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(BQ) Part 1 book Clinical manual and review of transesophageal echocardiography presents the following contents: Basic transesophageal echocardiography (fundamentals of ultrasound imaging, the basic tee exam), advanced transesophageal echocardiography (valvular heart diseases, ventricular function, pericardium).
CLINICAL MANUAL AND REVIEW OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY Second Edition Edited by Joseph P Mathew, MD, MHSc Chakib M Ayoub, MD Professor of Anesthesiology Chief, Division of Cardiothoracic Anesthesiology D u ke U n iversity Medical Center Durham, North Ca rolina Associate Professor Department of Anesthesiology America n U niversity of Beirut Medical Center Beirut, Lebanon Clinica l Assistant Professor Department of Anesthesiology Ya le U niversity School of Medicine New Haven, Connecticut Madhav Sw aminathan, MD, FASE, FAHA Associate Professor of Anesthesiology Director, Perioperative Echocardiog raphy D u ke U n iversity Medical Center Durham, North Ca rolina New York I Chicago I San Francisco I Lisbon I London I Madrid I Mexico City Milan I New Del h i I San Juan I Seoul I Singapore I Syd ney I Toronto Th McGrawãHIII Compontes Copyrightâ 2010 by The McGraw-Hill Companies, Inc All rights reserved Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher ISBN: 978-0-07-163628-5 11JIU): 0-07-163628-5 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07- I 63807-4, 11JIU): 0-07-163807-5 All trademarks are trademarks of their respective owners Rather than put a trademark symbol after eve1y occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trade mark Where such designations appear in this book, they have been printed with initial caps McGraw-Hill eBooks are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs To contact a representative please e-mail us at bulksales@mcgraw-hill.com Notice Medicine is an ever-changing science As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required The editors and the publisher of this work have checked with sources believed to be reliable in their efforts to pro vide information that is complete and generally in accord with the standards accepted at the time of publication However, in view of the possibility of human error or changes in medical sciences, neither the editors nor the publisher nor any other party who has been involved in the preparation or publication of this work waJTants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work Readers are encouraged to confirm the info1mation contained herein with other sources For example and in pa1ticular, readers are advised to check the product inf01mation sheet included in the package of each drug they plan to administer to be certain that the inf01mation contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for adminis tration This recommendation is of particular importance in connection with new or infrequently used dlugs TERMS OF USE This is a copyrighted work and The McGraw-Hill Companies, Inc ("McGraw Hill") and its licensors reserve all rights in and to the work Use of this work is subject to these terms Except as pe1mitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, trans mit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill's prior consent You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these terms THE WORK IS PROVIDED "AS IS." McGRAW-HILL AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, IN CLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WAR RANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE McGraw-Hill and its licensors not warrant or guarantee that the functions contained in the work will meet your requirements or that its operatio11 will be uninterrupted or error free Neither McGraw-Hill nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, conse quential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise Co nte nts vii xi xiii Contri b utors Fo rewo rd P refa ce BASIC TRANSESOPHAGEAL ECHOCARDIOGRAPHY Fundamentals of Ultrasound Imaging C h a pter PHYSICS OF ULTRASOUND IMAGING Brian P Barrick, Mihai V.Podgoreanu, and Edward K Prokop C h a pter UNDERSTANDING ULTRASOUND SYSTEM CONTROLS 16 Hillary Hrabak, Emily Forsberg, and David Adams C h a pter ANATOMIC VARIANTS AND ULTRASOUND ARTIFACTS 36 Wendy L Pabich and Katherine Grichnik C h a pter4 QUANTITATIVE ECHOCARDIOGRAPHY 63 Feroze Mahmood and Robina Matyal The Basic TEE Exam C h a pters TRANSESOPHAGEAL TOMOGRAPHIC VIEWS 87 Ryan Lauer and Joseph P Mathew C h a pter ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION 125 Linda D Gillam and Laura Ford-Mukkamala ADVANCED TRANSESOPHAGEAL ECHOCARDIOGRAPHY Valvular Heart Diseases C h a pter MITRAL VALVE 143 Johannes van der Westhuizen and Justiaan Swanevelder C h a pter MITRAL VALVE REPAIR 175 Ghassan Slei/aty, Iss am El Rassi, and Victor Jebara C h a pter AORTIC VALVE Mark A Taylor and Christopher A Troia nos 195 iv I Contents C h a pter TRICUSPID AND PULMONIC VALVES 222 George V Moukarbel and Antoine B Abchee C h a pter 1 PROSTHETIC VALVES 240 Blaine A Kent, Madhav Swaminathan, and Joseph P Mathew Ventricular Function C h a pter ASSESSMENT OF LEFT VENTRICULAR DIASTOLIC FUNCTION 266 Alina Nicoara and Wanda M.Popescu C h a pter EVALUATION OF RIGHT HEART FUNCTION 29 Rebecca A Schroeder, Shahar Bar-Yosef, and Jonathan B Mark C h a pter ECHOCARDIOGRAPHIC EVALUATION OF CARDIOMYOPATHIES 16 Andrew Maslow and Stanton K Shernan Pericardium C h a pter PERICARDIAL DISEASES 35 Nikolaos J Sku bas and Manuel L Fontes CLINICAL PERIOPERATIVE ECHOCARDIOGRAPHY C h a pter ECHOCARDIOGRAPHY FOR AORTIC SURGERY 370 Christopher Hudson, Jose Coddens, and Madhav Swaminathan C h a pter TRANSESOPHAGEAL ECHOCARDIOGRAPHY FOR HEART FAILURE SURGERY 87 Susan M Martinelli, Joseph G Rogers, and Carmela A Milano C h a pter TRANSESOPHAGEAL ECHOCARDIOGRAPHY FOR CONGENITAL HEART DISEASE 406 Stephanie S F Fischer and Mathew V Patteril C h a pter CARDIAC MASSES 440 Jose Coddens C h a pter 20 EPICARDIAL ECHOCARDIOGRAPHY AND EPIAORTIC ULTRASONOGRAPHY 454 Stan ton K Shernan and Kathryn E Glas C h a pter 21 TEE FOR NONCARDIAC SURGERY Angus Christie and Frederick W Lombard 462 Contents I v TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN NONOPERATIVE SETTINGS C h a pter 22 TEE IN THE CRITICAL CARE UNIT 475 Jordan Hudson and Andrew Shaw C h a pter 23 TEE IN THE EMERGENCY DEPARTMENT 84 Svati H Shah SPECIAL TOPICS C h a pter 24 EMERGING APPLICATIONS OF PERIOPERATIVE ECHOCARDIOGRAPHY 506 Carlo Marcucci, Bettina Jungwirth, Burkhard Macken sen, and Am an Mahajan C h a pter 25 THE NUTS AND BOLTS OF A PERIOPERATIVE TEE SERVICE 540 Shahar Bar- Yosef, Rebecca Schroeder, and Jonathan B Mark C h a pter 26 TRAINING AND CERTIFICATION IN PERIOPERATIVE TRANSESOPHAGEAL ECHOCARDIOGRAPHY 55 Jack Shanewise C h a pter THE TEE BOARD EXAM 565 Matthew Wood and Katherine Grichnik APPENDICES Appendix A NORMAL CHAMBER DIMENSIONS 57 Appendix B WALL MOTION AND CORONARY PERFUSION 573 Appendix( DIASTOLIC FUNCTION 575 AppendixD NATIVE VALVE AREAS, VELOCITIES, AND GRADIENTS 57 AppendixE MEASUREMENTS AND CALCULATIONS 86 AppendixF NORMAL DOPPLER ECHOCARDIOGRAPHIC VALUES FOR PROSTHETIC AORTIC VALVES AppendixG AppendixH 590 NORMAL DOPPLER ECHOCARDIOGRAPHY VALUES FOR PROSTHETIC MITRAL VALVES 595 MISCELLANEOUS 59 ANSWERS 600 INDEX 629 To my children, Jonathan, Eliza, and Susanna-dearly loved and precious gifts from God May you always walk in truth and grace knowing that the One who calls you is faithful and He also will bring it to pass joseph P Mathew To my wife, my closest friend, for her unconditional support To our children, for making it all worthwhile And to my mentors, for their remarkable vision Madhav Swaminathan To all four that are the most precious to me: My wife Aline It is her unconditional, never-ending love and support which make all things possible; My children Maurice the intellectual, for his compassionate and ambitious nature, Marc the charismatic, for his native wit, integrity, and determi nation, Paul, the rising star Chakib M Ayoub Co nt ributo rs Antoine B Abchee, MD, FACC Associate Professor of Clinical Medicine Department oflnternal Medicine American University of Beirut Beirut, Lebanon [10] David B Adams, RCS, RDCS [2] Duke University Medical Center Durham, North Carolina Brian P Barrick [1] Shahar Bar-Yosef, MD [13, 25] Assistant Professor Anesthesiology and Critical Care Medicine Duke University Medical Center Durham, North Carolina Angus Christie, MD [21] Associate Residency Director Department of Anesthesiology and Pain Management Maine Medical Center Portland, Maine Jose Coddens, MD [16, 19] Staff Anesthesiologist Anesthesia and Intensive Care Medicine Onze Lieve Vrouw Clinic Aalst, Belgium lssam EI-Rassi, MD [8] Senior Lecturer Cardiac Surgery Hotel-Dieu de France Hospital Beirut, Lebanon Stephanie S.F Fischer, MD [18] Cardiothoracic Anesthesiologist Private Practice Sea Point, South Africa Manuel L Fontes, MD [15] Associate Professor of Anesthesiology and Critical Care Anesthesiology New York, New York Laura Ford-Mukkamala, DO, FACC [6] Clinical Cardiologist Southeastern Cardiology Associates Columbus, Georgia Emily Forsberg, RDCS [2] Linda Gillam, MD, MPH Professor of Clinical Medicine Medicine Columbia University New York, New York [6] Kathryn E Glas, MD, MBA, FASE Associate Professor Anesthesiology Emory University Atlanta, Georgia Katherine Grichnik, MD, FASE Professor Anesthesiology Duke University Medical Center Durham, North Carolina [20] [3, 27] Hillary B Hrabak, BS, RDCS [2] Cardiac Sonographer Cardiac Diagnostic Unit Duke University Medical Center Durham, North Carolina Christopher Hudson [16] Jordan K C Hudson, MD, FRCPC Assistant Professor Deptartment of Anesthesiology Ottawa, Ontario Canada Victor Jebara, MD [8] Professor and Chief Thoracic and Cardiovascular Surgery Hotel Dieu de France Beirut, Lebanon [22] viii I Contri b utors Bettina Jungwirth, MD [8] Assistant Professor Department of Anesthesiology Klinik fuer Anaesthesiologie Muenchen, Germany Susan M Martinelli, MD Assistant Professor Anesthesiology University of North Carolina Chapel Hill, North Carolina Blaine A Kent, MD, FRCPC [11] Chief, Division of Cardiac Anestheisa Anesthesiology Capital District Health Authority/Dalhousie University Halifax, Nova Scotia Canada Andrew Maslow [14] Ryan E Lauer, MD [5) Assistant Professor Department of Anesthesiology Lorna Linda University Lorna Linda, California Willem Lombard [21] G Burkhard Mackensen, MD, PhD Associate Professor Anesthesiology Duke University Medical Center Durham, North Carolina Aman Mahajan, MD, PhD [24] Professor and Chief Cardiothoracic Anesthesiology Ronald Reagan UCLA Medical Center Los Angeles, California Feroze Mahmood [4] Assistant Professor Anesthesia and Critical Care Beth Israel Deaconess Medical Center Harvard Medical School Boston, Massachusetts Carlo E Marcucci [24] Director of Cardiothoracic Anesthesiology Anesthesiology University Hospital lausanne (CHUV) Lausanne, Vaud Switzerland Jonathan B Mark, MD [13, 25] Professor Anesthesiology Veterans Affairs Medical Center Durham, North Carolina [24] [17] Robina Matyal [4] George V Moukarbel, MD, FASE Advanced Echocardiography Fellow Cardiovascular Diseases Brigham and Women's Hospital Harvard Medical School Boston, Massachuserts Alina Nicoara, MD Assistant Professor Anesthesiology Branford, Connecticut [10] [12] Wendy Pabich [3] Mathew Patteril [18] Mihai V Podgoreanu, MD, FASE Assistant Professor Anesthesiology Duke University Durham, North Carolina Wanda M Popescu, MD [12] Assistant Professor Anesthesiology Yale University School of Medicine New Haven, Connecticut Edward K Prokop, MD [1 J Associate Clinical Professor Anesthesiology Hospital of St Raphael New Haven, Connecticut Joseph G Rogers, MD [17] Associate Professor Internal Medicine, CArdiology Division Duke University Medical Center Durham, North Carolina [1] Contri b utors I ix Rebecca A Schroeder, MD Associate Professor Anestehsiology Durk University School of Medicine Durham, North Carolina [13, 25] Svati H Shah, MD, MHS, FACC Assistant Professor of Medicine Medicine Duke University Medical Center Durham, North Carolina Ghassan Sleilaty, MD [8] Fellow Division of Cardiovascular and Thoracic Surgery Hotel Dieu de France Hospital Beirut, Lebanon [23] Justiaan Swanevelder [7] Mark A Taylor, MD, FASE [9] Assistant Professor Department of Anesthesiology The Western Pennsylvania Hospital-Forbes Regional Campus Monroeville, Pennsylvania Jack S Shanewise, MD, FASE [26] Professor of Clinical Anesthesiology Anesthesiology Columbia University Medical Center New York, New York Andrew Shaw, MB, FRCA, FCCM Associate Professor Anesthesiology Duke University Medical Center Durham, North Carolina [22] Stanton Shernan [14, 20] Nikolaos I Skubas, MD, FASE, DSc Associate Professor Anesthesiology Weill Cornell Medical College New York, New York [15] Christopher A Troianos, MD [9] Professor and Chair Department of Anesthesiology Western Pennsylvania Hospital Pittsburgh, Pennsylvania Johannes van der Westhuizen, MBChB, MMed(Anes) [7] Consultant Anesthesiologist Anesthesiology Haumann and Partners Bloemfontein, South Africa Matthew Wood, [271 354 C H A PTER thicker than mm considered abnormal • Multiple measurements should be performed to obtain an aver age thickness, and multiple views of the pericardium should be imaged because pericardial thickening may be asymmetric in distribution This heterogeneity of peri cardial involvement accounts for some of the limitations in diagnosing and detecting pericardial disease when using TIE Additional features of the echocardiographic examination that assist in the diagnosis of constrictive pericarditis include abnormal interventricular septal motion (see below) and atrial compression by the thick ened pericardium Examination of the venous inflow to the right and left heart (vena cava and pulmonary veins) also may assist in the diagnosis of pericardial disease As previ ously described, by advancing the probe to the ME depth and optimizing the view of LA and RA separated by the interatrial septum, the bicaval view can be imaged by rotating the multiplane angle forward to 90° The inferior vena cava (NC) will appear on the top left of the screen as it enters the atrium Maintaining this view while advancing the probe more distally into the esoph agus will demonstrate the entire length of the NC and the intrahepatic veins as they enter the NC A dilated and nonpulsatile NC is a nonspecific indicator of con strictive pericarditis Moreover, a decrease with sponta neous inspiration in NC diameter of less than 50% at the junction of the RA is a marker of elevated RA pres sure Similarly, variations in pulmonary vein flow veloc ities with respiration (see below) aid in the diagnosis of constriction M-mode On TIE M-mode echocardiography, diagnostic fea tures in constrictive pericarditis, include pericardial thickening, flattening of the LV inferolateral wall dur ing mid- to late diastole, LA enlargement, abnormal diastolic and systolic motions of the interventricular septum, atrial systolic notch (a posterior rather than the normal anterior interventricular septal motion occur ring after the onset of electrocardiographic P wave that terminates before the QRS complex) , and premature pulmonic valve closure 17 Diastolic septal motion is related primarily to the trans-septal pressure gradient, which in constrictive pericarditis is derived from the abrupt filling of the ventricles Therefore, during the early phase of diastole, the interventricular septum can exhibit a sudden posterior deflection followed by a more gradual posterior septal motion occurring later in diastole (atrial systolic notch) Whereas these findings may be apparent in constrictive pericarditis, Engel and associates reported a low sensitivity in the diagnosis of constrictive pericarditis with the use of M-mode 17 In a series of 40 patients with a diagnosis of constrictive pericarditis confirmed by hemodynamic criteria, surgi cal examination, or necropsy, the most common find ings by M-mode were abnormal septal motion and flat tening of the LV inferolateral wall motion in diastole 17 However, posterior septal motion abnormality is seen in other pathologic states including RV volume over load, ischemic heart disease, and in the setting of cardiac surgery Although the use of M-mode may have limitations in the assessment of constrictive pericarditis, in general, all patients with this pathol ogy will display abnormal findings on M-mode Thus, M-mode should be considered an adj unct to other modalities of echocardiographic diagnosis of constrictive pericarditis Pulsed-Wave Doppler Doppler examination of flow dynamics is often diag nostic of constrictive pericarditis and is an important adjunct in differentiating pericardial processes from myocardial pathology associated with diastolic dysfunc tion The Doppler findings characterize the flow dynamics due to the rigid, noncompliant pericardium encompassing both ventricles, minimizing their dias tolic volume, exaggerating their interdependence, and isolating them from intrathoracic respiratory changes RV and LV diastolic inflow velocities show high early inflow velocities (E wave) consistent with rapid early filling and rapid equalization of pressures This is a reflection of the restraining effect of the thickened peri cardium and of the decreased filling of the ventricles in mid- to late diastole The mitral and tricuspid late inflow velocities (A wave) are extremely low or virtually absent, as in a restrictive filling pattern, with the atrial contraction contributing little to LV filling In addi tion, the deceleration time of the E velocity is short In constrictive pericarditis, pulmonary vein flow dynamics should correlate with the expected findings of pericardial impediment of atrial filling during ventricu lar systole (blunting of the S wave), followed by rela tively larger diastolic flow (D wave) Although the D wave is greater in magnitude than the S, it also becomes limited by poor chamber compliance during the latter part of diastole as ventricular pressure rapidly equili brates with atrial pressure Consequently, atrial contrac tion will have little to no contribution to ventricular filling, resulting in redirection of blood flow from the atrium to the pulmonary vein depicted as a larger A wave.1 However, the clinical validity of Doppler find ings is highly dependent on the ultrasonographer's tech nical expertise, the clinical setting at the time of the examination (ie, loading conditions) , and, more impor tantly, its confirmation or support of other clinical or PERICARDIAL D I S EASES echocardiographic correlates of the underlying patho physiology The aforementioned findings are highly influenced by respiratory variations and by ventricular interaction (please refer to the Cardiac Tamponade section for additional details) Normally, decreases in intrathoracic pressure with spontaneous inhalation are transmitted to the heart and the pulmonary veins In healthy, sponta neously ventilating subjects, this decreased intrathoracic pressure results in minor decreases in pulmonary vein to LA pressure gradient, resulting in mild decrease in LV ftlling ( < Oo/o to 5% fluctuation of the mitral inflow E wave) In constrictive pericarditis, the thickened peri cardium isolates the intrapericardial cardiac chambers (but not the extrapericardially located pulmonary veins) from changes in intrathoracic pressure during the respi ratory cycle k a result, mitral inflow E and pulmonary vein D velocities decrease during inspiration This decrease in diastolic flow is due to a significant decrease in the pressure gradient between the pulmonary vein and the LA During spontaneous exhalation, mitral inflow E and pulmonary vein D velocities increase (>25% compared with the inspiratory values) as intratho racic pressure rises and the flow of blood previously pooled ill the lungs during inspiration increases 20 ,21 Reciprocal changes are seen on the right side of the heart such that RV filling increases with spontaneous inspira tion and decreases with exhalation A variation greater FIGURE 5-4 Transmitral flow pattern in constrictive pericarditis A decrease in the m itral E velocity with inspira tion g reater than 25% in a spontaneously ventilati ng patient poi nts to the presence of strictive pericarditis The spectral display in this patient has been inverted from the usual d i s play for tra ns esophageal echocardiography I 355 than 25% between mspiratory and expiratory velocities on the right side is also mdicative of constrictive pericarditis In addition, prominent hepatic vern diastolic flow reversal may be noticed as a result of mcreased RA pressure k compared with spontaneous breathing, positive pressure ventilation reverses the respiratory variation of mitral inflow and pulmonary vein inflow velocities in subjects with constrictive pericarditis.22 Relative to exha lation, a mechanical breath increases the intrathoracic pressure, leading to greater mitral inflow E and pul monary vein D velocities during Doppler examination Increased respiratory variation in mitral inflow E velocities in conjunction with pulmonary vein inflow velocity variation is virtually pathognomonic for con strictive pericarditis (Figure 5-4) This is an impor tant finding that helps to distinguish constrictive peri carditis from restrictive cardiomyopathy in which there is no respiratory variation in velocities, as well as no pericardia! thickening Of note, there is a subset of patients with constrictive pericarditis who not exhibit respiratory variation, namely those with atrial fibrillation or severely elevated LA pressures Tissue Doppler Doppler tissue imaging of the lateral mitral annulus in the ME four-chamber view allows the measure ment of myocardial wall velocities The diastolic E' and 356 C H A PTER A' velocities of Doppler tissue parallel transmitral E and A velocities, but are relatively independent of preload (see Chapter 2) Doppler tissue velocities reflect LV expansion and contraction and therefore aid in differ entiating constrictive pericarditis from restrictive car diomyopathy In constrictive pericarditis, E' tends to be preserved (>8 cm/s) despite increased LV filling pressure, whereas a significantly decreased E' ( 000 mL) with very little increase in pericardia! pressure and no symptomatology Con versely, rapid accumulations of very small volumes (50 to 00 mL) or a strategically located mass can lead to marked elevations in pericardial pressure and clini cal decompensation.24 Once pericardial collection exceeds the ability of pericardium to expand, the total intrapericardial vol ume (fluid/content and cardiac structures and volume) becomes constant throughout the cardiac cycle Because the intracardiac pressures vary during the cardiac cycle, the compressive effects of a pericardial fluid collection are seen first on low-pressure chambers, ie, atria during atrial relaxation (ie, ventricular systole) and ventricles during diastole Therefore, systolic atrial inversion will be noticed before diastolic RV outflow tract compres sion An increasing pericardial pressure also will equili brate more rapidly with the pressures of the thinner walled ri t heart than with the pressures of the lefr heart.25 •2 Coronary blood flow is reduced in cardiac tamponade, but this reduction is not sufficient to add an ischemic inj ury to the myocardium In the absence of coronary artery disease there is a proportionate decrease in both ventricular preload (decreased cham ber filling) and afterload As a consequence, myocar dial work and oxygen consumption are reduced However, patients with preexistent coronary artery disease may be at increased risk for myocardial ischemia and/ or infarction Under normal conditions, ventricular interaction is extremely important for maintenance of adequate car diac performance The average stroke volume of the RV equals the stroke volume of the LV; however, res piration causes cyclical differences in LV and RV stroke volumes During spontaneous inspiration, neg ative intrapleural pressure facilitates venous return to the right heart At the same time venous return to the left heart is diminished because ( ) lung expansion increases the pulmonary venous blood volume and (2) increase in RV filling causes the interventricular septum to "bulge" lefrward, thereby reducing LV dimension and altering its compliance and filling (ventricular interaction/interdependence) During spon taneous exhalation, the reverse process occurs This ventricular interdependence is exaggerated in cardiac tamponade, because the total cardiac volume is lim ited by the pressurized pericardial content As the intrapericardial content increases, it reaches a point at which the parietal pericardium cannot stretch com mensurate with the rising pressure Because of the fixed space within the pericardium, cardiac chamber dimensions become smaller Thus, the normal effects of respiration will be pronounced: the increased extra intrathoracic pressure gradient during spontaneous inspiration favors filling of RV at the expense of LV filling, while there is more LV filling during sponta neous exhalation (when there is less RV filling) Echocardiographic studies of patients with cardiac tamponade have described phasic respiratory changes in which LV filling (and mitral valve excursions) decreased during inspiration 25 In contrast, RV dimen sions increased in association with a shifring of the interventricular septum toward the LV In the case of cardiac tamponade, ventricular interaction involves not � PERICARDIAL D I S EASES only the interventricular septum but also other cardiac chambers, depending on the etiology of the tamponade (fluid vs clot; regional vs global tamponade) Therefore, the magnitude of diastolic changes is related to the severity of pericardia! fluid collection, chamber pres sure and volume, and transpulmonary pressures dur ing inspiration and exhalation Overall, the physiology of ventricular interaction in clinical cardiac tampon ade becomes more complex as the pressure-volume relation of mediastinal and chest structures is altered with each heartbeat and by respiratory and neuroen docrine influences Normally, there is an inspiratory decrease of less than mm Hg in the arterial systolic pressure and an accompanying inspiratory decrease in the venous pressure However, in patients with tamponade, there is pulsus paradoxus: an inspiratory decrease of arterial pressure greater than mm Hg with venous pressure that remains steady or increases 27 The mag nitude of paradoxical pulse is directly proportional to the inspiratory (spontaneous breathing) decrease of LV dimension, diastolic volume, and stroke vol ume Of importance, pulsus paradoxus and the pha sic respiratory changes in ventricular dimensions are not unique to cardiac tamponade These changes can be present in constrictive pericarditis and in a variety of clinical conditions in which intrapleural pressure is significantly diminished, such as respiratory dis tress, airway obstruction, chronic obstructive pul monary disease, and pulmonary embolism Of note, this clinical feature of cardiac tamponade may be absent in patients with chest wall trauma, neuromus cular disease, and pneumothorax because they can not produce sufficient negative intrapleural pressure during inspiration to produce changes in chamber dimension and decrease in LV stroke volume Simi larly, those under positive pressure mechanical venti lation or with severe aortic regurgitation may or may not exhibit hemodynamic findings s uggestive of pul sus paradoxus In the setting of cardiac surgery, cardiac tamponade can occur acutely over minutes or hours or after a few days postoperatively The reported incidence of acute cardiac tamponade is 0.5% to 8%.28•29 The typical patient has significant chest tube drainage (>200 mL!h) in the immediate postoperative period with or without hemodynamic signs of inadequate cardiac output Alternatively, the chest tubes may become obstructed by blood clots, thus impeding mediastinal drainage Delayed tamponade has been defined arbitrarily as car diac tamponade occurring more than to days after pericardiotomy.25·28•29 The incidence is 0.3% to 2.6% and is often misdiagnosed because of a low index of sus picion or because the clinical signs and symptoms are I 357 similar to those of congestive heart failure, pulmonary embolism, and generalized fatigue (ie, failure to thrive postoperatively) Thus, diagnosis of cardiac tamponade after cardiac surgery is often difficult and requires a high degree of clinical suspicion, proficient knowledge of pulmonary artery catheter derived hemodynamics, physical exami nation, and use of diagnostic tools such as echocardiog raphy, chest roentgenography, and magnetic resonance imaging (Figure 5-5) Relying on a single diagnostic modality can lead to inaccurate management and increased patient morbidity The classic teaching of equalization of diastolic blood pressures in cardiac tamponade (CVP PA diastolic pressure PAOP) is infrequently observed postoperatively because the peri cardium is left open As such, blood and clot not distribute around the heart homogeneously to produce equalization of pericardia! diastolic pressures In general, CVP is elevated, but PA diastolic pressure and the PAOP can be normal, elevated, or, in some cases, decreased Regional cardiac tamponade occurs when one or more cardiac chambers are compressed Postoperative RA hematomas often become localized to the anterior and lateral walls, whereas LA clots are found more com monly behind the left atrium in the oblique sinus.3° After cardiotomy, diastolic regional collapse of RA or RV is the most common echocardiographic finding in "early'' cardiac tamponade.29 -3 However, Russo and = FIGURE 5-5 = Pericardia! effusion seen on magnetic resonance imagi ng The pericard i u m is distended (large white arrows) and separated from the su rface of the heart (small arrows) by a fl uid collection 358 C H A PTER colleagues found that only 33% of patients with the diagnosis of cardiac tamponade had right heart catheterization findings that reflected equalization of diastolic blood pressures 32 Overall, 90% of patients with postcardiotomy cardiac tamponade had atypi cal clinical, hemodynami � , or echocardiographic findmgs Therefore, the dtagnosis of postoperative cardiac tamponade should be considered whenever hemodynamic deterioration is encountered, particu larly when reduction in cardiac output and blood pressure are not readily responsive to conventional management Selective compression of the right heart by hematoma becomes less prominent in "delayed" tamponade as the right heart becomes adherent or tethered to the anterior chest wall The clinical presentation in such a case may be mistaken for congestive heart failure, acute LV or RV infarc tion, septic shock, or pulmonary embolism In delayed tamponade, the complaints tend to be vague, and fewer hemodynamic data are available (ie, pul monary artery catheter) to allow prompt diagnosis of tamponade Although transthoracic echocardiography (TTE) is generally less invasive than TEE, imaging constraints in the post-cardiac surgical patient often leads to inconclusive diagnosis (see below) In contrast, TEE can be very helpful in diagnosis and clinical manage ment of tamponade Electrocardiography and chest roentgenography are adj unct diagnostic techniques Electrocardiographic changes seen with cardiac tam ponade include nonspecific ST- and T-wave abnormal ities, low-voltage QRS complex, signs of myocardial ischemia and pericarditis, and electrical alternans 33 The latter is seen in patients with large effusions and is characterized by beat-to-beat shifts in the electrical axis This beat-to-beat alteration may be due to the increased distance between the heart and the chest wall, resulting in a "pendulum" -like motion of the heart.25 • 33 However, it has been shown that minimal amount of pericardia! fluid removal abolishes electri cal alternans despite an enlarged pericardia! space Thus, the electrocardiographic changes of electrical alternans may reflect a hemodynamic pathology rather tha� � anatomic abnormality This finding, although tamponade, is not very specific sensltlve for cardtac (very few patients with tamponade present with elec trical alternans) On stand:rrd �nterior-posterior chest roentgenogra phy, the cardtac silhouette may appear normal in size or extremely enlarged depending on the acuity of the tam ponade process With large effusions, the cardiac sil houette will appear "widened" with or without features such as obscuring of the pulmonary vessels at the hilum and a globular or "water bottle" configuration of the heart Two-Dimensional Echocardiogra phy Several echocardiographic features of cardiac tampon ade may be detected by TTE and TEE: ( ) dimin ished LV dimension (and mitral valve excursion) during inspiration, (2) shift of the interventricular septum toward the LV, (3) changes in transvalvular (mitral and �artie) flow characteristics seen by J? oppler techmques (see below) , (4) diastolic paste nor monon of the RV wall, and (5) in some cases, a systolic notch on the RV epicardium Although many of the signs on a roentgenogram or echocardiogram can be suggestive of cardiac tamponade, it should be remembered that no finding by itself is 00% sensi tive and specific TIE can be compromised by postoperative fac tors: the su �gic � site may preclude use of an optimal transthoracic wmdow, chest tubes affect imaging and proper positioning of the patient, compression of the chest wall with the TIE probe may worsen incisional pain, and some loculated effusions may not be amenable to TTE imaging TEE can overcome many of these imaging constraints Pericardia! effusions can be readily seen and graded, and pericardia! blood clots can be visualized to compress the atria and the ventricle Detection of pericardia! effusion with two dimens io nal imaging may commence by advancing the TEE probe to obtain a transgastric midpapillary short-axis (SAX) view at 0° and assess for the presence of an echolucent fluid-filled space surrounding one or both ventricles (Figure 5-6) Hemorrhagic or puru lent fluid is more echogenic than serous collections Often, fibrin strands are visible Of note, the absence of pericardia! contents around the LV should not nec essarily exclude the absence of pericardia! collection around other heart structures such as the RV RV and LV function should be assessed in this view When the effusion is significant, ventricular function can be depressed if the pericardia! pressure overwhelms ven tricular diastolic pressures to the point that myocar dial blood flow is reduced Next, the transgastric two-chamber and long-axis (LAX) views are obtained by rotating the probe to about 90° to 1 0° In these views, the anterior and inferior walls of the LV are visualized and, if present, a pericardia! collection appe � rs as an echolucent space separating the afore mentioned LV walls from the parietal pericardium In all transgastric views, in the absence of previous sur gery or pericardia! disease, any pericardia! effusion will be diffuse, with clear separation between the parietal and visceral pericardia Diffuse collections are visualized first posterior to the heart, as the patient is usually supine during examination, and when small they are seen in systole only Pericardia! effusions are PERICARDIAL D I S EASES I 359 FIGURE 5-7 Pericardia I effusion detected on the m idpapil lary short-axis view The right ventricle is a l most obliterated and its cavity is barely visible Around both ventricles, there is a n echolucent space fi lled with fl uid (asterisk) The viscera l perica rd iu m is indistinguishable from the epicardial su rface of the two ventricles The parietal pericard i u m is the outer border of the pericardia! effusion The distance between the two pericardia! layers is em, so the pericardia! fl uid col lection is graded as moderate Notice the a bsence of electrical alternans i n the electrocard iog raphic tracing at the bottom of the picture (IVS, interventricular sep tum; RV, right ventricle; LV, left ventricle.) FIGURE 5-6 graded as minimal (50 to 00 mL) if the visceral and parietal pericardia! layers are separated by less than em in diastole, small ( 00 to 250 mL) if separated by to em, moderate (2 50 to 500 mL) if sepa rated by to em, and large (>500 mL) when greater than cm 34 The absence of pericardial effu sion in the transgastric views should not limit further echocardiographic examination because loculated pericardial collections (Figure 5-7) can exist around the RA or the LA (seen in the ME four-chamber view or the ME bicaval view) In the latter view, one can perform an M-mode examination through the RA free wall, to identify systolic RA free wall inversion or collapse The same can be done in the ME LAX view to diagnose RV o utflow tract diastolic collapse Sig nificant pericardia! effusion may also dilate potential spaces formed by the pericardial folds, such as the transverse sinus (Figure 5-8) , found between the posterior ascending aorta and the anterior LA wall (visualized in the ME LAX view, where one can see Right atrial compression b y a large localized thrombus i n a modified midesophagea l fou r cham ber view The arrow points to the invagination in the right atriu m wal l created by the throm bus Particu larly i n the post-card iac surgical setti ng, locu lated peri cardia I col lections can form around the right or left atriu m, restrict ventricular fil l i ng, and cause hemody namic col lapse (LA, left atri u m; RA, right atriu m; TV, tri cuspid va lve.) that the left atrium and ascending aorta are not next to each other but are separated by the dilated trans verse sinus) RA COLLAPSE The RA is a thin and flexible structure and, under nor mal conditions, brief wall inversion can occur fu a con sequence, the specificity of RA systolic collapse for tamponade increases when systolic compression persists for one-third or longer of the duration of the cardiac cycle.28 Atrial compression has a 95% sensitivity, 00% specificity, and positive predictive value of 90%.30 It is best visualized by TIE on parasternal LAX and apical four-chamber views; on TEE, the ME four-chamber view (Figure 5-9) or the ME bicaval views are recom mended RA systolic collapse is a sensitive sign in the diagnosis of tamponade and is best evaluated by using M-mode through the RA (Figure 5- 0) RV COLLAPSE RV collapse may occur when the pericardial pressure exceeds RV pressure This typically occurs during dias tole, when the RV pressure is at its lowest Diastolic RV collapse is more specific than RA collapse for confirm ing tamponade35 and can be identified by an abnormal posterior inward motion of the anterior RV wall during diastole (Figure 5- 1 ) 30.3 Timing of collapse may be 360 C H A PTER FIGURE 5-8 I n this mides ophageal long-axis view, peri cardia! effusion comp resses the free wa l l of the rig ht ven tricle and the right ventricular outflow tract The tra nsverse sinus (arrow), a potential space created by the perica r dia! folds between the left atriu m and the ascending aorta, is also filled with pericar dia! fl uid I n large pericardia I effusions, this space can be markedly di lated and serve as a helpful diag nostic finding (AO, ascending aorta; E, effu sion; LA, left atrium; RVOT, right ventricular outflow tract.) FIGURE 5-9 Right atrial collapse The left atriu m, right atrium, right ventricle, and left ventricle are seen in a mides ophageal fou r-chamber view with the probe rotated toward the right atrium There is pericardia I effusion around the heart (asterisk, outside the free wall of the right ventricle) The pictu re is significant because the free wall of the rig ht atriu m is i nverted (white arrow) d u ring systole (white mark on the electrocardiograph at the bottom of the echo display) Systolic right atrial collapse should always raise the suspicion of hemodynamically sig nificant pericardia I fluid collection (LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.) PERICARDIAL D I S EASES I 36 FIGURE 5- M-mode image of right atrial free wal l com pression i n ca rd iac tam ponade While i n the tra ns esophageal echoca rd iographic mid esophagea l fou r-cham ber view, the cu rsor l i n e is positioned so that it transects the left atri u m, i nteratria l septum, and the free wa l l of the right atri u m Dashed l i nes coi ncide with the systolic i nter va l on the electrocard iographic tracing The i nwa rd motion of the right atrial free wa l l d u ring systol e is apparent Although this may be normal if short lived, it is indicative of cardiac tam ponade if the d u ration of the inward motion lasts longer than one-third of the systol i c period (white arrow) (lAS, i nteratrial septum; LA, left atrium; RA, right atriu m ) FIGURE 5- Right ventricular d iastolic collapse The left and rig ht ventricles are seen in a transgastric short-axis view with a large pericardia I effusion detected anteriorly and posteriorly In the left panel the right ventricle is seen at end-systole; in the right panel, the right ventricle is i nverted d u ring d iastole (arrow) ( E, effusion; LV, left ventricle; RV, right ventricle.) C H A PTER 362 Table 5- Echoca rd i o g p h i c F i n d i n g s i n Ca rd ia c Ta m p o n a d e, Con strictive Perica rd itis, and Restri ctive C a rd i o myopathy 20 Cardiac Tamponade Constrictive Pericarditis Restrictive Cardiomyopathy Moderate to large pericardia I effusion Pericardia I thickening, sometimes (20%-30%) with calcification Small RA and LA Normal pericardium, thickened LV RA, LA, and RV free wall inversion (collapse) IVC plethora IVS moves towa rd the LV during spontaneous inspiration Major enlargement of RA and LA Relatively little IVS movement in most cases Doppler LV Inflow PVFiow Respiratory variation present: spontaneous exhalation E > inspiration E Respiratory variation present: spontaneous exhalation D > inspiration D MVAnnulus E variation: spontaneous exhalation > inspiration by �25% D variation: exhalation > inspiration by �25%, S:D >1 E' >8.0 cm/s Little respiratory variation, E:A �2.0, DT < 60 ms Little respiratory variation, S:D < E'