal limits
• Anticholinergic medications may be administered to maintain a NSR and slightly increase
the heart rate.
Maintenance
• Volatile and/or intravenous anesthetics may be utilized. Reductions in SVR are desirable to
facilitate forward flow; however, adequate cerebral and coronary perfusion should be
ensured. Total intravenous techniques may be associated with bradycardia, particularly if
utilizing high doses of remifentanil.
• Fluid balance includes maintaining normal preload and hematocrit >24–30 g/dL to
optimize forward flow and myocardial oxygen balance. Excessive preload may add to
regurgitant volume and cause LV failure.
Extubation/Emergence
No additional concerns

FOLLOW-UP

BED ACUITY
Depends on surgical procedure and severity of underlying disease
MEDICATIONS/LAB STUDIES/CONSULTS
Standard postoperative fluid and electrolyte management and related laboratory studies
COMPLICATIONS
Perioperative arrhythmia

REFERENCES
1. Odili AN, Amusa GA. Aortic aneurysm with valvular insufficiency: Is it due to Marfan
syndrome or hypertension? A case report and review of literature. J Vasc Nurs.
2011;29(1):16–22.
2. Singh JP, Evans JC, Levy D, et al. Prevalence and clinical determinants of mitral, tricuspid,
and aortic regurgitation. Am J Cardiol. 1999;83:897–902.
3. Maurer G. Aortic regurgitation. Heart. 2006;92(7):994–1000.
4. Dujardin KS, Enriquez-Sarano M, Schaff HV, et al. Mortality and morbidity of aortic
regurgitation in clinical practice: A long-term follow-up study. Circulation.
1999;99(14):1851–1857.

ADDITIONAL READING
• 2006 American College of Cardiology/American Heart Association Guidelines
• Van Dyck MJ, Watremez C, Boodhwani M, et al. Review articles: Transesophageal
echocardiographic evaluation during aortic valve repair surgery. Anesth Analg.
2010;111:59–70.

CODES

ICD9
• 395.1 Rheumatic aortic insufficiency
• 424.1 Aortic valve disorders
• 746.4 Congenital insufficiency of aortic valve

ICD10
• I35.1 Nonrheumatic aortic (valve) insufficiency
• I06.1 Rheumatic aortic insufficiency
• Q23.1 Congenital insufficiency of aortic valve

CLINICAL PEARLS
• Aortic regurgitation (AR) is most commonly an acquired disease but may be related to
congenital malformations and several systemic conditions such as Marfan syndrome.
• Significant signs and symptoms include shortness of breath, angina, syncope, and systolic
and diastolic congestive heart failure with eccentric hypertrophy and a dilated LV.
• Severity is classified by echocardiographic criteria; 60 mL or 50% regurgitant volume being
severe AR.
• Acute AR is life-threatening and often requires immediate surgical management.
• Chronic AR requires medical or surgical management and may be asymptomatic until late
stages. Symptomatic, severe AR with below normal LV EF requires urgent treatment and has
poorer prognosis.
AORTIC STENOSIS
Brian L. Marasigan, MD

BASICS
DESCRIPTION
• The aortic valve normally consists of 3 leaflets which open during ventricular systole with
an area of >2.5 cm2 and close during diastole. Since the aortic valve is the smallest area
through which blood leaves the heart, its diameter determines maximum blood flow.
• Aortic valve stenosis is a narrowing of this area at the valve itself. New recommendations
classify severe aortic stenosis (AS) as an area <1.0 cm2 with a transvalvular mean gradient
>40 mm Hg, although symptoms may begin at much earlier stages. It is the most common
valvular lesion in the US.
EPIDEMIOLOGY
Prevalence
• Congenital AS occurs in 4–8 per 1,000 live births.
• Congenitally bicuspid aortic valves occur in 1–2% of the US population and later in life
accounts for 30–40% of AS.
• >50% of AS is acquired.
Prevalence
Present in 2–4% of adults aged 65 years and older (1)[B].
Morbidity
• Risk for acute myocardial infarction, syncope, congestive heart failure (CHF), and
endocarditis
• Low-grade severe stenosis with preserved ejection fraction has similar outcomes to those
with moderate stenosis (2)[B].
• Asymptomatic very severe AS (area <0.75 cm2) has a very poor prognosis and rapid
deterioration; elective valve surgery should be considered (3)[A].
Mortality
• 9% mortality per year
• Symptomatic AS sudden death risk is 15–20% with a 3-year mortality of 75%.
• When symptoms of angina, syncope, or CHF are present, 50% mortality is seen at
approximately 5, 3, and 2 years, respectively.
ETIOLOGY/RISK FACTORS
• Age <70 years: The etiology of AS is more commonly rheumatic or bicuspid aortic valve
disease.
• Age >70 years: The etiology of AS is more commonly calcific AS.
• Risk factors are similar to vascular disease and may include hyperlipidemia, hypertension,
and diabetes.
PHYSIOLOGY/PATHOPHYSIOLOGY
• The basic pathophysiology of AS stems from obstruction of cardiac output with a highly
resistant valve opening. As the stenosis becomes more severe, the left ventricle (LV)
compensates with concentric hypertrophy to overcome the increasing afterload/tension;
stroke volume is maintained. Additionally, cardiac output becomes fixed and highly
dependent upon heart rate and filling (diastolic dysfunction).
• Myocardial oxygen supply and demand
– Supply decreases from: A thickened myocardium (coronary blood flow must
perfuse/penetrate), increased left ventricular end diastolic pressure (decreased coronary
diastolic perfusion pressure), and limited cardiac output.
– Demand increases from: A thickened myocardium (more muscle equals increased energy
consumption) and increased afterload.
• Over time, systolic function can decrease as the LV decompensates and dilates or becomes
ischemic. Ventricular systolic and diastolic dysfunction can lead to pulmonary congestion
and CHF. Additionally, sympathetic tone increases and may contribute to symptoms.
• A slow heart rate is desired to allow time for forward flow after an adequate LV pressure has
been attained. Maintaining a sinus rhythm is necessary, as LV hypertrophy impairs filling
and the atrial kick is needed to maintain adequate LV end diastolic volume (preload).
• Both normal and congenitally bicuspid valves undergo degeneration through which scarring,
calcification, and sclerosis become the most common cause of acquired AS.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Maintenance of cardiac output, coronary perfusion (diastolic perfusion pressure), normal
sinus rhythm, volume status, and prevention of cardiac decompensation are the primary
goals.
• Inotropic support may be necessary to prevent cardiovascular overload or collapse.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Severity of symptoms may be classified by NYHA I–IV. Early symptoms often include
exertional shortness of breath.
– Anginal pain may be an early symptom and may occur in the absence of coronary
occlusion.
– Syncope may occur due to a decrease in cardiac output and exertional systemic
vasodilation.
– CHF is often a late sign that signifies severe valve stenosis or cardiomyopathy.
History
• Commonly diagnosed after symptomatic exercising or during workup for diastolic or systolic
CHF
• May be discovered early after detailed physical exam and heart auscultation
Signs/Physical Exam
• Crescendo–decrescendo systolic murmur and decreased S2 sound
• Pulsus parvus et tardus with narrow pulse pressure
• Signs of CHF and increased sympathetic tone
TREATMENT HISTORY
Previous history of balloon aortic valvuloplasty or valve replacement
MEDICATIONS
• Antihypertensives including beta-blockers and calcium channel blockers
• Anti-anginals including nitrovasodilators
• Heart failure treatments including digoxin, ACEI/ARB, and diuretics
• Statin therapy
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Basic metabolic profile to monitor electrolytes and kidney function; aids with perioperative
management
• CBC: WBC to monitor for infection; Hct and platelet counts should be adequate for surgery.
• CXR to assess cardiopulmonary status
• Echocardiogram for diagnosis and classification of disease severity (valve area, transvalvular
gradient) and ventricular function
• Basic coagulation studies to evaluate liver function
CONCOMITANT ORGAN DYSFUNCTION
• Cardiac: LV hypertrophy, diastolic dysfunction, hypertension, aortic regurgitation (due to
poor valve closure), mitral stenosis, or regurgitation in rheumatic heart disease
• Pulmonary: Hypertension, congestion, and pleural effusion
• Renal insufficiency
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Decompensated CHF
• Sepsis or infection
• Unrelated end-organ failure
• Recent myocardial infarction or stroke
CLASSIFICATIONS
• AS severity by valve area:
– >2.5 cm2: Normal
– 1.5–2.0 cm2: Mild stenosis
– 1.0–1.5 cm2: Moderate stenosis
– <1.0 cm2: Severe stenosis
• AS severity by mean pressure gradient:
– <25 mm Hg: Mild stenosis
– 25–40 mm Hg: Moderate stenosis
– >40 mm Hg: Severe stenosis

TREATMENT

PREOPERATIVE PREPARATION
Premedications
Benzodiazepines may be useful to prevent anxiety and tachycardia; however, they should be
titrated cautiously to avoid sympatholysis.
Special Concerns for Informed Consent
• Risk for intraoperative stroke, myocardial infarction, and death should be discussed.
• Arterial line placement if needed
INTRAOPERATIVE CARE
Choice of Anesthesia
• Depends on the procedure: Sedation, general (endotracheal tube or laryngeal mask airway)
and peripheral nerve blocks may be utilized.
• Neuraxial techniques can result in a sympathectomy and decreased systemic vascular
resistance (SVR) that can impair coronary perfusion. This technique may be considered in
mild or moderate AS. Epidurals can allow for slower bolusing, time for fluid loading, and
treatment of hypotension with vasopressors (phenylephrine).
Monitors
• Standard ASA monitors
• 5-lead EKG for arrhythmia and ischemia
• Arterial line for beat-to-beat BP monitoring
• Invasive monitors may be chosen based upon the severity of AS and the surgical procedure.
Induction/Airway Management
A smooth, controlled induction should be performed to maintain vital signs within normal
limits (heart rate and SVR) and allow time for treatment.
Maintenance
• Volatile anesthetics, intravenous, or a combination may be utilized. The goal should be to
maintain normal sinus rhythm and SVR.
– Total intravenous anesthesia with propofol and high-dose narcotics can result in
bradycardia and hypotension; consider concurrent phenylephrine, ephedrine, or an
anticholinergic.
– Volatile agents can decrease SVR and myocardial contractility; consider concurrent
phenylephrine.
• Preload. Because stroke volume is fixed, adequate filling volumes are essential in
maintaining a stable cardiac output. For patients at risk for ischemic events, hematocrit
values may also be of concern.
• Rhythm, rate, blood pressure
– Normal sinus rhythm may be maintained by minimizing cardiac stress and avoiding pro-
arrhythmic drugs
– Slight bradycardia may improve coronary perfusion time and LV filling but may decrease
total cardiac output (stroke volume is fixed). Conversely, tachycardia increases myocardial
oxygen consumption along with decreases in LV filling time and diastolic coronary
perfusion time. Caution should be exercised when using powerful chronotropes or
anticholinergics.
– Hypotension and hypertension should be managed with rate and rhythm in mind. All
inotropes and vasopressors may be used with caution.
• Ischemia usually occurs with arrhythmia, tachycardia, or hypotension, and the treatment
usually lies in the reversal of those conditions.
Extubation/Emergence
• Avoid tachycardia and hypotension
• Use standard extubation criteria

FOLLOW-UP
BED ACUITY
Depends on surgical procedure, severity of underlying disease, and intraoperative events
MEDICATIONS/LAB STUDIES/ CONSULTS
Cardiology consult may be considered in severe disease if ischemic events occurred
intraoperatively.
COMPLICATIONS
• Perioperative arrhythmia
• Mental status changes and stroke
• Myocardial infarction

REFERENCES
1. Freeman RV, Otto CM. Spectrum of calcific aortic valve disease: Pathogenesis, disease
progression, and treatment strategies. Circulation. 2005;111(24):3316–3326.
2. Jander N, Minners J, Holme I, et al. Outcome of patients with low gradient “severe” aortic
stenosis and preserved ejection fraction. Circulation. 2011;123(8):887–895.
3. Rosenhek R, Zilberszac R, Schemper M, et al. Natural history of very severe aortic stenosis.
Circulation. 2010;121(1):151–156.

ADDITIONAL READING
• Andritsos M, Singh N, Patel P, et al. The year in cardiothoracic and vascular anesthesia:
Selected highlights from 2010. J Cardiothorac Vasc Anesth. 2011;25(1):6–15.
See Also (Topic, Algorithm, Electronic Media Element)
• Aortic regurgitation
• Aortic valve replacement

CODES

ICD9
• 395.0 Rheumatic aortic stenosis
• 424.1 Aortic valve disorders
• 746.3 Congenital stenosis of aortic valve

ICD10
• I35.0 Nonrheumatic aortic (valve) stenosis
• Q23.0 Congenital stenosis of aortic valve
• I06.0 Rheumatic aortic stenosis

CLINICAL PEARLS
• Severity is classified by valve area and transvalvular gradients; values <1.0 cm2 and a mean
pressure gradient of 40 mm Hg indicate severe AS.
• Maintenance of general anesthesia includes supporting cardiac systolic function, optimizing
fluid management, sustaining normal sinus rhythm, and monitoring for ischemia.
AORTIC VALVE REPLACEMENT
Sascha Beutler, MD, PhD
Daniel Castillo, MD

BASICS
DESCRIPTION
General
• Aortic valve replacement is an open, intracardiac surgery procedure in which the stenotic or
regurgitant aortic valve is replaced with a healthy valve. The 2 basic artificial heart valves
are mechanical and tissues valves.
• Following sternotomy, opening of the pericardium, and routine venous and arterial
cannulation, the patient is taken onto full cardiopulmonary bypass (CPB). After the heart is
arrested, the aorta is opened to expose the aortic valve. The valve leaflets are excised and
the annulus is debrided. The annulus is then measured to properly match the prosthetic
valve. Interrupted sutures are placed through the annulus for its entire circumference and
then passed through the sewing ring. The prosthesis is tied securely in place.
• Systemic rewarming is initiated during the final stages of the valve implantation, and the
left ventricle is allowed to fill during aortic closure. With the patient in the head-down
position, all remaining air is vented from the left heart and aorta. The cross-clamp is
removed.
• Pacing wires and chest tubes are placed and the patient is weaned from bypass. Once the
patient is stable, decannulation and heparin reversal are accomplished in routine manner.
• Concomitant root replacement may be necessary in patients with aortic stenosis secondary
to bicuspid valve pathology and concurrent aortic root dilations.
• Pulmonary autograft (Ross procedure) involves replacing the aortic valve with a pulmonary
valve autograft and right-sided reconstruction with a homograft; it is used in children and
adolescents.
• Minimally invasive aortic valve surgery through smaller incisions with specialized
instruments is being explored; for the surgery on the valve itself conventional instruments
and techniques are used.
– Only selected patients are eligible for these approaches.
– Initial results are favorable in regard to clinical outcome, perioperative complications and
cost.
– No randomized controlled trials are available comparing minimally invasive and open
surgery.
• Transcatheter aortic valve replacement is a new catheter-approach that obviates the need for
open heart surgery. It is being used in Europe and parts of the world, but only tested in
clinical trials in the US. The results for high-risk patients with severe aortic stenosis who are
not surgical candidates are promising (1)[B].
Position
• Supine, arms tucked
• Temporary Trendelenburg at the time of left ventricle de-airing, prior to coming off bypass
Incision
• Standard: Median sternotomy
• Alternative incision sites (e.g., right second intercostal anterior thoracotomy) are used as
part of “minimally invasive aortic valve surgery.”
Approximate Time
4–8 hours, depending on the experience of the team and technical difficulties
EBL Expected
• CPB machine leads to dilution.
• Blood loss typically ranges from 1,000 to 2,000 mL.
Hospital Stay
Typical length of stay in the surgical ICU is 1–3 days and 3–7 days in the hospital overall.
Special Equipment for Surgery
• Valve (mechanical or tissue)
• CPB machine (operated by perfusionist)
• Minimally invasive approaches require special equipment.
• Transesophageal echocardiography probe (intraoperative examination performed by echo
trained anesthesiologists or cardiologist)
EPIDEMIOLOGY
Prevalence
In 2009 approximately 70,000 patients underwent aortic valve replacement in the US.
Morbidity
• The 2008 ACC/AHA Valvular Disease guidelines refer to risk stratification models to
estimate the risk of in-hospital mortality and morbidity of valve surgery with or without
coronary artery bypass (2). All models have drawbacks such as estimating risk for only one
specific procedure or not including patient’s variable like nutritional status. There are 3
major models:
– The US-based registry by the Society of Thoracic Surgeons (STS) (3)[B]. It includes data
from nearly 90% of cardiac surgery providers in the US and may provide the most
accurate risk stratification for aortic valve replacement.
– The European System for Cardiac Operative Risk Evaluation (“EuroScore")
– The scoring system developed from Great Britain’s and Ireland’s national database
Mortality
• Varies significantly with age, comorbidities, type of valvular lesion, ventricular function,
other concomitant valvular surgery, and/or bypass surgery
• Risk stratification models are useful to predict mortality risk for the individual patient.
Example: Mortality <1% in a 65-year-old patient with symptomatic severe aortic stenosis,
normal left ventricular function and otherwise healthy; however, mortality increases >1%
for the same patient with hypertension and diabetes.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Hemodynamic stability from induction to the initiation of bypass. Management depends on:
The type of lesion (stenosis vs. regurgitation), right and left ventricular function, pulmonary
pressures, and other clinical factors.
• After successful replacement and completion of bypass, the goal is to maintain adequate
cardiac output and blood pressure; inotropes may be required if left ventricular function is
depressed.

PREOPERATIVE ASSESSMENT
SYMPTOMS
Vary depending on the type of lesion (stenosis vs. regurgitation) and the time course (acute
vs. chronic)
History
Determine if there is a history of esophageal strictures or other abnormality that would
prohibit placement of transesophageal echocardiography during the procedure.
Signs/Physical Exam
See “Aortic Stenosis” and “Aortic Regurgitation” chapters
MEDICATIONS
• Medical management depends on the type of lesion and other comorbidities.
• Initiation of statins may reduce the incidence of atrial fibrillation and mortality.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Preoperative transthoracic echocardiography and sometimes a transesophageal
echocardiography are performed.
• Coronary angiography is routinely performed since significant coronary artery disease is a
common comorbidity and may require concurrent coronary bypass grafting.
CONCOMITANT ORGAN DYSFUNCTION
• Renal dysfunction; further deterioration may be precipitated by contrast dye used during
catheterization (prior to the valve replacement) and increased bypass time.
• Chronic pulmonary disease may acutely worsen secondary to bypass and lead to hypoxemia
when coming off.
• Pre-existing neurologic deficits put the patient at great risk for further mental status
deterioration postoperatively.
TREATMENT

PREOPERATIVE PREPARATION
Premedications
Consider gentle anxiolysis with benzodiazepines
Special Concerns for Informed Consent
Morbidity and mortality risks vary with the extent of surgery (e.g., coronary bypass surgery
in addition to valve replacement) and pre-existing comorbidities.
Antibiotics/ Common Organisms
Skin flora poses the greatest concern; cefazolin is utilized if the patient is not a carrier of
multi-resistant bacteria and there is no allergy. It is administered intravenously within 60
minutes prior to incision and repeated q3–4h until chest closure.
INTRAOPERATIVE CARE
Choice of Anesthesia
• General anesthesia in the US
• There are case reports of open heart surgery performed under epidural with sedation in
other parts of the world.
Monitors
• ASA standard monitoring; core and shell temperatures are measured.
• Arterial line placement most often prior to induction; the absence of pulsatile blood flow
during bypass precludes noninvasive blood pressure measurement.
• Central venous access is usually obtained after induction; pulmonary artery catheter
placement may be considered.
• Transesophageal echocardiography is frequently used intraoperatively to guide and assess
aortic valve replacement.
Induction/Airway Management
• Goal is to provide hemodynamic stability throughout the induction period. Gentle propofol
administration (with vasopressors and inotropes as needed) or etomidate in combination
with fentanyl.
• In the event of hemodynamic instability CPB may be instituted immediately.
Maintenance
• Patients are usually maintained with oxygen/volatile agents and intermittent doses of
opioids and non-depolarizing muscle relaxants.
• During bypass, volatile agent is added to the blood by the perfusionist through the bypass
machine.
• The management of patients during bypass varies substantially by institution and
practitioner.
• On bypass the target mean arterial blood pressure is typically between 50 and 80 mm▒Hg.
• On bypass the patient’s body temperature is cooled at the beginning and warmed to normal
body temperature before termination of bypass.
Extubation/Emergence
• Patients remain intubated and are transferred to the ICU.
• Sedation is typically provided with propofol or dexmedetomidine infusion. The latter
appears to have a lower risk for the development of postoperative delirium.

FOLLOW-UP

BED ACUITY
• Surgical ICU
• The time to extubation varies from a few hours to 24 hours and even days, depending on the
patient’s hemodynamic status, respiratory status, bleeding/coagulation, and other organ
systems.
ANALGESIA
• Usually provided by intravenous opioids either as intermittent boluses or as continuous
infusion until extubation
• Once the patient is extubated and bowel function has returned, oral opioids can be given.
COMPLICATIONS
• Bleeding, reoperation, heart block (requires insertion of permanent cardiac pacemaker),
stroke, renal failure, prolonged ventilation, infection; the incidence varies depending on
preoperative status, length and type of operation.
• Atrial fibrillation
• Replacement of a diseased heart valve with a prosthetic valve exchanges the native disease
for complications that are unique to the prosthetic valve.
– Structural failure, though not uncommon with bioprosthesis, is very rare with mechanical
valves.
– Severe and recurrent bleeding due to anticoagulant therapy: Mechanical valves require
long-term anticoagulation therapy, most often with warfarin, while patients with
bioprosthetic valves usually receive anticoagulation with warfarin only for 6 weeks to 3
months postoperatively and then aspirin lifelong.
– Valvular thrombosis and thromboembolic events, especially in patients with mechanical
valves and inadequate anticoagulant therapy
– Severe hemolysis is seen mostly with mechanical valves
– Endocarditis
• Complications associated with open heart surgery and CPB
PROGNOSIS
As survival after a first valve replacement has improved, more patients require a second
operation for replacement (about 2–3% during the first 10 years).
REFERENCES
1. Leon MB, Smith CR, Mack M. Transcatheter aortic-valve implantation for aortic stenosis in
patients who cannot undergo surgery. N Engl J Med. 2010;363(17):1597–1607.
2. Bonow RO, Carabello BA, Chatterjee K, et al. Focused update incorporated into the
ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A
report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. Circulation. 2008;118:e523–e661.
3. Shahian DM, O’Brien SM, Filardo G, et al. The Society of Thoracic Surgeons 2008 cardiac
surgery risk models. Part 2: Isolated valve surgery. Ann Thorac Surg. 2009;88:S23–S42.

ADDITIONAL READING
• Tabata M, Umakanthan R, Cohn LH, et al. Early and late outcomes of 1000 minimally
invasive aortic valve operations. Eur J Cardiothorac Surg. 2008;33:537–541.
• www.sts.org/quality-research-patient-safety/quality/risk-calculator-and-models/risk-
calculator
• www.euroscore.org
• www.ucl.ac.uk/research/riskmodel/index.html
See Also (Topic, Algorithm, Electronic Media Element)
• Aortic valve stenosis
• Aortic valve regurgitation
• Cardiopulmonary bypass

CODES

ICD9
• V42.2 Heart valve replaced by transplant
• V43.3 Heart valve replaced by other means

ICD10
• Z95.2 Presence of prosthetic heart valve
• Z95.3 Presence of xenogenic heart valve
• Z95.4 Presence of other heart-valve replacement

CLINICAL PEARLS
• Aortic valve replacement is an open, intracardiac surgery requiring CPB. The standard
approach is a median sternotomy; newer minimally invasive techniques are on the rise.
• Risk stratification models can help predict mortality and morbidity for the individual
patient.
• There is a significant rate of structural failure of bioprosthetic valves within the first 10–15
years that can require reoperation.
AORTOCAVAL COMPRESSION OF PREGNANCY
Kanishka Monis, MD
Poovendran Saththasivam, MD

BASICS
DESCRIPTION
• Aortocaval compression refers to compression of the aorta and inferior vena cava (IVC) by
the gravid uterus.
• Supine hypotension syndrome describes the development of rapid hypotension or
cardiovascular collapse after placing the patient in a supine position with rapid recovery in
the lateral, sitting, or standing position. Classic signs and symptoms include bradycardia,
pallor, sweating, dizziness, and nausea.
EPIDEMIOLOGY
Prevalence
• 100% of parturients experience some degree of aortocaval compression at term.
• Approximately 15% of parturients experience supine hypotension syndrome at term.
Morbidity/Mortality
Compression of the aorta can lead to a decrease in uteroplacental perfusion and fetal
hypoxemia.
ETIOLOGY/RISK FACTORS
• Supine position
• Multiple gestations
• Obesity
• Polyhydramnios
• Uterine myomata (“fibroid tumors”)
• Fetal breech presentation, transverse and oblique, increases the risk of aortocaval
compression.
PHYSIOLOGY/PATHOPHYSIOLOGY
• Venous: Compression of the IVC leads to a decrease in venous return and an increase in
lower extremity venous pressure.
– The decreased preload can result in a 10–20% decline in stroke volume and cardiac
output.
– Blood return via collaterals (intraosseous vertebral veins, paravertebral veins, and epidural
veins) is less than would occur through the IVC.
• Aorta: Compression of the abdominal aorta can cause a decrease in peripheral perfusion.
– Uteroplacental insufficiency may be secondary to decreased perfusion pressure, and can
present as decelerations on the fetal heart monitor.
• Uterine contractions and fetal descent during labor typically reduce the risk of aortocaval
compression. However, there have been some case reports of aortocaval compression
occurring during labor and the postpartum period.
PREVENTATIVE MEASURES
• Avoid the supine position:
– A full lateral position minimizes aortocaval compression.
– A left uterine displacement (with a pelvic wedge or table tilt) may be reduced to 15° to
improve comfort or facilitate Cesarean delivery.
– Flexing of the legs may decrease lumbar lordosis, thus reducing vena cava compression.
– Crossing one leg over the other tilts the pelvis and can relieve vena cava compression.
• Ensure adequate intravascular volume and vascular tone; aortocaval compression is
enhanced during periods of maternal hypotension.
• The speed of delivering the fetus is important if a Cesarean section is planned. Minimize any
delays and consider a wedge or table tilt.

PREOPERATIVE ASSESSMENT
• The severity of the aortocaval compression is greatest at about 38 weeks and decreases after
the engagement of the fetal head into the maternal pelvis.
• The onset of the symptoms is usually rapid (average of 3–10 minutes).
• The syndrome is initiated by placing the patient in the supine position.
• Maternal heart rate is invariably increased in most cases. Maximum heart rate or abrupt
bradycardia can ensue just before syncope.
• Fetal heart tones will often demonstrate decelerations that signify fetal distress.
• Symptoms:
– Dyspnea
– Nausea/vomiting
– Diaphoresis
– Dizziness
– Anxiety/agitation
– Loss of consciousness
• Signs:
– Maternal tachycardia or bradycardia
– Hypotension
– Pallor/cyanosis
– Cold clammy skin
– Non-reassuring fetal heart tracing
– Distension of lower extremity veins
DIFFERENTIAL DIAGNOSIS
• Pulmonary thromboembolism
• Amniotic fluid embolism
• High neuraxial block
• Uterine rupture
• Placental abruption
• Myocardial infarction

TREATMENT

• Lateral position or left uterine displacement (LUD): Some parturients may still experience
supine hypotension syndrome in LUD.
• Fluid boluses can minimize aortocaval compression.
• Vasopressor boluses (phenylephrine or ephedrine) for treatment of hypotension

FOLLOW-UP

• Parturients in late pregnancy should be advised to recognize the symptoms of aortocaval


compression and avoid lying supine.
• The anesthesia provider should be vigilant and prepared to recognize aortocaval
compression in parturients who are placed in the supine position. In particular, placement
of a laboring epidural and bolusing can result in hypotension (sympatholysis) and enhance
the effects of compression.

ADDITIONAL READING
• Cyna AM, Andrew M, Emmett RS, et al. Techniques for preventing hypotension during
spinal anaesthesia for caesarean section. Cochrane Database Syst Rev. 2006;4:CD002251.
• Kinsella SM, Lohmann G. Supine hypotensive syndrome. Obstet Gynecol. 1994;83(5 Pt
1):774–788.
• Levy DM. Emergency caesarean section: Best practice. Anaesthesia. 2006;61(8):786–791.
• Ngan Kee WD. Prevention of maternal hypotension after regional anaesthesia for cesarean
section. Curr Opin Anaesthesiol. 2010;23(3):304–309.
See Also (Topic, Algorithm, Electronic Media Element)
• Cardiovascular physiology in pregnancy
• Preload
• Fetal heart tones

CODES

ICD9
• 459.2 Compression of vein
• 671.80 Other venous complications of pregnancy and the puerperium, unspecified as to
episode of care or not applicable
• 671.81 Other venous complications of pregnancy and the puerperium, delivered, with or
without mention of antepartum condition

ICD10
• I87.1 Compression of vein
• O22.8X9 Other venous complications in pregnancy, unsp trimester
• O22.8X1 Other venous complications in pregnancy, first trimester

CLINICAL PEARLS
• Aortocaval compression is present after 20 weeks gestation and reaches its maximum effect
at 38 weeks gestation.
• Aortocaval compression is lessened once the fetal head is engaged in the pelvis.
• Supine hypotension syndrome manifests as profound hypotension and bradycardia.
• Uteroplacental insufficiency caused by compression of the aorta can manifest via a non-
reassuring fetal heart tracing.
• Lateral position or left uterine displacement relieves aortocaval compression.
APNEA OF PREMATURITY
Joel Stockman, MD
Samuel H. Wald, MD

BASICS
DESCRIPTION
• Apnea of prematurity (AOP) is defined as the cessation of breathing in premature infants
which lasts for:
– >20 seconds, or
– >10 seconds if associated with bradycardia (<80 beats per minute [bpm]) or oxygen
desaturation (O2 saturation <80–85%)
• It is categorized as central, obstructive, or mixed, with mixed apnea making up the majority
of cases (1)[C].
EPIDEMIOLOGY
Prevalence
• >50% of preterm infants have clinically significant apnea, bradycardia, or oxygen
desaturation, with a peak incidence occurring between 5 and 7 days after birth (2)[C].
– Essentially affects all neonates weighing <1,000 g at birth (1)[C]
• Incidence is inversely related to gestational age and postconceptual age.
– Postoperative risk is <5% at a postconceptual age of 48 weeks and gestational age of 35
weeks.
– Postoperative risk is <1% at a postconceptual age of 56 weeks with a gestational age 32
weeks or postconceptual age of 56 weeks and gestational age of 32 weeks (3)[A].
Prevalence
• Significant AOP will resolve by 40 weeks postconceptual age for a majority of those infants
at risk (1)[C].
• Of note, most severely premature infants (24–28 weeks gestation) may have apnea
persisting beyond 40 weeks postconceptual age (4)[C].
Morbidity
AOP is seen in most high-risk neonates, so there is great difficulty in separating its effects
from the consequences of prematurity. However, it is thought to increase the incidence of
intraventricular hemorrhage (IVH), hydrocephalus, prolonged mechanical ventilation, and
abnormal neurologic development after the 1st year of life (5)[C].
Mortality
No direct correlation found
ETIOLOGY/RISK FACTORS
• An associated risk factor for postsurgical apnea is the presence of an apneic episode at
home.
• Anemia (hemoglobin <10 g/dL) is a significant risk factor, especially for neonates >43
weeks postconceptual age (3)[A].
PHYSIOLOGY/PATHOPHYSIOLOGY
• AOP reflects the immaturity of the respiratory control system, which manifests as an
unstable respiratory rhythm. The neonatal neurotransmission pathway is underdeveloped,
and both central and peripheral chemoreceptors are impaired.
– The preterm neonate’s ventilatory response to hypercapnia is significantly reduced.
– Preterm infants express a biphasic response to hypoxia, with the initial response being an
increase in ventilation for 1 minute, followed by a phase of decreased ventilation.
Severely preterm infants typically do not display a period of hyperventilation.
– There is an enhanced inhibitory response by upper and lower airway afferent innervation
secondary to stimulation (i.e., negative pressure and positive airflow) (6).
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Sedative drugs/anesthetic agents create a significant risk for development of apnea.
• At-risk infants must be admitted and monitored in the immediate postoperative setting.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Cessation of breathing for more than 20 seconds
• Cessation of breathing for more than 10 seconds if accompanied by:
– Bradycardia (>30 bpm below resting heart rate)
– Oxygen saturation <85% for >5 seconds
History
• Discuss presence of apneic events with the bedside caregivers to note severity
• Assess other comorbidities related to the premature infant
• Note the current duration of ventilatory support
Signs/Physical Exam
• Observe respiratory effort
• Assess for any upper airway abnormalities
• Assess for conditions that may affect breathing (e.g., neurologic disorders, pulmonary
disorders, CHD)
TREATMENT HISTORY
• History of mechanical ventilation/support
• Methylxanthines (e.g., caffeine, theophylline) administration.
MEDICATIONS
• Methylxanthines are the mainstay of treatment.
– These drugs are thought to stimulate breathing efforts by an unknown mechanism (may be
due to increased chemoreceptor responsiveness, enhanced respiratory muscle
performance, and generalized nervous system excitation).
– Adverse effects include feeding intolerance and tachycardia.
– Effective in reducing apneic episodes and ventilator use in the first 2–7 days of treatment
– Caffeine is the Preferred Drug Due to its lower toxicity (7)[A].
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• CBC
– A hemoglobin level <10 g/dL increases the risk of apnea to greater than the mean for
infants of all postconceptual ages (3)[A].
• Electrolyte panel
CONCOMITANT ORGAN DYSFUNCTION
• Respiratory distress syndrome
• Infections
• Hypoglycemia
• Neurologic dysfunction (e.g., IVH, hydrocephalus, stroke)
CIRCUMSTANCES TO DELAY/ CONDITIONS
• These infants should be cared for in an environment that has the capability to provide
continuous postoperative cardiorespiratory monitoring.
• Institutional practices may vary, but recommendations exist to delay elective cases up to 60
weeks postconceptual age. Clinicians must weigh the risk for unrecognized apnea versus the
cost savings through avoidance of overnight admission.
CLASSIFICATIONS
• Spontaneous:
– Minimal physiologic changes
– Events of brief duration and associated with self-recovery
– Events occurring once or twice in 24 hours
• Mild/moderate:
– Events involving apnea, bradycardia, and/or oxygen desaturation of intermediate duration
• Severe:
– Events of clinical significance with persistent bradycardia and oxygen desaturation
– Requires vigorous stimulation, oxygen administration, and/or assisted ventilation (2)[C]

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Consider:
– Atropine 10 mcg/kg
– Caffeine 10 mg/kg
Special Concerns for Informed Consent
• Need for possible continued postoperative intubation and ventilation
• Need for postoperative apnea monitoring
– Minimum observation period of 12–24 hours for those infants at increased risk
INTRAOPERATIVE CARE
Choice of Anesthesia
• Less oxygen desaturation/bradycardia is associated with procedures completed under
regional anesthesia (spinal/caudal) and without sedation (8)[A].
• Use short-acting anesthetic agents
• Minimize long-acting intravenous and oral anesthetics
Monitors
• Standard ASA monitors
• Appropriate IV access
Induction/Airway Management
Dictated by the patient’s comorbidities
Maintenance
Any form of sedation/general anesthesia carries an increased risk of postoperative apnea.
Extubation /Emergence
• Ensure the full reversal of muscle relaxant
• The preterm infant should be completely awake and vigorous prior to extubation.

FOLLOW-UP

BED ACUITY
Discharge to a monitored, inpatient unit for 12–24 hours
MEDICATIONS/LAB STUDIES/ CONSULTS
Postoperative respiratory support may be necessary, depending on the type of surgery.
COMPLICATIONS
Preterm infants may have a history of prior intubation and thus are at an increased risk for
subglottic stenosis.

REFERENCES
1. iner NN, Higgins R, Kattwinkel J, et al. Summary proceedings from the apnea-of-
prematurity group. Pediatrics. 2006;117:S47–S51.
2. Mayock DE. Apnea. University of Washington Division of Neonatology, 2011. Available at:
http://depts.washington.edu/nicuweb/NICU-WEB/apnea.stm
3. Cote CJ, Zaslavsky A, Downes JJ, et al. Postoperative apnea in former preterm infants after
inguinal herniorrhaphy: A combined analysis. Anesthesiology. 1995;82(4):809–822.
4. Baird TM, Martin RJ, Abu-Shaweesh JM. Clinical associations, treatment, and outcome of
apnea of prematurity. NeoReviews. 2002;3:66–70.
5. Butcher-Puech MC, Henderson-Smart DJ, Holley D. Relation between apnea duration and
type and neurological status of preterm infants. Arch Dis Child. 1985;60(10):953–958.
6. Mathew OP. Apnea of prematurity: Pathogenesis and management strategies. J Perinatol.
2010:1–9.
7. Henderson-Smart DJ, Steer PA. Methylxanthine treatment for apnea in preterm infants.
Cochrane Database Syst Rev. 2001;3:CD000140.
8. Krane EF, Haberkern CM, Jacobson LE. Postoperative apnea, bradycardia, and oxygen
desaturation in formerly premature infants: Prospective comparison of spinal and general
anesthesia. Anesth Analg. 1995;80:7–13.
See Also (Topic, Algorithm, Electronic Media Element)
• Pediatric respiratory physiology
• Caudal epidural

CODES

ICD9
770.81 Primary apnea of newborn

ICD10
P28.3 Primary sleep apnea of newborn

CLINICAL PEARLS
• The risk of AOP is inversely correlated to postconceptual age.
• The anesthetic should be tailored to the use of agents with the least respiratory depression.
• Postoperative intubation may be necessary in high-risk patients.
• Inpatient admission and/or postoperative respiratory monitoring are highly recommended
in at-risk patients.
APPENDECTOMY
Emily L. Drennan, MD

BASICS
DESCRIPTION
General
• Appendicitis is caused by an obstruction of the appendiceal lumen and can result in
inflammation, edema, and the potential for rupture of the viscus.
• Appendectomy is a surgical procedure that can be performed, open or laparoscopically, to
remove the appendix when infection and/or inflammation are suspected or present.
Removal is undertaken to avoid the complication of a ruptured appendix with resultant
peritonitis.
• Laparoscopic appendectomies are primarily performed today. Following trochar insertion
and the establishment of a pneumoperitoneum, the cecum is identified and retracted in
order to mobilize the appendix. An incision or window is made into the mesoappendix prior
to clamping and ligating the base. The appendix may be removed through the trochar or
placed into a bag depending on its size. Benefits over an open procedure include: Less
postoperative pain, smaller incisions (better cosmetic result), and reduced length of stay.
Drawbacks include: Greater cost, potentially longer operative time, and requirement of
general anesthesia due to insufflation.
• Open appendectomy involves adequate exposure of the cecum, followed by pulling of the
cecum through the incision site to expose the attached appendix. The base is clamped and
cut and drains are inserted prior to wound closure.
– Laparoscopic cases may be converted to open when operating conditions are suboptimal
for laparoscopy.
– It is commonly performed for complicated appendicitis or patients with extensive previous
intra-abdominal surgeries.
– May be performed under regional anesthesia for patients who are at high risk for
complications of general anesthesia (e.g., pregnancy, pulmonary hypertension).
Position
• Open: Supine with arms out or tucked
• Laparoscopy: Supine with arms tucked; surgeon stands on the left side of the patient.
Rightward tilt of the bed and Trendelenburg position may facilitate surgical exposure.
Incision
• Laparoscopy: 1 cm incision at the umbilicus, and two to three 5 mm incisions in the lower
abdomen for the insertion of trochars.
• Open: Transverse right lower quadrant incision (McBurney or Rockey-Davis)
Approximate Time
15–60 minutes for either approach
EBL Expected
Less than 75 mL
Hospital Stay
• 24 hours for uncomplicated appendicitis
• Ruptured or otherwise complicated appendicitis has an average length of stay of 5 days.
Special Equipment for Surgery
Laparoscopy equipment
EPIDEMIOLOGY
Prevalence
• In the US, ~250,000 cases of appendicitis annually
• Most common in 10–19 year olds
Prevalence
In the US, approximately 7% of people are affected at some point in their lives.
Morbidity
Varies from 5% to 11% and is related to the perforation of the appendix and degree of
peritonitis
Mortality
• Overall rate of 0.2–0.8% related to appendicitis, not surgical intervention
• Rate following appendectomy: 0–0.2%
• Elderly have the highest mortality rate.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Consider preoperative nasogastric tube placement to decompress the stomach
• Patient may be hypovolemic from vomiting and/or poor PO intake.
• Counsel pregnant patients about the risk for preterm labor; discuss the option of an open
procedure with neuraxial anesthesia.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Abdominal pain
• Anorexia
• Nausea
• Emesis
History
Periumbilical pain that migrates to the right lower quadrant (RLQ) is present in
approximately 50% of cases.
Signs/Physical Exam
• RLQ pain, tenderness
• Guarding, rebound on abdominal exam
• Pain with rectal exam
• Psoas sign; inflammation from retrocecal appendix
• Palpation of the mass in the RLQ
MEDICATIONS
Antibiotic therapy may be considered for nonsurgical candidates, such as those with severe
lung disease or recent myocardial infarction.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• KUB, ultrasound, and/or CT scan have reduced the incidence of “normal” appendixes
mimicking appendicitis.
• WBC count with differential
• Beta-HCG, to rule out ectopic pregnancy as a cause of pain in females
• Concomitant organ dysfunction may necessitate additional preoperative assessment such as
EKG, basic metabolic panel, etc.
Pregnancy Considerations
• Most common general surgery intervention during pregnancy with an incidence of 0.06–
0.1%
• Preoperative diagnosis is difficult in the setting of pregnancy. Additionally, the gravid
patient has an elevated WBC at baseline.
• An ultrasound diagnosis is preferred over CT scan to avoid radiation exposure.
• The appendix is located at the umbilical level in the second trimester and the RUQ in the
third trimester.
• 4% risk of pregnancy loss, 7% risk of early labor and delivery related to appendectomy

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• GI prophylaxis including a H2 blocker, non-particulate antacid, and possibly a pro-motility
agent
• Preoperative hydration and electrolyte repletion, as needed
Special Concerns for Informed Consent
Patient should be consented for laparoscopic as well as open appendectomy.
Antibiotics/ Common Organisms
• One dose is adequate for uncomplicated disease.
• Metronidazole plus a first-generation cephalosporin, aminoglycoside, or quinolone
• Common organisms are Escherichia coli, Bacteroides, Klebsiella, Enterococcus, and
Pseudomonas.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Laparoscopic appendectomy:
– General endotracheal anesthesia (GETA)
• Open appendectomy:
– GETA
– Spinal or epidural anesthesia with a T10 level is also possible.
Monitors
• Standard ASA monitors
• Foley, if patient has not voided in the immediate preoperative period, or per surgeon
request to improve visualization
Induction/Airway Management
• Sequential compression devices should be placed prior to induction.
• Rapid-sequence induction with endotracheal intubation is often required unless a difficult
airway is anticipated. If there is a potential for a difficult airway, consider an awake
fiberoptic intubation.
• Muscle relaxants: The speed of onset of succinylcholine is favorable; however, it may be
contraindicated in certain patients (e.g., children, stroke, etc.). Non-depolarizing muscle
relaxants administered at induction doses may not be reversible by the end of the case.
• Place an orogastric tube after intubation for gastric emptying
Maintenance
• Choice of inhalation agent
• Muscle relaxation can enhance surgical exposure. If succinylcholine was used at induction,
subsequent non-depolarizing administration may be needed.
• If a laparoscopic approach is used, the initial insufflation may lead to bradycardia from
vagal stimulation, which should resolve with time. Desufflation may be necessary if the
patient becomes hemodynamically unstable.
• As with other laparoscopic procedures, the pneumoperitoneum is created to enhance
visualization. However, it can impair ventilation by decreasing lung compliance and
functional residual capacity. Additionally, the Trendelenburg position is often implemented
to displace bowel with gravity and can further impair ventilatory efforts.
Extubation/Emergence
The patient should be fully awake, fully reversed, and capable of protecting their airway to
avoid aspiration.
Pediatric Considerations
• Appendicitis is more difficult to diagnose in children because of an inability to obtain a good
history. Younger children are more likely to present with perforated appendicitis because of
this diagnostic challenge.
• Surgery may be safely delayed until morning, without undertaking significant risk to the
child.
• Consider performing an ipsilateral transverse abdominal plane (TAP) block to improve pain
control and decrease postoperative narcotic requirements.

FOLLOW-UP

No need to continue antibiotics postoperatively for uncomplicated appendicitis


BED ACUITY
• Floor bed is typically sufficient.
• Telemetry or ICU may sometimes be necessary in the event of a perforated appendix or
other comorbid conditions.
ANALGESIA
• Generally mild-to-moderate pain, much improved after appendix removed
• Consider IV narcotic +/– ketorolac
• Regional techniques include TAP block or a thoracolumbar paravertebral block.
COMPLICATIONS
• Wound infection
• Intra-abdominal abscess
• Appendiceal stump leak
• Thromboembolism
• Injury to other structures in the surgical field

REFERENCES
1. Katkhouda N, Mason R, Towfigh S, et al. Laparoscopic vs. open appendectomy: A
prospective randomized double-blind study. Ann Surg. 2005;242(3):439–448.
2. McGory M, Zingmond D, Tillou A, et al. Negative appendectomy in pregnant women is
associated with a significant risk of fetal loss. J Am Coll Surg. 2007;205(4):534–540.
3. Sauerland S, Jaschinski T, Neugebauer EAM. Laparoscopic versus open surgery for
suspected appendicitis. Cochrane Database Syst Rev. 2010;10:CD001546.
4. Surana R, Quinn F, Puri P. Is it necessary to perform appendectomy in the middle of the
night in Children? BMJ. 1993;306(6886):1168.
See Also (Topic, Algorithm, Electronic Media Element)
Laparoscopy

CLINICAL PEARLS
• Appendicitis occurs most commonly in young patients; it has greater morbidity in those over
60 years of age.
• In the event of a ruptured appendix, immediate appendectomy is not the management of
choice. Antibiotic therapy, fluid resuscitation, and percutaneous drainage should be
undertaken with an interval appendectomy performed at a later date after the patient has
recovered.
• The open and laparoscopic approaches to an appendectomy are both appropriate; patient
comorbidities should play some role in the decision-making of the surgeon.
• A delay in proceeding to surgery does not affect patient outcome; it is a delay in diagnosis
that affects outcome.
ARTERIAL LINE WAVEFORM
John C. Frenzel, MD

BASICS
DESCRIPTION
• An arterial line is an invasive monitor that provides:
– Beat-to-beat numeric blood pressure values
– A waveform with arterial pressures (y-axis) as a function of time (x-axis)
– A means to attain arterial blood gas sampling
• An electromechanical transducer is coupled to the patient via a fluid column that is
generally composed of normal saline and heparin (4 units/mL).
PHYSIOLOGY PRINCIPLES
• During the cardiac cycle, blood ejected from the left ventricle (LV) flows into the vascular
tree. A pressure wave is transmitted through the vessels and temporally leads the flow of
blood.
– Measurement of pressure occurs at the level of the transducer, not the location of the
cannula. This is in contrast to noninvasive blood pressure (NIBP) measurements, where
measurement occurs at the level of the cuff.
– The arterial waveform is a measure of pressure and does not necessarily correlate to
cardiac output (flow). For example, in patients with poor cardiac output and a high
systemic vascular resistance (SVR), pressure will be normal but perfusion inadequate.
• Anacrotic limb describes the first phase of the arterial pulse cycle and represents ventricular
ejection of blood. The highest point corresponds to the systolic blood pressure.
– Steep slopes can correspond to increases in HR and inotropy.
– Dampened slopes can correspond to decreases in HR and contractility.

FIGURE 1. Arterial line waveform. Point 1 to 2 represents the anacrotic limb. Point 2 to 3 represents the dicrotic limb,
with the dicrotic notch found along the way.

• Dicrotic limb describes the downstroke of the waveform; it begins at the peak, continues
through the dicrotic notch, and ends at the diastolic baseline. The dicrotic notch coincides
with closure of the aortic valve and the end of LV ejection. It is a result of the reflection of
the pressure wave created when the forward flow of blood out of the LV stops and the
elastic recoil of the aorta forces blood back against the closed aortic valve. Pressure decay is
the drop in pressure over time (dP/dT) from the dicrotic notch to diastolic pressure; it is a
function of SVR.
– Steep slopes correspond to decreased SVR/afterload. The waveform appears narrow.
– Dampened slopes correspond to increased SVR/afterload. The waveform may appear
widened.
• The highest fidelity of readings and waveform data occurs when utilizing:
– The largest diameter catheter that does not obstruct the lumen of the vessel
– The shortest length of high pressure (stiff walled) tubing between the transducer and the
patient
– Tubing that is free of gas bubbles
– Tubing that is free of other obstructions such as clotted blood
– A catheter that is placed closer to the central vascular tree
• Reflection and deflection occur as blood flows through the vasculature. Because the arterial
system undergoes constant pressure adjustments as well as has several bends and branches,
the flow of blood is turbulent as well as laminar. Turbulent flow results in pressure waves
being reflected much like waves in a pool of water are reflected off the concrete side. This
results in increased systolic pressures and decreased diastolic pressures in the more distal
arteries; the mean pressure is only minimally affected. Alternatively, if the vessels were
straight, and had no branches, flow would be laminar and the pressures would not change
in the more distal arteries.

FIGURE 2. Arterial line tracing from proximal to distal sites. Systolic pressures increase, diastolic pressures decrease, while
mean pressures remain mostly unchanged.

ANATOMY
• Although any artery can be used, the risk of distal thrombosis limits catheter placement to
larger vessels with adequate collateralization.
• The radial artery is the most common location for arterial monitoring.
• The ulnar artery is more difficult to cannulate because it is deeper at the wrist. It should not
be used if the ipsilateral radial artery has been punctured.
– Some suggest the use of the Allen Test to assess the adequacy of collateralization of the
hand.
– Recent studies have called this into question and if there is doubt, vascular ultrasound
should be used (1).
• Use of the femoral artery must be balanced against concerns of site and line infection,
pseudo-aneurysm formation, or distal embolization from plaque rupture.
• Other less frequently used sites for arterial wave monitoring include axillary, brachial, and
dorsalis pedis vessels.
• In neonates temporal and umbilical arteries are used.
DISEASE/PATHOPHYSIOLOGY
• Dicrotic notch: The notch is a result of the reflection of the pressure wave created when the
forward flow of blood out of the LV stops and the elastic recoil of the aorta forces blood
back against the closed aortic valve.
– Patients with severe aortic insufficiency will have an indistinct notch. Since the aortic
valve is incompetent, blood flows freely backward, and no such pressure wave is
generated.
– A flat or absent notch may suggest low intravascular volume.
– A low or late notch may correlate to decreased SVR.
• Heparin-induced thrombocytopenia (HIT): In some patients, chronic exposure to heparin can
result in HIT (2). HIT results in thrombosis, not bleeding. Sodium citrate has been used as a
substitute for heparin in the flush (3).
• Thrombosis is an unusual complication but potentially devastating if it results in prolonged
ischemia (4). First-line therapy is systemic anticoagulation. Some studies have been
performed showing thrombolytics are effective as second-line therapy (5).
• Temporary occlusion of the radial artery following arterial line placement is not infrequent
and is reported in 1.5–35% (mean 19.7%) of studies on the subject. Generally temporary
occlusion has no serious consequences (6).
PERIOPERATIVE RELEVANCE
• Placement of arterial waveform monitoring is common when continuous beat-to-beat blood
pressure measurement is indicated. Changes in the waveform can be useful in cases where
rapid changes in volume status are occurring.
• Dampened waveforms result in underestimation of the blood pressure and can be seen with:
– Lumen occlusion due to thrombosis, clots, air bubbles, or kinking
– Loss of backpressure from the flush solution (low flush bag pressure, no fluid in pressure
bag)
– Troubleshooting involves inspection of the system starting from the placement site (if
possible) back to the electronics. On opening the transducer to air, the reading should
drop to zero. If not, this indicates the possibility of baseline drift and the system should be
re-zeroed. Next, the system should be flushed. If the reading does not move over 300
mm▒Hg, then the pressure bag should be checked. Otherwise the system should be
inspected distal to the transducer for obstructions, disconnections, or leaks.
– Tubing: overly compliant, distensible; incorrect tubing

FIGURE 3. Dampened tracing results in decreased systolic pressures, increased diastolic pressures, while mean pressures
remain mostly unchanged.

• Under-dampened or resonant waveforms result in overestimation of the blood pressure and


can occur due to:
– Tubing: Long, noncompliant, overly-stiff.
– “Ringing” describes exaggerated highs and lows that can occur when the measurement
system comes close to the natural underlying harmonic frequency of the waveform.
– Increased SVR

FIGURE 4. Under-dampened or resonant tracing results in increased systolic pressures, decreased diastolic pressures, while
mean pressures remain mostly unchanged.

• The electromechanical system must be zeroed prior to use by opening the transducer to air.
For neurosurgical cases, or cases where the patient is in the sitting position, the zero
reference is commonly set to the Circle of Willis at the level of the ear. Otherwise, the zero
reference is placed at the level of the heart. If the transducer is not physically attached to
the OR bed, the level must be adjusted when changes in patient position or vertical height
are made.
• Stroke volume variation describes changes in the systolic and diastolic pressure that
correlate with the respiratory cycle.
– Mechanical ventilation: Positive pressure inspiration corresponds with an increase in
airway pressures, compression of intrathoracic veins, and a decrease in transmural blood
flow. As a result, with inspiration, there is decreased preload that corresponds to
decreased blood pressure. Conversely, exhalation corresponds to a decrease in airway
pressures with increases in blood pressure.
– Spontaneous ventilation: Exhalation and the end of inspiration correspond to an increase
in airway pressures, compression of intrathoracic veins, and a decrease in transmural
blood flow.

FIGURE 5. Stroke volume variation with mechanical ventilation. Exhalation corresponds to decreased intrathoracic
pressures, allowing blood to return to the heart (increased preload, with resultant increase in cardiac output and blood
pressure). Inspiration corresponds to increased intrathoracic pressures with resultant decreases in blood return to the heart
(decreased preload that causes decreases in stroke volume, cardiac output, and blood pressure).

• Arterial line placement can be aided by ultrasound, but this is usually reserved for femoral
cannulation of pediatric patients and select adults.
• Newer methods of cardiac output monitoring use a peripheral arterial line and the pressure
waveform to calculate cardiac output. Unlike thermodilution methods, these devices use
advanced algorithms to assess vascular tone and sensing technology to indirectly measure
SVR.
• Arterial transducers are built to continually infuse a small volume (3 mL/hr) of flush
solution to reduce cannula thrombosis.
EQUATIONS
MAP = DBP(2/3) + SBP(1/3); where MAP is mean arterial pressure, DBP is diastolic blood
pressure, and SBP is systolic blood pressure. This represents the average, or mean, blood
pressure throughout the cardiac cycle.

REFERENCES
1. Jarvis MA, Jarvis CL, Jones PRM, et al. Reliability of Allen’s test in selection of patients for
radial artery harvest. Ann Thorac Surg. 2000;70(4):1362–1365.
2. Chong BH. Heparin-induced thrombocytopenia. J Thromb Haemost. 2003;1:1471–1478.
3. Branson PK, McCoy RA, Phillips BA, et al. Efficacy of 1.4 percent sodium citrate in
maintaining arterial catheter patency in patients in a medical ICU. Chest. 1993;103:882–
885.
4. Mangano DT, Hickey RF. Ischemic injury following uncomplicated radial artery
catheterization. Anesth Analg. 1979;58:55–57.
5. Geschwind JH, Dagli MS, Lambert DL, et al. Thrombolytic therapy in the setting of arterial
line-induced ischemia. J Endovasc Ther. 2003;10:590–594.
6. Scheer BV, Perel A, Pfeiffer UJ. Clinical review: Complications and risk factors of
peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and
intensive care medicine. Crit Care. 2002;6(3):199–204.
See Also (Topic, Algorithm, Electronic Media Element)
• Transducers
• Hypertension
• Heparin-induced thrombocytopenia

CLINICAL PEARLS
• Transducer systems can drift leading to erroneous readings. Leaving a NIBP cuff on the
patient and set to cycle every 15 or 30 minutes can help to more rapidly identify this
problem.
• Placing the pulse oximeter on the same hand as the arterial line can be helpful in
monitoring adequacy of perfusion distal to the arterial line.
• Check and tighten all connections after placement. Stopcocks that are not used for blood
sample draws should be taped in the vertical position and the draw port covered by a cap
and tape to avoid inadvertent injection of substances via the arterial line.
ASPIRATION
Kanishka Monis, MD
Poovendran Saththasivam, MD

BASICS
DESCRIPTION
• Aspiration is defined as the inhalation of gastric, oropharyngeal, or other foreign contents
into the larynx and lower respiratory tract. It can be divided into 2 broad categories:
– Aspiration pneumonitis: Inhalation of sterile acidic gastric contents resulting in chemical
injury to the lung; also known as Mendelson syndrome
– Aspiration pneumonia: An infectious, pathologic process caused by inhalation of secretions
that have been colonized by microorganisms
• Although aspiration is rare during anesthesia, it is an important cause of anesthesia-related
mortality and ventilator-associated pneumonia (VAP) in the ICU setting.
EPIDEMIOLOGY
Incidence
3.1–10.2 per 10,000 patients receiving general anesthesia
Morbidity
• Pneumonia
• Lung abscess and empyema
• Acute lung injury (ALI)
• Acute respiratory distress syndrome (ARDS)
Mortality
3.8–4.6%; massive aspiration can reach 25%
ETIOLOGY/RISK FACTORS
• Extremes of age
• Full stomach at the time of anesthesia
• Pregnancy
• Critical illness
• Emergency surgeries
• Gastroesophageal reflux disease
• Diabetic gastroparesis
• Obesity
• Difficult airway
• Acidic gastric content pH <2.5
• Gastric volume >0.4 mL/kg
• Loss of airway reflexes
– Drug/alcohol overdose
– Unconscious patient from general anesthesia, deep sedation, trauma
• Neurologic dysphagia
PHYSIOLOGY/PATHOPHYSIOLOGY
• There are several structures and reflexes that protect against aspiration.
– Upper esophageal sphincter (UES)
The cricopharyngeus muscle acts as the constrictor muscle of the pharynx and divides
the upper esophagus from the hypopharynx.
Decreased tone is seen with sodium thiopental, succinylcholine, midazolam, and
halothane.
Increased tone is seen with the use of ketamine.
– Lower esophageal sphincter (LES)
Located at the border between the stomach and the esophagus
Composed of the right crux of the diaphragm and the acute angle of the left margin of
the esophagus with the gastric fundus; it forms a sling around the lower esophagus.
Decreased tone is seen with opioids, inhalation agents, and sodium thiopental.
Increased tone is seen with antiemetics (metoclopramide), cholinergic drugs, and
succinylcholine.
– Airway reflexes
Laryngospasm: Hypoxia results from the closure of the false and true vocal cords;
however, this prevents aspiration of foreign contents.
Coughing: Forceful expiratory flow can aid with removal of foreign contents.
Expiration: Describes a forceful expiratory effort without preceding inspiration
Spasmodic panting: Episodes of shallow breathing result in rapid vocal cord opening and
closing and reduce the aspiration of foreign material.
• Consequences of aspiration
– Large particles will cause airway obstruction. Areas of lung that are not being ventilated
are still perfused leading to ventilation/perfusion (V/Q) mismatching, shunting,
hypoxemia, and death.
– In aspiration pneumonitis, acid-related effects of gastric contents will cause inflammatory
reactions and direct lung tissue injury, airway constriction, and edema. Release of
cytokines and chemokines attract inflammatory mediators, neutrophils, and macrophages.
Altered lung defenses may lead to bacterial infection.
– In aspiration pneumonia, the aspiration of oropharyngeal secretions and contaminated
gastric contents will elicit an acute inflammatory lung response to bacteria and bacterial
products. The pathogens that are frequently associated with aspiration pneumonia are
Gram-positive cocci, Gram-negative rods, and (rarely) anaerobes.
Pregnancy Considerations
• Pregnant patients in labor have an increased risk of aspiration due to:
– Slow gastric emptying time
– Increased gastric volume
– Relaxation of the LES due to progesterone’s effect and the upward pressure of the
enlarging uterus on the LES. Patients are typically considered a “full stomach” beginning
their second trimester.
PREVENTATIVE MEASURES
• Adequate preoperative fasting to control gastric content and volume:
See Table
• Decrease gastric acidity:
– Sodium citrate is a nonparticulate antacid that functions to raise gastric pH as well as
increase gastric motility.
– H2 antagonists inhibit secretion of acid, thereby reducing acidity of stomach contents and
gastric volume.
• Decrease gastric volume:
– Metoclopramide is an antidopaminergic and cholinergic which speeds gastric emptying
and increases LES tone.
– Nasogastric tube insertion and suctioning prior to or after induction for gastric
decompression
– In situ nasogastric tubes should be suctioned prior to induction. Of note, it can form a
mechanical barrier to LES protection against aspiration.
• Application of cricoid pressure/Sellick maneuver:
– Described by Sellick in 1961 as a way to prevent aspiration during the rapid sequence
induction phase of anesthesia
– The upward and backward directed pressure on the cricoid cartilage compresses the
esophagus against the vertebral bodies, thus occluding the esophagus. The recommended
pressure is 30–40 Newtons (difficult to ascertain while performing the technique).
– Theoretically, this will prevent passage of gastric content into the pharynx and subsequent
aspiration into the tracheobronchial tree.
– Minimizes gastric insufflation and aspiration in unconscious patients; however, it may also
prevent effective mask ventilation by reducing airway patency. It may cause discomfort to
the patient if applied too early.
• Early endotracheal intubation with a cuffed endotracheal tube will decrease but not
eliminate the risk of gastric aspiration.
– Excessive cuff pressure may compromise the microcirculation of tracheal mucosa leading
to necrosis. Insufficient cuff pressure may impair ventilation and allow leakage of
supraglottic material into the tracheobronchial tree.
– A better seal can be achieved by using the ultra thin cuff (low pressure, high volume). This
prevents the formation of folds that can lead to longitudinal channels for supraglottic
material to enter the tracheobronchial tree.
Pregnancy Considerations
• Consider all laboring patients as having a "full stomach," irrespective of the last meal time.
– Avoid general anesthesia, if possible
– If general anesthesia is necessary, consider metoclopramide, sodium citrate, and H2
antagonists.
• Semi-recumbent position has been endorsed by the Centers for Disease Control and
Prevention (CDC) as an effective measure to decrease the risk of aspiration and VAP.
– Reflux of gastric contents is counterbalanced by the effect of gravity in the semi-
recumbent position.
– Prone position in patients with ARDS has been reported to reduce gastric aspiration and
risk of VAP in some studies.

DIAGNOSIS
• Vomiting at the time of induction or following extubation
• Symptoms:
– Postoperative coughing, hoarseness, night sweats, shortness of breath, pleuritic chest pain,
myalgia, and malaise
• Signs:
– Intraoperatively: Hypoxemia, wheezing, bronchospasm/laryngospasm
– Postoperatively: Fever, cyanosis, tachypnea, inspiratory wheezing (in lesions where the
obstruction is in proximal trachea) or expiratory wheeze (distal obstruction), rales,
irritability
• Diagnostic tests and imaging:
– ABG with an increased alveolar–arterial oxygen gradient and hypoxia
– CXR may reveal consolidation and opacities. Changes may be delayed and not appear for
12–24 hours after initial aspiration.
– CBC with differential
– Sputum culture
DIFFERENTIAL DIAGNOSIS
• Pulmonary thromboembolism
• Pulmonary air embolism
• Pulmonary tuberculosis
• ARDS
• Drug reaction
• Asthma
• Bronchospasm
• Laryngospasm
• Myocardial infarction

TREATMENT

• Vomiting at induction
– Immediately place the patient in the Trendelenburg position to prevent aspiration into the
trachea
– Suction the upper airway
– Endotracheal intubation and inflation of the cuff
– Endotracheal suctioning with a soft suction tube; bronchoscopy and removal of large
inhaled particles
• Vomiting intraoperatively (with a supraglottic device or mask ventilation)
– Remove supraglottic device and have an assistant maintain cricoid pressure
– Head down/lateral position
– Suction and clear the upper airway
– Administer 100% oxygen
– Administration of succinylcholine and endotracheal intubation for airway protection
– Expedite surgery
• Vomiting at emergence
– Head down or lateral position to prevent the entry of aspirated contents into the airway
– Gentle suctioning of the pharynx
– Administer 100% oxygen
– Consider reintubation for airway protection
• There is no data to support the use of steroids in the treatment of aspiration.
– Antibiotics should be considered once a specific organism is identified.
– In situations that involve bowel obstruction and aspiration of bowel contents, Gram-
negative and Gram-positive antibiotic coverage should be considered if the patient
develops signs of aspiration pneumonia.
• There is no data to support use of steroids in treatment of aspiration pneumonitis or
pneumonia.

FOLLOW-UP

CLOSED CLAIMS DATA


• In 4,459 total anesthesia-related claims:
– Aspiration was the primary or secondary cause of morbidity in 158 (3.5%) of all claims.
– Aspiration was the primary source of adverse events in 1.75% of these patients.
– The majority of aspiration events (42%) occurred during the induction of anesthesia.
– Obstetrical related aspiration accounted for 21% of all claims.

REFERENCES
1. Yoshikawa H, Yamazaki S, Abe T. Acute respiratory distress syndrome in children with
severe motor and intellectual disabilities. Brain Dev. 2005;27(6):395–399.
2. Brownlee IA, Aseeri A, Ward C, et al. From gastric aspiration to airway inflammation.
Monaldi Arch Chest Dis. 2010;73(2):54–63.
3. Beck-Schimmer B, Bonvini JM. Bronchoaspiration: Incidence, consequences and
management. Eur J Anaesthesiol. 2011;28(2):78–84.
4. Paintal HS, Kuschner WG. Aspiration syndromes: 10 clinical pearls every physician should
know. Int J Clin Pract. 2007;61(5):846–852.
5. Kluger MT, Visvanathan T, Myburgh JA, et al. Crisis management during anaesthesia:
Regurgitation, vomiting, and aspiration. Qual Saf Health Care. 2005;14(3).

ADDITIONAL READING
• ASA NPO Guidelines
See Also (Topic, Algorithm, Electronic Media Element)
• Ventilator-associated pneumonia
• Asthma
• Venous air embolism

CODES

ICD9
• 482.9 Bacterial pneumonia, unspecified
• 507.0 Pneumonitis due to solids and liquids

ICD10
• J15.9 Unspecified bacterial pneumonia
• J69.0 Pneumonitis due to inhalation of food and vomit

CLINICAL PEARLS
• All patients with stroke should be screened for swallowing abnormalities to prevent
aspiration.
• Patients with decreased sensorium are unable to protect the airway, thus are at an increased
risk for aspiration.
• Mechanically ventilated patients with risk factors of aspiration should be nursed by placing
the head of the bed elevated at 30–35°.
ASSESSMENT OF ACUTE POSTOPERATIVE PAIN
Thomas Ledowski, MD, PD, DEAA, FANZCA

BASICS
DESCRIPTION
• Pain is defined as “an unpleasant sensory and emotional experience associated with actual
or potential tissue damage or described in terms of such damage” by the International
Association for the Study of Pain (ISAP).
• It is often referred to as the “fifth vital sign,” and relief from pain is seen as a basic human
right. Pain is by its very nature an entirely subjective experience and should always be
regarded as such!
• Anesthesia providers and pain medicine physicians encounter pain in the acute and chronic
setting:
– Acute pain is of recent onset and probable limited duration.
– Chronic pain commonly persists beyond the time of healing of an injury; frequently there
may not be any clearly identifiable cause.
EPIDEMIOLOGY
Prevalence
• Annually in the US, there are >73 million surgical procedures. An expected 80% of patients
experience acute pain with up to 87% of those being moderate and severe.
• Following an ICU stay, approximately 75% of patients report to have suffered from
moderate-to-severe pain.
• Children especially suffer from postoperative pain unnecessarily, with approximately 15%
experiencing severe pain.
Prevalence
Every day in the US, approximately 175,000 patients suffer from moderate or severe
postoperative pain.
Morbidity
• Under-treatment of acute pain has significant consequences:
– Increased length of hospital stay and rehabilitation leading to high socioeconomic cost
– Progression to chronic pain may result in catastrophic personal and socioeconomic
consequences.
– Triggering of sleep deprivation and anxiety disorders can result in significant personality
changes.
– Greatly decreased patient satisfaction
– Increased overall postsurgical stress response with elevated plasma levels of catabolic
hormones, hypercoagulopathy, and increased myocardial oxygen consumption
– There is no clear correlation between pain treatment and overall postsurgical mortality
due to a lack of randomized controlled studies.
• Over-treatment of acute and chronic pain also has undesired consequences:
– Respiratory depression with subsequent hypoxia that can lead to brain damage or death
may result from the inappropriate use of opioids; increased occurrence in high-risk
patients (e.g., sleep apnea, elderly).
– Other adverse events with opioid treatment include constipation, itching, nausea, and
vomiting.
– Adverse events with NSAIDs include GI ulceration and bleeding.
ETIOLOGY/RISK FACTORS
• Acute postoperative pain depends on the degree of surgical tissue trauma, but is also
affected by individual patient factors such as:
– Previous experiences
– Personality, anxiety, catastrophizing, neuroticism, depression
– Cultural background
• Risk factors for misdiagnosis of pain:
– Inability to communicate verbally (e.g., young children, patients with dementia or
delirium, and sedated patients in the ICU)
– Medical myths (e.g., infants do not feel pain as much as adults)
– Using “objective” physiologic parameters (heart rate, blood pressure) to assess the severity
of pain and make treatment decisions; pain is SUBJECTIVE!
PHYSIOLOGY/PATHOPHYSIOLOGY
Adverse physiologic effects in patients with postoperative pain include:
• Pulmonary system: Atelectasis, V/Q mismatching, hypoxemia, hypercapnia
• Cardiovascular system: Hypertension, tachycardia, increased myocardial oxygen demand
• Hematologic system: Decreased immune function, hypercoagulable state
• GI system: Ileus
PREVENTATIVE MEASURES
• The assessment of pain should be a holistic approach involving patient self-rating, whenever
possible. It should also include obtaining a thorough medical and pain history, behavioral
observation and, with caution, monitoring of physiologic parameters (e.g., blood pressure,
respiration rate).
• Pain assessment and treatment by a dedicated acute pain service may result in better pain
relief and less side effects.

PREOPERATIVE ASSESSMENT
• An initial assessment of postoperative pain must commence as early as possible and consists
of a medical (type of surgery, comorbidities) and pain history:
– Location
– Quality; dull visceral, stabbing, shooting, or neuropathic pain
– Intensity
– Provoking factors (coughing) versus continuous pain
– Chronic pain history; especially which medications have been used
– Factors influencing pain treatment; patient’s beliefs and expectations, knowledge, coping
strategies
• Reassessment should be repeated regularly at appropriate intervals (e.g., recovery room
every 3–5 minutes, ward every 0.5–4 hours).
• Physiologic parameters can be used as indicators of pain and include heart rate, blood
pressure, and respiration rate.
– Although physiologic parameters are often used as a “crutch” to assess pain in
unconscious patients, they should only be used with extreme caution to guide therapeutic
decisions. None of them have been validated as accurate measures of pain!
• A variety of pain scales are available. They range from scales “objectively” measuring pain
in conscious patients to scales used in unconscious and pediatric patients.
• Verbal descriptor scale (VDS): Conscious patients. Pain is described as absent, mild,
moderate, severe, and agonizing/unbearable.
– Quick and easy
– Useful in elderly patients with cognitive impairment; use familiar words such as no, mild,
moderate, unbearable (2)[C]
– Less sensitive to pain changes and dependent on higher verbal skills (e.g., a patient who
barely speaks English may not understand the term “agonizing”)
• Visual analogue scale (VAS): Conscious patients. Consists of a 100 mm long horizontal line
with the words “no pain” on the left (0) and “worst pain imaginable” on the right (100).
The patient marks his/her actual severity of pain on the scale (pen/paper or ruler/sliding
marker system).
– Helpful in most conscious subjects
– A reduction of pain by approximately 30% has been rated meaningful by patients.
– Clinical use may be hindered by anesthesia-related cognitive impairment in the immediate
postoperative period.
– Requires basic motor skills; 0–5 mm commonly signify “no”, 5–45 mm “mild”, 45–74 mm
“moderate” and 75–100 mm “severe” pain
• Numeric rating scale (NRS): Conscious patients. Commonly 0–10 points, hence an 11-point
scale. 0 means no pain, 10 worst pain imaginable; 4 is often used as the threshold for
treatment intervention (e.g., opioid administration).
– The NRS correlates well with the VAS but is easier to administer with consistent results.
• Multidimensional pain scales (e.g., McGill Pain Questionnaire); conscious patients
– Helpful to evaluate more complex pain issues (e.g., chronic or neuropathic pain)
– Due to their complexity, these pain scales are usually not useful in the acute postoperative
context.
• Functional pain scales: Conscious patients. Assesses a patient’s ability to perform certain
tasks (e.g., coughing, physiotherapy). Commonly rated as “no” (performance unhindered by
pain), “mild” (moderate-to-severe pain during task), and “significant” limitation (unable to
perform task).
– The ability to perform a certain task may be influenced by more factors than just pain, but
such scales can be useful to trigger pain therapeutic intervention.
• Behavioral pain scale (BPS): Sedated or semi-conscious patients. 3 components are analyzed:
Facial expression (relaxed, partially tightened, fully tightened, grimacing), upper limb
movement (none, partially bent, fully bent, permanently retracted), and compliance with
ventilation (tolerant, mostly tolerant, fighting ventilator, unable to control ventilation).
Each component is rated from 1 to 4; hence, a total BPS score of 12 (maximum pain) can be
achieved.
– BPS is reliable and valid for pain assessment in sedated adult ICU patients (3)[B].
• Critical care pain observation tool (CPOT): Sedated or semi-conscious patients. 4 domains:
Facial expression (relaxed, tense, grimacing), body movement (none, protective, restless),
muscle tension (relaxed, tense, rigid), compliance with ventilation (tolerant, coughing,
fighting), or, in extubated patients, vocalization (normal, moaning, crying); rated from 0 to
2 points each. CPOT ranges from 0 to 8 (maximum pain).
– The CPOT correlates with the VAS which supports its clinical use (4)[C].
• Premature infant pain profile (PIPP) has been validated for postoperative pain in both
premature infants and term newborns. Indicators: Gestational age, behavioral state, heart
rate, oxygen saturation, brow bulge, eye squeeze, nasolabial furrow; all marked with 0–4
points with a total score of 0–21 points (moderate-to-severe pain if >12).
• Children’s Revised Impact of Event Scale (CRIES). Indicators: Crying, oxygen requirement,
increased heart rate and blood pressure, expression, sleeplessness; all marked 0–2 points,
total score 0–10.
• Faces Legs Activity Cry Consolability Scale (FLACC). Indicators (1–3 year olds): Facial
expression, leg movement, overall activity, crying, consolability; each factor scores 0–2
points, with a total score of 0–10 points.
• Faces Pain Scale-Revised (FPS-R). Indicators (4–7 year olds): Showing 6 faces (very happy to
very sad/crying); shown to be equivalent to a 5-step scale graded 0–10 VAS on paper/ruler.
DIFFERENTIAL DIAGNOSIS
• When solely based on clinical observation and the monitoring of physiologic parameters,
pain assessment may be confounded by a range of other factors including:
– Arousal (potent sympathetic stimulus)
– Anxiety (especially children)
– Confusion (especially elderly patients, emergence delirium in children)
– Co-medication (antihypertensive drugs, sympatholytic [e.g., beta-blockers, clonidine] and
sympathomimetic drugs [e.g., catecholamines, ketamine])
• Hence, get a patient self-rating whenever possible.

TREATMENT

Consists of a multimodal approach including:


• Oral and parenteral analgesics (opioids, NSAIDs, acetaminophen)
• Patient-controlled analgesia (PCA)
• Regional and neuraxial blocks
• Non-conventional therapies (e.g., transcutaneous electrical nerve stimulation)
FOLLOW-UP

In-hospital postoperative patients may have their pain managed by either the surgical team,
primary service, anesthesia service, or acute pain team.
CLOSED CLAIMS DATA
• From 1985 to 2007, there were 150 out of 7,328 closed claims related to acute pain
(American Society of Anesthesiologists Closed Claims Project).
– Although this may appear to be a low percentage, the outcome in approximately 30% of
cases was death or brain damage.
– The median payment was $211,650 ($627–14,880,000).
• Pain mismanagement has been viewed as “unprofessional conduct” by state medical boards
with individual doctors being disciplined.

REFERENCES
1. esonen A, Kauppila T, Tarkkila P, et al. Evaluation of easily applicable pain measurement
tools for the assessment of pain in demented patients. Acta Anaesthesiol Scand.
2009;53:657–664.
2. Pesonen A, Suojaranta-Ylinen R, Tarkkila P, et al. Applicability of tools to assess pain in
elderly patients after cardiac surgery. Acta Anaesthesiol Scand. 2008;52:267–273.
3. ade CH. Clinical tools for the assessment of pain in sedated critically ill adults. Nurse Crit
Care. 2008;13:288–297.
4. Tousignant-Laflamme Y, Bourgault P, Gelinas C, et al. Assessing pain behaviours in healthy
subjects using the critical care pain observation tool (CPOT): A pilot study. J Pain.
2010;11:983–987.

ADDITIONAL READING
• Macintyre PE, Scott DA, Schug SA, et al. Acute pain management: Scientific evidence, 3rd
ed. Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine,
2010.
See Also (Topic, Algorithm, Electronic Media Element)
• Complex regional pain syndrome I
• Complex regional pain syndrome II
• Epidural

CODES

ICD9
338.18 Other acute postoperative pain

ICD10
G89.18 Other acute postprocedural pain

CLINICAL PEARLS
• Pain is a SUBJECTIVE experience.
• Pain is often misdiagnosed in young children, as well as demented and sedated patients.
• Pediatric pain scales should be age-adequate; there is no “one-fits-all” scale.
• Physiologic parameters as well as newly introduced monitoring solutions (e.g., skin
conductance or surgical pleth index) are influenced by many factors other than pain; if
used, they require caution and support from other methods of pain assessment (e.g.,
observation).
• The adequacy of pain relief should be checked regularly.
• Assessment alone is not enough. Clear orders and policies must also define which level of
pain triggers and which response/medication to alleviate it.
ASSIST CONTROL VENTILATION
Daniel Castillo, MD
Sascha Beutler, MD, PhD

BASICS
DESCRIPTION
• Assist control ventilation (A/C) or assisted mechanical ventilation (AMV) is a full support
mode of mechanical ventilation that is used preferentially across the intensive care units
(ICU) in the US and around the world (1)[B]. Spontaneous breathing modes have been
shown to decrease atelectasis and can improve V/Q matching.
• In this mode, the breath can be triggered by the set rate (ventilator-triggered) or by the
patient; the “interactive” element of this mode allows the patient to receive a “fully
supported” breath when they initiate one.
• Patients ventilated with A/C can go from total ventilatory rate control when apneic,
sedated, or paralyzed to full patient trigger rate control when spontaneously breathing (2)
[B],(3)[B]; this change will occur seamlessly without changing the ventilator settings.
• In A/C, as in other modes of ventilation, it is necessary to set parameters such as:
– FIO2
– Positive end expiratory pressure (PEEP)
– Pressure-targeted or volume-targeted
– Respiratory rate
– Mode of triggering: Negative pressure- triggering or flow-triggering
– Peak flow
PHYSIOLOGY PRINCIPLES
• Mechanical ventilation (MV) parameters: MV is based on the equation of motion, where
pressure, volume, and flow change continuously during the respiratory cycle, assuming that
compliance and resistance remain constant (4)[A].
• Physiologic ventilatory control: The respiratory center in the brain stem controls ventilation.
Signals are delivered to the respiratory muscles to contract and create a negative
intrapleural pressure, resulting in lung expansion and airflow entering the airways.
• Interactive components of AC ventilation: During MV, if the patient initiates a breath, the
ventilator is triggered to deliver a preset breath to the patient.
• Backup rate: When the patient is unable to initiate a breath, the set ventilatory rate delivers
the breaths. This functions as a backup or “safety-net” when the patient’s breathing rate
drops below the ventilator set rate (5)[C],(6)[B],(7)[B],(8)[B].
• Patient-triggered versus ventilator-triggered breaths: The delivered breath in A/C is equally
supported regardless if it is patient or ventilator initiated; they are identical in duration and
magnitude.
• Work of breathing: Contrary to popular belief, A/C does not abolish the work of breathing
because breaths remain initiated by the patient; it does, however, decrease it. As a result,
there is decreased fatigue and shallow breaths that can result in atelectasis and shunting.
• Settings:
– FIO2: As with most modes of ventilation, this needs to be selected. Patients are often
started at an FIO2 of 1.0 with downward titration to avoid oxygen toxicity and decreased
surfactant production.
– PEEP: Reduces atelectasis during expiration with resultant improvement in oxygenation,
lung volumes (by increasing FRC), and lung compliance. PEEP also antagonizes auto-
PEEP. In acute respiratory distress syndrome (ARDS), it can decrease atelectrauma (the
opening and closing of airways) and the effects of volutrauma. Initially, PEEP is typically
set at the lower inflection point (LIP) of a pressure-volume curve and then titrated
upwards to produce the best PaO2 with an FIO2 <0.6.
– Method of support (tidal volume vs. pressure targeted): In tidal volume support, a volume
is set for each breath. The volume set is delivered using a fixed flow (flow × time).
Airway pressure is not set and will depend on the elastic and resistance component of the
lung. Inspiratory time is determined by the VT delivered and the flow rate: Ti = VT/flow
rate. In pressure-targeted support, the ventilator utilizes flow (adjustable) to generate a set
pressure in the airway for a period of time determined by the inspiratory time of the I:E
(inspiration:expiration) ratio. The pressure generated is the same for patient- and
ventilator-initiated breaths. The VT generated is not fixed and will depend on the elastic
and resistance components of the lung. For ARDS patients, the goal is to attain a tidal
volume of 5–7 mL/kg with peak pressures <30 mm Hg.
– Respiratory rate: Some machines set a minute volume that determines the respiratory rate:
MV/VT.
– Mode of triggering: Negative pressure sensors are typically found on anesthesia machines
and are set at –2 cm H2O. However, because they place an unnecessary workload on
breathing, they have been replaced by flow triggers on ICU ventilators. Flow triggers
implement a continuous flow of gas and when patient-triggered inspiration (negative
pressure) deflects this flow, the ventilator is triggered. If the trigger is too sensitive, the
patient can hyperventilate. If it is not sensitive enough, the patient becomes
dyssynchronous.
– Peak flow is measured as liters per minute (L/min) and is typically set at 4 times the
minute ventilation; this parameter is utilized as opposed to an I:E ratio. In adults, 50
L/min is initially chosen; higher levels may be selected in patients with airflow
obstruction. If the flow rate is too high, the volume is rapidly delivered to the most
compliant lung tissues (not to the inelastic diseased tissues) at very high peak pressures. If
the peak flow is too low, the patient will demand more gas than the ventilator is setup to
supply and dyssynchrony with the machine occurs; this is referred to as “air hunger.”
Pressure augmentation allows the ventilator to sense that the patient’s demands exceed
the peak flow, and automatically increases the flow.
• Ventilatory settings are adjusted based upon the patient’s plateau pressure, inspiratory flow
demand, and blood gas targets.
ANATOMY
• The airway tree starts with the trachea and divides approximately 23 times (dichotomous
divisions) to form alveolar sacs that contain 17 alveoli in average.
• The average adult has a gas exchange surfaces in the lungs of about 50–100 m2 (300 million
alveoli).
PHYSIOLOGY/PATHOPHYSIOLOGY
• Respiratory failure: Respiratory rate >35 breaths/min or <6 breaths/min; oxygen
saturation <90% despite adequate supplemental oxygen; tidal volume <5 mL/kg; vital
capacity <15 mL/kg; pH <7.20; PaCO2 >50 mm Hg; A-a gradient >350 mm Hg on an
FIO2 1.0
• Pulmonary consequences and ventilator-associated lung injury
– Barotrauma can be seen with excessive pressures and can lead to pneumothorax,
pneumomediastinum, subcutaneous emphysema, and pneumopericardium.
– Volutrauma can be seen with high-end inspiratory volumes that can lead to alveolar stress
injury and increased lung water; can be reversed by PEEP.
– Atelectrauma; decreases in surfactant result in less “patent” alveoli, or alveolar collapse.
The repeated opening and collapsing results in shear stress to the alveoli.
– Biotrauma describes the maladaptive inflammatory release that occurs secondary to
mechanical factors or biophysical injury. Cytokines, complement, prostanoids,
leukotrienes, proteases, and reactive oxygen species can result in damage to distal organs.
Tissue injury can result from these inflammatory mediators as well as impaired oxygen
delivery and bacteremia.
– Hyperventilation and significant respiratory alkalosis can develop, particularly with CNS
disorders, febrile states, or sepsis. An alarm can be set if the ventilator cycles too
frequently.
– Air trapping and breath stacking can occur with obstructive airway disease or with
increased respiratory rates (not enough time to exhale the full tidal volume).
– Muscle atrophy resulting from disuse develops if used for long, thus the need for gradual
weaning of pressure or volume support before extubation.
• Cardiovascular effects: Increased intrathoracic pressure
– Decreases venous return to the right atrium (preload) and can potentially decrease cardiac
output. This can be significant in patients that are hypovolemic, have low ejection
fractions, or are preload-dependent (pericardial tamponade).
– Can decrease left ventricular afterload by increasing the transmural pressure (less
negative). In patients with LV dysfunction, the negative inspiratory pressures that are
needed to maintain adequate inspiratory volumes are greater (due to pulmonary edema,
the lung volume and compliance decrease). Positive pressure ventilation functions on the
principle of increasing intrathoracic pressures and hence makes the transmural pressure
less negative.
• Renal function has been shown to decrease with positive pressure ventilation (decreased
urine output and sodium excretion).
• Hepatic function may be affected due to decreased cardiac output, increased hepatic
vascular resistance, and elevated bile duct pressure.
PERIOPERATIVE RELEVANCE
• A/C is useful for rapid weaning at the end of a case where the patient is not yet breathing
spontaneously but expected to shortly (muscle relaxant reversal, decreasing volatile or IV
anesthetic levels). Patients can be extubated directly from A/C or switched to pressure
support prior to extubation.
• In patients not breathing spontaneously (neuromuscular blockade, opioids), there is no
difference in minute ventilation between SIMV, AC, or CMV.
EQUATIONS
Equation of motion of the airway: P = VT/C + R × F (P = transpulmonary pressure, VT =
tidal volume, C = compliance, R = resistance, F = flow) (3)[A]

Volume-targeted assist control ventilation. On the left, the patient is receiving controlled, set breaths at a rate of 12/min.
On the right, the patient is receiving assisted breaths as can be seen by the small downward deflection produced by a
patient-triggered breath. All breaths have an identical tidal volume.
Pressure-targeted assist control ventilation. On the left side, the peak flow is set at 30 L/min, and the scooped out
appearance of the pressure trace indicates that the patient is slightly dyssynchronous. On the right side, pressure
augmentation has been added and increases the peak flow rate in response to the patient’s demand. Results in improved
dynamics in regard to the pressure and flow waveforms and resembles pressure support, rather than assist control.

REFERENCES
1. steban A, Anzueto A, Alia I, et al. How is mechanical ventilation employed in the intensive
care unit? Am J Respir Crit Care Med. 2000;161(5):1450–1458.
2. hiumello D, Pelosi P, Calvi E, et al. Different modes of assisted ventilation in patients with
acute respiratory failure. Eur Respir J. 2002;20:925–933.
3. Tejeda M, Boix JH, Alvarez F, et al. Comparison of pressure support ventilation and assist-
control ventilation in the treatment of respiratory failure. Chest. 1997;111:1322–1325.
4. Nikischin W, Gerhardt T, Everett R, et al. A new method to analyze lung compliance when
pressure–volume relationship is nonlinear. Am J Respir Crit Care Med. 1998;158:1052–
1060.
5. Sassoon CSH, Zhu E, Caiozzo VJ. Assist-control mechanical ventilation attenuates
ventilator-induced diaphragmatic dysfunction. Am J Respir Crit Care Med.
2004;170(6):626–632.
6. Tobin MJ, Jubran A, Laghi F. Patient–ventilator interaction. Am J Respir Crit Care Med.
2001;163:1059–1063.
7. Tobin MJ. Mechanical ventilation N Engl J Med. 1994;330:1056–1061.
8. Toublanc B, Rose D, Glerant JC, et al. Assist-control ventilation vs. low levels of pressure
support ventilation on sleep quality in intubated ICU patients. Intensive Care Med.
2007;33(7):1148–1154.
See Also (Topic, Algorithm, Electronic Media Element)
• Continuous positive airway pressure
• Positive end expiratory pressure
• Acute respiratory distress syndrome
• Intubation and extubation criteria

CLINICAL PEARLS
• A/C does not abolish the work of breathing; it can reduce it.
• It provides a seamless transition from ventilator-controlled respiration to ventilator-
supported, patient-initiated breaths.
ASTHMA
Nina Singh-Radcliff, MD

BASICS
DESCRIPTION
• Asthma describes bronchial hyper-reactivity with reversible airflow obstruction in response
to various stimuli. Despite its reversible nature, chronic airway inflammation is a hallmark.
• A reactive airway, or bronchial hyper-responsiveness, is also seen in chronic bronchitis,
emphysema, allergic rhinitis, and respiratory infections.
EPIDEMIOLOGY
Prevalence
7% of US population, increasing yearly
Prevalence
• 1/2 of all cases develop before the age of 10 years
• 1/3rd occur after the age of 40 years
• 2:1 male:female preponderance up to the age of 30 years, then equalizes
Morbidity
• Perioperative occurrence is seen in 0.17–2.4% of asthmatics.
• 40,000 missed school or work days each day
• 30,000 asthma attacks daily
• 5,000 ER visits daily
• 1,000 hospital admissions daily
Mortality
5000/year
ETIOLOGY/RISK FACTORS
• Allergens
• Pharmacologic agents (aspirin, beta-blockers, NSAIDS, sulfa)
• Infections (viral airway infections increase airway resistance even in non-asthmatics,
possibly due to a cholinergic mechanism in the bronchial smooth muscles)
• Exercise (post-exercise)
• Emotional stress
• Cold weather
• Abnormal autonomic nervous system regulation
• Endotracheal tube, mucus, saliva (anesthetic related)
• Pregnant patients administered prostaglandins for abortion or operative delivery
PHYSIOLOGY/PATHOPHYSIOLOGY
• The above-mentioned triggers can elicit bronchial smooth muscle contraction. Additionally,
vagal and sympathetic factors directly modulate airway tone (1,2,3).
• Acutely, inflammatory edema and mucus plugging exacerbate airflow limitation.
Chronically, airway remodeling, thickening, and abnormal communications occur in the
epithelium of the injured airway and in the pulmonary mesenchyma; changes are
permanent and can result in progressive damage (1,2,3).
• Immunologic–inflammatory pathways involve lymphocytes, eosinophils, neutrophils, mast
cells, leukotrienes, and cytokines (1,2,3).
• Bronchoconstriction increases (3):
– Work of breathing
– Air trapping
– V/Q mismatch (reduced ventilation that causes shunting)
– Pulmonary vascular resistance (PVR)
– Right ventricle afterload
– Residual volume (RV)
– Functional residual capacity (FRC)
– Total lung capacity (TLC)
– Oxygen consumption
– Carbon dioxide production
• Bronchoconstriction decreases:
– Airflow
– FEV1
– Expiratory reserve volume (ERV)
– Inspiratory reserve volume (IRV)
– FEV1/FVC
– FEV25-75%
– Dynamic compliance of lungs
• Accessory muscles are recruited to preserve tidal volume (TV) despite increased ERV (from
increased FRC and air trapping) (1,2).
• Initially, hyperventilation causes respiratory alkalosis. Over time, increased air trapping and
respiratory muscle fatigue increase CO2 retention; therefore, normalization of PaCO2 reflects
decompensation. Extreme air trapping can restrict cardiac filling and “pulmonary
tamponade” that can result in pulse-less electrical activity.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Assess severity of disease, optimize pulmonary function, and treat acute exacerbation
• The anesthetic plan should prevent, suppress, and blunt airway hyper-reactivity; stimuli that
do not ordinarily evoke airway responses can precipitate life-threatening
bronchoconstriction in the asthmatic.
• Diagnose and treat perioperative bronchoconstriction

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Shortness of breath
• Chest tightness
• Cough
History
• Age of onset
• Triggers
• Treatment history
– Frequency of exacerbations
– Nighttime awakenings
– Rescue inhaler use
– Steroids pulse dose
– ER visits
– Hospitalizations
– ICU admissions
– Intubations
Signs/Physical Exam
• Expiratory wheezing
• Accessory muscle use
• Tachypnea
• Diminished or inaudible breath sounds
MEDICATIONS
• “Controller” to modify airway environment
– Inhaled steroids
– Theophylline
– Leukotriene modifiers
– Cromolyn
• “Rescue” for acute bronchospasm (quick onset)
– Beta-adrenergic agonists
– Anticholinergics
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Pulmonary function tests can aid with diagnosis, and objectively assess severity and
response to treatment (FEV, FEV1/FVC)
• CXR (hyperventilation, pneumonia, CHF)
• EKG (acute right heart failure, PVCs)
• Eosinophilia
• ABGs (pCO2 and pO2)

CONCOMITANT ORGAN DYSFUNCTION


77% have gastroesophageal reflux disease (GERD); control of GERD may improve asthma
symptoms.
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Acute exacerbation
• Chronic sinus infection
• Upper respiratory infection
• Pneumonia
CLASSIFICATIONS
• Based on symptoms, nighttime awakenings, short-acting beta-agonist symptoms,
interference with normal activity, lung function, oral steroid use
– Mild
– Moderate
– Marked
– Severe/status asthmaticus

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Consider beta-agonists (MDI, nebulizer)
• Consider a steroid stress dose (avoid Addisonian crisis if recent therapy and major surgery)
• Consider a steroid pulse dose (avoid perioperative exacerbation in severe disease, or major
surgery)
• Anxiolysis
INTRAOPERATIVE CARE
Choice of Anesthesia
• Consider regional anesthesia to avoid airway instrumentation and stage II emergence
(increased risk for bronchoconstriction)
• Consider LMA, which sits supraglottically and is associated with less airway irritation than
ETT
Monitors
• Standard ASA monitors
• Consider augmenting the ETCO2 waveform to improve detection of obstruction; a slow rise
to the peak indicates expiratory obstruction.
• Consider an arterial line in high-risk patients to allow for ABG monitoring
Induction/Airway Management
• Laryngoscopy, intubation, suctioning, and cold inspired gases can exacerbate hyper-
reactivity.
• Patient should be “deep” prior to airway instrumentation. Ensure that an adequate dosage of
induction medications and neuromuscular blockade have been administered, as well as an
appropriate amount of time for onset. Induction medications should be titrated to blunt
bronchial smooth muscle responsiveness, and NMBD should be titrated to block coughing,
gagging, or bucking. Although these are skeletal muscle phenomenon, when provoked, they
can precipitate irritant receptors and airway hyper-reactivity.
• Consider bag mask ventilating with volatile agents (potent bronchodilators) for 2–3 minutes
prior to airway instrumentation
• Ketamine is the only bronchodilating IV induction agent; propofol and etomidate blunt
airway reflexes to a greater extent than thiopental.
• Lidocaine blunts airway response to irritation. However, caution is advised when topically
applied; spraying can cause irritation and precipitate bronchospasm.
• Succinylcholine has histamine release; however, studies have not shown this to be clinically
relevant.
• When considering a RSI, the risk of aspiration needs to be weighed against the risk of
bronchoconstriction from airway manipulation prior to the patient being “deep.”
Maintenance
• Keep the patient “deep” or adequately anesthetized. Otherwise, innocuous stimuli can result
in increased airway resistance (saliva, mucus, ETT).
• I:E ratio should be reduced (increased time for exhalation to avoid air trapping; similar to
phenomenon of “pursed lip breathing” in patients with emphysema).
• Humidify, warm inspiratory gases
• Fluid hydration to soften mucus secretions
Extubation/Emergence
• Consider “deep” extubation (removing airway while anesthetic is sufficient to suppress
hyper-reactivity)
• When it is unwise to extubate before the patient is fully awake, consider suppressing airway
reflexes (IV lidocaine, bronchodilators, epinephrine IV/SQ, dexmedetomidine).
• Neostigmine may bronchoconstrict if not administered with adequate antimuscarinics.
• Antimuscarinics can thicken secretions.

FOLLOW-UP

BED ACUITY
• Vigilance for bronchospasm
• Consider supplemental oxygen (nasal cannula, face mask)
• Consider scheduled bronchodilator treatments
• Incentive spirometry and deep breathing
• Early mobilization
• Good pain control
• Control GERD
COMPLICATIONS
• Intraoperative bronchospasm is diagnosed by:
– Increased peak inspiratory pressures (PIP)
– ETCO2 sloping
– Expiratory wheezing
• Treatment consists of:
– Deepening the anesthetic with inhaled volatile agents. Volatile agents are potent
bronchodilators and cause direct bronchial smooth muscle cell dilation by altering
intracellular calcium regulation. However, if there is little or no airway movement, this
may not be effective.
– Deepening the anesthetic with intravenous agents. Propofol does not bronchodilate, but it
can suppress airway reflexes.
– Inhaled beta-agonists. Albuterol causes bronchodilation, but may require several puffs (8–
10) to ensure delivery through a long narrow ETT. There are several devices available that
can facilitate delivery.
– Steroids intravenously. Administration should not preclude more immediate therapy.
– Epinephrine (IV bolus, SQ, drip); sympathomimetic that decreases bronchospasm via beta-
2 agonist.
– Theophylline may be considered; however, it is more common for symptom control and
prevention. Additionally, it has a narrow therapeutic index and levels need to be
monitored if continued postoperatively.
– Heliox can promote laminar airflow, but reduces FIO2, and has not been shown to be
therapeutic.
– Magnesium (drowsiness and NMBD potentiation)
– Avoid histamine-releasing medications (e.g. morphine, vancomycin)

REFERENCES
1. Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and
bronchospasm. Br J Anaesth. 2009;103(S1):i57–i65.
2. Fanta CH. Asthma. N Engl J Med. 2009;360:1002–1014.
3. Tirumalasetty J, Grammer LC. Asthma, surgery, and general anesthesia: A review. J
Asthma. 2006;43(4):251–254.

ADDITIONAL READING
• Asthma and Allergy Foundation of America
• Burburan SM, Xisto DG, Ferreira HC, et al. Lung mechanisms and histology during
sevoflurane anesthesia in a model of chronic allergic asthma. Anesth Analg.
2007;104(3):631–637.
• Overview of Changes to Asthma Guidelines. www.aafp.org
See Also (Topic, Algorithm, Electronic Media Element)
• Ventilation perfusion matching
• Ventilation perfusion mismatching
• Pulmonary function tests
• Functional residual capacity
• End tidal CO2
• I:E ratio
• Deep extubation
• Laminar flow

CODES

ICD9
• 493.90 Asthma,unspecified type, unspecified
• 493.92 Asthma, unspecified type, with (acute) exacerbation

ICD10
• J45.901 Unspecified asthma with (acute) exacerbation
• J45.909 Unspecified asthma, uncomplicated

CLINICAL PEARLS
• Assess the severity of disease in order to plan an appropriate anesthetic technique.
• Stimuli that do not ordinarily evoke airway responses can precipitate life-threatening
bronchoconstriction in asthmatics. Ensure that the patient is adequately induced prior to
airway manipulation, as well as remains adequately anesthetized during the surgery;
consider a “deep" extubation.
• Intraoperative bronchoconstriction presents as increased PIP, a sloping ETCO2 waveform,
and wheezing.
• All that wheezes is not asthma; rule out other causes prior to treating for bronchospasm.
• Asthma increases the risk of bronchospasm, hypoxemia, hypercapnia, inadequate cough,
atelectasis, and pulmonary infection following surgery.
ATELECTASIS
Arun Alagappan, MD
Stephen P. Winikoff, MD

BASICS
DESCRIPTION
• Atelectasis refers to a collapse of lung tissue from compression, absorption, or loss of
surfactant; it is very common in the perioperative setting.
• Atelectasis from anesthesia:
– Occurs with both inhalational and intravenous anesthetics
– Appears within minutes after induction (1)
– Occurs with spontaneous and mechanical ventilation
– Primarily affects lung tissue in the basal regions adjacent to the diaphragm
– Can be worsened with positioning (supine and Trendelenburg)
– Can persist for days after major surgery
EPIDEMIOLOGY
Prevalence
• Atelectasis is found in 90% of anesthetized patients (2).
• Infants are at a greater risk secondary to their decreased lung compliance relative to their
chest wall. Additionally, their closing volume is greater due to incomplete development of
the elastic supporting structures of the lung, and as a result, they are at risk for airway
closure during tidal volume breathing (2).
• Atelectasis is most common after cardiac surgery with CPB (3).
Prevalence
• Observed in all age groups
• Magnitude is independent of age in adults (2).
Morbidity
Hypoxemia, right ventricular dysfunction, lung injury
Mortality
Pulmonary complications account for 24% of deaths within 6 days of surgery (2). Atelectasis
causes physiologic impairments that contribute to the development of these pulmonary
complications.
ETIOLOGY/RISK FACTORS
• There are 3 mechanisms by which atelectasis can develop:
– Compression
– Absorption
– Loss of surfactant
• Compression atelectasis: Occurs when the transmural pressure that distends the alveolus is
reduced. During anesthesia, the diaphragm is relaxed and is cephaledly displaced making it
less effective at maintaining distinct pressures in the extrathoracic and abdominal cavities.
Abdominal pressures are transmitted to the pleural space and promote collapse of adjacent
lung units (3).
• Absorption atelectasis: Occurs when less gas enters the alveolus than is removed by uptake
of blood. This can happen when there is complete airway occlusion creating a pocket of
trapped gas in a distal lung unit that continues to be perfused. Gas uptake from the pocket
continues without inflow of gas, and the pocket collapses. Alternately, in the absence of
complete airway occlusion, if the VA/Q is reduced, there is a point reached at which the
rate of inspired gas entering the alveolus is balanced by gas uptake from the alveolus. Below
this critical ratio, the lung unit will collapse. This becomes more likely with increasing FIO2
(2). May be seen when nitrous oxide is changed to 100% oxygen at the end of a case.
• Loss-of-surfactant atelectasis: Occurs when the alveolar-stabilizing function of surfactant is
depressed by anesthesia or by a lack of intermittent deep breaths. Surfactant is a surface-
active lipoprotein that is produced by alveolar type 2 cells and acts to reduce alveolar
surface tension. The surface tension of the alveolar air–water interface provides a retractive
force opposing lung inflation. The presence of surfactant can lower the air–water surface
tension to near zero, ensuring that the alveolar space remains open. Abnormalities in the
amount or composition of surfactant are seen in certain conditions including neonatal
respiratory distress syndrome and acute respiratory distress syndrome (ARDS), as well as
secondarily from inflammatory processes in the lung (4).
• Other contributing factors to atelectasis under general anesthesia include:
– Obesity: The weight of the chest wall and abdomen makes diaphragmatic excursion more
difficult and promotes atelectasis (5). Studies have shown that atelectasis resolves more
slowly compared to nonobese patients.
– Positioning: In the supine position, abdominal contents have cephalad invasion against the
relaxed diaphragm. In Trendelenburg, gravity further accentuates this.
– Laparoscopy: Pneumoperitoneum promotes atelectasis. Studies have also shown that it is
associated with an increased incidence of postoperative atelectasis (5).
PHYSIOLOGY/PATHOPHYSIOLOGY
• Atelectasis causes several physiologic impairments in respiratory function resulting in a
range of clinical findings including:
– Hypoxemia
– Decreased pulmonary compliance
– Right ventricular dysfunction
– Worsening of lung injury
• Hypoxemia results from ventilation perfusion mismatching or shunt. Perfusion to the
alveolar unit continues despite the lack of ventilation.
• Decreased pulmonary compliance is primarily through a reduction in lung volume (3). This
increases the work of breathing by requiring an increased transpulmonary pressure to
achieve a given tidal volume.
• Right ventricular dysfunction: Atelectasis contributes to regional hypoxia that in turn
contributes to hypoxic pulmonary vasoconstriction and increased pulmonary vascular
resistance. This can result in right ventricular dysfunction and increased microvesicular
leakage (3).
• Lung injury: Atelectasis can potentiate existing lung injury in both high and low tidal
volume ventilation strategies. In high tidal volume ventilation with zero PEEP, atelectasis
causes increased serum cytokine concentrations as well as impaired lung compliance (3).
During low tidal volume ventilation in the presence of atelectasis, there was shown to be a
decrease in survival (3).
• Chronic obstructive pulmonary disease actually reduces the amount of atelectasis that
develops due to hyperinflation of the lungs and prevents lung collapse. However, these
patients develop a more severe V/Q mismatch (2).
PREVENTATIVE MEASURES
Prevention of atelectasis starting at induction of anesthesia is important.
• Induction:
– Application of CPAP (6 cmH2O) for 5 minutes prior to induction, followed by mechanical
ventilation with PEEP has been suggested to be superior to PEEP alone (1).
– Although studies have suggested that using lower FIO2 during preoxygenation prevents
atelectasis formation during induction, it is not recommended. The apnea time before
hypoxia develops is decreased; hence the margin of safety is decreased (6).
• Intraoperative:
– Lower levels of FIO2 may decrease absorption atelectasis (6).
– Application of PEEP (6 cmH2O) can prevent formation of atelectasis and reduction of FRC
(increased lung volume and oxygen storage) (2). It may also be an effective strategy to
avoid atelectasis when higher FiO2 is required.

PREOPERATIVE ASSESSMENT
• Atelectasis should be considered whenever there are alterations in lung physiology in a
setting where atelectasis is likely.
• Hypoxemia secondary to atelectasis is reflected in an increased A-a gradient. It is important
to note other causes of hypoxemia, as seen below in differential diagnosis.
• Confirmation of the diagnosis, if needed, can be obtained with imaging.
– On CXR, atelectasis will have features similar to consolidation with opacification of the
lung parenchyma (3).
– CT scan is superior to CXR based on the resolution, and ability to measure whole and
regional lung volumes. Atelectasis on CT scan has been defined as pixels with attenuation
values of –100 to +100 Hounsfield units (a measure of density as seen on CT) (3).
– Thoracic ultrasound is emerging as a way to rapidly assess regional consolidation (3).
DIFFERENTIAL DIAGNOSIS
Atelectasis should be distinguished from other causes of hypoxemia including:
• Hypoxic delivery
• Hypoventilation
• Diffusion impairment
• Right-to-left intracardiac shunting

TREATMENT

• A vital capacity maneuver (VCM) can offset the atelectasis that develops after induction of
general anesthesia. A pressure of 40 cmH2O maintained for 7–8 seconds is needed to re-
expand previously collapsed lung tissues (2).
– Laparoscopy: The recruitment effect of a single VCM may be lost after pneumoperitoneum
and requires additional maneuvers to keep the alveoli open (5).
– Lower FIO2: When the inflation and succeeding ventilation are performed with a lower
FIO2, atelectasis reappears more slowly. One study demonstrated that when 40% was
used, only 20–25% of the initial area was atelectatic 40 minutes after the VCM. When
100% oxygen was used, however, atelectasis recurred within 5 minutes (7).
– Drawbacks of VCM include a decreased preload, and potentially cardiac output.
• A PEEP of 10 cmH2O will consistently reopen collapsed lung tissue. However, those lung
units may re-collapse after discontinuation of PEEP. It has been shown that PEEP applied
immediately following a VCM will completely prevent recurrence of atelectasis, even when
100% oxygen is used (2).
• Postoperatively, techniques or devices that encourage or force patients to inspire deeply are
beneficial, with a goal of producing a large, sustained increase in transpulmonary pressure
to distend and re-expand collapsed lung units. Techniques include intermittent positive-
pressure breathing, deep-breathing exercises, incentive spirometry, and chest physiotherapy.
All these techniques were shown to be equally efficacious in reducing the frequency of PPC
following abdominal surgery (3).

FOLLOW-UP

• Most perioperative atelectasis resolves within 24 hours after surgery (2). However, the
normal coordination of respiratory muscle action is disrupted in the postoperative period,
and this predisposes to decreases in FRC and VC which can contribute to development of
atelectasis for days following major surgery (8).
• Patients should be monitored for development of postoperative pulmonary complications.

REFERENCES
1. rismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with
muscular relaxation: A proposal of atelectasis. Anesthesiology. 1985;62:422–428.
2. Magnusson L, Spahn DR. New concepts of atelectasis during general anesthesia. Br J
Anesth. 2003;91:61–72.
3. Duggan M, Kavanagh BP. Pulmonary atelectasis. Anesthesiology. 2005;102:838–854.
4. Griese M. Pulmonary surfactant in health and human lung diseases: State of the art. Eur
Resp J. 1999;13:1455–1476.
5. Talab HF, Zabani IA, Abdelrahman HS, et al. Intraoperative ventilatory strategies for
prevention of pulmonary atelectasis in obese patients undergoing laparoscopic bariatric
surgery. Anesth Analg. 2009;109(5):1511–1516.
6. Reber A, Englberg G, Wegenius G, et al. Lung aeration: The effect of pre-oxygenation and
hyperoxygenation during total intravenous anaesthesia. Anaesthesia. 1996;51:733–737.
7. Rothen HU, Sporre B, Engbert G, et al. Prevention of atelectasis during general anesthesia.
Lancet. 1995;345:1387–1391.
8. Weiskopf RB. Preventing postoperative pulmonary complications. Anesthesiology.
2000;92:1467–1472.
9. Ho-Tai LM, Devitt JH, Noel AG, et al. Gas leak and gastric insufflations during controlled
ventilation: Face mask versus laryngeal mask airway. Can J Anaesth. 1998;45:206–211.
10. Hedenstierna G, Edmark L. Mechanisms of atelectasis in the perioperative period. Best
Pract Res Clin Anesth. 2010;24:157–169.
See Also (Topic, Algorithm, Electronic Media Element)
• Pulmonary ventilation perfusion matching
• Functional residual capacity
• Surfactant
• Hypoxemia intraoperatively
• Postoperative pulmonary complications

CODES

ICD9
518.0 Pulmonary collapse

ICD10
J98.11 Atelectasis

CLINICAL PEARLS
• Ketamine is the only anesthetic that does not produce atelectasis when used alone (3).
• Infants are at a greater risk for atelectasis secondary to decreased lung compliance relative
to the chest wall (2).
• Gastric insufflation may result from the application of PEEP during induction if peak
pressures exceed 20 mm Hg (9).
ATRIA
Ali Salehi, MD

BASICS
DESCRIPTION
• The atria:
– House the sinoatrial (SA) node that initiates electrical impulses
– Are responsible for the active filling of the ventricles during diastole
– Play an important role in the neurohormonal regulation of sodium (Na+) and fluid
balance
PHYSIOLOGY PRINCIPLES
• SA node: The primary pacemaker of the heart; located at the junction of the superior vena
cava (SVC) and the right atrium (RA). The action potential is initiated in the SA node which
has an automaticity of 70–80 pulse per minute (ppm) and a conduction velocity of 0.05
m/s.
• Internodal bundles: There are 3 bundles that connect the SA node to the atrioventricular
(AV) node (anterior internodal bundle of Bachman, middle internodal bundle of
Wenckebach, and posterior internodal bundle of Thorel). The action potential is conducted
via these bundles through both atria to the AV node simultaneously. The conduction
velocity in these bundles is 0.8–1 m/s.
• AV node: Located in the right posterior portion of the interatrial septum (IAS). It is the only
conducting pathway between the atria and the ventricles. Its conduction velocity is slower
(0.02–0.05 m/s) than the rest of the heart, allowing the ventricles sufficient diastolic filling
time. The AV node can act as a latent pacemaker with an automaticity of 40–60 ppm.
• His bundle: Divides at the top of the interventricular septum into the left bundle branch and
right bundle branch; has an automaticity rate of 40 ppm. The left bundle divides into
anterior and posterior fascicles. These bundles run subendocardially and come in contact
with Purkinje fibers that spread throughout the myocardium. Conduction velocity in this
system is fast (1–1.5 m/s for the bundles and 3–3.5 m/s for Purkinje fibers).
• Innervation: Embryologically, the SA node develops from the structures on the right side of
the heart and the AV node from the left side of the heart. This results in the SA node being
innervated by the right vagus nerve and the AV node by the left vagus nerve. Sympathetic
innervations (T1–T4, cardioaccelerator fibers) follow the same distribution. The majority of
sympathetic fibers come from the ipsilateral stellate ganglion.
• Endocrine physiology: Atrial myocytes are responsible for the production and release of
atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). ANP and BNP are
polypeptides that are released from the atria in response to increases in extracellular fluid
(ECF) volume due to Na+ retention. They function to increase the glomerular filtration rate
(GFR) via renal glomerular afferent arteriole vasodilatation and efferent arteriole
vasoconstriction; decrease the reabsorption of Na+ from the distal convoluted tubule and
collecting ducts (causing a net increase in Na+ excretion and volume loss); and increase
capillary permeability and relax vascular smooth muscle in arterioles and venules, causing
decreases in blood pressure.
ANATOMY
• The walls of all heart chambers consist of 3 layers: Endocardium (inner layer of the heart,
comprises endothelial cells and subendocardial connective tissue), myocardium (middle
layer of the heart, comprises myocardial muscle cells), and epicardium (outer layer of the
heart, formed by the visceral layer of the pericardium).
• Right atrium: The chamber forming the right upper border of the heart.
– Systemic venous return from the SVC and inferior vena cava (IVC) enter the posterior,
smooth wall of the RA (SVC enters at the level of the 3rd costal cartilage; IVC enters at the
level of the 5rd costal cartilage on the same line as the SVC). The coronary sinus (CS)
carries cardiac venous return into the posterior wall between the orifice of the IVC and
tricuspid valve. The IVC is protected by the Eustachian valve and the CS is protected by
the Thebesian valve.
– Pectinate muscles are found on the anterior portion of the RA; they are rough,
trabeculated, and made of parallel muscle bundles.
– The anterior and posterior portions are separated on the right by the sulcus terminalis
externally and crista terminalis internally.
– The posteromedial wall of the RA is the IAS.
– The base of the RA is the tricuspid valve and has 3 leaflets (anterior, posterior, and
septal).
• Left atrium (LA): A smooth-walled chamber that forms the base of the heart.
– Receives pulmonary venous return through the right upper and lower pulmonary veins
(RUPV, RLPV) and the left upper and lower pulmonary veins (LUPV, LLPV).
– The left atrial auricle (LAA), or appendage, forms the superior part of the left border of
the LA and has a rough trabeculated wall comprising pectinate muscles.
– The LA wall is slightly thicker than the RA.
– Unlike the right-sided veins, pulmonary veins do not have valves.
• Interatrial septum: Separates the 2 chambers and extends posteriorly and to the right
causing most of the LA to be posterior to the RA.
– Embryologically, the IAS is formed by the septum primum and septum secundum (1).
– The septum primum starts to develop in the 5th week of gestation and grows towards the
endocardial cushion (1).
– The septum secundum, at the same time, develops to the right of the septum primum as an
invagination of the atrial wall. It stops growing in the 7rd week of gestation. It leaves a
posterior inferior gap called the “fossa ovalis (1).”
– The lower portion of the septum primum persists into adulthood as the “flap valve." Upon
birth and expansion of the lungs, right-sided pressures drop below left-sided pressures and
the flap valve is pressed against the septum secundum. In 66% of people they fuse
together forming the “fossa ovalis." In 33% they fail to fuse resulting in a “patent foramen
ovale” (PFO) (1).
DISEASE/PATHOPHYSIOLOGY
• Abnormal pulmonary venous return (congenital defect): One or more pulmonary veins that
carry oxygenated blood from the lungs enter the RA instead of the LA; this can be partial
anomalous pulmonary venous return (PAPVR) or total anomalous pulmonary venous return
(TAPVR). PAPVR presents with symptoms of right-sided volume overload, pulmonary
hypertension, and right heart failure. TAPVR is a cyanotic disorder and a true surgical
emergency needing an atrial septostomy in the newborn. Since all of the pulmonary venous
flow returns to the RA, presence of an atrial septal defect (ASD) or patent ductus arteriosus
(PDA) is essential to sustain life after birth.
• Atrial septal defect: An abnormal connection between the LA and RA that is associated with
a left-to-right shunt. Patients present with symptoms of right-sided volume overload (JVP
elevation, hepatic congestion, lower extremity edema, shortness of breath, pulmonary
congestion). Over time, if not corrected, it can cause right ventricle (RV) failure and
elevation of RA pressures with resultant shunt reversal (right-to-left shunt; Eisenmenger’s
syndrome). This will lead to hypoxemia and cyanosis. There are 4 major types:
– Septum secundum ASD: Results from inadequate growth of the septum secundum,
enlarged foramen ovale, or excessive absorption of the septum primum. Most common
ASD (80–90%), usually seen in women in the 5th or 6th decade of life, and rarely
associated with other cardiac defects (1).
– In addition to the septum primum, the endocardial cushion is responsible for the
development of the medial portion of the mitral and tricuspid valves, and the inlet portion
of the interventricular septum. A complete endocardial cushion defect is associated with a
septum primum ASD, a common AV valve, and an inlet VSD. It comprises 2–3% of all
ASDs and can be associated with a mitral (anterior leaflet) or tricuspid valve (septal
leaflet) cleft (1).
– Sinus venosus ASD: The failure in separation between the right-sided pulmonary veins and
the SVC, IVC, or RA. It comprises 2–10% of all ASDs. The superior type is a defect at the
junction of the SVC and RA leading to anomalous pulmonary venous return of the RUPV
into the RA. The inferior type is a defect in the junction of the IVC and RA leading to
anomalous pulmonary venous return of the RLPV into the RA (1).
– Coronary sinus ASD: Results from the unroofing of the CS which leads to a connection
between the inferior part of the LA and CS; associated with left-sided SVC. It is the least
common form.
• Atrial bradycardia: Sinus bradycardia (SB) is a heart rate <60 bpm. It can be seen normally
in athletes due to preconditioning and increased stroke volume due to exercise. SB can also
result from conditions involving the SA node such as inferior myocardial infarction;
medications (beta-blockers, inhalational anesthetic agents, narcotics, anticholinesterase
agents, and succinylcholine); and vagus nerve stimulation from carotid sinus message,
tension on the extra-ocular muscles (oculocardiac reflex) or omentum. Additionally, reflex
bradycardia can result from a sudden rise in BP that is detected by the carotid sinus. Causes
include a rise in intracranial pressure (Cushing’s reflex from tumors, intracranial bleed), use
of alpha-agonists (phenylephrine, norepinephrine), and increases in cardiac output.
• Atrial tachycardia is a heart rate >100 bpm with a narrow complex QRS on ECG.
– Sinus tachycardia is due to an increase in output (automaticity rate) of the SA node. Heart
rate is usually 100–180 bpm with a “P” wave seen on the ECG. Common causes include
sympathetic stimulation (hypoxia, hypercarbia, acidosis, ischemia), hypotension or
hypovolemia, anemia, anxiety, fever, anaphylactic reactions, sepsis, medications
(dopamine, epinephrine), hyperthyroidism, and physical activity.
– Supraventricular tachycardia (SVT) includes all forms of tachycardia originating above the
bifurcation of the His bundle. They have a regular rate of 150–220 bpm. The most
common type is AV nodal re-entrant tachycardia (60%). Another 30% are due to an AV
re-entry pathway connecting the atria to the ventricles. The remaining etiologies include
pre-excitation syndromes such as Wolff–Parkinson–White and paroxysmal atrial
tachycardia.
– Atrial flutter occurs at a rate of 200–350 bpm. It is usually associated with a circuit
movement of the right atrial tissue causing the saw tooth pattern on ECG. Atrial flutter is
almost always associated with a 2:1 or greater AV block because the AV node is not able
to conduct more than 220 bpm.
– Atrial fibrillation occurs at a rate of 300–500 bpm in a completely irregular and
disorganized fashion. It is the result of multiple, concurrent, circulating re-entrant
excitation waves in both atria; seen as an irregular pattern of AV node conduction at
irregular intervals about 80–160 bpm. A-fib can be acute, chronic, or paroxysmal. Most of
the foci responsible for a-fib appear to originate from atrial smooth muscle at the junction
of the pulmonary veins and the LA. Other foci that can be involved include the mitral
valve isthmus, orifice of CS, and SVC.
• Conduction abnormalities:
– First-degree heart block: All impulses are conducted to the ventricles but the PR interval
on the ECG is prolonged.
– Second-degree heart block (2 types): Type 1 (Wenckebach) is associated with gradual
prolongation of the PR interval and eventual drop of a ventricular beat. Type 2 has a
normal PR interval with sudden dropped ventricular beats; it has the potential to progress
into complete heart block.
– Third-degree (complete) heart block is associated with total dissociation of the atria and
ventricles. The ventricles beat at a rate lower than the atrial rhythm. The block can be at
the level of the AV node (nodal block) or lower (infranodal). In nodal block the remaining
AV node becomes the pacemaker of the ventricles at a rate of 40–50 bpm. In infranodal
block the pacemaker will be further down the conduction system with a lower rate of 15–
30 bpm which can result in significant hypotension, dizziness, and syncope. Complete
heart block usually occurs due to myocardial infarction, cardiac surgery, or ventricular
septal defects.
– Right or left bundle branch block (RBBB, LBBB): Impulse is conducted through the intact
bundle into the normal side and then through the ventricular myocardium to the blocked
side. Ventricular rate is normal but there is a wide QRS complex on the ECG.
PERIOPERATIVE RELEVANCE
• Sinus bradycardia: Intraoperative medical management should be administered when
associated with hemodynamic changes; treatment may include anticholinergic agents
(atropine, glycopyrrolate), beta-agonists (isoproterenol), and volume resuscitation. If
medical management fails, the use of temporary pacing devices should be considered, such
as cutaneous pacing pads, esophageal pacing leads, intravenous pacing wires and pacing
pulmonary artery catheters (PAC, or epicardial pacing placed prior to closure of the chest in
cardiac surgery).
• LBBB: Avoid placement of a PAC due to the risk of complete heart block. Detection of a new
onset LBBB in the perioperative period is suggestive of an ischemic event.
• Atrial contraction (P wave on ECG) is responsible for 20% of LV filling during diastole. This
percentage increases in patients with mitral stenosis (30%) and aortic stenosis (40%), so
maintaining sinus rhythm in these patients is of utmost importance. If a-fib or atrial flutter
occurs, medical or electrical cardioversion should be attempted. If attempts for
cardioversion are unsuccessful, ventricular response rate should be controlled to allow for
adequate ventricular filling.
• Atrial tachycardias in the perioperative period should be managed based upon the
appropriate ACLS protocols.
• Serum BNP level is an indicator of heart failure. Normal serum BNP levels are <100 pg/dL.
Levels >100 pg/dL suggest heart failure. Its sensitivity, specificity, and positive predictive
value are higher than cardiomegaly on CXR or rales on physical exam in diagnosing heart
failure. It also serves as an objective means to assess treatment.
GRAPHS/FIGURES

• SVC: Superior Vena Cava


• AAo: Ascending Aorta
• RAA: Right Atrial Appendage
• CT: Crista Terminalis
• ER/EV: Eustachian Valve/Eustachian Ridge
• CS/ThV: Coronary Sinus/Thebesian Valve
• SI: Septal Isthmus
• STV: Septal leaflet of Tricuspid Valve
• RV: Right Ventricle
• RCA: Right Coronary Artery
• OF: Oval Fossa (Fossa Ovalis)

REFERENCES
1. Rojas CA, El-Sherif A, Medina HM, et al. Embryology and Developmental defects of the
interatrial septum. Am J Roentgenol. 2010;195(5):1100–1104.
2. Linton NWF, Dubrey SW. Narrow complex tachycardias. Postgrad Med J. 2009;85:546–
551.

ADDITIONAL READING
• Costanzo LS. Physiology, 4th ed. Philadelphia, PA: Elsevier, 2010, chap. 4, 111–181.
• Ganong WF. Review of medical physiology, 20th ed. New York, NY: McGraw-Hill
Companies, 2001, chap. 24, 439–451.
• Ganong WF. Review of medical physiology, 20th ed. New York, NY: McGraw-Hill
Companies, 2001, chap. 28, 528–544.
• Moore KL, Dalley AF, Agur AMR. Clinically oriented anatomy, 6th ed. Philadelphia, PA:
Lippincott Williams & Wilkins, 2010, chap. 1, 135–160.
See Also (Topic, Algorithm, Electronic Media Element)
• Atrial fibrillation
• AV conduction blocks
• Vagal response
• Tachycardia
• Bradycardia

CLINICAL PEARLS
The atria of the heart function as priming pumps, house the sinoatrial node, and are involved
in several congenital and rhythm disturbances.
ATRIAL FIBRILLATION
Andrea Vanucci, MD, DEAA
Ivan M. Kangrga, MD, PhD

BASICS
DESCRIPTION
• Atrial fibrillation (AF) is a supraventricular arrhythmia characterized by uncoordinated
atrial activation and consequent deterioration of mechanical function.
• AF is associated with a high risk of stroke as well as increased mortality and health
expenditures; as such, it is a major public health issue.
EPIDEMIOLOGY
Incidence
• General population: ∼1% per year
– Age <40 years: ∼0.1% per year
– Age >80 years: ∼2% per year (1)[A]
• Postoperatively:
– Noncardiac surgery: Up to 8%
– Thoracic surgery: Up to 30%
– Cardiac surgery: Up to 46% (2)[A]
Prevalence
About 2.2 million patients in the US and 4.5 million in the European Union have either
persistent or paroxysmal AF (1)[A]
Morbidity
• Stroke, cerebral thromboembolic complications, myocardial ischemia, CHF, hypotension
• Ischemic stroke: 5% per year (2–7 times more frequently than those without AF)
Mortality
• Doubled compared to age-matched controls in NSR
• Related to the severity of underlying heart disease
• Congestive heart failure is a strong predictor of mortality
• Only a minority of patients die of thromboembolic complications
ETIOLOGY/RISK FACTORS
• Cardiovascular: HTN, CAD, CHF, valvular (mitral stenosis), and pericardial heart disease
• Non-cardiovascular: DM, hyperthyroidism, alcohol abuse, COPD, age
• Iatrogenic: Surgery, medications (beta-agonists, cold medications, antihistamines, local
anesthetics)
• Familial: Na+ and K+ channel mutations
• Perioperative: Atrial injury or ischemic inflammation, increased adrenergic tone, atrial
stretch from volume overload, and electrolyte disturbances
PATHOPHYSIOLOGY
• Re-entry is the main electrophysiologic mechanism of AF, and is secondary to structural or
electrical remodeling.
• Atrial dilation and inflammation can result in interstitial fibrosis and is the most common
substrate predisposing to AF.
• Channelopathies involving both K+ and Na+ channels are responsible for most familial
forms of AF.
• Triggers include alcohol, sleep deprivation, emotional stress, caffeine, and exercise.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Maintain rate control in patients presenting with AF; maintain NSR in patients with
recurrent or paroxysmal AF.
• Perioperative anticoagulation strategy should balance the risk of bleeding related to the type
of surgery and the individual patient’s risk of thrombosis (3)[B].
• Optimization of comorbidities
• Implement preventative strategies in surgical patients who are at a high risk for the
development of AF (e.g., thoracic and cardiac procedures).

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Palpitations, shortness of breath
• Neurologic symptoms
History
• Duration and type of AF (see “Classification”)
• Assess CHADS2 score
Signs/Physical Exam
• Irregularly irregular heart rate
• Signs of CHF, orthopnea, heart murmurs and gallop, rales and crackles
• Consider common comorbidities: COPD, hyperthyroidism, DM, valvular disease
TREATMENT HISTORY
• Length of treatment
• Antiarrhythmics: Class, efficacy, side effects
• Previous electrical cardioversion
• Electrophysiological ablation
• Percutaneous closure of the left atrial appendix
• Anticoagulation regimen; INR if on warfarin
MEDICATIONS
• For rhythm control, Class III antiarrhythmics (amiodarone, sotalol) are preferred due to
their decreased toxicity, however they should be used with caution in patients with LQT.
For rate control, beta-blockers, calcium channel blockers, and digitalis are commonly used.
• Amiodarone is effective for both rate control and pharmacological cardioversion (up to 90%
success if bolused followed by infusion). It is considered safe in patients with LV
dysfunction, unlike class IC drugs. Acute side effects: Hypotension, bradycardia.
• CHADS2 provides an objective score for estimating the risk of stroke in non-valvular AF.
Points for individual stroke risk factors are assigned as follows: 1 point is assigned for CHF,
HTN, age >75, or DM; and 2 points are assigned for a history of CVA/TIA. A CHADS2 score
of 0 denotes low risk, 1–2 intermediate risk, and 3–6 high risk of stroke (4)[A].
• Anticoagulation regimens are based upon the risk of stroke (CHADS2 or other scores) and
are balanced against the risk of bleeding.
– Aspirin if CHADS2 score ≤1
– Warfarin if CHADS2 score ≥2
– Dabigatran is a direct selective thrombin inhibitor. Stroke prevention is equal to that of
warfarin and fewer bleeding complications are seen with low doses. It is dosed twice per
day, orally. For a CHADS2 score = 1, the dose is 110 mg PO and for a CHADS2 score ≥2,
the dose is 150 mg PO (4)[A].
– The CHADS2 score has not been validated in valvular AF where there is a high risk of
stroke; thus, anticoagulation is always required.
• Statins
DIAGNOSTIC TESTS & INTERPRETATION
• Palpation or auscultation: Irregular heart rate
• EKG: Uneven R-R interval with occasional f waves
• CXR: Pulmonary vasculature congestion and cardiomegaly
• Echocardiogram and stress testing may be considered to rule out underlying structural or
ischemic myocardial disease, left atrial enlargement, thrombus, RV strain if PE is suspected.
• Holter monitor in suspected paroxysmal AF or if evaluating the efficacy of rate control
treatment
• Pacemaker may be in place.
Labs/Studies
• Serum or whole-blood (point-of-care) INR if on warfarin, or PTT/ACT if on heparin; there is
no valid point-of-care test for direct thrombin inhibitors.
• Electrolytes, including magnesium
• Digoxin levels
• Thyroid function tests if on amiodarone
• EP studies, if available
CONCOMITANT ORGAN DYSFUNCTION
Evaluate cardiopulmonary, neurologic, and endocrine systems for known associated
comorbidities
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Poor rate control
• Signs and symptoms of CHF
• New-onset AF of unknown etiology (rule out ischemic or structural heart disease)
• Delay DC cardioversion until therapeutic INR or TEE evidence of atrial thrombus
CLASSIFICATIONS
• Newly discovered AF is the first presentation of AF for which the actual onset is not known.
• Paroxysmal and persistent AFs are both recurrent, but the former is self-terminating within
7 days, while the latter requires cardioversion to restore sinus rhythm.
• Permanent AF describes unsuccessful or abandoned attempts to convert to sinus rhythm.
• Etiologically, AF can be valvular or non-valvular. Patients with mitral valve disease are at an
increased risk for stroke.

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Anxiolysis as needed
• Caution with possible triggering agents (glycopyrrolate, albuterol)
• Ideal resting heart rate is 60–80 bpm. Consider optimizing existing antiarrhythmic therapy.
• In cardiac surgery, corticosteroids should be considered; they have been shown to reduce
the incidence of AF postoperatively (5)[A].
• Statins, given 7 days preoperatively, reduce the incidence of postoperative AF in thoracic
and cardiac surgery, and should be considered (5)[A].
Special Concerns for Informed Consent
• Increased risk of thromboembolic or hemorrhagic (if on anticoagulant) complications
• Increased risk of ventricular arrhythmias, CHF
• Possible need for intraoperative DC cardioversion in recurrent AF
• Possible TEE to rule out atrial clots in a patient who is not anticoagulated
INTRAOPERATIVE CARE
Choice of Anesthesia
• Regional or neuraxial anesthesia may be contraindicated due to anticoagulants. If warfarin
has been held for surgery, PT/PTT/INR should be checked prior to placement. In patients
with thrombin inhibitors (Dabigatran) ASRA recommends against the use of neuraxial
anesthesia.
• For MAC cases, consider dexmedetomidine to maintain rate control.
Monitors
• Noninvasive BP measurement is adequate for most routine cases. Highly irregular pulses
may result in the NIBP cuff reading taking more time to cycle and may give unreliable
measurements.
• Arterial line is not necessary in stable hemodynamics and routine cases. However, a lower
threshold should exist for placing an arterial line when hemodynamic instability is
anticipated.
• Central venous catheters, pulmonary artery catheters, and TEE may be indicated based on
the type of surgery and comorbidities. TEE is a superior monitor of preload and
contractility, particularly in the absence of atrial contraction. TEE may be beneficial in
guiding fluid administration and vasopressor therapy in critical patients with AF.
• Esophageal Doppler and arterial pressure based cardiac output monitors do not work well in
AF.
Induction/Airway Management
• Avoid excessive sympathetic stimulation prior to airway management by ensuring adequate:
– Depth of anesthesia with induction agents, volatile agents, opioids, and lidocaine
– Oxygenation and ventilation
– Time for full onset of muscle relaxants when intubating
• Have rate control drugs ready and available
Maintenance
• MAC/sedation: Caution with, or avoidance of, epinephrine in local anesthesia
• General anesthesia may be provided with either a balanced inhalational or intravenous
technique.
• Rate control: Adequate depth of anesthesia, cautious use of positive chronotropes (e.g.,
ephedrine, albuterol, vagolytic agents, etc.)
• Rapid ventricular rate (RVR) with instability warrants immediate DC cardioversion.
• For RVR with hemodynamic stability, rate control may begin with diltiazem or beta-
blockers. Reserve amiodarone for patients with poor LV function. Caution: Amiodarone may
convert into NSR and “eject” a clot into the systemic circulation.
• New-onset AF: Pharmacological conversion if stable, DC cardioversion if unstable. Caution:
Successful DC cardioversion may still require anticoagulation due to atrial stunning.
Extubation/Emergence
• Avoid excessive sympathetic stimulation (see “Induction”)
• Slow titration of reversal agents
• Consider deep extubation, if appropriate, to avoid coughing and bucking

POSTOPERATIVE CARE
BED ACUITY
• Routine postoperative care is usually appropriate in stable patients.
• Telemetry or ICU care may be warranted in poorly controlled AF and hemodynamic
instability.
MEDICATIONS/LAB STUDIES/ CONSULTS
• Reinstitute rate control, antiarrhythmic, and/or anticoagulants as soon as appropriate
• Labs: Electrolytes, glucose in DM, INR/PTT
• Troponins if underlying cause for AF is CAD
COMPLICATIONS
• RVR with hypotension, CHF
• Ventricular arrhythmias
• Myocardial ischemia
• Bleeding versus stroke and other thrombotic complications
• Postoperative cognitive dysfunction

REFERENCES
1. Fuster V, Ryden L, Cannom D, et al. 2011 ACCF/AHA/HRS Focused Updates Incorporated
Into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial
Fibrillation: A Report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines. Circulation. 2011;123(10): e269–e367.
2. Mayson SE, Greenspon AJ, Adams S, et al. The change in face of postoperative atrial
fibrillation prevention. Cardiol Rev. 2007;15:231–241.
3. Mannucci C, Douketis JD. The management of patients who require temporary reversal of
vitamin K antagonists for surgery: A practical guide for clinicians. Intern Emerg Med.
2006;1:96–104.
4. Medi C, Hankey G, Freedman S. Stroke risk and antithrombotic strategies in atrial
fibrillation. Stroke. 2010;41:2705–2713.
5. Jongnaranggsin K, Hakan O. Postoperative atrial fibrillation. Med Clin N Am. 2008;92:87–
99.

ADDITIONAL READING
• Horlocker T, Wedel D, Rowlingson J, et al. Regional anesthesia in the patient receiving
antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and Pain
Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med. 2010;35:64–
101.
• Kaatz S, Douketis JD, Zhou H, et al. Risk of stroke in patients with and without chronic
atrial fibrillation. J Thromb Haemost. 2010;8:884–890.
• Lip GH, Huang-Fat T. Management of atrial fibrillation. Lancet. 2007;370:604–618.
See Also (Topic, Algorithm, Electronic Media Element)
• Atrial flutter
• Cerebrovascular disease
• Postoperative stroke
• Perioperative statins

CODES

ICD9
427.31 Atrial fibrillation
ICD10
• I48.0 Paroxysmal atrial fibrillation
• I48.2 Chronic atrial fibrillation
• I48.91 Unspecified atrial fibrillation

CLINICAL PEARLS
• Assess for the underlying structural, valvular, or coronary artery ischemic disease.
• Perioperative anticoagulation and rate control management should be addressed in
consultation with the surgeon, anaesthetist, and cardiologist.
• Risk of stroke is higher in valvular AF.
• Atrial thrombi may be seen in 14% of patients in whom AF lasted >2 days.
• Statins may be protective: Risk of postoperative AF is inversely related to the duration of
preoperative statin prophylaxis. Additionally, statins improve outcomes in the surgical
ablation of AF.
ATRIAL FLUTTER
Mirsad Dupanovic, MD
Svjetlana Tisma-Dupanovic, MD

BASICS
DESCRIPTION
• Atrial flutter (AFL) is a paroxysmal, regular, macro re-entrant arrhythmia most often
occurring in patients with structural heart disease. The re-entrant circuit is classically
confined to the right atrium with typical rates from 240 to 320 beats per minute (bpm).
• Ventricular rate is determined by AV node conduction; thus a 2:1 AV block results in a
ventricular rate of 120–160 bpm. Rapid AV node conduction is responsible for
hemodynamic deterioration and AFL-related fatalities.
• AFL is usually short-lived and closely related to atrial fibrillation (AF). If present for a
prolonged period, AFL usually evolves to AF.
EPIDEMIOLOGY
Incidence
• Incidence of ∼1% in the general population
• Incidence >5% in patients >80 years old
Prevalence
Uncertain since AFL is rarely a chronic condition
Morbidity/Mortality
• Based on the integrity of the myocardial conduction system, ventricular function, age at
presentation, duration of arrhythmia, and presence of other coexisting diseases.
• Associated with a 1.7-fold increase in mortality over a mean period of 3.6 years. The risk is
higher if AFL coexists with AF.
ETIOLOGY/RISK FACTORS
• Male gender: AFL ∼5-fold more common in men.
• Cardiac procedures:
– Pericarditis following cardiac surgery can lead to atrial inflammation and AFL.
– Myocardial scar formation following atrial ablation procedures can instigate AFL.
• Cardiovascular diseases:
– Structural heart disease leading to right atrial enlargement (valvular heart disease,
pulmonary embolism, or cardiomyopathy).
– Slowing of cardiac conduction (fibrosis or antiarrhythmic agents).
• Other disease: Chronic obstructive pulmonary disease (COPD), thyrotoxicosis, and chronic
alcoholism.
• Iatrogenic: Digitalis toxicity.
PATHOPHYSIOLOGY
• AFL describes a class of re-entrant arrhythmias localized to the atria.
– Typical AFL (isthmus-dependent, Type I): Right atrial re-entrant circuit that travels around
the tricuspid valve either counterclockwise or clockwise.
The flutter wave circuit is bounded by the caval veins, crista terminalis, and the
Eustachian ridge (the “isthmus” of slow conduction).
The direction of the re-entry circuit determines polarity of typical “sawtooth” flutter
waves (Ta). The Ta waves, which reflect atrial repolarization, are positive in the inferior
leads with counterclockwise re-entry. Clockwise re-entry results in negative Ta deflection
in the inferior leads. If discernable, P’ waves (atrial depolarization) have reverse polarity
in the same leads.
Cycle length of 200–400 ms depends on atrial size and the presence of antiarrhythmic
drugs.
– Atypical AFL (non-isthmus dependent, Type II): Right or left atrial re-entrant circuits that
travel around a region of atrial scarring.
Atrial scar secondary to myocardial disease, surgical procedure, or extensive
radiofrequency atrial ablation.
Difficult to treat: Ablation, cardioversion, and pharmacologic interventions are often
unsuccessful.
• AV conduction ratio (1:1, 2:1, 4:1, 6:1) influences the physiologic consequences of AFL.
– 1:1 AV node conduction results in a rapid ventricular rate and hemodynamic compromise.
Occurs in the setting of accessory pathways or exogenous catecholamines.
Rapid ventricular rate may lead to myocardial ischemia, malignant ventricular
arrhythmias, and death.
– 2:1 AV node conduction results in a fixed and regular ventricular rate.
– Variable AV block produces an irregular ventricular rhythm.
Occurs with nodal disease, increased vagal tone, and in the presence of nodal blocking
agents.
• AFL and AF have similar pathophysiology and coexist in many patients.
– ∼50% of patients with AFL will develop AF over a 5-year period.
– The arrhythmia-related “remodeling” caused by one arrhythmia AFL leads to progression
of the other AF. “Remodeling” is characterized by structural (increased atrial size),
electrical (shortening of atrial refractory period), and ultrastructural (promoting atrial
fibrosis) changes.
Pediatric Considerations
• AFL with atrial rates of 400–600 bpm and 2:1 conduction is common in neonates.
Termination of the arrhythmia can be accomplished with transesophageal pacing or external
synchronized cardioversion.
• Mustard, Senning, or Fontan cardiac procedures dramatically increase the risk for
development of AFL.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• The underlying medical condition or inciting event should be optimized.
• Control the ventricular rate to enhance ventricular filling and sufficient stroke volume.
– Calcium channel blockers or beta-blockers can be used to increase AV conduction block
and slow ventricular rate.
– Carotid sinus massage may increase the AV conduction ratio and temporarily slow the
ventricular rate.
• Conversion to sinus rhythm via synchronized cardioversion:
– Monophasic shocks in the following sequence: 100 J, 200 J, 300 J, 360 J.
– If AFL duration is >48 hours, confirmation via transesophageal electrocardiography (TEE)
to confirm the absence of atrial thrombus and/or anticoagulation must precede
cardioversion.
• Anticoagulation is typically via heparin or warfarin.
– Patients with AFL are at similar risk of stroke as patients with AF and should be
anticoagulated if AFL lasts >48 hours.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• The hemodynamic consequences of AFL depend on the flutter rate, AV conduction ratio,
ventricular rate, and presence of ventricular dysfunction.
• Symptoms depend on the ventricular rate.
– Increased ventricular rates (1:1 or 2:1 AV conduction) are often perceived as palpitations,
chest discomfort, or dizziness.
– Decreased ventricular rates (8:1 AV conduction) may manifest as fatigue and exercise
intolerance.
History
• Evaluation of risk factors: Open heart surgery, cardiac valvular disease, myocardial
ischemia, pulmonary embolism, COPD, hyperthyroidism, and/or digitalis toxicity.
• History of AFL: Duration, current management, and previous treatment.
• Presence of coexisting diseases: Pharmacologic management depends on myocardial
function.
Signs/Physical Exam
• Tachycardia with regular, usually fixed, ventricular rate of 140–160 bpm. Irregularly
irregular pulse is rare, but may occur if AV conduction ratio is variable.
• Rapid, rippling flutter waves may be seen in the jugular venous pulse with an AV
conduction ratio of 4:1 but not with 2:1 ratio.
• Cardiac decompensation leads to dyspnea, hypoxemia, rales, and crackles.
• Previous radiofrequency ablation
– AFL ablation has a >90% long-term success rate. Best results are seen with isthmus-
dependent AFL, normal right atrial size, and no history of AF.
MEDICATIONS
• Rate control: Amiodarone, diltiazem, verapamil, or beta-adrenergic blockers slow down AV
conduction and control the ventricular rate.
– Amiodarone, diltiazem, and digoxin are preferred in the presence of impaired myocardial
function.
– Beta-blockers are effective in the setting of increased sympathetic tone and thyrotoxicosis.
– Vagolytic effects of class I antiarrhythmic drugs administered for AFL may result in
reduction of atrial rate to 180-200 bpm, consequential 1:1 AV nodal conduction, and
resultant increase of ventricular rate. Thus, AV blocking drugs should be administered
before the administration of class I antiarrhythmic drugs.
• Convert rhythm: Ibutilide, amiodarone, dofetilide, sotalol, flecainide, propafenone,
procainamide, and disopyramide have variable success (50–60%) in terminating AFL.
• Approximately 15% of patients treated with class IC antiarrhythmic agents or amiodarone
for AF will develop AFL. This led to the development of a “hybrid" management strategy of
antiarrhythmic drugs to treat AF with subsequent ablation to treat AFL.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Labs: Electrolytes, cardiac enzymes, digoxin level, and thyroid function tests.
• ECG: Atrial rate ranges from 240 to 340 bpm, “sawtooth” pattern in the inferior leads, and
regular ventricular response with a discernable and consistent relationship between flutter
waves and QRS complexes.
– Flutter waves can be obscured by the T waves. Infusion of adenosine or vagal maneuvers
will briefly stop or decrease AV conduction, allowing recognition of the flutter waves.
– In the setting of an accessory pathway, the ECG pattern is indistinguishable from
ventricular tachycardia, even with 2:1 conduction.
– Atrial rate of >340 bpm may be seen with atypical AFL.
• Echocardiogram: Evaluate atrial size and ventricular function
– TEE is used to evaluate for the presence of atrial thrombus prior to synchronized
cardioversion in patients with AFL lasting longer than 48 hours.
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Uncontrolled ventricular rate, myocardial ischemia, or cardiac decompensation.
• Synchronized cardioversion in hemodynamically unstable patients.

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Anxiolytics can decrease sympathetic output.
• Rate control: Calcium channel blockers or beta-adrenergic blockers can be titrated to effect.
Special Concerns for Informed Consent
• Increased risk of intraoperative rapid ventricular rate, myocardial ischemia, cardiac
decompensation, and thromboembolic events.
• Risks and benefits of delaying the surgery to evaluate and treat paroxysmal AFL must be
explained. Non-urgent surgery should be postponed until adequate control of the ventricular
rate has been achieved.
INTRAOPERATIVE CARE
Choice of Anesthesia
Insufficient evidence to suggest that either general or regional anesthesia is preferred for
patients with AFL.
Monitors
• Standard ASA monitors including ECG with ST segment analysis.
• Arterial catheter for close monitoring of blood pressure or frequent blood gas evaluation.
• Central venous catheter for infusion of vasopressors or transvenous pacing.
• Pulmonary artery catheter for evaluation of cardiac output or mixed venous oxygenation, if
indicated.
• Transesophageal echocardiography, if indicated.
Induction/Airway Management
• Risk of hemodynamic instability
– Vasodilation and myocardial depression from induction agents (propofol and thiopental).
– Sympathetic stimulation from laryngoscopy.
– Dexmedetomidine is associated with prolonged hypotension and increased AV nodal
blockade.
• Avoid pharmacologic agents associated with sympathetic activation (ketamine) or vagolytic
effects (pancuronium).
Maintenance
• Use of either volatile anesthetic or total intravenous anesthetic is acceptable.
• Conservative fluid management in the setting of reduced myocardial function.
• Intraoperative occurrence may be treated with rate control medications, vagal maneuvers,
or cardioversion if the patient is hemodynamically unstable.
Extubation/Emergence
• Avoid sympathetic stimulation.
• Ensure adequate analgesia.
• Balance reversal of neuromuscular block (excessive anticholinergics can provoke AFL);
consider slow titration to reduce incidence.

POSTOPERATIVE CARE
BED ACUITY
ICU with hemodynamically unstable or poorly controlled AFL
MEDICATIONS/LAB STUDIES/ CONSULTS
• Medications: Rate control agents and anticoagulation as indicated.
• Labs: Electrolytes, digoxin level, cardiac enzymes, and thyroid function tests.
COMPLICATIONS
• Systemic thromboembolism
• Coronary and/or cerebral ischemia secondary to hemodynamic insufficiency
• Tachycardia-induced cardiomyopathy
• Sinus bradycardia following administration of AV nodal blocking agents

REFERENCES
1. Lee KW, Yang Y, Scheinman MM. Atrial flutter: A review of its history, mechanism, clinical
features, and current therapy. Curr Probl Cardiol. 2005;30:121–168.
2. Nattel S, Singh BN. Evolution, mechanisms, and classification of antiarrhythmic drugs:
Focus on class III actions. Am J Cardiol. 1999;84:11R–19R.
3. Van Gelder IC, Hagens VE, Bosker HA, et al. Pharmacologic versus direct-current electrical
cardioversion of atrial flutter and fibrillation. Am J Cardiol. 1999;84:147R–151R.
See Also (Topic, Algorithm, Electronic Media Element)
• Atrial fibrillation
• Electrical cardioversion
• Wolff–Parkinson–White

CODES

ICD9
427.32 Atrial flutter

ICD10
• I48.3 Typical atrial flutter
• I48.4 Atypical atrial flutter
• I48.92 Unspecified atrial flutter

CLINICAL PEARLS
• Atrial flutter (AFL) commonly occurs in patients after open heart surgery and those with
underlying cardiac disease.
• ECG manifestations include flutter waves with variable AV conduction.
• Ventricular rate control is achieved with beta-blockers or calcium channel blockers.
• Hemodynamically unstable patients require immediate synchronized cardioversion.
ATRIAL SEPTAL DEFECT (ASD)
Jason Choi, MD
John G. T. Augoustides, MD, FASE, FAHA

BASICS
DESCRIPTION
• A defect of the interatrial septum that allows communication between the right and left
atria. It is the most common congenital heart defect in adults.
• 3 types:
– Ostium secundum (75% of all ASDs): Patent foramen ovale (PFO) is a subtype of ostium
secundum and is the most common ASD.
– Ostium primum (15%): Associated with mitral regurgitation from the cleft mitral valve
– Sinus venosus (10%): Associated with anomalous partial drainage of the pulmonary veins
into the right atrium or superior vena cava
• ASD is often benign and asymptomatic until the 4th or 5th decade of life. Virtually all adults
with an ASD become symptomatic by the 6th decade.
– Moderate or severe defects present in a child with congestive heart failure (CHF).
– First presentation of ASD in adults may be a stroke or transient ischemic attack (TIA).
– Diagnosis is common during pregnancy due to increased blood volume.
• Clinical sequelae of ASD correspond to the degree and direction of shunting.
– Most common is left-to-right cardiac shunt.
– Right-to-left shunt indicates a more severe disease.
– PFO is the main cause of transient right-to-left shunt and paradoxical emboli.
EPIDEMIOLOGY
Incidence
ASD is diagnosed in 1 out of 1,500 live births.
Prevalence
• ASDs account for 10% of all congenital heart diseases and 30% of adult congenital heart
diseases (1)[A].
• ASDs are 2–3 times more common in women.
• PFOs present in about 25% of adults (2)[A]. A majority of PFOs are undiagnosed.
Morbidity
• ASDs have low morbidity.
• Pulmonary hypertension is rarely seen before the 3rd decade of life (3)[B].
Mortality
• ASDs are associated with low mortality.
• Decreased life expectancy is seen with ASD, but patients can reach advanced age without
intervention. Mortality rate from ASD repair is close to zero if performed before the 4th
decade in patients without significant pulmonary hypertension (2)[B].
ETIOLOGY/RISK FACTORS
• Spontaneous genetic mutations lead to aberrant embryologic septal development (4)[B].
• Inheritance of ASD is not fully understood.
• Ostium primum is associated with Down syndrome.
• CHF symptoms in an infant with ASD indicate additional congenital heart defects (3)[C].
PATHOPHYSIOLOGY
• Size of defect, ventricular compliance, and direction of venous inflow determine the degree
and direction of interatrial shunting.
– Defects <5 mm are hemodynamically insignificant, while defects >20 mm cause
clinically significant shunting (1)[A].
• Left-to-right shunt is a result of greater right ventricle compliance and lower pulmonary
vascular resistance (PVR).
– Chronic left-to-right shunt increases pulmonary blood flow and can lead to pulmonary
vascular congestion and right ventricular strain.
– Severe pulmonary hypertension and right heart failure may develop. Pulmonary flow can
reach 4 times that of systemic flow in severe disease. Right-to-left shunt (Eisenmenger
syndrome) can develop over time secondary to increased pulmonary pressures. This
“shunt reversal” results in cyanosis as a significant fraction of blood bypasses the
pulmonary circulation and gets ejected into the systemic circulation, unoxygenated.
• Patients most commonly present with dyspnea, palpitations, and decreased exercise
tolerance. Atrial arrhythmias, especially atrial fibrillation, are commonly seen in the 4th
decade.
• PFO is unique as a dynamic shunt occurring under certain physiologic situations that
transiently elevate right atrial pressures (e.g., coughing, Valsalva maneuver, and increased
PVR).
– All other ASDs can have transient right-to-left shunting, but usually shunt left-to-right
continuously.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Decrease the risk of paradoxical emboli (e.g., avoid air entry in IV lines).
• To prevent worsening of left-to-right shunt, avoid increases in systemic vascular resistance
(SVR), fluid overload, steep Trendelenburg positioning, and over-transfusion.
• Be aware of scenarios that cause transient right-to-left shunting: Pulmonary embolism, high
positive end-expiratory pressure (PEEP), venous air embolism, pneumoperitoneum with
laparoscopy, and cardiac tamponade.
• Be prepared to treat pulmonary hypertension with direct pulmonary vasodilators.

PREOPERATIVE ASSESSMENT
SYMPTOMS
• ASD is an acyanotic defect (left-to-right shunt).
• Cyanosis and clubbing with only an ASD reflect right-to-left shunt and severe disease.
• Atrial fibrillation
• CHF symptoms: Orthopnea
History
• Clinical presentations of ASD vary.
• ASD is often undiagnosed until adulthood due to a lack of symptoms and physical findings.
• Rule out a history of stroke, TIA, new onset dyspnea on exertion, and palpitations from
atrial arrhythmias.
• Assess progression/worsening of symptoms.
• Ask about a history of murmur or previous assessment by a cardiologist.
Signs/Physical Exam
• Fixed-split S2 heart sound on auscultation is pathognomonic for ASD.
• Systolic ejection murmur is heard from increased output through the pulmonic valve.
• Ostium primum is associated with significant mitral regurgitation.
• S4 heart sound reflects right ventricular hypertrophy and pulmonary hypertension.
TREATMENT HISTORY
Closure of the defect with open heart surgery or cardiac catheterization. If the patient has not
had an ASD closure, they are most often asymptomatic.
MEDICATIONS
There is no specific medical therapy.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• ECG: Incomplete right bundle branch block (invariably present), atrial arrhythmia (e.g.,
atrial fibrillation), prolonged PR interval, right ventricular hypertrophy, or right axis
deviation
• CXR: Prominent pulmonary vasculature often noted from vascular congestion
• Echocardiography: Important to note the degree of shunting, size and strain of right
ventricle, and pulmonary artery pressures
– TEE with bubble study is the gold standard diagnostic study (4)[A].
• Cardiac catheterization: Pulmonary artery pressures should be recorded.
CONCOMITANT ORGAN DYSFUNCTION
Other organ dysfunction, such as pulmonary edema, pulmonary hypertension, or
complications of right heart failure, is only seen with moderate/severe disease from ASD.
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Presence of right-to-left shunt requires correction or medical optimization prior to elective
surgery (4)[B].
• Pulmonary blood flow >1.5 times the systemic flow warrants closure of the ASD (1)[A].
CLASSIFICATIONS
• Asymptomatic
• Symptomatic left-to-right shunt
• Right-to-left shunt with pulmonary hypertension

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• For most patients with ASD, there is no restriction on premedication.
• Premedication with midazolam can help with facilitating parental separation in the
pediatric population.
Special Concerns for Informed Consent
Risk of paradoxical emboli leading to stroke is minimal but present.
INTRAOPERATIVE CARE
Choice of Anesthesia
For the typical asymptomatic ASD patient, choice of anesthesia and technique can be tailored
to provider and/or patient preference.
Monitors
• Standard ASA monitoring
• Monitors should be tailored to extent of surgery and its risks.
• For open ASD repair on bypass, TEE, arterial line, and central line +/– pulmonary artery
catheter are recommended for intra-operative management.
Induction/Airway Management
• No special airway considerations
• Drug dilution occurs from increased pulmonary blood flow, but is unlikely to have clinical
relevance or to affect induction time.
• There is no indication for endocarditis prophylaxis (4)[B], unless concomitant valvular
disorder warrants it.
Maintenance
• Imperative to prevent air emboli
• Prevent increases to the left-to-right shunt
– Use techniques that decrease the SVR (promotes forward flow into the aorta) or increase
the PVR
– Avoid a high FiO2 and hyperventilation; they can cause pulmonary vasodilatation.
– Maintain higher mean airway pressures
– Avoid fluid overload and over-transfusion
Extubation/Emergence
Bucking and coughing upon emergence increases the risk of paradoxical emboli by causing
transient right-to-left shunting.

POSTOPERATIVE CARE
BED ACUITY
ICU postoperative care is not warranted unless the patient has significant pulmonary
hypertension or has had closure of the ASD.
MEDICATIONS/LAB STUDIES/ CONSULTS
If symptoms or complications of ASD manifest during the perioperative period, cardiology
should be consulted.
COMPLICATIONS
• Paradoxical embolism: Stroke, TIA, fat embolism
• Transient supraventricular dysrhythmias and atrioventricular conduction defects are
common post-closure of ASD.
• Post-ASD closure, interpretation of central venous pressure (CVP) must account for a
previously dilated right atrium. Maintaining normal CVP values may cause volume
overload.

REFERENCES
1. Rigatelli G, Ronco F. Patent foramen ovale: A comprehensive review for pulmonologist.
Curr Opin Pulm Med. 2010;16:442–447.
2. ensley FA, Martin DE, Gravlee GP. A practical approach to cardiac anesthesia, 3rd ed.
Philadelphia: Lippincott Williams and Wilkins, 2003.
3. Augoustides JG, Ochroch EA. Assessment of intracardiac shunts: Perioperative
echocardiography. Int Anesthesiol Clin. 2008;46:83–95.

ADDITIONAL READING
• Warnes CA, Williams RG, Bashore TM, et al. ACC/AHA 2008 guidelines for the management
of adults with congenital heart disease: Executive summary. A report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2008;118(23):2395–2451.
See Also (Topic, Algorithm, Electronic Media Element)
• Ventricular septal defect
• Cardiopulmonary bypass
• Patent foramen ovale
• Venous air embolism
• Chest x-ray

CODES
ICD9
• 745.5 Ostium secundum type atrial septal defect
• 745.8 Other bulbus cordis anomalies and anomalies of cardiac septal closure

ICD10
• Q21.1 Atrial septal defect
• Q21.2 Atrioventricular septal defect

CLINICAL PEARLS
• 25% of adults have patent foramen ovale (PFO) and most are undiagnosed.
• Avoid air entry in IV lines in ASD patients.
• A fixed-split S2 heart sound is pathognomonic for ASD.
• PFOs can transiently shunt right-to-left during the anesthetic course (high peak inspiratory
pressure [PIP], coughing, abdominal insufflation, Trendelenburg positioning, etc).
ATRIAL TACHYCARDIAS
Svjetlana Tisma-Dupanovic, MD
Mirsad Dupanovic, MD

BASICS
DESCRIPTION
• Atrial tachycardias (ATs) encompass several types of arrhythmias driven by one or more
ectopic sources outside the sinus node and do not require the participation of the AV node
for maintenance of tachycardia. ATs may be based on micro-reentrant, triggered, or
automatic mechanisms causing focal atrial tachycardia (FAT) or multifocal atrial
tachycardia (MAT) (1)[A].
• FAT may present as transient, recurrent, sustained, and incessant with usual rates of 130–
250 bpm. MAT may be persistent and easily misinterpreted as atrial fibrillation (2)[A].
EPIDEMIOLOGY
Prevalence
FAT accounts for 5–15% of patients undergoing electrophysiologic studies. The rates are
higher in children (1)[A].
Prevalence
• FAT: 0.34% in asymptomatic individuals and 0.46% in symptomatic patients (1)[A]
• MAT in the hospitalized population has been estimated to be 0.05–0.32% (2)[A].
Morbidity/Mortality
• Incessant AT may result in dilated cardiomyopathy, which may be reversible after the
tachycardia has been terminated.
• Patients being hospitalized with MAT are usually elderly and may have high mortality as a
consequence of underlying chronic obstructive pulmonary disease (COPD) (2)[A].
ETIOLOGY/RISK FACTORS
• FAT: Open heart surgery (especially for correction of CHD), younger age, and disturbances
of the autonomic nervous system
• MAT: COPD, congestive heart failure (CHF), hypoxemia, use of theophylline, electrolyte
abnormalities (hypomagnesemia, hypokalemia), and increased age (2)[A].
PHYSIOLOGY/PATHOPHYSIOLOGY
• FAT is characterized by atrial activation starting rhythmically at a small area (focus) from
which it spreads out centrifugally. Usual locations of such foci are the area along the crista
terminalis and near the right and left pulmonary veins. It may be caused by micro-reentrant,
triggered, or automatic mechanisms (3)[A].
– Micro-reentry may be initiated and terminated with programmed electrical stimulation.
Verapamil, adenosine, and dipyridamole can terminate this arrhythmia.
– Triggered activity may also be initiated and terminated with electrical stimulation (atrial
extrastimuli or rapid atrial pacing). Verapamil, propranolol, adenosine, carotid sinus
massage, and dipyridamole can terminate triggered FAT.
– Automatic FAT cannot be initiated or terminated with programmed electrical stimulation,
but it can be initiated by isoproterenol infusion and terminated with propranolol. The
rhythm is insensitive to adenosine, verapamil, and carotid sinus massage. Episodes of
automatic FAT commonly show a “warm-up” phenomenon at the beginning (the rate
gradually increases) and a “cool-down” phenomenon at termination (the rate gradually
slows down with transition to normal sinus rhythm). Since automaticity decreases with
aging, automatic FAT is less common in geriatric patients (1)[A].
• MAT (chaotic AT) may be initiated by delayed after-depolarizations arising from multiple
atrial foci. The definition of MAT requires at least 3 distinct P’ wave morphologies (2)[A].
Pediatric Considerations
FAT during infancy is typically incessant. Patients often present with tachycardia-induced
cardiomyopathy. MAT is an uncommon, well-tolerated, and self-limiting rhythm in most
pediatric patients.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Drugs that modulate the autonomic nervous system may be useful in the anesthetic regimen
of patients presenting with FAT.
• Treatment of the underlying medical diseases is the primary and the most successful therapy
for MAT. It is also important to avoid hypoxemia as well as medications or procedures that
could worsen the pulmonary status.
• Cardioversion has no effect on the sites of ectopy that produce automatic FAT and is not
effective in converting MAT to sinus rhythm (1)[A], (2)[A].

PREOPERATIVE ASSESSMENT
SYMPTOMS
• Symptoms of ATs may range from none to syncope to symptoms of heart failure.
• The severity of FAT presentation depends on the ventricular rate and presence of ventricular
dysfunction.
• The gradual increase in heart rate at the beginning and slowing at termination may make it
difficult for a patient to recognize the tachycardia.
• Some patients may perceive fast ventricular rates as palpitations, chest discomfort, or
dizziness. Exercise intolerance results from the inappropriately high ventricular rate that
does not change with increasing workload.
• Symptoms or signs of CHF are due to decreased left ventricular contractility, AV valve
regurgitation, and atrial dilatation.
History
• Review for presence of a cardiac or pulmonary disease, recent heart surgery, and the
arrhythmogenic effects of current medications.
• Review for previous episodes, management, and current duration of AT.
• FAT may resolve spontaneously. However, failure to perceive the FAT of incessant nature
can lead to depression of myocardial function and tachycardia-induced cardiomyopathy. If
the tachycardia is not treated aggressively, the myocardial function can continue to decline,
resulting in an irreversible cardiomyopathy. This occurs in 80% of cases due to FAT of
abnormal automaticity. Patients with faster rates may be at higher risk (1)[A].
• The MAT usually occurs in elderly and seriously ill patients. It may resolve within days
following successful management of the underlying disease. If management of the
underlying disease is not successful, onset of MAT implies a poor prognosis. MAT may be
preceded by or progress to atrial fibrillation or atrial flutter in 50% of cases. The choice of
pharmacologic agents may depend on the presence of coexisting medical diseases.
Signs/Physical Exam
• The pulse rate may not be reflective of the atrial rate because of variable AV node
conduction.
• The heart rates seen in FAT vary based on the patient’s age and catecholamine state. In case
of chronic FAT the rate tends to vary from hour to hour influenced by a variety of
physiologic factors modifying autonomic tone. Ventricular rate is usually regular.
• In MAT, the rhythm is irregular and the physical examination findings clinically resemble
atrial fibrillation.
• Dyspnea, hypoxemia, rales, and crackles are signs of cardiac decompensation.
TREATMENT HISTORY
• Review type, length, success of treatment, and recurrence of symptoms
• History of interventional management: Overdrive pacing and cardioversions are usually not
successful in automatic FAT and MAT.
• History of arrhythmia ablation: The treatment of choice for poorly controlled FAT and MAT
has become radiofrequency catheter ablation.
MEDICATIONS
• Termination of AT using adenosine makes it highly unlikely that automatic FAT is present.
• Primary acute treatment strategy of FAT is slowing or terminating the tachycardia. AV nodal
blocking is the secondary strategy. IV beta-adrenergic blockers may terminate automatic
FAT while nonautomatic FATs are frequently terminated by verapamil (1)[A].
• Class I antiarrhythmic medications may decrease automaticity, prolong refractory period,
and can terminate FAT.
• Class III drugs that slow myocardial conduction and AV conduction have had modest success
in treatment of ATs. These medications, except amiodarone, have the potential to decrease
myocardial performance and must be used with caution in patients with decreased LV
function.
• Digoxin slows AV conduction by enhancement of vagal activity and is a positive inotropic
agent.
• Calcium channel blockers (Class IV drugs) slow the AV conduction, but are negative
inotropes and should be used selectively and cautiously.
• The management strategies of MAT also rely on suppression of the tachycardia focus and/or
slowing of AV conduction. It may take a combination of drugs to control the rate.
• Metoprolol and high doses of IV magnesium can be useful in treating MAT.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Electrolytes, digoxin level
• The majority of FATs can be diagnosed from the ECG; however, differentiation from other
forms of supraventricular tachycardia (SVT) may be difficult.
– FAT presents on the ECG with P’ waves that generally show an abnormal axis and
configuration, but remain similar in shape. When the focus arises from the left atrium, the
P’ wave is negative in lead I; those with focus in the low right atrium show a negative P’
wave axis in the lead aVF with a positive wave in lead I. Occasionally, the focus is in an
area close to the sinus node or in the high right atrium and the P’ wave axis is similar to
sinus tachycardia. When the rhythm resembles sinus tachycardia, it can lead to a delay in
diagnosis and institution of therapy.
– The atrial rate during FAT is generally between 100 and 180 bpm. Each P’ wave is usually
followed by a QRS complex, and the PR interval is typically not prolonged. Thus the P’P’
intervals do not vary by more than 50 ms unless an exit block from the focus of FAT is
present.
– AV block may be present during FAT and is due to decreased sympathetic tone or digitalis
toxicity.
– Tachycardia-induced ST segment depression and T wave inversion may occur and may
persist for some time after the cessation of long-lasting FAT.
– During MAT there are ≥3 distinct P’ waves of varying morphology in the same ECG lead;
there is no dominant atrial pacemaker (difference from sinus rhythm with frequent
premature atrial complexes and focal AT); AV conduction may be variable; and there is an
isoelectric baseline with varying PP, PR, and RR intervals. Multiple P’ wave morphologies
and variable P-R and R-R intervals may contribute to confusion of MAT and atrial
fibrillation. The ventricular rate is usually 100–150 bpm but may be as high as 250 bpm.
• Ambulatory (Holter) monitoring is very helpful in establishing the FAT diagnosis.
• Exercise testing is frequently not useful because the sinus heart rate increases and the
automatic focus is suppressed.
CONCOMITANT ORGAN DYSFUNCTION
• COPD, pulmonary infection
• Congestive heart failure
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Uncontrolled ventricular rate, hemodynamic instability, signs of myocardial ischemia, or
cardiac decompensation
• Cardiac consultation may be necessary.
CLASSIFICATIONS
Varies; depends on pathophysiologic characteristics or clinical presentation
TREATMENT

PREOPERATIVE PREPARATION
Premedications
• A combination of benzodiazepines and opioids will decrease anxiety and modulate
sympathetic tone.
• Anticholinergic agents may worsen AT.
• Consider medications that decrease automaticity and AV conduction without decreasing
cardiac output.
Special Concerns for Informed Consent
Increased risk of cardiac complications
INTRAOPERATIVE CARE
Choice of Anesthesia
Depends on the surgical procedure. There is insufficient evidence to suggest that either
general or regional anesthesia is more beneficial for patients with ATs.
Monitors
• Standard ASA monitors including ECG with ST segment and T wave trends
• Arterial catheter for cases of expected blood pressure instability or need for frequent blood
gas evaluation (COPD)
• Central venous catheter is optional, but if utilized, intracardiac stimulation should be
minimized during catheter placement.
• Pulmonary artery catheter may be used in cases of cardiomyopathy.
Induction/Airway Management
• Increased risk of hemodynamic instability due to cardiac depression caused by intravenous
or inhalational anesthetics
• Consider administration of higher doses of benzodiazepines and opioids to decrease
sympathetic tone
• Dexmedetomidine, an alpha-2 agonist, may be useful in decreasing the sympathetic tone and
the heart rate, but the loading dose may cause significant hypotension.
• Ketamine and pancuronium are relatively contraindicated.
• Minimize the length of laryngoscopy or avoid laryngoscopy with the use of a laryngeal mask
airway or intravenous sedation.
Maintenance
• Neither propofol nor volatile agents have significant electrophysiologic effects and are
adequate maintenance agents.
• Conservative fluid management in case of cardiomyopathy
Extubation/Emergence
• Balanced reversal of neuromuscular block, with slow administration
• Avoid sympathetic stimulation
• Complications:
– Hemodynamic instability, coronary ischemia
– Tachycardia-induced cardiomyopathy

FOLLOW-UP

BED ACUITY
Poorly controlled AT will dictate ICU care.
MEDICATIONS/LAB STUDIES/CONSULTS
• Rate control as indicated
• Electrolytes, digoxin level, cardiac enzymes
COMPLICATIONS
• Hemodynamic instability, coronary ischemia
• Tachycardia-induced cardiomyopathy

REFERENCES
1. Roberts-Thomson KC, Kistler PM, Kalman JM. Atrial tachycardia: Mechanisms, diagnosis
and management. Curr Probl Cardiol. 2005;30:529–573.
2. McCord J, Borzak S. Multifocal atrial tachycardia. Chest. 1998;113:203–209.
3. Saoudi N, Cosio F, Waldo A, et al. A classification of atrial flutter and regular atrial
tachycardia according to electrophysiological mechanisms and anatomic bases. Eur Heart
J. 2001;22:1162–1182.

CODES

ICD9
427.89 Other specified cardiac dysrhythmias

ICD10
I47.1 Supraventricular tachycardia

CLINICAL PEARLS
• FAT usually occurs in young patients and may resolve spontaneously; however, failure to
perceive an incessant FAT (e.g., in small children) can lead to a cardiomyopathy that may
become irreversible if the tachycardia is not aggressively pharmacologically treated.
• MAT usually occurs in elderly and seriously ill patients. It may resolve within days following
successful management of the underlying disease. If management of the underlying disease
is not successful, onset of MAT implies a poor prognosis.
• Cardioversion has no effect on the sites of ectopy that produce automatic FAT and is not
effective in converting MAT to sinus rhythm. Radiofrequency catheter ablation may be
curative.
AUTOLOGOUS BLOOD TRANSFUSION
Andrew A. Klein, MD

BASICS
DESCRIPTION
• Transfusion of the patient’s own blood or blood components back to them has the
theoretical advantages of:
– No risk of transmission of infection
– No blood transfusion reaction
– No graft versus host disease
– No storage of blood required (except with preoperative autologous blood donation
[PABD])
• There are 4 types of autologous blood transfusion:
– Preoperative autologous blood donation
– Intraoperative hemodilution
– Cell salvage or saver
– Postoperative blood collection and re-transfusion
• Allogeneic transfusions are the “opposite” of autologous transfusions and involve giving a
patient blood collected from another person and has been stored in the blood bank.
• “You know what you’ve got inside you and therefore what you’re getting.”
PHYSIOLOGY PRINCIPLES
• Oxygen-carrying capacity: In a normal person breathing room air, arterial blood carries
approximately 20 mL O2/100 mL; 19.7 mL combined with hemoglobin (Hb) and only 0.3
mL dissolved in plasma. Hemoglobin molecules within red blood cells contain iron that can
bind reversibly to oxygen molecules to form oxyhemoglobin. Normal Hb is 13–16 g/dL in
men and 12–16 g/dL in women.
• Viscosity is the tendency of fluids to resist flow. Blood viscosity depends largely on
hematocrit (increasing exponentially as hematocrit increases), red cell characteristics, and
blood protein concentration. Increasing viscosity (from blood transfusion) leads to reduced
flow, especially in vessels <0.3 mm in diameter. This causes an increase in resistance with
a resultant increase in blood pressure (blood pressure is equal to cardiac output multiplied
by resistance: BP = CO × R).
• Transfusion, even of autologous blood, should be reserved for when it is needed, and local
protocols should be followed. The ACC/AHA Guidelines recommend that blood is given
when the Hb <6 g/dL; as this is described as lifesaving. They also state that transfusion in
most postoperative patients with a Hb <7 g/dL is reasonable and that in select patients
with critical end-organ ischemia, it may be necessary to transfuse at a Hb of 10 g/dL.
• Preoperative autologous blood donation (PABD): 1–2 units of blood are collected from the
patient 2–4 weeks before surgery.
– The goal is to remove red blood cells and plasma, process it, and store it until the day of
surgery. The blood is not separated into components and is re-administered as whole
blood. Thus, it contains some or all of the blood components needed by the patient.
– Preoperative donation allows the patient time to recover and begin red cell regeneration,
provided that iron stores are adequate. Thus, levels should be checked and iron
supplementation administered if necessary.
– Guidelines state that patients should be in good health to tolerate phlebotomy of around
450 mL and autologous blood collection should only be offered to those patients in whom
there is a reasonable expectation that blood will be required.
– Patients who would not normally require cross-matched blood (e.g., Group and Save only)
should not be considered, unless there is a specific clinical reason. Direct patient requests
should be discouraged after adequate explanation.
– Contraindications include anemia (Hb <11 g/dL), current infection, no definite surgical
date, severe cardiac, respiratory, or cerebrovascular disease, and pregnancy.
– Autologous blood should be stored in a refrigerator at a controlled temperature between 2
and 8°C, with alarms set at 3–7°C, and physically separated from homologous blood stocks
and cross-matched blood. This refrigerator should be equipped with a recorder and an
alarm similar to those on other fridges used for blood storage.
– The autologous label for each unit should include all necessary information for correct
identification of the patient and should have a suitable adhesive for refrigerated storage.
• Intraoperative hemodilution consists of blood collection immediately before surgery (usually
after induction of anesthesia), followed by IV fluid replacement to prevent hypovolemia.
Blood is then re-infused at the end of, or after, surgery. Blood is kept warm in the operating
theatre (can be stored for up to 8 hours in blood collection [containing citrate] bags without
refrigeration).
– Popular in cardiac surgery before or immediately after commencing cardiopulmonary
bypass
– Usually acceptable to Jehovah’s Witnesses if blood is kept in continuous contact with the
patient
– Less metabolic derangements due to the shorter storage time; hyperkalemia does not
develop in <24 hours but hemolysis can occur during blood removal if too small a line is
used.
– Hematocrit before blood removal should be >30%, and generally >36%. After blood
removal, hematocrit should be >24%.
• Cell salvage is the most common method of autologous blood transfusion. Blood lost during
or immediately after surgery is suctioned and collected into a designated reservoir. Heparin
is added to prevent clotting and is processed and transfused back to the patient.
– May commonly be utilized in cardiac, vascular, and orthopedic surgery
• Postoperative blood collection (most often after orthopedic surgery) and re-transfusion of
unprocessed blood back to the patient. It has been used in cardiac and orthopedic surgery,
as well as traumatic hemothorax. During total knee replacement, the surgery is most
commonly performed with a tourniquet in place, and this is then deflated at the end of the
procedure after a drain has been placed in the joint. This drain is then opened after 30–60
minutes, and the blood collects into a specifically designed collection reservoir (bellows)
using vacuum suction (as opposed to wall suction). The collected blood is filtered before
being immediately transfused back to the patient; this is performed on an hourly basis. This
system is low-cost, easy to perform, and with minimal side effects. Blood is
defibrinogenated and thus does not require anticoagulation prior to transfusion;
additionally, it is sterile.
• Autologous platelet-rich plasma is collected from the patient intraoperatively via apheresis
equipment. When used for cardiac surgery patients, it is removed prior to heparin
administration and the onset of cardiopulmonary bypass. It is returned after heparin
reversal. Studies have not shown improved benefit in regard to hemostasis and/or decreased
need for transfusion.
PHYSIOLOGY/PATHOPHYSIOLOGY
• PABD can have disadvantages, problems, and/or challenges including:
– Wastage of blood due to cancellation of surgery
– Inability to utilize the blood for another patient, in the event that it is not given to the
donor patient. A small number of autologous units are administered to other patients;
however, due to the donor’s comorbidities, autologous units are often unsuitable for
allogeneic donation.
– The need for storage
– Metabolic derangements still exist, such as hyperkalemia and loss of 2,3 DPG (related to
length of storage)
– Potential for administrative error
– Blood must still be warmed during infusion to prevent hypothermia.
– Donation may predispose to deterioration in medical condition (e.g., severe ischemic heart
disease).
– Contraindicated in patients with anemia
– Unacceptable to Jehovah’s Witnesses
– Not often practiced due to logistical reasons, particularly scheduling of surgery, collecting,
and storing blood (different locations)
– Does not guarantee that allogeneic blood will not be transfused
– Vasovagal reactions during collection from hypotension and bradycardia
– Increased cost compared to allogeneic blood units
• Intraoperative hemodilution can have disadvantages including:
– Hemodynamic instability: Removal of up to 500 mL of blood is possible; however, loss of
volume may cause hypotension unless fluid is replaced immediately.
– Precipitation of myocardial ischemia or worsening tissue oxygenation from acute anemia
– Need for wide-bore vascular access; central venous may be necessary if the arm IV is
insufficient or unreliable.
– Blood storage time is limited to a few hours. It should not be stored in the blood fridge,
but kept in the patient’s immediate vicinity and transfused within 8 hours.
• Cell salvage can have disadvantages including:
– Loss of plasma containing clotting factors and platelets leading to coagulopathy and
bleeding. This is only relevant after at least 50% of a patient’s blood volume has been
processed.
– Requires “enough” blood loss in order to prepare a unit
• Postoperative blood collection can have disadvantages including:
– Risks of fluid overload with rapid re-infusion
– Clotting of blood in re-transfusion bag if not administered to patient immediately after
filtration
• Direct re-infusion of shed mediastinal blood from postoperative chest tube drainage is not
recommended as a means of blood conservation and may cause harm (Level B evidence).
PERIOPERATIVE RELEVANCE
• Autologous transfusion can optimize or increase Hb while reducing the risk and amount of
allogeneic blood transfusion.
• Allogeneic blood is strongly associated with increased risk of death (1)[B] and
complications, including postoperative infection (2)[A], cancer recurrence, acute lung injury
(TRALI) (3)[B], and increased length of stay in the intensive care unit and hospital. Risk
correlates with the number of units of allogeneic blood transfused and length of time that
the blood is stored (4)[B]. These risks are NOT associated with autologous transfusion.
• Needs advance planning and preparation before surgery
• Discuss with the surgeon and patient

REFERENCES
1. Karkouti K, Wijeysundera DN, Yau TM, et al. The independent association of massive blood
loss with mortality in cardiac surgery. Transfusion. 2004;44:1453–1462.
2. Duffy G, Neal KR. Differences in post-operative infection rates between patients receiving
autologous and allogenic blood transfusion: A meta-analysis of published randomized and
nonrandomized studies. Transfusion Med. 1996;6:325–328.
3. Brander L, Reil A, Bux J, et al. Severe transfusion-related acute lung injury. Anesth Analg.
2005;101:499–501.
4. Koch CG, Li L, Sessler DI, et al. Duration of red-cell storage and complications after cardiac
surgery. N Engl J Med. 2008;358:1229–1239.
See Also (Topic, Algorithm, Electronic Media Element)
• Cell salvage
• Blood transfusions
• Transfusion-related infections
• Blood substitutes

CLINICAL PEARLS
• Autologous blood transfusion is commonly considered in coronary artery bypass, major
vascular surgery, primary and revision hip or total knee replacements, hepatic resections,
radical prostatectomies, and major spine surgery with instrumentation.
• Directed donation describes blood donated by a friend or family member for a designated
patient. This may be used when the patient’s health or baseline hemoglobin may not be
suitable for autologous donation. Drawbacks, however, are that it is not as safe as the
patient’s own blood and is handled as an autologous donation.
AUTONOMIC HYPERREFLEXIA
John F. Bebawy, MD
Antoun Koht, MD

BASICS
DESCRIPTION
• Autonomic hyperreflexia (AH) is a syndrome characterized by profound and imbalanced
reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) at or above
the T6 level.
– Inciting stimulus ranges from innocuous to noxious.
– Unchecked sympathetic discharge occurs below the level of injury in response to a
stimulus also below the level of injury.
– Compensatory hemodynamic responses occur above the level of injury.
– Also known as “autonomic dysreflexia”
• Patients with SCI commonly present to the operating room for urologic and other lower
extremity procedures (e.g., decubitus ulcers) that can elicit AH.
EPIDEMIOLOGY
Prevalence
• Associated with the incidence of SCI at or above the T6 level; in the US, there are 12,000
new cases of SCI annually.
• Pregnant women with SCI at or above the T6 level: 2/3rd can experience AH during labor.
Prevalence
• 48–90% of patients with SCI at or above the T6 level
• Males:females 4:1
Morbidity
Primarily due to uncontrolled hypertension leading to myocardial infarction, cerebral
hemorrhage, seizures
Mortality
Rare as a direct result of AH
ETIOLOGY/RISK FACTORS
Any stimulation below the level of SCI. Most commonly:
• Bladder distension
• Bowel distension
• Surgery
• Pressure sores
• Urinary tract infection (UTI)
• Cholelithiasis
• Sexual intercourse
PHYSIOLOGY/PATHOPHYSIOLOGY
• AH can be seen after the initial spinal shock phase of SCI, when autonomic reflexes return.
• Injury at or above the T6 level is above major splanchnic sympathetic outflow (T6 to L2).
• Sensory input below the level of injury is transmitted via peripheral nerves to the
spinothalamic tract and posterior columns of the spinal cord, and activates sympathetic
neurons.
• However, normal, descending inhibitory outflow is blocked at the level of injury; this leads
to unopposed and abnormal sympathetic discharge and elevated blood pressure (due to
unopposed vasoconstriction).
• Brainstem and carotid baroreceptor reflexes above the level of injury attempt to compensate
for the elevation in blood pressure (below the level of injury) by increasing parasympathetic
discharge to the heart via the vagus nerve; this leads to bradycardia and compensatory
vasodilation above the level of injury.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Despite the possible loss of sensation, anesthesia for procedures below the level of SCI is
advisable to prevent AH.
– General anesthesia and spinal anesthesia are preferred methods.
– Epidural anesthesia may also be beneficial, but to a lesser extent due to reduced block
density and sacral nerve sparing.
• Be prepared to treat manifestations of AH (e.g., with short-acting and direct-acting
antihypertensives).

PREOPERATIVE ASSESSMENT
SYMPTOMS
Headache, blurred vision, nasal congestion, chest pain, anxiety
History
• Ascertain the level, age, completeness, and stability of the SCI.
• In cervical injury, assess if spinal fixation has been performed.
• Frequency and inciting events for AH (e.g., urinary catheterization, bowel distension, etc.)
Signs/Physical Exam
• Asymptomatic in between episodes of AH
• During an episode of AH:
– Below the level of SCI: Elevated blood pressure, cool to touch, piloerection
– Above the level of SCI: Flushing and sweating, bradycardia, cardiac arrhythmias (atrial
fibrillation, premature ventricular contractions, AV conduction abnormalities)
TREATMENT HISTORY
• Prophylactic efforts include the removal of inciting stimulus:
– Bladder catheterization, fecal disimpaction, etc.
• Sitting patient up from the supine position, legs down
MEDICATIONS
No specific routine medications
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
Depend upon the surgical procedure and other patient comorbid conditions
CONCOMITANT ORGAN DYSFUNCTION
• Decubitus ulcers
• Contractures and deconditioning
• Frequent UTIs
• Pulmonary impairment
CIRCUMSTANCES TO DELAY/ CONDITIONS
• Acute episodes of AH should trigger a search for, and removal of, inciting stimulus, and/or
postponement of nonemergent surgical interventions.
• Emergent surgical intervention during an AH episode should be performed under spinal or
general anesthesia.
CLASSIFICATIONS
None

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Anxiolytics as appropriate
• Vasodilators if acutely hypertensive
Special Concerns for Informed Consent
• Cases planned to involve sedation should include the caveat that a spinal or general
anesthetic may be used to treat an acute AH episode.
• Morbidity of an acute AH episode should be reviewed, especially for lower body surgery.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Spinal anesthesia may be preferred since it blocks descending spinal cord reflexes directly
(1)[C].
• General anesthesia, at adequate levels, can inhibit reflex spinal sympathetic discharge.
• Epidural anesthesia may be used but could be less effective in severe AH cases.
Monitors
• Standard ASA monitors
• Consider an arterial line if the patient is at high risk (e.g., lower body surgery, prolonged
surgery) for, or has had a confirmed AH episode.
Induction/Airway Management
• Awake fiberoptic intubation or other alternative airway devices may be preferred in patients
with previous cervical fusion and limited neck mobility, or in those patients with an
unstable cervical spine.
• Induction drugs should not aggravate pre-existing hypertension, nor should they cause
excessive hypotension, since vascular tone below the level of SCI is lower at baseline (but
higher during an acute AH episode).
• Avoid succinylcholine; a proliferation of extrajunctional receptors due to disuse can result in
massive amounts of potassium extravasating from the muscle with the use of a depolarizing
muscle relaxant.
Maintenance
• General anesthesia should be maintained at adequate levels to inhibit reflex sympathetic
discharge.
• Epidural catheters should be appropriately redosed with local anesthetics or have an
infusion started in order to maintain adequate block density.
• An AH episode should be immediately treated with:
– Direct-acting vasodilators: Calcium channel blockers, nitrates, hydralazine
– Beta-blockers are second-line because of their potential to cause unopposed alpha-related
vasoconstriction.
– Central-acting vasodilators (e.g., clonidine) may be less effective.
Extubation/Emergence
• Short-acting antihypertensives should be immediately available to treat emergence-related
hypertension.
• Extubation of patients with cervical fusion should be performed when the patient is
oxygenating and ventilating independently and following commands.

FOLLOW-UP
BED ACUITY
Following an episode of AH, monitor blood pressure and heart rate in a monitored setting for
at least 2 hours.
MEDICATIONS/LAB STUDIES/ CONSULTS
• If the patient had an intraoperative episode of AH, antihypertensives should be continued,
as appropriate
• If myocardial ischemia is suspected:
– Electrocardiogram
– Troponin levels
– Opioids, nitrates, oxygen, vasopressors, as needed
– Cardiology consultation
COMPLICATIONS
Profound sympathetic discharge can result in (2):
• Cardiac ischemia
• Cerebral edema
• Cerebral hemorrhage
• Renal failure
• Ophthalmic/retinal disease
• Pulmonary edema

REFERENCES
1. Khastgir J, Drake MJ, Abrams P. Recognition and effective management of autonomic
dysreflexia in spinal cord injuries. Expert Opin Pharmacother. 2007;8(7):945–956.
2. Kirshblum SC, Priebe MM, Ho CH, et al. Spinal cord injury medicine: Rehabilitation phase
after acute spinal cord injury. Arch Phys Med Rehabil. 2007;88(3 Suppl 1):S62–S70.

ADDITIONAL READING
• Mallory B.Autonomic dysfunction in spinal cord disease. In: Lin VW, Cardenas DD, Cutter
NC, et al., eds. Spinal cord medicine: Principles and practice, 1st ed. New York: Demos,
2003.
See Also (Topic, Algorithm, Electronic Media Element)
• Spinal shock
• Autonomic nervous system

CODES

ICD9
337.3 Autonomic dysreflexia

ICD10
G90.4 Autonomic dysreflexia

CLINICAL PEARLS
• Autonomic hyperreflexia (AH) is a syndrome characterized by profound and imbalanced
reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) at or above
the T6 level.
• An AH episode is characterized by any of the following: Headache, blurred vision, nasal
congestion, chest pain, anxiety, elevated blood pressure, bradycardia, flushing and sweating
above level of SCI, piloerection, or cardiac arrhythmias.
• Treatment of an AH episode involves the administration of antihypertensives, removal of the
inciting stimulus (bladder catheterization, fecal disimpaction, etc.), sitting the patient up
from the supine position, placing the legs down, and loosening of any tight clothing.
• For all lower body surgeries, even in the absence of sensation, the provision of an anesthetic
should be considered.
AUTONOMIC NERVOUS SYSTEM
Anthony H. Guarino, MD

BASICS
DESCRIPTION
• The autonomic nervous system (ANS) regulates individual organ function and homeostasis
and, unlike the somatic nervous system, is not under voluntary control. It comprises the:
– Sympathetic system
– Parasympathetic system
– Enteric nervous system: Not frequently discussed; a meshwork of nerve fibers that
innervate the GI tract, pancreas, and gallbladder.
• The sympathetic nervous system can be therapeutically blocked via neuraxial techniques
(spinal and epidural), localized paravertebral ganglia blocks, and regional IV sympatholytic
injections.
PHYSIOLOGY PRINCIPLES
• Sympathetic nervous system (SNS): The SNS is continuously maintaining homeostasis in the
body. When stress is encountered there is increased activity resulting in the increased
release of catecholamines (“fight or flight”).
– Preganglionic neurons originate in the thoracic and lumbar spinal cord. Their axons
project to a paravertebral sympathetic trunk (or chain) that extends from C2 to the
coccyx. Most preganglionic neurons synapse with postganglionic neurons within the
trunk. Some preganglionic neurons travel to other ganglia outside of the sympathetic
chain and synapse there.
– Postganglionic neurons from the sympathetic trunk (as well as outside ganglia) travel to
the target organ.
– Neurotransmitters:
Preganglion and postganglion synapses: Acetylcholine
Postganglion and target organ: Norepinephrine. An exception is sweat glands that utilize
acetylcholine.
– Effects on organs:
Eyes: Dilates pupils
Heart: Tachycardia and increased force of contractions (increases systolic blood pressure)
Vasculature: Increases the tone (vasoconstriction) and hence diastolic blood pressure
Pulmonary: Dilates bronchioles
Gastrointestinal: Inhibits peristalsis
Renal: Increases renin secretion which retains sodium and water
Penis: Promotes ejaculation
• Parasympathetic nervous system (PNS): The PNS works complementary to the ANS in
maintaining homeostasis in the body. It is generally thought to guide vegetative functions
(“rest and digest”).
– Preganglion neurons originate in the medulla (cranial nerves III, VII, IX, and X) as well as
the cervical and sacral spinal cord. Their axons project to ganglia close to the target organ
where they synapse with postganglionic neurons; they have a longer course compared to
preganglionic sympathetic neurons. Of note, ∼75% of the parasympathetics travel with
the vagus nerve.
– Postganglionic neurons have a short distance that they travel to the target organ.
– Neurotransmitters:
Preganglion to postganglion synapses: Acetylcholine
Postganglion to target organ synapses: Acetylcholine
– Effects on organs:
Eyes: Constricts pupils
Heart: Decreases the heart rate
Vasculature: Decreases tone (vasodilation)
Pulmonary: Constricts bronchioles
Gastrointestinal: Promotes peristalsis
Penis: Promotes erections
• Adrenal medulla: Develops tandemly in utero with the SNS and acts as a modified
sympathetic ganglion. Synapses occur between preganglionic and postganglionic neurons
within it, but the postganglionic neurons do not leave the medulla; instead they directly
release norepinephrine and epinephrine into the blood.
DISEASE/PATHOPHYSIOLOGY
• Complex regional pain syndrome I and II is a chronic neuropathic pain disorder. Although
the exact pathophysiology remains unknown, manifestations are secondary to ANS
dysfunction. CRPS I and II are characterized by pain in a nondermatomal pattern. Signs and
symptoms of neuropathic pain include intense burning pain, hyperalgesia, allodynia, local
edema, sweating, skin color changes, and temperature disturbances in the affected
extremity.
• Peripheral vascular disease refers to arterial obstruction outside the heart. It can cause
ischemia and is believed to be associated with dysfunction of the ANS.
• Raynaud’s disease is an exaggerated and reversible vasospasm of digital arteries in response
to cold or stress. The etiology is believed to be secondary to ANS dysfunction.
PERIOPERATIVE RELEVANCE
• Propofol, at clinically relevant concentrations for sedation, does not alter central
sympathetic outflow at the spinal cord level. However, at deeper levels of sedation and
induction doses, it can depress central sympathetic activity and is likely to lead to
hypotension (decreases preload, afterload, and contractility).
• Ketamine causes direct, dose-dependent stimulation of the CNS that leads to increased SNS
outflow. Consequently, cardiovascular effects resemble SNS stimulation: Increases in
systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and
myocardial oxygen requirements. Systemic vascular resistance and LV end diastolic pressure
are normally unchanged. In the critically ill, it has a negative inotropic effect.
• Etomidate maintains hemodynamic stability through preservation of both sympathetic
outflow and autonomic reflexes.
• Opioids generally have a dose-dependent sympatholytic effect.
• Benzodiazepines can influence autonomic neurocardiac regulation, probably through their
interaction with the gamma-aminobutyric acid A-receptor (GABAA) chloride ion channel
complex. They act in a biphasic manner: Initially causing a reduction in central vagal tone
followed by decreasing the cardiac pacemaker directly. Induction doses can reduce blood
pressure but not to the same degree as propofol.
• Anticholinesterases enhance PNS activity and will cause bradycardia, hypotension,
hypersecretion, bronchoconstriction, GI tract hypermotility, and decrease intraocular
pressure.
• Anticholinergics inhibit parasympathetic nerve impulses by selectively blocking
acetylcholine receptor binding at nerve junctions.
• Inhaled volatile anesthetics generally suppress the ANS components in a dose-dependent
manner.
• Neuraxial blocks: Local anesthetics injected into the epidural or intrathecal space produce a
differential blockade. Nerve fibers have different sensitivities due to their location in the
spinal cord, diameter, and the presence or absence of myelin. Sympathetic nerve fibers are
blocked first, and are usually followed by pain, sensory, and motor nerves.
• Sympathetic blocks: Performed to interrupt nociceptive pathways as well as vasomotor,
sudomotor, and visceromotor nerves. Low concentrations of local anesthetics block small
myelinated A-delta and unmyelinated C fibers with a minimal effect on other parts of the
peripheral nerves. They may be performed as a diagnostic tool to determine if sympathetic
input is a contributor to the pain state. Thus, they help guide decisions on whether a more
permanent intervention would be helpful (e.g., neurolysis or surgery).
• Horner syndrome is seen with interscalene brachial plexus blocks, due to the nerve’s
proximity. Manifests as ptosis, miosis, enophthalmos, conjunctival injection, nasal
congestion, and facial anhidrosis.
GRAPHS/FIGURES
FIGURE 1. Sympathetic nervous system. Preganglionic neurons originate in the thoracic and lumbar spinal cord and
synpase with postganglionic neurons in the paravertebral sympathetic trunk.

FIGURE 2. Parasympathetic nervous system. Preganglionic neurons originate in the medulla and cervical and sacral spinal
cord and then synapse with postganglionic neurons near the target organ.

REFERENCES
1. Marx JL. New information about the development of the autonomic system. Science.
1979;206(4417):434–437.
2. Burnstock G. Autonomic innervation and transmission. Br Med Bull. 1979;35(3):255–262.
3. Burnstock G. Review lecture: Neurotransmitters and trophic factors in the autonomic
nervous system. J Physiol. 1981;313:1–35.
4. Burnstock G. The changing face of autonomic neurotransmission. Acta Physiol Scand.
1986;126(1):67–91.
5. Hirst GD, Choate JK, Cousins HM, et al. Transmission by post-ganglionic axons of the
autonomic nervous system: The importance of the specialized neuroeffector junction.
Neuroscience. 1996;73(1):7–23.

ADDITIONAL READING
• http://www.sciencedaily.com/articles/s/sympathetic_nervous_system.htm
• http://www.ehs.net/2231/pdf/autonomic.pdf
See Also (Topic, Algorithm, Electronic Media Element)
• Complex regional pain syndrome I
• Complex regional pain syndrome II
• Epidural
• Raynaud phenomenon
CLINICAL PEARLS
• Sympathetic blocks can aid an anesthetic as well as reduce pain during postoperative care.
• Autonomics affect every organ system in some manner or form.
AWAKE CRANIOTOMY
R. Alexander Schlichter, MD

BASICS
DESCRIPTION
General
• Evidence of trephinated skulls dates back to prehistoric times. The modern era of awake
craniotomies began with cocaine local anesthesia in 1886; sedation was added in the 1930s.
• Today, awake craniotomies are performed when patients have tumors or epileptic foci near
eloquent areas of the brain (Broca, Wernicke).
• Variations in anesthetic technique depend upon the patient as well as the surgeon’s
preference. During cognitive testing and tumor resection, the patient must be awake.
However, line and block placement, craniotomy, bone flap removal, as well as dural closure
can be performed with an adequate level of sedation versus general anesthesia (“asleep-
awake-asleep” technique).
Position
• In “asleep-awake-asleep” techniques, the patient is positioned after induction, whereas with
sedation the patient’s comfort is assessed before deeper levels are administered.
• Supine, with a bump under the left side so that the patient is facing the anesthesiologist.
• The patient’s left arm is folded over the patient and the right arm is abducted out. Pressure
points are padded.
• The patient is placed in a Mayfield frame. In sedated patients, the scalp block is first tested
and additional local anesthetic is added at pin sites.
• The patient is draped such that there is a window for the patient to communicate with the
anesthesiologist. This also allows emergent access to the airway.
• For the rare right-sided awake craniotomy, the above positioning is reversed.
Incision
Temporal incision: Temporalis flap, Burr hole, bone flap and then excision of the dura
Approximate Time
3–5 hours. The anesthesia and surgical preparatory time is longer than it is for a standard
craniotomy.
EBL Expected
300–500 mL. More bleeding can occur, so adequate venous access and blood products should
be available.
Hospital Stay
3–5 days for uncomplicated surgeries
Special Equipment for Surgery
• Mayfield frame
• Stealth/MRI
• Surgical microscope
• Special surgical drape for access to the patient
• Speech mapping electrodes and neuromonitoring personnel
• Ice cold saline in case of seizure
EPIDEMIOLOGY
Incidence
• The incidence of these lesions being removed under awake craniotomy is neurosurgeon- and
institution-driven, and therefore varies from center to center.
• Improvements in anesthetic techniques have resulted in an increased incidence of awake
craniotomies being performed.
Prevalence
• Dependent on type of lesion and location
• Most epileptic syndromes are treated medically. The prevalence of operable epilepsy is
institutionally dependent.
Morbidity
Low. Patient selection for awake craniotomies provides a healthier cohort. Tumors are also
usually smaller but in strategic brain tissue.
Mortality
Low
ANESTHETIC GOALS/GUIDING PRINCIPLES
• The choice of sedation and analgesic drugs may vary by institution; the ideal drug for the
procedure should be quick in onset, short in duration, and easy to titrate.
• The choice between deep sedation versus “asleep-awake-asleep” technique depends upon the
patient’s, as well as the surgeon’s preference. Sedation is possible because a scalp block is
capable of providing adequate anesthesia for scalp incision/craniotomy and the brain has no
intrinsic nociception. Oversedation can lead to obstruction, apnea, loss of airway, or
hypoventilation with resultant increases in CBF and/or ICP.
• Personal reassurance and communication are powerful tools in keeping patients calm.
Consider meeting the patient in a preoperative visit, the night before, or having a phone
discussion prior to the day of surgery.
• Seizure, stroke, and oversedation can occur quickly. Emergency airway drugs and
equipment must be readily available.

PREOPERATIVE ASSESSMENT
SYMPTOMS
Cognitive speech dysfunction, either expressive (Broca) or receptive (Wernicke)
History
• History of cognitive speech dysfunction, seizures.
• The tumor may be an incidental finding on brain imaging for an unrelated complaint.
• Mental capacity, claustrophobia, anxiety, drug and alcohol abuse, sleep apnea, acid reflux,
and BMI need to be assessed.
Signs/Physical Exam
• Full neurologic exam including speech
• Auscultation of heart and lungs
• Airway exam
MEDICATIONS
• Dexamethasone decreases vasogenic tumor edema.
• Anticonvulsants (phenytoin, levetiracetam)
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• CBC, Type and Screen
• Chemistry panel, coagulation panel
• Head CT, MRI, functional MRI (fMRI)
CONCOMITANT ORGAN DYSFUNCTION
Most patients are relatively healthy from a cardiovascular profile. Most complain of
headaches, seizures, or cognitive speech dysfunction.

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• A dexmedetomidine bolus should be followed by an infusion.
• When sedation is utilized, a small dose of midazolam may be considered prior to line and
Foley catheter placement. Low-dose remifentanil infusion may be started prior to the scalp
block.
• Antiemetic prophylaxis should be administered with non-sedating drugs such as 5-HT3A and
dexamethasone (also given to treat cerebral edema). Dexamethasone should be slowly
infused in awake patients as it can cause severe rectal itching and burning.
• Antiepileptic loading
• Anticholinergics should be avoided unless necessary. Patients may complain of dry mouth
during cognitive testing if used.
Special Concerns for Informed Consent
• The patient must be counseled that they will be awake during significant parts of the
surgery. Emphasize that open communication with the anesthesiologist is always possible.
• Risk of seizure and intubation is possible.
• Blood consents for possible transfusion are needed.
Antibiotics/Common Organisms
Gram-positive coverage for skin flora (cephalosporin, vancomycin for allergies)
INTRAOPERATIVE CARE
Choice of Anesthesia
• Sedation involves the administration of IV sedative and analgesic medications (most
commonly dexmedetomidine, remifentanil, and propofol). Propofol and remifentanil alone
can be used, but are associated with deeper sedation, hypercarbia, and airway problems.
Neuroleptic analgesia with droperidol and an opioid has been associated with dysphoria,
oversedation, and hypotension.
• “Asleep-awake-asleep" is often performed with a combination of dexmedetomidine,
remifentanil, and propofol at higher doses than sedation and then resumed after tumor
excision.
Monitors
• Standard ASA monitors
• Arterial line for beat-to-beat monitoring, labs
• 2 large-bore IVs (14–18) for rapid resuscitation and blood transfusion
• Central venous access is only necessary in patients with poor venous access. Awake
placement can be stressful for the patient.
• Foley catheter with urometer. In awake patients, especially in males, urethral lidocaine can
ease discomfort of placement and maintenance.
• Bispectral analysis can help guide the depth of anesthesia during GA or deep sedation.
• Neuromonitoring with speech mapping electrodes and appropriate personnel
Induction/Airway Management
• Scalp block: Usually done while the patient is lightly sedated (and before the patient is
induced for the “asleep-awake-asleep”) to monitor for local anesthetic toxicity. Often
performed with 0.5% bupivacaine or ropivacaine. The surgeon can infiltrate pin sites,
incision sites, and dura with 1% lidocaine.
• Sedation: Oxygen delivery via nasal cannula, facemask, or non-rebreather facemask
• “Asleep-awake-asleep": An LMA is often placed with either spontaneous ventilation or
controlled ventilation. Controlled ventilation is associated with lower CO2 levels.
Alternatively, a sphenopalatine block with bilateral placement of nasal trumpets can allow
spontaneous ventilation and a lighter depth of anesthesia than an LMA. The nasal trumpets
can be left in place, allowing the patient to phonate during testing. Obstruction is still
possible.
Maintenance
• Sedation: Dexmedetomidine 1 mcg/kg over 10 minutes followed by an infusion of 0.2–0.5
mcg/kg/hr. Remifentanil 0.01–0.05 mcg/kg/min. For sedation only, propofol should be
used sparingly if at all. Patients may find manipulation of the dura, in particular traction,
painful.
• “Asleep-awake-asleep": Dexmedetomidine 1 mcg/kg over 10 minutes followed by an
infusion of 0.2–0.5 mcg/kg/hr. Remifentanil 0.01–0.05 mcg/kg/min and propofol at 40–80
mcg/kg/min. Titrate to respiratory rate, and ETCO2. If using an LMA, control CO2 with
pressure support ventilation. Turn propofol off for emergence to “awake” portion.
• Brain relaxation: Mannitol and/or loop diuretic for diuresis. Diuresis can offset reductions in
brain relaxation that can result form higher CO2 tensions.
• Cognitive testing: The patient is awake, responsive, and able to participate in testing. If the
patient is under general anesthesia with an LMA or ETT, a smooth emergence should be the
goal to avoid coughing, laryngospasm, bucking, or delirium. Testing consists of a series of
neurologic tests: Counting, ABC’s, names, word association, pictures, and simple motor
commands. During these simple tests, the neurosurgeon electrically stimulates portions of
the brain to determine if it is safe to excise.
• Tumor excision: After testing, the patient remains conversant as the tumor is excised to
assure that eloquent tissue is not removed.
• Seizure precautions: Because the brain is being directly stimulated, the risk of seizure is
significant. Anticonvulsants should be loaded at the beginning of the case. Ice cold saline
should be available to the surgeon to flood the field. Emergency airway drugs and
equipment should be immediately available.
• After tumor removal, the patient can be placed under heavy sedation or GA until the end of
the procedure with appropriate airway protection in place.
Extubation/Emergence
• “Asleep-awake-asleep": Medications should be discontinued and the LMA removed when the
patient is breathing and following commands. Patients with nasal airways can have them
removed when they are awake.
• Neurologic exam should be performed to confirm that no changes in neurocognitive
function occurred during closure.

POSTOPERATIVE CARE
BED ACUITY
ICU: Quick discharge if the patient has no neurologic changes
ANALGESIA
• Pain is typically mild since the residual scalp block and dexmedetomidine can provide relief.
• Short-acting IV opioids and oral opioids
• Oral, rectal, and IV acetaminophen
COMPLICATIONS
• Cerebral edema can occur postoperatively. Any changes in neurologic exam need to be
examined and the patient should be sent to neuroimaging.
• Postoperative seizures (1–11% incidence) can be treated with appropriate anticonvulsants.
Continue the patient’s regular medication regimen.
• Postoperative nausea and vomiting should be treated with non-sedating antiemetics.
PROGNOSIS
Good: Residual seizure activity or regrowth of tumor may require additional surgery.

REFERENCES
1. Bonhomme V, Franssen C, Hans P, et al. Awake craniotomy. Eur J Anesthesiol.
2009;26(11):906–912.
2. Bulsara KR, Johnson J, Villavicencio AT, et al. Improvements in brain tumor surgery: The
modern history of awake craniotomies. Neurosurg Focus. 2005;18(4):e5.
3. Mack PF, Perrine K, Kobylarz E, et al. Dexmeditomidine and neurocognitive testing. J
Neurosurg Anesthesiol. 2004;16:20–25.
4. Sarang A, Dinsmore J. Anaesthesia for awake craniotomy—evolution of a technique that
facilitates awake neurological testing. BJA. 2003;90:161–165.
See Also (Topic, Algorithm, Electronic Media Element)
• Seizure disorder

CLINICAL PEARLS
• Patient refusal is a contraindication to an awake craniotomy. Patients with drug or alcohol
abuse, obesity, mental retardation, anxiety, claustrophobia, sleep apnea, and
gastroesophageal reflux should be scrutinized.
• Communication and reassurance are paramount in keeping the patient calm and
cooperative.
• Adequate scalp block and additional local anesthetic in the field can improve success.
• Alpha-2 agonists (dexmedetomidine) have been shown to improve sedation with less
respiratory depression.
• Seizure and loss of airway are a constant risk. Have airway drugs and equipment
immediately available.
AWARENESS UNDER ANESTHESIA
Dave Nisha Davendra, PharmD, DO
Stephen P. Winikoff, MD

BASICS
DESCRIPTION
• The term “awareness” during anesthesia implies that during a period of intended general
anesthesia, the brain is aroused by stimuli that are stored in memory for future explicit
recall.
• The term “awake paralysis” is also included as an anesthesia awareness claim and refers to
errors in the administration of neuromuscular blocking agents, resulting in paralysis of the
unanesthetized patient.
• Despite the infrequent occurrence, awareness is of significant concern to patients and is
associated with significant adverse psychological sequelae.
– Closed Claims Data identified 2 main causes of awareness:
– Light anesthesia (“not enough")
– Anesthetic delivery problems
EPIDEMIOLOGY
Prevalence
• Awareness during anesthesia may affect as many as 60,000 adults each year in the US.
• Explicit recall is estimated to occur in 0.13% of patients (2).
• Awareness with surgical procedures:
– Trauma surgeries: 11–43%
– Cardiac surgeries: 1.5%
– Obstetric emergencies: 0.4%
• Children have an increased incidence of 0.6–2.7%.
• Awareness accounts for 2% of all claims in the Closed Claims database.
Prevalence
The majority of patients in the Closed Claims database are female, ASA class I–II, <60 years
of age, and had elective surgery.
Morbidity
• Postoperative sequelae that may persist for varying durations (33–69%):
– Sleep disturbances including nightmares
– Prone to daytime anxiety and panic attacks, and in the worst case, post-traumatic stress
disorder (PTSD). 10–25% of patients who experience PTSD will not recover and will
require treatment.
– Avoidance of future medical care including any future anesthetic exposure
• Patients, who experience the inability to move or feelings such as helplessness, have a
significant increase in the persistence of late psychological sequelae such as PTSD.
ETIOLOGY/RISK FACTORS
• Light anesthesia increases the risk for awareness. However, in certain patient populations,
the administration of even small doses of anesthetic agents can result in deleterious
hemodynamic consequences.
– Limited cardiac reserve: Cardiac tamponade, coronary artery disease
– Hypovolemia: Sepsis, trauma
– Cesarean sections: Attempts to reduce uterine relaxation, fetal hazard, and hypotension
can result in the administration of low concentrations of volatile anesthetics and the
avoidance of benzodiazepines.
– Cardiopulmonary bypass: Low concentrations of volatile agents and high-dose opioids are
often administered to preserve hemodynamics. Because hypothermia while on pump can
“provide MAC,” volatile anesthetics may be discontinued.
• Anesthetic delivery problems.
– Malfunctioning machines will disrupt the administration of anesthesia. Vaporizer and
circuit leaks prevent administration of full doses of anesthetic agents to the patient.
– Drug administration errors increase the risk of awareness. Accidental administration of
muscle relaxant to an awake/conscious patient will cause awareness.
• Reliance of nitrous, opioids, or muscle relaxants for anesthesia increases the risk of
awareness. Volatile anesthetics are markedly more effective in producing amnesia. Use of
neuromuscular blocking agents will mask physical signs of light anesthesia.
• Premature discontinuation of anesthetics in attempts to awaken the patient more quickly
increases the risk of awareness at the end of the surgical case.
• Difficult intubations may entail repeated attempts to secure the airway, and supplemental
agents may not have been administered.
• Populations with increased anesthetic requirements may be underdosed when normal
concentrations of anesthetic agents are administered. They include:
– Pediatric patients
– Chronic alcohol abusers
– Opioid and cocaine abusers
– Polypharmacy: Cytochrome P450 induction will enhance drug metabolism.
• Patients on beta-blockers and calcium channel blockers can have their physiologic response
to inadequate anesthesia masked.
• Previous history of awareness under anesthesia can be an indication of increased risk for
future awareness.
PHYSIOLOGY/PATHOPHYSIOLOGY
• Interactions between analgesics and hypnotics are fundamental in the depth of anesthesia
and physiology of awareness.
– Hypnotic drugs are capable of producing CNS depression.
– The net effect of analgesics and hypnotics is to increase the depth of anesthesia and
decrease the probability of responsiveness.
– The use of systemic analgesics and local anesthetics attenuates surgical stimulation before
reaching the cortical level and causing awareness.
• Awareness is the postoperative recall of events occurring during general anesthesia. A
spectrum of cognitive activity, including awareness with, or without, explicit memory, and
unconscious awareness with implicit memory have been reported during the administration
of drugs that are intended to induce and maintain general anesthesia.
– Explicit memory is the conscious recollection of previous experiences.
– Implicit memory is changes in performance or behavior that are produced by previous
experiences but without any conscious recollection of those experiences.
• Perceptions of awareness are variable:
– Most common: Sounds, conversations, sensation of paralysis, anxiety, helplessness, pain,
and panic
– Least common: Visual perception, intubation, and feeling the operation without pain
• Physical and physiologic responses have been reported that may indicate perception of
painful stimulation whether conscious or unconscious.
– Purposeful movement indicates motor response to awareness and surgical stimuli.
– Rate and volume of ventilation in spontaneously breathing subjects, as well as heart rate
and blood pressure, will increase indicating a physiologic response to awareness.
PREVENTATIVE MEASURES
• The incidence of awareness has decreased substantially over recent decades with improved
appreciation of the complications and its morbidity as well as understanding of risk factors
and causes.
• Preoperative measures include patient and equipment assessment:
– Review patient medical records for previous occurrences of awareness or potential risk
factors.
– Interview the patient to assess the level of anxiety and previous experience with
anesthesia.
– Inform high-risk patient of the possibility of intraoperative awareness, consent, and
reassure the patient, as appropriate.
– Conduct a preoperative checklist-based anesthesia machine and equipment check to
ensure that the desired anesthetic drugs and dosages will be delivered. These procedures
should be extended to include proper functioning of intravenous access, infusion pumps,
and their connections.
• Intraoperative measures include the adequate use of medications and monitors.
– Amnestic agents should be strongly considered in anticipation or the possibility of a
patient in whom light anesthesia is required (benzodiazepines, scopolamine).
– Adequate doses of induction agents should be administered (also allow an adequate
amount of time for onset). In rapid-sequence intubations, consider more than just a “sleep
dose” of intravenous induction agents.
– Difficult intubation (anticipated or unexpected) can require supplemental doses of an
induction agent.
– Volatile agents should be maintained at least at 0.8–1.0 MAC; monitor the end-tidal
concentrations.
– Muscle relaxant use should be minimized if not necessary for the surgical procedure since
movement is the best indicator of light anesthesia.
– Nitrous oxide and opioid anesthesia should be supplemented with a potent volatile agent
to decrease the high incidence of awareness.
– Suspected inadequate anesthesia should be immediately addressed with deepening of the
anesthetic and a benzodiazepine.
– A bispectral index (BIS) is a processed electroencephalogram that provides a single
dimensionless number, which ranges from 0 (equivalent to EEG silence) to 100
(equivalent to fully awake and alert). Values of 65–85 have been advocated as a measure
of sedation, whereas values of 40–65 have been recommended for general anesthesia. The
FDA states that the use of BIS monitoring to guide anesthetic administration may be
associated with a reduction in the incidence of awareness with recall in adults during
general anesthesia and sedation. However, studies have shown that awareness can occur
at a BIS value <65, so the standard of care of this monitoring technique is equivocal.
– Modulate operating room behavior. Patients tend to remember auditory perceptions.

PREOPERATIVE ASSESSMENT
Conduct a postoperative interview with the modified Brice Questionnaire.
• What was the last thing you remembered before going to sleep?
• What was the last thing you remembered on waking?
• Do you remember anything between going to sleep and waking?
• While you were sleeping during the operation, did you dream?

TREATMENT

• A discussion with the patient should take place to obtain a detailed account of the patient’s
experience.
• An occurrence report regarding the event should be completed for the purpose of quality
management.
• Apologize to the patient, and offer counseling or psychological support to the patient.
• Notify the patient’s surgeon, nurse, and other key personnel about the incident and
interview.
• Patient should be informed of the Anesthesia Awareness Registry and encouraged to join the
registry by calling (206) 616-2669 and request a paper enrollment packet. Eligibility
includes the following:
– Surgery must be under general anesthesia.
– Patient must be 13 years or older.
– Patient must have the ability to read and understand English.
– Awareness of recall of events or sensations during surgery when you should have been
asleep and unaware.

FOLLOW-UP

CLOSED CLAIMS DATA


• Awareness claims accounted for 79 (1.9%) of 4,183 claims in the database.
• There were 18 claims for awake paralysis, most of which represented substandard care
involving errors in labeling and administration.
• There were 61 claims for recall during general anesthesia, most of which were likely in
women with nitrous–narcotic–relaxant techniques.

REFERENCES
1. merican Society of Anesthesiologists Task Force on Intraoperative Awareness. Practice
advisory for intraoperative awareness and brain function monitoring. Anesthesiology.
2006;104:847–864.
2. Sebel PS, Bowdle TA, Ghoneim MM, et al. The incidence of awareness during anesthesia: A
multicenter United States study. Anesth Analg. 2004;99(3):833–839.
3. Sandin RH, Enlund G, Samuelsson P, et al. Awareness during anesthesia: A prospective case
study. Lancet. 2000;355:707–711.
4. Domino KB, Posner KL, Caplan RA, et al. Awareness during anesthesia: A closed claims
analysis. Anesthesiology. 1999;90:1053–1061.
5. Spitellie PH, Holmes MA, Domino KB. Awareness during anesthesia. Anesthesiology Clin N
Am. 2002;20:555–570.
6. Mashour GA, Wang LY, Turner CR, et al. A retrospective study of intraoperative awareness
with methodological implications. Anesth Analg. 2009;108:521–526.

ADDITIONAL READING
• Myles P, Leslie K, McNeil J, et al. A randomised controlled trial of BIS monitoring to prevent
awareness during anaesthesia: The B-Aware Trial. Lancet. 2004;363:1757–1763.
• Webb RK, Currie M, Morgan CA, et al. The Australian Incident Monitoring Study: An
analysis of 2000 incident forms. Anaesth Intens Care. 1993;21:520–528.

CLINICAL PEARLS
• Awareness during general anesthesia is unintentional consciousness or awareness of events
happening during an operation either with or without pain sensations. It is a frightening
experience that can lead to debilitating emotional injury and even post-traumatic stress
disorder.
• ASA guidelines suggest considering premedication with amnestics, particularly when light
anesthesia is anticipated, administering more than a “sleep dose” of induction agent, and
avoiding muscle paralysis unless necessary.
• Light anesthesia is the most common cause of awareness.
BARIATRIC SURGERY
John D. Kot, MD
Judith A. Turner, MD, PhD

BASICS
DESCRIPTION
General
• Bariatric surgery includes a variety of surgical weight loss procedures indicated in the
treatment of morbid obesity (defined as an absolute BMI ≥40 kg/m2 or BMI ≥35 kg/m2
combined with obesity-related comorbidities). Surgical intervention for less obese
individuals who do not meet these criteria is controversial.
• Bariatric surgery may be classified as malabsorptive, restrictive, or mixed.
– Malabsorptive procedures, such as biliopancreatic bypass, are rare due to problems
associated with severe malabsorption.
– Restrictive procedures diminish gastric volume and include gastric banding and sleeve
gastrectomy.
– Roux-en-Y gastric bypass (RYGB) has become the “gold standard,” and combine gastric
restriction with minimal malabsorption.
• Laparoscopy is the preferred and more common approach due to a significant reduction in
postoperative complications and length of hospital stay as compared to an open procedure.
• Medical problems associated with obesity may include hypertension, heart disease, stroke,
type 2 diabetes, metabolic syndrome, obstructive sleep apnea (OSA), respiratory
insufficiency, pulmonary hypertension, thromboembolism, hepatic steatosis, certain cancers,
osteoarthritis, and depression.
• Eligible patients usually have failed supervised medical treatment, have undergone
psychological screening, and have demonstrated lifestyle changes for a specified length of
time in order to optimize surgical benefit.
Position
• Reverse Trendelenburg position (RTP) with back extension for laparoscopic surgery
• Supine for open procedures
• Adequate patient straps and padding of pressure points due to increased risk of slipping and
neuropathy
Incision
• 4–6 port sites for laparoscopy
• Midline for open
Approximate Time
2–4 hours
EBL Expected
25–100 mL
Hospital Stay
2–3 days
Special Equipment for Surgery
• Large OR table with an optional inflatable mat in place to facilitate patient movement after
surgery
• Laparoscopic equipment (including adequately long instruments) or large retractors
• Orogastric (OG) tube with inflatable gastric balloon
EPIDEMIOLOGY
Prevalence
Laparoscopic RYGB is currently the most common bariatric procedure.
Prevalence
In the US in 2008, it is estimated that >200,000 total bariatric procedures were performed
(and has been increasing yearly).
Morbidity
• Wound infection: 10% with open versus 1% with laparoscopic
• Hernia: 8% with open versus <1% with laparoscopic
Mortality
• Overall risk is <1%.
• Mortality risk factors include age >45 years, hypertension, male sex, risk factors for PE, and
BMI >50 kg/m2.
– 4 or more risk factors increase mortality risk to 2.4%.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Patient population with significant comorbidities
• Preoperative airway examination is critical, and additional airway equipment should be
readily available.
• High risk for DVT/PE, thus preoperative heparin SC and/or an IVC filter are essential. IVC
filters are typically reserved for patients with a history of DVT, PE, or BMI near 60 kg/m2.
• Except for succinylcholine, drug dosing should be based upon lean body mass (LBM).
• Special attention should be made to patient positioning and padding of pressure points to
mitigate nerve injury.
• Avoid endogastric tubes, other than the intragastric balloon tube that may be placed at the
surgeon’s request; this includes esophageal temperature probes.
• Judicious use of sedatives and analgesics to minimize respiratory impairment

PREOPERATIVE ASSESSMENT
SYMPTOMS
As related to comorbidities: Chest pain, dyspnea, somnolence, GERD
History
• Careful assessment of comorbidities especially cardiopulmonary
• Known difficult airway
• Previous bariatric surgery
• History of DVT or PE
Signs/Physical Exam
• Thorough airway examination
• Any evidence of cardiac failure: Pulmonary rales, additional heart sounds, increased JVD
MEDICATIONS
• Weight loss medications: Sibutramine may worsen hypertension, and orlistat may lead to
deficiencies in fat-soluble vitamins (A, D, E, K).
• Consider holding diuretics and ACE inhibitors given bowel prep and the potential for
hypotension especially if the procedure is in the reverse Trendelenburg position.
• Hold oral diabetic medications on the morning of surgery.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Check blood glucose
• Electrolytes if renal insufficiency
• PT/PTT, INR if taking orlistat or previous bariatric surgery given potential for chronic
vitamin K deficiency
• Consider liver function tests
• Consider baseline ABG if respiratory impairment is significant
• EKG, further cardiac testing (Echo, Stress) as indicated
• Consider CXR as indicated
CONCOMITANT ORGAN DYSFUNCTION
• Neurologic: Cerebrovascular disease
• Cardiac disease: Hypertension, coronary artery disease
• Respiratory impairment: Restrictive disease, OSA with possible pulmonary hypertension
(chronic hypoxia)
• Renal insufficiency
• Hepatic steatosis
• Metabolic: Diabetes, hypercholesterolemia

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Heparin SC to decrease risk of DVT
• Antacid as indicated
• Judicious use of anxiolytics
Special Concerns for Informed Consent
• Potential to convert to open
• Potential for postoperative intubation
Antibiotics/Common Organisms
Cefoxitin unless precluded by drug allergies
INTRAOPERATIVE CARE
Choice of Anesthesia
• General endotracheal anesthesia
• Epidural for postoperative analgesia if an open procedure is planned
Monitors
• Standard ASA monitors
• May need to place a NIBP cuff on the wrist or ankle given body habitus
• Avoid esophageal temperature monitoring since the probe may become inadvertently
entrapped
• Invasive monitors only as indicated and central venous catheter if peripheral access proves
difficult
• Foley catheter to monitor urine output for adequate volume resuscitation
Induction/Airway Management
• Pre-oxygenation in RTP to maximize FRC. Some anaesthetists administer CPAP for several
minutes prior to induction, as this may decrease atelectasis after the induction of anesthesia.
• Awake fiberoptic intubation if warranted
• Rapid-sequence intubation if indicated
• Proper patient positioning is crucial to facilitate direct laryngoscopy. The upper thorax is
“ramped” with either blankets or by elevating the back of the table 30–40° and extending
the head until the external auditory meatus is level with the sternal notch.
• Additional difficult airway equipment should be readily accessible.
• Drug dosing should be based on LBM, rather than ideal or total body weight (IBW, TBW);
LBM is calculated by adding approximately 20–50% of the difference between TBW and
IBW to IBW.
• Only succinylcholine is dosed based on TBW as pseudocholinesterase levels increase
proportionate to body weight.
Maintenance
• Any anesthetic technique is acceptable although desflurane may improve recovery time.
• Ventilation.
– An FiO2 of 0.5 may decrease atelectasis (the nitrogen in air prevents absorption
atelectasis; it is poorly soluble in blood and thus serves as a “filler" within alveoli, hence
keeping them open).
– PEEP is often administered to decrease atelectasis; increased values may be needed but
must be balanced with decreasing venous return to the heart.
– Recruitment maneuvers may be necessary to address atelectasis.
– Adjust ventilation accordingly to maintain normocapnia during laparoscopic CO2
insufflation.
• Avoid N2O due to the possibility of bowel distention, high oxygen demands of the obese,
and worsening of any underlying pulmonary hypertension.
• Muscle relaxation is required to facilitate surgery and ventilation.
• The surgical team will request the placement of oral intragastric tubes to help size the
gastric pouch, as well as perform leak tests with methylene blue. Lubrication, neck flexion,
and the use of a laryngoscope may be appropriate. No other tubes should be in the
esophagus/stomach.
• Narcotics should be judiciously administered to avoid postoperative respiratory
complications; remifentanil may be preferable intraoperatively.
• Fluids. Address NPO and bowel prep, as well as increased maintenance fluid requirements to
prevent postoperative ATN.
Extubation/Emergence
• Full reversal of neuromuscular blockade is essential.
• Place the patient in RTP to maximize FRC and minimize work of breathing.
• Antiemetics to mitigate PONV risk
• Consider the placement of an airway exchange catheter if airway management was difficult.

FOLLOW-UP

BED ACUITY
• Need for mechanical ventilation and/or ICU care is rare but more common after an open
procedure.
• Patients with known or suspected OSA will require a monitored bed. CPAP and BiPAP have
been shown to be safe although there is theoretical concern of anastomotic injury due to the
pressurized air.
ANALGESIA
• Pain is typically mild with laparoscopic procedures.
• Local anesthetic infiltration at incision sites may be helpful initially.
• If the procedure was open, an epidural catheter or dexmedetomidine may be preferable to
limit respiratory depression.
• Avoid NSAIDs given the risk for gastric ulceration.
COMPLICATIONS
• Anastomotic leak (2%) and stricture (10%)
• Respiratory complications (most common)
• Venous thromboembolism
• Laparoscopy related: Gas embolism, pneumothorax, pneumomediastinum
• Stricture or obstruction
• Wound infection (increased with open)
• Incisional hernia (increased with open)
• Dumping syndrome and malnutrition with bypass procedures
PROGNOSIS
• RYGB yields an average loss of 50–60% excess body weight and BMI decrease of 10 kg/m2
within the first 12–24 months.
• Majority experience resolution of other comorbidities: Diabetes (90%), hypertension and
hyperlipidemia (70%), and OSA.
• Overall, significantly reduced long-term mortality

REFERENCES
1. Bguyen NT, Goldman C, Rosenquist CJ, et al. Laparoscopic versus open bypass: A
randomized study of outcomes, quality of life, and costs. Ann Surg. 2001;234:279–291.
2. Demaria EJ, Murr M, Byrne TK, et al. Validation of the obesity surgery mortality risk score
in a multicenter study proves it stratifies mortality risk in patients undergoing gastric
bypass for morbid obesity. Ann Surg. 2007;246(4):578–582.
3. Huerta S, DeShields S, Shipner R, et al. Safety and efficacy of postoperative continuous
positive airway pressure to prevent pulmonary complications after Roux-en-Y gastric
bypass. J Gastrointest Surg. 2002;6:354–358.
4. Larson CP, Dutson E. The bariatric challenge. Curr Rev Clin Anesth. 2010;30:207–214.
5. NIH conference: Gastrointestinal surgery for severe obesity—Consensus Development
Conference Panel. Ann Intern Med. 1991;115:956–961.
6. Ogunnaike BO, Jones SB, Jones DB, et al. Anesthetic considerations for bariatric surgery.
Anesth Analg. 2002;95:1793–1805.
See Also (Topic, Algorithm, Electronic Media Element)
• Continuous positive airway pressure (CPAP)
• Laparoscopy
• Diabetes mellitus
• Laryngoscopy positioning

CODES

ICD9
• 278.01 Morbid obesity
• V45.86 Bariatric surgery status

ICD10
• E66.01 Morbid (severe) obesity due to excess calories
• Z98.84 Bariatric surgery status

CLINICAL PEARLS
• Patient population with significant comorbidities, including cardiovascular disease
• Preoperative airway examination is critical; additional airway equipment should be readily
available.
• High risk for DVT/PE; preoperative heparin SC and/or IVC filter are essential.
• Judicious use of sedatives and analgesics to minimize respiratory impairment
• Laparoscopy is the preferred and more common approach due to a significant reduction in
postoperative complications and hospital stay as compared to an open procedure.
Laparoscopic RYGB is the “gold standard” bariatric procedure.
BIER BLOCK
Angela T. Hsu, MD

BASICS
DESCRIPTION
• Intravenous regional anesthesia (IVRA) involves the administration of local anesthetic distal
to a tourniquet. It is a simple, safe, and reliable technique to provide anesthesia for
extremity surgery.
• The technique is also known as a Bier block, named after the German surgeon August Bier,
who first described the technique in 1908.
• Benefits of this technique:
– Easy to perform; it requires only the ability to perform venipuncture.
– Low failure rate
– Fast and reliable onset within 5 minutes
– Provides muscle relaxation for a surgical procedure
– Rapid recovery
• Limitations of this technique:
– Anesthesia is limited to the area distal to the tourniquet.
– The maximum duration of anesthesia is usually limited to 1 hour, secondary to the onset
of tourniquet pain.
– There is a concern for systemic toxicity if inadequate tourniquet inflation, early deflation,
or inadvertent deflation occurs.
– Lack of postoperative pain relief
PHYSIOLOGY PRINCIPLES
• The mechanism whereby IVRA provides anesthesia is controversial.
• Via studies using radioisotope-labeled local anesthetic, the following mechanism has been
proposed:
– Initially, the local anesthetic works on free nerve endings by binding to intracellular
sodium channels and inhibiting the initiation and propagation of nerve impulses.
– This is later followed by blockade of proximal nerve trunks, as the local anesthetic travels
from superficial veins to deep venules of nerve trunks. The theory of nerve trunk site of
action has been further supported because distal extremity anesthesia is achieved despite
application of an additional distal tourniquet that would inhibit medication distribution to
these tissues.
• Ischemia and compression of nerve trunks have been proposed as a late mechanism of
anesthesia and paralysis.
ANATOMY
• Bier block can be performed for upper extremity surgery below the elbow, or lower
extremity surgery below the knee.
– This technique is particularly suitable for surgery of distal extremities: hand, forearm,
foot, and ankle.
PHYSIOLOGY/PATHOPHYSIOLOGY
• Local anesthetic systemic toxicity can result from early tourniquet deflation, inadequate
inflation, or inadvertent premature deflation.
– After tourniquet release, patients may complain of dizziness, tinnitus, and perioral
numbness.
– Tourniquet malfunction may lead to the premature release of local anesthetic to the
systemic circulation, resulting in severe local anesthetic toxicity with seizures and
cardiovascular instability.
PERIOPERATIVE RELEVANCE
• IVRA is ideal for outpatient surgical procedures of the distal extremity. It provides a
bloodless surgical field and anesthesia that is reliable in onset and offset. In comparison to
general anesthesia, patients may be discharged earlier and have a decreased incidence of
postoperative nausea and vomiting.
• Patient selection:
– Patients with significant anxiety are unlikely to tolerate tourniquet-related pain.
Administering IV anxiolytic may help, but this may negate the benefits in discharge time
and cost.
– Procedure duration: Procedures longer than 60–90 minutes are not well tolerated
secondary to tourniquet pain.
• Contraindications:
– Avoid this technique in patients who cannot tolerate extremity ischemia from the
tourniquet.
Raynaud’s disease
Homozygous sickle cell disease (usually tolerated in heterozygous sickle cell disease)
Caution in crush injuries (viable tissues will be subjected to further ischemia)
• Medication selection:
– Prilocaine and lidocaine are commonly used due to their high therapeutic index.
– Prilocaine:
Usual adult dose is 40 mL of 0.5% prilocaine.
Recommended maximum dose is 6 mg/kg.
Because of concerns with methemoglobinemia, prilocaine is not as popular as lidocaine
in clinical practice. However, methemoglobinemia is usually not a concern until
prilocaine levels reach 10 mg/kg.
– Lidocaine:
Usual adult dose is also 40 mL of 0.5% lidocaine.
Recommended maximum dose is 5 mg/kg.
– Bupivacaine is not recommended secondary to its cardiotoxic potential, and reports of
several deaths.
– Ensure that the local anesthetic is preservative-free and does not contain epinephrine.
– Several adjuvants (e.g., clonidine, narcotics, neostigmine, muscle relaxants, ketorolac)
have been studied to improve block quality, tourniquet pain, or postoperative analgesia.
• Technique:
– Prepare equipment: Test the double-lumen tourniquet and ensure that resuscitative
equipment is nearby.
– In the extremity being operated on, place a 20–22 g IV in a vein distal to the surgical site.
– Place a 2nd IV in another limb for administration of fluids or other IV medications that
will be used during the procedure.
– Place a double-lumen tourniquet on the upper arm or thigh; do not inflate. Avoid
tourniquet placement on the forearm or lower leg since arterial compression is inadequate
at these locations.
– The extremity is then elevated and exsanguinated beginning distally via an Esmarch or
rubber bandage. Ensure that even the digits are exsanguinated.
– The proximal tourniquet is inflated to 100 mm Hg above pulse-occlusion pressure. The
pulse-occlusion pressure is best determined by loss of the pulse oximeter signal on the
finger or toe.
– Remove the Esmarch or rubber bandage. Confirm the absence of the radial or dorsalis
pedis pulse.
– Inject local anesthetic slowly (in the distal IV catheter of the operative extremity). Remove
the IV catheter and hold pressure at the IV site.
– The patient should be ready for surgical incision within a few minutes.
– When the patient complains of tourniquet pain, the distal cuff is inflated. The proximal
cuff is released after distal cuff inflation.
– After the surgery is completed, gradual release of the distal lumen is advised. The
minimum recommended time before the tourniquet can be deflated is 20 minutes to avoid
local anesthetic toxicity.

REFERENCES
1. Blackburn EW, Shafritz AB. Why do Bier blocks work for hand surgery… most of the time?
J Hand Surg Am. 2010;35(6):1022–1024.
2. Brown EM, McGriff JT, Malinowski RW. Intravenous regional anaesthesia (Bier block):
Review of 20 years’ experience. Can J Anaesth. 1989;36(3):307–310.
3. Rawal N. Intravenous regional anesthesia. Tech Reg Anesth Pain Manage. 2000;4(1):51–53.
See Also (Topic, Algorithm, Electronic Media Element)
• Local anesthetic systemic toxicity
• Methemoglobinemia

CLINICAL PEARLS
• Bandage wrapping during exsanguination can cause significant pain in a fractured
extremity. An alternative is to elevate the extremity for 30 seconds while applying firm
pressure to occlude the brachial or femoral artery. The tourniquet is then inflated after this
method of extremity exsanguination.
• Typically for upper extremity block, 40 mL of 0.5% lidocaine or prilocaine is used. For
larger or muscular patients, the dose can be increased to 50 mL. For small or frail patients,
the volume can be decreased to 30 mL.
• For the lower extremity, usually a larger volume is utilized to assure adequate distribution
of drug. One technique is 150 mL of 0.25% lidocaine.
• Make sure the local anesthetic contains no epinephrine. It is also recommended to have
preservative-free local anesthetic, although a review of 1,906 cases using local anesthetic
with preservative did not reveal ill-effects.
• Inform the patient that with this regional technique, the extremity may feel warm, numb, or
tingly. The skin will also appear mottled. This is normal.
• Maximum continuous tourniquet inflation time should be limited to 90 minutes secondary
to concern of extremity ischemia.
• Procedures longer than 90 minutes using Bier block as anesthesia are possible with a short
period of tourniquet release. In these cases, the IV cannula is kept in place during surgery.
After 1 hour, the tourniquet is deflated for 5 minutes. The surgeon elevates the arm and
applies a sterile Esmarch bandage, reinflates the tourniquet, and administers 50% of initial
local anesthetic dose. This may be repeated if necessary.
BLALOCK-TAUSSIG (BT) SHUNT
Alison R. Perate, MD

BASICS
DESCRIPTION
General
• Surgeon Alfred Blalock and cardiologist Helen Taussig developed the procedure after noting
that cyanotic children with a patent ductus arteriosus (PDA) did better than those without a
PDA. The first Blalock–Taussig (BT) shunt was performed in 1944 on a human with
Tetralogy of Fallot (TOF).
• The BT shunt is a palliative surgery for cyanotic heart defects with limited pulmonary blood
flow/ductal dependant lesions.
– Single ventricle physiology (most common indication)
– Tetralogy of Fallot
– Tricuspid atresia
– Ebstein anomaly
– Small pulmonary arteries
– Pulmonary stenosis
• The shunt connects the right subclavian artery to the right pulmonary artery (PA); the left
PA can be used as well. This increases the amount of deoxygenated blood directed to the
lungs.
– Classic BT shunt: The subclavian or carotid artery is anastomosed directly to the PA.
– Modified BT shunt uses artificial material (GORTEX) 4–5 mm in diameter to make the
aorticopulmonary connection.
Position
Supine, fully prepped from neck to groin for cardiopulmonary bypass (CPB) or extracorporeal
membrane oxygenation (ECMO) access if needed
Incision
• Historically, the procedure was performed via a lateral thoracotomy at the level of the 4th
intercostal space. However, this approach had limited access to small neonatal anatomy,
commits the surgeon to the side of entry, makes it difficult to ligate the PDA if done via a
right thoracotomy, and has a risk of flail scapula from an incision through the latissimus
dorsi muscle.
• Most institutions now use a median sternotomy; this approach allows for improved access,
easier conversion to CPB, augmentation for diminutive PAs, and less distortion of vascular
anatomy.
Approximate Time
Dependent on the surgeon’s experience; approximately 2–3 hours
EBL Expected
• Surgeon dependant
• Typically minimal (∼50 mL) when only a BT shunt is being performed
• May need to transfuse blood to maintain euvolemia
Hospital Stay
• Highly dependant on the underlying congenital heart disease that necessitated the shunt
• If the shunt remains patent and there are no complications, discharge to home is usually
between 8 and 15 days.
• Most surgeons require the patient to stay reasonably close to the hospital for the first few
weeks due to the risk of shunt occlusion.
Special Equipment for Surgery
• CPB machine should be in the room, prepped, and ready to use.
• ECMO back-up/capability
EPIDEMIOLOGY
Incidence
• Unknown number worldwide
• All congenital heart disease (CHD) = 8/1,000
• Cyanotic CHD is estimated at 25% of all CHD; corresponds to 2/1,000.
• Most registry data (Canada and Europe) quote an annual incidence of 1.5/1,000 live births.
Prevalence
Overall prevalence is increasing as therapies improve.
Morbidity
• Morbidity is largely related to the experience of both the surgeon and anesthesiologist as
well as the postoperative care (ICU).
• Risk of neurologic sequelae from surgery
Mortality
• Dependant on the complexity of the underlying heart defect/comorbidities
• Highest mortality of the 3 stages of the Fontan procedures
• Increased when performed in neonates compared to older children
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Patients have “duct-dependent” lesions; therefore, pulmonary blood flow can be tenuous.
Prevent any condition that would increase pulmonary vascular resistance (PVR), such as
hypothermia, acidosis, hypercapnia, or hypoxia.
• The maintenance of adequate pressures is necessary to prevent shunt occlusion. This is
accomplished via adequate blood volume as well as vasopressors if necessary.

PREOPERATIVE ASSESSMENT
SYMPTOMS
Because CHD presents in the neonatal period, feeding intolerance is a common symptom
reflecting decreased exercise tolerance.
History
• With improvements in fetal ultrasound technology, many lesions are now detected in utero.
• Those who are postnatally diagnosed are often cyanotic at birth, or when the PDA closes.
Signs/Physical Exam
• Murmur—with a diastolic component
• PaO2 <150 mm Hg on 100% FiO2
• Tachypnea, diaphoresis, central cyanosis
• Hepatomegaly
MEDICATIONS
Patients arrive on prostaglandins to maintain PDA patency. Most cyanotic heart disease is due
to inadequate blood flow to the lungs; If the ductus closes, pulmonary blood flow will be
inadequate and cardiopulmonary collapse will occur.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Chest radiograph: Look for signs of heart failure and lung congestion/fluid accumulation
• Echocardiogram: To determine the exact cardiac anatomy and nature of the lesion causing
the cyanosis
• CBC, chemistry, coagulation panel
• Cardiac MRI now gaining popularity
CONCOMITANT ORGAN DYSFUNCTION
• Heart failure
• Acidosis from malperfusion/hypoxemia

TREATMENT

PREOPERATIVE PREPARATION
Premedications
• Anxiolytics are not usually necessary due to the young age of the patient. If the patient is
older, midazolam or pentobarbital may be considered.
• Maintain the prostaglandin infusion
Special Concerns for Informed Consent
Parents should be made aware of the risk of complications/death.
Antibiotics/Common Organisms
• Important in the modified BT shunt due to placement of the indwelling gortex graft
• Skin flora
INTRAOPERATIVE CARE
Choice of Anesthesia
General endotracheal anesthesia
Monitors
• Standard ASA monitors
• Arterial line on the contralateral side of the shunt can be placed postinduction.
• 2 well-functioning IVs; if performed in the immediate postnatal period, an umbilical vein
line allows for the measurement of venous pressures.
• Surgeon may place right atrial lines prior to chest closure for right-sided pressures.
• Urine Foley catheter
Induction/Airway Management
• Bag mask ventilation and intubation should avoid hypercapnia, hypoxia, or coughing and
bucking as these derangement increase the pulmonary vascular resistance.
• Aggressive hydration is not usually needed as TOF repair is most commonly done as a
single-stage operation and does not undergo BT shunts anymore. In the TOF subset, there is
concern for RVOT obstruction in the face of inadequate intravascular volume. Adequate, but
not overaggressive, hydration is required to prevent this.
Maintenance
• Gas (isoflurane usually) with fentanyl or other short-acting opioids
• Standard paralysis doses of pancuronium or vecuronium as most of these patients are
extubated at the conclusion of surgery.
• Hypotension is often caused by surgical manipulation of great vessels.
• Neuromonitoring is not currently used, but is an evolving area of research.
• On clamping of the PA, some patients (in particular neonates) may develop profound
desaturation due to increases in dead space. This can also cause increases in the PaCO2,
causing the PVR to rise even further and reversing flow through the PDA (ceases pulmonary
blood flow). This will require going on CPB for the completion of surgery.
• Good surgical technique will minimize the effect of traction on the lung.
• In classical BT shunt, arterial flow to the ipsilateral arm is often compromised and can result
in ischemia. Modified BT shunt decreases this risk by maintaining flow to the arm.
• Ionotropes (such as epinephrine) are often utilized when weaning from CPB, until the blood
pressure is stabilized.
• Heparin is utilized to prevent clot formation during clamping of arteries; this can increase
the patient’s risk of bleeding.
• If the shunt is too large, overcirculation of the pulmonary vasculature can occur, resulting in
pulmonary edema and desaturation.
Extubation/Emergence
• Depending on the underlying heart defect, most can be extubated immediately after surgery.
• Patient must be strong, awake, and able to protect their airway in order to be extubated.
Hemodynamics should also be stable, with minimal ionotropic support. ABG results should
not reveal acidosis, which could reflect underperfusion of tissues.

FOLLOW-UP

BED ACUITY
Cardiac ICU
ANALGESIA
• IV opioids: morphine is often administered (easy to titrate); however other opioids are
acceptable and based upon practitioner and institution preferences. If the patient is older
(mental capacity >7 years of age), PCA may be considered.
• No current studies in the pediatric population for regional techniques
COMPLICATIONS
• Shunt occlusion—surgical emergency
• Pseudoaneurysm—can compress mediastinal structures
• Excessive pulmonary blood flow leading to pleural effusions
• Decreased diastolic pressures
• Congestive heart failure
• Distortion of vascular anatomy
• Pulmonary artery hypoplasia
• Phrenic/vagus/recurrent laryngeal nerve injury
• Arrhythmias
PROGNOSIS
• Dependant on the complexity of the underlying heart defect
• It is considered a palliative procedure, not curative; if done for single ventricle pathology,
this is the first of 3 steps to a Fontan completion.

REFERENCES
1. Kandakure PR, Dharmapuram AK, Ramadoss N, et al. Sternotomy approach for the
modified Blalock-Taussig Shunt: Is it a safe option? Asian Cardiovasc Thorac Ann.
2010;18(4):368–372.
2. Mavroudis C, Backer C. Pediatric cardiac surgery. Philadelphia: Mosby, 2003.Van Arsdell
GS, Maharaj GS, Tom J, et al. What is the optimal age for repair of tetralogy of Fallot?
Circulation. 2000;102(19 Suppl 3):III123–III129.Alkhulaifi AM, Lacour-Gayet F, Serraf A,
et al. Systemic pulmonary shunts in neonates: Early clinical outcome and choice of surgical
approach. Ann Thorac Surg. 2000;69(5):1499–1504.
3. Pearl JM, Nelson DP, Schwartz SM, et al. First-stage palliation for hypoplastic left heart
syndrome in the twenty-first century. Ann Thorac Surg. 2002;73(1):331–339; discussion
339–340.
See Also (Topic, Algorithm, Electronic Media Element)
• Fetal cardiovascular physiology
• Cardiopulmonary bypass
• Extracorporeal membrane oxygenator

CODES

ICD9
746.89 Other specified congenital anomalies of heart.

ICD10
Q24.8 Other specified congenital malformations of heart

CLINICAL PEARLS
• It is critical to maintain patency of the shunt in the postoperative period. Maintain adequate
blood pressure and volume. Shunt occlusion is a life-threatening surgical emergency.
• Patients may become severely hypoxic upon clamping of the PA. CPB must be on standby
and ready to cannulate.
• An A-line should be placed on the opposite side of the shunt. Otherwise when the artery is
clamped, the arterial line will be useless.
BLOOD COAGULATION PHYSIOLOGY IN PREGNANCY
Andrew Geller, MD
Mark Zakowski, MD
Sivam Ramanathan, MD

BASICS
DESCRIPTION
• Normal pregnancy becomes a hypercoagulable state at 6–8 weeks of gestation and returns to
the pre-pregnancy state in the 1st month after delivery (1).
• Hypercoagulability during pregnancy minimizes blood loss during delivery and in the
postpartum period (2).
PHYSIOLOGY PRINCIPLES
• Hypercoagulability during pregnancy is achieved via several mechanisms:
– Increased levels of procoagulants: Factors V, VII, VIII, IX, X, and XII; vWF; fibrinogen;
prothrombin.
– Decreased levels of anticoagulants: Factors XI and XIII; protein S.
– Decreased fibrinolysis is caused by increased concentrations of plasminogen activator
inhibitors 1 and 2 (1,3).
DISEASE/PATHOPHYSIOLOGY
• Thromboembolism: Deep venous thrombosis (DVT) and pulmonary embolism (PE) are the
greatest cause of morbidity and mortality in the parturient, occurring in 1 in 1,600
pregnancies.
– Contributing factors include: Hypercoagulable state, increased venous distention and
obstruction due to compression of the inferior vena cava by the gravid uterus.
– Thrombus primarily occurs in the venous system of the legs or, less commonly, in the
pelvic veins.
– Diagnostic tests include ultrasound imaging of the deep venous system of the lower
extremities and D-dimer levels. If PE is suspected, V/Q scan, MRI/MRA, or CT angiogram
is indicated.
– Prophylaxis is recommended for women at high risk for thromboembolism (e.g., bed rest,
postsurgical procedure, or pre-existing hypercoagulable disease state).
Thromboprophylaxis is accomplished with heparin SQ q12h (adjusted to the mid-range
of therapeutic PTT), dalteparin 200 U/kg SQ q24h, or enoxaparin 1 mg/kg q12h.
Thromboprophylaxis is discontinued at the time of delivery.
• Gestational thrombocytopenia: Platelet counts 70,000–150,000/μL.
– Occurs in ∼10% of pregnancies, usually in the third trimester.
– Proposed etiology includes increased plasma volume (dilutional) and increased platelet
clearance.
– Condition usually does not require treatment.
• Idiopathic thrombocytopenia purpura (ITP)
– Occurs in ∼3% of pregnancies, usually manifests in the first or second trimester.
– Treatment is with corticosteroids and/or intravenous IgG.
• Hemolysis, Elevated Liver enzymes, Low Platelet counts (HELLP) Syndrome
– Form of severe preeclampsia that can start after 20 weeks of gestation and up to 2 days
post-delivery.
– Thrombocytopenia results from increased anti-platelet IgG levels, activation of the
coagulation cascade (platelet consumption), and platelet sequestration in the spleen (4,5).
– Mortality results from liver rupture, disseminated intravascular coagulation (DIC), acute
renal failure, acute respiratory distress syndrome (ARDS), shock, and stroke.
– Management is supportive care.
Seizure prophylaxis with intravenous magnesium sulfate.
Blood pressure control for systolic pressure >160 mm Hg or diastolic pressure >90
mm Hg.
– Definitive treatment is delivery of the fetus and placenta.
• Thrombotic thrombocytopenia purpura (TTP)
– Thrombocytopenia is a result of platelet aggregation due to impaired vWF protease.
– Occurs anytime during pregnancy (first trimester through postpartum period).
– Severe cases can be treated with plasmapheresis.
• Hemolytic uremic syndrome (HUS)
– Microangiopathic hemolytic anemia from microvascular injury (6).
– 90% of cases occur postpartum with a mean onset of 26 days postdelivery (7).
– May require plasmapheresis
PERIOPERATIVE RELEVANCE
• Hypercoagulable states increase the risk of thromboembolism.
– Complications include uteroplacental thrombosis, fetal loss, DVT, PE, CVA, and cortical
venous thrombosis.
– Prophylaxis against thromboembolism (following surgical procedures and Cesarean
section) include: Graduated compression stockings, sequential leg compression devices,
early ambulation, and thromboprophylaxis.
• Some inherited congenital coagulopathies may improve or worsen depending on whether
the given factor increases or decreases with pregnancy.
– Hypofibrinogenemia and von Willebrand disease may improve.
– Factor XI deficiency may worsen.
• Hypocoagulable states may cause:
– Increased risk of postpartum hemorrhage
– Increased risk of placental abruption
– Increased risk of non-reassuring fetal status during labor
– A contraindication to neuraxial anesthesia due to increased risk of bleeding and epidural
hematoma formation.
Generally a stable platelet count >80,000/mL is sufficient for neuraxial anesthesia.

ALERT
• Management of anticoagulation pre-delivery
– Low molecular weight heparin (LMWH) should be switched to SQ or IV unfractionated
heparin 36 hours before elective induction or C-section.
– Many prefer to switch to unfractionated heparin at 36 weeks, to avoid going into labor on
LMWH, which might delay or preclude epidural placement.
– IV heparin should be turned off 4–6 hours before anticipated delivery.
• Management of anticoagulation prior to neuraxial block
– SQ heparin is not a contraindication for neuroaxial anesthesia if the total daily dose is
<10,000 U divided q12h.
– Conventional doses of fractionated LMWH require waiting at least 12 hours after the last
dose to perform a regional block; if higher doses are used, wait 24 hours.
– IV heparin can be administered 1 hour after a neuraxial block is in place.
– Removal of epidural catheters should occur at least 2–4 hours after the last heparin dose
(PTT measurement may be warranted).
– Restart fractionated or unfractionated (regular) heparin (for DVT prophylaxis) at least 2
hours after removal of the epidural catheter. Doses of heparin (5,000 U SQ q12h) and
LMWH (e.g., enoxaparin 1 mg/kg SQ q24h) should not increase the risk of hematoma
formation with neuraxial blockade after delivery if guidelines are strictly observed.
• Postoperative anticoagulation guidelines:
– Prophylaxis: Wait 12 hours after vaginal delivery to restart heparin and 24 hours after
Cesarean delivery for LMWH.
– Therapeutic: Wait 24 hours after delivery (8).

REFERENCES
1. Brenner B. Haemostatic changes in pregnancy. Thromb Res. 2004;114:409–414.
2. Crowley JP. Coagulopathy and bleeding in the parturient patient: Recent information has
helped in the identification of individuals at special risk. R I Med J. 1989;72:135–143.
3. Cerneca F, Ricci G, Simeone R, et al. Coagulation and fibrinolysis changes in normal
pregnancy: Increased levels of procoagulants and reduced levels of inhibitors during
pregnancy induce a hypercoagulable state, combined with a reactive fibrinolysis. Eur J
Obstet Gynecol Reprod Biol. 1997;73:31–36.
4. Leduc L, Wheeler JM, Kirshon B, et al. Coagulation profile in severe preeclampsia. Obstet
Gynecol. 1992;79:14–18.
5. Burrows RF, Hunter DJ, Andrew M, et al. A prospective study investigating the mechanism
of thrombocytopenia in preeclampsia. Obstet Gynecol. 1987;70:334–338.
6. McCrae KR, Cines DB. Thrombotic microangiopathy during pregnancy. Semin Hematol.
1997;34:148–158.
7. Esplin MS, Branch DW. Diagnosis and management of thrombotic microangiopathies
during pregnancy. Clin Obstet Gynecol. 1999;42:360–367.
8. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving
antithrombotic or thrombolytic therapy. American Society of Regional Anesthesia and Pain
Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med. 2010;35:64–
101.
ADDITIONAL READING
• Chestnut D, Polley L, Tsen L, et al. Chestnut’s obstetric anesthesia, 4th ed., 2009, chap. 43.
• Hoffman R, Benz EJ, Shattil SJ, et al. Hematology: Basic principles and practice, 5th ed.
Churchill Livingstone, chap. 161.
See Also (Topic, Algorithm, Electronic Media Element)
• Pulmonary embolism
• Preeclampsia
• Thrombocytopenia

CLINICAL PEARLS
• Patients with a history of an early pregnancy loss need to be worked up for genetic disorders
of coagulation.
• Hypercoagulable states are a leading cause of maternal mortality in the world because of the
risk of PE.
• Symptoms of DVT, PE, and cortical vein thrombosis need to be evaluated and have a low
threshold for workup.
• DIC in pregnancy is associated with dead fetus syndrome, preeclampsia, HELLP syndrome,
placental abruption, massive transfusion, uterine rupture, and amniotic fluid embolism.
• Pregnant women on anticoagulants need coordination and correct timing of medication,
regional anesthesia, and delivery per guidelines.
BLOOD FLOW RESISTANCE
Teodora Orhideea Nicolescu, MD

BASICS
DESCRIPTION
• Blood flow resistance (BFR) is the impedance offered by the blood vessels and its
interactions with the flowing blood. Conductance is the reciprocal of BFR.
• The basics of BFR are adapted from Ohm’s impedance law in electricity: R = V/I where R is
resistance, V is voltage, and I is current. Extrapolation of these factors and concepts to the
vascular system is as follows:
– Resistance (R): Equivalent to the vascular resistance and measured in dynes ×
seconds/cm5 (or Woods units)
– Voltage (V): Equivalent to the pressure difference across the area being discussed and
referred to as the ΔP
– Current (I): Equivalent to the cardiac output and measured as liters/minute
– R = ΔP/CO
• Resistance to flow can also include additional elements; for example, when expressed across
a valve it will be related to the valve size as well.
PHYSIOLOGY PRINCIPLES
• BFR is expressed as the ratio between the pressure gradient (arterial and venous pressure
difference) and the flow of blood. Factors affecting vascular resistance are arteriole radius,
viscosity, and length.
• Arteriole radius: Resistance is inversely proportional to the fourth power of the radius (r4).
Radius is affected by:
– Autonomic control
– Hormones: Angiotensin II, norepinephrine, and epinephrine
– Metabolites:
Adenosine
Serotonin
Endothelium-derived relaxing factor (EDRF)
Prostacyclin
Nitric oxide (NO)
– Autoregulation is present in critical organs including the cerebral, myocardial, hepatic,
and renal circulations to maintain a constant (and adequate) blood flow and delivery of
oxygen and glucose across a range of mean arterial pressures. Increased flow elicits
vasoconstriction and decreases blood flow, whereas decreased flow results in vasodilation
to increase blood flow.
• Viscosity describes the tendency of a fluid to resist flow. It is affected by the hematocrit,
temperature, and flow state.
• Length: Does not appreciably change in vivo; this is more applicable to airflow.
• Blood flow patterns and resistance:
– Laminar flow describes low-resistance, straight-line flow. Under ideal laminar flow
conditions, resistance is mostly dependent on the radius. Poiseuille’s law can be applied to
measure the resistance: R = (8 × L × n)/r4, where L is length, n is viscosity, and r is
radius.
– Turbulent flow describes high-resistance, high-velocity flow that creates eddy currents
(whirls of blood); overall flow is decreased at any given perfusion pressure compared to
laminar flow.
ANATOMY
• Vessel diameter has a direct effect on the resistance of the vessel.
• Arteries have 3 layers:
– Intima is a smooth layer that essentially helps lower BFR (low friction).
– Media has 2 components: An elastic component that is predominant in the large arteries
and is responsible for the stretch-recoil vessel properties, and a muscular component
predominantly present in medium-size arteries and arterioles which is responsible for
changing the vessel size.
– Adventitia bestows a protective and tissue-securing role; it thereby plays no role in BFR.
DISEASE/PATHOPHYSIOLOGY
• Chronic hypertension: In primary hypertension, the cardiac output increases initially, while
the systemic vascular resistance (SVR) remains normal. Eventually, the cardiac output
returns to normal and the SVR remains elevated.
• Pulmonary hypertension: Results from an imbalance in vasoactive peptides (prostacyclin,
endothelin 1, NO), which initiates smooth muscle proliferation followed by vasoconstriction
and right heart pressure overload.
• Temperature: Hypothermia increases blood viscosity and decreases vessel radius via
vasoconstriction (in order to preserve warmth).
• Hematocrit: Hemoconcentration and polycythemia vera increase blood viscosity. Anemic
patients, conversely, have a decrease in blood viscosity with a consequent decrease in
resistance; transfusion can, in addition to increasing oxygen-carrying capacity, increase
resistance and improve blood pressure in hypotensive patients.
• Prosthetic valves: As the cross-sectional area of the valve decreases from stenosis or
prosthetic valve housing, BFR increases, velocity increases, and pressure decreases across
the valve. This translates into a need for a large systolic pressure to drive blood forward.
A1V1 = A2V2, where A = cross-sectional area and V = velocity across the valve.
• Sepsis and anaphylaxis: Vasodilation decreases the BFR.
PERIOPERATIVE RELEVANCE
• BFR is often considered and discussed in regard to:
– SVR: Represents the change in pressure after being ejected from the left ventricle to the
pressure upon returning to the right atrium. SVR = (MAP – CVP)/CO, where MAP is
mean arterial pressure, CVP is central venous pressure, and CO is cardiac output. Normal
values range from 1,200 to 1,500 dynes × seconds/cm5.
– Pulmonary vascular resistance (PVR): Represents the change in pressure from the
beginning (pulmonary arteries) to the end (left atrium) of the pulmonary circulation. PVR
= (PAP – LAP)/CO, where PAP is the mean pulmonary artery pressure, LAP is left atrial
pressure, and CO is cardiac output. Normal values range from 100 to 300 dynes ×
seconds/cm5.
– Across heart valves: Stenotic valves and prosthetic heart valves can impose increased
resistance to flow. Transvalvular gradients can be measured via cardiac catheterization or
estimated/calculated with echocardiogram.
• Vasopressors and inotropes
– Phenylephrine: A synthetic, selective, and pure alpha-1 agonist. Receptor binding
increases the release of calcium from the sarcoplasmic reticulum and causes contraction of
vascular smooth muscle. This results in increased preload from venoconstriction and
afterload from vasoconstriction.
– Norepinephrine: Endogenously, it is released by the postsynaptic terminal of the
sympathetic nervous system. When exogenously administered, it has strong alpha-1
receptor agonism at veins and arteries, resulting in increased preload and afterload.
Coronary blood flow increases due to the increase in diastolic blood pressure. Side effects
include an increase in PVR, mesenteric ischemia, renal failure, decreased hepatic blood
flow, and peripheral hypoperfusion (digit necrosis).
– Dopamine: When exogenously administered, it causes alpha-1 agonism at higher dosages
(>10 mcg/kg/min). Initially, the vasoconstricting effects predominate in the skeletal
muscle vascular beds; with increasing doses, circulation in the limbs may become
compromised.
– Epinephrine: When exogenously administered, it causes alpha-1 agonism at higher
dosages.
– Vasopressin: V1 receptor agonism functions to increase sarcoplasmic release of calcium
and vascular smooth muscle constriction, primarily in capillaries and small arterioles. This
functions to shift blood flow away from splanchnic, muscle, fat and skin tissues to vital
organs.
– Phosphodiesterase inhibitors block enzymatic breakdown of cAMP to cGMP. In the
myocardium, this results in increased intracellular calcium with resultant enhanced
inotropy. However, in vascular smooth muscle, increased cAMP results in vasodilation.
• Vasodilators
– Nitrovasodilators: Nitroglycerin breaks down into NO, which consequently causes calcium
sequestration within vascular smooth muscle. At lower doses, venous and coronary
arteries are primarily affected; at higher doses, arterial dilation occurs. Nitroprusside
similarly breaks down into NO, but has a greater effect on arterial smooth muscle.
– Angiotensin-converting enzyme inhibitors (ACE I) block the conversion of angiotensin I to
angiotensin II. Angiotensin II is a potent endogenous vasoconstrictor.
– Angiotensin II receptor blockers (ARBs) competitively antagonize angiotensin II binding to
receptors on blood vessels.
– Calcium channel blockers (CCB) block voltage-gated calcium channels in the sarcoplasmic
reticulum, resulting in decreased intracellular calcium and decreased vasomotor tone.
– Hydralazine is a direct vasodilator. It increases cGMP levels with resultant decreases in
calcium release from the endoplasmic reticulum causing arterial vessel dilation (diastolic
pressure is decreased to a greater extent than systolic blood pressure) and venodilation.
• Anesthetic medications with vasodilatory properties:
– Propofol
– Volatile agents
– Lidocaine
• Resistance to blood flow also provides the basis for calculations obtained from pulmonary
artery catheter data.
EQUATIONS
• Ohm’s law: R = V/I, where R is resistance, V is voltage, and I is current
• Fluid dynamics extrapolation: R = ΔP/CO, where R is resistance, ΔP is change in pressure,
and CO is cardiac output
• Poiseuille’s law: R = (8 × L × n)/r4, where R is resistance, L is length, n is viscosity, and r
is radius

REFERENCES
1. Khalafbeigui F, Suga H, Sagawa K. Left ventricular systolic pressure-volume area correlates
with oxygen consumption. Am J Physiol. 1979;237:H566–H569.
2. Maughan WL, Sunagawa K, Burkhoff D, et al. Effect of arterial impedance changes on the
end-systolic pressure-volume relation. Circ Res. 1984;54:595–602. [A]
3. Rose WC, Shoukas AA. Two-port analysis of systematic of systemic venous and arterial
impedances. Am J Physiol. 1993;265:H1577–H1587. [C]
4. Sasse SA, Chen PA, Mahutte CK. Relationship of changes in cardiac output to changes in
heart rate in medical ICU patients. Intens Care Med. 1996;22:409–414.
5. Suga H. Total mechanical energy of a ventricle model and cardiac oxygen consumption.
Am J Physiol. 1979;236:H498–H505.
6. Sunagawa K, Sagawa K. Models of ventricular contraction based on time-varying elastance.
Crit Rev Biomed Eng. 1982;6:193–228.
7. Wallace A, Lam HW, Mangano DT. Linearity, load dependence, hysteresis, and clinical
association of systolic and diastolic indices of left ventricular function in man. Multicenter
Study of Perioperative Ischemia (McSPI) Research Group. J Card Surg. 1995;10:460–467.
[B]
See Also (Topic, Algorithm, Electronic Media Element)
• Laminar flow
• Cardiac output
• Cerebral blood flow
• Septic shock
• Anaphylactic shock

CLINICAL PEARLS
• Circulation is influenced by the resistance of the vascular bed against which the heart is
pumping. Cardiac output is directly influenced by BFR.
• The most important determinant of BFR is vessel radius, which is regulated by the
sympathetic nervous system (SNS), hormones, metabolites, and autoregulation. The SNS can
increase the blood pressure 3-fold via increasing the heart rate, inotropy, and both arterial
and venous resistances.
• Therapy for arterial blood pressure management is aimed at changing the BFR (changing the
vessel radius or blood flow viscosity).
• Pulmonary artery catheter data and its calculations, as well as echocardiography imaging,
aid with clinical decision-making and guidance of therapy.
• Several anesthetic medications cause vasodilation, with resultant decreases in BFR.
BLOOD OXYGEN CARRYING CAPACITY
Onyi Onuoha, MD, MPH
Nina Singh-Radcliff, MD

BASICS
DESCRIPTION
• The blood oxygen-carrying capacity is the milliliters of oxygen present in 1 deciliter of
blood.
• In blood, oxygen can exist in 2 forms: Dissolved and attached to hemoglobin. Hemoglobin is
the primary transporter of oxygen in mammals.
• In the event of decreased oxygen delivery, the blood provides a limited cushion against
hypoxia.
PHYSIOLOGY PRINCIPLES
• Oxygen is necessary for aerobic metabolism and cell integrity. However, despite its absolute
necessity, the body only has minimal storage capacity (unlike glucose). When apneic,
oxygen stores are limited to the oxygen in the lungs (FRC) and the blood; both of which are
unable to sustain life beyond a few minutes.
• In a healthy adult at rest, oxygen consumption is ∼200–250 mL O2/min and oxygen
delivery is ∼950–1,150 mL O2/min. Thus, ∼25% of the arterial oxygen is used every
minute, and the deoxygenated blood returning to the lungs has ∼75% saturation (mixed
venous oxygen saturation) (1).
• Hemoglobin provides the most efficient means of carrying and transporting blood. At full
oxygen saturation, 1 g of hemoglobin in 1 dL of blood is capable of carrying 1.34 mL of O2.
Thus, Hgb × 1.34 × SaO2 determines the milliliters of oxygen bound to hemoglobin in 1
dL of blood. Oxygen bound to hemoglobin does not exert partial pressure.
• Oxygen is poorly soluble in blood with a coefficient of 0.003 milliliters of oxygen per
deciliter of plasma per millimeter of mercury oxygen. Hence, a patient breathing room air
with an approximate PaO2 of 100 mm Hg has 0.3 mL of oxygen dissolved in 1 dL of blood.
• Oxygen–hemoglobin (O2–Hgb) dissociation curve: PaO2 on the x-axis, and SaO2 on the y-
axis. As PaO2 increases, SaO2 increases. The curve is not linear, but sigmoid in shape. This
represents hemoglobin’s desire to be fully bound or fully dissociated from oxygen; it is
unstable in intermediate states. This characteristic facilitates its physiologic function; at the
lungs, hemoglobin will fully saturate and at the tissue level, it will easily dissociate and
unload to oxygenate the tissues.
• Assuming normal hemoglobin moieties and conditions, the PaO2 is in equilibrium with
oxyhemoglobin and dissolved oxygen. For example, a PaO2 of 100 mm Hg has an SpO2 of
98% and 0.3 mL O2/dL of blood. A PaO2 of 500 mm Hg has an SpO2 of 100% and 1.5 mL
O2/dL of blood.

ANATOMY
• Hemoglobin is an iron-containing protein that is composed of 4 polypeptide chains or
subunits. The iron-containing heme group of each polypeptide reversibly binds up to 4
molecules of oxygen (2).
• The adult hemoglobin (HbA) molecule is made of 2α globin and 2β globin subunits.
• The binding of the first oxygen molecule to hemoglobin induces conformational changes in
the structure of the hemoglobin that allows the binding of other molecules of oxygen more
readily. At normal resting conditions, 25% of the oxygen bound to hemoglobin is extracted
by the tissues (equivalent to a partial pressure of 40 mm Hg).
• Fetal hemoglobin (HbF), on the other hand, has 2α and 2γ subunits that possess a strong
affinity for oxygen. The fetus is exposed to much lower oxygen pressures from the placenta;
∼21% of the level found in the adult lung (1).
DISEASE/PATHOPHYSIOLOGY
• Low oxygen-carrying capacity is the result of a low PaO2, low hemoglobin, impaired
oxygen-to-hemoglobin binding, or an increased oxygen demand/consumption.
– Low PaO2: Hypoxic mixture (low inspired oxygen), hypoventilation, V/Q mismatching,
shunting, impaired diffusion
– Low hemoglobin: Chronic or acute anemia
– Impaired oxygen-to-hemoglobin binding: Abnormal hemoglobins (fetal, thalassemia, sickle
cell disease), carboxyhemoglobin, cyanhemoglobin, methemoglobin, sulfhemoglobin
– Increased oxygen demand/consumption: Hyperthermia, hyperthyroidism, sepsis,
pregnancy, vigorous exercise
• Acute anemia: The initial hemodynamic response is a fall in systemic vascular resistance
(SVR) that is partly due to the decrease in blood viscosity and in part, the result of nitric
oxide-mediated vasodilation. The decrease in SVR reduces blood pressure and causes a
baroreceptor-mediated neurohormonal activation, identical to that seen in patients with
severe low-output heart failure. Eventually, sympathetic and renin–angiotensin–aldosterone
activity cause peripheral vasoconstriction and decrease in renal blood flow and glomerular
filtration rate. Kidneys retain salt and water (3).
• Chronic anemia results in hemodynamic and non-hemodynamic (erythropoiesis)
compensatory responses to enhance oxygen-carrying capacity (2,4).
– Hemodynamic responses are complex and involve a vasodilation-mediated high-output
state with neurohormonal activation (as described above in acute anemia). The high-
output state initially helps to increase oxygen transport. However, compensatory
mechanisms have deleterious long-term consequences and could contribute to anemia’s
role as an independent risk factor for adverse outcomes.
– Non hemodynamic responses: Increased levels of 2,3-diphosphoglycerate (2,3-DPG) shift
the O2–Hgb dissociation curve to the right. This is the least energy-consuming mechanism
to support increased oxygen delivery to the tissues (lacks significant increase in cardiac
output). Erythropoiesis also serves to increase red blood cell production.
• In elevated altitudes, ventilation and heart rate are elevated with a minimum reduction in
stroke volume. In addition, plasma volume is reduced over 24–48 hours to improve the
oxygen-carrying capacity of the blood. Prolonged sojourn at altitudes is compensated for
with enhanced erythropoiesis and a larger hemoglobin mass, allowing for a partial or full
restoration of the blood volume and arterial oxygen content.
PERIOPERATIVE RELEVANCE
• General anesthesia causes a 15% reduction in metabolic rate and a subsequent decrease in
oxygen requirement. Artificial ventilation further decreases the oxygen requirement by 6%
with the removal of the work of breathing. Anesthetic agents, however, do not affect the
transport of oxygen by hemoglobin or its solubility in blood.
• The increased utilization of oxygen when metabolic rate is increased (postoperative
shivering, malignant hyperthermia, etc.) leads to a decrease in PaO2 which activates normal
protective responses to hypoxia (aortic and carotid chemoreceptors, sympathetic nervous
system) to increase cardiac output. However, these protective responses are usually reduced
by anesthetic drugs intraoperatively, and can extend into the postoperative period.
• Blood transfusion: It remains the clinician’s responsibility to determine the transfusion
“trigger” for an individual patient based on multiple elements that determine the demand
for the delivery of oxygen and the physiological reserve. The decision should be based on
the premise that the oxygen-carrying capacity is increased to prevent oxygen consumption
from exceeding oxygen delivery. Additionally, the following should be considered:
– Theoretically, the oxygen-carrying benefit of red blood cells should hasten recovery from
respiratory failure, and transfusion would therefore be expected to shorten the duration of
mechanical ventilation. However, evidence to the contrary has been reported.
– Storage of packed red blood cells (pRBCs) is associated with a decline in 2,3-DPG that
leads to a subsequent left shift of the O2–Hgb dissociation curve. Therefore, while
transfusion increases the patient’s hemoglobin, it results in a less efficient oxygen delivery
when compared to the native hemoglobin at that same hematocrit. 2,3-DPG levels return
to normal over 12–24 hours.
– The need to restore blood viscosity may precede the need to restore oxygen-carrying
capacity during hemodilution or anemic conditions. A minimum level of blood viscosity
appears to be necessary for generating shear stress and stimulating the release of
vasoregulatory factors such as nitric oxide and prostacyclin (3).
– Studies in subpopulations (renal failure, Jehovah’s Witnesses, military casualties) have
shown that considerably greater amounts of anemia than was previously believed can be
well tolerated.
– Patients that are unable to increase their cardiac output (coronary artery disease,
prior/acute myocardial infarction, beta-adrenergic blockade, decreased SVR such as sepsis
or post-cardiopulmonary bypass) or have impaired oxygenation (pulmonary disease, high
altitude) have limited compensatory responses to hypoxia.
• Isovolemic hemodilution to hemoglobin levels of 5 g/dL in normal volunteers is well
tolerated. A robust cardiovascular response manifested by increases in heart rate and stroke
volume leads to compensation.
• Blood substitutes are being investigated to increase oxygen-carrying capacity. At this time,
there are no available products for clinical use.
EQUATIONS
• Oxygen content = [(Hgb × 1.39 × SaO2) + (PaO2 × 0.003)]. Units are as follows: Hgb is
in g/dL; 1.39 is mLO2/dL; SaO2 is % (0.01) but no units (5).
• Oxygen arterial content (CaO2) = [(Hgb × 1.39 × SaO2) + (PaO2 × 0.003)] (5).
• Oxygen venous content (CvO2) = [(Hgb × 1.39 × SvO2) + (PvO2 × 0.003)]. If obtained
at the pulmonary artery (PAC), it is a representation of the true mixed venous oxygen (5).
• Oxygen delivery (DO2) (mL/min) = cardiac output (CO) × blood oxygen content

GRAPHS/ FIGURES
Oxygen–hemoglobin dissociation curve

REFERENCES
1. aw R, Biukwirwa H. The physiology of oxygen delivery. Update Anaesth. 1999;10(3):1–2.
2. reacher DF, Leach RM. Oxygen transport. BMJ. 1998;317(7168):1302–1306.
3. abrales P, Martini J, Intaglietta M, et al. Blood viscosity maintains microvascular
conditions during normovolemic anemia independent of blood oxygen-carrying capacity.
Am J Physiol Heart Circ Physiol. 2006;291(2):H581–H590. Anand IS. Heart failure and
anemia: Mechanisms and pathophysiology. Heart Fail Rev. 2008;13:379–386.
4. Martin L. The four most important equations in clinical practice. Available at:
http://www.globalrph.com/martin_4_most2.html

ADDITIONAL READING
• Bartsch P, Saltin B. General introduction to altitude adaptation and motion sickness. Scand J
Med Sci Sports. 2008;18(Suppl 1):1–10.
• Henig NR, Pierson DJ. Mechanism of hypoxemia. Respir Care Clin N Am. 2000;6(4):501–
521.
• Ouellette DR. The impact of anemia in patients with respiratory failure. Chest. 2005;128(5
Suppl 2):576S–582S.
See Also (Topic, Algorithm, Electronic Media Element)
• Blood substitutes
• Isovolemic hemodilution
• Mixed venous oxygen saturation

CLINICAL PEARLS
• Pulse oximetry is not a reliable monitoring modality in the presence of dyshemoglobins
(hemoglobin that is unable to bind to oxygen). The 2 major dyshemoglobins seen in clinical
practice are carboxyhemoglobin (COHb) and methemoglobin (MetHb). Co-oximeters are
able to separate out oxyhemoglobin from MetHb and COHb and are therefore more accurate
for quantifying oxygen-carrying capacity/content.
• Blood substitutes: Include hemoglobin-based oxygen carriers (HBOCs) which transport
oxygen when introduced intravenously. Synthetic analogs, such as perfluorocarbon
emulsions (PFCs), have also been used as substitutes. These chemicals are able to dissolve
large amount of gases such as oxygen. Unlike blood, PFCs exhibit a linear oxygen
dissociation curve with an increase in PaO2 enhancing oxygen transport by these molecules
and increasing the driving pressure of diffusion of oxygen into tissues. With a linear
relationship however, the need for oxygen remains greater since most of the oxygen is
released prior to the arrival of the oxygen-laden molecule to the capillary network where
the partial pressure of oxygen is low. These also require high FiO2 to dissolve adequate
amounts of oxygen. However, optimal oxygen transport still remains difficult to reproduce
and continues to differentiate real blood from blood substitutes and volume expanders.
BLOOD PRESSURE
Mitesh Patel, MD
Lydia A. Conlay, MD, PhD

BASICS
DESCRIPTION
• Blood pressure (BP) is the pressure exerted by circulating blood upon the walls of blood
vessels and is one of the principal vital signs.
• During each heartbeat, BP varies between a maximum (systolic) and a minimum (diastolic)
pressure.
• The mean BP is a function of pumping by the heart and resistance to flow in blood vessels; it
decreases as the circulating blood moves away from the heart through arteries (1,2).
PHYSIOLOGY PRINCIPLES
• Mean arterial pressure (MAP) is the average pressure over a cardiac cycle and is determined
by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure
(CVP); it can be calculated by the equation MAP = (CO × SVR) + CVP.
• Pulse pressure (PP) is the difference between systolic and diastolic BP which results from the
pulsatile nature of cardiac output. PP = SBP − DBP.
• BP regulation is modulated by several reflexes on a minute-to-minute basis.
– Arterial baroreflex is mediated by stretch-sensitive sensory nerve endings located in the
carotid sinuses and the aortic arch. The rate of firing of these baroreceptors increases with
arterial pressure, and the net effect is a decreased sympathetic outflow, resulting in
decreased arterial pressure and heart rate.
– The renin–angiotensin–aldosterone system contributes to the regulation of arterial
pressure primarily via the vasoconstrictor properties of angiotensin II and the sodium-
retaining properties of aldosterone (3).
– Chemoreceptors located in the carotid and aortic bodies regulate BP by monitoring blood
pO2, pCO2, and pH.
• Diastolic BP plays an important role in coronary perfusion pressure. Coronary perfusion
pressure (CPP) is the difference between the aortic diastolic pressure and left ventricular
end-diastolic pressure (LVEDP). CPP = DBP − LVEDP.
• Manual intermittent measurement techniques: Auscultation remains the most widely used
and was originally described by Nikolai Korotkoff in 1905. A sphygmomanometer, cuff, and
stethoscope measure BP by auscultating sounds generated by turbulent arterial flow beyond
the partially occluding cuff. The first sound is heard at the systolic pressure (phase I). Its
character progressively changes (phases II and III), becomes muffled (phase IV), and is
finally absent (phase V). Diastolic pressure is recorded at phase IV or V.
• Automated intermittent measurement techniques: Most automated noninvasive BP devices
are based on oscillometry, where variations in cuff pressure resulting from arterial
pulsations during cuff deflation are sensed. The pressure at which the peak amplitude of
arterial pulsations occurs corresponds closely to MAP; systolic and diastolic pressures are
derived from proprietary formulas that examine the rate of change of the pressure
pulsations.
• Direct measurement techniques of arterial BP: Arterial cannulation with continuous pressure
transduction and waveform display remains the accepted reference standard for BP
monitoring. It is invasive, more costly, and requires technical expertise to perform (4).
DISEASE/PATHOPHYSIOLOGY
• Acute hypertension is a risk factor for myocardial ischemia, stroke, and bleeding from the
surgical sites.
• Chronic hypertension doubles the risk of cardiovascular disease including coronary heart
disease (CHD), congestive heart failure (CHF), ischemic and hemorrhagic stroke, renal
failure, and peripheral arterial disease. Because most patients with long-standing
hypertension are assumed to have some element of coronary disease and cardiac
hypertrophy, excessive BP elevations are undesirable.
• Uncontrolled hypertension (>180/120 mm Hg) and/or clinical signs and symptoms of
hypertensive emergency warrant cancellation of elective surgery until the BP is optimized.
Patients should receive emergency medical care and not simply be sent home. Warning
signs and symptoms of hypertensive emergency include:
– Headache
– Confusion
– Visual changes
– Seizures
– Focal neurologic changes
– Nausea and vomiting
– Papilledema
– Exudative hemorrhages
– Shortness of breath
– Chest pain
– Azotemia, oliguria, and proteinuria
PERIOPERATIVE RELEVANCE
• In the operative setting, systolic and diastolic pressures should generally be kept within 10–
30% of preoperative levels (5).
• The systolic BP (generated from myocardial ventricular contraction) helps estimate the risk
for a heart attack or stroke according to the Framingham study. Intraoperatively, systolic BP
correlates with the amount of surgical bleeding.
• MAP is commonly referred to during cardiac surgery (particularly during bypass) and is a
determinant of cerebral perfusion pressure (CPP = MAP – ICP). Cerebral blood flow is
autoregulated between MAPs of 60 and 180 mm Hg; should the MAP fall below 60 mm Hg,
the cerebral blood flow becomes severely decreased. In hypertensive patients, the
autoregulation curve is shifted to the right (6).
• Severe intraoperative hypotension is an anesthetic emergency, and treatment is vital to
ensure adequate organ blood flow, particularly to the brain, heart, kidneys, and the placenta
in pregnancy. Consequences of hypotension can include stroke, myocardial infarction, acute
tubular necrosis, fetal compromise, acidosis, and death. Because hypotension can be
harmful, this symptom is often treated before the cause has been ascertained. Hypotension
can result from abnormalities in preload, contractility, afterload, heart rate, cardiac rhythm,
intravascular volume, or SVR. Common causes of hypotension include:
– Hypovolemia can reduce preload and may be due to hemorrhage, vomiting, diarrhea,
burns, or sepsis.
– Increased intrathoracic pressure, as seen with positive pressure ventilation and tension
pneumothorax, can reduce preload.
– Spinal and epidural anesthesia cause vasodilatation and decreased preload due to
sympathetic block; if the block is above T4, it may also result in decreased myocardial
contractility and bradycardia.
– Excessive anesthesia: General anesthetics (both inhalation and intravenous) may cause
hypotension by reducing CO and SVR.
– Obstruction of major vessels can increase afterload and cause pump failure. Causes include
pulmonary embolism or aortocaval compression by tumor or pregnancy.
– Decreased myocardial contractility, as from beta-blockers, cardiac arrhythmias, cardiac
tamponade, and myocardial infarction
– Bradycardia, as from heart block or vagal overtone
– Shock, as from spinal, cardiogenic, or anaphylaxis shock or sepsis
• Treatment of intraoperative hypotension often precedes treating the cause:
– Optimize preload: Administer an intravenous fluid bolus.
– Elevate legs or head down tilt to improve venous return.
– Reduce anesthetic agent if appropriate.
– Use sympathomimetic drugs.
• Causes of intraoperative hypertension include:
– “Light” anesthesia or pain
– Hypercarbia
– Medication error (inadvertent administration of pressors)
– Preeclampsia/eclampsia
– Acute increase in intracranial pressure
– Volume overload
– Full bladder
– Pheochromocytoma
– Autonomic hyperreflexia
– Decreased vascular compliance (arteriosclerosis)
– Disorders with increased cardiac output (aortic regurgitation, thyrotoxicosis)
– Renal parenchymal diseases
– Aortic coarctation
– Medications (such as monamine oxidase inhibitors, cocaine, or methamphetamine)
• Autonomic hyperreflexia or dysreflexia (AD) is a life-threatening condition which occurs
most often in individuals with spinal lesions above the T6 spinal cord level. At this level, the
lesion is cephalad to the sympathetic cell bodies in the spinal cord and is believed to disrupt
descending CNS impulses that normally regulate sympathetic outflow. AD is a reaction of
the autonomic (involuntary) nervous system to overstimulation which is characterized by
severe hypertension, (reflex) bradycardia, profuse sweating, vasodilation above the level of
the lesion (including flushing of the skin, nasal stuffiness, severe headaches), apprehension,
anxiety, and occasionally cognitive impairment. AD is believed to be triggered by afferent
stimuli originating below the level of the lesion, which increase BP via sympathetically
mediated vasoconstriction in muscle, skin, and splanchnic vascular beds (7). The stimuli
that trigger AD often result from the distension of a viscous such as the bladder or intestine.
GRAPHS/FIGURES
See Table
See Table

REFERENCES
1. Health and Life. Normal blood pressure range adults. Available at:
http://healthlifeandstuff.com/2010/06/normal-blood-pressure-range-adults/
2. labunde R. Cardiovascular physiology concepts. Lippincott Williams & Wilkins, 2005.
3. Klabunde RE. Cardiovascular physiology concepts: Mean arterial pressure. Available at:
http://www.cvphysiology.com/Blood%20Pressure/BP006.htm [Accessed September 29,
2008; Archived version October 3, 2009.
4. Karlsson AK. Autonomic dysreflexia. Spinal Cord. 1999;37:383–391.
5. Rohrig R, Junger A, Hartmann B, et al. The incidence and prediction of automatically
detected intraoperative cardiovascular events in noncardiac surgery. Anesth Analg.
2004;98(3):569–577.

ADDITIONAL READING
• Morgan GE, Mikhail MS, Murray MJ. Anesthesia for patients with cardiovascular diseases.
In: Clinical Anesthesiology, 4th ed., McGraw Hill, 2005, chapter 20.
See Also (Topic, Algorithm, Electronic Media Element)
• Autonomic hyperreflexia
• Controlled hypotension
• Arterial waveform
• Perioperative hypertension
• Mean arterial pressure

CLINICAL PEARLS
• Maintaining an adequate BP is essential to maintain perfusion to vital organs. BP should be
maintained within 10–30% of the patient’s baseline.
• The consequences of hypotension are sufficiently serious to potentially warrant treatment
even before the cause of the hypotension is ascertained. Intraoperative hypotension most
commonly reflects “deep” anesthesia, hypovolemia, or the use of specific drugs or anesthetic
techniques.
• Uncontrolled hypertension is associated with an increase in perioperative morbidity and
mortality. Elective cases should be cancelled when a patient demonstrates signs of a
hypertensive emergency. Anesthesiologists are often faced with the decision to cancel or
proceed with uncontrolled BPs exceeding 180/110 mm Hg.
• Titrating therapies to traditional endpoints such as blood pressure does not ensure that the
microvascular bed is being adequately perfused. For example, a normal or high blood
pressure may be a vasoconstrictive response to a low cardiac output state.
BLOOD SUBSTITUTES
Jonathan S. Jahr, MD
Dayna Zimmerman, BS

BASICS
DESCRIPTION
• “Blood substitutes” have been studied for >50 years and are either derivatives of
hemoglobin or perfluorocarbons; they are designed to carry and offload oxygen to tissues.
– Hemoglobin-based oxygen carriers are termed (HBOCs); attained from human or bovine
sources.
– Perfluorocarbon-based oxygen carriers are termed (PFBOCs).
• No products discussed are FDA approved for human use. One product (Hemopure®, OPK
Biotech, Cambridge, MA) has been approved in South Africa and Russia. Another product
(Oxyglobin®, OPK Biotech) is FDA and European Union approved for canine anemia.
PHYSIOLOGY PRINCIPLES
• Blood substitutes have been designed to carry oxygen to ischemic tissue as well as tested as
a resuscitation fluid.
• HBOCs are:
– Synthesized from human or bovine blood cells in a process that removes the red cell
membrane, purifies and deactivates pathogens (prions), and re-polymerizes the purified
hemoglobin (via glutaraldehyde pegylation, encapsulation, or zero-link polymerization).
– Prepared as a bag of solution around 250–500 mL, or the equivalent amount of
hemoglobin as a unit of packed red blood cells. Some of the HBOCs offload oxygen more
easily and may be more efficient than banked blood.
– Newer generations have attempted to link oxygen carrying with diminished extravasation
from the vascular compartment, block nitric oxide scavenging, and serve as anti-
inflammatory agents to diminish the deleterious effects of ischemia.
• “First-generation” HBOCs are designed to have a normal hemoglobin (10–13 g/dL), normal
viscosity, elevated colloid oncotic pressure, shift the oxyhemoglobin dissociation curve to
the right, and a normal Hill coefficient.
– They include α-α cross-linked hemoglobin, 2,3 diaspirin cross-linked hemoglobin
(HemAssist®, Baxter, Deerfield, IL), and hemoglobin raffimer (Hemolink™, Hemosol,
Toronto, ON).
• “Second-generation” HBOCs are designed with the same goals as first-generation HBOCs but
with fewer side effects. They too have a normal hemoglobin (10–13 g/dL), normal viscosity,
elevated colloid oncotic pressure, shift the oxyhemoglobin dissociation curve to the right,
and a normal Hill coefficient. To date, they remain the most successful HBOCs.
– Human polyhemoglobin (PolyHeme®, Northfield, Evanston, IL) and hemoglobin glutamer
(bovine) 200 and 250 (Hemopure® and Oxyglobin®, OPK Biotech) have completed FDA
Phase III testing but were not approved in the US.
• “Third-generation” HBOCs have a low hemoglobin (5–6 g/dL), normal to high viscosity,
lower colloid oncotic pressure, shift the oxyhemoglobin dissociation curve to the left, and a
normal Hill coefficient.
– There are a number of “third-generation” HBOCs currently undergoing preclinical and
clinical testing (Maleimide-Polyethylene Glyco-modified Hemoglobin [MP4], Hemospan®,
Sangart, San Diego, CA; Zero-linked Hemoglobin Polymer Oxyvita®, OXYVITA, New
Windsor, NY).
DISEASE/PATHOPHYSIOLOGY
• “First-generation” HBOCs had serious complications including renal failure and increased
mortality