HEMODYNAMIC ROUNDSInterpretation of Cardiac Pathophysiology fromPressure Waveform Analysis

THIRD EDITION

Edited by

Morton J. Kern, MDDivision of Cardiology

University of California, Irvine

Michael J. Lim, MDJ.G. Mudd Cardiac Cath Lab

St. Louis University Health Sciences Center

James A. Goldstein, MDWilliam Beaumont Hospital

Royal Oak, Michigan

InnodataFile Attachment9780470930502.jpg

HEMODYNAMIC ROUNDS

HEMODYNAMIC ROUNDSInterpretation of Cardiac Pathophysiology fromPressure Waveform Analysis

THIRD EDITION

Edited by

Morton J. Kern, MDDivision of Cardiology

University of California, Irvine

Michael J. Lim, MDJ.G. Mudd Cardiac Cath Lab

St. Louis University Health Sciences Center

James A. Goldstein, MDWilliam Beaumont Hospital

Royal Oak, Michigan

Copyright r 2009 by John Wiley & Sons, Inc. All rights reserved

Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientific, Technical, and Medical business with

Blackwell Publishing.

Published by John Wiley & Sons, Inc., Hoboken, New Jersey

Published simultaneously in Canada

No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical,

photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act,

without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright

Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, (978) 750-8400, fax (978) 750-4470, or on the web at www.copyright.com.

Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken,

NJ 07030, (201) 748-6011, fax (201) 748-6008, or online at http://www.wiley.com/go/permission.

Limit of Liability/Disclaimer of Warranty: While the publisher and author have used their best efforts in preparing this book, they make no

representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied

warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written

sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional

where appropriate. Neither the publisher nor author shall be liable for any loss of profit or any other commercial damages, including but not

limited to special, incidental, consequential, or other damages.

For general information on our other products and services or for technical support, please contact our Customer Care Department

within the United States at (800) 762-2974, outside the United States at (317) 572-3993 or fax (317) 572-4002.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic formats.

For more information about Wiley products, visit our web site at www.wiley.com.

ISBN: 978-0-470-08576-9

Library of Congress Cataloging-in-Publication Data is available.

Printed in the United States of America

10 9 8 7 6 5 4 3 2 1

http://www.copyright.comhttp://www.wiley.com/go/permissionhttp://www.wiley.com

To Margaret and Anna Rose, the systole of my life. MJKTo Amy, Parker, and Taylor – the essential pieces to my life. MJLTo my wife Cindy, who keeps life fun while I am working. JAG

HEMODYNAMIC ROUNDS 2007

The following citations have been used in the chapters identified by chapter number. These chapters were originallypublished in Catheterization and Cardiovascular Diagnosis and comprise the basis for most of the chapters inHemodynamic Rounds, Third Edition.

Chapter 1 Kern MJ, Aguirre FV, Donohue TJ. Hemodynamic rounds: Interpretation of cardiac pathophysiologyfrom pressure waveform analysis: Pressure wave artifacts. Cathet Cardiovasc Diagn 27:147–154, 1992.

Chapter 2 Kern MJ. Pitfalls of right heart hemodynamics. Cathet Cardiovasc Diagn 43:90–94, 1998.

Chapter 3 Kern MJ, Deligonul U. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis. II. The tricuspid valve. Cathet Cardiovasc Diagn 21:278–286, 1990.

Chapter 4 Kern MJ. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressure waveformanalysis. The left-side V wave. Cathet Cardiovasc Diagn 23:211–218, 1991.

Chapter 5 Kern MJ. The LVEDP. Cathet Cardiovasc Diagn 44:70–74, 1998.

Chapter 6 Kern MJ, Donohue TJ, Bach R, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac patho-physiology from pressure waveform analysis: Simultaneous left and right ventricular pressure measure-ments. Cathet Cardiovasc Diagn 28:51–55, 1992.

Chapter 7 Kern MJ, Aguirre FV, Hilton TC. Hemodynamic rounds: Interpretation of cardiac pathophysiologyfrom pressure waveform analysis. The effects of nitroglycerin. Cathet Cardiovasc Diagn 25:241–248, 1992.

Chapter 8 Schoen WJ, Talley JD, Kern MJ. Hemodynamic rounds: Interpretation of cardiac pathophysiology frompressure waveform analysis: Pulsus alternans. Cathet Cardiovasc Diagn 24:315–319, 1991.

Chapter 9 Kern MJ. Editorial comments for hemodynamic rounds: Interpretation of cardiac pathophysiology frompressure waveform analysis: Acute aortic insufficiency. Cathet Cardiovasc Diagn 28:244–249, 1993.

Chapter 10 Kern MJ, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis: Aortic regurgitation. Cathet Cardiovasc Diagn 26:232–240, 1992.

Chapter 11 Kern MJ, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis: aortic regurgitation. Cathet Cardiovasc Diagn 26:232–240, 1992.

Chapter 12 Kern MJ, Aguirre FV, Guerrero M. Abnormal hemodynamics after prosthetic aortic root reconstruction:Aortic stenosis or insufficiency? Cathet Cardiovasc Diagn 44:336–340, 1998.

Chapter 13 Godlewski KJ, Talley JD, Morris GT. Interpretation of cardiac pathophysiology from pressure waveformanalysis: Acute aortic insufficiency. Cathet Cardiovasc Diagn 28:244–248, 1993.

Chapter 14 Kern MJ, Aguirre FV, Donohue TJ, Bach RG. Hemodynamic rounds: Interpretation of cardiac patho-physiology from pressure waveform analysis: Multivalvular regurgitant lesions. Cathet Cardiovasc Diagn28:167–172, 1993.

Chapter 15 Suh WM, Kern MJ. Modified and reproduced from Cathet Cardiovasc Intervent 71: 944–949, 2008.

Chapter 17 Kern MJ, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis: Mitral valve gradients, part I. Cathet Cardiovasc Diagn 26:308–315, 1992.

Chapter 18 Kern MJ. Mitral stenosis and pulsus alternans. Cathet Cardiovasc Diagn 43:313–317, 1998.

Chapter 19 Azrak E, Kern MJ, Bach RG, Donohue TJ, Hemodynamic evaluation of a stenotic bioprosthetic mitralvalve. Cathet Cardiovasc Diagn 45:70–75, 1998.

Chapter 20 Kern MJ. Left ventricular puncture for hemodynamic evaluation of double prosthetic valve stenosis.Cathet Cardiovasc Diagn 43:466–471, 1998.

Chapter 22 Freihage JH, Joyal D, Arab D, Dieter RS, Loeb HS, Steen L, Lewis B, Liu JC, Leya F, et al. Invasiveassessment of mitral regurgitation: Comparison of hemodynamic parameters. Cathet CardiovascIntervent 69:303–312, 2007.

Chapter 23 Kern MJ. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressure waveformanalysis. The pulmonary valve. Cathet Cardiovasc Diagn 24:209–213, 1991.

Chapter 24 Kern MJ, Bach RG. Pulmonic balloon valvuloplasty. Cathet Cardiovasc Diagn 44:227–234, 1998.

Chapter 25 Kern MJ, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis: Mitral valve gradients, part II. Cathet Cardiovasc Diagn 27:52–56, 1992.

Chapter 29 Kosmicki L, Michaels AD. Cathet Cardiovasc Intervent 2008, in press.

Chapter 30 Higano ST, Azrak E, Tahirkheli NK, Kern MJ. Hemodynamics of constrictive physiology: Influence ofrespiratory dynamics on ventricular pressures. Cathet Cardiovasc Intervent 46:473–486, 1999.

Chapter 32 Kern MJ, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis: Pericardial compressive hemodynamics. Part II, Cathet Cardiovasc Diagn 26:34–40,1992.

Chapter 33 Kern MJ, Aguirre FV. Hemodynamics rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis: Pericardial compressive hemodynamics. Part III. Cathet Cardiovasc Diagn 26:152–158, 1992.

Chapter 34 Kern MJ, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis: Pericardial compressive hemodynamics. Part I. Cathet Cardiovasc Diagn 25:336–342,1992.

Chapter 35 Azrak EC, Kern MJ, Bach RG. Hemodynamics of cardiac tamponade in a patient with AIDS-relatednon-Hodgkin’s lymphoma. Cathet Cardiovasc Diagn 45:287–291, 1998.

Chapter 36 Strote JA, Dean LS, Goldberg SL, Krieger EV, Stewart DK. A novel assessment for a constrictive peri-carditis. In press. 2008.

Chapter 38 Kern MJ, Donohue TJ, Bach RG, Aguirre FV. Hemodynamic rounds: Interpretation of cardiac patho-physiology from pressure waveform analysis: Cardiac arrhythmias. Cathet Cardiovasc Diagn 27:223–227,1992.

Chapter 39 Kern MJ, Deligonul U. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis. Pacemaker hemodynamics. Cathet Cardiovasc Diagan 24:22–27, 1991.

Chapter 40 Kern MJ, Puri S, Donohue TJ, Bach RG. Hemodynamics of dual-chamber pacing and Valsalva man-euver in a patient with hypertrophic obstructive cardiomyopathy. Cathet Cardiovasc Diagn 44:438–442,1998.

Kern MJ, H, Bach RG. Hemodynamics effects of alcohol-induced septal infarction for hypertrophicobstructive cardiomyopathy. Cathet Cardiovasc Intervent 47:221–228, 1999.

Chapter 41 Kern MJ. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressure waveformanalysis. Coronary hemodynamics: I. Coronary catheter pressures. Cathet Cardiovasc Diagn 25:57–60,1992.Kern MJ. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressure waveformanalysis. Coronary hemodynamics part II. Patterns of coronary flow velocity. Cathet Cardiovasc Diagn25:154–160, 1992.Kern MJ, Aguirre FV, Donohue TJ, Bach RG. Hemodynamic rounds: Interpretation of cardiacpathophysiology from pressure waveform analysis. Coronary hemodynamics part III: Coronaryhyperemia. Cathet Cardiovasc Diagn 26:204–211, 1992.Kern MJ, Puri S, Craig WR, Bach RG, Donohue TJ. Coronary hemodynamics for angioplasty andstenting after myocardial infarction: Use of absolute, relative coronary velocity and fractional flowreserve. Cathet Cardiovasc Diagn 45:174–182, 1998.

Chapter 44 Kern MJ, Aguirre FV, Donohue TJ, Bach RG. Hemodynamic rounds: Interpretation of cardiacpathophysiology from pressure waveform analysis: adult congenital anomalies. Cathet Cardiovasc Diagn27:291–297, 1992.

Chapter 46 Kern MJ, Deligonul U, Miller L. Hemodynamic rounds: Interpretation of cardiac pathophysiology frompressure waveform analysis. IV. Extra hearts: Part I. Cathet Cardiovasc Diagn 22:197–201, 1990.Kern MJ, Deligonul U. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis. IV. Extra hearts: Part II. Cathet Cardiovasc Diagn 22:302–306, 1990.Kern MJ, Deligonul U. Hemodynamic rounds: Interpretation of cardiac pathophysiology from pressurewaveform analysis. IV. Extra hearts: Part III. Cathet Cardiovasc Diagn.

CONTENTS

CONTRIBUTORS xiii

PREFACE xv

INTRODUCTION xvii

SECTION I: FUNDAMENTALS AND CLINICAL APPLICATIONS OF HEMODYNAMICS 1

PART 1: HEMODYNAMIC WAVEFORMS: NORMAL AND PATHOPHYSIOLOGIC 7

1 Pressure Wave Artifacts: Measurement Systems and Artifacts 9

Morton J. Kern and Steven Appleby

2 Pitfalls of Right-Heart Hemodynamics 17

Morton J. Kern and Steven Appleby

3 The Tricuspid Valve 23

Morton J. Kern and Steven Appleby

4 The Left-Sided V Wave 33

Morton J. Kern and Steven Appleby

5 The LVEDP 43

Morton J. Kern and Steven Appleby

6 Simultaneous Left and Right Ventricular Pressure Measurements 49

Morton J. Kern and Steven Appleby

7 Effects of Nitroglycerin 55

Morton J. Kern and Steven Appleby

8 Pulsus Alternans 63

Morton J. Kern and Steven Appleby

ix

PART 2: VALVULAR HEART DISEASE 69

9 Aortic Stenosis 71

Abhay Laddu and Michael J. Lim

10 Aortic Regurgitation 89

Robert H. Neumayr and Michael J. Lim

11 Aortic Regurgitation—Case Presentations 97

Morton J. Kern

12 Abnormal Hemodynamics After Prosthetic Aortic Root Reconstruction: Aortic Stenosisor Insufficiency? 105

Morton J. Kern, Frank V. Aguirre, and Marco Guerrero

13 Acute Aortic Insufficiency—Case Presentation 111

Krystof J. Godlewski, J. David Talley, and Glenn T. Morris

14 Multivalvular Regurgitant Lesions 117

Morton J. Kern, Frank V. Aguirre, Thomas J. Donohue, and Richard G. Bach

15 The Hemodynamic Dilemma of Combined Mitral and Aortic Stenosis 123

William M. Suh and Morton J. Kern

16 Determination of the Source and Severity of a Transvalvular Left Ventricular Outflow Tract Gradientin Patients with a Prosthetic Aortic Valve 129

Michael Ragosta, D. Scott Lim, and James Bergin

17 Mitral Valve Gradients—Section I 135

Morton J. Kern and Frank V. Aguirre

18 Mitral Valve Gradients—Section II: Mitral Stenosis and Pulsus Alternans 143

Morton J. Kern

19 Mitral Valve Gradients—Section III 149

Elie Azrak, Morton J. Kern, Richard G. Bach, and Thomas J. Donohue

20 Mitral Valve Gradients—Section IV: Left Ventricular Puncture for Hemodynamic Evaluationof Double Prosthetic Valve Stenosis 155

Morton J. Kern

21 Simplified Mitral Valve Gradient Calculation by Cui et al. 161

Morton J. Kern

22 Invasive Assessment of Mitral Regurgitation: Comparison of Hemodynamic Parameters 163

Morton J. Kern

23 The Pulmonary Valve 167

Morton J. Kern

24 Percutaneous Balloon Valvuloplasty 173

Zoltan Turi and Morton J. Kern

x CONTENTS

PART 3: VALVULOPLASTY 197

25 Mitral Valve Gradients and Valvuloplasty 199

Morton J. Kern and Frank V. Aguirre

26 Reduction of Mitral Regurgitation After Aortic Valvuloplasty 205

Ted Feldman

27 Aortic Valvuloplasty in a Very Elderly Woman 211

Ted Feldman

28 Mitral Valve Gradient with Dobutamine Stress Testing 217

Ted Feldman

29 Left-Heart Catheterization and Mitral Balloon Valvuloplasty in a Patient with a MechanicalAortic Valve 223

Douglas L. Kosmicki and Andrew D. Michaels

PART 4: HEMODYNAMICS OF PERICARDIAL CONSTRAINT, MYOCARDIAL RESTRICTION,AND TAMPONADE 229

30 Constrictive Physiology 231

Stuart T. Higano, Elie Azrak, Naeem K. Tahirkheli, and Morton J. Kern

31 Post-Cardiac Surgical Constrictive Pericardial Disease 247

Elie Azrak and Morton J. Kern

32 Pericardial Compressive Hemodynamics 253

Morton J. Kern and Frank V. Aguirre

33 Unusual Hemodynamics of Constrictive Physiology 261

Morton J. Kern and Frank V. Aguirre

34 Cardiac Tamponade 269

Morton J. Kern and Frank V. Aguirre

35 Tamponade in a Patient with AIDS-Related Non-Hodgkin’s Lymphoma 277

Elie Azrak, Morton J. Kern, and Richard G. Bach

36 A Novel Assessment for Constrictive Pericarditis in a Complex Patient 283

Justin A. Strote, Larry S. Dean, Steven L. Goldberg, Eric V. Krieger, and Douglas K. Stewart

37 Why Does Kussmal’s Sign and Pulsus Paradoxus Occur? 289

Morton J. Kern

PART 5: ARRYTHMIAS 293

38 Cardiac Arrhythmias 295

Morton J. Kern, Thomas J. Donohue, Richard G. Bach, and Frank V. Aguirre

39 Pacemaker Hemodynamics 301

Morton J. Kern and Ubeydullah Deligonul

CONTENTS xi

PART 6: HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY 307

40 Hypertrophic Cardiomyopathy 309

Morton J. Kern, Steven Appleby, and Ted Feldman

PART 7: CORONARY HEMODYNAMICS 337

41 Coronary Hemodynamics 339

Morton J. Kern

42 Hemodynamic and Intravascular Ultrasound Assessment of an Ambiguous Left Main CoronaryArtery Stenosis 367

Massoud A. Leesar and Garry S. Mintz

43 Renal Hemodynamics: Theory and Practical Tips 379

Tariq S. Siddiqui, Ziad Elghoul, Syed T. Reza, and Massoud A. Leesar

PART 8: ADULT CONGENITAL ANOMALIES 387

44 Adult Congenital Anomalies 389

Morton J. Kern, Robin Abdulmalek, Frank V. Aguirre, Thomas J. Donohue, and Richard G. Bach

45 Case Studies in Congenital Cardiac Anomalies 399

Ralf J. Holzer and Ziyad M. Hijazi

PART 9: EXTRA HEARTS 409

46 Extra Hearts: Unusual Hemodynamics of Heterotopic Transplant and Ventricular Assist Devices 411

Morton J. Kern, Ubeydullah Deligonul, and Leslie Miller

PART 10: RIGHT VENTRICULAR DYSFUNCTION 427

47 Hemodynamic Manifestations of Ischemic Right-Heart Dysfunction 429

James A. Goldstein

SECTION II: CLINICAL AND BEDSIDE APPLICATIONS OF HEMODYNAMICS 437

48 Hemodynamic Evaluation of Dyspnea 445

James A. Goldstein

49 Bedside Evaluation of Low-Output Hypotension 449

James A. Goldstein

50 Hemodynamic Evaluation of Right-Heart Failure 455

James A. Goldstein

INDEX 459

xii CONTENTS

CONTRIBUTORS

Robin Abdelmalik, MD, Resident Internal Medicine,University California Irvine, 101 The City Drive,Orange, CA 92868

Elie Azrak, MD, Cardiology Consultants, St. Louis,MO 63110

Frank V. Aguirre, MD, Prarire Cardiovascular Associ-ates Spramfield, Illinois

Steven Appleby, MD, Fellow in Cardiology, UniversityCalifornia Irvine, 101 The City Drive, Orange, CA92868

Richard G. Bach, MD, Washington University, St.Louis, MO

James Bergin, MD, Cardiovascular Division, Univer-sity of Virginia Health System, Cardiovascular Division,Box 800158, Charlottesville, Virginia, 22908

Jeff Ciaramita, MD, Fellow in Cardiology, St. LouisUniversity, 1325 S. Grand Ave. St. Louis, Missouri63110

Larry S. Dean, MD, Professor of Medicine, Director,UW Regional Heart Center, Division of Cardiology,University of Washington, 1959 NE Pacific Ave, Box356422, Seattle, WA 98195

Ubeydullah Deligonul, MD, Cardiovascular Consul-tants, St. Louis, MO

Thomas J. Donohue, MD, St. Raphael’s Hospital, NewHavern, CT

Ziad Elghoul, MD, Division of Cardiology, Universityof Louisville, 323 E. Chestnut St., Louisville, KY 40292

Ted Feldman, MD, Director Invasive Cardiology, Evan-ston Hospital, 2650 Ridge Avenue, Evanston, IL 60201

Krystof J. Godlewski, MD, University of Louisville,Louisville, KY

Steven L. Goldberg, MD, Clinical Associate Professor,Director, Cardiac Catheterization Laboratory, Divisionof Cardiology, University of Washington, 1959 NEPacific Ave, Box 356422, Seattle, WA 98195

James A. Goldstein, MD, Director, Cardiovascular Re-search, William Beaumont Hospital, 3601 W. ThirteenMile Rd Royal Oak, MI 48073

Marco Guerrero, MD, Fellow in Cardiology, St. LouisUniversity, St. Louis, MO 63110

Stuart T. Higano, MD, Cardiovascular Consultants,St. Louis, MO

Ziyad M. Hijazi, MD, FSCAI, Director, Rush Centerfor Congenital & Structural Heart Disease, Professor ofPediatrics & Internal Medicine, Chief, Section of Pedia-tric Cardiology, Rush University Medical Center, Suite770 Jones 1653 W. Congress Parkway, Chicago, IL60612

Ralf J. Holzer, MD, MSc. Assistant Director, CardiacCatheterization & Interventional Therapy, AssistantProfessor of Pediatrics, Cardiology Division, The OhioState University, The Heart Center, Columbus Chil-dren’s Hospital, 700 Children’s Drive, Columbus, OH43205

John Kern, MD, Department of Cardiothoracic Sur-gery, University of Virginia Health System, Cardio-vascular Division, Box 800158, Charlottesville, VA22908

Morton J. Kern, MD, Professor of Medicine, AssociateChief of Cardiology, University of California, Irvine,CA 90803

Douglas L. Kosmicki, MD, Fellow in Cardiology, Uni-versity of Utah, 30 North 1900 East, Room 4A100, SaltLake City, UT 84132-2401

Eric V. Krieger, MD, Cardiology Fellow, Division ofCardiology, University of Washington, 1959 NE PacificAve, Box 356422, Seattle, WA 98195

Abhay Laddu, MD, Resident InternalMedicine, St. LouisUniversity, 1325 S. Grand Ave. St. Louis, MO 63110

Massoud A. Leesar, MD, Division of Cardiology, Uni-versity of Louisville, 323 E. Chestnut St., Louisville, KY40292

xiii

D. Scott Lim, MD, Cardiovascular Division, Universityof Virginia Health System, Cardiovascular Division,Box 800158, Charlottesville, VA 22908

Michael J. Lim, MD, Director Interventional Cardiol-ogy, St. Louis University, 1325 S. Grand Ave. St. Louis,MO 63110

Andrew D. Michaels, MD, Associate Professor of Med-icine, Director, Cardiac Catheterization Laboratory andInterventional Cardiology, University of Utah, 30 North1900 East, Room 4A100, Salt Lake City, UT 84132

Leslie Miller, MD, Washington Hospital, Washington,DC

Robert H. Neumayr, St. Louis University, St. Louis,MO

Gary S. Mintz, MD, Chief Medical Officer, Cardiovas-cular Research Foundation, 111 E 59th St, 11th Floor,New York, NY 10022 212 851 9395

Glenn T. Morris, MD, University of Louisville, Louis-ville, KY

Michael Ragosta, MD, Director, Cardiac Cath Lab,Cardiovascular Division, Associate Professor of Medi-cine, Director, Cardiac Catheterization Laboratories,University of Virginia Health System, CardiovascularDivision, Box 800158, Charlottesville, VA 22908

Syed T. Reza, MD, Division of Cardiology, Universityof Louisville, 323 E. Chestnut St., Louisville, KY 40292

Tariq S. Siddiqui, MD, Division of Cardiology, Uni-versity of Louisville, 323 E. Chestnut St., Louisville, KY40292

Douglas K. Stewart, MD, Professor, University of Wa-shington Medical Center, Director, Interventional Car-diology Fellowship, Division of Cardiology, Universityof Washington, 1959 NE Pacific Ave, Box 356422,Seattle, WA 98195

George A. Stouffer, MD, Professor of Medicine, Direc-tor of Interventional Cardiology, CB 7075, University ofNorth Carolina, Chapel Hill, NC 27599

Justin A. Strote, MD, Interventional CardiologyFellow, Division of Cardiology, University of Washing-ton, 1959 NE Pacific Ave, Box 356422, Seattle, WA98195

Williams M. Suh, MD, Fellow in Cardiology, Univer-sity California Irvine, 101 The City Drive, Orange, CA92868

Naeem K. Tahirkheli, MD, Fellow in Cardiology, MayoClinic Rochester, MN

J. David Talley, MD, University of Louisville, Louis-ville, KY

Joshua W. Todd, MD, Fellow, Division of Cardiology,CB 7075, University of North Carolina, Chapel Hill, NC27599

Zoltan Turi, MD, Professor of Medicine, Robert WoodJohnson Medical School, Director, Structural HeartDisease Program, Cooper University Hospital, D-427,One Cooper Plaza, Camden, NJ 08103

xiv CONTRIBUTORS

PREFACE

As noted in the textbooks of cardiology, hemodynamicscontinue to be an integral part of the training experienceand comprise validation for much of the pathophysiologyobtained from clinical examination, echocardiographicstudy, and new imaging modalities. With the increasedattention to visual medicine and angiography, the gra-phics of hemodynamics have been in decline. However,hemodynamics remain useful for diagnosis and treatmentof the multitude of various and unusual cardiovascularconditions. It remains true that in today’s modern cardi-ology, hemodynamics are still critical to the diagnosis ofvalvular disorders and unusual cardiomyopathic condi-tions contributing to cardiac disability.

The first edition of Hemodynamic Rounds emphasizedthe interpretation of hemodynamic waveforms for clinicaldecision-making as presented from a series of casespublished in the journal of ‘‘Catheterization and Cardio-vascular Diagnosis,’’ now renamed ‘‘Catheterization andCardiovascular Intervention.’’ The case-based format lim-ited itself to description of individual hemodynamic tra-cings, but was not presented in a formalized textbookfashion. The second edition of Hemodynamic Roundsextended this work and enlarged and reorganized it intonew sections providing a more logical approach to thestudy of pressure waveforms and the associated pathology.

In the present edition of Hemodynamic Rounds, afurther thematic approached to the understanding ofpathophysiologic waveforms is provided. The text hasbeen divided into 10 major parts (comprising Section Iof this edition) incorporating the previously publishedworks with new and dynamic tracings and incorporatingthe latest publications regarding hemodynamic topics asthey have evolved into our modern practice.

Part 1 describes normal and pathophysiologic hemo-dynamic waveforms and is organized to the study ofpressure wave measurement systems, artifacts, and nor-mal waveforms. The hemodynamics of the tricuspidvalve, the mitral valve, and left-sided V waves arereviewed. LV end-diastolic pressure, simultaneous right-and left-heart pressures, and effects of nitroglycerin andpulsus alternans are also discussed.

Parts 2 and 3 cover valvular and valvuloplasty hemo-dynamics. In Part 4, constrictive and restrictive

physiologic waveforms are described in detail. Cardiacarrhythmias are dealt with in Part 5. Hypertrophic ob-structive cardiomyopathy is presented in Part 6. Coronaryhemodynamics in Part 7 has also been expanded. The newconcepts involving absolute and relative coronary reserveand pressure-derived fractional flow reserve are comparedwith the intent to help the practitioner understand practicein the laboratory on a daily basis. These findings can beused for decision-making during coronary angiography.

Parts 8 and 9 deal with particularly unusual hemo-dynamic problems involving adult congenital anomaliesand hemodynamics, extra hearts and transplants, intra-aortic balloon pumps, and circulatory assist devices.Finally, in Part 10, right ventricular infarction is de-scribed by one of the world’s experts, Dr. Goldstein.

As a new and important aspect of hemodynamicrounds, Dr. Goldstein (in Section II of this edition)has undertaken the compilation of clinical and bedsideapplications of hemodynamics describing the correlationbetween the anatomic and pathophysiologic presenta-tions of dyspnea, edema and Anasarca, syncope, hypo-tension, and low cardiac output in four distinct blocks,presenting correlative findings between anatomy, hemo-dynamics, and clinical manifestations.

It is the hope of the authors that this work will be oflasting value to students, trainees, practicing physicians, andall related health-care personnel dealing with the importantsubject of cardiac hemodynamics. I continue to thank Dr.Frank Hildner, first editor and founder of Catheterizationand Cardiovascular Interventions, formerly Catheterizationand Cardiovascular Diagnosis for his involvement with thiswork, without whom this book would never have beenpublished.

I would like to thank Margaret and Anna Rose, thecontinuing systole of my life as noted in our first edition,and I would like to extend my deepest appreciation tomy co-editors and contributors to this work and to myfellows in training without them, there would be nopoint in these exercises.

MORTON J. KERN, MDProfessor of Medicine

Associate Chief Cardiology

University of California, Irvine

xv

INTRODUCTION

MORTON J. KERN, MD, AND FRANK J. HILDNER, MD

HISTORICAL REVIEW

On February 28, 1733, the president of the Council ofthe Royal Society, Sir Hans Sloane, requested thatStephen Hales, one of the counselors, present his in-formation on the mechanics of blood circulation from aprevious presentation of a series of hemodynamic ex-periments reported in his book Haemastaticks [1]. Mr.Hales took his place in medical history next to WilliamHarvey with regard to studies of the human and animalcirculation. De Motu Cordis [2] and Haemastaticksstimulated scientists interested in the newly developedprinciples and mathematical computations of fluid me-chanics as applied to circulatory physiologic events. Thesimple measurement of blood pressure now became asubject of great scientific interest.

From such basic interests, experimental physiologistsat Oxford University in the 1800s, investigating thephysiology of the circulation, began estimating theoutput of ventricular contraction and velocity of bloodflow in the aorta based on relatively primitive measure-ments of cardiovascular structures. These data remainvalid and correspond to currently accepted data ob-tained by computerized quantitative techniques. Cardi-ologists interested in hemodynamics should continue toemulate Stephen Hales, who relied on direct measure-ments and observations repeatedly checked and appliedon simple and repeatedly confirmed computations. Thenumerous original achievements in hemodynamics pro-vided to us by Hales are remarkable even by today’ sstandards and included the first direct and accuratemeasurement of blood pressure in different animals(see Figure) under different physiologic conditionssuch as hemorrhage and respiration; cardiac outputestimated by left ventricular systolic stroke volumemeasured from the diastolic volume after death of theanimal; calculations of pressure measured on the inter-nal surface of the left ventricular at the beginning of

systole; and determination of blood flow velocity in theaorta approximating 0.5m/sec. Stephen Hales intro-duced the concept of the wind castle or capacitanceeffect in the transformation of pulsatile flow in largevessels to continuous flow in smaller vessels. Hales alsomade the first direct measurement of venous bloodpressure and correct interpretation of venous return oncardiac output in relation to contraction and respira-tions. Since recording equipment documenting the ob-servations of Hales was lacking, understanding theunique collection of data depends on interpreting de-scriptive material.

Our current appreciation of hemodynamics asprovided in this book stems directly from a small groupof modern physiologists active in the 1920s, amongwhom Dr. Carl Wiggers, from Western ReserveUniversity in Ohio, emerges. Major advances in hemo-dynamic research arose from the development of record-ing instruments with improved fidelity able to captureand reproduce the waveforms of rapidly changingpressures during the various phases of cardiac contrac-tions in the various heart chambers. Dr. Wiggers andcolleagues also employed the newly developed electro-cardiogram to obtain simultaneous pressure wave-forms and electrical activity and thus, establish thefundamental electrical–mechanical intervals and rela-tionships which are the benchmark against which theobservations of the pressure tracings of classical diseasedconditions, some of which are described herein, can becompared [3].

An interval of sixty years separates the originators ofclinical cardiovascular anatomy and physiology frompresent day practitioners. What happened during thattime should not be forgotten because it still affects ustoday. However, some of the lessons that have beenlearned, while still valid, tend to be ignored. From thetime Claude Bernard coined the phrase ‘‘cardiac

xvii

catheterization’’ (1840) [4], laboratories of that type andname have been hemodynamic and physiology labora-tories. Mter Forssman performed the first documentedhuman cardiac catheterization-on himself [5]—the nat-ure of the work did not change, only the subjects. In thelate 1930s, Cournand and Ranges [6] used the new rightheart catheterization technique to investigate pulmonaryphysiology. With World War II, the scope and directionof their work changed to include hemorrhagic shock anddrug effects on the circulation. But in those days, themost serious problems presented by patients related tocongenital and rheumatic heart disease. Accordingly,laboratories around the world began publishing dataon the hemodynamics and physiology of atrial septal

defects [7], ventricular septal defects [8], stenotic andinsufficient mitral and aortic valves and ventricularfunction. The beginning of invasive cardiology hadcome to an end.

Without doubt, the most important and crucialdevelopment needed for the advancement of the fieldof cardiovascular diseases was the cathode ray tube, adirect result of the war. Before the image intensifier[9, 10], cardiac fluoroscopy utilized high-dose radiationand required the physician to accommodate his eyesto a green fluorescent screen by wearing red goggles for15–20 minutes before starting. Indeed, the faintly glow-ing image in a completely dark room frequently failed toreveal even the position of the catheter [11]. Without the

Drawing depicting Dr. Stephen Hales (seated) directing and observing the measurementof arterial pressure in a sedated horse circa 1730. (Reproduced with permission from:Medicine: An Illustrated History, Lyons AS, Petrucelli RJ II (eds.), New York, Harry N.Abrams, Inc., 1987.)

xviii INTRODUCTION

additional light provided by the image intensifier,‘‘angiocardiography’’ was nothing more than a simpleflat-plate radiograph, or perhaps a sequence of cut filmsobtained on the newly developed serial film changer [12].Cineangiography was developed in the late 1950sthrough the persistent efforts of lanker (1954) [13] andSones (1958) [14]. The addition of advanced imagingspurred the progress of catheter invasive techniques,which then permitted investigation of heretofore unap-proachable anatomical sites, clinical conditions, anddisease entities which in turn resulted in effective cardiacsurgery. Once again, hemodynamic analysis was neededto explain what was being newly observed and to assistthe development of medical and surgical interventions.After the basic mechanics of congenital anomalies andrheumatic abnormalities were confirmed, conditionsrelated to occlusive coronary artery disease such asmyocardial infarction, left ventricular aneurysms, mitralchordal, and septal rupture were investigated. Soonthereafter, newer concepts of systolic and diastolicmyocardial mechanical function, hypertrophic obstruc-tive and nonobstructive cardiomyopathy, electrophysio-logic relations, and other previously unappreciatedconditions came under scrutiny. The final result was abody of knowledge that permitted development and useof the newly conceived noninvasive techniques includingadvanced physical examination (phonocardiographs,ballistocardiographs, etc.), exercise stress testing, radio-nuclide imaging, and echocardiography. In this age ofimaging, even as it was during the previous fifty or sixtyyears, hemodynamic analysis remains absolutely neces-sary for a proper understanding and appreciation of allcardiovascular conditions and situations.

APPROACH TO HEMODYNAMIC WAVEFORMINTERPRETATION

With this background, we turn our attention frompressure waveforms to the interpretation of cardiacpathophysiology. Each chapter has been published orwill soon appear in Catheterization and CardiovascularDiagnosis and will serve to provide both novice andadvanced cardiologists with classical and, at times,unique pressure tracings to emphasize the value ofcareful observation as the waveforms relate to differentcardiac pathophysiology states.

It is clear that good-quality hemodynamic data arerequired for the quantitative determinations of patho-physiologic conditions for most cardiovascular maladies.As in the days of Dr. Hales, some hemodynamic data areextraordinarily simple, such as using a sphygmoman-ometer for indirect assessment of systemic arterial pres-sure. Some hemodynamic data may also be complex,

requiring catheterization with placement of multiplecatheters within several chambers of the heart. Suchdata can then be used in the precise computations ofpressure and flow to determine valvular gradients, myo-cardial contraction, relaxation, compliance, impedanceand work [15–17]. Additional techniques, unknown tophysiologists and cardiologists in decades earlier, haverecently provided insight into the physiology of thecoronary circulation. Intracoronary Doppler and vascu-lar ultrasound imaging catheters can now provide infor-mation complementary to but previously unavailablethrough traditional angiographic methodologies.

As with all laboratory data, the significance of var-ious hemodynamic findings should be placed in contextof the ancillary historical, clinical, echocardiographic,roentgenographic, and electrocardiographic data. Act-ing on isolated laboratory values is dangerous and hasbeen the nemesis of all technical innovations inmedicine.

METHODOLOGIES INVOLVEDIN HEMODYNAMIC DATA COLLECTION

Each laboratory, and preferably all physicians, shouldestablish protocols for right and left heart catheteriza-tion. A uniform and consistent approach to data collec-tion insures complete, accurate and reliable data for themajority of clinical problems. The standardized routinealso obviates missing easily overlooked data collectionsteps. Time is also saved during procedure setup anddata recording. The technical staff does not have torethink what will happen for a unique and personalhemodynamic protocol of each different operator.Right-heart catheterization, sometimes performed se-quentially with left-heart catheterization, may often becombined simultaneously with left-heart catheterizationto provide the most complete data. In most academiclaboratories, a combined methodology is preferred.

The methodology for performing right-heart cathe-terization has been reviewed previously [18], but theindications have become a subject for controversy [18,19]. While some quarters feel routine right-heart cathe-terization is unjustified, others are equally adamant thatpatient care demands our maximum effort to provideoptimum results. Unexpected congenital and hemody-namic abnormalities are found at right heart catheter-ization even with previous echocardiography. This hasbeen pointed out by Shanes et al. [20] and Barron et at[21], even though they come to opposite opinions.However, there is no debate if right-heart catheterizationis performed to evaluate patients with previous conge-nital heart disease, valvular heart disease, left- orright-heart failure, previous myocardial infarction,

METHODOLOGIES INVOLVED IN HEMODYNAMIC DATA COLLECTION xix

cardiomyopathy, or any unexplained significant clinicalhistorical or physical findings.

Left-heart hemodynamic protocols most often use asingle pressure transducer, but simultaneous measure-ments of left ventricular and arterial pressure can easilybe obtained through the side arm of an arterial sheathand the smaller catheter residing within using twotransducers. Pressure obtained from an arterial sheathis satisfactory when at least a one French size largersheath than the arterial catheter is used. After collectingthe hemodynamic data, computations are made toclarify and enhance quantitative cardiac function. Mea-surements of cardiac work, calculation of flow resis-tance, valve areas, and shunt calculations are based onaccurate hemodynamic data, arterial and venous bloodoxygen saturations, and cardiac output determinations.

If the information is considered important enough toperform hemodynamic measurements, the operatorsshould take the time to obtain pressure waveforms thatare reliable and unequivocal, separating artifact frompathology. To achieve this goal, operators must befamiliar with the equipment producing the waveformsand the sources of error found in recording techniques,tubing, transducers and catheters. The foHowing sectionwill highlight the important considerations for equip-ment used in daily hemodynamic measurements.

EQUIPMENT FOR HEMODYNAMIC STUDIES

A set of transducers, tubing and manifolds are employedfor hemodynamic measurements which should be costefficient, familiar, accurate, and simple to use for thelaboratory. Although a variety of manifolds exist whichare both disposable and reusable, the variety of trans-ducers, tubing, and injection syringes should be costefficient and easy to operate. Optimal hemodynamicpressure waves should be properly damped to reducesinusoid ‘‘ringing’’ or overshoot artifact. Short, stifftubing with a minimal distance from the end of thecatheter to the transducer is desirable. Long tubingcontributes to poor-quality tracings, introducing ‘‘fling’’artifact due to the momentum of fluid through the tube.The zero position for hemodynamic measurements isalso important. In some laboratories, the zero level is setat mid chest, measured in the AP diameter of the patient(divided by 2) with the transducer connected by a fluid-filled tube to the zero level fixed at the table. When thetransducer is raised above the zero level, pressure islower. When the transducer is lower than the zero level,the pressure is higher. Setting an accurate zero beforeand at the conclusion of each measurement is minimallytime-consuming and assures accuracy by eliminatingrecordings with erroneous zero baselines or transducer

systems that have zero drift errors over time. The zeroposition at the mid-chest level can also be obtained byusing two fluid-filled tubes connected to transducers.One tube is placed on top of the chest and the other atthe back. The zero line manifold is then set at bedsideheight so that the two pressures are equidistant from thisheight. Artifacts related to under- and overdamping andsuggestions to reduce these artifacts are described inChapter 2.

Pressure Transducers

For most laboratories, table-mounted fluid-filled trans-ducers produce acceptable clinical studies. Other devicesare available which are suitable for special situations orrequirements. Among these are miniaturized transducersmounted on the pressure manifold or placed in thepressure line. Some are disposable which obviates theneed for sterilization but also adds to the cost. Othertransducers are mounted on the end of the catheter andare inserted into the vessel or chamber being studied.These can be zeroed but require another pressure-sensing device for calibration. The specialized reusablemicromanometer transducer-tipped catheters producinghigh-fidelity pressure recordings are required in thecomputation of the rate of rise of pressure with time(dP/dt) or relaxation (�dP/dt). Catheter reuse requirescareful and meticulous cleaning, which is difficult andtedious at best. The cost of these devices usually preventsuse in other than investigational pursuits.

Pressure Manifolds

Three- and four-port manifolds are available in dispo-sable or reusable plastic configurations. In general, mostlaboratories set the first three ports for pressure, flushsolution, and radiographic contrast media. A four-portmanifold is also available and offers ‘the advantage of anattached fourth port closed system for disposal of flushsolutions. The waste fluid port (fourth port) minimizescontamination of personnel and laboratory equipment.The clear plastic manifolds are safe, practical, anddisposable.

Physiologic Recorders

Every laboratory is equipped with a physiologic recorderwith a multichannel photographic oscilloscope, electro-cardiographic and pressure amplifiers and hard-copyprinter capability. Most now use analog-to-digital signalconverters to store and reproduce waveforms. A varietyof specialized amplifiers (e.g., green dye curve calcula-tors or signal differentiators) permit additionaldata collection. Multichannel (2–20 channels) units can

xx INTRODUCTION

process, display, and record electrocardiographic, pres-sure signals and direct inputs from a variety of externalsources. Although the number of recorded channels maybe less than the number that can be displayed, forroutine cardiac catheterization at least one electrocar-diogram and one to three pressure signals are required.In complex cases such as electrophysiologic studies,congenital, valvular heart disease or hemodynamicresearch studies it is common to use between 6 and18 channels. The physiologic recorder should be set upwith amplifiers calibrated to reference pressure or vol-tage standards before each case. After the recorder isready, pressure transducers are calibrated to a commonpressure source. Differences in amplifiers or transducerscan then be easily identified.

Recording artifacts may be responsible for confusingdata. Examples of recording artifacts producing abnor-mal hemodynamic tracings are included in several chap-ters. The recording technician should demonstratepressure scale changes and ensure correct time-linepositioning to assist the physician in observing andcollecting accurate and complete information.

CARDIAC OUTPUT METHODOLOGY

Critical to the calculations of nearly all hemodynamicdata (systemic and pulmonary vascular resistances, aswell as valve areas) is the accurate determination ofcardiac output. The two methods most widely acceptedfor determining cardiac output have been reviewed[15, 16]. The Fick method assesses oxygen consumptionwith a polarographic cell or Douglas bag and bloodoxygen saturations. The second method is indicatordilution technique, most commonly employing roomtemperature or iced saline using cold as the indicator.Green dye cardiac output curves are equally accuratebut no longer used. Methods and limitations of thesetechniques have been described in detail [22]. Theoperators in the cardiac catheterization laboratoryshould familiarize themselves with the limitations andpotential sources of error with both techniques.

REVIEWING WAVEFORMS

Pressure waveforms may be confusing for the cardio-vascular fellow-in-training. After an intense trainingperiod in which the components of all pressure wavesfound in cardiovascular structures are incorporated, theyoung physician must be encouraged to continue practi-cing pattern recognition and deductive analysis. Heshould continue to strengthen his skills by performingsystematic analysis of complete pressure data obtained

on all indicated cases. This systematic examinationincludes a comparison of the pressure values acrossvalves, an analysis of the pressure in all adjacentchambers, and the determination of whether the ab-normalities are internally consistent with the clinicalquestions to be addressed. Finally, pressure calculationof resistance values and valve areas need to be confirmed(manual calculations to verify computer-managed datawill, at times, be required). When reviewing physiologictracings, every operator, whether expert or novice,should consider the following key points.

First, identify the cardiac rhythm. Most cardiacevents can be identified by their timing from within theR–R cycle. Hemodynamic data qbtained during ar-rhythmias may be confusing since the various irregularcontraction sequences distort pressure waves. Next,determine the pressure scale on which the waveform isrecorded and verify the pressure per division to becertain there is no recording artifact. Also, note therecording speed to assess the appropriate cardiac rhythmand timing of events occurring within one cardiac cycle.The comparison of waveforms for the chamber ofinterest should be made against known waveforms ofnormal physiology. The right atrial A and V waves arecommonly deformed by various arrhythmias, valvulardisease, or pericardial and respiratory pathophysiologicstates. Right and left ventricular waveforms are gener-ally unaffected by most diseases, but the rate andposition of the upslope and downslope of the pressurewaves (relative to each other) should be brisk andcharacteristic. Electrocardiographic conduction ab-normalities may alter the activation sequence of ventri-cular pressure. The presence of an exaggerated A wavein the ventricular tracings may identify chamber stiffnessincreased above normal limits. The early appearance ofthe A wave may also indicate first degree AV conductionblock, a commonly observed phenomenon. Pressureartifacts should then be differentiated from true patho-physiologic waveforms. The type of artifacts due tocatheter fling, over or underdamping will be discussedin Chapter 2.

Finally, the interpretation of the waveforms should bemade in conjunction with the clinical presentation andsuspected diseased conditions of the patient. A large Vwave does not always represent valvular regurgitation.The equilibration of right and left ventricular diastolicpressures may be hypovolemia rather than pericardialconstriction. Consider alternative clinical and physiolo-gic explanations.

The examination and consideration of possible me-chanisms of the various waveform phenomena forms thebasis for the chapters in this book. The information willhopefully enhance the reader’s appreciation of seeminglytrivial, but often important confirmatory data for

REVIEWING WAVEFORMS xxi

patients in discovery and confirmation of their cardiacpathophysiology.

REFERENCES

1. Hales S (ed.). Statical Essays: Containing Haemastaticks.

New York: Hafner Publishing Company, Inc., 1964.

2. Harvey W (ed.). Movement of the Heart and Blood in

Animals. Springfield, IL: Charles C Thomas, 1962.

3. Wiggers CJ (ed.). The Pressure Pulses in the Cardiovascular

System. New York: Longmans, Green and Co., 1928.

4. Grmek MD. Catalogue des manuscrits de Claude Bernard.

Paris: Masson et Cie, 1967.

5. Forssman W. Die sondierung des rechten herzens. Klin

Wochenschr 8:2085–2087, 1929.

6. Cournand A, Ranges HA. Catheterization of the right

auricle in man. Proc Soc Exp Bioi Med 46:462, 1941.

7. Brannon ES, Weens HS, Warren JV. Atrial septal defect.

Study of hemodynamics by the technique of right heart

catheterization. Am J Med Sci 210:480, 1945.

8. Baldwin E deF, Moore LV, Noble RP. The demonstration

of ventricular septal defect by means of right heart

catheterization. Am Heart J 32:152, 1944.

9. Sturm RE, Morgan RH. Screen intensification systems and

their limitations. Am J Roentgenol 62:617, 1949.

10. Moon RJ. Amplifying and intensifying fluoroscopic

images by means of scanning X-ray tube. Science

112:339, 1950.

11. Zimmerman HA. Presentation at the Twenty-second An-

nual Scientific Session of the American Heart Association,

Atlantic City, NJ, June 4, 1949.

12. Sanchez-Perez JM, Carter RA. Time factors in cerebral

angiography and an automatic seriograph. Am J Roent-

genol 62:509–518, 1949.

13. Janker R. Roentgenotogische Funktionsdiagnostic Wupper.

Elberfeld: Garandit, 1954.

14. Sones FM Jr. Cinecardioangiography. Pediatr Clin North

Am 5:945, 1958.

15. Grossman E, Baim DS (eds.). Cardiac Catheterization,

Angiography and Intervention, 4th ed., Philadelphia: Lea

& Febiger, 1991.

16. Pepine CJ, Hill JA, Lambert CR (eds.). Diagnostic and

Therapeutic Cardiac Catheterization. Baltimore: Williams

& Wilkins, 1989.

17. Miller G (ed.). Invasive Investigation of the Heart. London:

Blackwell Scientific Publications, 1989.

18. Green DG Society for Cardiac Angiography officers and

Trustees. Right heart catheterization and temporary pace-

maker insertion during coronary arteriography for sus-

pected coronary artery disease. Cathet Cardiovasc Diagn

10:429–430, 1984.

19. Samet P. The complete cardiac catheterization. Cathet

Cardiovasc Diagn 10:431–432, 1984.

20. Shanes JG, Stein MA, Dierenfeldt BJ, Kondos GT. The

value of routine right heart catheterization in patients

undergoing coronary arteriography. Am Heart J

113:1261–1263, 1987.

21. Barron JT, Ruggie N, Uretz E, Messer JV. Findings on

routine right heart catheterization in patients with sus-

pected coronary artery disease. Am Heart J 115:1193, 1988.

22. Kern MJ, Deligonul U, Gudipati C. Hemodynamic

and ECG data. In: Kern MJ (ed.). The Cardiac Catheter-

ization Handbook. St. Louis: Mosby–Year Book, 1991,

pp. 119–177.

xxii INTRODUCTION

SECTION I

FUNDAMENTALS AND CLINICAL APPLICATIONSOF HEMODYNAMICS:

UNDERSTANDING THE PRESSURE WAVESIN THE HEART: THE WIGGER’S DIAGRAM

Everything you want to know about hemodynamicsstarts here. All pressure waves of the cardiac cycle canbe understood by reviewing and knowing how electricaland mechanical activity of the heart’s contraction andrelaxation are related.

Every electrical activity is followed normally by amechanical function (either contraction or relaxation)resulting in a pressure wave. The timing of mechanicalevents can be obtained by looking at the ECG andcorresponding pressure tracing.

The ECG ‘‘P’’ wave, the QRS, and the ‘‘T’’ wave areresponsible for atrial contraction, ventricular activation,and ventricular relaxation, respectively. The periodsbetween electrical activation reflect impulse transmissiontimes to different areas of the heart. These time delayspermit the mechanical functions to be in synchrony andgenerate efficient cardiac output and pressure. When thenormal sequence of contraction and relaxation of theheart muscle are disturbed by arrhythmia, cardiac func-tion is inefficient or ineffective as demonstrated on thevarious pressure waveforms associated with thearrhythmia.

The cardiac cycle is begun with the P wave. TheP wave is the electrical signal for atrial contraction. Theatrial pressure wave (‘‘A’’ wave, point #1 in Figure I.1)follows the P wave by 30–50msec. Following the A wavepeak, the atrium relaxes and pressure falls, generatingthe x-descent (point b).

The next event is the depolarization of the ventricleswith the QRS (point b). The LV pressure after the ‘‘A’’wave is called the end-diastolic pressure. It can bedenoted by a vertical line dropped from the R wave tothe intersection of the LV pressure (point b). About 15–30msec after the QRS, the ventricles contract and boththe LV and RV pressures increase rapidly. This periodwith rise in LV pressure without change in LV volume iscalled the isovolumetric contraction period (interval b–c).

When LV pressure rises above the pressure in the aorta,

the aortic valve opens and blood is ejected into the

circulation (point c). This point is the beginning of

systole. Some hemodynamicists include isovolumetric

contraction as part of systole.About 200–250msec after the QRS, the heart begins

relaxing and repolarization starts, there by generating a

‘‘T’’ wave. At the end of the ‘‘T’’ wave (point e), the LV

contraction has ended and LV relaxation produces a fall

in the LV (and aortic pressure). When the LV pressure

falls below the aortic pressure, the aortic valve closes

(point e). Systole is concluded and diastole is underway.

After aortic valve closure the ventricular pressure con-

tinues to fall. When the LV pressure falls below the LA

pressure, the mitral valve opens and the LA empties into

the LV (point f). The period from aortic valve closure to

mitral valve opening is called the isovolumetric relaxation

period (interval e–f). Diastole is the period from mitral

valve opening to mitral valve closing.Following the atrial pressure wave across the cycle, it

should be noted that after the A wave, pressure slowly

rises across systole, continuing to increase until the end

of systole when the pressure and volume of the LA are

nearly maximal, producing a ventricular filling wave, the

‘‘V’’ wave. The ‘‘V’’ wave (point f, #4) peak is followed

by a rapid fall when the mitral valve opens. This V wave

pressure descent is labeled the ‘‘y’’-descent. The peaks

and descents of the atrial pressure waves are changed by

pathologic conditions and used to support the diagnosis

of these pathologies, as will be seen in the examples

dealing with heart failure, constrictive physiology, and

RV infarction.After the ‘‘V’’ wave, the LV is filled by the small

pressure gradient assisting blood flow from the atria into

the ventricles over the diastolic period (called diastasis)

until the cycle begins again with atrial pressure building

until activated to contract and generate the A wave,

ejecting atrial blood into the LV.To appreciate valve function and dysfunction, we

study the pressure changes that normally open and closethe valves. The aortic and pulmonary valves open in

Hemodynamic Rounds: Interpretation of Cardiac Pathophysiology fromPressure Waveform Analysis, Third Edition, edited by Morton J. Kern,Michael J. Lim, and James A. Goldstein.Copyright r 2009 John Wiley & Sons, Inc.

3

systole, when ventricular pressure exceeds aortic pres-sure (and RV exceeds PA pressure). Stenosis of thesevalves produces high-velocity systolic murmurs.

The mitral and tricuspid valves are closed in systolewhen LV pressure is greater than atrial pressure. Amitral or tricuspid regurgitant valve that fails to closeis characterized by a low-velocity systolic murmur with arumbling quality.

Conversely, incompetent aortic valves failed to sealand let blood continue to rush backward into the LV indiastole. The blood rushes into the LV with a diastolicmurmur. At the beginning of diastole, LA pressure is atits highest. If the mitral valve is stenotic, the high LApressure emptying into the LV produces a diastolicrumble.

When reviewing the cardiac hemodynamics, we canalways refer to the Wigger’s diagram to determine whatthe expected normal hemodynamic responses should be.

The Wigger’s diagram with periods of systole, dia-stole, and isovolumetric contraction and relaxationperiods identified on Figure I.2.

Fig. Section I.2. Wigger’s diagram.

Fig. Section I.1. The cardiac cycle.

4 UNDERSTANDING THE PRESSURE WAVES IN THE HEART: THE WIGGER’S DIAGRAM

A normal right atrial (RA) and pulmonary capillarywedge (PCW) pressure tracing (used as left atrial pres-sure) is shown in Figure I.3 demonstrating normal ‘‘A’’

and ‘‘V’’ waves with the associated ‘‘x’’- and ‘‘y’’-descents.

Fig. Section I.3. Normal RA, PCW and LV pressure waveforms. LV, left ventricule;

0–40mmHg scale.

UNDERSTANDING THE PRESSURE WAVES IN THE HEART: THE WIGGER’S DIAGRAM 5