The Practice of Clinical Echocardiography

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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The Practice of Clinical Echocardiography III

Second Edition Catherine M. Otto MD Professor of Medicine Acting Director, Division of Cardiology Director, Training Programs in Cardiovascular Disease Associate Director, Echocardiography Laboratory University of Washington Seattle, Washington

W.B. SAUNDERS COMPANY An Imprint of Elsevier Science Philadelphia•London•New York•St. Louis•Sydney•Toronto

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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W.B. SAUNDERS COMPANY An Imprint of Elsevier Science The Curtis Center Independence Square West Philadelphia, Pennsylvania 19106 Library of Congress Cataloging-in-Publication Data The practice of clinical echocardiography / [edited by] Catherine M. Otto.—2nd ed. p. cm. Includes bibliographical references and index. ISBN 0-7216-9204-4 1. Echocardiography. I. Otto, Catherine M. [DNLM: 1. Echocardiography. WG 141.5.E2 P8942 2002] RC683.5.U5 C57 2002 616.1'207543-dc21 2001049709 Acquisitions Editor: Richard Zorab Production Editor: Robin E. Davis Production Manager: Mary Stermel Illustration Specialist: Rita Martello Book Designers: Catherine Bradish and Lynn Foulk THE PRACTICE OF CLINICAL ECHOCARDIOGRAPHY, Second Edition ISBN 0-7216-9204-4

Copyright © 2002, 1997 by W.B. Saunders Company. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Printed in the United States of America. Last digit is the print number: 9 8 7 6 5 4 3 2 1

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Contributors

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Gerard P. Aurigemma MD Professor of Medicine and Radiology, University of Massachusetts Medical School; Director, Noninvasive Cardiology, University of Massachusetts Medical Center, Worcester, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas J. Benedetti MD Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Ann F. Bolger MD Associate Clinical Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco General Hospital, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of

Echocardiography Hans G. Bosch MSc Senior Staff Member, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographic Digital Image Processing and Approaches to Endocardial Edge Detection Ian G. Burwash MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Benjamin F. Byrd III MD Associate Professor of Medicine, Division of Cardiology, Vanderbilt University School of Medicine; Director, Echocardiography Laboratory, Vanderbilt University Medical Center, Nashville, Tennessee Maintaining Quality in the Echocardiography Laboratory Kwan-Leung Chan MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Edmond W. Chen MD Fellow, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic

Embolic Event John S. Child MD Professor, University of California, Los Angeles, School of Medicine; Co-Chief, Division of Cardiology, Director, Ahmanson/UCLA Adult Congenital Heart Disease Center, UCLA Medical Center, Los Angeles, California Echocardiographic Evaluation of the Adult with Postoperative Congenital Heart Disease Joseph A. Diamond MD Assistant Professor of Medicine, Mount Sinai School of Medicine; Assistant Attending, The Mount Sinai Medical Center, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Pamela S. Douglas MD Tuchman Professor of Medicine; Head, Cardiovascular Medicine Section, University of Wisconsin Medical School, Madison, Wisconsin Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas R. Easterling MD Associate Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Peter J. Fitzgerald MD, PhD Associate Professor of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical

Applications Kirsten E. Fleischman MD, MPH Assistant Professor in Residence, University of California, San Francisco, School of Medicine; Attending Physician, University of California, San Francisco, Medical Center, San Francisco, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome Elyse Foster MD Professor of Clinical Medicine, University of California, San Francisco, School of Medicine; Director, Adult Echocardiography Laboratory, Moffitt-Long Hospital, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myicardial Infarction, Detection of Complications, and Prognostic Implications

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William H. Gaasch MD Professor of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts; Director, Cardiovascular Research, Lahey Clinic, Burlington, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Edward F. Gibbons MD Assistant Clinical Professor of Medicine, University of Washington School of Medicine; Director of Echocardiography, Director of Inpatient Cardiology Services, Virginia Mason Medical Center, Seattle, Washington

Education and Training of Physicians and Sonographers John S. Gottdiener MD Professor of Medicine, State University of New York at Stony Brook, School of Medicine; Director, Noninvasive Cardiac Imaging, St. Francis Hospital, Roslyn, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Brian P. Griffin MD Director, Cardiovascular Disease Training Program, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning and Intraoperative Evaluation of Mitral Valve Repair Sheila K. Heinle MD Clinical Assistant Professor of Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas Quantitation of Valvular Regurgitation: Beyond Color Flow Mapping Mary Etta E. King MD Associate Professor of Pediatrics, Harvard Medical School; Director, Pediatric Echocardiography, Massachusetts General Hospital, Boston, Massachusetts Echocardiographic Evaluation of the Adult with Unoperated Congenital Heart Disease Tim Kinnaird MB Fellow in Cardiovascular Medicine, London Chest Hospital, London, United Kingdom Pericardial Disease

Katsuhiro Kitamura MD Research Fellow in Medicine, Stanford University Medical Center, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Allan L. Klein MD Professor of Medicine, Ohio State University College of Medicine; Director, Cardiovascular Imaging Research, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Carol Kraft RDCS Lead Cardiac Sonographer, Virginia Mason Medical Center, Seattle, Washington Education and Training of Physicians and Sonographers Carolyn K. Landolfo MD Assistant Professor of Medicine, Duke University School of Medicine; Director, Adult Echocardiography, Duke University Medical Center, Durham, North Carolina The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation Jannet F. Lewis MD Professor of Medicine, George Washington University Medical Center; Director of Echocardiography, George Washington University Hospital, Washington, D.C. Doppler and Two-Dimensional Echocardiographic Evaluation in Acute and Long-term Management of the Heart Failure Patient David T. Linker MD

Associate Professor of Medicine, Division of Cardiology; Adjunct Associate Professor of Bioengineering; University of Washington School of Medicine, Seattle, Washington Principles of Intravascular Ultrasound Warren J. Manning MD Associate Professor of Medicine and Radiology, Harvard Medical School; Section Chief, Non-invasive Cardiac Imaging, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Pamela A. Marcovitz MD Director, Clinical Cardiology Fellowship Program; Director, Echocardiographic Research, William Beaumont Hospital, Royal Oak, Michigan Exercise Echocardiography: Stress Testing in the Initial Diagnosis of Coronary Artery Disease and in Patients with Prior Revascularization or Myocardial Infarction Roy W. Martin PhD Research Professor, Department of Anesthesiology and Center for Bioengineering, Applied Physics Laboratory, University of Washington School of Medicine, Seattle, Washington Interaction of Ultrasound with Tissue, Approaches to Tissue Characterization, and Measurement Accuracy Thomas H. Marwick MD, PhD Professor of Medicine, Head of Section, University of Queensland Department of Medicine; Director of Echocardiography, Princess Alexandra Hospital, Brisbane, Queensland, Australia Stress Echocardiography with Nonexercise Techniques: Principles, Protocals, Interpretation, and Clinical Applications David J. Meier MD

Cardiology Fellow, University of Michigan Health System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention of Chronic Mitral and Aortic Regurgitation

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Bradley I. Munt MD Clinical Instructor, The University of British Columbia Department of Medicine; Cardiologist, Providence Healthcare and St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Danielle Noll MD Department of Cardiology, Echocardiography, Medizinische Klinik, Klinikum Innentadt, Munich, Germany Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Catherine M. Otto MD Professor of Medicine; Acting Director, Division of Cardiology; Director, Training Programs in Cardiovascular Disease; Associate Director, Echocardiography Laboratory, University of Washington School of Medicine, Seattle, Washington Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making; The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy; Echocardiographic Findings in Acute and Chronic Pulmonary Disease Donald C. Oxorn MD

Associate Professor of Anesthesiology, Adjunct Associate Professor of Medicine, University of Washington School of Medicine, Seattle, Washington Monitoring Ventricular Function in the Operating Room: Impact on Clinical Outcome Abraham C. Parail MD Fellow in Cardiology, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Robert A. Phillips MD, PhD Associate Professor of Medicine, Mount Sinai School of Medicine; Director, Department of Medicine, Lenox Hill Hospital, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Thomas R. Porter MD Associate Professor, University of Nebraska College of Medicine, Diagnostic Cardiac Ultrasound and Noninvasive Diagnostics, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Harry Rakowski MD Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Rita F. Redberg MD

Associate Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic Embolic Event Johan H. C. Reiber PhD Professor of Medical Imaging, Director, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographi Digital Image Processing and Approaches to Endocardial Edge Detection Cheryl L. Reid MD Associate Professor of Medicine, University of California, Irvine College of Medicine; Director, Non-invasive Cardiology, University of California, Irvine, Medical Center, Orange, California Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy: Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Carlos A. Roldan MD Associate Professor of Medicine, University of New Mexico School of Medicine; Staff Cardiologist, Director, Echocardiography Laboratory, Veterans Affairs Medical Center; Staff Cardiologist, University of New Mexico Health Sciences Center, Albuquerque, New Mexico Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Elizabeth W. Ryan MD

Research Fellow in Cardiology, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of Echocardiography Kiran B. Sagar MD Professor of Cardiology and Medicine, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Nelson B. Schiller MD Professor of Medicine, Radiology, and Anesthesia, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco Veterans Affairs Medical Center; Attending Physician, Cardiology, Echocardiography, and Adult Congenital Heart Disease, Moffitt-Long Hospital, San Francisco, California Clinical Decision Making in Endocarditis Ingela Schnittger MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Douglas S. Segar MD Clinical Associate Professor of Medicine, Indiana University School of Medicine, Indiana Heart Institute, Indianapolis, Indiana The Digital Echocardiography Laboratory

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David M. Shavelle MD

Interventional Cardiology Fellow, Good Samaritan Hospital, Los Angeles, California Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making Florence H. Sheehan MD Research Professor of Medicine, Division of Cardiology, University of Washington School of Medicine, Seattle, Washington Quantitative Evaluation of Regional Left Ventricular Systolic Function; Three-Dimensional Echocardiography: Approaches and Applications Bruce K. Shively MD Associate Professor of Cardiology, Oregon Health and Science University; Co-Director, Echocardiography Laboratory, Oregon Health and Science University Hospital, Portland, Oregon Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Mikel D. Smith MD Professor of Internal Medicine/Cardiology, University of Kentucky College of Medicine; Director, Adult Echocardiography Laboratory, Gill Cardiovascular Institute, Albert B. Chandler Medical Center, Lexington, Kentucky Left Ventricular Diastolic Function: Clinical Utility of Doppler Echocardiography A. Rebecca Snider MD Consultant, Pediatric Cardiology, Monmouth Junction, New Jersey General Echocardiographic Approach to the Adult with Suspected Congenital Heart Disease Mark R. Starling MD Professor of Internal Medicine,

Director of Cardiology Training Program, Associate Chief of Cardiology, University of Michigan Medical School; Chief, Cardiology Section, VA Ann Arbor Healthcare System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation William J. Stewart MD Associate Professor of Medicine, Department of Cardiology, Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Marcus F. Stoddard MD Professor of Medicine, University of Louisville School of Medicine; Director, Noninvasive Cardiology, University of Louisville Hospital, Louisville, Kentucky Echocardiography in the Evaluation of Cardiac Disease Due to Endocinopathies, Renal Disease, Obesity, and Nutritional Deficiencies Maran Thamilarasan MD Assistant Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Christopher R. Thompson MD, CM Clinical Associate Professor of Medicine (Cardiology), Director, Echocardiography Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Aneesh V. Tolat MD

Clinical Fellow in Medicine, Harvard Medical School; Clinical Fellow in Cardiovascular Diseases, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Brandon R. Travis PhD School of Chemical Engineering, Georgia Institute of Technology, Atlanta, Georgia Fluid Dynamics of Prosthetic Valves Zian H. Tseng MD Cardiology Fellow, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myocardial Infarction, Detection of Complications, and Prognostic Implications Hannah A. Valantine MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Samuel Wang MD Assistant Professor of Clinical Internal Medicine, University of California, Davis, School of Medicine; Attending Physician, University of California, Davis, Medical Center, Sacramento, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome E. Douglas Wigle MD Professor of Medicine, University of Toronto; Staff Cardiologist,

Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Selwyn P. Wong MD Cardiologist, Middlemore Hospital, Auckland, New Zealand Echocardiographic Findings in Acute and Chronic Pulmonary Disease Anna Woo MD Assistant Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy

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Feng Xie MD Research Assistant Professor, Cardiology, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Paul G. Yock MD Professor of Medicine, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Ajit P. Yoganathan PhD Regents Professor of Biomedical Engineering, The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia

Fluid Dynamics of Prosthetic Valves Miguel Zabalgoitia MD Professor of Medicine; Director, Echocardiography Laboratory, University of Texas Health Science Center, San Antonio, Texas Echocardiographic Recognition and Quantitation of Prosthetic Valve Dysfunction William A. Zoghbi MD Professor of Medicine, Director of Echocardiography Research, Baylor College of Medicine; Associate Director, Echocardiography Laboratory, The Methodist Hospital, Houston, Texas Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Preface Echocardiography increasingly has become a key component in the routine evaluation of patients with suspected or known cardiovascular disease. As this technique has evolved and matured, the role of the echocardiographer has shifted from simply providing a description of images to providing an integrated assessment of echocardiographic data in conjunction with the other clinical data from each patient. In effect, echocardiography has become a specialized type of cardiology consultation. The information now requested by the referring physician includes not only the qualitative and quantitative interpretation of the echocardiographic images and Doppler flow data but also a discussion of how this information might affect clinical decision making. Specific examples include decisions regarding medical or surgical therapy (e.g., treatment of endocarditis, surgery for aortic dissection), optimal timing of intervention in patients with chronic cardiac diseases (e.g., valvular regurgitation, mitral stenosis), prognostic implications (e.g., heart disease in pregnancy, heart failure patients), and the possible need for and frequency of periodic diagnostic evaluation (e.g., congenital heart disease, the postoperative patient). This book reflects our role as clinicians with specialized expertise in echocardiography and is of value to cardiology fellows pursuing advanced training in echocardiography, cardiologists in clinical practice, researchers using echocardiographic techniques, and other individuals using echocardiographic approaches in the clinical setting (including anesthesiologists, radiologists, emergency medicine physicians, and obstetricians), as well as to cardiac sonographers, cardiovascular technologists, and nursing professionals.

Each chapter provides an advanced level of discussion, written by an expert in the field, building upon the basic material in the Textbook of Clinical Echocardiography (C. M. Otto, 2nd Edition, WB Saunders, Philadelphia, 2000). The emphasis is on optimal data acquisition, results of recent studies, quantitative approaches to data analysis, potential technical limitations, and areas of active research, in addition to a detailed discussion of the impact of echocardiographic data on patient management. Tables, line drawings, echocardiographic images, and Doppler tracings are used to summarize and illustrate key points. In this Second Edition, the text has been revised to reflect recent advances, illustrations and tables have been updated, and new references have been added to each chapter. The book is organized into sections based on major diagnostic categories. In this new edition, an introductory section on transesophageal echocardiography has been added. Chapters include basic principles of transesophageal imaging, monitoring of ventricular function in the operating room, and a discussion of echocardiographic evaluation of aortic dissection and trauma. Other detailed information on the role of transesophageal echocardiography is integrated into subsequent chapters, which are organized by disease categories. The next section focuses on the left ventricle, with chapters spanning the spectrum from emerging new techniques (e.g., myocardial contrast echocardiography, automated edge detection, tissue characterization, three-dimensional echocardiography) to critical appraisals of quantitative techniques (e.g., left ventricular geometry and systolic function, evaluation of regional function, and assessment of diastolic function). The section on ischemic heart disease includes chapters on the role of echocardiography in the emergency room and coronary care unit, stress echocardiography (exercise and nonexercise), and the basic principles, instrumentation, and clinical applications of intravascular ultrasound in patients with coronary artery disease. The critical role that echocardiography now plays in management of patients with valvular heart disease is evident in a section of chapters on technical aspects of echocardiographic evaluation, optimal timing of surgery and periodic evaluation of patients with valvular regurgitation, management of patients undergoing balloon mitral commissurotomy, clinical decision making in patients with endocarditis, evaluation of disease severity, progression in valvular aortic stenosis, and evaluation of prosthetic valves. The following clinically oriented sections bring together data from both the

echocardiographic and general cardiology literature to discuss the role of echocardiography in patients with cardiomyopathies (heart failure, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and the posttransplant patient) and pericardial disease, pregnant patients with cardiac disease, and a wide range of other vascular and systemic diseases that lead to cardiac dysfunction (hypertension, aortic dissection, pulmonary disease, systemic immune-mediated diseases, renal disease, aging, systemic embolic events, and cardiac arrhythmias). In recognition of the increasing number of adult patients presenting with congenital heart disease, either as a new diagnosis or following prior surgical procedures, three chapters are devoted to this topic. In addition, a new section has been added on the echocardiography laboratory to address issues that increasingly affect our clinical practice, including education and training of echocardiographers, quality improvement in the echocardiography laboratory, and the transition to a digital laboratory. It is hoped that this book will provide the needed background to support and supplement clinical experience and expertise. Of course, competency in the acquisition and interpretation of echocardiographic and Doppler data depends on appropriate clinical education and training as detailed in accreditation requirements for both physicians and technologists, and as recommended by professional societies including the American Society of Echocardiography, the American College of Cardiology, and the American Heart Association. I strongly support these educational requirements and training recommendations; XII

readers of this book are urged to review the relevant documents. In addition, there continue to be advances both in the the technical aspects of image and flow data acquisition and in our understanding of the clinical implications of specific echocardiographic findings. This book represents our knowledge base at one point in time; readers should consult the current literature for the most up-to-date information. Although an extensive list of carefully selected references is provided with each chapter, the echocardiographic literature is so robust that it is impractical to include all relevant references; the reader can use an online medical literature search if an all-inclusive listing is desired. Catherine M. Otto MD

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Acknowledgments

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Sincere thanks are due to the many individuals who made this book possible. Primary recognition goes to the chapter contributors who provided scholarly, thoughtful, and insightful discussions and who integrated the clinical and echocardiographic information into a format that benefits our readers. The support staff at each of our institutions deserves our appreciation for manuscript preparation and providing effective communication, with special thanks to Sharon Kemp and Bev Bubela. The many research subjects who contributed to the data on which our current understanding is based certainly are worthy of our appreciation. The cardiac sonographers at the University of Washington Medical Center (Rachel Elizalde, RDCS; Michelle C. Fujioka, RDMS; Carolyn J. Gardner, RDCS; Caryn D'Jang, RDCS; Scott Simicich, RDCS; David Stolte, RDCS; Rebecca G. Schwaegler, RDMS; Erin Trent, RDCS; and Todd R. Zwink, RDMS) merit acknowledgment. In addition, gratitude is due to Richard Zorab and the production team at W.B. Saunders. Finally, I thank my family for their constant encouragement and support.

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NOTICE Medicine is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the treating physician, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the Publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this publication. THE PUBLISHER

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Section 1 - Transesophageal Echocardiography

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Chapter 1 - Indications, Procedure, Image Planes, and Doppler Flows Ian G. Burwash MD Kwan-Leung Chan MD

Transesophageal echocardiography (TEE) has become a valuable diagnostic imaging modality for the dynamic assessment of cardiac anatomy and function. Since the initial description of esophageal echocardiography in 1976,[1] the potential role and utility of TEE in the evaluation of diseases of the heart and great vessels have expanded to involve all aspects of cardiac disease. The close proximity of the esophagus to the heart and great vessels provided the echocardiographer with an easily accessible window with the potential for excellent visualization of cardiac structures, avoiding the intervening lung and chest wall tissues that limit transthoracic imaging. The potential of TEE to provide a valuable imaging tool became widely recognized in the 1980s with advancements in TEE probe technology, including the availability of single-plane phased array transducers and the addition of color flow and continuous wave Doppler imaging technology. TEE does not supplant transthoracic echocardiography

(TTE), however; it is a complementary imaging modality with its own strengths and weaknesses. The 2

introduction of biplane TEE transducers in the late 1980s and multiplane transducers in the 1990s has resulted in a further expansion of potential diagnostic applications. Perhaps the best evidence of TEE's diagnostic utility and value in patient management is the widespread use of this technology. TEE is found in the inpatient and outpatient ambulatory setting, in the operating room, in the intensive care unit, and in the emergency department. Currently, TEE accounts for approximately 5% to 10% of all echocardiography studies performed. The indications and utility of TEE will likely expand in the future with new technologic advancements such as three-dimensional echocardiography.

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Performance of Transesophageal Echocardiography Transesophageal echocardiography is a semi-invasive procedure that should be performed only by a properly trained physician who understands the indications for and potential complications of the procedure. Both technical and cognitive skills are required for the competent performance and interpretation of TEE studies (Table 1-1) , and guidelines on training have been published.[2] The physician should be assisted by an experienced sonographer whose tasks are to ensure that optimal images are obtained by adjusting the controls of the echocardiographic system and to ensure safety by monitoring the responses of the patient during the procedure. Although family members or friends are usually not allowed in the room when the procedure is being performed, there are situations in which their presence can be helpful. The presence of a parent can have a calming effect when one is dealing with an apprehensive teenager. A friend or a relative who speaks the same language can relieve much of the anxiety when dealing with an anxious patient who is not fluent in English. Transesophageal echocardiography should be performed in a spacious room that can comfortably accommodate a stretcher. The room should be equipped with an oxygen outlet and suction facilities. A pulse oximeter should be available, to be used mainly in cyanotic patients and patients with severe lung disease. The TEE probe should be carefully examined prior to each use. In addition to visual inspection, it is important to palpate the probe, particularly the flexion portion, to ensure that there is no unusual wear and tear of the probe.[3] Stretching of the steering cables may result in increased flexibility and mobility of the probe tip with buckling of the probe tip within the esophagus.[4] This phenomenon is associated with a poor TEE image and resistance to probe withdrawal. The probe should be advanced into the stomach and straightened by retroflexion of the extreme antiflexed probe tip. We have also detected perforation of the TEE probe sheath by a ruptured steering cable and recommend inspection of the casing for any protruding wires prior to probe insertion.[3] The flexion controls

need to be tested on a regular basis. Anterior flexion should exceed 90 degrees, and right and left flexion should approach 90 degrees. TABLE 1-1 -- Cognitive and Technical Skills Required for the Performance of Transesophageal Echocardiography (TEE) Cognitive Skills Knowledge of appropriate indications, contraindications, and risks of TEE Understanding of differential diagnostic considerations in each clinical case Knowledge of physical principles of echocardiographic image formation and blood flow velocity measurement Familiarity with the operation of the ultrasonographic instrument, including the function of all controls affecting the quality of the data displayed Knowledge of normal cardiovascular anatomy, as visualized tomographically Knowledge of alterations in cardiovascular anatomy resulting from acquired and congenital heart diseases Knowledge of normal cardiovascular hemodynamics and fluid dynamics Knowledge of alterations in cardiovascular hemodynamics and blood flow resulting from acquired and congenital heart diseases Understanding of component techniques for general echocardiography and TEE, including when to use these methods to investigate specific clinical questions Ability to distinguish adequate from inadequate echocardiographic data and to distinguish an adequate from an inadequate TEE examination Knowledge of other cardiovascular diagnostic methods for correlation with TEE findings Ability to communicate examination results to patient, other health care professionals, and medical record Technical Skills Proficiency in performing a complete standard echocardiographic examination, using all echocardiographic modalities relevant to the case Proficiency in safely passing the TEE transducer into the esophagus and

stomach and in adjusting probe position to obtain the necessary tomographic images and Doppler data Proficiency in correctly operating the ultrasonographic instrument, including all controls affecting the quality of the data displayed Proficiency in recognizing abnormalities of cardiac structure and function as detected from the transesophageal and transgastric windows, in distinguishing normal from abnormal findings, and in recognizing artifacts Proficiency in performing qualitative and quantitative analysis of the echocardiographic data From Pearlman AS, Gardin JM, Martin RP, et al: J Am Soc Echocardiogr 1992;5:187–194. Preparation of Patient Patients should be contacted at least 12 hours before the procedure and instructed to fast for at least 4 hours before the procedure. They are informed that they should be accompanied, because they will not be able to drive or return to work for several hours owing to the lingering effect of sedation. On the day of the study, the procedure is explained in greater detail, and informed consent is obtained. Patients are told to expect mild abdominal discomfort and gagging following the insertion of the probe and are reassured that these responses are transient. A 20-gauge intravenous cannula is then inserted for administration of medications and contrast agents, if necessary. Lidocaine hydrochloride spray is routinely used for topical anesthesia, which should cover the posterior pharynx and the tongue. We usually use diazepam 2 to 10 mg intravenously 3

for sedation.[5] Midazolam at 0.05 mg/kg, with a total dose between 1 and 5 mg, can also be used. Sedation is used in about 85% of our patients and should be more sparingly used in elderly patients, because they tend to be more stoic and the effect of sedation is more likely prolonged. On the other hand, sedation is essential in young anxious patients and when the study is expected to be protracted. We aim for light sedation so that at the end of the procedure the patients are awake and can leave with an escort. Heavy sedation is needed in situations in which blunting the hemodynamic responses to the procedure is desirable. One obvious example is a patient undergoing TEE for suspected aortic

dissection.[6] It has not been our practice to use anticholinergic agents such as glycopyrrolate to decrease salivation. In the rare circumstances in which there is excessive salivation, it is usually adequate to simply instruct the patient to let the saliva dribble onto the towel placed under the chin, or the saliva can be removed by intermittent suction. Bacteremia is not a significant risk in TEE, and we do not use antibiotic prophylaxis to prevent endocarditis even in patients with prosthetic heart valves.[7] [8] Esophageal Intubation We perform the TEE study with the patient in the left decubitus position. The physician, the sonographer, and the echocardiographic system are all positioned on the left-hand side of the patient.[5] Artificial teeth or dentures are routinely removed. The flexion controls should be unlocked to allow for maximum flexibility of the probe when it is being inserted. The patient's head should be in a flexed position. The tip of the probe is kept relatively straight and gently advanced to the back of the throat. It should be maintained in a central position, because deviation to either side increases the likelihood that it may become lodged in the piriform fossa. The operator can facilitate this process by inserting one or two fingers into the patient's oropharynx to direct the path of the probe. Gentle pressure is exerted and the patient is instructed to swallow. The swallowing mechanism helps guide the probe into the esophagus. In older patients, cervical spondylosis with prominent protrusion into the posterior pharynx can create difficulty with passage of the probe.[5] Manually depressing the back of the tongue provides more room, allowing the TEE probe to assume a less acute angle and facilitating the intubation of the esophagus. If significant resistance is encountered when the probe is advanced, it is prudent to withdraw the probe and then initiate a new attempt. Esophageal intubation is more difficult with the multiplane probe than with the smaller monoplane and biplane probes.[9] [10] The latter can be used, if available, when esophageal intubation cannot be achieved with a multiplane probe. In experienced hands, the rate of failure of esophageal intubation should be less than 2%.[5] [9] [11]

A bite guard should always be used, except in edentulous patients. Our practice is to put it between the patient's teeth after the TEE probe has been successfully passed into the esophagus. Patients with a very sensitive pharynx may close their mouths involuntarily during esophageal intubation. In these patients, it is safer to insert the bite guard before the insertion of

the TEE probe. The patient should be instructed to keep the guard between the teeth throughout the procedure, and regular checks should be made to ensure that it is in the proper position to prevent damage to the probe or injury to the patient. Even when the probe is inserted without difficulties, it is not uncommon for the patient to develop nausea with or without mild retrosternal or abdominal discomfort. We find it useful to pause for 10 to 15 seconds to allow these symptoms to subside before proceeding with echocardiographic imaging. Our practice is to start with images acquired from the esophagus before advancing the probe into the stomach for the gastric views. The gastroesophageal sphincter is usually reached when the probe is advanced 40 cm from the teeth. Gentle pressure is all that is required to advance the probe through the gastroesophageal sphincter. The patient may again experience nausea and mild discomfort, and it may be advisable to pause momentarily for these symptoms to subside. Imaging of the proximal descending thoracic aorta and aortic arch is generally reserved for the end of the study, because the probe needs to be positioned in the upper esophagus and the patient is generally more aware of the probe at this position and tends to have more discomfort and gagging. Inadvertent passage of the probe into the trachea can occur, particularly in deeply sedated patients. The development of stridor and incessant cough should alert the operator of this possibility. Furthermore, it would be difficult to advance the probe beyond 30 cm from the teeth and the image quality is usually poor.[5] In patients on mechanical ventilation, esophageal intubation is more difficult. We usually introduce the probe with the patient lying supine, because the airway is protected and aspiration is unlikely. The probe is positioned behind the endotracheal tube and gently advanced. It is helpful to have the patient's mandible pulled forward when the probe is being advanced. If there is undue resistance at about 25 to 30 cm from the teeth, slight deflation of the cuff of the endotracheal tube can be considered to ease the passage of the probe. We do not usually remove the gastric tube, which can be used as a guide to help in the proper positioning and passage of the TEE probe. In a minority of intubated patients, successful esophageal intubation may be achieved only with direct laryngoscopy. Image Format There is no general agreement on how the imaging planes should be

displayed. Our preference is to orient the images such that the right-sided structures are on the left side of the screen and the left-sided on the right. The apex of the imaging plane with the electronic artifact is at the top of the screen. Thus, in the longitudinal views, superior structures are to the right of the screen and the inferior to the left.[12]

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TABLE 1-2 -- Standard Imaging Planes with Multiplane Transesophageal Echocardiography (TEE) at the University of Ottawa Heart Institute

Imaging View Basal

Fourchamber

Standard Imaging Plane Aortic valve

Angle of Imaging Array (degrees) 0–60

Atrial septum

90–120

Pulmonary bifurcation

0–30

Left ventricle

0–180

Mitral valve

0–180

Left ventricular outflow tract

120–160

Transgastric Left ventricle Mitral valve

0–150 0–150

Main Cardiac Structures Aortic valve, coronary arteries, left atrial appendage, pulmonary veins Fossa ovalis, superior vena cava, inferior vena cava Pulmonic valve, main and right pulmonary arteries, proximal left pulmonary artery Left ventricle (regional and global function), right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles, chords Aortic valve, ascending aorta, left and right ventricular outflow tracts, pulmonic valve, main pulmonary artery Left ventricle, right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles,

Aortic

Coronary sinus Descending thoracic aorta Aortic arch

0

chords Coronary sinus, tricuspid valve

0

Entire descending thoracic aorta

90

Aortic arch, arch vessels, left pulmonary artery

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Standard Imaging Planes Advances in TEE transducer technology have culminated in the development of the multiplane probe capable of two-dimensional and color flow imaging in multiple planes. The imaging plane can be steered electronically from 0 to 180 degrees by means of a pressure-sensitive switch, providing views unattainable by monoplane and biplane probes. The following discussion focuses only on standard imaging views routinely performed at the University of Ottawa Heart Institute using multiplane TEE (Table 1-2) . These views are considered "standard" because they have important clinical relevance and can be obtained in most patients with specific imaging planes. Four basic maneuvers are used to obtain specific tomographic views with TEE.[13] The first relates to the positioning of the probe by advancement or withdrawal of the probe. Although this is a simple maneuver, it is the most crucial, and the imaging views can be conveniently categorized according to the location of the TEE probe within the esophagus or stomach (Fig. 11) . The second maneuver involves rotation of the probe from side to side. This is particularly useful when using longitudinal imaging planes, which provide a better demonstration of the continuity between vertically aligned structures such as the superior vena cava and the arch vessels.[12] [13] Steering the imaging plane using the pressure-sensitive switch is the third maneuver to obtain different tomographic views. The ability to image cardiac structures from 0 to 180 degrees not only enhances understanding of cardiac anatomy but also provides a ready means for three-dimensional reconstruction. [14] [15] The fourth maneuver involves manipulation of the anterior-posterior and right-left flexion control knobs. The availability of a steerable imaging plane has drastically reduced the need to use the flexion knobs, but there are situations in which these knobs play a crucial role in obtaining proper tomographic views.[10] [13] The versatility of multiplane TEE provides an almost infinite number of

imaging planes. In our experience, it is useful to categorize them into four groups: basal, four-chamber, transgastric, and aortic views (see Fig. 1-1) . Table 1-2 summarizes the standard imaging planes and the cardiac structures evaluated in these four groups of views. Basal Views The basal group of views is obtained with the TEE probe located in the midesophagus. The base of the heart, Figure 1-1 Diagram showing the transesophageal echocardiography transducer locations for the four standard imaging views: basal (A), fourchamber (B), transgastric (C), and aortic (D).

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particularly the aortic valve, is well seen. The relationship of the two great arteries can be very well defined and followed cephalad to at least the level of the pulmonary bifurcation. Beyond this level, the interposing trachea make imaging impossible. Three tomographic planes are found to be particularly useful and are routinely performed at our laboratory. Aortic Valve

A short-axis view of the aortic valve can be obtained with the probe at about 30 to 35 cm from the teeth. The left coronary cusp often appears to have nodular thickening if the aortic valve is cut obliquely, which is often the case at 0 degrees.[12] Steering the imaging plane to 30 to 60 degrees should eliminate this artifact by providing an optimal short-axis view of the aortic valve (Fig. 1-2) . [13] A slight pull-back of the transducer should allow visualization of both the left and right coronary arteries. The left coronary artery can be followed to its bifurcation into the left anterior descending and circumflex arteries (Fig. 1-3) . The right coronary artery is more difficult to display, and usually only the proximal 2 to 3 cm is seen (Fig. 14) . Other structures well seen in this view are the left atrial appendage and the left pulmonary veins. The partition between these structures can be quite bulbous and should not be confused with an abnormal intracardiac mass (see Fig. 1-4) .[16] Rotating the probe to the right should reveal the right pulmonary veins.

We like the horizontal plane in imaging the four pulmonary veins. The left and right pulmonary veins are imaged separately. It is difficult to image the upper and lower pulmonary veins, left or right, in the same view because the veins are not located in the same plane with the lower pulmonary veins posterior and inferior to the upper pulmonary veins.[17] When one pulmonary vein is identified, a slight translational movement of the probe should bring out the other, because the orifices of the upper and Figure 1-2 The aortic valve was imaged with the imaging plane at about 60 degrees, showing the three cusps in systole. LA, left atrium; RA, right atrium; RV, right ventricle.

Figure 1-3 The left coronary artery (arrows) was imaged at 0 degrees. Ao, aorta; LA, left atrium.

lower pulmonary veins are in close proximity. The lower pulmonary veins run horizontal to the imaging plane, whereas the upper veins are more anterior and at an obtuse angle, making them more suitable for Doppler assessment. The right and left atrial appendages wrap around the great arteries anteriorly. The left atrial appendage is more prominent and can consist of multiple lobes.[18] A comprehensive interrogation using multiple imaging planes should be performed to exclude left atrial appendage thrombus in the appropriate clinical setting. The right atrial appendage is smaller and triangular in shape (Fig. 1-5) . The endocardial surfaces of both appendages are corrugated and should not be confused with small thrombi.[16] A long-axis view of the aorta can be achieved with the imaging plane at about 120 degrees. A more rightward imaging plane, such as 150 degrees, may be Figure 1-4 The proximal right coronary artery (small arrows) and the bulbous partition between the left atrial appendage and the left upper pulmonary vein (large arrow) are demonstrated. Ao, aorta; LA, left atrium.

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Figure 1-5 The atrial septum was preferentially imaged using the longitudinal plane to demonstrate its relation with the superior vena cava (SVC). LA, left atrium; RA, right atrium; RAA, right atrial appendage.

needed if the ascending aorta is dilated and tortuous. This view allows the visualization of a longer length of the ascending aorta and thus significantly reduces the blind spot caused by the interposing trachea. Atrial Septum

We prefer to image the atrial septum using the longitudinal plane at 90 to 120 degrees. The fossa ovalis, which is the thinnest part of the atrial septum, and the continuity of the superior vena cava with the right atrium are very well demonstrated in this view (see Fig. 1-5) . This view is particularly valuable in demonstrating the sinus venosus atrial septal defect, which is usually located just inferior to the entrance of the superior vena cava.[19] [20] The foramen ovale, if present, is located at the superior aspect of the fossa ovalis and is readily seen in this view. It is important to advance the probe to the level of the inferior vena cava so as not to neglect the inferior aspect of the atrial septum.[21] Careful sweep of the atrial septum with left-right rotation is needed to visualize the entire atrial septum. Continuous rotation from right to left will sequentially demonstrate the left ventricular outflow tract and the right ventricular outflow tract. Rotating the probe to the right shows the right upper pulmonary vein and provides parallel alignment for Doppler assessment. Pulmonary Bifurcation

The pulmonary bifurcation view is achieved by withdrawal of the probe with the imaging plane at 0 degrees. The pulmonic valve and main pulmonary artery are best seen slightly superior to the aortic valve (Fig. 16) . The pulmonic valve is thinner than the aortic valve and is usually difficult to image in a true cross section. Further slight withdrawal allows imaging the pulmonary bifurcation. The entire length of the right pulmonary artery but only the very proximal portion of the left pulmonary artery can be seen. The right pulmonary artery can usually be followed to its first bifurcation by rotation of the probe rightward, but this maneuver is better performed with the longitudinal plane at 90 degrees. Gradual rotation from left to right provides good visualization in cross section of the entire right pulmonary artery and its first bifurcation. This is an important view in

the detection of proximal pulmonary emboli.[22] [23] Four-Chamber Views Four-chamber views are obtained with the transducer within the middle to lower esophagus. It is difficult to image the left ventricle in its true long axis. Excessive anterior flexion should be avoided to prevent foreshortening of the ventricles. Indeed, to optimize visualization of the left ventricle, it is advisable to withdraw the probe slightly and at the same time attempt gentle retroflexion while maintaining adequate contact between the imaging surface and the esophagus. In the setting of a dilated and unfolded aorta, rotating the imaging plane to about 20 to 30 degrees may be necessary to obtain the four-chamber view without the aorta obscuring the tricuspid valve and part of the right ventricle. Left Ventricle

The inferior septum and anterolateral wall are usually seen in the fourchamber view (Fig. 1-7) . The left ventricular apex is difficult to visualize, particularly in patients with a dilated left ventricle. In addition to retroflexion, rightward flexion can often be helpful to minimize foreshortening of the left ventricle. Far-field imaging can be improved by decreasing the transmission frequency. A continuous sweep from 0 to 180 degrees should be performed to examine the different left ventricular segments Figure 1-6 The bifurcation of the main pulmonary artery (MPA) into the right (RPA) and left (LPA) pulmonary arteries was imaged using the transverse plane. Ao, aorta.

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Figure 1-7 The four-chamber view showing the left ventricle (LV) and mitral valve. LA, left atrium; RA, right atrium; RV, right ventricle.

so as to have a comprehensive assessment of left ventricular global and regional function (Fig. 1-8) .

Mitral Valve

The mitral valve is well seen using the four-chamber view, but the depth of the imaging plane should be reduced to enhance the resolution of the image ( see Fig. 1-7 and Fig. 1-8 ). To identify the individual scallops of the anterior and posterior mitral leaflets, a careful sweep from 0 to 180 degrees should be made. The technique of visualizing specific scallops of the mitral leaflets have been published,[24] but patient-to-patient variation should be kept in mind. The presence of a good long-axis view of the aortic valve and proximal ascending aorta, usually at Figure 1-8 The left ventricle and mitral valve can be comprehensively assessed by a continuous sweep of the imaging plane, which was about 100 degrees in this example. LA, left atrium; LV, left ventricle.

120 degrees, is a good indication that the middle scallops of both the anterior and the posterior mitral leaflets are imaged and provides the internal reference for the analysis of the other imaging planes. Both papillary muscles can be imaged but usually not in the same plane. The subvalvular chords are seldom completely imaged because they are frequently obscured by the mitral leaflets. The morphologic information obtained from this view should be corroborated by the short-axis view of the mitral valve obtained from the transgastric view, which also allows a better assessment of the subvalvular structures, including the papillary muscles and chords. Four-chamber views are ideal for the assessment of mitral regurgitation in relation to the number of regurgitant jets, the direction of the regurgitant jets, and the severity of regurgitation. [25] [26] Left Ventricular Outflow Tract

We like to image the left ventricular outflow tract at 120 to 160 degrees, because the outflow tract has a horizontal alignment in this plane that may allow optimal imaging even in the setting of a prosthetic aortic valve (Fig. 1-9) . The opening and closing of the aortic valve as well as the presence or absence of aortic regurgitation can be well visualized. The proximal ascending aorta is present in this view. A slight withdrawal of the probe will allow more of the ascending aorta to be visualized (Fig. 1-10) . A slight rotation to the left will show the right ventricular outflow tract with the thin pulmonic valve. Both the motion of the pulmonic valve and the presence or absence of pulmonic regurgitation can be adequately assessed

using this view. Transgastric Views There is slight resistance during the passage of the TEE probe through the gastroesophageal junction, and the Figure 1-9 The left ventricular outflow tract was well seen with the imaging plane at about 120 degrees. Ao, aorta; LA, left atrium; LV, left ventricle; RVOT, right ventricular outflow tract.

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Figure 1-10 Slight withdrawal of the probe relative to the probe position used to acquire the image shown in Figure 1-9 showed the right pulmonary artery (RPA) in short axis and more of the ascending aorta (Ao). LA, left atrium.

appearance of the liver is a clear indication that the probe is in the stomach. Anterior flexion, often with leftward rotation and flexion, is required to achieve good contact between the imaging surface and the gastric wall. Extreme anterior flexion with further advancement of the probe can sometimes produce images similar to the five-chamber views obtained from the subxiphoid surface approach. Left Ventricle

Multiple cross sections of the left ventricle can usually be obtained using the transgastric approach ( Fig. 1-11 and Fig. 1-12 ). These are the views commonly used in the intraoperative assessment of left ventricular function.[24] Optimization of the short-axis views of the left ventricle Figure 1-11 Transgastric short-axis view of the left ventricle (LV) at the papillary muscle level.

Figure 1-12 Transgastric long-axis view of the left ventricle (LV) with

visualization of the apex.

can be achieved with leftward rotation accompanied by leftward flexion. To visualize the left ventricular apex, gentle advancement of the probe is required together with slight retroflexion. In our experience, the short-axis view of the left ventricular apex can be obtained in about 60% of cases. Another way to visualize the left ventricular apex is to use the longitudinal plane at about 90 degrees (see Fig. 1-12) . Careful lateral rotation can be used to obtain comprehensive regional assessment of the left ventricle. Leftward rotation of this imaging plane can yield a good alignment with the left ventricular outflow tract and aortic valve to allow accurate measurement of the transaortic pressure gradients in the setting of aortic stenosis (Fig. 1-13) . [27] The right ventricle can be seen with rightward rotation of the probe. Both short- and long-axis views of the tricuspid valve are achievable, although Figure 1-13 Transgastric transesophageal echocardiography approach to assess the severity of aortic stenosis using continuous wave Doppler echocardiography.

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the tricuspid valve and its papillary muscles are better assessed with the long-axis plane. Mitral Valve

The mitral valve can be best assessed using the horizontal imaging plane with the transducer brought up to near the gastroesophageal junction (Fig. 1-14) . Anterior flexion and leftward flexion are usually required to optimize this view. Adjusting the imaging plane to about 20 degrees will help to bring out the lateral commissure. This view provides unambiguous assessment of the individual scallops of both the anterior and posterior mitral leaflets and thus should be attempted in all patients with myxomatous mitral valve degeneration. In our experience, this view is achievable in about 70% of patients. Both the papillary muscle and chords can be demonstrated, and the continuity between these structures and the mitral leaflets is best seen in the long-axis plane. Coronary Sinus

The coronary sinus comes into view when the probe is withdrawn to be near the gastroesophageal junction and the flexion knobs are in relatively neutral positions (Fig. 1-15) . This view can also be achieved by retroflexion with the probe in the lower esophagus. The coronary sinus is seen as a vascular structure located posterior to the left ventricle at the atrioventricular groove draining into the right atrium. The tricuspid valve can be visualized to the right and anterior. A dilated coronary sinus should raise the possibility of the presence of a persistent left superior vena cava, which is the most common cause. Leftward rotation while following the coronary sinus may sometimes demonstrate this anomalous vein. In the esophageal views, the left superior vena cava is usually sandwiched between the left atrial appendage and the left upper pulmonary vein.[28] Figure 1-14 The mitral valve was demonstrated in the short axis showing the anterior (arrows) and posterior (arrowheads) mitral leaflets.

Figure 1-15 The coronary sinus (CS) was demonstrated with the probe at the gastroesophageal junction. LV, left ventricle; RV, right ventricle.

Aortic Views The thoracic aorta is well assessed by TEE because of its close proximity to the esophagus. Descending Thoracic Aorta

The best way to assess the descending thoracic aorta is to use the horizontal imaging plane with the transducer rotated leftward and posterior, followed by slow withdrawal from the level of the diaphragm to the aortic arch (Fig. 1-16) .[16] Because of the relationship between the Figure 1-16 The descending aorta was imaged in the short axis to allow good visualization of entire circumference.

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Figure 1-17 The aortic arch (AA) was imaged using the longitudinal plane, showing the origin of the left subclavian artery (LSA).

esophagus and the aorta, slight rotational adjustment is required to visualize the entire circumference of the aortic wall as the probe is slowly withdrawn.[29] If the aorta is dilated or tortuous, proper short-axis views of the descending aorta will require adjustment of the imaging plane by 0 to 90 degrees. Aortic Arch

The longitudinal imaging plane at 90 degrees is preferred in imaging the aortic arch because it allows visualization of the entire circumference of the aorta (Fig. 1-17) .[29] Anterior rotation of the longitudinal plane should visualize the entire aortic arch, but the proximal aortic arch may not be visualized when the aortic arch is unfolded. The transducer will need to be withdrawn slightly to image the arch vessels, which course superiorly. In one third of patients, all three arch vessels can be imaged, but in the other two thirds of patients, only the two distal arch vessels can be imaged. It is rare not to be able to image at least one arch vessel. As a rule, the brachiocephalic artery, which is anterior and more rightward, is the most difficult to image because of the interposing trachea. The transverse plane in a more superior location may sometimes show the three arch vessels in their short axis. Advancing the probe by 1 to 2 cm so that the imaging plane is just inferior to the aortic arch can frequently image the proximal left pulmonary artery. It is sometimes possible to follow it to the first bifurcation. This view should be sought in the assessment of patients suspected of having pulmonary embolism.

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Doppler Examination Transesophageal echocardiography can be used to assess the flow patterns across the four cardiac valves, but it does not provide additional information to TTE. Furthermore, good alignment with the transvalvular flows may not be feasible because of the anatomic confines of the esophagus. On the other hand, intracardiac flows such as pulmonary vein flow and left atrial appendage flow are best evaluated by TEE and provide important insight into intracardiac hemodynamics. Pulmonary Vein Flow The pulmonary veins are imaged from the midesophagus level. Pulmonary vein flow can be assessed by placing the pulsed Doppler = sample=20 volume 0.5 to 1.0 cm into the pulmonary veins. The anterior to posterior = direction of the left and right upper pulmonary veins allows the Doppler = ultrasound beam to be aligned parallel to blood flow. This often cannot = be=20 achieved when interrogating the left and right lower pulmonary = veins. The normal pulmonary venous flow pattern can be = divided=20 into three phases: (1) antegrade systolic flow, (2) antegrade diastolic = flow,=20 and (3) retrograde atrial contraction flow reversal (F= ig.=20 1-18) . Two phases of antegrade systolic flow can usually be = appreciated on=20 transesophageal study. Systolic flow is dependent on apical displacement = of the=20 annulus, which is predominantly determined by left ventricular function, = atrial=20 relaxation, and atrial compliance.[3= 0]=20 [3= 1]=20 Left atrial pressure also affects antegrade systolic flow, with = increases in=20 left atrial pressure reducing systolic flow.[3= 0]=20 [3= 1]=20 Mitral regurgitation increases left atrial pressure during systole and = may=20 result in systolic flow reversal in one or all pulmonary=20 veins.[3= 0]=20 [3= 1] =20 Diastolic antegrade flow occurs as the mitral valve opens and left = atrial=20 pressure falls. The diastolic flow profile is dependent on left atrial = pressure,=20 left ventricular relaxation, and ventricular compliance. = [3= 0] =20 [3= 1]=20 Atrial contraction flow reversal is dependent on atrial contractility, = atrial=20 systolic pressure, and left ventricular compliance. The normal pulmonary = venous=20 flow pattern is dependent on heart rate and age.[3= 1]=20 [3= 2]=20 Higher systolic pulmonary venous flow velocities, higher atrial reversal = velocities, and smaller diastolic flow velocities=20

Figure = 1-18 Normal pulmonary venous flow showing two antegrade = flows in=20 ventricular systole and diastole, with a diminutive retrograde flow = caused by=20 atrial contraction. .

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patients younger than 50 years of=20 age.[3= 1]=20 [3= 2]=20 Left Atrial Appendage Flow The left atrial appendage can be imaged from = the=20 midesophagus

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aortic valve short-axis view (30 to 60 degrees) or the = midesophagus=20 two-chamber view (80 to 100 degrees). Left atrial appendage flow should = be=20 recorded by positioning the color flow sector over the left atrial = appendage and=20 placing the pulsed-Doppler sample volume at the site of maximal flow = velocity.=20 This usually occurs in the proximal or middle third of the left atrial=20 appendage. Velocity recordings from the distal third of the left atrial=20 appendage frequently incorporate wall motion artefacts and are usually=20 unsatisfactory. Low-velocity flow may be present, and wall filters = should be set=20 low. The pattern of left atrial appendage flow is = dependent on=20 cardiac rhythm.[3= 3]=20 In patients with sinus rhythm, four left atrial appendage flow waves = have been=20 described (F= ig.=20 1-19) : (1) a large positive wave after the electrocardiographic = P-wave,=20 which represents left atrial appendage contraction and emptying; (2) a = large=20 negative early systolic wave immediately following the QRS complex = representing=20 left atrial appendage filling; (3) alternating positive and negative = waves of=20 decreasing velocity throughout the remainder of systole representing = passive=20 flow in and out of the appendage; and (4) a low-velocity positive = emptying wave=20 in early diastole coinciding with rapid left ventricular filling. In = addition, a=20 low-velocity middiastolic negative filling wave representing appendage = filling=20 from the pulmonary veins may follow the early diastolic atrial appendage = emptying wave. The normal velocities are as follows: left atrial = appendage=20 contraction, 60 =B1 14; left atrial appendage filling, 52 =B1 13; and = early=20 diastolic filling, 20 =B1 11 cm per second.[3= 3]=20 [3= 4] =20 In patients with atrial fibrillation, a regular = atrial=20 contraction wave is absent. However, the left atrial appendage continues = to=20 contract, resulting in irregular oscillating positive and negative = emptying and=20 filling waves with variable velocities. The velocities are usually = larger during=20 ventricular diastole when the mitral valve is open, and=20

Figure = 1-19 Normal left atrial appendage flow pattern in sinus = rhythm,=20 showing prominent atrial emptying and filling = velocities.

smaller during systole when the mitral valve is closed. = Of note,=20 mean left atrial appendage velocities tend to be lower with higher heart = rates=20 because of the smaller proportion of time spent during diastole.

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The = early=20 diastolic appendage emptying wave, which coincides with early rapid left = ventricular filling, may still be visualized in atrial fibrillation. In = patients=20 with atrial flutter, the velocity waves are more regular and tend to be = of=20 greater velocity because of the slower atrial contraction rate.=20 Factors other than cardiac rhythm that may = affect left=20 atrial appendage velocities have recently been reviewed and include age, = heart=20 rate, left atrial contractility, left atrial pressure, left ventricular = systolic=20 and diastolic function, mitral stenosis, and mitral=20 regurgitation.[3= 3]=20 The potential clinical utility of assessing = left atrial=20 appendage velocities relates to the association of left atrial appendage = velocities with left atrial spontaneous echo contrast and left atrial = appendage=20 thrombus.[3= 3]=20 [3= 5]=20 [3= 6]=20 Atrial fibrillation patients with a left atrial appendage contraction = velocity=20 of less than 20 cm per second are more likely to have left atrial = appendage=20 thrombus and have a greater risk of ischemic stroke compared with = patients with=20 left atrial appendage velocities of 20 cm per second or=20 greater.[3= 5]=20 [3= 6]=20 Lower left atrial appendage velocity has also been observed in stroke = patients=20 with normal sinus rhythm.[3= 7]=20 Other potential utilities may relate to an ability of left atrial = appendage=20 velocities to predict the success of maintaining sinus rhythm following=20 cardioversion of atrial fibrillation.[3= 3]=20 [3= 8]=20 Coronary Artery Flow The assessment of coronary artery flow may be = limited by=20 motion of the heart during the cardiac cycle and difficulties aligning = the=20 Doppler ultrasound beam parallel to coronary blood flow. Coronary artery = blood=20 flow and coronary artery blood flow reserve are best measured in the = distal left=20 main coronary artery or proximal left anterior descending artery using = the=20 midesophagus aortic valve short-axis view, in which the pulsed-Doppler=20 ultrasound beam can be aligned parallel to coronary blood flow. The = ultrasound=20 beam can only rarely be aligned parallel to flow in the left circumflex = artery,=20 and the right coronary artery cannot be imaged in up to half of all = patients.=20 The normal Doppler flow signal is characterized by a large diastolic = component=20 and small systolic component moving away from the transducer. In = general, normal=20 diastolic velocities are 60 cm per second or less, and diastolic = velocities=20 greater 100 cm per second

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suggest significant obstruction in the=20 artery.[3= 9]=20 [4= 0]=20 [4= 1]=20 Additionally, coronary artery flow reserve can be assessed by measuring = peak or=20 mean diastolic coronary flow velocities at rest and then following = dipyridamole=20 or adenosine infusion. [4= 0]=20 [4= 2]=20 Transaortic and Transpulmonary Flow Transaortic flow can be assessed by imaging the = left=20 ventricular outflow tract and aortic valve in the transgastric long-axis = view=20 (100 to 135 degrees) or deep transgastric long-axis view (0 degrees), in = which=20 the probe is=20 12

advanced deep into the stomach = adjacent=20 to the left ventricular apex and anteflexed until the imaging plane is = directed=20 superiorly to the base of the heart. In these views, the pulsed-Doppler = or=20 continuous wave Doppler beam can be aligned parallel to blood flow to = measure=20 transaortic velocity. Stroke volume can be derived with the additional=20 measurement of either the midesophagus left ventricular outflow tract = diameter=20 or the short-axis aortic valve orifice area at valve leaflet=20 level.[4= 3]=20 [4= 4]=20 In patients with aortic stenosis or other forms of left ventricular = outflow=20 tract obstruction, the transvalvular pressure gradients can be derived = using the=20 simplified Bernoulli equation and continuous wave Doppler signals = obtained from=20 the transgastric longaxis or deep transgastric long-axis view.=20 [2= 7]=20 Transpulmonary flow has been measured by = combining either=20 pulsed Doppler or continuous wave Doppler velocity measurements of = pulmonary=20 artery flow obtained from mid-esophagus short- axis images of the main = pulmonary=20 artery and measurements of the main pulmonary artery=20 diameter.[4= 5]=20 [4= 6]=20 Transmitral and Transtricuspid Flow In the midesophageal four-chamber view or = long-axis view,=20 the pulsed Doppler ultrasound beam can be aligned parallel to = transmitral flow=20 to accurately measure transmitral filling velocities. The pulsed Doppler = sample=20 volume should be kept small (3 to 5 mm) and positioned at the mitral = valve=20 leaflet tips for the evaluation of diastolic function and filling=20 pressures.[3= 0]=20 In contrast, transmitral stroke volume is measured by placing the sample = volume=20 at the mitral

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valve annulus, so that velocity and annular dimensions are = measured at the same location.[4= 7]=20 [4= 8]=20 Transtricuspid filling can be assessed by = pulsed Doppler=20 measurements obtained in the midesophageal four-chamber view. However, = it is=20 frequently not possible to align the Doppler ultrasound beam parallel to = blood=20 flow. The transtricuspid filling pattern is similar to the transmitral = filling=20 pattern, although lower velocities are present.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Indications for Transesophageal Echocardiography The potential utility of TEE in the assessment and management of patients with suspected and overt cardiac disease is wide-ranging and encompasses the spectrum of cardiac problems encountered in clinical cardiology. TEE can be performed on patients in the ambulatory setting, intensive care unit, coronary care unit, or operating room. In general, TTE should be employed as the initial diagnostic investigation, as this technique is noninvasive and will entail no risk to the patient. Patient factors such as obesity, emphysema, or chest deformities frequently limit ultrasound penetration, resulting in nondiagnostic TTE studies. Surgical bandages may limit the number of available acoustic windows, and mechanical ventilation and surgical devices, such as traction and intra-aortic balloon pumps, may limit the ability to properly position the patient. Subcutaneous emphysema may result in the complete TABLE 1-3 -- Common Indications for Transesophageal Echocardiography Nondiagnostic transthoracic echocardiogram Assessment of native valve disease Assessment of prosthetic valves Assessment of infective endocarditis Assessment of a suspected cardioembolic event Assessment of cardiac tumors Assessment of atrial septal abnormalities Assessment of aortic dissection, intramural hematomas, and aortic rupture Evaluation of congenital heart disease Detection of anatomic coronary artery disease Stress echocardiography

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Evaluation of pericardial disease Evaluation of critically ill patients Intraoperative monitoring Monitoring during interventional procedures inability of TTE to visualize cardiac structures. TEE should be considered in these patients to obtain the necessary diagnostic information. Despite an adequate TTE study, TEE may be indicated to assess cardiac structures not usually seen by TTE, such as the superior vena cava, pulmonary veins, and the descending thoracic aorta, or to provide improved anatomic details such as the detection of flail mitral valve leaflet scallops and valvular vegetations, which are not consistently detected by TTE. Finally, TEE has important applications in the operating room, which are discussed in Chapter 2 and Chapter 19 . The common clinical indications for TEE are given in Table 1-3 . Native Valve Disease The presence, etiology, and severity of native valve disease can usually be determined by TTE. TEE should be reserved for the clinical situation in which TTE findings are inconclusive or a more precise characterization of the valve lesion will alter the patient management plan. Excellent visualization of the mitral valve anatomy is possible by TEE because of the close proximity of the mitral valve to the TEE transducer and the ability to image with high-frequency transducers. The mitral annulus, leaflets, chordal structures, and papillary muscles can all be visualized and evaluated. The use of a multiplane transducer allows a comprehensive, detailed examination of the valve to determine the location and mechanism of mitral regurgitation (see Chapter 19) . Ruptured chordae tendineae can be visualized, and precise anatomic localization of prolapsing or flail leaflet scallops is possible to predict the potential for successful mitral valve repair.[25] [49] [50] Abnormalities of the papillary muscles, such as a partial or complete rupture, are better visualized by TEE than TTE.[51] The severity of mitral valve regurgitation can be quantified using the methods employed for TTE,[52] but color Doppler velocity regurgitant jet areas tend to be larger in size on TEE than TTE because higher transducer frequencies are used and because of the close proximity of the transducer to

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the regurgitant jet.[53] Pulmonary vein flow can be assessed in nearly all patients and provides 13

a valuable measure of mitral regurgitation severity.[54] [55] Regurgitant vena contracta width, regurgitant volumes, and regurgitant orifice areas using the proximal flow convergence zone can be obtained by TEE.[56] [57] In mitral stenosis, TTE is usually satisfactory in assessing the valve morphology and severity of stenosis (see Chapter 20) . TEE appears equivalent to TTE in assessing valve mobility and leaflet thickening, but subvalvular disease and calcification may be underestimated owing to the shadowing effect of thickening and calcification of the mitral leaflets and annulus in the esophageal views.[58] Transvalvular pressure gradients can be measured by aligning the continuous wave Doppler beam parallel to left ventricular inflow through the mitral valve in the midesophageal views.[59] Effective orifice areas can be derived by the pressure half-time method,[59] the proximal flow convergence method, or orifice planimetry.[60] Orifice planimetry requires a tomographic cut of the distal or most narrow mitral orifice, however, which is technically more difficult to obtain by TEE and frequently not possible. The potential suitability of a patient for percutaneous balloon mitral valvuloplasty usually incorporates a detailed TEE assessment of the left atrial chamber and appendage to identify thrombus, in addition to an evaluation of the mitral valve morphology score and mitral regurgitation severity.[61] Transthoracic echocardiography can adequately visualize most aortic valve abnormalities, and only rarely is TEE required for assessment. However, subvalvular abnormalities such as subaortic membranes frequently require TEE for definitive diagnosis. [62] The assessment of aortic regurgitation severity only rarely necessitates a TEE evaluation (see Chapter 17) . Standard Doppler methods used for TTE may be employed using TEE.[63] One of the best measures, the ratio of color jet area to left ventricular outflow tract area, can be obtained from esophageal short-axis images of the outflow tract immediately inferior to the aortic valve. Jet height to outflow tract height can be obtained from esophageal long-axis images. Holodiastolic flow reversal in the descending aorta is always present with severe aortic regurgitation and can be detected by biplane or multiplane TEE using pulsed Doppler.[64] Aortic regurgitation severity may also be quantified by TEE using proximal flow convergence methods and vena

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contracta width.[65] [66] The severity of aortic stenosis is best quantified using transvalvular pressure gradients or valve areas derived by TTE (see Chapter 22) . Continuous wave Doppler interrogation of the aortic valve is possible by TEE using the transgastric long-axis view (100 to 135 degrees) or deep transgastric long-axis view (0 degrees) in which the probe is advanced deep into the stomach adjacent to the left ventricular apex and anteflexed until the imaging plane is directed superiorly to the base of the heart (see Fig. 113) . Good correlations between TTE and TEE gradients have been reported, despite the limited TEE windows.[27] Anatomic orifice area can be derived by planimetry of the maximum systolic aortic valve orifice visualized from esophageal short-axis images. Proper transducer position should be confirmed by rotating to the longitudinal plane and verifying that the leaflet tips are being imaged. Aortic valve areas derived by orifice planimetry correlate well with valve areas derived by TTE using the continuity equation and Gorlin equation valve areas.[27] , [67] [68] Valve calcification may affect the accuracy of TEEmeasured orifice areas.[69] Importantly, orifice planimetry is often more feasible and accurate using multiplane than biplane TEE.[68] Prosthetic Valves Transesophageal echocardiography is an extremely valuable technique in the assessment of prosthetic valve function, because TTE visualization of the prosthetic valve components and function is often limited by the echogenicity of the prosthetic components (see Chapter 24 and Chapter 25) . Reverberation artifacts, attenuation artifact, and acoustic shadowing obscure visualization of the prosthetic components and limit the visualization of structures beyond the prosthesis. Thickening and calcification of the leaflets, or the presence of a torn or flail bioprosthetic leaflet, are better appreciated on TEE. The structure and motion of the occluding device of a mechanical prosthesis may also be better evaluated. TEE provides increased sensitivity for detecting abnormalities of bioprosthetic and mechanical prostheses when compared to TTE.[70] [71] Small abnormalities of prosthetic valves such as leaflet thickening, flail leaflets, vegetations, thrombi, and filamentous strands can be missed on TTE but appreciated on TEE.[70] [71] [72] [73] [74] [75] [76] [77] TEE can be used to distinguish pannus from thrombus formation[78] and to guide thrombolytic therapy use in patients with the latter condition.[79] TEE is especially valuable in assessing mitral prostheses, as the transducer's posterior

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position provides excellent visualization of vegetations and thrombi, which usually locate on the left atrial aspect of the prosthesis.[70] [73] However, the ventricular aspect of a mitral prosthesis may not be adequately seen, and so TTE should complement the TEE assessment. [80] Transesophageal echocardiography can differentiate between normal variant and pathologic prosthetic valve regurgitation.[71] [72] [73] [74] [75] [81] Prosthetic mitral regurgitation is frequently better evaluated by TEE than TTE,[71] [72] [74] because TEE provides excellent visualization of the left atrial cavity without any intervening prosthetic material. TEE should be performed in patients in whom significant mitral regurgitation is not seen on TTE but is a clinical concern. Importantly, TEE allows characterization of mitral regurgitation jets as paravalvular or transvalvular in origin, which may modify the surgical procedure.[72] [74] [82] Multiplane TEE appears to better delineate paraprosthetic mitral regurgitation as compared with biplane TEE.[82] The incremental benefit of TEE in the assessment of regurgitation severity is less clear for aortic prostheses because the aortic regurgitation jet is usually well seen on TTE, and TEE visualization of prosthetic aortic regurgitation may be compromised by partial obstruction of the aortic regurgitation jet by either a mitral or aortic prosthesis in the esophageal views.[75] All bioprostheses and mechanical prostheses are inherently stenotic. The degree of stenosis is dependent on the prosthesis type and size and the presence of an associated pathologic condition such as leaflet calcification, pannus formation, or valve thrombosis.[83] In general, TTE is sufficient to assess the severity of prosthetic aortic or mitral 14

stenosis, but only TEE has sufficient resolution to distinguish these pathologic conditions.[78] In patients with inadequate TTE findings, TEE can quantify prosthetic mitral stenosis by measuring diastolic pressure gradients, pressure half-time, and effective orifice area using the proximal flow convergence method, as described for native mitral stenosis.[60] [84] Prosthetic aortic stenosis can be assessed by measuring transvalvular pressure gradients, as described for native aortic stenosis. [27] Importantly, flow through certain mechanical aortic prostheses results in localized pressure gradients and significant pressure recovery, which may lead to a discrepancy between Doppler and catheterization pressure gradients and an apparent "overestimation" of Doppler gradients.[85]

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Infective Endocarditis The presence of a vegetation is a hallmark finding of infective endocarditis, and its identification in the clinical setting of suspected endocarditis confirms the diagnosis[86] (see Chapter 21) In native valve endocarditis, the sensitivity of TTE for the detection of vegetations was 28% to 63%, and the sensitivity of TEE was 86% to 98%. [87] [88] [89] [90] [91] The specificity of the TTE and TEE findings for a vegetation appears similar and exceeds 90% when strict echocardiographic criteria are used for diagnosis.[87] [88] [90] Smaller vegetations are more likely to be detected by TEE than TTE.[88] Isolated case reports have suggested that pulmonic valve vegetations may also be better seen by TEE.[92] TEE does not appear to have an increased sensitivity compared with TTE, however, in the detection of tricuspid valve vegetations.[93] Prosthetic valve endocarditis is more difficult to diagnose using either TTE or TEE. The reported sensitivity of TTE for detecting vegetations was 0 to 43%, and the sensitivity of TEE was superior at 33% to 86%.[70] [89] [94] , [95] Thus, TEE should be performed in patients with suspected prosthetic valve endocarditis if the TTE procedure does not identify a vegetation. Although TEE has an improved sensitivity for detecting vegetations compared with TTE, the impact of TEE on diagnosis appears to be greatest in patients with suspected endocarditis with an intermediate clinical probability of endocarditis, especially patients with prosthetic valves.[96] Importantly, the absence of a vegetation on TEE makes the diagnosis of endocarditis unlikely (<10%), and alternative diagnoses should be considered.[95] [97] However, false-negative TEE studies have been reported, and patients with a high index of suspicion of endocarditis, prosthetic valves, or a persistent bacteremia may benefit from follow-up TEE if the initial study was negative.[95] [97] The complications of infective endocarditis, including abscess formation, leaflet diverticula, leaflet perforation, fistula tracts, mycotic aneurysms, and pseudoaneurysm formation, are better detected by TEE than TTE.[89] [98] [99] [100] [101] In a large series of patients with infective endocarditis, only 28% of surgically or autopsy confirmed abscess cavities were identified by TTE, as opposed to an 87% detection rate by TEE.[98] The specificity of both techniques in the detection of abscess formation exceeded 90%. Thus, patients with a suspected abscess based on clinical grounds or persistent bacteremia should undergo TEE.

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The role or potential utility of TEE in uncomplicated confirmed endocarditis is controversial. TEE may provide the clinician with prognostic information. Larger, mobile vegetations on TEE are associated with systemic embolization.[91] Additionally, complications including embolism, abscess formation, need for valve replacement, and death may be more likely to occur in patients with a vegetation that fails to decrease in size with therapy.[102] At this time, we do not perform routine follow-up TEE for cases of uncomplicated confirmed endocarditis. Suspected Cardioembolic Event The potential for a cardioembolic event should be considered in patients suffering cerebral ischemia or a peripheral arterial embolus. The Cerebral Embolism Task Force has suggested that cardiac emboli account for 15% of cerebral ischemic events.[103] Several cardiac abnormalities have a strong association with cardioembolic events and are considered a major risk source (see Chapter 37) . These abnormalities include atrial fibrillation, left atrial or left ventricular thrombi, vegetations, intracardiac tumor, mitral stenosis, mechanical valves, recent myocardial infarction, dilated cardiomyopathy, and intra-aortic debris.[104] Minor risk sources with weaker associations include cardiac abnormalities such as atrial septal aneurysms, patent foramen ovale, spontaneous echo contrast, mitral annular calcification, and mitral valve prolapse.[104] Many of these conditions can be diagnosed by clinical assessment, but echocardiography is frequently required for the diagnosis of many of the anatomic abnormalities. Approximately 7% of patients with a suspected cardioembolic event will have left atrial thrombus in the absence of atrial fibrillation and mitral stenosis. [105] The thrombus is frequently located in the left atrial appendage, a region poorly visualized on TTE. The sensitivity of TTE in detecting left atrial thrombus has been reported to be only 0 to 53%, whereas TEE has a sensitivity of 93% to 100% and a specificity exceeding 95%.[106] [107] In contrast, left ventricular thrombi may be better appreciated by TTE than TEE because of the close proximity of the left ventricular apex to the TTE transducer and the far field position and frequent apical foreshortening of the left ventricular apex on TEE.[108] However, TEE assessment may be beneficial if the TTE findings are inconclusive. [109] Left atrial spontaneous echo contrast is rarely appreciated on TTE, but well seen on TEE because of the close proximity of the left atrium to the TEE transducer and use of higher frequency transducers.[110] TEE may better detect small myxomas and aid in the diagnosis and management by better characterizing the

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attachment site.[111] [112] Similarly, TEE is superior in the detection of patent foramen ovale and atrial septal aneurysms.[113] [114] The size of the patent foramen ovale is associated with the cardioembolic risk and can better be appreciated by TEE.[115] A comprehensive characterization of aortic arch atheroma is rarely possible by TTE alone and requires TEE assessment.[35] [116] [117]

The indication for performing a TEE in patients with a suspected cardioembolic event is controversial. Although TEE has a better sensitivity than TTE for detecting potential 15

cardioembolic abnormalities, the yield for identifying a major risk source is limited. An analysis of pooled data from more than 30 cross-sectional studies suggested an overall detection rate for intracardiac masses of 4% for TTE and 11% for TEE.[104] However, the yield was greater in patients with evidence of cardiac disease. TTE and TEE identified an intracardiac mass in 13% and 19% of patients with cardiac disease and only 0.7% and 1.6% in patients without cardiac disease, respectively. In addition, the information obtained by TEE, which may include the identification of minor risk sources, may not significantly alter patient management.[104] [118] Many management decisions will be predetermined by the clinical setting (e.g., the patient with atrial fibrillation requires anticoagulation), and the management of patients with minor-risk cardiac abnormalities is frequently controversial. Thus, TEE should only be performed if the results have a reasonable chance of altering patient management or therapy. In this regard, TEE may have the greatest impact on patient management in the clinical setting of patients younger than 55 years of age with unexplained cerebral ischemia, in patients having recurrent events, or in patients with suspected endocarditis. Atrial Septal Abnormalities Transesophageal echocardiography provides excellent visualization of the atrial septum because of the atrial septum's close proximity to the transducer and perpendicular orientation to the ultrasound beam. Abnormalities of the atrial septum, including atrial septal defects, atrial septal aneurysms, and patent foramen ovale, are identified more frequently by TEE than by TTE.[19] [113] [114] , [119] [120] Sinus venosus defects and associated anomalous pulmonary venous drainage are frequently not

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identified on transthoracic imaging but can be easily detected on TEE study. [19] [20] TEE can be used to assess the severity of left-to-right shunting across the defect, determine the potential for percutaneous closure by accurate localization and characterization of the defect, and be used to assist in proper device placement during percutaneous closure.[121] [122] TEE can also detect thrombus formation within an atrial septal aneurysm and paradoxic emboli across an atrial septal defect.[115] [120] Cardiac Tumors For detecting intracardiac tumors, TEE appears superior to TTE, computed tomography, angiography, and magnetic resonance imaging.[112] [123] The sensitivity of TTE and TEE for the detection of atrial myxomas has been reported to be 95% and 100%, respectively.[123] Nonmyxomatous intracardiac tumors are identified by TTE and TEE in 91% and 100% of patients, respectively.[123] Pericardial or paracardial tumors are detected in only 67% by TTE and 97% by TEE.[123] TEE appears especially valuable in the detection of tumors located at the base of the heart, adjacent to the great vessels, or adjacent to the right heart.[112] [123] In addition, TEE is superior to TTE in characterizing features of a cardiac tumor that may assist in the diagnosis and management, such as the involvement of multiple chambers, the site of tumor attachment, the presence of multiple tumors, infiltration of adjacent structures, tumor calcification, or cyst formation.[112] [123] TEE has been used to guide percutaneous biopsy of intracardiac tumors.[124] However, the size and extent of paracardial involvement is not well assessed by TTE or TEE. In this setting, tomographic imaging with a wider field of view (magnetic resonance imaging or computed tomography) is needed. Aortic Dissection, Intramural Hematoma, and Rupture Aortic dissection can be detected by TEE with a high degree of accuracy and is the diagnostic investigation of choice for suspected aortic dissection in many institutions (see Chapter 3) . [125] The ascending aorta, aortic arch, and descending thoracic aorta can be visualized with excellent resolution owing to the close proximity of the aorta to the transducer and the use of high-frequency transducers. Importantly, a small segment of the superior ascending aorta cannot be visualized using TEE owing to the interposition of the air-filled trachea and bronchus. The sensitivity of monoplane and biplane TEE for the diagnosis of aortic dissection has been reported to be 97% to 100%, with a specificity that has ranged from 77% to 100%.[125] [126] [127] [128] The specificity was found to be greater than 95%, except in one

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study.[126] Multiplane TEE has been associated with similar sensitivities and specificities of 98% to 100% and 94% to 95%, respectively.[129] [130] The sensitivity and specificity of TEE compares favorably with those of other technologies, including aortography, computed tomography, and magnetic resonance imaging.[126] [127] [128] In addition to diagnosis, TEE can determine the extent of the dissection, differentiate the true and false lumens, identify thrombus within the false lumen, identify the site of the intimal tear, and assess for aortic valve involvement. [125] , [126] Involvement of the arch vessels and coronary arteries can also be determined.[125] Additionally, TEE can detect findings of aortic rupture, such as a pericardial effusion, pleural effusion, or mediastinal hematoma, which may significantly alter surgical therapy.[125] Aortic complications after repair may also be detected.[131] Associated aortic abnormalities, such as intramural hematoma and penetrating aortic ulcers, may have a similar presentation to aortic dissection and can be diagnosed using TEE.[128] [129] [132] TEE appears to have a high sensitivity and specificity for the detection of intramural hematoma, [129] but the diagnostic accuracy in the detection of penetrating aortic ulcers is unclear. In the largest series of 12 patients, penetrating aortic ulcers were identified by TEE in 83% of patients.[132] Transesophageal echocardiography has been used in the setting of chest trauma for the diagnosis of traumatic aortic rupture. The reported sensitivity and specificity for the detection of traumatic aortic rupture has ranged from 63% to 100% and 84% to 100%, respectively.[117] [133] However, TEE cannot consistently visualize the superior ascending aorta and aortic arch branch vessels, a frequent site of traumatic injury.[134] Thus, the role of TEE in the diagnostic evaluation of chest trauma patients remains undefined. Congenital Heart Disease

16

Transesophageal echocardiography commonly adds information to the preoperative, intraoperative, and postoperative assessment and management of patients with congenital heart disease[135] [136] (see Chapter 39 , Chapter 40 , Chapter 41 ). TEE can better appreciate abnormalities of the atrial septum and pulmonary veins, and it can be used to guide percutaneous

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closure of atrial septal defects.[19] [20] [119] , [121] [122] [124] In patients with atrioventricular canal defects, the atrioventricular valves and site of chordal insertion can be visualized to determine the potential for surgical valvuloplasty. [137] TEE provides good visualization of an atrial baffle and can detect stenoses or leaks.[138] Complications of a Fontan procedure, such as obstruction or thrombosis, can be evaluated.[139] TEE can characterize right and left ventricular outflow tract obstructions.[62] [135] [137] Abnormalities of the aorta, including aortic coarctation and patent ductus arteriosus, are also better appreciated by TEE than by TTE.[140] [141] Coronary Artery Disease Transesophageal echocardiography can be employed for the diagnosis of coronary artery disease by (1) visualization of coronary stenoses in the proximal vessels or (2) detection of stress-induced regional wall motion abnormalities. The left main coronary artery can be visualized in more than 85% of patients.[39] [142] [143] [144] [145] The proximal left anterior descending artery and proximal left circumflex artery can also be visualized in most patients.[142] [143] [144] The proximal right coronary artery is more difficult to visualize but may still be seen in 50% of patients or more.[142] [144] Several studies have examined the accuracy of TEE in identifying coronary stenoses in the proximal segments of the coronary arteries using two-dimensional and color flow imaging. In patients with visualized vessels, the sensitivity of TEE in identifying significant left main coronary stenoses has been reported to be 91% to 100%, with specificities greater than 90%.[39] [142] [143] [144] [145] The sensitivity for detecting significant proximal left anterior descending artery disease, left circumflex artery disease, and right coronary artery disease has been reported to be 78% to 100%, 50% to 89%, and 82% to 100%, respectively.[142] [143] [144] The sensitivity for detecting coronary artery stenoses significantly decreases, however, if patients with nonvisualized segments are included in the analysis.[144] One author has reported employing TEE and the continuity equation to quantify the severity of stenoses in the left anterior descending artery.[41] In addition, coronary artery flow reserve can be measured using TEE, and differences in flow reserve can be detected in patients with left anterior descending artery stenoses.[40] [42] TEE should not replace coronary angiography in the diagnosis of proximal coronary artery stenoses, but it may be useful in assessing angiographically questionable stenoses involving the left main ostium or the left anterior descending artery in centers in which

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intravascular ultrasonography is not available.[146] Stress echocardiography with TEE imaging has been used to evaluate patients with suspected or confirmed coronary artery disease.[147] [148] TEE provides high-quality images with excellent endocardial resolution. Stress techniques employed to induce ischemia have included transesophageal atrial pacing and pharmacologic methods using either dobutamine or dipyridamole.[147] [148] These techniques have been shown to be highly accurate in the detection of coronary artery disease and to provide information useful in risk stratification, and they may be useful in the assessment of myocardial viability in patients with left ventricular dysfunction.[147] [148] TEE is an invasive procedure with potential risks, however, and stress echocardiography with TEE imaging should be reserved for patients who have poor TTE images. Additional applications of TEE in the assessment of coronary artery disease include the detection of anomalous coronary arteries and the detection and mapping of coronary artery fistulas.[149] Pericardial Disease Pericardial effusions and cardiac tamponade are usually easily diagnosed on TTE and do not require TEE (see Chapter 29) . However, the detection of cardiac tamponade after cardiac surgery can be difficult to diagnose by TTE. Local compression of the right atrium by extracardiac thrombus may not be apparent on TTE because of the posterior position of the thrombus and poor TTE images related to suboptimal patient position, surgical bandages, and drainage tubes. TEE circumvents these problems and can better detect extracardiac compression.[150] Constrictive pericarditis and restrictive physiologic diseases can usually be differentiated on TTE using respiratory monitoring. In patients with nondiagnostic TTE, however, TEE with respiratory monitoring may be useful in differentiating these diseases. [151] Pericardial thickening can be measured by TEE and correlates with computed tomography. [152] In one study, TEE was shown to be superior to TTE in assessing pericardial thickening, intrapericardial metastases, intrapericardial thrombus, and pericardial cysts.[150] Intensive Care Unit The TTE images obtained in the intensive care unit are frequently inadequate because of poor acoustic penetration, limited windows from surgical bandages and drains, mechanical ventilation, and an inability to

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properly position patients. In this setting, TEE can provide essential information that alters patient management. TEE has been shown to be valuable in the assessment of the patient with unexplained hypotension, pulmonary edema, and hypoxia.[153] [154] TEE provides information on myocardial function, valve function, and volume status, which is critical in evaluating the patient with unexplained hypotension or unexplained pulmonary edema. TEE can detect right-to-left intracardiac shunting through a patent foramen ovale, which may occur in ventilated patients requiring high levels of pressure support and right ventricular infarction. [155] [156] The presence of massive or proximal pulmonary emboli can be diagnosed by TEE.[22] [23] Potential complications of myocardial infarction, including left ventricular 17

dysfunction, papillary muscle rupture, and myocardial rupture, may be detected. Intraoperative Monitoring Intraoperative TEE can provide detailed information on cardiac anatomy and function not obtainable by other monitoring technologies and can obtain this information without disrupting the surgical procedure.[157] [158] TEE can evaluate global and segmental left ventricular function, detect intraoperative myocardial ischemia, and monitor hemodynamics, including cardiac output, left ventricular filling pressures, and volume status. The cause of hemodynamic disturbances can be determined and intraoperative complications identified. Importantly, the adequacy of valve repairs or replacements and surgical reconstructions for congenital and acquired diseases can be evaluated prior to leaving the operating room. In 1996, the American Society of Anesthesiologists published recommendations for performing TEE based on the strength of supporting evidence and expert opinion that TEE improved clinical outcome.[157] The complete list of potential indications for TEE in the intraoperative period is extensive and is discussed in more detail in Chapter 2 and Chapter 19 . Monitoring During Interventional Procedures Transesophageal echocardiography is a valuable adjunct to percutaneous mitral valvuloplasty. TEE can guide catheter placement during trans-septal puncture, assist in proper balloon placement, evaluate the valvuloplasty result, identify complications, and shorten procedure and fluoroscopy

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times.[121] [159] It has been used to assist in right ventricular biopsies and biopsies of intracardiac masses.[124] [160] TEE may assist in trans-septal puncture and proper catheter position for radiofrequency ablation.[161] TEE has been used to guide catheter position for percutaneous closure of atrial septal defects, patent ductus arteriosus, ventricular septal defects, and coronary artery fistulas.[122] [162] [163] [164] TEE has also been found to be useful in the pediatric population during creation or enlargement of an interatrial communication or balloon dilation of obstructive left heart lesions. [165] Electrical cardioversion of atrial fibrillation without prolonged anticoagulation has been proposed as a safe procedure if TEE excludes left atrial thrombus.[166] However, this management scheme is controversial and requires further investigation (see Chapter 38) .[167]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Contraindications to Transesophageal Echocardiography Patients undergoing TEE should be kept on NPO (nothing by mouth) status for 4 to 6 hours prior to the procedure because of the potential for vomiting and aspiration. However, urgent procedures can likely be performed earlier with minimal risk of vomiting and aspiration if there has been only clear fluid intake up to 2 hours prior to the procedure.[168] TEE should not be performed in the uncooperative patient. Patients who are uncooperative should either have the study deferred or be sedated and paralyzed, if necessary. Patients with a tenuous cardiorespiratory status should be intubated and ventilated to avoid decompensation during the procedure. To avoid esophageal rupture, TEE should not be attempted in a patient with esophageal obstruction caused by a stricture or mass. The presence of an esophageal diverticulum should also be considered a relative contraindication because of the possibility of the probe entering and perforating the diverticulum. TEE is contraindicated in the patient with a perforated viscus or active gastrointestinal bleed. Esophageal varices are not a contraindication to TEE. However, the potential additive information should be weighed against the small risk of major bleeding. Severe cervical arthritis or dislocation of the atlantoaxial joint, in which flexion of the neck is severely limited or impossible, should be considered a relative contraindication to TEE. TEE can be performed safely in patients receiving anticoagulation therapy.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Complications of Transesophageal Echocardiography Transesophageal echocardiography is a relatively safe procedure with a low complication rate. Procedural complications have been observed in 0.47% to 2.80% of patients with successful esophageal intubation, however (Table 1-4) .[5] [9] [11] [169] The vast majority of complications are minor. Major complications, defined in one study as death, laryngospasm, sustained ventricular tachycardia, or congestive heart failure, occur in approximately 0.3% of patients.[169] In the Multicenter European Survey of 10,419 examinations, the TEE examination had to be interrupted prior to completion in 0.88% of studies.[11] Patient TABLE 1-4 -- Procedural Complications with Transesophageal Echocardiography Major Complications Death Esophageal rupture Laryngospasm or bronchospasm Congestive heart failure or pulmonary edema Sustained ventricular tachycardia Minor Complications Excessive retching or vomiting Sore throat Hoarseness Minor pharyngeal bleeding Blood-tinged sputum Nonsustained or sustained supraventricular tachycardia Atrial fibrillation

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Nonsustained ventricular tachycardia Bradycardia or heart block Transient hypotension Transient hypertension Angina Transient hypoxia Parotid swelling Tracheal intubation

18

intolerance of the probe, including excessive retching or vomiting, was the most common complication, resulting in premature termination of the procedure.[11] In the largest series, deaths have been reported in 0 to 0.03% of patients.[5] [9] [11] , [169] Cardiac complications reported include nonsustained and sustained supraventricular tachycardias or atrial fibrillation, nonsustained and sustained ventricular tachycardia, bradycardia, transient hypotension or hypertension, angina pectoris, congestive heart failure, and pulmonary edema. Pulmonary complications have included transient hypoxia and laryngospasm. Bleeding complications have included minor pharyngeal bleeding or blood-tinged sputum, MalloryWeiss tear, and severe hematemesis in a patient with a malignant tumor invading the esophagus. A minor sore throat may be present for 24 hours after the procedure. Adverse reactions may occur as a result of intravenous sedation, topical anesthesia, or drying agents such glycopyrrolate. Intravenous sedation may result in respiratory depression and hypoxia, hypotension, or paradoxical reactions. Topical anesthesia with benzocaine or lidocaine may result in acute toxic methemoglobinemia, a rare condition in which hemoglobin is oxidized by the topical anesthesia agent and is unable to carry oxygen to the tissues.[170] The partial pressure of oxygen in the blood is normal, but oxyhemoglobin levels are decreased. Patients usually develop cyanosis and dyspnea. On pulse oximetry, oxygen saturation often appears only mildly reduced because this technique cannot distinguish methemoglobin and reduced hemoglobin. The diagnosis can be confirmed with an arterial blood gas sample with measurement of methemoglobinemia. Methylene blue (1

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Transesophageal echocardiography is a very powerful tool that provides a unique acoustic window to assess cardiac structure and function. In our view, a comprehensive study should include the standard views discussed in this chapter. When dealing with specific clinical problems, additional views should be used to obtain the necessary diagnostic information. In critically ill patients, we believe that the initial views should be those that are most pertinent to the clinical question. Adequate diagnostic information would then have been obtained even if the study needs to be terminated prematurely. Finally, we need to be mindful that TEE is a semi-invasive procedure and is not free of risks. Clear and convincing indications should be present before a TEE study is performed.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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and biplane versus multiplane transesophageal imaging: A review of 2947 consecutive studies. Can J Cardiol 1997;13:81–84. 10. Yvorchuk K, Sochowski R, Chan K: A prospective comparison of the multiplane

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21. Fagan S, Veinot JP, Chan KL: Residual sinus venosus atrial septal defect following

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30. Nishimura RA, Tajik AJ: Evaluation of diastolic filling of left ventricle in health

and disease: Doppler echocardiography is the clinician's Rosetta stone. J Am Coll Cardiol 1997;30:8–18. 31. Klein AL, Tajik AJ: Doppler assessment of pulmonary venous flow in healthy

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velocity patterns in normal subjects. J Am Soc Echocardiogr 1996;9:274–280. 35. The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography: Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. Ann Intern Med 1998;128:639–647. 36. Goldman ME, Pearce LA, Hart RG, et al: Pathophysiologic correlates of

thromboembolism in nonvalvular atrial fibrillation: I. Reduced flow velocity in the left atrial appendage (The Stroke Prevention in Atrial Fibrillation [SPAFF-III] study). J Am Soc Echocardiogr 1999;12:1080–1087. 37. Kamalesh M, Copeland TB, Sawada S: Severely reduced left atrial appendage function: A cause of embolic stroke in patients in sinus rhythm? J Am Soc Echocardiogr 1998;11:902–904. 38. Verhorst PM, Kamp O, Welling RC, et al: Transesophageal echocardiographic

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with left main coronary artery stenosis by transesophageal Doppler color flow echocardiography. J Am Coll Cardiol 1991;17:87–93. 40. Kozakova M, Palombo C, Pratali L, et al: Assessment of coronary reserve by

transoesophageal Doppler echocardiography: Direct comparison between different modalities of dipyridamole and adenosine administration. Eur Heart J 1997;18:514– 523.

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41. Isaaz K, da Costa A, de Pasquale JP, et al: Use of the continuity equation for

transesophageal Doppler assessment of severity of proximal left coronary artery stenosis: A quantitative coronary angiography validation study. J Am Coll Cardiol 1998;32:42–48. 42. Redberg RF, Sobol Y, Chou TM, et al: Adenosine-induced coronary vasodilation during transesophageal Doppler echocardiography: Rapid and safe measurement of coronary flow reserve ratio can predict significant left anterior descending coronary stenosis. Circulation 1995;92:190–196. 43. Feinberg MS, Hopkins WE, Davila-Roman VG, et al: Multiplane transesophageal

echocardiographic Doppler imaging accurately determines cardiac output measurement in critically ill patients. Chest 1995;107:679–673. 44. Katz WE, Gasior TA, Quinlan JJ, et al: Transgastric continuous-wave Doppler to

determine cardiac output. Am J Cardiol 1993;71:853–857. 45. Gorscan J III, Diana P, Ball BA, et al: Intraoperative determination of cardiac

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output by transesophageal pulsed Doppler echocardiography. Anesthesiology 1991;74:9–14. 47. Hozumi T, Shakudo M, Applegate R, et al: Accuracy of cardiac output estimation

with biplane transesophageal echocardiography. J Am Soc Echocardiogr 1993;6:62– 68. 48. Pu M, Griffin BP, Vandervoort PM, et al: Intraoperative validation of mitral inflow

determination by transesophageal echocardiography: Comparison of single-plane, biplane and thermodilution techniques. J Am Coll Cardiol 1995;26:1047–1053. 49. Foster GP, Iselbacher EM, Rose GA, et al: Accurate localization of mitral

regurgitation defects using multiplane transesophageal echocardiography. Ann Thorac Surg 1998;65:1025–1031. 50. Grewal KS, Malkowski MJ, Kramer CM, et al: Multiplane transesophageal

echocardiographic identification of the involved scallop in patients with flail mitral valve leaflet: Intraoperative correlation. J Am Soc Echocardiogr 1998;11:966–971. 51. Moursi MH, Bhatnagar SK, Vilacosta I, et al: Transesophageal echocardiographic

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evaluation of mitral regurgitation: The twenty-four signs of severe mitral regurgitation. Cardiol Clin 1993;11:399–408. 53. Smith MD, Harrison MR, Pinton R, et al: Regurgitant jet size by transesophageal

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patterns in detecting mitral regurgitation and left ventricular abnormalities. Can J Cardiol 1999;15:665–670. 56. Grayburn PA, Fehske W, Omran H, et al: Multiplane transesophageal

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score by transthoracic and transesophageal echocardiography. Am J Cardiol 1991;68:1106–1107. 59. Stoddard MF, Prince CR, Tuman WL, et al: Angle of incidence does not affect accuracy of mitral stenosis area calculation by pressure half-time: Application to Doppler transesophageal echocardiography. Am Heart J 1994;127:1562–1572. 60. Degertekin M, Basaran Y, Gencbay M, et al: Validation of flow convergence

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the assessment of percutaneous mitral commissurotomy. Eur Heart J 1991;12(suppl B):61–65. 62. Essop MR, Skudicky D, Sareli P: Diagnostic value of transesophageal versus

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by transesophageal echocardiography: Correlation with angiographic determination. Echocardiography 1993;10:269–278. 64. Sutton DC, Kluger R, Ahmed SU, et al: Flow reversal in the descending aorta: A

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65. Sato Y, Kawazoe K, Nasu M, et al: Clinical usefulness of the proximal isovelocity

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orifice area determined by transesophageal echocardiography in patients with eccentric aortic regurgitation. J Heart Valve Dis 1997;6:580–586. 67. Hoffmann R, Flachskampf FA, Hanrath P: Planimetry of orifice area in aortic stenosis using multiplane transesophageal echocardiography. J Am Coll Cardiol 1993;22:529–534. 68. Kim KS, Maxted W, Nanda NC, et al: Comparison of multiplane and biplane

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echocardiography in determining aortic valve area in aortic stenosis. Am J Cardiol 1996;77:882–885. 70. Daniel WG, Mugge A, Grote J, et al: Comparison of transthoracic and

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71. Alton ME, Pasierski TJ, Orsinelli DA, et al: Comparison of transthoracic and

transesophageal echocardiography in evaluation of 47 Starr-Edwards prosthetic valves. J Am Coll Cardiol 1992;20:1503–1511. 72. Daniel LB, Grigg LE, Weisel RD, et al: Comparison of transthoracic and

transesophageal assessment of prosthetic valve dysfunction. Echocardiography 1990;7:83–95.

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73. Khandheria BK, Seward JB, Oh JK, et al: Value and limitations of transesophageal

echocardiography in the assessment of mitral valve prosthesis. Circulation 1991;83:1956–1968. 74. Chaudhry FA, Herrera C, DeFrino PF, et al: Pathologic and angiographic

correlations of transesophageal echocardiography in the prosthetic heart valve dysfunction. Am Heart J 1991;122:1057–1064. 75. Karalis DG, Chandrasekaran K, Ross JJ Jr, et al: Single-plane transesophageal

echocardiography for assessing function of mechanical or bioprosthetic valves in the aortic valve position. Am J Cardiol 1992;69:1310–1315. 76. Gueret P, Vignon P, Fournier P, et al: Transesophageal echocardiography for the

diagnosis and management of nonobstructive thrombosis of mechanical mitral prosthesis. Circulation 1995;91:103–110. 77. Orsinelli DA, Pearson AC: Detection of prosthetic valve strands by

transesophageal echocardiography: Clinical significance in patients with suspected cardiac source of embolism. J Am Coll Cardiol 1995;26:1713–1718. 78. Barbetseas J, Nagueh SF, Pitsavos C, et al: Differentiating thrombus from pannus

formation in obstructed mechanical prosthetic valves: An evaluation of clinical, transthoracic and transesophageal echocardiographic parameters. J Am Coll Cardiol 1998;32:1410–1417. 79. Ozkan M, Kaymaz C, Kirma C, et al: Intravenous thrombolytic treatment of

mechanical prosthetic valve thrombosis: A study using serial transesophageal echocardiography. J Am Coll Cardiol 2000;35:1881–1889. 80. Tenenbaum A, Fisman EZ, Vered Z, et al: Failure of transesophageal

echocardiography to visualize a large mitral prosthesis vegetation detected solely by transthoracic echocardiography. J Am Soc Echocardiogr 1995;8:944–946. 81. Flachskampf FA, O'Shea JP, Griffin BP, et al: Patterns of transvalvular

regurgitation in normal mechanical prosthetic valves. J Am Coll Cardiol 1991;18:1493–1498. 82. Flachskampf FA, Hoffmann R, Franke A, et al: Does multiplane transesophageal

echocardiography improve the assessment of prosthetic valve regurgitation? J Am Soc Echocardiogr 1995;8:70–78. 83. Reisner SA, Meltzer RS: Normal values of prosthetic valve Doppler

echocardiographic parameters: A review. J Am Soc Echocardiogr 1998;11:201–210.

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84. Gorscan J III, Kenny WM, Diana P, et al: Transesophageal continuous-wave

Doppler to evaluate mitral prosthetic stenosis. Am Heart J 1991;121:911–914. 85. Baumgartner H, Khan S, DeRobertis M, et al: Effect of prosthetic aortic design on

the Doppler-catheter gradient correlation: An in vitro study of normal St. Jude, Medtronic-Hall, Starr-Edwards, and Hancock valves. J Am Coll Cardiol 1992;19:324– 332. 86. Durak DT, Lukes AS, Bright DK: New criteria for diagnosis of infective

endocarditis: Utilization of specific echocardiographic findings. Am J Med 1994;96:200–209. 87. Birmingham GD, Rahko PS, Ballantyne FE: Improved detection of infective

endocarditis with transesophageal echocardiography. Am Heart J 1992;123:774–781. 88. Erbel R, Rohmann S, Drexler M, et al: Improved diagnostic value of

echocardiography in patients with infective endocarditis by transesophageal approach: A prospective study. Eur Heart J 1988;9:43–53. 89. Taams MA, Gussenhoven EJ, Bos E, et al: Enhanced morphologic diagnosis in

infective endocarditis by transoesphageal echocardiography. Br Heart J 1990;63:109– 113. 90. Shively BK, Gurule FT, Roldan CA, et al: Diagnostic value of transesophageal

compared with transthoracic echocardiography in infective endocarditis. J Am Coll Cardiol 1991;18:391–397. 91. Mügge A, Daniel WG, Frank G, et al: Echocardiography in infective endocarditis:

Reassessment of prognostic implications of vegetation size determined by the transthoracic and the transesophageal approach. J Am Coll Cardiol 1989;14:631–638. 92. Shapiro SM, Young E, Ginzton LE, et al: Pulmonic valve endocarditis as an underdiagnosed disease: Role of transesophageal echocardiography. J Am Soc Echocardiogr 1992;5:48–51. 93. San Roman JA, Vilacosta I, Zamorano JL, et al: Transesophageal

echocardiography in right-sided endocarditis. J Am Coll Cardiol 1993;21:1226–1230. 94. Zabalgoitia M, Herrera CJ, Chaudhry FA, et al: Improvement in the diagnosis of

bioprosthetic valve dysfunction by transesophageal echocardiography. J Heart Valve Dis 1993;2:595–603. 95. Lowry RW, Zoghbi WA, Baker WB, et al: Clinical impact of transesophageal

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echocardiography in the diagnosis and management of infective endocarditis. Am J Cardiol 1994;73:1089–1091. 96. Lindner JR, Case RA, Dent JM, et al: Diagnostic value of echocardiography in

suspected endocarditis: An evaluation based on the pretest probability of disease. Circulation 1996;93:730–736. 97. Sochowski RA, Chan K-L: Implication of negative results on a monoplane

transesophageal echocardiographic study in patients with suspected infective endocarditis. J Am Coll Cardiol 1994;21:216–221. 98. Daniel WG, Mugge A, Martin RP, et al: Improvement in the diagnosis of abscesses

associated with endocarditis by transesophageal echocardiography. N Engl J Med 1991;324:795–800. 99. Massey WM, Samdarshi TE, Nanda NC, et al: Serial documentation of changes in

a mitral valve vegetation progressing to abscess rupture and fistula formation by transesophageal echocardiography. Am Heart J 1992;124:241–248. 100. Castro SD, Cartoni D, d'Amati G, et al: Diagnostic accuracy of transthoracic and

multiplane transesophageal echocardiography for valvular perforation in acute infective endocarditis: Correlation with anatomic findings. Clin Infect Dis 2000;30:825–826. 101. Vilacosta I, San Roman JA, Sarria C, et al: Clinical, anatomic, and

echocardiographic characteristics of aneurysms of the mitral valve. Am J Cardiol 1999;84:110–113. 102. Rohmann S, Erhel R, Darius H, et al: Effect of antibiotic treatment on vegetation

size and complication rate in infective endocarditis. Clin Cardiol 1997;20:132–140. 103. Cerebral Embolism Task Force: Cardiogenic brain embolism: The second report

of the Cerebral Embolism Task Force. Arch Neurol 1989;46:727–743. 104. Kapral MK, Silver FL, with the Canadian Task Force on Preventive Health Care:

Preventive health care, 1999 update: 2. Echocardiography for the detection of a cardiac source of embolus in patients with stroke. Can Med Assoc J 1999;161:989– 996. 105. Dressler FA, Labovitz AJ: Systemic arterial emboli and cardiac masses:

Assessment with transesophageal echocardiography. Cardiol Clin 1993;11:447–460. 106. Hwang JJ, Chen JJ, Lin SC, et al: Diagnostic accuracy of transesophageal

echocardiography for detecting left atrial thrombi in patients with rheumatic heart

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disease having undergone mitral valve operations. Am J Cardiol 1993;72:677–681. 107. Manning WJ, Weintraub RM, Wakomonski CA, et al: Accuracy of

transesophageal echocardiography for identifying left atrial thrombi. A prospective intraoperative study. Ann Intern Med 1995;123:817–822. 21

108. Mugge A, Daniel WG, Haverich A, et al: Diagnosis of noninfective cardiac mass

lesions by two-dimensional echocardiography: Comparison of the transthoracic and transesophageal approaches. Circulation 1991;83:70–78. 109. Chen C, Koschyk D, Hamm C, et al: Usefulness of transesophageal

echocardiography in identifying small left ventricular apical thrombus. J Am Coll Cardiol 1993;21:208–215. 110. Black IW, Hopkins AP, Lee LCL, et al: Left atrial spontaneous echo contrast: A

clinical transesophageal echocardiographic analysis. J Am Coll Cardiol 1991;18:398– 404. 111. Rittoo D, Cotter L: Detection of a small left atrial myxoma: Value and limitations

of four imaging modalities. J Am Soc Echocardiogr 1997;10:874–876. 112. Mügge A, Daniel WG, Haverich A, et al: Diagnoses of noninfective cardiac mass

lesions by two-dimensional echocardiography: Comparison of the transthoracic and transesophageal approaches. Circulation 1991;83:70–78. 113. Siostrzonek P, Zangeneh M, Gössinger H, et al: Comparison of transesophageal

and transthoracic contrast echocardiography for detection of a patent foramen ovale. Am J Cardiol 1991;68:1247–1249. 114. Pearson AC, Nagelhout D, Castello R, et al: Atrial septal aneurysm and stroke: A

transesophageal echocardiographic study. J Am Coll Cardiol 1991;18:1223–1229. 115. Hausmann D, Mügge A, Daniel WG: Identification of patent foramen ovale

permitting paradoxical embolism. J Am Coll Cardiol 1995;26:1030–1038. 116. Tunick PA, Kronzon I: Atheromas of the thoracic aorta: Clinical and therapeutic

update. J Am Coll Cardiol 2000;35:545–554. 117. Willens HJ, Kessler KM: Transesophageal echocardiography in the diagnosis of

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diseases of the thoracic aorta: Part II—atherosclerotic and traumatic diseases of the aorta. Chest 2000;117:233–243. 118. Rauh G, Fischereder M, Spengel FA: Transesophageal echocardiography in

patients with focal cerebral ischemia of unknown cause. Stroke 1996;27:691–694. 119. Mehta RH, Helmcke F, Nanda NC, et al: Transesophageal Doppler color flow

mapping assessment of atrial septal defect. J Am Coll Cardiol 1990;16;1010–1016. 120. Mugge A, Daniel WG, Angermann C, et al: Atrial septal aneurysm in adult

patients: A multicenter study using transthoracic and transesophageal echocardiography. Circulation 1995;91:2785–2792. 121. Rittoo D, Sutherland GR, Shaw TR: Quantification of left-to-right shunting and

defect size after balloon mitral commissurotomy using biplane transesophageal echocardiography, color flow Doppler mapping, and the principle of proximal flow convergence. Circulation 1993;87:1591–1603. 122. Ewert P, Berger F, Daehnert I, et al: Transcatheter closure of atrial septal defects

without fluoroscopy: Feasibility of a new method. Circulation 2000;101:847–849. 123. Engberding R, Daniel WG, Erbel R, et al: Diagnosis of heart tumours by

transoesophageal echocardiography: A multicentre study in 154 patients. Eur Heart J 1993;14:1223–1228. 124. Beaver TA, Robb JF, Teufel EJ, et al: Right ventricular outflow tract obstruction

in an older woman: Facilitated diagnosis with transesophageal echocardiographyguided biopsy. J Am Soc Echocardiogr 2000;13:622–625. 125. Cigarrao JE, Isselbacher EM, DeSanctis RW, et al: Diagnostic imaging in the

evaluation of suspected aortic dissection: Old standards and new directions. N Engl J Med 1993:328:35–43. 126. Nienaber CA, von Kodolitsch Y, Nicolas V, et al: The diagnosis of thoracic aortic

dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1–9. 127. Bansal RC, Chandrasekaran K, Ayala K, et al: Frequency and explanation of false

negative diagnosis of aortic dissection by aortography and transesophageal echocardiography. J Am Coll Cardiol 1995;25:1393–1401. 128. Willens HJ, Kessler KM: Transesophageal echocardiography in the diagnosis of

diseases of the thoracic aorta: Part I—aortic dissection, aortic intramural hematoma, and penetrating atherosclerotic ulcer of the aorta. Chest 2000;116:1772–1779.

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129. Keren A, Kim CB, Hu BS, et al: Accuracy of biplane and multiplane

transesophageal echocardiography in diagnosis of typical acute aortic dissection and intramural hematoma. J Am Coll Cardiol 1996;28:627–636. 130. Sommer T, Fehske W, Holzkuecht N, et al: Aortic dissection: A comparative

study of diagnosis with spiral CT, multiplanar transesophageal echocardiography and MR imaging. Radiology 1996;199:347–352. 131. Masani ND, Banning AP, Jones RA, et al: Follow-up of chronic thoracic aortic

dissection: Comparison of transesophageal echocardiography and magnetic resonance imaging. Am Heart J 1996;131:1156–1163. 132. Vilacosta I, San Roman JA, Aragoncillo P, et al: Penetrating atherosclerotic aortic

ulcer: Documentation by transesophageal echocardiography. J Am Coll Cardiol 1998;32:83–89. 133. Smith MD, Cassidy JM, Souther S, et al: Transesophageal echocardiography in

the diagnosis of traumatic rupture of the aorta. N Engl J Med 1995;332:356–362. 134. Ahrar K, Smith DC, Bansal RC, et al: Angiography in blunt thoracic aortic injury.

J Trauma 1997;42:665–669. 135. Ritter SB: Transesophageal real-time echocardiography in infants and children

with congenital heart disease. J Am Coll Cardiol 1991;18:569–580. 136. Weintraub R, Shiota T, Elkadi T, et al: Transesophageal echocardiography in

infants and children with congenital heart disease. Circulation 1992;86:711–722. 137. Sreeram N, Stumper OF, Kaulitz R, et al: Comparative value of transthoracic and

transesophageal echocardiography in the assessment of congenital abnormalities of the atrioventricular junction. J Am Coll Cardiol 1990;16:1205–1214. 138. Kaulitz R, Stümper OFW, Geuskens R, et al: Comparative values of the

precordial and transesophageal approaches in the echocardiographic evaluation of atrial baffle function after an atrial correction procedure. Am J Coll Cardiol 1990;16:686–694. 139. Stümper O, Sutherland GR, Geuskens R, et al: Transesophageal echocardiography

in evaluation and management after a Fontan procedure. J Am Coll Cardiol 1991;17:1152–1160. 140. Engvall J, Sjoqvist L, Nylander E, et al: Biplane transoesophageal

echocardiography, transthoracic Doppler, and magnetic resonance imaging in the

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assessment of coarctation of the aorta. Eur Heart J 1995;10:1399–1409. 141. Andrade A, Vargas-Barron J, Rijlaarsdam M, et al: Utility of transesophageal

echocardiography in the examination of adult patients with patent ductus arteriosus. Am Heart J 1995;130:543–546. 142. Tardif JC, Vannon MA, Taylor K, et al: Delineation of extended lengths of coronary arteries by multiplane transesophageal echocardiography. J Am Coll Cardiol 1994;24:909–919. 143. Reichert SL, Visser CA, Koolen JJ, et al: Transesophageal examination of the left

coronary artery with a 7.5 MHz annular array two-dimensional color flow Doppler transducer. J Am Soc Echocardiogr 1990;3:118–124. 144. Samdarshi TE, Nanda NC, Gatewood RP Jr, et al: Usefulness and limitations of

transesophageal echocardiography in the assessment of proximal coronary artery stenosis. J Am Coll Cardiol 1992;19:572–580. 145. Yoshida K, Yoshikawa J, Hozumi T, et al: Detection of left main coronary artery

stenosis by transesophageal color Doppler and two-dimensional echocardiography. Circulation 1990;81:1271–1276. 146. Firstenberg MS, Greenberg NL, Lin SS, et al: Transesophageal echocardiography

assessment of severe ostial left main coronary stenosis. J Am Soc Echocardiogr 2000;13:696–698. 147. Panza JA: Transesophageal echocardiography with stress for the evaluation of

patients with coronary artery disease. Cardiol Clin 1999;17:501–520. 148. Madu EC: Transesophageal dobutamine stress echocardiography in the evaluation

of myocardial ischemia in morbidly obese subjects. Chest 2000;117;657–661. 149. Lin FC, Chang HJ, Chern MS, et al: Multiplane transesophageal

echocardiography in the diagnosis of congenital coronary artery fistula. Am Heart J 1995;130:1236–1242. 150. Hutchison SJ, Smalling RG, Albornoz M, et al: Comparison of transthoracic and

transesophageal echocardiography in clinically overt or suspected pericardial heart disease. Am J Cardiol 1994;74:962–965. 151. Klein AL, Cohen GI, Pietrolungo JF, et al: Differentiation of constrictive

pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol 1993;22:1935–1943.

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152. Ling LH, Oh JK, Tei C, et al: Pericardial thickness measured with

transesophageal echocardiography: Feasibility and potential clinical usefulness. J Am Coll Cardiol 1997;29:1317–1323. 153. Heidenreich PA, Stainback RF, Redberg RF, et al: Transesophageal

echocardiography predicts mortality in critically ill patients with unexplained hypotension. J Am Coll Cardiol 1995;26:152–158. 154. Vignon P, Mentec H, Terre S, et al: Diagnostic accuracy and therapeutic impact of

transthoracic and transesophageal echocardiography in mechanically ventilated patients in the ICU. Chest 1994;106;1829–1834. 155. Dewan NA, Gayasaddin M, Angelillo VA, et al: Persistent hypoxemia due to

patent foramen ovale in a patient with adult respiratory distress syndrome. Chest 1986;89:611. 156. Bansal RC, Marsa RJ, Holland D, et al: Severe hypoxemia due to shunting

through a patent foramen ovale: A correctable complication of right ventricular infarction. J Am Coll Cardiol 1985;15:499–504. 157. American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography: Practice guidelines for perioperative transesophageal echocardiography. Anesthesiology 1996;84:986–1006. 158. Kolev N, Brase R, Swanevelder J, et al: The influence of transoesophageal

echocardiography on intra-operative decision making: A European multicentre study. European Perioperative TOE Research Group. Anaesthesia 1998;53:767–773. 159. Park SH, Kim MA, Hyon MS: The advantages of on-line transesophageal

echocardiography guide during percutaneous balloon mitral valvuloplasty. J Am Soc Echocardiogr 2000;13:26–34. 160. Pytlewski G, Georgeson S, Burke J, et al: Endomyocardial biopsy under

transesophageal echocardiographic guidance can be safely performed in the critically ill cardiac transplant recipient. Am J Cardiol 1994;73:1019–1020. 161. Kantoch MJ, Frost GF, Robertson MA: Use of transesophageal echocardiography

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in radiofrequency catheter ablation in children and adolescents. Can J Cardiol 1998;14:519–523. 162. Tumbarello R, Sanna A, Cardu G, et al: Usefulness of transesophageal

echocardiography in the pediatric catheterization laboratory. Am J Cardiol 1993;71:1321–1325. 163. van der Velde ME, Sanders SP, Keane JF, et al: Transesophageal

echocardiographic guidance of transcatheter ventricular septal defect closure. J Am Coll Cardiol 1994;23:1660–1665. 164. McElhinney DB, Burch GH, Kung GC, et al: Echocardiographic guidance for

transcatheter coil embolization of congenital coronary arterial fistulas in children. Pediatr Cardiol 2000;21:253–258. 165. Cheung YF, Leung MP, Lee J, et al: An evolving role of transesophageal

echocardiography for the monitoring of interventional catheterization in children. Clin Cardiol 1999;22:804–810. 166. Manning WJ, Silverman DI, Gordon SP, et al: Cardioversion from atrial

fibrillation without prolonged anticoagulation with use of transesophageal echocardiography to exclude the presence of atrial thrombi. N Engl J Med 1993;328:750–755. 167. Moreyra E, Finkelhor RS, Cebul RD: Limitations of transesophageal

echocardiography in the risk assessment of patients before nonanticoagulated cardioversion from atrial fibrillation and flutter: An analysis of pooled trials. Am Heart J 1995:129:71–75. 168. Greenfield SM, Webster GJ, Brar AS, et al: Assessment of residual gastric

volume and thirst in patients who drink before gastroscopy. Gut 1996;39:360–362. 169. Khandheria BK, Seward JB, Tajik AJ: Concise review for primary-care

physicians: Transesophageal echocardiography. Mayo Clin Proc 1994;69:856–863. 170. Grauer SE, Giraud GD: Toxic methemoglobinemia after topical anesthesia for

transesophageal echocardiography. J Am Soc Echocardiogr 1996;9:874–876.

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23

Chapter 2 - Monitoring Ventricular Function in the Operating Room Impact on Clinical Outcome Donald C. Oxorn MD

Since being introduced into anesthetic practice in the late 1980s, transesophageal echocardiography (TEE) for intraoperative monitoring during cardiac surgery has gained wide acceptance. In 1995, Poterack[1] reported a national survey of anesthesia residency program directors in which 91% reported its use. TEE is relatively noninvasive, can be used in the vast majority of patients, and does not interfere physically with most surgical procedures. In some centers, TEE is used routinely for all cases involving cardiopulmonary bypass, whereas it is used more selectively at others. The usefulness of TEE during noncardiac surgery has been less thoroughly investigated, although if one extrapolates from the experience with hemodynamically unstable intensive care unit patients,[2] its utility in the differential diagnosis of intraoperative hemodynamic instability would appear intuitive. In this chapter, after I offer a general approach to and a personal philosophy on intraoperative TEE, the focus will be on the assessment of cardiac

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function in the setting of both cardiac and noncardiac surgery. In addition, the impact intraoperative TEE has had on the quality of perioperative care is discussed. Intraoperative assessment of valvular function, chamber size, masses, and great vessels are covered in other sections of the book.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

An Approach to Intraoperative Transesophageal Echocardiography Intraoperative TEE has become inextricably linked with cardiac anesthesiology. Over the past decade, guidelines for physician training in TEE have been directed primarily at cardiologists[3] [4] [5] and have stressed a background in transthoracic echocardiography, the acquisition of both cognitive and technical skills, and an ongoing program of maintenance of competence (see Chapter 42) . What is the standard that anesthesiologists should hold themselves up to? No written standard exists, although there are several distinct levels of expertise. Some individuals have taken advanced training that has included the performance and interpretation of surface studies under the tutelage of cardiologists and sonographers; others have studied TEE in the operating room during cardiac anesthesiology fellowships or "on the job"; and many have taught themselves by observation in the operating room, attendance at educational symposia, and the study of text and videotape. The educational program for intraoperative TEE at the Cleveland Clinic is a joint effort between cardiac anesthesiologists and cardiologists and is designed to train individuals to the highest level.[6] There are now two examinations of special competence under the auspices of the National Board of Echocardiography. The curriculum for the intraoperative examination focuses primarily on TEE, whereas the curriculum for the examination in general echocardiography emphasizes a broad knowledge of most aspects of echocardiography, both transthoracic and transesophageal. I believe that anesthesiologists who wish to practice intraoperative TEE should adhere to several tenets. Firstly, although attendance at lectures and reviewing written matter is important, didactic material should not

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replace direct interaction with knowledgeable colleagues. My personal experience suggests that beginning with transthoracic echocardiography is an invaluable first step. Secondly, it must be recognized that there will be different comfort levels among practitioners, and consultation with more skilled colleagues, be they anesthesiologists or cardiologists, should be encouraged. Even if intraoperative TEE is used solely as a monitor of ventricular function, it behooves the practitioner to perform a complete examination and to recognize that unexpected pathologic lesions, when present, may necessitate consultation. And lastly, all practitioners who are involved with TEE would serve themselves and their institutions by striving to pass one of the examinations of special competence. A working group of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists developed guidelines for performing a comprehensive intraoperative TEE examination.[7] Their recommendations are summarized in Figure 2-1 (Figure Not Available) . It is the committee's contention that if the practitioner performs a careful and systematized examination every time the probe is inserted, the chance of missing important findings is minimized, and the potential for teaching is enhanced. Figure 2-1 (Figure Not Available) Twenty cross-sectional views composing the recommended comprehensive transesophageal echocardiography examination. The icon adjacent to each view indicates the approximate multiplane angle. ME, midesophageal; LAX, long axis; TG, transgastric; SAX, short axis; AV, aortic valve; RV, right ventricle; asc, ascending; desc, descending; UE, upper esophageal. (From Shanewise JS, Cheung AT, Aronson S, et al: Anesth Analg 1999;89:870.)

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluation of Intraoperative Ventricular Function Left Ventricular Filling In the operating room, rapidity is needed in the assessment of preload during periods of hemodynamic instability. Since the introduction of the pulmonary artery catheter in the 1970s, measurement of pulmonary capillary wedge pressure as a surrogate of left ventricular end diastolic volume has been the intraoperative practice standard; however, it is recognized that especially in situations of decreased ventricular compliance, the pulmonary capillary wedge pressure is an inaccurate estimate of preload.[8] TEE has the potential to refine this measurement by allowing Doppler estimation of left atrial pressure, two-dimensional measurement of left ventricular cross-sectional area, and calculation of left ventricular volume. Left Atrial Pressure

Left atrial pressure can be estimated with Doppler TEE by several methods. If mitral regurgitation is present, 25

measurement of the peak velocity of the regurgitant jet and application of the modified Bernoulli equation allows calculation of the left ventriculoatrial pressure gradient; subtraction of this number from the peak systolic blood pressure yields left atrial pressure[9] (Fig. 2-2) . Certain mitral inflow and pulmonary venous variables also correlate with left atrial pressure; Kuecherer et al[10] found that in patients undergoing cardiovascular surgery, changes in the systolic fraction of the pulmonary venous tracing correlated inversely and strongly with pulmonary capillary wedge pressure, and they theorized that this related to decreased atrial compliance. Nomura et al[11] found that in patients with ejection fractions

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less than 35%, the deceleration time of the early velocity of mitral inflow correlated with pulmonary capillary wedge pressure, and that a deceleration time greater than 150 msec was strongly predictive of a pulmonary capillary wedge pressure of less than 10 mm Hg. There are a number of caveats related to the intraoperative estimation of left atrial pressure with TEE. Patients with a rhythm other than sinus or with valvular regurgitation were excluded in most studies; these are the very patients in whom preload estimates are often crucial. In suitable patients, correlations but not absolute values of left atrial pressure are usually yielded. Use of the mitral regurgitation jet to calculate left atrial pressure dictates that mitral regurgitation must be present. And finally, an estimate of left atrial pressure, whether obtained by Doppler echocardiography or by pulmonary artery catheter, may still yield inaccurate estimates of preload in patients with decreased ventricular compliance. End-Diastolic Area and End-Systolic Area

A number of authors have examined the intraoperative relationship between end-diastolic and end-systolic area Figure 2-2 Measuring the peak velocity (V) of the mitral regurgitation (MR) jet and applying the modified Bernoulli equation yields a pressure gradient (PG) between the left atrium and ventricle of 56 mm Hg. Subtracting this value from the systolic arterial pressure of 86 mm Hg gives a left atrial pressure (LAP) of 30 mm Hg. BP, blood pressure.

measured at the transgastric midpapillary level and cardiac volume status. Cheung et al[12] performed an elegant study examining the effect of graded hypovolemia produced by autologous blood collection on hemodynamic and TEE-derived indices of left ventricular preload in patients undergoing coronary artery bypass surgery. Patients with valvular insufficiency, rhythms other than sinus, and overt congestive heart failure were excluded. Patients were stratified on the basis of resting left ventricular function. Enddiastolic area, end-systolic area, pulmonary capillary wedge pressure, and measures of end-diastolic and end-systolic wall stress decreased linearly as blood volume was reduced from 0 to 15% in all patients; however, in patients with impaired left ventricular function, only the TEE-derived indices maintained linearity (Fig. 2-3) (Figure Not Available) . Other studies have also demonstrated that single plane areas, although not

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predictive of absolute left ventricular volumes,[13] [14] can generally be used to monitor for a trend toward increased or decreased volume.[15] [16] [17] It must also be remembered that the presence of a small end-diastolic area or end-systolic area does not always reflect decreased intravascular volume. Small left ventricular volumes can be seen with restrictions to filling, as in pericardial disease, or decreased right heart function, as in right ventricular infarction or large pulmonary embolus[18] (Fig. 2-4) . Patients presenting for cardiac surgery often have preexisting impairment of diastolic function. De Hert et al[19] obtained transmitral flow signals with TEE and high-fidelity recordings of left ventricular pressure in patients anesthetized for coronary bypass. A subset of patients was identified in whom leg elevation resulted in a decreased dP/dt; those same patients developed a restrictive pattern on mitral inflow. Diastolic function is worsened to a variable degree following cardiopulmonary bypass.[20] This explains the frequent inadequacy of left ventricular filling despite seemingly adequate filling pressures.

26

The presence of end-systolic obliteration of the left ventricular cavity, although usually associated with hypovolemia (Fig. 2-5) , may also be associated with increased inotropy, or redistribution of blood out of the thoracic cavity.[21] Left Ventricular Volumes

In an in vitro study using silicone rubber models of the left ventricle, the calculation of left ventricular volumes using multiplane TEE and the disk summation method[22] was found to be highly accurate.[23] However, problems related to the moving heart, exclusion of akinetic segments of the left ventricle, and difficulty in getting a true long-axis view of the left ventricle have led to disappointing Figure 2-3 (Figure Not Available) End-diastolic area (EDA) and end-systolic area (ESA) in response to graded hypovolemia yielded estimated blood volume (EBV) deficits of 0 to 15%. Patients had either normal left ventricular (LV) function or reduced LV function. Control patients were not subjected to hypovolemia. (From Cheung AT, Savino JS, Weiss SJ, et al: Anesthesiology 1994;81:376–387.)

Figure 2-4 Transgastric image of a transesophageal echocardiography

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scan obtained in a patient who had suffered massive fat embolism. Increased pulmonary vascular resistance and subsequent right ventricular (RV) dilation led to impaired left ventricular (LV) filling.

results when used in the perioperative setting.[14] [24] Technologic advances such as three-dimensional TEE,[25] harmonic imaging,[26] and automated border detection may lead to improved intraoperative accuracy. In summary, the assessment of preload with intraoperative TEE is in most cases a semiquantitative estimate based on visual inspection of enddiastolic and end-systolic areas and on temporal comparison with the use of videotape or stored cine loops. Confounding conditions such as right ventricular failure or the administration of inotropic agents must be considered. Global Systolic Function Cardiac Output

Ventricular filling, contractility, wall stress, and heart rate all influence cardiac output. Thus, cardiac output is the measurement most often used in anesthetic and critical care practice as a guide to therapeutic manipulations of cardiac function. Despite its limitations,[27] [28] thermodilution cardiac output measurement has been considered the "gold standard" since being popularized in the early 1970s. Doppler transesophageal echocardiography has the potential to be used in the intraoperative setting for the continuous measurement of cardiac output. These methods utilize the concept that the cross-sectional area of a conduit within the cardiovascular system multiplied by the Doppler-derived timevelocity integral yields the stroke volume through that conduit. When the result is multiplied by heart rate, the product is cardiac output. Several important assumptions are inherent to this approach. Valid area formulas must be applicable to the anatomic site being analyzed. The velocity profile across the valve must be flat and devoid of skew.[29] [30] Whichever anatomic area is chosen, the ability to consistently obtain the image and to interrogate parallel to flow is mandatory. Pulmonary Artery.

With the probe at 0 degrees and retroflexed, the main pulmonary artery and pulmonic valve can be imaged at the base of the heart (Fig. 2-6) . This

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Figure 2-5 Transesophageal echocardiogram from a hypovolemic patient. During systole, the posteromedial and anterolateral papillary muscles touch. LV, left ventricle; RV, right ventricle.

Figure 2-6 Imaging at the base of the heart of the main pulmonary artery (PA) and its branches. Pulsed Doppler velocity time integral (VTI) and diameter measurement are used to calculate stroke volume. MnGRAD, mean gradient; PGRAD, peak gradient; PV, pulmonary valve; Vmax, maximum velocity.

28

site has been examined with pulsed wave Doppler,[30] [31] [32] and in a study by Gorcsan et al,[33] using both pulsed wave and continuous wave methodologies, pulmonary artery diameter was measured just distal to the pulmonic valve. Interobserver variability was low in all studies, and correlation with thermodilution was strong in all but the study by Muhiudeen et al,[31] in which patients with inaccurate thermodilution measurements may have been included. The major limitation with using the pulmonary artery is the inability to obtain an adequate two-dimensional image for diameter measurement in up to 25% of patients. Right Ventricular Outflow Tract.

With the probe turned rightward and flexed, the right ventricular outflow tract is imaged from the stomach between 0 and 120 degrees (Fig. 2-7) . Imaging frequency must usually be reduced to ensure optimal penetration. Maslow et al[34] found excellent correlation between cardiac output calculated with pulsed wave Doppler and thermodilution. Patients with pulmonary hypertension, significant tricuspid regurgitation, and non-sinus rhythms were excluded. Again, in a significant percentage (16%) of patients, the two-dimensional image was not suitable. Left Ventricular Outflow Tract.

With the probe in the stomach, turned leftward, in the flexed position, and at low imaging frequency, the aortic valve and left ventricular outflow tract

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can usually be imaged between 0 and 140 degrees (Fig. 2-8) (Figure Not Available) . Imaging from the stomach allows parallel pulsed Doppler interrogation of the left ventricular outflow tract, and its diameter, obtained from either the stomach or the midesophageal 120-degree view, allows calculation of the cross-sectional area and cardiac output (Fig. 2-9) . Strong correlation with thermodilution and low interobserver variability have been described.[35] [36] To avoid contamination of the Doppler signal by the region of flow acceleration adjacent to the aortic Figure 2-7 Pulsed wave (PW) Doppler measurement from the right ventricular outflow tract (RVOT) (color plate). RV, right ventricle.

valve orifice, the sample volume must be placed precisely in the left ventricular outflow tract. Aortic Valve.

Using the transgastric view described for left ventricular outflow tract, several investigators have studied the combination of continuous wave Doppler positioned through the left ventricular outflow tract and aortic valve and cross-sectional area of the aortic valve using the triangle method (Fig. 2-10) .[37] [38] In brief, the triangular shape of the aortic valve orifice at mid-systole is assumed to represent the time averaged value for the aortic valve area. Strong correlation with thermodilution and low interobserver variability were again obtained (Fig. 2-11) . As continuous wave Doppler is used, it is important to confirm that the maximal peak velocity is occurring at the aortic valve. The triangle method is limited to patients with unrestricted aortic valve opening. Mitral Valve.

Using the mitral valve for calculation of cardiac output has the advantages of consistent imaging and parallel Doppler alignment. However, the saddle shape of the mitral annulus makes the area measurement unpredictable, and the cross-sectional velocity skew[29] is of concern when using pulsed wave Doppler. Practical Considerations.

For intraoperative transesophageal Doppler calculation of cardiac output, the left ventricular outflow tract method is the most reproducible. Adjustments in the degree of probe flexion and imaging angle should be

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made to ensure that the aortic valve and ascending aorta are clearly visualized and that the Doppler intercept angle is small (see Fig. 2-9) . Several measurements should be made and averaged, this being especially important when dealing with rhythms other than sinus. In practical terms, Doppler measurement of cardiac output is used when a pulmonary artery catheter is not in place, or when conditions such as severe tricuspid regurgitation render thermodilution inaccurate. There is a need for 29

Figure 2-8 (Figure Not Available) Transesophageal echocardiography imaging from the stomach allows parallel alignment with the ascending aorta. (From Perrino AC Jr., Harris SN, Luther MA: Anesthesiology 1998;89:350–357.) Figure 2-9 Transgastric imaging of the left ventricular outflow tract (LVOT). The ascending aorta is well visualized, and the Doppler intercept angle is small. Pulsed Doppler velocity time integral (VTI) and diameter measurement are used to calculate stroke volume. MnGRAD, mean gradient; PGRAD, peak gradient; Vmax, maximum velocity.

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Figure 2-10 The triangle method of aortic valve area measurement. (From Darmon PL, Hillel Z, Mogtader A, et al: Anesthesiology 1994;80:796–805.)

further validation of this approach in patients with a spectrum of cardiovascular diseases. Ejection Fraction and Stroke Volume

Although it is somewhat load dependent and therefore not a pure index of "left ventricular function,"[39] ejection fraction is often assumed to reflect ventricular contractility. During intraoperative TEE, the fractional area of change measured at the transgastric midpapillary level is often used interchangeably with ejection fraction, although gauging volume in a potentially asymmetric Figure 2-11 Regression analysis: thermodilution cardiac output (TCO)

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and Doppler cardiac output (DCO) using the aortic valve triangle method. (From Darmon PL, Hillel Z, Mogtader A, et al: Anesthesiology 1994;80:796– 805.)

chamber based on a measure of area has obvious limitations.[40] [41] A number of studies report the relationship between TEE-derived fractional area of change and radionuclide-derived ejection fraction. Clements et al[42] examined the relationship in 12 patients having abdominal aortic aneurysm surgery. There was excellent correlation in patients with both normal and abnormal left ventricular function. In patients with ventricular dyssynergy, fractional area of change led to a slight overestimate of ejection fraction. Urbanowicz et al[13] found strong correlation in 10 patients following coronary artery bypass grafting. In a series of 15 patients following coronary artery bypass grafting, Ryan et al[14] measured TEE ejection fraction using volumes calculated from the modified Simpson's and arealength methods[43] in addition to TEE-derived fractional area of change and radionuclide-derived ejection fraction. Unlike previous studies, variability was calculated and found to be small and not significantly different between the three measurement techniques. Not surprisingly, the TEE volumetric results were more representative of radionuclide ejection fraction than fractional area of change. Smith et al[24] also found that ejection fraction based on TEE volumetric methods were comparable to those obtained with angiography. In an attempt to develop online methods of intraoperative functional assessment, the technique of automated border detection has been used (see Chapter 7) . Automated border detection is based on the principle of acoustic quantification of ultrasonic back scatter signals to detect the bloodtissue interface and thereby define the endocardial edge.[44] Measurements correlate closely to those obtained by manual tracing of the endocardial border. [45] [46] [47] Gorcsan et al[17] examined stroke area, defined as the difference between end-systolic area and end-diastolic area measured at the midpapillary level, and compared the results to stroke volume measured in the ascending aorta by an electromagnetic flow probe in nine patients undergoing coronary artery bypass. Preoperative left ventricular function was largely preserved. Measurements were made before and after cardiopulmonary bypass. There was a strong correlation between the measurements at all periods of the study. Katz et al[48] compared stroke volume as measured by thermodilution to stroke volume obtained with automated border detection determination of end-systolic and end-diastolic areas and volumetric formulas (Fig. 2-12) ; these latter measurements were

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made at the two-chamber and four-chamber midesophageal views. There was a close correlation between stroke volumes obtained by the two methods, but whereas the two-chamber view led to an average underestimate of 0.4 L, the four-chamber view led to an average underestimate of 1.9 L. In a similar study, Greim et al[49] used the twochamber view alone. Directional changes in stroke volume between thermodilution and automated border detection again correlated closely; however, the automated border detection technique significantly underestimated stroke volume. Ejection fraction has been estimated using automated border detection derived measurements of fractional area of change at the midpapillary level and compared to radionuclide-derived ejection fraction.[45] [46] [47] Although the directionality of change was significantly 31

Figure 2-12 An example of transesophageal echocardiography automated border detection from the four-chamber view with ventricular volume estimated on line by the area length method. (From Katz WE, Gasior TA, Reddy SC, et al: Am Heart J 1994;128:389–396.)

correlated, fractional area of change derived by automated border detection consistently overestimated radionuclide-derived ejection fraction. It would appear that fractional area of change more closely estimates ejection fraction in patients with normal ventricular function. The use of TEE-derived volumetric data to estimate ejection fraction is more accurate, but the cumbersome calculations involved do not lend themselves to rapid intraoperative derivation. The use of automated border detection algorithms and programmed volume calculations may prove superior but are largely untested in clinical practice. At present, the intraoperative assessment of ejection fraction is impractical, and stroke volume measurement is best accomplished with either Doppler or thermodilution methodology. Contractility

The end-systolic pressure-volume relationship and resultant end-systolic elastance defines contractility in a load-independent fashion[50] and would therefore be of potential use in the estimation of intraoperative left ventricle contractility and in the quantification of changes resulting from manipulations such as cardiopulmonary bypass.

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A number of surrogates of this relationship have been described to facilitate the practical acquisition of this information in an operating room setting. The substitution of femoral arterial pressure for left ventricular end-systolic pressure,[51] end-systolic area for end-systolic volume,[20] [52] [53] and endsystolic wall stress for end-systolic pressure[53] have been made. Although these substituted measurements are not construed as replacements for traditional measures of pressure and volume, their directional change suggests that in cardiac surgical patients undergoing cardiopulmonary bypass, they may be used as an alternative way of assessing loadindependent left ventricular function. The changes in contractility as a result of cardiopulmonary bypass[20] [54] and the administration of anesthetic agents[52] appear better assessed with estimates of end-systolic elastance than with more traditional indices of ventricular performance such as fractional area of change. Figure 2-13 illustrates the decrease in elastance (Ees) and increased chamber stiffness (Kc) that occur following cardiopulmonary bypass, and the mitigating effect of volume loading prior to bypass termination. At present, the methods for data analysis are prohibitively complex.[55] [56] Right Ventricular Function

In the setting of cardiopulmonary bypass, the evaluation of right ventricular function is important. Right ventricular dysfunction often occurs secondary to the inadequate delivery of cardioplegia[57] and to the embolization of intracardiac air down the right coronary artery following separation from cardiopulmonary bypass. The triangular shape of the right ventricle makes its global function hard to quantitate with TEE, and the abnormal septal motion often seen following cardiopulmonary bypass[58] compounds this difficulty. Rafferty et al[59] measured planimetered areas and major and minor axes in both long-axis and short-axis images of the right ventricle with TEE, before and after cardiopulmonary bypass. Unfortunately, the echo measurements, obtained offline, were not compared in a meaningful way to results obtained by thermodilution. Semiquantitative analysis of right ventricular function with TEE has also been attempted with the analysis of hepatic venous flow.[60] Many factors other than right ventricular systolic function, however, affect hepatic venous flow. In patients with diverse causes of right ventricular dysfunction, Vignon et al[61] demonstrated the ability to 32

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Figure 2-13 Effect of cardiopulmonary bypass (CPB) on elastance (Ees) and chamber stiffness (Kc) of the left ventricle. Times of measurement were before the start of CPB (baseline); immediately after separation from CPB (time 0); and 5 minutes (time 5), 10 minutes (time 10), and 15 minutes (time 15) later. In protocol 1, preload was optimized just before the start of the separation procedure from CPB. In protocol 2, preload was optimized 10 minutes before the anticipated separation time. Data are shown as mean ± SEM. In protocol 1, ventricular function after separation from CPB was impaired, with a decrease in Ees and an increase in Kc, and a progressive improvement of ventricular function within the first 10 minutes after separation from CPB. These findings were not seen in protocol 2, in which ventricular function remained unchanged and comparable to baseline values. *Difference between both groups is statistically significant at P < 0.01. (From De Hert SG, Rodrigus IE, Haenen LR, et al: Anesthesiology 1996;85:1063–1075.)

quantitate right ventricular function with color kinesis and surface echocardiography. This method of examining right ventricular function has not been evaluated in an intraoperative setting with TEE. At the present time, TEE assessment of intraoperative right ventricular function is best accomplished by visual inspection and semiquantitative assessment in both the transgastric and the four-chamber views. Excellent transgastric views of all three leaflets of the tricuspid valve and the entire free wall of the right ventricle are best obtained by scanning at approximately 40 degrees (Fig. 2-14) . Regional Wall Motion The suggestion of a link between perioperative myocardial ischemia and cardiac morbidity[62] [63] has led to an intensive search for accurate methods of its intraoperative detection (Fig. 2-15) (Figure Not Available) . Visual inspection of ST segment changes has been the foundation upon which the newer technologies of automated ST analysis and TEE detection of regional wall motion abnormalities have been added. There are several points on which to judge the merits of TEE: Applicability, accuracy, reproducibility, cost, expertise required for interpretation, and prognostic importance. Segmental analysis is most frequently undertaken using the 16-segment model first proposed by Schiller et al[64] and later modified for TEE by Shanewise et al[7] (Fig. 2-16) (Figure Not Available) . Excellent inter- and intraobserver variability has been documented when six segments at the midpapillary level were analyzed offline by an anesthesiologist trained in

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TEE and an echocardiographer.[65] The recognition that coronary occlusion leads to the immediate development of regional wall motion abnormalities[66] and their frequent regression following revascularization[67] has prompted investigators to examine the usefulness of intraoperative TEE as a monitor of ischemia. The paucity of contraindications to TEE means that it can be used in most patients undergoing general anesthesia. The midpapillary view is generally easy to obtain and demonstrates areas of myocardium subtended by the three major coronary arteries. Interpretation is rarely confounded by rhythm disturbances, as is the case for automated ST analysis. TEE cannot be used, however, in patients receiving regional anesthesia, and, because the probe is not inserted until after anesthetic induction, it cannot detect changes during this vulnerable period. Assessment of the accuracy of TEE in the detection of myocardial ischemia has been limited somewhat by the lack of a reliable reference standard. Smith et al[68] found that in patients at high risk of myocardial ischemia who were analyzed offline, wall motion changes could be detected Figure 2-14 Transgastric image of the right ventricular (RV) free wall, septum, and the leaflets of the tricuspid valve.

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Figure 2-15 (Figure Not Available) Causes of ischemic changes on intraoperative monitors (color plate). (From Fleisher LA: Anesthesiology 2000;92:1183–1188.)

more quickly and commonly than ST segment changes. Conflicting studies[69] [70] regarding the prognostic importance of regional wall motion abnormalities were subsequently published. In a study by London et al,[69] 156 patients undergoing noncardiac surgery who were at high risk for coronary artery disease were studied. Specific clinical, electrocardiographic, or hemodynamic events prompted analysis of stored images. The number of new wall motion abnormalities detected was low, and discordance with electrocardiographic findings was significant (Table 2-1) . The number of postoperative cardiac complications was low. In the

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study by Leung et al,[70] patients undergoing coronary artery bypass were examined with electrocardiography and TEE. Although prebypass ischemia was rare, postbypass ischemia was more common and postoperative cardiovascular complications were associated more closely with TEE findings than with electrocardiography alone. It is now accepted that regional wall motion abnormalities, although often the result of myocardial ischemia, may be due to hypovolemia, tethering of nonischemic myocardium, and myocardial stunning after cardiopulmonary bypass.[71] [72] Offline analysis has been employed in most of the large-scale studies involving comparison of TEE with other methods of ischemia detection, but extrapolation to the accuracy of real-time TEE analysis should not be assumed. Regional wall motion abnormalities that subtend the anatomic distribution of coronary TABLE 2-1 -- Comparison of Transesophageal Echocardiography (TEE) and Intraoperative Electrocardiography (ECG) Monitoring for Myocardial Ischemia * TEE + TEE ECG + 8 (1 MI) 11 ECG 24 (2 MI, 1 UA) MI, myocardial infarction; UA, unstable angina. From London MJ, Tuban JF, Wong MG, et al: Anesthesiology 1990;73 (4):644. * P < 0.05.

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Figure 2-16 (Figure Not Available) A 16-segment model of the left ventricle. A, Fourchamber views show the three septal and three lateral segments. B, Two-chamber views show the three anterior and three inferior segments. C, Long-axis views show the two anteroseptal and two posterior segments. D, Middle short-axis views show all six segments at the midpapillary level. E, Basal short-axis views show all six segments at the basal level. (From Shanewise JS, Cheung AT, Aronson S, et al: Anesth Analg 1999;89:870–884.)

artery flow are more often a result of ischemia than those that do not.

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Comunale et al[73] also documented the poor concordance between the TEE and electrocardiography and attributed this finding to the lack of standard definitions of significant regional wall motion abnormalities and ischemic ST changes, the exclusion of longitudinal TEE views, and the use of different models of segment nomenclature. The role of intraoperative monitoring of myocardial ischemia with TEE remains unclear. Intraoperative TEE monitoring is better suited to patients undergoing cardiac as opposed to noncardiac surgery and to those patients in whom more traditional methods of ischemia are deemed inadequate. The ability to monitor additional tomographic planes,[74] [75] the use of cine loops for comparison, and the advent of new technologies such as automated border detection and Doppler tissue imaging should improve accuracy. Regional wall motion abnormalities precede electrocardiographic changes, [76] and, once ischemia is diagnosed, TEE can be used to directly monitor the effects of intervention. Personnel with expertise in the online assessment of wall motion abnormalities are needed, however. Lastly, studies examining the outcomes of patients monitored for myocardial ischemia with TEE are needed. Intraoperative Assessment of Coronary Reserve Dobutamine stress echocardiography is a well-established technique for diagnosing coronary artery disease and predicting the improvement of dysfunctional myocardium postoperatively (see Chapter 14) .[77] [78] The ability to predict the reversibility of left ventricular dysfunction with the use of intraoperative low-dose dobutamine TEE was examined by Aronson et al[79] in the setting of coronary artery bypass grafting. The odds ratios for early and late improvement in myocardial function were 20.7 and 34.6 times higher if preoperative low-dose dobutamine produced improved function than if it did not. The instances when this intraoperative strategy might supplant the normal preoperative assessment of myocardial viability by transthoracic dobutamine stress echocardiography[78] or low-dose dobutamine technetium-99m sestamibi scintigraphy[80] have yet to be determined.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Use of Transesophageal Echocardiography to Monitor Intraoperative Cardiac Function in Specific Clinical Entities The use of TEE has improved our ability to intelligently manage postcardiopulmonary bypass instability. It has allowed us to understand the intraoperative changes that occur during some of the newer techniques in coronary revascularization and can guide us in placement of numerous intracardiac and intravascular devices. Its use in monitoring cardiac function during noncardiac surgery is most advantageous in the diagnosis of sudden and unexplained hemodynamic instability. Separation from Cardiopulmonary Bypass At the time of separation of the patient from cardiopulmonary bypass, the use of TEE may guide the anesthesiologist in the use of pharmacologic and nonpharmacologic therapies and can maximize the likelihood of a smooth transition. Intracardiac Air

Left-sided intracardiac air is ubiquitous following procedures in which leftsided chambers have been open to atmosphere and is identified by its characteristic "firefly" appearance. Air is often seen entering the left atrium from the pulmonary veins or enmeshed in the mitral subvalvular apparatus (Fig. 2-17) . Echocardiographic inspection is carried out in the fourchamber and transgastric long-axis views. Careful evacuation by the surgeon is important and involves suctioning on the aortic root vent or needle aspiration of the left ventricular apex to evacuate trapped pockets. As well as guiding evacuation, TEE is 35

Figure 2-17 Four-chamber midesophageal view. As the patient is being

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separated from cardiopulmonary bypass (CPB), a pocket of air enmeshed in the left ventricular subvalvular apparatus is noted (asterisk), with numerous bubbles emanating from it. LA, left atrium; LV, left ventricle.

useful in diagnosing the consequences of embolization through the right coronary ostium, which results in ventricular dysfunction in a right coronary distribution. Cardiac Output

There are a number of potential causes of low cardiac output immediately following cardiopulmonary bypass: perioperative infarction, coronary air emboli, metabolic abnormalities, hypovolemia, left ventricular outflow tract obstruction, and inadequate myocardial protection. It seems intuitive that the yield of TEE when it is used during hemodynamic instability during and after cardiac surgery would be high. Two published series[81] [82] have demonstrated the myriad diagnoses that have been made TABLE 2-2 -- Relevant Intraoperative Transesophageal Echocardiograph Findings Categorized by Indication Indication, n

Finding Severe left ventricular dysfunction ± regional wall motion abnormality Aortic dissection ± aortic regurgitation Significant mitral regurgitation Intracardiac/great vessel shunt Hyperdynamic left ventricular function

HEMODYNAMIC SURGICAL INSTABILITY PLANNING TRAUMA HYPOXEMIA 15 2

1

13

4

2

1

1

2

TOTA NO. O PATIE

2 1

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Severe right 2 1 ventricular dysfunction Extracardiac clot 2 Significant aortic 2 regurgitation Significant 1 tricuspid regurgitation Pericardial 1 tamponade No relevant 5 1 4 3 findings From Brandt RR, Oh JK, Abel MD, et al: J Am Soc Echocardiogr 1998;1 (10):972. and the ability to intervene on many (Table 2-2) . No attempt was made to compare TEE with other diagnostic modalities, although the speed with which information is made available appears hard to supersede. The use of myocardial contrast echocardiography has improved our understanding of the distribution of cardioplegia delivered by both anterograde and retrograde routes. The ability to predict the adequacy of delivery based on knowledge of coronary anatomy and the presence of angiographically demonstrated collateral flow is marginal at best.[83] It is also clear that retrograde cardioplegia does not reliably perfuse the right ventricular free wall,[57] [84] and, in some centers, this observation has led to a strategy of early cardioplegia administration down a vein graft to the right coronary artery.[85] In the future, the use of myocardial contrast echocardiography may help to 36

Figure 2-18 A, Transesophageal echocardiography to investigate hypoxia revealed an expanding ascending aortic aneurysm with main pulmonary artery (PA) compression. B, Normal image for comparison. LA, left atrium; SVC, superior vena cava.

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differentiate postbypass stunning, which would be treated with cardiopulmonary support, from graft obstruction, which would be treated with surgical correction.[86] [87] Off-Pump Coronary Bypass Surgery The off-pump bypass surgical approach to coronary revascularization involves bypassing coronary arteries without cardiopulmonary bypass, otherwise known as the "beating heart" operation. TEE can detect regional wall motion abnormalities during intermittent coronary occlusion and cardiac lifting, which, if persistent, may necessitate the institution of cardiopulmonary bypass. The use of color kinesis to better define regional wall motion abnormalities intraoperatively has been described [88] but is limited somewhat by cardiac translocation during surgical manipulation. Cardiac Function in Noncardiac Surgery The use of TEE to monitor cardiac function in noncardiac surgery has been described largely in anecdotal form. In most of the case reports, unexplained hypotension prompted the use of TEE, and subsequent diagnoses have included massive pulmonary embolism,[89] [90] intracardiac tumor extension,[91] retroperitoneal hemorrhage,[92] cardiac tamponade,[93] main pulmonary artery obstruction by an expanding aortic aneurysm[94] (Fig. 2-18) , traumatic cardiac injury,[95] [96] [97] ventilator-induced systemic air embolism,[98] [99] and a case of venous air embolism during pelvic surgery, which resulted in pulseless electrical activity until open cardiac aspiration was undertaken (Fig. 2-19) . Positioning of Intravascular Devices Intraoperative TEE can be used to guide the positioning of a number of intravascular devices: Central Venous Pressure Air Aspiration Catheters.

These are often used during sitting craniotomies to aspirate air that has gained access to the venous circulation. Correct positioning is at the right atrial-superior vena caval junction, and imaging is best in the midesophagus with rightward rotation and a transducer angle of approximately 90 degrees (Fig. 2-20) . Intra-aortic Balloon Pump.

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The benefits of intra-aortic balloon pump have been demonstrated with TEE and include improved left ventricular function and decreased wall stress. [100] [101] The balloon pump is best imaged in the descending aorta in a vertical plane. Correct positioning is at the inferior border of the transverse aortic arch.[102] Once the tip of the balloon is visualized at a transducer angle of approximately 90 degrees, the probe marking at the teeth is noted. The probe is slowly withdrawn until the left subclavian artery orifice is seen; the marking is again noted. The distance between the balloon and the subclavian orifice should be approximately 5 cm (Fig. 2-21) . Left Ventricular Assist Device.

As the left ventricular assist device withdraws blood from the left ventricle, left atrial pressure falls below right atrial pressure. It is important Figure 2-19 During pelvic surgery, massive amounts of air are seen entering the right atrium (RA) via the inferior vena cava (IVC).

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Figure 2-20 A catheter inserted from the arm is positioned at the junction of the right atrium (RA) and superior vena cava (SVC) to evacuate any air that gains access to the venous circulation during sitting craniotomy. LA, left atrium.

to determine whether a patent foramen ovale is present, as right-to-left shunting will invariably occur. The orifice of the ventricular apical cannula should be imaged in the four-chamber view, and the lack of obstruction by adjacent walls should be ascertained[103] (Fig. 2-22) . Right Ventricular Assist Device.

In positioning the right atrial drainage cannula, it is preferable to avoid impingement on the tricuspid valve (Fig. 2-23) . Minimally Invasive Cardiac Surgery.

Port access surgery

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Figure 2-21 Intra-aortic balloon pump (IABP) positioned in the descending thoracic aorta. The left subclavian artery is visualized and not encroached upon.

involves the performance of a variety of surgical procedures through small thoracic ports or very limited incisions. Cannulation for the purposes of cardiopulmonary bypass and cardioplegic arrest is achieved percutaneously. TEE is used to position the various endovascular catheters and to monitor their position during surgery[104] [105] (Fig. 2-24) (Figure Not Available) . Some surgeons prefer an upper sternotomy incision. Cannulation is then achieved directly, except for the retrograde cardioplegia cannula, 38

Figure 2-22 The drainage component of the left ventricular assist device (LVAD) is seen to freely enter the apical region of the left ventricle (LV). LA, left atrium.

which is inserted through blind right atrial puncture and maneuvered into the coronary sinus under TEE guidance[106] (Fig. 2-25) . Left Ventricular Vent.

A left ventricular vent is placed through the right upper pulmonary vein into the left atrium and advanced through the mitral valve into the left ventricle to drain excess ventricular volume on bypass (Fig. 2-26) . Transplant Surgery Transesophageal echocardiography can be used to assess the function of the donor heart prior to procurement and after separation from cardiopulmonary bypass, when Figure 2-23 (color plate.) The drainage component of the right ventricular assist device (RVAD) enters the right atrium (RA) through the appendage (left, arrow). The tip is seen in the right atrium and free of the tricuspid valve on TEE (right). PA, pulmonary artery. Figure 2-24 (Figure Not Available) The various endovascular cardiopulmonary

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bypass catheters for post-access surgery are depicted. (From Siegel LC, St. Goar FG, Stevens JH, et al.: Circulation 1997;96:562–568.)

the effects of the ischemic time may become evident. During lung transplantation, the use of TEE has been described in the evaluation of vascular anastomoses,[107] and a recent case report documented a diagnosis of post-transplant pulmonary venous obstruction.[108] Laparoscopic Surgery As laparoscopic surgery has grown in its application, so has the realization that the associated pneumoperitoneum 39

Figure 2-25 During minimally invasive cardiac surgery, the coronary sinus catheter is seen entering the right atrium (RA) and passing into the coronary sinus. LA, left atrium.

leads to increased left ventricular wall stress[109] and decreased fractional area of change.[110] Following release of the pneumoperitoneum, higher than baseline fractional area of change has been described.[110] These hemodynamic alterations have been attributed to the physical effect of increased intra-abdominal pressure and to the associated neurohumoral changes. TEE has also been used to monitor for intraoperative gas embolization.[111]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Transesophageal Echocardiography as a Monitor of Intraoperative Ventricular Function: Impact on Perioperative Complications and Cost-Effectiveness Medical technology assessment has become an important step in the introduction and clinical use of increasingly sophisticated and costly methods of monitoring and diagnosis.[112] In anesthetic and critical care practice, no technology has engendered more controversy than the use of pulmonary artery catheterization, which has become an established monitor of cardiovascular function, despite the lack of significant outcome and costeffectiveness data.[113] [114] The use of TEE to monitor intraoperative ventricular function varies significantly between institutions[1] [115] and relates in part to the experience of the operator, the type of surgical procedure, and the cardiopulmonary reserve of the patient. For TEE to be deemed an effective mode of intraoperative monitoring, it must be shown to provide at least the same if not more information than currently accepted monitoring techniques, have a reasonable cost profile, involve acceptable risk, and alter outcome in a positive way. Kato et al[116] demonstrates the ability to diagnose and effectively manage intraoperative ischemia under TEE guidance, but, as is the case with many subsequent studies, their study falls short in not evaluating the effects of intraoperative TEE monitoring on patient outcome. Several studies have addressed the impact of intraoperative TEE monitoring of ventricular function during coronary bypass surgery. Bergquist et al[117] studied the concordance between real-time intraoperative TEE interpretation by five cardiac anesthesiologists and offline analysis by two blinded investigators in the assessment of left ventricular filling, ejection fraction area, and regional wall motion. Results obtained by the two methods were within 10% of each other 75% of the time with respect to ejection fraction and filling. The accuracy of regional assessment

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Figure 2-26 A left ventricular (LV) vent is seen passing into the left atrium (LA) via a right-sided pulmonary vein. MV, mitral valve.

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TABLE 2-3 -- Surgical Management Alterations During Coronary Artery Bypass Grafting Based on Transesophageal Echocardiographic Findings

Before CPB, n 2 NA NA 0 8

Before CPB After CPB After Total No. Separation, Separation, CC, of n n n Patients NA NA NA 2 NA 3 1 4 NA NA 2 2 0 0 1 1 2 3 1 12

Alteration Rush to CPB Return to CPB Reopen LVAD/ECMO Additional redo grafts IABP 4 3 2 0 9 CC, chest closure; CPB, cardiopulmonary bypass; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic balloon pump; LVAD, left ventricular assist device; NA, not applicable. From Savage RM, Lytle BW, Aronson S, et al: Ann Thorac Surg 1997;64(2):368. was variable: more accurate for normal than for abnormal wall motion and better in anesthesiologists with more advanced echocardiographic training. In the second part of the study,[118] TEE was found to be the most important factor in guiding hemodynamic interventions in 17% of cases examined. What is lacking is a clear demonstration that the TEE assessments were correct and that the same interventions would not have been undertaken if guided by more traditional monitors. Cost and outcome were not examined. Savage et al,[87] at the Cleveland Clinic, examined the use of intraoperative

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TEE monitoring in a group of high-risk patients undergoing coronary artery bypass grafting. As well as documenting numerous management changes related to TEE-derived information (Table 2-3) , they documented lower short-term morbidity and mortality rates as compared with a historical group of patients with similar severity scores[119] who were not monitored with TEE (Table 2-4) . An individual not part of the anesthetic or surgical team read the TEE scan; it is uncertain whether someone involved in direct patient management would have as readily garnered the information. In studies from Australia,[120] Europe,[121] Canada,[122] and India,[123] the realtime accrual of information with TEE was demonstrated to be of value in the management of hemodynamic perturbations and the planning of the surgical procedure in coronary bypass grafting as well as other cardiac surgical procedures Table 2-5 , Table 2-6 , and Table 2-7 ). No assessment of the effect of intraoperative TEE TABLE 2-4 -- Patient Outcomes with and without Intraoperative Transesophageal Echocardiography (TEE) Management without TEE 478 64.8 5.9 18 (3.8) 14 (3.5)

Variable Management with TEE Patients, n 82 Age, y 68.4 Severity score 6.1 Hospital deaths, n (%) 1 (1.2) Myocardial Infarction, n 1 (1.2) (%) Cardiac morbidity, n (%) 1 (1.2) 7 (1.5) ICU CNS morbidity, n (%) 3 (3.6) 18 (3.8) Hospital CNS morbidity, n 1 (1.2) 16 (3.3) (%) CNS, central nervous system; ICU, intensive care unit. From Savage RM, Lytle BW, Aronson S, et al: Ann Thorac Surg 1997; 64(2):368.

monitoring on patient outcome was made. These studies are summarized in Table 2-8 . The impact of monitoring of ventricular function during noncardiac surgery

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has not been studied as closely. In a retrospective review by Suriani et al, [124] the use of TEE was associated with some alterations in anesthetic and surgical management in a majority of cases. However, the indications for TEE were subjective, and neither the cost-effectiveness nor the effect on outcome was studied.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Has the burden of proof been met with respect to intraoperative TEE as a monitor of ventricular function? If one adopts the premise that rigorously designed, randomized, controlled clinical trials are society's benchmark,[125] TABLE 2-5 -- Impact of Routine Transesophageal Echocardiographic (TEE) Findings on Medical and Surgical Management: Coronary Artery Bypass Grafting After Cardiopulmonary Bypass (N = 120) Clinical Problem/TEE Finding (no. of patients) Consequence (no. of patients) Acute SWMA (8), acute Graft revision (3), papaverine (1), SWMA and medical therapy (5) moderate/severe mitral regurgitation (1) IABP not in optimal position (2) IABP not in descending aorta ST depression (II and V5)/no SWMA (3) Pulmonary

Impact E (3) * †

IABP advanced

I (6) V (2) ‡

IABP reinserted

V (1)

De-cannulation-good outcome

I (3)

Medical therapy for ischemia, not protamine reaction

I (1)

hypertension 3 minutes post protamine/

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widespread SWMA, moderate to severe mitral regurgitation E, essential; I, informative; IABP, intra-aortic balloon pump; SWMA, segmental wall motion abnormality; V, valuable. From Sutton DC, Kluger R: Anaesth Intensive Care 1998;26(3):287. * One patient also classified as valuable for IABP not in descending aorta. † One patient also classified as informative for ST depression without SWMA. ‡ Two patients also classified as informative in problems separating from CPB.

41

TABLE 2-6 -- Influence of Intraoperative Transesophageal Echocardiogra as the Driving Force on Interventions Compared with Other Monito Monitor Intervention, n (%) TEE ELECTROCARDIOGRAPHY Fluid bolus 275 0 (28) Anti-ischemic 207 114 (31) therapy (56) Vasopressor 56 3 (1) or inotrope (16) therapy Change in 4 0 anesthetic (2) depth Vasodilator 6 9 (6) therapy (4) Antiarrythmic 0 55 (89) therapy

ARTERIAL CATHETER 129 (13)

PULMONARY ARTERY OTH CATHETER 73 (7)

11 (3)

31 (8)

183 (51)

27 (7)

164 (78)

2 (1)

96 (68)

13 (9)

0

0

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Surgical 9 17 (33) 12 (23) 0 intervention (17) Miscellaneous 3 2 (6) 27 (75) 3 (8) (8) Total 560 200 (9) 622 (28) 149 (7) (25) From Kolev N, Brase R, Swanefelder J, et al: Anaesthesia 1998;53(8):76 *Indicates that the interventions were not based on information from the four monitors studied. More than half of these interventions were transfusion of blood for low hematocrit.

TABLE 2-7 -- Summary of Surgical Modifications Related to the Intraoperative Use of Transesophageal Echocardiography Modification Number Return on bypass for revision of coronary artery bypass graft 4 Modification of planned surgery: Valvular replacement cancelled 5 Valvular replacement or repair 11 Pleural drainage 3 Detection of air emboli before aortic unclamping 2 Surgical exploration for hemodynamic instability 7 Femoral artery bypass for aortic dissection 2 Others: Ventricular aneurysm resection 1 Aortoplasty 1 Cancellation of aortic dissection (diagnostic error) 1 Left ventricular assist device 1 Total 38 From Couture P, Denault AY, McKenty S, et al: Can J Anaesth 2000;47 (1):20.

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TABLE 2-8 -- Summary of Studies Examining the Alterations in Therapy During Cardiac Surgery with the Use of Intraoperative Transesophageal Echocardiography Altered Therapy, Study Population Surgery n/% 98/17% of all Bergquist n = 75, 584 C[118] Interventions revasc interventions et al Savage et n = 82 "High CSurgical change: [87] al risk" revasc 27/33% of patients Hemodynamic change: 42/51% of patients Sutton & n = 120 C16/13% of all patients Kluger revasc

Outcome Reported No Compared to historical controls

No

[120]

C-all 560/25% of all No Kolev et n = 224, [121] 2232 NC interventions al interventions Couture n = 851 C-all 125/15% of all No [122] et al patients Mishra et n = 5016 C-all 1146/23% of all No [123] al patients C-all, coronary and non-coronary cardiac surgery; C-revasc, coronary revascularizations; NC, noncardiac surgery.

42

then the jury is still out. The cost-effectiveness data that have been generated by studies of the use of TEE in congenital cardiac surgery,[126] preparation for elective cardioversion,[127] and determination of antibiotic treatment duration in endocarditis[128] have not yet demonstrated the benefits of monitoring of ventricular function in cardiac or noncardiac surgery. The data collected for studies are often reviewed offline, whereas clinical utility comes from online interpretation. Outcome data are scarce and sometimes conflicting. The "division of labor" in the operating room is also important, as too much attention to TEE may distract the anesthesiologist from other

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monitoring tasks.[129] Transesophageal echocardiography is an expensive undertaking and is not practically carried into the postoperative phase of patient management. Case studies and observational data cannot be dismissed, however. [130] [131] TEE has a unique ability to facilitate the rapid diagnosis of circulatory instability, and a number of observational studies show that information gained during intraoperative TEE frequently guides subsequent therapeutic maneuvers. In response, most fellowships in cardiac anesthesiology have incorporated instruction in the monitoring of ventricular function with intraoperative TEE. It must be emphasized that appropriate physician training and quality assurance[132] are crucial to the correct interpretation of data. Further technologic advancements such as color kinesis, automated border detection, and the use of loop storage for comparison should improve accuracy. Studies examining cost-effectiveness and outcome are needed.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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References 1. Poterack KA: Who uses transesophageal echocardiography in the operating room?

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9. Gorcsan JD, Snow FR, Paulsen W, et al: Noninvasive estimation of left atrial

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transmitral flow velocity patterns. Anesthesiology 2000;93:374. 20. De Hert SG, Rodrigus IE, Haenen LR, et al.: Recovery of systolic and diastolic left

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31. Muhiudeen IA, Kuecherer HF, Lee E, et al: Intraoperative estimation of cardiac

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Comparison of short axis imaging and simultaneous radionuclide angiography. Br J Anaesth 1990;64:331. 43. Wyatt HL, Haendchen RV, Meerbaum S, et al: Assessment of quantitative methods

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54. Gorcsan J 3rd, Gasior TA, Mandarino WA, et al: Assessment of the immediate effects of cardiopulmonary bypass on left ventricular performance by on-line pressurearea relations. Circulation 1994;89:180. 55. Deneault LG, Kancel MJ, Denault A, et al: A system for the on-line acquisition,

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wall motion abnormalities with transesophageal echocardiography. Can J Anaesth

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1999;46:827. 66. Tennant R, Wiggers CJ: The effect of coronary occlusion on myocardiol

contraction. Am J Physiol 1935;112:351. 67. Koh TW, Pepper JR, Gibson DG: Early changes in left ventricular anterior wall

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74. Koide Y, Keehn L, Nomura T, et al: Relationship of regional wall motion

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wall-motion abnormalities by transesophageal echocardiography: The incremental value of additional cross sections in the transverse and longitudinal planes. Anesth Analg 1996;83:1141. 76. Hauser AM, Gangadharan V, Ramos RG, et al: Sequence of mechanical,

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dobutamine technetium-99m sestamibi scintigraphy with low-dose dobutamine echocardiography for predicting functional recovery after revascularization. Am J Cardiol 2000;86:153. 81. Chan KL: Transesophageal echocardiography for assessing cause of hypotension

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antegrade and retrograde cardioplegia: A contrast echo study. Ann Thorac Surg 1999;68:955.

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86. Aronson S, Savage R, Toledano A, et al: Identifying the cause of left ventricular

systolic dysfunction after coronary artery bypass surgery: The role of myocardial contrast echocardiography. J Cardiothorac Vasc Anesth 1998;12:512. 87. Savage RM, Lytle BW, Aronson S, et al: Intraoperative echocardiography is

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intraoperative pulmonary embolism. Anesth Analg 1995;81:188. 91. Plowman AN, Bolsin SN, Patrick AJ: Unusual cause of intraoperative hypotension

diagnosed with transoesophageal echocardiography in a patient with renal cell carcinoma. Anaesth Intensive Care 1999;27:63. 92. Yamaura K, Okamoto H, Maekawa T, et al: Detection of retroperitoneal

hemorrhage by transesophageal echocardiography during cardiac surgery. Can J Anaesth 1999;46:169. 93. Hsin ST, Luk HN, Lin SM, et al: Detection of iatrogenic cardiac tamponade by

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with a left ventricular assist device in a patient with multiple trauma. J Thorac Cardiovasc Surg 1999;118:189. 96. Weiss RL, Brier JA, O'Connor W, et al: The usefulness of transesophageal

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critical care. Can J Surg 1999;42:171.

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98. Ibrahim AE, Stanwood PL, Freund PR: Pneumothorax and systemic air embolism

during positive-pressure ventilation. Anesthesiology 1999;90:1479. 99. Ho AM, Ling E: Systemic air embolism after lung trauma. Anesthesiology

1999;90:564. 100. Cheung AT, Savino JS, Weiss SJ: Beat-to-beat augmentation of left ventricular

function by intraaortic counterpulsation. Anesthesiology 1996;84:545. 101. Reichert CL, Koolen JJ, Visser CA: Transesophageal echocardiographic

evaluation of left ventricular function during intraaortic balloon pump counterpulsation. J Am Soc Echocardiogr 1993;6:490. 102. Shanewise JS, Sadel SM: Intraoperative transesophageal echocardiography to

assist the insertion and positioning of the intraaortic balloon pump. Anesth Analg 1994;79:577. 103. Scalia GM, McCarthy PM, Savage RM, et al: Clinical utility of echocardiography

in the management of implantable ventricular assist devices. J Am Soc Echocardiogr 2000;13:754. 104. Siegel LC, St. Goar FG, Stevens JH, et al: Monitoring considerations for port-

access cardiac surgery. Circulation 1997;96:562. 105. Coddens J, Deloof T, Hendrickx J, et al: Transesophageal echocardiography for

port-access surgery. J Cardiothorac Vasc Anesth 1999;13:614. 106. Secknus MA, Asher CR, Scalia GM, et al: Intraoperative transesophageal

echocardiography in minimally invasive cardiac valve surgery. J Am Soc Echocardiogr 1999;12:231. 107. Michel-Cherqui M, Brusset A, Liu N, et al: Intraoperative transesophageal

echocardiographic assessment of vascular anastomoses in lung transplantation. A report on 18 cases. Chest 1997;111:1229. 108. Huang YC, Cheng YJ, Lin YH, et al: Graft failure caused by pulmonary venous

obstruction diagnosed by intraoperative transesophageal echocardiography during lung transplantation. Anesth Analg 2000;91:558. 109. Branche PE, Duperret SL, Sagnard PE, et al: Left ventricular loading

modifications induced by pneumoperitoneum: A time course echocardiographic study. Anesth Analg 1998;86:482.

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110. Harris SN, Ballantyne GH, Luther MA, et al: Alterations of cardiovascular

performance during laparoscopic colectomy: A combined hemodynamic and echocardiographic analysis. Anesth Analg 1996;83:482. 111. Fahy BG, Hasnain JU, Flowers JL, et al: Transesophageal echocardiographic

detection of gas embolism and cardiac valvular dysfunction during laparoscopic nephrectomy. Anesth Analg 1999;88:500. 112. Fleisher LA, Mantha S, Roizen MF: Medical technology assessment: An

overview. Anesth Analg 1998;87:1271. 113. Connors AF Jr, Speroff T, Dawson NV, et al: The effectiveness of right heart

catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996;276:889. 114. Robin ED: Death by pulmonary artery flow-directed catheter: Time for a

moratorium? Chest 1987;92:727. 115. London MJ, Shroyer AL, Grover FL, et al: Evaluating anesthesia health care

delivery for cardiac surgery: The role of process and structure variables. Med Care 1995;33(10 suppl):OS66. 116. Kato M, Nakashima Y, Levine J, et al: Does transesophageal echocardiography

improve postoperative outcome in patients undergoing coronary artery bypass surgery? J Cardiothorac Vasc Anesth 1993;7:285. 117. Bergquist BD, Leung JM, Bellows WH: Transesophageal echocardiography in

myocardial revascularization: I. Accuracy of intraoperative real-time interpretation. Anesth Analg 1996;82:1132. 118. Bergquist BD, Bellows WH, Leung JM: Transesophageal echocardiography in

myocardial revascularization: II. Influence on intraoperative decision making. Anesth Analg 1996;82:1139. 45

119. Higgins TL, Estafanous FG, Loop FD, et al: Stratification of morbidity and

mortality outcome by preoperative risk factors in coronary artery bypass patients: A clinical severity score. JAMA 1992;267:2344. 120. Sutton DC, Kluger R: Intraoperative transoesophageal echocardiography: Impact

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on adult cardiac surgery. Anaesth Intensive Care 1998;26:287. 121. Kolev N, Brase R, Swanevelder J, et al: The influence of transoesophageal

echocardiography on intra-operative decision making: A European multicentre study. European Perioperative TOE Research Group. Anaesthesia 1998;53:767. 122. Couture P, Denault AY, McKenty S, et al: Impact of routine use of intraoperative

transesophageal echocardiography during cardiac surgery. Can J Anaesth 2000;47:20. 123. Mishra M, Chauhan R, Sharma KKHP, et al: Real-time intraoperative

transesophageal echocardiography: How useful? Experience of 5,016 cases. J Cardiothorac Vasc Anesth 1998;12:625. 124. Suriani RJ, Neustein S, Shore-Lesserson L, et al: Intraoperative transesophageal

echocardiography during noncardiac surgery. J Cardiothorac Vasc Anesth 1998;12:274. 125. Pocock SJ, Elbourne DR: Randomized trials or observational tribulations?

[editorial; comment]. N Engl J Med 2000;342:1907. 126. Siwik ES, Spector ML, Patel CR, et al: Costs and cost-effectiveness of routine

transesophageal echocardiography in congenital heart surgery. Am Heart J 1999;138(4 Pt 1):771. 127. Seto TB, Taira DA, Tsevat J, et al: Cost-effectiveness of transesophageal

echocardiographic-guided cardioversion: A decision analytic model for patients admitted to the hospital with atrial fibrillation. J Am Coll Cardiol 1997;29:122. 128. Rosen AB, Fowler VG Jr, Corey GR, et al: Cost-effectiveness of transesophageal

echocardiography to determine the duration of therapy for intravascular catheterassociated Staphylococcus aureus bacteremia. Ann Intern Med 1999;130:810. 129. Weinger MB, Herndon OW, Gaba DM: The effect of electronic record keeping

and transesophageal echocardiography on task distribution, workload, and vigilance during cardiac anesthesia. Anesthesiology 1997;87:144. 130. Benson K, Hartz AJ: A comparison of observational studies and randomized,

controlled trials [see comments]. N Engl J Med 2000;342:1878. 131. Concato J, Shah N, Horwitz RI: Randomized, controlled trials, observational

studies, and the hierarchy of research designs. N Engl J Med 2000;342:1887. 132. Rafferty T, LaMantia KR, Davis E, et al: Quality assurance for intraoperative

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46

Chapter 3 - Aortic Dissection and Trauma Value and Limitations of Echocardiography Elizabeth W. Ryan MD Ann F. Bolger MD

The rate of mortality with acute aortic dissection escalates hourly, [1] reaching 50% by 48 hours. Immediate diagnosis and therapy are critical for survival. Two thousand new cases of acute dissection are reported in the United States per year[2] the true incidence, including the large numbers of patients who die from unrecognized dissection, has been estimated at more that 10,000 per year.[3] Further, 10% to 30% of acute dissections occurring in the hospital may be misdiagnosed. Prompt diagnosis is a clinical challenge because patient's presenting symptoms may be nonspecific or even misleading. Aortic dissection must be included in the differential diagnosis of chest pain in many patients at risk for dissection and also when simultaneous acute involvement of multiple organ systems does not have a ready explanation. Acute dissection of the aorta can share many of the features of acute myocardial infarction: pain (related to the dissection itself or to myocardial ischemia), electrocardiographic abnormalities consistent with ischemia (resulting from involvement of the coronary ostia in proximal dissection),[4] and elevated serum creatinine kinase levels.[5] True myocardial ischemia is a potential component of the syndrome of aortic dissection. On pathologic examination, Hirst et al[6] found

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involvement of the coronary arteries in 39 of 505 cases of acute dissection (7.7%). Confusion of acute dissection with myocardial infarction not only delays appropriate treatment but also may lead to disastrous consequences if thrombolytic agents are administered.[7] [8] Thrombolysis impedes compensatory thrombosis of the false channel and promotes uncontrollable hemorrhage in the event of aortic rupture. Given that the incidence of aortic dissection is far less than that of myocardial infarction (0.26% of 5011 patients in the Anglo-Scandinavian Study of Early Thrombolysis trial[7] ) and that ST segment elevation is a relatively rare finding in patients with aortic dissection, classic electrocardiographic changes without physical findings suggesting dissection will rarely mislead clinicians toward thrombolysis.[9] Maintenance of a high suspicion for dissection must be paired with highly reliable tests to avoid such infrequent but catastrophic misdiagnoses. The optimal diagnostic test for acute aortic dissection, therefore, must be accurate, safe, and immediately applicable in a broad range of medical environments. The limited sensitivity of echocardiography for dissection from the transthoracic approach has been greatly improved by transesophageal approaches; transesophageal examinations can be performed within minutes in the emergency department, operating room, or intensive care unit and provides high-quality images of the thoracic aorta as well as of other cardiac and vascular structures at risk. The advantages and limitations of echocardiographic techniques 47

in the management of patients with aortic dissection have been carefully investigated at many centers, and, as a result, their strengths and weaknesses relative to other imaging techniques are being better defined. Ongoing advances in transesophageal probe technology and other ultrasonographic imaging methods are proceeding rapidly, with smaller transducers, multiple and variable imaging planes, and wider ranges of frequencies being made available. These improvements are solidifying the already well-established role of echocardiography in the diagnosis and follow-up of aortic dissection.

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Pathophysiology of Aortic Dissection Anatomy and Histology The aortic wall consists of three layers: the intima, which is a single layer of vascular endothelium; the media, with concentric layers of smooth muscle cells, collagen, elastin, and extracellular matrix proteoglycans; and the peripheral adventitia, consisting of loose connective tissue that anchors the aorta in surrounding tissues. The vaso vasorum, which perfuses the aortic wall, is contained within the adventitia. Of the three layers of the aortic wall, the structure of the media dominates the wall's mechanical properties.[10] Medial smooth muscle directly influences wall stiffness by contraction. In addition, smooth muscle cells are the major source of the extracellular matrix components. These include the elastin fibers, which can be stretched to 300% of their resting length without rupturing[11] and are important contributors to the normal pulsatile behavior of the vessel. Elastin is less important to the overall strength of the aorta than collagen, however, which is both stiffer and much stronger than elastin. The components of the media vary from vessel to vessel and change with age. In the aortas of older patients, the elastin content decreases and the collagen content increases, resulting in increased vascular stiffness.[12] The mechanical properties of the vasculature are also almost always disturbed in cases of systemic hypertension.[13] Mechanical and Shear Stresses The aortic wall is subjected to mechanical stresses of several forms. Stress, which is expressed as force per unit area, may occur in radial, circumferential, or longitudinal directions.[14] The normal intima bears little of the aorta's stress load. It is exposed to shear stresses, however, which are forces applied parallel to the vessel wall as a result of the viscous effects of blood flow. The amount of these shear stresses varies with the distribution of velocity across the vessel lumen and with local vessel geometry.

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Circumferential stress predominantly affects the media. This type of stress (δ) increases with the radial pressure from the aortic lumen (P) and the aortic radius (r), and decreases with increasing wall thickness (h): δ = Pr/h The danger of aortic dilation can therefore be understood: in dilated, thinwalled aortas, the circumferential stresses may be increased many times above normal. In addition, the geometry of the dilating aorta changes progressively from the normal cylinder to an ellipsoidal or even spherical shape. This slowly increases the circumferential stress but quickly exacerbates longitudinal stress. Most atraumatic aortic tears are caused by longitudinal stress, which explains why they are generally transverse in orientation.[15] The ascending aorta experiences additional longitudinal stress owing to the motion of the aortic annulus. Finally, dilated or aneurysmal vessels demonstrate marked stiffness, in part because of loss of elastin.[16] Combined aortic dilation, wall thinning, and shape change sets the stage for intimal rupture and the initiation of dissection. Intimal or medial abnormalities of the aorta increase the resistance to both shear and circumferential stresses. Stress failures of both types may play a role in aortic dissection. Circumferential stress failure can occur when the stresses caused by intraluminal pressure are greatly magnified in the thin fibrous cap of an atheromatous lesion. If the lesion fractures and a small crack develops, the circumferential stress will cause it to extend through the wall.[10] Shear stress failure is due to inhomogeneity in the properties of the vessel wall. Even under normal conditions, mural stresses are greater on the inner than on the outer wall.[15] In the presence of atherosclerosis, incremental variations in the shear resistance between contiguous regions of diseased and normal wall occur. The progression of aortic dissection probably represents an example of shear failure, in which the interface between two such aortic segments with different stiffness leads to separation of medial and intimal layers: the two layers slide relative to one another, because the "glue" of the extracellular matrix cannot withstand the shear stress.[10] Once initiated, dissections behave like a two-ply tube. The intima and the internal elastic lamina of the media form the inner layer, and the outer layer consists of the external elastic lamina and the adventitia. A velocitydependent shear force will then further separate the two layers, creating a false lumen separated from the true lumen by the intima and internal elastic

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lamina.[15] Experimentally, it has been demonstrated that the work per unit area of tissue required to propagate a tear in the aorta is small (15.9 ± 0.9 mJ cm2 ), and independent of the depth of the tear.[17] These concepts of shear and tensile failure are the basis for understanding why different patient populations are at increased risk for aortic dissection. Medial elastic tissue degeneration resulting from hereditary defects of the arterial wall creates the substrate for dissection in patients with Marfan's syndrome, Turner's syndrome,[18] Noonan's disease, Ehlers-Danlos syndrome, and osteogenesis imperfecta.[15] [19] In these patients, as well as in other groups, dilation of the aorta is an important source of tensile failure and a precursor to dissection. Both wall abnormalities (shear failure) and increased wall stress (tensile failure) caused by dilation are important in nonhereditary risk groups. Dissection occurring in hypertensive patients is generally based on 48

high blood pressure, moderate aortic dilation, and medial muscular degeneration predisposing the internal layer to tear.[15] The contribution of shear stress in those patients is infrequent and unpredictable. Atherosclerosis In atherosclerosis, both generalized and focal manifestations can predispose to dissection. True aortic aneurysms are caused by atherosclerotic degeneration of the media and progress to involve all three layers of the vessel wall and to gradual dilation. Increasing risk accompanies diameters exceeding 10 cm, rapid expansion, or symptoms. Formation of laminar thrombus within the aneurysm does not decrease the wall stress. The 1-year survival rate in patients with thoracic aortic aneurysms is less than 60%, and the 5-year survival rate is approximately 20%. False aneurysms are created by through-and-through disruption of the media, with the adventitia alone confining the extravasation.[20] The risk of rupture is even higher in this setting. A third type of atherosclerotic aortic abnormality is penetrating aortic ulceration.[21] [22] In this case, rupture of atherosclerotic plaque causes fissuring into the media and creation of an intramural hematoma, which may progress to rupture or pseudoaneurysm formation. Trauma

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Trauma is another important cause of dissection. Dissection may occur in external, accidental trauma and be difficult to assess in the setting of major multisystem injuries. The region most prone to traumatic injury is the aortic isthmus, where relative tethering by the spinal arteries and ligamentum arteriosum resists abrupt deceleration more than the more mobile transverse arch.[23] Other vulnerable sites include the origin of the innominate artery, particularly with vertical forces from falls, and the ascending aorta above the sinus of Valsalva. [24] Traumatic injuries to the aorta may result in intimal tears, recognizable on transesophageal echocardiography (TEE) scans as mobile flaps. Thrombus may be seen protruding into the lumen; in other cases, intramural hematoma without apparent intimal discontinuity is seen. Although very minor lesions such as minimal hematomas may regress spontaneously, the prognosis of significant aortic trauma is grave. Without repair, there is a 30% rate of mortality within the first 24 hours. Within 1 week, the mortality rate is greater than 50%.[25] Prompt recognition is therefore critical to patient outcome. TEE has been shown to be safe and highly sensitive for aortic trauma after motor vehicle accidents, equivalent to angiography and more expeditiously applied.[26] TEE may also detect other signs of cardiac trauma, including wall motion abnormalities, pericardial effusion, and valvular insufficiency. When the suspicion of aortic rupture in the territory of the transverse arch remains high, computed tomography (CT) may provide better images of those territories. Other sources of trauma include the Heimlich maneuver for respiratory obstruction and cardiovascular procedures. Operative sources of tears in the aorta include cannulation sites for cardiopulmonary bypass, aortic transections for valve or aortic segment replacement, and proximal anastomotic sites for coronary bypass grafts.[27] [28] Very uncommonly, aortic catheterization for angiography may traumatize an atherosclerotic region and prompt dissection.[29] Angioplasty procedures of coronary or renal vessels can also initiate the process.[30] A history of these procedures may be important in alerting the clinician to the possibility of dissection in these patients. Pregnancy Although aortic dissection is mostly a disease of middle-aged or elderly men, women and children can also experience dissection. It has been claimed that half of all aortic dissections occurring in women younger than 40 years of age are associated with pregnancy, particularly during the third trimester or the postpartum period.[31] [32] [33] This finding has been disputed

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by Oskoui and Lindsay,[34] who reviewed their own experience and published a series of 1253 dissections in consecutive patients (868 men and 385 women), with no cases occurring in pregnancy. They concluded that most women experiencing aortic dissection in pregnancy had other risk factors such as hypertension or Marfan's syndrome, and that the apparent association could result from selective reporting and coincidental occurrence of dissection with the very common condition of pregnancy. There are also other well-recognized causes of aortic dissection (Table 31) .[35] [36] [37] [38] [39] [40] [41] [42] [43] Genetic Diseases Of the genetic causes of aortic medial disease and aortic dissection, Marfan's syndrome is the most common and best studied. Although a clinical diagnosis, Marfan's syndrome can be confirmed by linkage to the dominantly inherited gene MFS-1 on 15q21 or by determination of the specific family mutation.[44] Histologic examination of the aortic wall in patients with Marfan's syndrome reveals fragmentation of aortic components, especially the elastic fibers,[45] and abnormal accumulation of collagenous and mucoid materials in the media.[46] Fragmentation of elastinassociated microfibrils also occurs in aortic valve leaflets. [47] The disruption and loss of elastic tissue of the media is attributed to a deficiency of fibrillin, a microfibrillar protein that scaffolds the elastic lamellae in the aortic wall.[48] [49] These changes are greatest in the ascending aorta, which is subject to the greatest pulsatile expansion and therefore the highest stress in systole.[15] The alterations in aortic wall components are associated with abnormal functional properties: aortic elasticity is abnormal in patients with Marfan's syndrome, irrespective of the aortic diameter. [50] A comparative study of aortic wall dynamics between patients with Marfan's syndrome and normal control subjects confirmed that, in both groups, stiffness of the wall increases with age and aortic diameter, but at all ages the patients in the Marfan's syndrome group exhibit a stiffer aorta for a given diameter than the control subjects do.[51] Furthermore, Marfan's syndrome patients have large ascending aortic diameters, but not 49

TABLE 3-1 -- Patient Populations at Risk for Aortic Dissection Genetic disorders (medial abnormalities)

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Marfan's syndrome Turner's syndrome Noonan's disease Ehlers-Danlos syndrome Osteogenesis imperfecta Congenital disorders Aortic coarctation Unicuspid or bicuspid aortic valve Degenerative disorders Hypertension Atherosclerotic vascular disease Aortic ulcer Aortic aneurysm Non-Marfan's syndrome cystic medial necrosis Traumatic causes Deceleration injury Penetrating injury Heimlich maneuver Postprocedural causes Cardiac surgery Cannulation Cross-clamping Aortic valve replacement Angioplasty Coronary Renal Inflammatory disorders Syphilis Giant cell arteritis Other conditions

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Pregnancy Weight lifting Cocaine use Discontinuation of beta blockers Polycystic kidney disease abdominal aortic size, after correction for body surface area.[50] Dissection occurs in Marfan's syndrome patients because of this dilation in combination with wall weakness; mural stress increases dramatically with increasing radius and becomes self-perpetuating[15] (Fig. 3-1) . Echocardiographic evidence of aortic root dilation is present in 60% to 80% of patients with Marfan's syndrome.[52] [53] In one series, aortic dilation was generalized in 51% and localized in 28% of patients.[54] Localized dilation did not appear to represent an earlier stage of aortic involvement, as the patient ages in both groups were identical, as was the duration of follow-up. It could not be determined whether generalized dilation reflected more severe underlying cystic medial necrosis from different specific mutations in fibrillin. Generalized dilation, however, was associated with higher rates of expansion as well as aortic regurgitation. In Marfan's syndrome patients, aortic insufficiency has been associated with decreased survival.[43] The existence of mitral valve prolapse does not appear to be an independent predictor of outcome. The clinical course of patients with Marfan's syndrome with respect to progressive aortic dilation and dissection is variable[55] increased risk has been associated with older age,[54] [55] male gender, aortic root diameters exceeding 60 mm,[56] aortic growth rate,[54] [55] and a family history of dissection.[57] Of great concern is the observation that aortic dissection can occur in Marfan's syndrome patients even in the absence of aortic root dilation.[58] Medical management of Marfan's syndrome patients with aortic dilatation involves beta blockers and observation of aortic root diameter to determine the timing of elective surgery aimed at preventing aortic dissection. Longterm fatality rates are improved with prophylactic aortic root replacement; the 5-year survival rate approximates 97% for elective surgery versus only 51% with emergency surgery for dissection.[59] Operative mortality in experienced centers for elective surgery in Marfan's syndrome patients is low (1.3% to 1.5% 30-day mortality rate versus 11.7% for emergency surgery).[60] [61] In patients with normal aortic valve leaflets, elective aortic valve-sparing surgery may provide better clinical outcomes than aortic root

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replacement,[62] although in this retrospective review, patients undergoing aortic root replacement with aortic valve replacement had more cardiac comorbidities than the patients in whom valve-sparing surgery was possible. The size of aneurysm often determines the feasibility of valvesparing surgery; therefore, some centers recommend elective surgery when the aortic root reaches 50 mm.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Spectrum of Aortic Dissection The primary entry tear that initiates aortic dissection is usually transverse and involves more than half of the circumference of the aorta. In 65% of cases, it occurs within 3 cm of the coronary ostia. Ten percent of tears occur in the descending thoracic aorta and another 10% in the arch. Primary tears are rare in the abdominal aorta.[63] Whatever the location of the initial tear, dissections may extend caudally, proximally, or occasionally in both directions. Figure 3-1 Type A aortic dissection (arrows indicate intimal flap) in a patient with Marfan's syndrome. Prolapse of the posterior mitral valve leaflet is also noted.

Anatomic Classification

50

There are several widely used classification systems for dissection (Table 3-2) . The DeBakey classification divides dissections with involvement of the ascending aorta into type I, which extends into the transverse arch and distal aorta, type II, which is confined to the ascending aorta, and type III, which involves the descending aorta only.[64] The Stanford classification[65] was developed from a functional approach based on whether the ascending aorta is involved, regardless of the site of primary intimal tear and irrespective of the extent of distal propagation. This reflects clinical observations that the biologic behavior of the dissection, the clinical prognosis, and how the patient should be managed pivot almost exclusively on whether the ascending aorta is involved.[66] [67] [68] This system of nomenclature describes type A dissections as any with involvement of the

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ascending aorta (including DeBakey types I and II), and type B dissections as dissection limited to the descending aorta (DeBakey type III). The clinical classification schemes described do not emphasize the location of the primary entry tear or the extent of the distal propagation of the dissection. These two factors are of less prognostic value and can be technically difficult to determine.[69] [70] When identification of the entry site is possible, the culprit primary intimal tear is more easily resected. Although successful resection of the primary tear does not appear to affect early or late survival rates, it may decrease the incidence of late reoperation.[71] Some cases of aortic dissection will present with multiple "primary" tears. Two separate dissections in the same patient may be more common than previously reported. Roberts and Roberts[72] reported that 3 of 40 necropsy patients had separate proximal and distal thoracic dissections. Although all fatal events were caused by rupture of the acute proximal dissections, a separate distal dissection may still pose a risk for late complications, and therefore recognizing two separate dissections may have important implications in terms of follow-up and therapy.[73] Multiple distal "exit" tears, which decompress the false lumen, are extremely common. Time Course Dissections are also differentiated with respect to their time course. Acute dissections are detected within 14 days of the onset of initial symptoms. Chronic dissections TABLE 3-2 -- Nomenclature of Aortic Dissection Dissection Type Ascending aorta involved

Ascending aorta not involved

Classification Stanford type A DeBakey I DeBakey II University of Alabama "ascending"[56] Massachusetts General Hospital "proximal"[57] Stanford type B DeBakey III University of Alabama "descending"[56] Massachusetts General Hospital "distal"[57]

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present more than 2 weeks after onset.[68] [74] This division is arbitrary; it may primarily reflect the fact that the majority of type A dissection patients will die within 2 weeks if untreated.[75] Chronic dissections may be detected because of symptoms or may be an incidental finding. They are differentiated from aortic aneurysms by the presence of an intimal flap and false lumen. These may not be easy to recognize when the false lumen is largely thrombosed. Pronounced atherosclerotic changes may be present in the false lumen in chronic dissections, even when the true lumen walls appear normal and hyperlipidemia is absent.[76] Sequelae The concomitant sequelae of aortic dissection are many and varied. Obstruction of branch vessels may explain acute myocardial ischemia and infarction of cerebral, spinal, bowel, and renal territories. Aortic valve dehiscence with regurgitation, cardiac tamponade from retrograde extension into the pericardium, and frank aortic rupture are all highly morbid consequences.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography in Aortic Dissection Time is of the essence when aortic dissection is suspected, and the entire thoracic aorta must be visualized. Transthoracic echocardiography is immediately available, and, in some cases of proximal dissection, it may visualize the ascending aortic intimal flap and false lumen, or a flap in the descending aorta may be visible from the suprasternal (Fig. 3-2) or subcostal windows. Other clues to dissection available from transthoracic approaches include pericardial effusion with or without tamponade, aortic valve insufficiency with or without leaflet dehiscence, aortic root dilation, or regional wall motion abnormalities. Given the variable occurrence of any of these abnormalities, it is not surprising that the sensitivity of transthoracic echocardiography has been limited (Table 3-3) . Transesophageal Imaging Transesophageal echocardiography has elevated ultrasonic diagnosis of dissection into the first line of clinical options (Fig. 3-3) . Multiple studies have documented specificity and sensitivity in the range of 98% and 99%, respectively. The recognized blind spot of TEE, involving the distal ascending aorta and superior aspect of the arch, is an important limitation, especially because entry tears in this region are important to clinical management. The goal of imaging the entire thoracic aorta may therefore require a combination of modalities and approaches, including transthoracic views (often from the suprasternal notch), transesophageal windows, and often direct epiaortic or epicardial views at the time of surgery. Transesophageal echocardiography has many discrete advantages in the diagnosis of acute aortic dissection, the most important of which is its documented accuracy. Erbel 51

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Figure 3-2 Suprasternal views of the transverse and descending aorta demonstrate the intimal flap (A, arrows) as well as an entry tear with systolic flow from the true lumen into the false lumen (B) (color plate).

et al,[77] reporting for the European Cooperative Study Group for Echocardiography on a series of 164 patients suspected of acute dissection, demonstrated sensitivity and specificity rates of 99% and 98%, respectively. Another large study by Nienaber et al[78] compared TEE with magnetic resonance imaging (MRI). Both TEE and MRI had perfect sensitivity; the 100% specificity of MRI exceeded the 68% specificity of TEE. The authors suggested that TEE's limited visualization of common ascending aorta pathologic lesions might have accounted for the higher rate of false-positive findings. In that study, strict criteria for diagnosing dissection were not applied (see later discussion); more stringent criteria could minimize false-positive results. Transthoracic echocardiography TABLE 3-3 -- Imaging Modalities for Aortic Dissection

Study Appelbaum et al[67] Miller[66] Daily et al

Modality TTE

Positive Negative Sensitivity, Specificity, Predictive Predictive A % % Value, % Value, % 77 93 — —

TTE TTE

59 83

83 63

— 80

— 70

Miller[66] TEE Chirillo et TEE al[1] Daily et al TEE

98 98

77 97

— 98

— 97

100

68

82

100

88

94

96

84

88

97

97

85

100

100

100

100

98

98

—

—

[65]

[65]

DeBakey Aortography et al[64] Chirillo et Aortography al[1] Daily et al MRI [65]

Miller[66]

MRI

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83

100

100

86

94

87

—

—

[83]

Erbel et al CT [94]

CT, computed tomography; MRI, magnetic resonance imaging; TE transesophageal echocardiography; TTE, transthoracic echocardiograp from the suprasternal notch provides additional views of this vulnerable area. The sequential use of TEE and CT, aortography, or MRI is clearly extremely powerful in clarifying suspicious or clinically incongruous results.[79] [80] Transesophageal echocardiography provides additional information about left and right ventricular wall motion and global function and aortic and mitral valve competence. Importantly, with acute type A dissections, TEE is able to detect and determine the severity and mechanism of aortic valve regurgitation[81] and may influence the decision to replace or repair the valve. An important advantage of TEE in cases of dissection is its rapid and safe performance in a wide range of clinical environments, including emergency departments, 52

Figure 3-3 Examining the aorta in multiple planes is essential. In this case, the short-axis view (A) suggests an abscess cavity. The long-axis view (B), however, demonstrates a longitudinal dissection flap (arrows). Ao, aorta; LA, left atrium.

intensive care units, and the operating room. TEE requires minimal patient preparation, avoids the contrast agent and x-ray exposure associated with CT and angiography, and eliminates the time delays and practical encumbrances of MRI. Choice of a "best test" must always take into account the individual center's track record with each modality, as well as access issues. Safety of Transesophageal Echocardiography The safety of transesophageal examinations depends on adequate patient

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preparation with respect to pain, anxiety, and airway protection. Careful monitoring of the electrocardiogram and blood pressure is critical to avoiding adverse affects of TEE. In a study of 54 ambulatory patients, TEE was accompanied by an increase in systolic pressure in 77% of patients. This elevation was moderate (average increase of 16 mm Hg) in most patients, but some patients had acute increases of as much as 51 mm Hg.[82] Abrupt increases of blood pressure must clearly be avoided in any patient suspected of having a dissection. Serial blood pressure monitoring, pulse oximetry, intravenous sedation, topical anesthesia, and control of blood pressure with intravenous vasodilators and beta blockers, if needed, are important to patient safety. With these precautions, the majority of patients can undergo esophageal intubation with minimal distress and good hemodynamic stability. Even so, there has been a reported case of aortic rupture occurring during TEE in a patient with an acute dissection, which might have been elicited by retching and elevated blood pressure.[83] Other commonly reported adverse events during transesophageal studies that must be anticipated and avoided are nonsustained atrial and ventricular arrhythmias, excessive vagotonia with transient atrioventricular block, and arterial hypoxemia.[84] Diagnostic Features The diagnosis of aortic dissection is most secure when very specific criteria are met. Identification of an intimal flap, seen as a mobile, linear echo within the vascular lumen, and flow in the true and false channels on either side of the flap are highly sensitive features of dissection. The motion of the intimal flap toward the false lumen during systole may be a helpful feature. A thickening of the aortic wall in excess of 15 mm has also been used as a sign of dissection, suggesting thrombosis of a false channel, which makes the intimal flap difficult to recognize.[85] Strict adherence to these criteria can avoid confusion with imaging artifacts and manifestations of other types of disease and minimize false-positive results.[86] This is particularly important because most patients suspected of having an aortic dissection have evidence of vascular disease involving the thoracic aorta. In one series of 40 patients evaluated for dissection, abnormal aortic findings (including atherosclerotic plaques, intravascular and extravascular masses, thrombi, and dilation) were found in 16 of 17 patients in whom aortic dissection and coronary artery disease were excluded as explanations for their chest pain.[87] Other underlying aortic abnormalities such as coarctation or prior surgical repair may affect clinical management, but they are also important potential sources of misdiagnosis.

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Doppler Findings Color Doppler flow imaging during TEE is an excellent descriptor of aortic flow patterns with acute dissection. Flow in the false channel is variable and complicated; the true lumen, which is often dwarfed by the false channel, is identified by forward systolic flow (Fig. 3-4) . With large proximal entry tears, flow in the nearby segments of the false lumen may have the same direction and timing as the true lumen flow and may reverse in diastole.[88] [89] With 53

Figure 3-4 A short-axis transesophageal echocardiographic view of the descending aorta shows a small anterior true lumen and a larger posterior false lumen that is partially thrombosed (left, arrow). A pulsed Doppler signal from the true lumen, oriented from a long-axis view (right), demonstrates forward systolic flow.

smaller or more distal tears, false lumen flow is less similar to true lumen flow: it may be directed in the opposite direction, and peak velocity may occur later in the cardiac cycle, representing delay of flow into the false lumen. Many areas will show extremely slow, swirling flow with spontaneous echo contrast or partial thrombosis (Fig. 3-5) . These segments tend to be remote from large entry or exit sites, where high-velocity flow keeps these changes from occurring. Finally, areas of complete thrombosis are also seen, and care must be taken to ascertain that the hematoma is entirely intravascular and not actually Figure 3-5 Transesophageal echocardiogram of the descending thoracic aorta demonstrates the true lumen anteriorly and a thrombosing false lumen posteriorly in a patient with acute aortic dissection. As the false lumen thrombosis proceeds, the only clue to dissection may be the apparent "thickening" of the aortic wall.

the result of adventitial rupture, pseudoaneurysm formation, or intramural hematoma (Fig. 3-6) . Multiple communications between the true and false lumens are often identified on careful scanning of the entire thoracic aorta. Some will represent entry sites with flow from the true toward the false channel, and others will be exit sites or have bidirectional flow (Fig. 3-7) . Exit tears,

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where flow re-enters the true lumen from the false lumen, may occur at one or multiple sites. The exact location of a given tear can be estimated from the depth of probe insertion from the incisors, an arbitrary but 54

Figure 3-6 Transesophageal view of the descending aorta at 40 cm from the incisors in a patient with a prior proximal dissection and repair. There is discontinuity of the posterior aortic wall and a large thrombus extending into the periaortic tissues. This was confirmed to be a descending thoracic aortic rupture on subsequent surgery.

convenient reference point. Recording this information at the time of the procedure and on the written report not only is helpful in the surgical correction of dissection, but also is extremely important for comparison with postoperative follow-up TEE studies, in which many of the original tears may still be detectable. Identification of the primary entry site must be deduced from location, size, and flow patterns. In some cases, the primary tear cannot clearly be assigned to any one tear, either because of multiple tears as described Figure 3-7 A short-axis transesophageal echocardiographic view of the descending aorta with a large entry tear in the intimal flap. Pulsed Doppler echocardiography demonstrates flow from true to false lumen during systole. FL, false lumen; TL, true lumen.

earlier or, in some cases, because of the TEE blind spot. Adachi et al[90] were able to identify the entry site in 50 of 57 patients with acute dissection. They were more successful in this with type B dissections (90%) than with type A (83%). As mentioned previously, identification of the primary tear is mostly important because ensuring that the surgical repair resects the primary entry site may decrease the incidence of late reoperation. Complications of Dissection An important goal of echocardiographic imaging in aortic dissection is identifying associated complications. Type A dissections may produce acute aortic insufficiency because of annular dilation or disruption of leaflet suspension. TEE can provide detailed morphologic information regarding

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the quality of the leaflet tissue and the mechanism of aortic insufficiency; these can help in the decision regarding valve resuspension versus replacement. Pericardial effusion and tamponade are manifestations of aortic rupture with dissection and are often readily identified on transthoracic views. The Doppler manifestations of pericardial tamponade may be best obtained from external apical views and may obviate preoperative TEE in the interest of moving the patient emergently to the operating room. Small effusions unassociated with tamponade physiology may not be related to rupture and can be evaluated with contrast echocardiography if time and patient stability allow (Fig. 3-8) . Other rupture syndromes can occur at different sites. Uncontained rupture into the mediastinum or pleural space causes sudden death. Some ruptures are contained by the aortic adventitia, resulting in pseudoaneurysm formation or hematoma. In these cases, TEE can detect the intimal breach as well as the extension of the hematoma into the surrounding tissues; contrast can be helpful in delineating protuberant thrombus and rupture (Fig. 3-9) . An important proviso is to image the aorta at an adequate imaging depth so that such a hematoma 55

Figure 3-8 A four-chamber transesophageal echocardiographic view during contrast injection (Optison) shows contrast in the left ventricular cavity but not in the small pericardial effusion (arrow), which was unassociated with tamponade physiology.

can be recognized. These extravasations can be missed if the imaging field is restricted to the expected aortic contours; disastrous consequences can ensue if the site of the extravasation is not corrected along with the proximal aortic repair. Intramural Hematoma A small number of aortic dissections, estimated at 3% to 5%, occur without apparent intimal disruption.[6] [91] The pathologic process in these cases is rupture of the vasa vasorum into a region of medial degeneration, or possibly rupture of atherosclerotic plaque. Patients with this form of disease tend to be older (mean age, 70 years versus 56 years for communicating dissection) and have frequently had long-term hypertension. Transesophageal images

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Figure 3-9 A transesophageal echocardiographic view of the ascending aorta suggests an intimal flap with possible lumen rupture. Contrast injection (A, Optison) does not confirm extravasation outside the aorta (B, arrow).

demonstrate a thickened aortic wall with intramural echo-free spaces, an increased distance from the TEE probe to the inner aortic wall, and focal distortion of the transverse circular configuration of the aorta. This process has been described on CT images as well, seen as circular high-intensity areas along the aortic wall. [92] In their series, Mohr-Kahaly et al[93] described this type of noncommunicating aortic dissection as a dissection membrane without intimal tear and often involving the entire descending thoracic aorta. Early prognosis in those patients was somewhat better than in those with acute "communicating" dissections; this may reflect the tendency for the noncommunicating medial space to heal with complete thrombus formation.[94] These intramural hematomas may progress to typical dissection (in 33%) or to rupture (in 27%) and therefore usually require surgical rather than medical management.[95] Coronary Artery Involvement Involvement of coronary arteries by aortic dissection is an important issue, and one that raises the question of whether preoperative coronary angiography is mandatory. Involvement of one or both coronary arteries by acute aortic dissection has been estimated to occur in 10% to 20% of cases. [96] In a series of 34 aortic dissection patients, Ballal et al[97] detected coronary involvement with TEE in six of seven surgically documented dissected coronary arteries. Of note, electrocardiographic changes were demonstrated in only two of the six patients with coronary involvement. Adequate views of the ostia and proximal vessel were obtained for 88% of left main arteries and 50% of right coronary arteries overall. Visualization of the ostia and proximal coronary arteries continues to improve as variable imaging plane TEE probes are utilized and higher frequencies become available (Fig. 3-10) . A separate but related issue is whether concomitant coronary artery disease, independent of coronary dissection, is an important consideration that should prompt routine angiography. Given the underlying vascular disease 56

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Figure 3-10 A short-axis transesophageal echocardiographic view of the aortic root demonstrates an intimal flap in proximity to the left coronary ostium. LC, left coronary.

that affects many patients with dissection, it is not surprising that coronary disease has been found in up to 43% of patients with aortic dissection. The benefits of addressing potentially important coronary stenoses must be weighed against the risk of delays and aortic manipulation during acute dissection and adjusted for the patient's baseline likelihood of coronary disease. A series of 122 patients from the Cleveland Clinic found no difference in the in-hospital mortality rate between patients who had emergency coronary arteriography before dissection repair and those who did not. Three fourths of all coronary artery bypass procedures performed in that series were done because of coronary dissection rather than obstruction owing to coronary artery disease.[98]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Surgical Considerations The planning of surgical correction of aortic dissection is heavily influenced by many of the features discussed earlier. The extent of the dissection, the location of primary tears, and concomitant valvular insufficiency and coronary disease are all critically important to the surgical team. In addition, safe cannulation sites, aortic valve repair strategies, need for coronary reimplantation with root replacement, and confirmation of adequate cardiopulmonary bypass and even intra-aortic balloon function can all be addressed with intraoperative ultrasonography (Table 3-4) . Transesophageal imaging during surgery has the advantage of being nonobtrusive (at least for the surgeon, if not for the anesthesiologist) and is commonly also used as an accurate monitor of left ventricular wall motion and volume status. Intraoperative Echocardiographic Monitoring An additional tool for completing the scan of the aorta is intraoperative imaging from the epicardium or surface of the aorta. The unlimited number of acoustic windows from this approach allows careful interrogation of the aortic root, origins of the great vessels, cardiac valves, and left ventricular wall motion. The transesophageal blind spots in the ascending aorta and transverse arch can be thoroughly inspected from the epicardium, and potential aortic cannulation sites can be evaluated from the exterior aortic surface (Fig. 3-11) . Epicardial views give much greater freedom of visualization and measurement of the aortic valve and allow precise annular sizing before cardiopulmonary bypass to expedite selection of the valvular prosthesis. The position of the coronary ostia relative to the dissection and the annulus can be defined precisely with epicardial views, which may also aid in surgical decisions regarding valve-graft conduit placement or coronary ostial reimplantation. The amount of time required for imaging in the surgical field can be limited

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to a few minutes, but this achievement requires an experienced team with a surgeon or cardiologist familiar with the epicardial techniques and TABLE 3-4 -- Operative Uses of Transesophageal Echocardiography in Aortic Dissection Site Feature Pre–Cardiopulmonary Bypass Assessment Aorta Intimal flap Entry tear * Intramural hematoma Aortic rupture Aortic pseudoaneurysm Distal extent of extension Additional tears False lumen flow patterns, including thrombus Branch vessel involvement * Coronary situs and dissection Involvement of origins of great vessels Underlying pathologic condition Atheromatous disease Coarctation Sites of previous repairs Cannulation and cross-clamp sites Aortic valve Insufficiency Suitability for repair vs. replacement Sizing for allograft replacement Mitral valve Insufficiency Suitability for repair vs. replacement Left and right ventricle Wall motion abnormalities Pericardium Effusion Post–Cardiopulmonary Bypass Assessment Aorta Confirm competency of proximal anastomosis

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Establish baseline for false lumen flow and distal tears Aortic valve Confirm competency of repaired valve Mitral valve Confirm competency Left and right ventricle Wall motion Intra-aortic balloon Confirm position in true lumen * Epicardial and/or epiaortic scanning may be important in fully defining these features.

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Figure 3-11 Intraoperative epiaortic view of the transverse aortic arch in a patient with acute proximal aortic dissection. The intima is widely dissected and highly mobile. Note the linear streaking artifact from electrocautery.

views. The combination of epicardial and transesophageal techniques ensures that a high-quality ultrasonographic image is acquired of all segments of the aorta above the diaphragm and eliminates any uncertainty regarding involvement of the ascending aorta. Post-cardiopulmonary bypass images from the epicardium can also be extremely helpful in reassessing proximal tears and interrogating suture lines between aorta and conduit. Transesophageal views at the conclusion of cardiac surgery confirm aortic valve or prosthetic valve competency and allow prompt reinstitution of support if significant aortic insufficiency demands surgical revision. Intraaortic balloon pump position can be assessed with TEE (Fig. 3-12) ; accidental placement of the balloon in the false lumen can be disastrous if not immediately recognized.[99] Finally, postoperative TEE images of the graft and native aorta create a baseline for subsequent follow-up studies. Choice of Surgical Procedure The goal of surgical correction of aortic dissection is to prevent the most common causes of death. For type A dissections, death is caused by

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intrapericardial rupture and tamponade in 80% to 90% of cases and by extrapericardial rupture in 5% to 10%. For type B dissection, rupture causes 60% to 70% of deaths. A localized and conservative operative procedure prevents most deaths and is associated with the lowest number of operative risks. This generally consists of resection of a limited segment of aorta containing the worst damage, including the primary intimal tear if possible, and reconstruction of the local pathologic lesion. If required, however, extensive aortic reconstruction for dissection has been reported with longterm survival rates of 88.5% at 1 year and 81.7% at 9 years in a small series of Marfan's syndrome patients.[100] Coexisting Aortic Insufficiency Aortic valve insufficiency complicating aortic dissection has negative effects on outcome and may dictate important issues in the surgical approach. Preservation of the native aortic valve is possible in 86% of type A dissections with excellent results.[101] If the aortic annulus is abnormal because of Marfan's syndrome or annuloaortic ectasia, aortic valve replacement is preferred because of the limited long-term durability of aortic valve reconstruction in these patients. Initiation of cardioplegia for cardiopulmonary bypass usually depends on a competent aortic valve to allow antegrade perfusion of the coronary arteries; in the presence of significant aortic insufficiency, therefore, individual ostial cannulation or coronary sinus retroperfusion may be indicated. The specific causes of aortic insufficiency are also important[81] normal-appearing leaflets with a prolapsing cusp caused by avulsion of the leaflet base may be amenable to aortic repair with resuspension. Other cases may require aortic valve replacement. The specific involvement of the adjacent aortic root is also critical and may require a variable extent of prosthetic conduit. In some cases, human aortic allografts are used, which have the advantage of supplying both natural aortic valve and root. In proximal aortic involvement, the position and involvement of the coronary ostia are important. Ostial reimplantation may be necessary; coronary bypass grafting may be unavoidable if the coronary arteries are dissected. Coronary arteries may be reattached by direct reimplantation with or without a surrounding button of aortic tissue, reattached to a piece of prosthetic conduit (the Cabrol procedure), or completely bypassed with saphenous vein or internal mammary artery grafts. Figure 3-12 The position of the intra-aortic balloon pump (bright echo,

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upper right) can be confirmed with transesophageal echocardiography. This balloon is placed correctly in the anterior true lumen.

Coexisting Mitral Regurgitation

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Mitral regurgitation is a different example of a valvular abnormality associated with aortic dissection. New insufficiency may result from wall motion abnormalities induced by coronary involvement in the dissection, or from acute left ventricular dilation induced by aortic insufficiency. In other cases, mitral regurgitation is part of the underlying disorder, as is the case with Marfan's syndrome with mitral valve prolapse. Identification of the etiologic factors in the mitral insufficiency (e.g., leaflet degeneration, ventricular dilation, papillary muscle ischemia) will influence the need for repair or prosthetic replacement. Confirmation of results on early postcardiopulmonary bypass images is important, especially when the decision is made to leave the mitral valve alone despite some insufficiency in hopes that correction of acute ischemia or dilation will remedy it. Perfusion of Distal Vascular Beds In an acute aortic dissection, organs may be perfused by either the true or the false lumen flow. Organ under-perfusion may occur if flow to the source lumen is compromised. During surgery, malperfusion may be caused by flow reversal when cardiopulmonary bypass is established by cannulation of the femoral artery, with obliteration of major communications between the two lumens from cross-clamping, or with repair of the dissection itself. Neustein et al[102] describe a case in which femoral cardiopulmonary bypass compressed the true lumen and created severe malperfusion once the dissection was repaired. Perfusion through the new ascending aortic graft allowed immediate reinstitution of forward flow.

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Follow-up of Patients after Repair of Aortic Dissection Persistent Intimal Flaps Despite successful surgical repair of aortic dissection, the aorta retains many abnormalities of structure and Figure 3-13 (color plate.) Distal tears are frequently present in aortic dissection. A, During systole, flow crosses from the true lumen into the false lumen. B, During diastole, flow reverses as the false lumen decompresses. C, Tears are usually multiple; here, two discrete tears with systolic flow into the false lumen are seen at the same level of the aorta. TRUE, true lumen; FALSE, false lumen; DESC AO, descending aorta.

flow. Distal to the repair, the intimal flap and false lumen persist. The false lumen may thrombose, or it may retain flow along with entry and exit flow through multiple fenestrations (Fig. 3-13) . One study detected persistent flap and false lumen in 100% of post-repair patients by MRI.[103] Persistent flow in the false lumen can be detected with TEE in the majority of patients after surgical repair. Mohr-Kahaly et al[89] found persistence of the false lumen in 71% of their postoperative patients at a follow-up interval of 1 to 41 months, and in 82% of their medically treated patients. Dinsmore and Willerson[104] have suggested that long-term survival is poorer in patients with persistent flow in the false lumen. Thrombosis of the false channel seems to be protective, a "natural buttress against future or further extension of the dissection." TEE confirms that sites without communications develop low-velocity flow and thrombus, whereas "healing" changes are less likely to occur in regions with significant tears and persistent flow. TEE also demonstrates aggressive atherosclerotic changes and calcification of the "neointima" lining the false channel. Progression of Disease

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Patients with previous dissection may develop progressive abnormalities of both operated and nonoperated aortic segments. Twenty-five to 40% of original dissections will enlarge over time, and the rate and extent of enlargement are primary factors driving the need for reoperation.[96] In addition, dilation of noncontiguous, nonoperated aortic segments develops in 17% of patients with prior acute type A dissections. Early recognition of this progressive downstream aortic pathology allows reoperation in hopes of preventing rupture or redissection.[105] The concern regarding disease progression commits these patients to routine follow-up studies indefinitely. Pseudoaneurysm Formation Pseudoaneurysms form in 7% to 25% of patients with composite grafts, such as a Bentall procedure, secondary to hemorrhage at a suture line dehiscence. [106] Blood between 59

the graft and aortic wall can create supravalvular aortic stenosis.[107] Both of these complications can be detected and completely delineated by TEE,[108] as well as by CT, angiography, and MRI.[109] [110] Color flow Doppler will demonstrate blood flow into the echo-free space between the graft and the aortic wall. Other postoperative complications include endocarditis and the development of an aneurysm in the sinus of Valsalva.[111] Recurrent Disease Because the symptoms of acute redissection or expansion of a chronic dissection are nonspecific, the ability to reassess rapidly and compare the current findings with previous images is extremely important. Younger patients, those with Marfan's syndrome, and those with primary tears involving the transverse arch are particularly prone to progression of their disease.[112] Because TEE may not be able to reproducibly measure the true transverse diameter of an ectatic aorta, suspicion of chronic expansion usually requires additional confirmatory tests such as CT or MRI. Excellent definition of the intimal flap, false channel thrombi and flow patterns, and consistent reference landmarks for serial sizing over time make MRI a highly reliable method. When recurrent chest pain or hemodynamic instability suggests acute redissection, TEE can rapidly define the new pathologic abnormality and its extent. Changes from baseline postoperative or postdissection images can be extremely helpful in clarifying the etiologic

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Limitations of Transesophageal Echocardiography False-Negative Results The interposition of the trachea between the esophagus and the heart creates a blind spot that obscures portions of the distal ascending aorta, superior transverse arch, and origins of the great vessels. As a result, a dissection limited to these areas could be missed by transesophageal imaging alone. This is of concern because the clinical behavior and therapeutic approach to the patient depends largely on whether the proximal aorta is involved in the dissection. The occurrence of this extremely limited type of dissection must be very rare, because the incidence of false-negative studies has been minimal in large series.[76] In addition, large series have not confirmed a positive angiographic or CT result when the initial TEE result was negative. The involvement of the great vessels may not modify the surgical approach and can be assessed at operation.[113] The combination of transesophageal imaging with transthoracic imaging from suprasternal and parasternal windows yields a much more thorough assessment of the arch. CT, MRI, or angiography can also be used to assess this area when there is persistent clinical suspicion of a dissection that is not detectable by TEE. False-Positive Results The path of ultrasound through the esophageal wall and surrounding tissues may generate near-field artifacts that are often disconcertingly linear and run parallel to the aortic wall, mimicking an intimal flap. In patients with severe atherosclerotic disease, calcification in the wall can present similar artifacts and shadows. Abrupt aortic dilation can create a "shelf," which can resemble a flap as well. Determining that these do not represent true intimal flaps depends on recognizing the minimal mobility of these "structures" and the homogeneity of flow on both sides of the line. The ability to change to a second imaging plane, as is possible with biplane or multiple-plane TEE

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probes, is extremely helpful in resolving the issue of artifactual "flaps."[86] [114] Multiple-plane imaging also allows better visualization of the proximal ascending aorta, where atherosclerosis and ectasia can be misinterpreted as dissection.[77] Aneurysmal dilation of the aorta is another source of false-positive TEE studies for dissection. Flow in aneurysmal areas is often low-velocity and swirling, similar to the flow in false channels. The absence of an intimal flap is important in avoiding misdiagnosis in this situation. The possibility that the intimal flap is not seen because the false channel has thrombosed must be excluded by carefully scanning up and down the aorta from the abnormal site. An intimal layer identified proximally or distally may be followed back to the suspicious dilated segment to suggest dissection.

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Alternative Approaches to the Diagnosis of Dissection Echocardiography is only one of several diagnostic tests for dissection. The choice of imaging procedure, as well as the clinical confidence in positive or negative results, needs to be gauged relative to the test's performance (see Table 3-3) . Angiography is a time-honored diagnostic method for aortic dissection that may identify the intimal flap and false lumen. In addition, it can define coronary and great vessel ostial involvement. Its sensitivity and specificity for dissection (88% and 94%, respectively) are limited by false lumen thrombosis, intramural hematomas, and equal flow in true and false lumens.[115] [116] The last case is also an important limitation for CT studies, in which differential flow may not be detectable even with dynamic CT imaging.[117] The lower sensitivity (83%) of CT reflects its poor definition of the intimal flap and entry tear. Despite CT's high specificity (90% to 100%), a negative CT result in the presence of high clinical suspicion of dissection requires a second confirmatory test. Extremely slow, swirling flow within a segment of the false channel may not be completely differentiated from thrombus by MRI.[118] MRI's excellent definition of the important components of aortic dissection have resulted in its excellent sensitivity, however, which approaches 100%.[119] The pragmatic issues of imaging acutely ill patients with needs for hemodynamic monitoring or infusion of medications or those at risk for hemodynamic collapse continue to make TEE preferable in many acute settings. As mentioned earlier, MRI may be the procedure of choice for the follow-up of patients with repaired or chronic dissections.

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In their comparison of angiography, TEE, CT, and MRI techniques for aortic dissection, Barbant et al[120] used data from several published series to compare the accuracy and predictive value of these tests in populations

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with high, intermediate, and low prevalence of disease. For populations with a high risk of dissection, positive predictive values for all tests exceeded 85%. In intermediaterisk populations (prevalence, 10%), positive predictive values were greater than 90% for CT, MRI, and TEE but less than 65% for angiography. When the disease prevalence was low (1%), as it probably is in most clinical applications of these tests, the positive predictive values were less than 50% for angiography, CT, and TEE, and remained high only for MRI (100%). In any population, the negative predictive value was greater than or equal to 85% for all tests. These results suggest that TEE and other imaging techniques may not perform as well in a low-risk ambulatory population, as suggested by published results from higher-prevalence populations.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Research Applications and Future Directions Transesophageal echocardiographic images provide excellent spatial resolution, especially with the higher frequencies that are becoming available. Combining this with the high temporal resolution of M-mode methods has allowed investigation of aortic distensibility in normal patients, in patients at risk for vascular disease, and after repair of aneurysms or dissection. These types of methods have documented decreases in elastic aortic properties after aortic surgery, which predispose patients to redissection.[121] Two-dimensional echocardiographic assessments of aortic distensibility have been shown to estimate changes in aortic mechanical properties resulting from increasing age[122] Doppler estimates of pulse wave velocity Figure 3-14 Three-dimensional constructed views of the aorta in shortaxis (left) and long-axis (right) orientations demonstrate the intimal flap separating true and false lumens.

are also being investigated as measures of aortic compliance.[123] Animal models for validation of these parameters include chronic models of accelerated atherogenesis, as well as acute aortic ischemia and decreased distensibility generated by removal of the vasa vasorum.[124] High-frequency ultrasonic integrated backscatter methods are also being applied to the aortic wall (see Chapter 9) . Recchia et al[125] detected sixfold decreases in backscatter and 15-fold decreases in anisotropy, suggesting marked disorganization of the three-dimensional aortic architecture in the aortas of