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Playground Games 1st Edition Tracy Nelson Maurer
Digital Instant Download
Author(s): Tracy Nelson Maurer
ISBN(s): 9781615904730, 1615904735
Edition: 1
File Details: PDF, 2.47 MB
Year: 2011
Language: english
1600 John F. Kennedy Boulevard
Philadelphia, PA 19103

TEXTBOOK OF CLINICAL HEMODYNAMICS ISBN: 978-1-4160-4000-2

Copyright # 2008 by Saunders, Inc., an affiliate of Elsevier Inc.

All rights reserved. No part of this publication may be reproduced or transmitted in any form
or by any means, electronic or mechanical, including photocopying, recording, or any
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Notice
Knowledge and best practice in this field are constantly changing. As new research and expe-
rience broaden our knowledge, changes in practice, treatment and drug therapy may become
necessary or appropriate. Readers are advised to check the most current information provided
(i) on procedures featured or (ii) by the manufacturer of each product to be administered, to
verify the recommended dose or formula, the method and duration of administration, and
contraindications. It is the responsibility of the practitioner, relying on their own experience
and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment
for each individual patient, and to take all appropriate safety precautions. To the fullest extent
of the law, neither the Publisher nor the Authors assumes any liability for any injury and/or
damage to persons or property arising out of or related to any use of the material contained
in this book.
The Publisher

Library of Congress Cataloging-in-Publication Data

Ragosta, Michael.
Textbook of clinical hemodynamics / Michael Ragosta. – 1st ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4160-4000-2
1. Hemodynamics. 2. Cardiovascular system–Diseases–Diagnosis. I. Title.
[DNLM: 1. Hemodynamic Processes. 2. Heart Diseases–diagnosis.
3. Heart Function Tests. WG 106 R144t 2008]
RC670.5.H45R34 2008
616.10 0754–dc22
2007022989

Executive Publisher: Natasha Andjelkovic


Project Manager: Mary Stermel
Design Direction: Steve Stave
Marketing Manager: Todd Liebel

Printed in China.
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Contributors

VISHAL ARORA, MD RAJAN A.G. PATEL, MD


Fellow, Interventional Cardiology Fellow, Cardiology
University of Virginia Health System University of Virginia Health System,
Charlottesville, VA Charlottesville, VA

BRANDON BROWN, MD MICHAEL RAGOSTA, MD, FACC, FSCAI


Fellow, Interventional Cardiology Associate Professor of Medicine
University of Virginia Health System Director, Cardiac Catheterization
Charlottesville, VA Laboratories
University of Virginia Health System
HOWARD P. GUTGESELL, MD Charlottesville, VA
Professor of Pediatrics
University of Virginia Health System
Charlottesville, VA

D. SCOTT LIM, MD
Assistant Professor of Pediatrics
University of Virginia Health System
Charlottesville, VA

v
Acknowledgments

This book originated from a desire to deepest gratitude goes also to the many
assemble the wisdom I gained from patients suffering from cardiovascular
two of the most remarkable mentors disorders who I had the distinct privi-
I had as a cardiology fellow and young lege of serving and whose hemody-
faculty member at the University of Vir- namic waveforms are included in this
ginia. Over the many years I worked text from which future generations can
with these talented individuals, first learn. Most importantly, I want to thank
as a student and then as a colleague, my wife, Kiyoko, and my three marvel-
Dr. Eric R. Powers and Dr. Ian J. Sarem- ous children, Nick, Tony, and Sachi, for
bock taught me a deep appreciation their support and patience and for the
of the value of careful hemodynamic precious time I stole from them while
assessment in understanding cardiovas- writing this text.
cular pathophysiology, and I wish to
thank them for all they taught me. My Michael Ragosta, MD, FACC, FSCAI

vii
Preface

Systematic analysis of pressure wave- physiologic impact of a specific disease


forms generated in the cardiac catheteri- entity. Thus, it is imperative for an astute
zation laboratory led to our current cardiologist to be well versed in clinical
understanding of the pathophysiology hemodynamics and invasive physiologic
of many valvular, congenital, myocar- assessment in order to correctly use and
dial and pericardial diseases. Assessment interpret diagnostic tests and to diagnose
of hemodynamics has become an estab- and treat many cardiac diseases.
lished component of cardiac catheteri- It is the goal of this textbook to pro-
zation protocols and, along with vide instruction in clinical hemodynam-
angiography, forms the basis of invasive ics from the analysis of waveforms
cardiovascular diagnostic testing. How- generated in the cardiac catheterization
ever, many cardiologists and cardiology laboratory. Normal physiology and com-
training programs currently neglect clas- mon pathophysiologic states encoun-
sic hemodynamic assessment, empha- tered in the cardiac catheterization
sizing instead the skills involved in laboratory and intensive care unit are
angiography and intervention. Patients covered extensively and illustrated with
undergoing cardiac catheterization may authentic hemodynamic waveforms col-
be misdiagnosed or their condition mis- lected in routine clinical practice demon-
characterized because of errors in hemo- strating all important findings. This book
dynamic measurement or interpretation. is designed primarily as a resource for
In addition, recent advances in cardio- cardiologists in training, practicing cardi-
vascular imaging and diagnostics have ologists, and cardiac catheterization labo-
transformed the practice of cardiology ratory nurses and technicians, but may
to rely more heavily on echocardio- also prove useful for anyone involved in
grams, magnetic resonance images, and the care of cardiac patients, including
computed tomographic scans. Although cardiology nurse practitioners, physician
these techniques offer unprecedented assistants, coronary care unit nurses,
and exquisite anatomical details of the and both internal medicine and critical
cardiovascular system, they have limita- care physicians.
tions regarding their ability to assess the
Michael Ragosta, MD, FACC, FSCAI

ix
Table of Contents

Introduction to Hemodynamic Assessment in the cardiac catheterization Laboratory


Michael Ragosta, MD 1

Normal Waveforms, Artifacts, and Pitfalls


Michael Ragosto, MD 16

cardiac Outputs and Shunts


Vishal Arora, MD 38

Mitral Valve Disorders


Michael Ragosta, MD 50

Aortic Valve Disease


Michael Ragosta, MD 68

Hypertrophie cardiomyopathy and Related Conditions


Michael Ragosta, MD 91

Right-Sided Heart Disorders: Hemodynamics of the Tricuspid


and Pulmonic Valves and Pulmonary Hypertension
Michael Ragosta, MD 108

Pericardial Disease and Restrictive cardiomyopathy


Michael Ragosta, MD 123

Shock, Heart Failure, and Related Disorders


Michael Ragosta, MD 148

Complications of Acute Myocardiallnfarctîon


Brandon Brown, MD 164

Congenital Heart Disease


Rajan A.G. Patel, MD D. Scott Lim, MD 178
Coronary Hemodynamics
Michael Ragostal MD 199

Advanced Hemodynamic Assessment of Ventricular Function


D. Scott Liml MD Howard P. Gutgeselll MD 219

Miscella neous Hemodynamic Conditions


Michael Ragostal MD 226

Index 239
series of complicated biochemical steps,
CHAPTER 1 and muscle cells exert their cumulative
toil through the elegant dance of com-
Introduction to plex protein molecules. The latter secrets
eluded physicians and scientists, until
Hemodynamic only recently, when highly sophisticated
Assessment in the tools became available to reveal the intri-
cate and minute processes.
Cardiac Many of the mechanical processes
Catheterization inherent to cardiac physiology can be
understood by measuring changes in
Laboratory blood pressure and blood flow; the term
MICHAEL RAGOSTA, MD hemodynamics refers to this discipline.
Numerous brilliant investigators over
many years applied the study of hemo-
dynamics to collectively expand our
‘‘Look into any man’s heart you please, knowledge of cardiovascular physiology
and you will always find, in every one, in both normal and pathologic condi-
at least one black spot which he has to tions. The lessons learned from these
keep concealed.’’ generations of researchers rapidly became
Pillars of Society, act III assimilated into the contemporary prac-
Henrik Ibsen, 1877 tice of clinical cardiology. Currently,
hemodynamics is considered indispens-
Despite the exhortations of poets and able to the clinician managing patients
philosophers, the heart is, after all, sim- with cardiovascular disease and forms
ply a pump. The ability to ‘‘look into the foundation of invasive diagnostic
any man’s heart’’ with the goal of under- cardiology.
standing the function of this mysterious
organ circumvented early generations of
scientists and physicians. It would not A Brief History of
take long, however, for science to garner Hemodynamic Assessment
the tools needed to peer into the hearts
of men. Many of the major functions of All important human endeavors possess
the cardiovascular system important to histories replete with colorful anecdotes
our understanding of health and disease and legendary characters. The saga of
states are based on mechanical processes. cardiac catheterization is no exception.
Cardiac chambers contract and relax, The practical measurement of hemody-
valves open and close, and blood ebbs namics in humans required several crucial
and flows based upon elementary princi- developments. These included the inven-
ples of hydraulics. Contrast this with tion of safe and reliable catheterization
most other organ systems that exploit techniques to access and study the right
complex cellular and biochemical pro- and left sides of the heart, the ability to
cesses to accomplish their designated image catheter position, and the creation
functions. For example, the kidneys bal- of devices to convert pressure changes
ance fluid and electrolytes and excrete into an interpretable graphic form.
waste via an elaborate cellular array; Insertion of tubes into the bladders and
the liver, pancreas, and intestinal cells rectums of living persons and the blood
digest food and absorb nutrients by a vessels of cadavers had been achieved

1
2 Textbook of Clinical Hemodynamics

since primitive times.1 The first cardiac be the first to record intracardiac pressure
catheterization and pressure measure- using an early pressure recording system
ment performed on a living animal is connected to the end of a glass tube
attributed to the English physiologist inserted into a dog’s right ventricle.
Stephen Hales early in the 1700s and Later in the 1800s, in an attempt to
reported in the book Haemastaticks in address the controversy regarding the
1733. By accessing the internal jugular nature and timing of the cardiac apex
vein and carotid artery of a horse, Hales beat, the French veterinarian Jean Bap-
performed his experiments using a brass tiste Auguste Chauveau and physician
pipe as the catheter connected by a flexi- Étienne Jules Marey performed catheter-
ble goose trachea to a long glass column ization using rubber catheters placed
of fluid. The pressure in the white mare’s from a horse’s jugular vein and carotid
beating heart raised a column of fluid in artery. These meticulous scientists recog-
the glass tube over 9 feet high.1 nized the importance of obtaining the
As early as 1844, the famous French highest quality data and recorded pres-
physiologist Claude Bernard performed sures in various cardiac chambers with
numerous animal cardiac catheterizations clever mechanical devices invented by
designed to examine the source of meta- others but modified to suit their needs.2
bolic activity. Many prominent scientists The graphic recordings obtained from
theorized that ‘‘combustion’’ occurred in these early transducers and physiologic
the lungs. Using a thermometer inserted recorders appear remarkably similar to
in the carotid artery, Bernard2 compared those obtained in today’s cardiac cathe-
the temperature of blood in a living terization laboratories (Figure 1-1).
horse’s left ventricle to blood in the right From these early explorations of car-
ventricle, accessed from the internal diac pressure measurement evolved an
jugular vein, and showed slightly higher interest to quantify blood flow. In 1870,
right-sided temperatures, indicating that the German mathematician and physiol-
metabolism occurred in the tissues, not ogist Adolph Fick3 published his famous
in the lungs. Bernard2 also appeared to formula for calculating cardiac output

Or D

'''

Vent D D

''''

Vent G D'

FIGURE 1-1. Early pressure recordings obtained from the cardiac chambers of a horse by Marey and Chauveau. (Repro-
duced with permission, Mueller RL, Sanborn TA. The history of interventional cardiology: Cardiac catheterization, angio-
plasty, and related interventions. Am Heart J 1995;129:146–172.)
Chapter 1—Introduction to Hemodynamic Assessment 3

(oxygen consumption divided by arterio-


venous oxygen difference). However,
Fick had more interest in the conceptual
aspects of cardiac output determination
than in its validation or application. The
experiments necessary for validation of
Fick’s principle would fall to others more
than 60 years later. Fick3 also contributed
to the emerging field of hemodynamics
with his valuable work of refining early
pressure recording devices.
Despite numerous animal studies over
many years, the placement of a catheter
into the deep recesses of a living human
heart would have to wait for an accurate
method to image the course and position
of the catheter. This would, ultimately, be
feasible only after Wilhelm Roentgen’s
discovery of X-rays in 1895 (Figure 1-2).
The invention of an apparatus allowing
us to peer inside the living human body
FIGURE 1-2. Wilhelm Konrad Roentgen, discoverer of
for the first time represented one of the X-ray. (With permission, from Edward P, Thompson D:
the greatest medical advances in human Roentgen Rays and Phenomena of the Anode and Cathode.
VanNorstrand Co., NY, 1896.)
history. At the start of the 20th century,
it became possible to consider applying
the lessons learned from animal research
to humans. However, great trepidation into the heart because Bleichroeder
remained among cardiovascular research- reported the development of chest pain.
ers because most considered the place- They could not prove this theory because
ment of a catheter into a living, beating they failed to document the catheter
human heart foolhardy with potentially position by x-ray or pressure recording
deadly consequences. and never published their observations,
Although the historical record best- attempting to gain credit only after
ows acclaim for the first human cardiac Forssmann received his in 1929.1
catheterization to Werner Forssmann The account of Forssmann’s first car-
(performed on himself in 1929), his diac catheterization on himself, for
accomplishment may have been trumped which he was awarded the Nobel Prize
by the little known, often disputed, and in Medicine and Physiology in 1956,
poorly documented efforts of fellow along with André Frederic Cournand
Germans Fritz Bleichroeder, E. Unger, and and Dickinson Woodson Richards,2,4–7
W. Loeb1,2 in 1905. In an effort to deliver has been recounted numerous times
therapeutic injections close to the targeted and with several versions, some more
organ, these physicians attempted to engaging and colorful than others. The
place catheters, without radiologic guid- consistently told elements of his narra-
ance, into the central venous circulation tive are nearly unimaginable to contem-
via the basilic and femoral veins. During porary physicians familiar with the
one attempt made on his colleague Blei- existing training, medicolegal, and prac-
chroeder, Unger may have actually gotten tice environments.
4 Textbook of Clinical Hemodynamics

The essential facts of Forssmann’s story human experimentation by Schneider,


are as follows. After graduating medical he decided to carry out his project in
school, Forssmann began training as a secret. Forssmann recruited a colleague,
surgical intern at the Auguste-Viktoria Peter Romeis, and a surgical nurse, Gerda
Hospital in Eberswalde, Germany, a Ditzen, to assist him. Forssmann’s first
small community hospital outside Berlin attempt failed. Peter Romeis performed
(Figure 1-3). Forssmann’s6 motivation to the cutdown on his cubital vein and
pursue a means of instrumenting the advanced the catheter 35 cm, but he lost
right heart is unclear; he reported that it courage, believing it too dangerous to con-
evolved from the desire to find a method tinue, and stopped the experiment even
of infusing lifesaving drugs into the heart though Forssmann felt fine. A week later,
safer than by direct intramyocardial injec- Forssmann chose a quiet afternoon when
tion. Forssmann discussed his interest most of the hospital staff napped, and
with his chief, Dr. Richard Schneider, but together with his nurse accomplice gath-
Schneider banned the enthusiastic intern ered the surgical instruments in an empty
from pursuing this work, largely because room to perform the procedure. Gerda
he thought it unlikely that mainstream, Ditzen insisted on being the first sub-
German academic medicine would accept ject and Forssmann played along, fully in-
medical research from a community tending to perform the procedure on
hospital. In addition, many considered himself. After restraining the nurse to
placement of a catheter into the heart the table and preparing her incision site
very dangerous; Schneider did not wish with iodine, Forssmann turned from her,
notoriety for his hospital in the event quickly performed the venous cutdown
that these investigations ended poorly. on his own left arm and inserted the ure-
Undeterred by the prevailing lack of teral catheter 65 cm. Ditzen became angry
support, Forssmann first placed catheters when she realized the deceit but quickly
into the heart of cadavers from an arm helped him walk down a corridor and
vein then, impressed with the ease at two flights of stairs to the X-ray suite,
which the catheters advanced, decided to where Forssmann confirmed the position
perform the experiment on himself. As of the catheter tip in his right atrium.
he was forbidden to proceed with any Romeis apparently intercepted him in
the X-ray suite to try to abort the experi-
ment, but, according to one account, ‘‘. . .
the only way Forssmann could hold him
off was by kicking him in the shins.’’4
In his published account of his self-
experimentation, Werner Forssmann8 also
describes a case where he used the catheter
to deliver a solution of glucose, epineph-
rine, and strophanthin into the heart of a
patient gravely ill with purulent peritoni-
tis from a ruptured appendix. The patient
died shortly after a brief period of improve-
ment, and the autopsy confirmed the
FIGURE 1-3. Werner Forssmann performed the first catheter position in the right atrium.
catheterization on himself at this hospital in Eberswalde, Forssmann’s stunt did little to advance
Germany. (Reproduced with permission, Forssmann-Falck
R. Werner Forssmann: A pioneer of cardiology. Am J Cardiol the field of cardiac catheterization beyond
1997;79:651–660.) the bold demonstration that a catheter
Chapter 1—Introduction to Hemodynamic Assessment 5

could actually be positioned safely in the


human right atrium. No pressure mea-
surements were made, and the catheter
was not positioned in any other cardiac
chambers. However, Forssmann had
crossed the threshold and introduced the
world to the potential of human cardiac
catheterization.
Great turmoil and controversy followed
Forssmann’s publication. He failed to
gain support from the medical com-
munity, and, while he continued in-
vestigations in cardiac catheterization
(including at least six more self-experi-
ments),2 he became increasingly discour-
aged by the rigid, hierarchical nature of
German academic medicine and became FIGURE 1-4. Winner André F. Cournand, MD, along
a urologist in private practice. with Dickinson W. Richards and Werner Forssmann, of
the Nobel Prize in Medicine, 1956. (Reproduced with per-
In the immediate years following mission, Enson Y, Chamberlin MD. Cournand and
Forssmann’s success, a few isolated inves- Richards and the Bellevue Hospital Cardiopulmonary Lab-
oratory. Columbia Magazine, Fall 2001.)
tigators dabbled in right-heart catheteri-
zation experiments.1,2 However, nearly
a decade would pass before there emer- catheterization had been established and
ged a systematic discipline of right-heart Columbia became recognized as the first
catheterization exemplified by the ‘‘cardiopulmonary laboratory’’ capable of
classical work of André F. Cournand applying these techniques to the study
(Figure 1-4) and Dickinson W. Richards of cardiac and pulmonary diseases. With
at Columbia University’s First Medical the onset of worldwide hostilities and
Division of Bellevue Hospital. Develop- imminent war, the group first directed
ment of right-heart catheterization arose their efforts to the analysis of blood flow
out of Cournand and Richards’s interest in traumatic shock, making important
in pulmonary function, measurement of observations valuable in wartime. After
blood flow, and the interactions between the war, Cournand, Richards, and others
the heart and lungs in both health from their group published many land-
and disease. In the early 1930s, the group mark articles describing the hemodyna-
desired to measure pulmonary blood mic findings in congenital heart disease,
flow using the direct Fick method; how- cor pulmonale, valvular heart disease,
ever, this would require measuring and pericardial restrictive disease. Much
mixed venous blood from the right heart, of our current understandings of these
a feat considered too dangerous. Aware conditions evolved from this important
of Werner Forssmann’s act, the group body of work.
first demonstrated safety in animals and Growing confidence and experience in
then placed modified urethral catheters right-heart catheterization techniques
in the right atrium of humans, sampling led to interest in catheterization of the
blood for oxygen content and making left heart. Catheter access to the left heart
determinations of blood flow using offered unique challenges and a much
Fick’s principle. By the early 1940s, a safe greater concern about safety, and initial
and valuable methodology of right-heart adventures in accessing the left heart
6 Textbook of Clinical Hemodynamics

proved highly dangerous. Proposed and and massaged. This resulted in the
attempted methods to access the left restoration of a sinus rhythm, but the
ventricle included direct apical puncture, ventricular contractions were feeble and
retrograde access from puncture of the fifteen minutes after the onset of ventricular
thoracic or abdominal aorta, and a sub- fibrillation the heart ceased beating.9
xiphoid entry first into the right ventricle
and then followed by puncture of the With a failure rate of 100% in normal
interventricular septum. Methods to patients and an initial procedural mor-
directly access the left atrium included tality of nearly 10%, it is a wonder that
a transbronchial approach via a broncho- further attempts at retrograde left-heart
scope and a direct, posterior paraverte- catheterization were made. However,
bral left atrial puncture. It is interesting perseverance improved the safety and
that reports of experiments involving success at retrograde left-heart catheteri-
self-catheterization similar to Werner zation to its currently recognized form.
Forssmann’s involving the left heart are Additional advances included the devel-
noticeably absent from the literature. opment of trans-septal catheterization
Henry Zimmerman et al.9 reported the techniques, simultaneous right- and
first series of retrograde left-heart cathe- left-heart catheterization, and, of course,
terizations from a left ulnar artery cut- angiography. By the end of the 1950s,
down. This report noted failure to pass right- and left-heart catheterization had
a catheter across the aortic valve from become firmly established clinical tech-
a retrograde approach in five normal sub- niques for the evaluation of valvular,
jects, theorizing that the normal aortic structural, and congenital heart disease.
valve prevented ‘‘against the stream’’ With most of the basic elements of
passage of the catheter so they turned catheterization techniques in place,
their attention to patients with aortic investigators turned to refinement in
insufficiency. Zimmerman successfully equipment and techniques. Catheter
entered the left ventricle in 11 patients design represented one of the first impor-
with syphilitic aortic insufficiency. How- tant refinements. The stiff, unwieldy
ever, in a single patient with rheumatic catheters available to earlier generations
aortic insufficiency, the attempt proved of cardiovascular researchers required
fatal. Present-day cardiologists engaged substantial manipulative skill to position
in the regular performance of left-heart and often caused significant arrhythmia.
catheterization would find their account The invention of the balloon flotation
shocking. While attempting to pass the catheter exemplified by the Swan-Ganz
catheter into the left ventricle: catheter represented the innovation lead-
ing to the universal acceptance and
. . . the subject suddenly complained of widespread practical application of hemo-
substernal chest pain and the dynamic assessment. The balloon flota-
electrocardiogram which was being recorded tion catheter became a clinical reality
showed the abrupt appearance of from the desire of Dr. Harold JC Swan,
ventricular fibrillation. The catheter was professor of medicine at the University of
immediately withdrawn. Nine cubic California, Los Angeles, and director of
centimeters of 1 percent solution of procaine cardiology at Cedars-Sinai Medical Cen-
with 0.5 cc of a 1:1000 solution of ter, to apply cardiac catheterization tech-
adrenalin were injected directly into the niques to study the physiology of acute
heart without effect on the cardiac myocardial infarction (Figure 1-5). In the
mechanism. The heart was then exposed early 1960s, cutting-edge hospitals began
Chapter 1—Introduction to Hemodynamic Assessment 7

The answer to Swan’s dilemma pro-


vides an entertaining and often told
example of the near magical ability of
the human mind to solve problems.
Recalling this delightful story in his own
words in 199111:

In the fall of 1967, I had occasion to take


my (then young) children to the beach in
Santa Monica. On the previous evening,
I had spent a frustrating hour with an
extraordinary, pleasant but elderly lady in
an unsuccessful attempt to place one of
FIGURE 1-5. HJC Swan, MD, co-developer of the popu- Bradley’s catheters. It was a hot Saturday
lar Swan-Ganz catheter. (Reproduced with permission and the sailboats on the water were
from U.S. National Library of Medicine.)
becalmed. However, approximately half a
mile offshore, I noted a boat with a large
to develop specialized coronary care units spinnaker well set and moving through the
to care for patients with acute myocar- water at a reasonable velocity. The idea
dial infarction. Designed primarily to then came to put a sail or a parachute on
monitor and treat arrhythmias, coronary the end of a highly flexible catheter and
care units also became an obvious place thereby increase the frequency of passage of
to study the physiology of acute myocar- the device into the pulmonary artery. I felt
dial infarction. Early efforts to measure convinced that this approach would allow
hemodynamics in unstable patients with for rapid and safe placement of a flotation
acute myocardial infarction with stiff catheter without the use of fluoroscopy and
catheters and the primitive techniques would solve the problem of arrhythmias.
available at that time induced life-threat-
ening arrhythmias. Cardiologists consid- Edwards Laboratories worked with
ered catheterization dangerous during Swan to create the first five prototype
the acute phase of infarction and that it catheters that relied on a balloon to
carried an unacceptable risk. accomplish flotation rather than para-
Swan became aware of the work of chutes or sails. (Interestingly, an early
Ronald Bradley,10 who reported the use form of a balloon flotation catheter was
of very small tubing to safely instrument described by Lategola and Rahn and
the pulmonary artery and measure pres- failed to gain the attention of cardiovas-
sures in ‘‘severely ill’’ patients. When cular investigators; it did, however, pre-
Swan attempted this technique, how- vent Swan from obtaining a patent on
ever, he found little success in passing the idea11).
the flimsy, small-caliber catheters from a Swan had previously hired William
peripheral vein to the pulmonary artery. Ganz, an immigrant from the former
In addition to the dearth of techniques Czechoslovakia and survivor of the
to access a central vein, the most likely World War II labor camps, to work in the
explanation for Swan’s lack of success experimental laboratory at Cedars of
related to the low output state of his Lebanon Hospital. The first animal experi-
patients compared to those of Bradley, ments performed by Ganz with the proto-
preventing flotation of the catheter type catheters were a brilliant success.
along the blood flow stream. Once the catheter was advanced into the
8 Textbook of Clinical Hemodynamics

right atrium and the balloon inflated, the Roentgen’s discovery of X-rays or Werner
catheter quickly migrated across the tri- Forssmann’s audacious self-experiments.
cuspid valve and out the pulmonary We take for granted the formidable task
artery to the wedge position, confirming of translating a pressure wave sampled at
Swan’s notion. The catheters were tried the tip of the catheter to a graphic repre-
in humans with similar success and led sentation plotted as pressure versus time.
to the landmark publication in the New The early pioneers of heart catheteriza-
England Journal of Medicine.12 The group tion recorded intracardiac pressures in
further refined the catheter’s design, and animals with primitive transducers
Ganz added a thermistor to measure car- consisting of elastic membranes attached
diac output by the thermodilution tech- to the catheter and using water-filled
nique. Swan recognized that the catheter manometers that recorded pressure via
and procedure’s success as a universally a system of levers to a chart recorder
accepted bedside tool required that the (sphygmograph).2 Springs and other clever
technique be safe, easy to use, and not mechanical adaptations to the devices
interfere with routine nursing care in the improved their performance. Early in
intensive care unit. According to Swan11: the 20th century, several individuals
made key contributions in this field.
. . . right heart catheterization became so Carl J. Wiggers13 represents one of the
routine and simple that the then Director of key innovators in the development of
the Diagnostic Catheterization Laboratory, high-fidelity pressure recording instru-
Dr. Harold Marcus, stated that he would ments. He is credited with the invention
ban the device because it was impossible to of the Wiggers manometer, the first
train the cardiac fellows in the appropriate optical manometer. The optical manom-
manipulations of right heart catheters. eter was based on work originally
conceptualized by Otto Frank. Wiggers
The core elements of diagnostic car- spent time in Frank’s Munich lab but
diac catheterization and hemodynamic was quite taken aback by Frank’s secretive
assessment have changed little since nature. Wiggers noted13:
the 1970s. Innumerable additional con-
tributors have refined catheterization Such a restrictive attitude in sharing newly
techniques and expanded our knowl- developed apparatus was contrary to my
edge of hemodynamics in health and scientific upbringing and threatened to
disease; the valuable contributions of frustrate my future use of them. Therefore,
these notable leaders will be presented I connived with the laboratory mechanic
in subsequent chapters of this book. who could use some extra money to make
While the bulk of attention is paid copies for me. In a sense, therefore, I
to the colorful pioneers of cardiac cathe- smuggled the equipment I needed out of
terization, the important role of the the laboratory.
unglamorous physiologic recorder in
the advancement of the science of hemo- The configuration of Wiggers’s optical
dynamics is often ignored. In fact, the manometer consisted of the catheter
development of accurate physiologic attached to a fluid-filled chamber. At the
recording equipment provided substan- end of small side arm from this chamber
tial challenges. The contributions made was an elastic membrane. A small mirror
by mostly anonymous geniuses are easily attached to this membrane reflected
forgotten but were as crucial to the a light focused onto a light-sensitive
development of cardiac catheterization as recording paper. In this way, pressure
Chapter 1—Introduction to Hemodynamic Assessment 9

changes from the catheter would be be captured with a handheld mirror and
transmitted to the fluid-filled chamber adjusted to strike the paper. Researchers
and then to the membrane. The light could then record intravascular pressures.
beam essentially functioned as a weight-
less lever arm and a very sensitive Advances in electronics changed
method of reproducing rapid pressure the physiologic recorder. Oscilloscopes
changes. This innovation allowed the replaced the Hamilton manometer; the
first high-fidelity measurements of intra- new systems converted catheter pre-
cardiac pressure (Figure 1-6). Subsequent ssure to an electrical output displayed
modifications by William F. Hamilton14 on cathode ray tubes. Many of us still
provided the essential equipment used recall the old-fashioned chart recorders
in Cournand and Richards’s laboratory that used mechanical stylets to trace
at Bellevue. Measuring and recording the pressure contour onto heat-sensitive
hemodynamics in that era required great paper for later analysis and storage
patience and effort as demonstrated in (Figure 1-7). These apparatuses have
this description14: been replaced by tiny, cheap, and dis-
posable table-mounted pressure transdu-
Once the catheter was in place, all lights cers capable of converting a mechanical
in the room were turned off, and the force to an electrical one, with sub-
Hamilton manometer (which focused a sequent conversion of this electrical sig-
light on sensitive paper to record the nal in the ‘‘black box’’ of an advanced
pressure contour) was attached to the computer to the colorful graphic display
catheter and manipulated in absolute to that we have become accustomed
darkness so that its light output could (Figure 1-8).

FIGURE 1-6. High-fidelity re- 3 4


1 5
cordings obtained by Carl Wiggers 2
in 1921 from the right atrium 6
(top), pulmonary artery (middle),
and right ventricle (bottom) of a
dog, using the optical manometer.
(Reproduced with permission,
Reeves JT. Carl J. Wiggers and the
pulmonary circulation: A young C
man in search of excellence. Am J D
Physiol [Lung Cell Mol Physiol]
1998;18:L467–474.) B

D
A
E

1 2 3 4 5
10 Textbook of Clinical Hemodynamics

performed each day in the United States


measure left ventricular and aortic pres-
sures; nearly a third of these also include
assessment of right heart pressures and
cardiac output. Many additional patients
undergo right-heart catheterization alone
in the cardiac catheterization laboratory.
Medical, surgical, and coronary intensive
care units contribute innumerable addi-
tional right-heart catheterization pro-
cedures performed at the bedside in
critically ill patients, and anesthesiolo-
gists rely on right heart pressure monitor-
ing during many high risk surgical
procedures in the operating room. Thus,
hemodynamic assessment has become
an integral and established part of the
daily practices of cardiologists, pulmo-
nologists, anesthesiologists, surgeons,
and intensivists.
There are many indications for inva-
sive hemodynamic assessment. For
FIGURE 1-7. Mechanical recorder used to collect hemo- patients referred to the cardiac catheteri-
dynamics and popular in the 1980s and early 1990s.
zation laboratory, right- and left-heart
catheterization is often performed for
the evaluation and management of heart
failure syndromes, shock, unexplained
dyspnea, hypotension, respiratory fail-
ure, renal failure, edema, valvular heart
disease, pericardial disease, hypertrophic
cardiomyopathy, or congenital heart
disease. Patients with unusual chest pain
syndromes may require right-heart cath-
eterization to exclude pulmonary hyper-
tension. Most patients who undergo
cardiac catheterization mainly for the
FIGURE 1-8. Modern cardiac catheterization laboratory evaluation of the coronary arteries, as seen
outfitted with computerized hemodynamic monitoring in stable angina, abnormal stress tests,
systems used by the University of Virginia Cardiac Cathe-
terization Laboratories, circa 2006. acute coronary syndromes, or uncom-
plicated myocardial infarction, require
Hemodynamic Assessment only measurement of left heart and aor-
in Modern Clinical Practice tic pressure. However, postmyocardial
infarction patients who exhibit hypo-
The ease at which we can now assess tension, serious arrhythmia, or heart fail-
cardiovascular hemodynamics has estab- ure, or in the case of a suspected
lished cardiac catheterization as a routine complication such as right ventricular
diagnostic procedure. Nearly all of the infarction, ventricular septal defect or
thousands of cardiac catheterizations mitral regurgitation should also undergo
Chapter 1—Introduction to Hemodynamic Assessment 11

a careful right-heart catheterization. Pati- analyze, print, and store the hemody-
ents under evaluation for heart or lung namic waveforms generated.
transplantation often undergo right-heart A variety of catheters are available for
catheterization to identify pulmonary pressure sampling (Figure 1-9). The opti-
hypertension and, if present, a determina- mal catheter for hemodynamic measure-
tion of reversibility by pharmacologic ments is stiff to transmit the pressure
administration of a vasodilator agent. wave to the transducer without absorp-
Common indications for the bedside tion by the catheter, is easy and safe to
use of right-heart catheterization in position, and has a relatively large lumen
patients with cardiac disease include the opening to an end hole. The use of an
differentiation of cardiogenic from non- end-hole catheter is especially important
cardiogenic causes of pulmonary edema, when sampling pressures within small
profound hypotension or shock and the chambers or when discerning pressure
guidance of therapy in patients with gradients over relatively small areas. An
heart failure, pulmonary edema, pulmo- end-hole catheter may lead to damping
nary hypertension or shock particularly or other artifact if the end-hole comes
if there is renal impairment. Detailed into contact with the wall of the cardiac
recommendations on the indications chamber. The commonly used ‘‘pig-tail’’
and use of bedside right-heart catheteriza- catheter has multiple side-holes and sam-
tion have been provided.15 ples pressure at each of these openings,
resulting in a tracing representing a mix-
ture of the pressure waves collected at
Equipment each opening. Such catheters are ade-
quate if sampling pressure in a large,
The essential components of a hemo- uniform chamber such as the aorta or left
dynamic monitoring system include a ventricle. It will not, however, have the
catheter, a transducer, fluid-filled tubing required resolution to discern pressure
to connect the catheter to the transdu- gradients within the left ventricle. Cathe-
cer, and a physiologic recorder to display, ters with an end-hole and side-holes at

A B
FIGURE 1-9. Catheters used for collecting hemodynamic measurements. A, The popular Swan-Ganz catheter. This
model has four ports consisting of a proximal lumen (a), a distal lumen (b), and the balloon port (c), which inflates the
balloon mounted at the tip of the catheter. There is an extra infusion port (d) on this model. The thermistor for perfor-
mance of thermodilution cardiac outputs connects to the computer via a connecting plug (e). The catheter has 10-cm
increments marked by lines (arrow). B, Example of a Berman catheter. This is used for hemodynamics but also for angi-
ography. There is a port connecting to the distal lumen (a) and a balloon inflation port (b). There are multiple side-holes
to allow angiography at the tip of the catheter (c).
12 Textbook of Clinical Hemodynamics

just the tip prevent damping or artifac- balloon flotation to assist in catheter posi-
tual waveforms due to positioning of tioning and must be directed carefully
the catheter tip against the chamber wall through the cardiac chambers under fluo-
and are useful for collecting samples for roscopic guidance by the operator. These
oxygen saturation. The Swan-Ganz cath- include the Layman catheter and Cour-
eter is the most commonly used catheter nand catheter consisting of an end-hole,
for measuring right-heart pressures. In the NIH catheter that contains multiple
addition to the balloon at the tip for flo- side-holes near the tip but no end-hole,
tation, it consists of an end-hole (distal and the Goodale-Lubin catheter consist-
port), a side-hole 30 cm from the cathe- ing of an end-hole and two single side-
ter tip (proximal port), and a thermistor holes near the tip and used mostly for
for measurement of thermodilution car- blood sampling.
diac output. This catheter is used exten- Transducers and tubing constitute
sively in modern cardiac catheterization the next important component of the
laboratories as well as at the bedside for hemodynamic measurement system.
invasive monitoring. Other balloon flo- Table mounted, fluid-filled transducers
tation catheters include the Berman currently used by most catheterization
catheter, which is constructed of multi- laboratories and intensive care units are
ple side-holes near the tip and no end- inexpensive and disposable (Figure 1-10).
hole or thermistor and is used principally The pressure wave is transmitted through
for performance of angiography, and the the fluid-filled catheter to a membrane in
balloon-wedge catheter, which contains the transducer and deforms the mem-
an end-hole similar to the Swan-Ganz brane resulting in a change in electrical
catheter but no thermistor for cardiac resistance. This electrical signal is trans-
output measurement or additional infu- mitted to the analyzing computer and
sion or pressure monitoring ports. Other converted to a graphic representation of
catheters rarely used today for pressure the pressure wave. These relatively inex-
measurement or for blood sampling dur- pensive transducers are factory calibrated
ing right-heart catheterization do not use but require ‘‘zeroing.’’ They sometimes

FIGURE 1-10. Setup for a table-mounted transducer used for pressure measurement in the cardiac catheterization lab-
oratory. A, The general configuration. The catheter used to sample pressure is connected to a high-pressure tubing
(arrow). A close-up view of the transducer is shown in B (arrow). The high-pressure tubing connecting to the patient
attaches by a stopcock to the transducer (a). Another stopcock allows flushing and equilibration with air (b). The trans-
ducer connects by a cable to the hemodynamic computer (c).
Chapter 1—Introduction to Hemodynamic Assessment 13

do not hold calibration or a ‘‘zero’’ during identified if there is catheter whip or


use so should be replaced if suspicious or marked respiratory variation. It is impor-
faulty data are obtained. tant for the operator to compare his or
Fluid-filled systems are acceptable for her own interpretation of the waveforms
clinical purposes but are subject to mea- with the numbers provided by the
suring artifact. The catheter and connect- computer to ensure accurate reporting of
ing tubing should be stiff; soft tubing will these values.
absorb the pressure wave, damping and
distorting it. In addition, the catheter as
well as the tubing connecting the cathe- Catheterization Protocols
ter and transducer should be as short as
possible, with as few connections as pos- During a complete right- and left-heart
sible to prevent timing delays, pressure catheterization, the following routine
damping, and a potential source of air is generally followed (Table 1-1). After
bubbles. Great care should be taken to obtaining arterial and venous access, the
prevent kinking of the catheter or intro- physician positions the Swan-Ganz cath-
ducing air or clot within the catheter or eter in the pulmonary artery and a pigtail
tubing because this will distort the wave- catheter in the aorta. Thermodilution
form and lead to inaccuracies. Under cer- cardiac output is measured and blood
tain circumstances, pressure may be sampled from the aorta and the pulmo-
measured directly in the cardiac chamber nary artery to calculate cardiac output
or vessel by use of a tiny transducer using the Fick principle and to screen
(micromanometer) mounted at the tip for an intracardiac shunt. Aortic and pul-
of a catheter, avoiding the limitations of monary artery pressures are measured
a fluid-filled system. This is often the case and then the pigtail catheter advanced
when precise hemodynamic measure- in a retrograde fashion across the aortic
ments are required as part of a research valve and into the left ventricle. The
study but also form the basis of the Swan-Ganz catheter is advanced to the
pressure wire used for measurement of
intracoronary pressure, which will be
discussed in a later chapter. TABLE 1-1. Components of a Routine
Finally, a variety of proprietary com- Complete Right- and Left-Heart
puter systems are available for displaying, Catheterization
printing, and storing hemodynamic 1. Position pulmonary artery (PA) catheter.
waveforms. The major systems in use are 2. Position aortic (AO) catheter.
universally excellent and perform many 3. Measure PA and AO pressure.
4. Measure thermodilution cardiac output.
of the analyses and calculations previ- 5. Measure oxygen saturation in PA and AO blood
ously done manually. These systems ana- samples to determine Fick output and screen for
shunt.
lyze the waveforms and automatically 6. Enter the left ventricle (LV) by retrograde
identify systolic and diastolic pressure crossing of the AO valve.
7. Advance PA catheter to pulmonary capillary
values. It is important to note, however, wedge position (PCWP).
that the recognition algorithms in these 8. Measure simultaneous LV-PCWP.
9. Pull back from PCWP to PA.
systems occasionally misidentify wave- 10. Pull back from PA to right ventricle (RV) to
forms, particularly if there is artifact in screen for pulmonic stenosis and record RV.
the waveform or on the electrocardio- 11. Record simultaneous LV-RV.
12. Pull back from RV to right atrium (RA) to screen
gram. For instance, left ventricular end for tricuspid stenosis and record RA.
diastolic pressure or pulmonary artery 13. Pull back from LV to AO to screen for aortic
stenosis.
systolic pressure may not be properly
14 Textbook of Clinical Hemodynamics

pulmonary capillary wedge position


and simultaneous left ventricular and TABLE 1-2. Some Potential Risks of Right- and
Left-Heart Catheterization
pulmonary capillary wedge pressure
1. Access site complications
measured to screen for the presence of Bleeding
mitral stenosis. Pressure recordings are Hematoma
obtained from each chamber as the Vessel injury
Nerve injury
right-sided catheter is withdrawn with Infection
careful attention paid as the catheter Pseudoaneurysm formation
Arteriovenous fistula formation
crosses the pulmonic and tricuspid valves Pneumothorax (for internal jugular vein
to screen for valvular lesions. Simulta- puncture)
Inadvertent arterial puncture
neous right ventricular and left ventricu- 2. Arrhythmia
lar pressure recordings are obtained to Ventricular tachycardia, ventricular fibrillation
Atrial arrhythmia, supraventricular
screen for restrictive/constrictive physi- tachycardia
ology. Finally, careful observation of the Transient bundle branch block
pressure waveform, as the left ventricular Heart block
3. Myocardial infarction
catheter is pulled back into the aorta, 4. Stroke
serves as a screen for aortic valve stenosis. 5. Infection
Bacteremia
As in most procedures, there are few Endocarditis
‘‘absolute’’ contraindications to cardiac 6. Pulmonary embolism/infarction
7. Pulmonary artery rupture
catheterization. The risk-benefit ratio 8. Vessel or cardiac chamber perforation
should be carefully considered in each 9. Catheter entrapment
10. Cholesterol embolization
individual. Relative contraindications 11. Renal failure
for invasive hemodynamic assessment 12. Death
relate to patient features that increase
procedural risk. While generally consid-
ered safe, there are multiple, serious abnormalities. Catheter placement in the
potential complications from right- and right ventricular outflow tract can lead
left-heart catheterization (Table 1-2). to right bundle branch block; left bundle
The most commonly observed complica- branch block may arise when the aortic
tions relate to the access site, with hema- valve is crossed. Thus, patients with exist-
toma, bleeding, and vessel injury not ing left bundle branch block may
infrequent. Thus, significant coagulopa- develop complete block when right-heart
thy or thrombocytopenia or treatment catheterization is performed; similarly,
with anticoagulant or thrombolytic patients with underlying right bundle
drugs increases the risk of the procedure. branch block may develop complete
Careful consideration should be made heart block when the catheter crosses
in patients with active infections, par- the aortic valve during a left-heart cathe-
ticularly bacteremia. Left-heart cathe- terization. Normal conduction is gener-
terization is frequently avoided in ally restored with prompt removal of
patients with known left ventricular the offending catheter but may persist for
thrombus or active aortic valve endocar- some time and even require placement
ditis to minimize the risk of emboliza- of a temporary pacemaker. Catheteriza-
tion. Arrhythmias are commonly seen tion should be postponed, if possible, in
during catheterization; most are due to patients with serious electrolyte or meta-
catheter position, are transient, and of bolic disarray because these may pre-
no clinical consequence. However, high- dispose the patient to development of
grade atrioventricular block can arise ventricular or atrial arrhythmias during
if the patient has underlying conduction catheterization.
Chapter 1—Introduction to Hemodynamic Assessment 15

References 9. Zimmerman HA, Scott RW, Becker NO. Catheteriza-


tion of the left side of the heart in man. Circulation
1950;1:357–359.
1. Mueller RL, Sanborn TA. The history of interven- 10. Bradley RD. Diagnostic right heart catheterization
tional cardiology: Cardiac catheterization, angio- with miniature catheters in severely ill patients.
plasty, and related interventions. Am Heart J 1995; Lancet 1964;284:941–942.
129:146–172. 11. Swan HJC. The pulmonary artery catheter. Disease-
2. Cournand AF. Cardiac catheterization. Acta Med a-Month 1991;37:478–508.
Scand 1975;579(Suppl):7–32. 12. Swan HJ, Ganz W, Forrester J. Catheterization of
3. Acierno LJ. Adolph Fick: Mathematician, physicist, the heart in man with use of a flow-directed
physiologist. Clin Cardiol 2000;23:390–391. balloon-tipped catheter. N Engl J Med 1970;283:
4. Fenster JM. Mavericks, Miracles and Medicine. The 447–451.
Pioneers Who Risked Their Lives to Bring Medicine into 13. Reeves JT, Carl J. Wiggers and the pulmonary circu-
the Modern Age. Carroll and Graf Publishers, NY, lation: A young man in search of excellence. Am J
2003. Physiol (Lung Cell Mol Physiol) 1998;18:L467–474.
5. Fontenot C, O’Leary JP. Dr. Werner Forssman’s self- 14. Enson Y, Chamberlin MD. Cournand and Richards
experimentation. Am Surg 1996;62:514–515. and the Bellevue Hospital Cardiopulmonary Labo-
6. Steckelberg JM, Vlietstra RE, Ludwig J, Mann RJ. ratory. Columbia Magazine, Fall 2001.
Werner Forssmann (1904–1979) and his unusual 15. Mueller HS, Chatterjee K, Davis KB, et al. Present use
success story. Mayo Clin Proc 1979;54:746–748. of bedside right heart catheterization in patients
7. Forssmann-Falck R. Werner Forssmann: A pioneer with cardiac disease. J Am Coll Cardiol 1998;32:
of cardiology. Am J Cardiol 1997;79:651–660. 840–864.
8. Forssmann W. Die Sondierung des rechten Herzens.
Klin wochenschr 1929;8:2085–2087.
catheter (micromanometer) within the
CHAPTER 2 chamber or, more commonly, the pres-
sure transducer is outside of the body,
Normal Waveforms, and a pressure waveform is transmitted
from the catheter tip to the transducer
Artifacts, and Pitfalls through a column of fluid. These transdu-
MICHAEL RAGOSTA, MD cers consist of a diaphragm or membrane
attached to a strain-gauge-Wheatstone
bridge arrangement. When a fluid wave
strikes the diaphragm, an electrical cur-
The proper collection and interpreta- rent is generated with a magnitude de-
tion of hemodynamic waveforms are pendent on the strength of the force that
important components of cardiac cathe- deflects the membrane. The output cur-
terization often overshadowed by more rent is amplified and displayed as pressure
glamorous aspects of invasive cardio- versus time.
logy, such as angiography and coronary During the cardiac cycle, changes in
intervention. Accurate intracardiac pres- pressure occur rapidly, corresponding
sure measurements provide invaluable with various physiologic events. The
physiologic information in both normal force wave created by these events gen-
and pathologic states; poorly gathered erates a spectrum of wave frequencies.
or erroneously interpreted waveforms Consider, for example, the different
may lead to an incorrect diagnosis or a events that occur within the aorta
poor clinical decision. It is imperative throughout a single cardiac cycle. Begin-
that competent cardiologists understand ning with left ventricular ejection, the
normal and abnormal hemodynamic aortic valve opens, causing pressure to
waveforms and are capable of trouble- rise in the aorta, rapidly reaching a peak,
shooting problems and recognizing then falling quickly following peak ejec-
common artifacts and potential pitfalls tion. Closure of the aortic valve repre-
during the collection of hemodyna- sents another event, marking the end
mic data. of systole, and is associated with a slight
rise in pressure followed by pressure
decay during ventricular diastole until
Generation of Pressure the next ventricular contraction. All of
Waveforms these events occur rapidly and are asso-
ciated with varying wave frequencies.
The goal of a hemodynamic study is When the force wave strikes the trans-
to accurately reproduce and analyze the ducer, it should precisely reproduce all
changes in pressure that occur during of these events. The full range of fre-
the cardiac cycle within a cardiac cham- quencies needed to reproduce all of
ber. These rapidly occurring events rep- these force waves requires a sensing
resent mechanical forces and require membrane capable of a rapid frequency
conversion to an electrical signal to be response (0–20 cycles/second in the
transmitted and subsequently translated human heart). However, the physical
into an interpretable, graphic format. properties of a membrane capable of
The pressure transducer is the essential such a wide frequency response might
component that translates the mechani- resonate, creating artifacts. This phe-
cal forces to electrical signals. The trans- nomenon is similar to the sound that
ducer may be located at the tip of the a bell makes, continuing to oscillate

16
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 17

after initially struck. Resonation artifact Calibration, Balancing,


appears on the waveform as excessive and Zeroing
‘‘noise,’’ but reverberations can also lead
to harmonic amplification of the wave- Previous generations of transducers
form overestimating systolic pressure required calibration against a mercury
and underestimating diastolic pressure manometer; the factory-calibrated, dis-
(Figure 2-1). Therefore, hemodynamic posable, fluid-filled transducers in clinical
measurement systems need to provide use today no longer need this. Table-
some level of ‘‘damping’’ to reduce reso- mounted transducers do require bal-
nation artifacts. Damping is a method ancing or ‘‘zeroing,’’ which refers to the
of eliminating the oscillation; it may be establishment of a reference point for
done by the introduction of friction subsequent pressure measurements. The
to reduce the oscillation of the sensing reference or ‘‘zero’’ position should be
membrane, or it may be accomplished determined before any measurements
electrically by damping algorithms. are made. By convention, it is defined at
However, note the importance that the patient’s midchest in the anteropos-
damping reduces the frequency response terior dimension at the level of the ster-
and may result in loss of information. nal angle of Louis (fourth intercostal
Over-damping results in loss of rapid, space) (Figure 2-2). This site is an estima-
high-frequency events (for example, the tion of the location of the right atrium
dicrotic notch on the aortic waveform), and is also known as the phlebostatic axis.
causing underestimation of the systolic A table-mounted transducer is placed at
pressure and overestimation of the dia- this level and the stopcock is opened to
stolic pressure. The ideal pressure tracing air (atmospheric pressure) and set to zero
has the proper balance of frequency by the hemodynamic system. The system
response and damping. is now ready for pressure measurements.

180
Under-damped
160 Correct waveform
Over-damped
140

120

100
mmHg

80

60

40

20

0
FIGURE 2-1. Schematic representation of the effects of over- or under-damping on the pressure waveform. An under-
damped waveform will overestimate systolic pressure and underestimate diastolic pressure, whereas over-damping will
have the opposite effects. In addition, the over-damped waveform obscures subtle hemodynamic findings, such as the
dicrotic notch.
18 Textbook of Clinical Hemodynamics

A B
FIGURE 2-2. A, Demonstration of the ‘‘zero’’ position or phlebostatic axis representing a point midway in the antero-
posterior chest dimension at the fourth intercostal space. B, Table-mounted transducers are positioned at this point using
a level to ensure accuracy.

The tradition of using the midaxillary in patients who are unable to lie flat or
line as the zero position has been called who are at the extremes of body weight.
into question. Because of the influence A transducer placed above the true
of hydrostatic pressure, in the supine posi- zero position will furnish a measured
tion, and use of fluid-filled transducers, pressure lower than the actual pressure;
some physicians believe that setting the a transducer placed below the true zero
zero position as the upper border of the position will result in a pressure measure-
left ventricle is more accurate.1 The dif- ment higher than the actual pressure.
ference between this location and the These small pressure changes caused
conventional location provides greatest by improper zeroing may lead to signifi-
accuracy in diastolic pressure measure- cant errors in diagnosis and, perhaps,
ments. However, most routine labs find inappropriate therapy.
this approach impractical because it Transducer drift refers to either the
requires the use of echocardiography to loss of calibration or loss of balance after
determine the precise location; it is more initially setting the zero level. This is
applicable to research investigations. not uncommon. Many patients have
A major advantage of the midchest posi- been started on pressors for hypoten-
tion is that it has been shown to correlate sion or a patient falsely diagnosed with
with the position of the left atrium by mitral stenosis because of inaccurate
magnetic resonance imaging studies transducer balancing, improper zero
regardless of the patient’s age, gender, positioning, or transducer drifting. Care-
body habitus, or presence of chronic lung ful attention to this aspect is important
disease.2 Frequently, busy catheterization for proper interpretation.
laboratories might position the trans-
ducer at the same level for all patients or Normal Physiology and
from a measured, fixed distance from Waveform Characteristics
either the table or from the top of the
patient’s chest, without taking into con- Interpretation of pressure waveforms
sideration the variations in patient posi- requires a consistent and systematic
tion or body habitus. This practice will approach (Table 2-1). After confirming
lead to marked inaccuracies, particularly the zero level, the scale of the recording
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 19

under-damping. Each pressure event


TABLE 2-1. A Systematic Approach to should be timed with the electrocardio-
Hemodynamic Interpretation
gram (ECG). Finally, the operator should
1. Establish the zero level and balance transducer.
2. Confirm the scale of the recording. review the tracings for the presence of
3. Collect hemodynamics in a systematic method common artifacts that might lead to
using established protocols.
4. Critically assess the pressure waveforms for
misinterpretation.
proper fidelity. Note the importance of multiple
5. Carefully time pressure events with the ECG. events and their interrelationship to
6. Review the tracings for common artifacts.
properly interpret pressure waveforms,
particularly in disease states. Figure 2-3
is noted and a recording sweep speed is demonstrates the three basic waveforms
determined. Establishing standard pro- (atrial, ventricular, and arterial) and
tocols is helpful to ensure that all ne- their relationships to key electrical and
cessary information is collected in a physiologic events during the normal
systematic format (see Chapter 1). Care- cardiac cycle. Each waveform will be
ful scrutiny of the waveform ensures a described in detail in the following
high-fidelity recording without over- or sections.

1 2 3 4 5 6 7

Phase

Dicrotic
notch

Aortic

Left V
A C
ventricular

Left
atrial
FIGURE 2-3. Timing of the major electrical and mechanical events during the cardiac cycle. Phase 1 ¼ atrial contraction;
Phase 2 ¼ isovolumic contraction; Phase 3 ¼ rapid ejection; Phase 4 ¼ reduced ejection; Phase 5 ¼ isovolumic relaxation;
Phase 6 ¼ rapid ventricular filling; and Phase 7 ¼ reduced ventricular filling.
20 Textbook of Clinical Hemodynamics

Right Atrial Waveform

The normal right atrial pressure is


2–6 mmHg and is characterized by a
and v waves and x and y descents
(Figure 2-4). The a wave represents the
pressure rise within the right atrium
due to atrial contraction and follows
the P wave on the ECG by about
80 msec. The x descent represents the
pressure decay following the a wave and
reflects both atrial relaxation and the
sudden downward motion of the atrio-
ventricular (AV) junction that occurs FIGURE 2-5. Right atrial waveform obtained in a patient
with chronic atrial fibrillation, demonstrating persistence
because of ventricular systole. An a wave of the x descent despite loss of the a wave.
is usually absent in atrial fibrillation, but
the x descent may be present because
of this latter phenomenon (Figure 2-5).
A c wave is sometimes observed after
the a wave and is due to the sudden The next pressure event is the v wave.
motion of the tricuspid annulus toward A misunderstanding exists regarding the
the right atrium at the onset of ventric- v wave. Although this event is occurr-
ular systole. The c wave follows the a ing at the same time as ventricular sys-
wave by the same time as the PR inter- tole, when the tricuspid valve is closed,
val on the ECG; the first-degree AV the pressure rise responsible for the
block results in a more obvious c wave v wave is due to passive venous filling
(Figure 2-6). When a c wave is present, of the atrium, representing atrial dias-
the pressure decay following it is called tole. Increased filling of the right atrium
an x1 descent. results in greater prominence of the v
wave. The peak of the right atrial v wave
occurs at the end of ventricular systole,
when the atria are maximally filled and
corresponds with the end of the T wave
on the surface ECG. The pressure decay
that occurs after the v wave is the y
descent and is due to rapid emptying
of the right atrium when the tricuspid
valve opens. Atrial contraction follows
this event and the onset of another car-
diac cycle. In normal right atrial wave-
forms, the a wave typically exceeds the
v wave. During inspiration, the mean
right atrial pressure decreases due to
the influence of decreased intratho-
racic pressure, and there is augmenta-
FIGURE 2-4. An example of a normal right atrial pres- tion of passive right ventricular filling;
sure waveform. Note the timing from the electro-
cardiographic P and T waves to the hemodynamic a and the y descents become more prominent
v waves, respectively. (Figure 2-7).
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 21

FIGURE 2-6. Example of a right


atrial waveform with prominence 1 OT
of the c wave due to the presence
of first-degree AV block.
1 mV

a
v v
a v v
a a

0.19 mmHg/mm
1 2 3 4 5 6

tracings exhibit the characteristic fea-


tures of ventricular waveforms with
rapid pressure rise during ventricular
contraction and rapid pressure decay
during relaxation with a diastolic phase
characterized by an initially low pressure
that gradually increases (Figure 2-8). The
right atrial pressure should be within
a few mmHg of right ventricular end-
diastolic pressure unless there is tricuspid
FIGURE 2-7. With inspiration, the x and y descents
become more prominent on the right atrial waveform.
stenosis. With atrial contraction, an a
wave may appear on the ventricular
waveform at end-diastole (Figure 2-9),
Right Ventricular Waveform which is not a normal finding because
the normal, compliant right ventricle
The normal right ventricular systolic typically absorbs the atrial component
pressure is 20–30 mmHg, and the nor- without a significant pressure rise. There-
mal right ventricular end-diastolic pres- fore, the presence of the a wave on
sure is 0–8 mmHg. Right ventricular a right ventricular waveform usually
22 Textbook of Clinical Hemodynamics

FIGURE 2-8. Example of a normal right ventricular FIGURE 2-10. An example of a normal pulmonary
waveform. artery waveform. Note the dicrotic notch (arrow).

FIGURE 2-9. Right ventricular waveform obtained in a FIGURE 2-11. Respiratory variation in a pulmonary
patient with pulmonary hypertension and right ventricular artery pressure wave.
hypertrophy, demonstrating prominent a waves.

indicates decreased compliance from pul- other arterial waveforms, with a rapid
monary hypertension, right ventricular rise in pressure, systolic peak, a pressure
hypertrophy, or volume overload. decay associated with a well-defined
dicrotic notch from pulmonic valve clo-
sure, and a diastolic trough. Peak sys-
Pulmonary Artery Waveform tolic pressure occurs within the T wave
on the surface ECG.
The normal pulmonary artery systolic The pulmonary artery waveform, like
pressure is 20–30 mmHg, and the nor- other right heart chamber pressure wave-
mal diastolic pressure is 4–12 mmHg forms, is subject to respiratory changes
(Figure 2-10). A systolic pressure differ- (Figure 2-11). Inspiration decreases in-
ence should not exist between the right trathoracic pressure, and expiration
ventricle and the pulmonary artery increases intrathoracic pressure. The pres-
unless there is pulmonary valvular or sure changes associated with respiration
pulmonary artery stenosis. The pulmo- transmitted to the cardiac chambers are
nary artery pressure tracing is similar to often small and of little consequence.
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 23

However, patients on mechanical ventila- Pulmonary Capillary Wedge


tors, with pulmonary disease or morbid Pressure Waveform
obesity or in respiratory distress, may gen-
erate substantial changes in intrathoracic The normal mean pulmonary capillary
pressure, resulting in marked differences wedge pressure, or PCWP, is 2–14 mmHg
in pulmonary artery pressures during the (Figure 2-13). A true PCWP can be
respiratory phases (Figure 2-12). Most measured only in the absence of antero-
experts consider end-expiration to be the grade flow in the pulmonary artery and
proper point to assess pulmonary artery with an end-hole catheter, such that
(and other cardiac chamber) pressures pressure is transmitted through an unin-
because it is at this phase that intratho- terrupted fluid column from the left
racic pressure is closest to zero.3 The pul- atrium, through the pulmonary veins
monary artery end-diastolic pressure is and pulmonary capillary bed to the cath-
sometimes used as an estimation of the eter tip wedged in the pulmonary artery.
left atrial pressure; however, it is highly Under these circumstances, the PCWP is
inaccurate, especially if the pulmonary a reflection of left atrial pressure with
vascular resistance is abnormal.4 a and v waves and x and y descents.
The PCWP tracing exhibits several
important differences from a directly
measured atrial pressure waveform. The
c wave, sometimes identified in an atrial
waveform, is absent because of the
damped nature of the pressure wave.
The v wave typically exceeds the a wave
on the PCWP tracing. Because the pres-
sure wave is transmitted through the
pulmonary capillary bed, a significant
time delay occurs between an electrocar-
diographic event and the onset of the
corresponding pressure wave. The delay
may vary substantially, depending on
the distance the pressure wave travels.

FIGURE 2-12. Marked respiratory variation in pulmo-


nary artery pressure. A, A patient with marked pulmonary FIGURE 2-13. A normal pulmonary capillary wedge
hypertension. B, A patient with morbid obesity. pressure waveform with distinct a and v waves.
24 Textbook of Clinical Hemodynamics

Shorter delays are observed when the to reflect. In general, the mean PCWP is
PCWP is obtained with the catheter tip within a few millimeters of mercury of
in a more distal location. Typically, the the mean left atrial pressure, especially if
peak of the a wave follows the P wave the wedge and pulmonary artery systolic
on the ECG by about 240 msec rather pressures are low.6 High pulmonary
than 80 msec, as seen in the right atrial artery pressure creates difficulty in
tracing.5 Similarly, the peak of the v obtaining a true ‘‘wedge,’’ falsely elevat-
wave occurs after the T wave has already ing the pulmonary capillary wedge pres-
been inscribed on the ECG. The relation sure relative to the left atrial pressure.
between a true left atrial pressure and Obtaining an accurate and high-qual-
the PCWP is shown in Figure 2-14. Note ity PCWP tracing is not always easy or
the time delay between the same physi- possible. An existing uninterrupted fluid
ologic events and the ‘‘damped’’ nature column between the catheter tip and
of the PCWP relative to the left-atrial the left atrium is important. However,
(LA) waveform, with a pressure slightly the lung consists of three distinct physio-
lower than the left atrium it is meant logic pressure zones with a different rela-
tion between the alveolar, pulmonary
artery, and pulmonary venous pressures
(the lung zones of West) (Figure 2-15).7
Zone 1 is typically present in the apex of
the lungs, where the alveolar pressure is
greater than the mean pulmonary artery
and pulmonary venous pressures. Zone
2 is located in the central portion of
the lung, and pulmonary artery pressure
exceeds alveolar pressure, which, in turn,
is greater than the pulmonary venous
pressure. These zones are not acceptable
for estimation of the PCWP because cap-
FIGURE 2-14. Relationship between the left atrial (LA)
and pulmonary capillary wedge pressure (PCWP) wave- illary collapse is present based on these
forms. Note the time delay on the PCWP for the same pressure relations, and a direct column
events and the relatively ‘‘damped’’ appearance of the
PCWP tracing with a slightly lower pressure compared of blood does not exist between the
with the LA pressure. left atrium and the wedged catheter tip.

FIGURE 2-15. Schematic representa-


tion of the three lung zones of West.
Zone1 PA > Pa > Pv PA ¼ alveolar pressure, Pa ¼ pulmo-
nary artery pressure, Pv ¼ pulmonary
venous pressure. A true wedge pressure
can be obtained only when an uninter-
rupted column of blood exists from the
pulmonary vein to the pulmonary artery.
Zone 2 Pa > PA > Pv In zone 1, alveolar pressure is the highest
pressure compressing both vessels; in
zone 2, although pulmonary arterial pres-
sure exceeds pulmonary alveolar pres-
sure, the pulmonary venous system is
Zone 3 Pa > Pv > PA compressed by the higher alveolar pres-
sures. Zone 3 is the only area where alve-
olar pressure is lower than pulmonary
venous pressure and does not interfere
with the column of blood, thus allowing
an accurate wedge pressure.
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 25

Lung zone 3 is represented by the base fatal complication of pulmonary artery


of the lung, where alveolar pressure is catheterization. Over-wedging causes a
lower than both pulmonary arterial and false PCWP measurement without dis-
pulmonary venous pressure, allowing tinct a and v waves and a tracing that
pressure transmission directly from the does not reflect left atrial pressure.
left atrium to the wedged catheter tip. The mean PCWP is approximately
Lung zone 3 is where PCWP accurately 0–5 mmHg lower than the pulmonary
reflects left atrial pressure. Fortunately, artery diastolic pressure, unless there
in most patients in the supine position is increased pulmonary vascular resis-
on a cardiac catheterization table, most tance. Obtaining a suitable and accu-
of the lung is in zone 3. In addition, rate wedge pressure may be difficult or
because most blood flows to that area, impossible in patients with pulmonary
the catheter tip of a balloon flotation hypertension. Accordingly, if it is impor-
catheter usually ends up in zone 3. Situa- tant to measure the left atrial pressure
tions associated with catheter tip loca- accurately, such as during evaluation
tion in a non–zone 3 location include of mitral stenosis, and if the operator
the use of positive end expiratory is unable to confirm the wedge
pressure (PEEP), mechanical ventilation pressure, then a transseptal catheteriza-
(alveolar pressure increased and less of tion with direct measurement of the left
lung is zone 3), and hypovolemia. atrial pressure is necessary. Similar to
Demonstrating that the catheter tip is other right-sided pressure tracings, the
below the level of the left atrium, how- end-expiratory wedge pressure is most
ever, ensures a zone 3 location and representative of the true hemodynamic
greater accuracy.3 status if there is a great deal of respira-
Characteristics of a high-quality PCWP tory variation.
include (1) presence of well-defined a Overall, a good correlation exists be-
and v waves (note that the a wave is tween the pulmonary capillary wedge,
absent in atrial fibrillation and phasic left atrial, and left ventricular end-
waves may not be distinct at low pres- diastolic pressures. The PCWP does not
sures); (2) appropriate fluoroscopic con- correlate with left ventricular end-
firmation with the catheter tip in the diastolic pressures when there is mitral
distal pulmonary artery and no appar- stenosis, severe mitral or aortic regurgi-
ent motion of the catheter with the tation, pulmonary venous obstruction,
balloon inflated; (3) an oxygen satura- marked increase in positive end-
tion obtained from the PCWP position expiratory pressure, left atrial myxoma,
is greater than 90%; and (4) a distinct, marked left ventricular noncompliance,
abrupt rise in mean pressure is observed or non–zone 3 location of the catheter
when the balloon is deflated or the tip.8 In patients with large v waves, the
catheter is withdrawn from the PCWP trough of the x descent is the best predic-
position to the pulmonary artery. Of all tor of the left ventricular end-diastolic
these signs, obtaining an oxygen satura- pressure.9
tion greater than 90% from the catheter Determination of the PCWP in pati-
tip is the most confirmatory of a true ents on a ventilator with PEEP poses a
PCWP. An ‘‘over-wedged’’ pressure occurs common clinical dilemma. Positive end-
when the catheter tip is in a peripheral expiratory pressure increases alveolar
pulmonary artery and the balloon is over- pressure, reducing the proportion of
inflated; this catheter position may lead lung zone 3. In addition, the positive
to pulmonary artery rupture, a potentially pressure is transmitted to the central
26 Textbook of Clinical Hemodynamics

circulation, directly affecting right-sided ventricular ejection. However, identifica-


pressures and leading to an overestima- tion of the left ventricular end-diastolic
tion of the PCWP. The extent to which pressure (LVEDP) can sometimes be diffi-
PEEP increases right-sided chamber pres- cult. A late diastolic pressure rise may
sures is not predictable and depends become incorporated into the left ven-
on such variables as compliance of the tricular upstroke, obscuring the LVEDP
cardiac chamber, chest wall and lung, (Figure 2-17). Again, in the presence of
volume status, and existing filling pres-
sures. The general consensus is that
PEEP less than 10 cm H2O does not sig-
nificantly affect the PCWP. Still, debate
exists on methods to correct the PCWP
when PEEP exceeds 10 cm H2O. The
effect of PEEP on intrathoracic pressure
can be determined by subtracting the
esophageal pressure from the PCWP but
this method is not practical in most coro-
nary care units or cardiac catheterization
laboratories. One suggested method for
correction is based on the observation
that PCWP rises 2–3 cm for every 5 cm
H2O increment in PEEP.8 FIGURE 2-16. An example of a high-fidelity left ventric-
ular pressure waveform. An a wave is present on this
tracing, which is not always seen on left ventricular pres-
sure waves, unless diminished compliance of the left
ventricle is present.
Left Ventricular Waveform

The normal left ventricular systolic pre-


ssure is 90–140 mmHg, and the normal
end-diastolic pressure is 10–16 mmHg.
The left ventricular waveform is charac-
terized by a very rapid upstroke during
ventricular contraction, reaching a peak
systolic pressure, and then the pressure
rapidly decays (Figure 2-16). The pressure
in early diastole is typically very low and
slowly rises during diastole. Abnormal-
ities in ventricular relaxation are apparent
when early diastolic pressure is high
and declines during diastole.10 Similar
to the right ventricular waveform, an a
wave may be seen in the left ventricular
tracing at end-diastole; however, this is
usually abnormal and implies a noncom-
pliant left ventricle. Left ventricular end-
diastolic pressure is defined as the pressure
just after the a wave and before the abrupt FIGURE 2-17. Marked elevation of the LVEDP (arrow) in
rise in systolic pressure coinciding with a patient with heart failure.
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 27

large and prominent a waves, the pres- Central Aortic Pressure Waveform
sure just after the a wave represents the
LVEDP (Figure 2-18). Intrathoracic pres- The normal aortic systolic pressure is
sure changes due to the respiratory phases 90–140 mmHg, and the normal diastolic
can also affect LVEDP, the pressure at pressure is 60–90 mmHg. Central aortic
end-expiration (Figure 2-19). waveforms have a rapid upstroke, a sys-
tolic peak, and a clearly defined dicrotic
notch due to closure of the aortic valve
during pressure decay (Figure 2-20).
The peak systolic pressure equals the
peak left ventricular systolic pressure,
unless there is obstruction within the
left ventricle, at the aortic valve, or
within the proximal aorta. An anacrotic
notch may be apparent during the sys-
tolic pressure rise (Figure 2-21), as a

FIGURE 2-18. Large a wave on left ventricular pressure


wave. When a large a wave is present, the LVEDP is iden-
tified as the pressure just after the a wave and before the
LV systolic pressure rise (arrow).

FIGURE 2-20. An example of a normal, high-fidelity


aortic pressure waveform. Note the dicrotic notch (arrow).

FIGURE 2-21. This waveform demonstrates an example


FIGURE 2-19. Marked respiratory variation on a left of a prominent anacrotic ‘‘notch’’ or ‘‘shoulder’’ (arrow) in
ventricular pressure wave. The LVEDP should be measured a patient with severe aortic regurgitation. An anacrotic
at end-expiration. In this case, the LVEDP is nearly notch may also be observed in patients with severe aortic
50 mmHg. stenosis and indicates turbulence during ejection.
28 Textbook of Clinical Hemodynamics

result of turbulent flow during ejection, peripheral vascular disease, aortic or ilio-
and indicates an abnormality in the aor- femoral obstruction, or tortuosity and
tic valve or proximal aorta. arterial vasoconstriction. Factors asso-
The measured central aortic pressure ciated with diminished reflected waves
is composed of two components: the include vasodilation, hypovolemia, and
pressure wave generated from forward hypotension. The reflected wave is typi-
flow from left ventricular ejection and cally apparent late in the aortic wave-
the summation of pressure waves gener- form due to the time delay from its
ated from ‘‘reflected’’ waves. Reflected generation to its summation with the
waves result because as blood is ejected forward waves.
forward, it meets areas of resistance such The effect of reflected waves is particu-
as branch points or tortuous vessels. larly notable in peripheral arterial wave-
When the pressure wavefront strikes forms (brachial, femoral, and radial)
these areas, additional pressure waves are (Figure 2-22). Peak systolic press-
generated and directed back to the heart. ure exceeds central aortic pressure by
These pressure waves strike the aortic 10–20 mmHg due to peripheral amplifi-
valve, generating additional, forward- cation from reflected waves. The contour
directed, smaller pressure waves. There- of the waveform changes further from
fore, the sampled pressure waveform the aortic valve, with a steeper upstroke,
represents a summation of all of the narrower systolic portion (spiked appear-
forward impulses. ance), and markedly diminished or
This phenomenon is less apparent absent dicrotic notch.
when pressure is sampled closer to the
aortic valve. The effect increases further
from the aortic valve but is usually Measurement of
negligible. Under some circumstances, Simultaneous Pressures in
however, the reflected waves may be Two or More Chambers
of significant dimension. Factors that
increase the effect of reflected waves Cardiac catheterization protocols col-
include heart failure, aortic regurgita- lect simultaneous pressure in two
tion, systemic hypertension, increased or more chambers for the purpose of
aortic stiffness from advanced age or screening for several specific conditions.

FIGURE 2-22. A, A simultaneous central aortic pressure and femoral artery sheath pressure obtained in a patient with
aortic stenosis. Compared to the central aortic pressure, the femoral artery pressure wave exhibits a time delay, peripheral
amplification with higher systolic pressure, and a ‘‘damped’’ appearance with loss of the dicrotic notch. B, A simultaneous
central aortic and radial artery pressure showing the typical ‘‘spiked’’ appearance of a peripheral waveform.
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 29

Simultaneous left and right ventricular


pressures and simultaneous left ventric-
ular and PCWP recordings should be
obtained on all patients who undergo a
complete hemodynamic study that
involves a right and left heart catheteri-
zation. The purpose of these two man-
euvers is to screen for the presence of
occult restrictive/constrictive physiol-
ogy and mitral stenosis, respectively.
Additional simultaneous pressure mea-
surements include the collection of left
ventricular and either central aortic or
FIGURE 2-23. Simultaneous left and right ventricular
femoral arterial pressure when enter- waveforms in a patient with heart failure and pulmonary
taining the diagnoses of aortic stenosis, hypertension, showing the normal relationship between
the two chambers. The systolic pressures rise and
left ventricular outflow tract obstruc- fall together during the respiratory cycle, and diastolic
tion, or coarctation of the aorta, and pressures are more than 5 mmHg apart.
simultaneous right ventricular and pul-
monary artery pressures collected if there these relationships are observed in con-
is pulmonic valve or pulmonary artery strictive pericarditis and restrictive car-
stenosis. Simultaneous left atrial and left diomyopathy. A detailed discussion of
ventricular pressures are performed to these interactions and the hemody-
assess for mitral stenosis when a PCWP namic effects of pericardial and restric-
is not adequate or possible. tive myocardial diseases is the subject
of Chapter 8.
The hemodynamic effect of conduc-
Combination Left tion abnormalities is often reflected in
Ventricular and Right simultaneous right and left ventricular
Ventricular Pressures pressure tracings. Normally, the right
ventricular waveform sits within the
This maneuver is performed to screen confines of the left ventricular wave
for the presence of restrictive or con- (Figure 2-24, A). A right bundle branch
strictive physiology and should be a part block delays right ventricular contrac-
of all complete, hemodynamic evalua- tion relative to left ventricular contrac-
tions. Fairly complex interactions occur tion, resulting in a delay in the right
between the cardiac chambers, the peri- ventricular pressure wave and a shift to
cardium, and the intrathoracic cavity the right (Figure 2-24, B). The opposite
during the respiratory cycle. In general, occurs with a left bundle branch block
in patients without constrictive physiol- (Figure 2-24, C).
ogy, the net effect of these interactions
causes left and right ventricular diastolic Combination Pulmonary
pressures to differ by at least 5 mmHg, Capillary Wedge
with variation during the respiratory (or Left Atrial) and Left
cycle. Peak systolic pressure changes Ventricular Pressure
during inspiration and expiration in
the right and left ventricle parallel each The purpose of this maneuver is to
other (Figure 2-23). Abnormalities in screen for the presence of mitral valve
30 Textbook of Clinical Hemodynamics

A B

C
FIGURE 2-24. Effect of conduction abnormalities on simultaneous right and left ventricular pressure waveforms.
A, Normally, the right ventricular pressure wave sits within the left ventricular pressure contour. B, In the presence of a
right bundle branch block, the right ventricular wave is shifted to the right. Note how a premature ventricular contraction
returns the right ventricular tracing to a more normal appearance. C, A left bundle branch block or intraventricular con-
duction delay interrupts left ventricular contraction relative to the right ventricle, causing the right ventricular waveform
to shift to the left.

stenosis. In addition, simultaneous LV- may be problematic if a large v wave exists,


PCWP is needed to determine the mitral because it may be confused with a diasto-
valve orifice area in patients with known lic gradient (Figure 2-26). However, note
mitral stenosis. Normally, no gradient the location of the v wave on a true left
should exist between PCWP and LVEDP atrial waveform obtained by transseptal
(Figure 2-25). A small gradient may be dis- catheterization (Figure 2-27). The true
cernible only early in diastole. The time position of the v wave as seen on the left
delay associated with the PCWP tracing atrial waveform is during ventricular sys-
causes the a and v waves to appear later tole and the y descent correlates with the
in the left ventricular waveform. This decay in left ventricular pressure. Thus, if
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 31

FIGURE 2-27. This simultaneous left ventricular and


left atrial pressure tracing was obtained in a patient with
significant mitral regurgitation using a transseptal ap-
FIGURE 2-25. Simultaneous left ventricular and PCWP proach to measure left atrial pressure. A prominent v wave
tracings obtained during a routine cardiac catheterization is apparent, but no mitral gradient is present. Note
protocol as a screening test for mitral stenosis. As shown the timing of the v wave on the left atrial pressure tracing
here, no pressure gradient normally exists late in diastole relative to the left ventricular pressure waveform. As
between the two chambers. shown in Figure 2-26, the time delay inherent to PCWP
recordings causes the v wave of a PCWP to appear later
in diastole and may lead to a false diagnosis of a mitral
gradient.

Combination Central Aorta


(or Femoral Artery) and Left
Ventricular Pressure
Simultaneous left ventricular and cen-
tral aortic pressures are recorded in cases
of known or suspected aortic stenosis
as a method of determining the trans-
valvular gradient necessary to estimate
valve area. Often, simultaneous left ven-
tricular and femoral arterial sheath pres-
sures are used for this purpose. However,
discrepancies between central aortic and
FIGURE 2-26. Simultaneous left ventricular and pulmo- femoral arterial sheath pressures are
nary capillary wedge pressure tracings obtained in a commonly observed (see Figure 2-22,
patient with severe mitral regurgitation, demonstrating a
very large v wave. The time delay inherent to the wedge
A). These include peripheral amplifica-
pressure waveform suggests the presence of a mitral gra- tion resulting in a higher sheath than
dient during diastole. Phase shifting the wedge tracing central aortic pressure, and peripheral
to the left corrects this false gradient.
vascular disease, catheter thrombosis,
there is a large v wave on the PCWP, or kinking of the sheath resulting in
the time delay can be corrected by higher central aortic than sheath pres-
shifting the PCWP to the left, allowing sure. Additional details regarding this
proper alignment with the left ventricular assessment will be provided in a later
waveform. chapter.
32 Textbook of Clinical Hemodynamics

Common Errors and Artifacts kink, or blood clot anywhere along the
line from the catheter tip to the sensing
Most errors in the collection and inter- membrane. Similarly, a loose connec-
pretation of hemodynamic data are tion or stopcock can cause inaccuracy.
related to one of the reasons listed in Transducers may be defective or poorly
Table 2-2. Erroneous data due to calibrated, which should be considered
an improper zero level or unbalanced when there is difficulty maintaining
transducer might lead to patient mis- transducer balance or if the data obtained
management. With the commonly used appear inconsistent. The frequency res-
fluid-filled systems, artifacts and errors ponse of most clinically used systems
may be caused by a small air bubble, may be exceeded in the presence of
marked tachycardia, preventing the col-
lection of high-fidelity tracings. Mech-
Common Sources of Error or anical ventilators and extreme changes
TABLE 2-2. Inaccuracy in Hemodynamic in intrathoracic pressure can make inter-
Assessment pretation difficult. Finally, several arti-
1. Improper zero level or transducer balancing facts frequently thwart an unsuspecting
2. Air bubbles, clots, or kinks in the system clinician.
3. Loose connections
4. Defective transducers
Probably the most commonly observed
5. Tachycardia and loss of frequency response artifacts relate to an improper degree
6. Mechanical ventilators and excessive of damping. The over-damped tracing
intrathoracic pressure changes
7. Artifacts: (Figure 2-28) indicates the presence of
Over-damping excessive friction absorbing the force of
Overshoot or ‘‘ring’’ artifact
Catheter whip or ‘‘fling’’ the pressure wave somewhere in the line
Catheter entrapment from the catheter tip to the transducer.
Hybrid waveforms
The tracing lacks proper fidelity and

FIGURE 2-28. A, A damped aortic pressure waveform due to the presence of an air bubble in the catheter. This tracing
has poor fidelity, a smooth appearance, and lacks a dicrotic notch. B, Following vigorous flushing and removal of the
offending air bubble, a high-fidelity tracing is apparent with return of a dicrotic notch.
Chapter 2—Normal Waveforms, Artifacts, and Pitfalls 33

appears smooth and rounded because pressure during the systolic pressure rise
of loss of frequency response. This will with similar, negatively directed waves
result in loss of data and will falsely lower overshooting the true pressure contour
peak pressures. Typically, the dicrotic during the downstroke. This artifact
notch on the aortic or pulmonary artery may lead to overestimation of the peak
waveforms is absent, and the right atrial
or PCWP waveforms will lack distinct a
and v waves. The diastolic pressure tracing
on an over-damped ventricular waveform
will be smooth, preventing recognition of
an a wave and making determination of
end-diastolic pressure difficult. This arti-
fact is usually caused by sloppy operators
or air bubbles in the tubing, catheter, or
transducer, or a loose connection any-
where in the system. The operator should
also be aware that a thrombus or kink in
the catheter may also cause this artifact
as well as the presence of high viscosity
radiographic contrast agents in the cathe-
ter. For the latter reason, hemodynamic
data should always be collected with
saline, and not contrast, in the catheter.
Under-damping causes overshoot or FIGURE 2-29. ‘‘Ring’’ artifact is a very common artifact,
usually due to the presence of a small bubble somewhere
ring artifact (Figures 2-29 and 2-30). This in the system between the catheter tip and the transducer.
artifact typically appears as one or more The small bubble oscillates, causing the high-frequency,
spiked artifact shown here (arrow). This can usually be
narrow ‘‘spikes’’ overshooting the true corrected by flushing the catheter or introducing a filter.

A B
FIGURE 2-30. A commonly seen ‘‘overshoot’’ artifact in a right ventricular pressure tracing. A, The overshoot portion
(arrow) may provide the false impression that (B) the right ventricular pressure exceeds pulmonary artery pressure, lead-
ing to an erroneous diagnosis of pulmonary artery or pulmonic valve stenosis.
Exploring the Variety of Random
Documents with Different Content
the contest really lay; and again the duke proved victorious. The
conqueror made his “joyous entry” into Le Mans, and sent for the
little Margaret to be kept under his own protection until her marriage
could take place. But before the wedding-day arrived she lay in her
grave at Fécamp; Walter and Biota had already come to a
mysterious end; and the one gallant Cenomannian who held out
when Walter and all else had yielded—Geoffrey of Mayenne—was at
length compelled to surrender.[505] Thenceforth William ruled Maine
as its Conqueror, and as long as he lived, save for one brief moment,
the homage due to Anjou was heard of no more.

[502] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p. 532. The


story is somewhat suspicious, because Orderic tells it not in its
proper place, but in a sort of summary of Cenomannian history,
introductory to the war of 1073; so that it looks very much like a
confused anticipation of the treaty of Blanchelande (see below, p.
223). Still there is nothing intrinsically impossible in it, and I do
not feel justified in rejecting it without further evidence.

[503] Will. Poitiers (Duchesne, Hist. Norm. Scriptt.), p. 190.

[504] On the pedigree of the house of Maine see note D at end


of chapter.

[505] Will. Poitiers (Duchesne, Hist. Norm. Scriptt.), pp. 190,


191. Will. Jumièges, l. vii. c. 27 (ib. p. 283). Ord. Vit. (ibid.) pp.
487, 488.

The rapid decline of the Angevin power after Geoffrey Martel’s


death was due partly to the reaction which often follows upon a
sudden rise, partly to the exceptional greatness of the rival with
whom the Angevin count had to deal in the person of William the
Conqueror. But behind and beyond these two causes lay a third
more fatal than either. The house of Anjou was divided against itself.
From the hour of Martel’s death, a bitter dispute over his
testamentary dispositions had been going on between his nephews.
To young Fulk it seemed an unpardonable wrong that he was left
without provision—for even Saintonge, as we have seen, had now
slipped from his grasp—while his elder brother was in full possession
not only of the paternal county of Gâtinais but also of their uncle’s
heritage. In later days Fulk went so far as to declare that his uncle
had intended to make him sole heir, to the complete exclusion of
Geoffrey the Bearded.[506] Fulk is in one aspect a very interesting
person. Almost the sole authority which we possess for the history of
the early Angevin counts is a fragment written in his name. If it be
indeed his work—and criticism has as yet failed to establish any
other conclusion—Fulk Rechin is not merely the earliest historian of
Anjou; he is well-nigh the first lay historian of the Middle Ages.[507]
But in every other point of view he deserves nothing but aversion
and contempt. His very surname tells its own tale; in one of the most
quarrelsome families known to history, he was pre-eminently
distinguished as “the Quarreller.”[508] With the turbulence, the greed,
the wilfulness of his race he had also their craft and subtlety, their
plausible, insinuating, serpent-like cleverness; but he lacked the
boldness of conception, the breadth of view and loftiness of aim, the
unflinching perseverance, the ungrudging as well as unscrupulous
devotion to a great and distant end, which lifted their subtlety into
statesmanship and their cleverness into genius. The same qualities
in him degenerated into mere artfulness and low cunning, and were
used simply to meet his own personal needs and desires of the
moment, not to work out any far-reaching train of policy. He is the
only one of the whole line of Angevin counts, till we reach the last
and worst of all, whose ruling passion seems to have been not
ambition but self-indulgence. Every former count of Anjou, from Fulk
the Red to Geoffrey Martel, had toiled and striven, and sinned upon
occasion, quite as much for his heirs as for himself: Fulk Rechin
toiled and sinned for himself alone. All the thoroughness which they
threw into the pursuit of their house’s greatness he threw simply into
the pursuit of his own selfish desires. Had Geoffrey the Bearded
possessed the highest capacities, he could have done little for his
own or his country’s advancement while his brother’s restless
intrigues were sowing strife and discontent among the Angevin
baronage and turning the whole land into a hotbed of treason.[509]
Geoffrey’s cause was however damaged by his own imprudence. An
act of violent injustice to the abbey of Marmoutier brought him under
the ban of the Church;[510] and from that moment his ruin became
certain. From within and without, troubles crowded upon the
Marchland and its unhappy count. The comet which scared all
Europe in 1066 was the herald of evil days to Anjou as well as to the
land with which she was one day to be linked so closely. In that very
year a Breton invasion was only checked by the sudden death of
Duke Conan just after he had received the surrender of
Châteaugonthier.[511] Next spring, on the first Sunday in Lent,
Saumur was betrayed by its garrison to Fulk Rechin;[512] on the
Wednesday before Easter he was treacherously admitted into
Angers, and Geoffrey fell with his capital into the clutches of his
brother.[513] The citizens next day rose in a body and slew the chief
traitors;[514] the disloyalty of Saumur was punished by the duke of
Aquitaine, who profited by the distracted state of Anjou to cross the
border and fire the town;[515] while the remonstrances of Pope
Alexander II. soon compelled Fulk to release his brother.[516] Next
year, however, Geoffrey was again taken prisoner while besieging
Fulk’s castle of Brissac.[517] This time the king of France, alarmed no
doubt by the revelation of such a temper among his vassals, took up
arms for Geoffrey’s restoration, and he was joined by Count Stephen
of Blois, the son of Theobald from whom Geoffrey Martel had won
Tours. Fulk bought off both his assailants. Stephen, who was now
governing the territories of Blois as regent for his aged father, was
pacified by receiving Fulk’s homage for Touraine; the king was
bribed more unblushingly still, by the cession of what was more
undeniably Geoffrey’s lawful property than any part of the Angevin
dominions—his paternal heritage of the Gâtinais.[518] It thus became
Philip’s interest as well as Fulk’s to keep Geoffrey in prison. For the
next twenty-eight years he lay in a dungeon at Chinon,[519] and Fulk
ruled Anjou in his stead.

[506] See note B at end of chapter.


[507] “It needs some self-sacrifice to give up the only lay
historian whom we have come across since the days of our own
Æthelweard.” Freeman, Norm. Conq., 3d ed. vol. ii. p. 638.

[508] This seems to be the meaning of “Rechin.”

[509] Gesta Cons. (Marchegay, Comtes), pp. 138, 139.

[510] Gesta Cons. (Marchegay, Comtes), pp. 134–137. See


also Rer. Gall. Scriptt., vol. xii. p. 664, note.

[511] Will. Jumièges, l. vii. c. 33 (Duchesne, Hist. Norm.


Scriptt., p. 286). Chron. Brioc. and Chron. Britann. a. 1066
(Morice, Hist. Bret., preuves, vol. i. cols. 36, 102). Chronn. Rain.
Andeg., S. Serg. and Vindoc. a. 1067 (Marchegay, Eglises, pp.
12, 137, 168)—which, however, means 1066, as all these
chronicles place both the comet and the conquest in the same
year.

[512] Chron. S. Maxent. a. 1067 (Marchegay, Eglises, pp. 403,


404). This was February 25 (ibid.).

[513] Chronn. Rain. Andeg., S. Albin., S. Serg., Vindoc. a.


1067 (ib. pp. 12, 25, 137, 138, 168). Gesta Cons. (Marchegay,
Comtes, pp. 138, 139), antedated by a year.

[514] Chronn. Rain. Andeg., S. Albin. (as above); S. Serg. (ib.


p. 138); Vindoc. (ib. pp. 168, 169).

[515] Chron. S. Maxent. a. 1067 (ib. p. 404).

[516] Fulk Rechin (Marchegay, Comtes), p. 379.

[517] Ib. pp. 379, 380. Chronn. Rain. Andeg., S. Albin., S.


Serg. and Vindoc. a. 1068 (Marchegay, Eglises, pp. 12, 26, 138,
169).

[518] Gesta Cons. (Marchegay, Comtes), p. 139. Chron. Turon.


Magn. a. 1067 (Salmon, Chron. de Touraine, p. 125)—a date
which must be at least a year too early.

[519] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), pp. 723, 818.
He makes it thirty years, but the dates are undoubtedly 1068–
1096.
That time was a time of shame and misery such as the Marchland
had never yet seen. Eight years of civil war had fostered among the
barons of Anjou and Touraine a spirit of turbulence and lawlessness
which Fulk, whose own intrigues had sown the first seeds of the
mischief, was powerless to control. Throughout the whole of his
reign, all southern Touraine was kept in confusion by a feud among
the landowners at Amboise;[520] and it can hardly have been the
only one of its kind under a ruler who, instead of putting it down with
a strong hand, only aggravated it by his undignified and violent
intermeddling. Nor were his foreign relations better regulated than
his home policy. For a moment, in 1073, an opportunity seemed to
present itself of regaining the lost Angevin overlordship over Maine.
Ten years of Angevin rule had failed to crush out the love of
independence among the Cenomannian people; ten years of
Norman rule had just as little effect. While their conqueror was
busied with the settlement of his later and greater conquest beyond
sea, the patriots of Maine seized a favourable moment to throw off
the Norman yoke. Hugh of Este or of Liguria, a son of Herbert Wake-
the-dog’s eldest daughter Gersendis, was received as count under
the guardianship of his mother and Geoffrey of Mayenne. But
Geoffrey, who in the hour of adversity ten years before had seemed
little short of a hero, yielded to the temptations of power; and his
tyranny drove the Cenomannians to fall back upon the traditions of
their old municipal freedom and “make a commune”—in other words,
to set up a civic commonwealth such as those which were one day
to be the glory of the more distant Cenomannian land on the other
side of the Alps. At Le Mans, however, the experiment was
premature. It failed through the treachery of Geoffrey of Mayenne;
and the citizens, in the extremity of despair, called upon Fulk of
Anjou to save them at once from Geoffrey and from William. Fulk
readily helped them to dislodge Geoffrey from the citadel of Le
Mans;[521] but as soon as William appeared in Maine with a great
army from over sea Fulk, like his uncle, vanished. Only when the
conqueror had “won back the land of Maine”[522] and returned in
triumph to Normandy did Fulk venture to attack La Flèche, a castle
on the right bank of the Loir, close to the Angevin border, and held by
John, husband of Herbert Wake-dog’s youngest daughter Paula.[523]
At John’s request William sent a picked band of Norman troops to
reinforce the garrison of La Flèche; Fulk at once collected all his
forces and persuaded Hoel duke of Britanny to bring a large Breton
host to help him in besieging the place. A war begun on such a scale
as this might be nominally an attack on John, but it was practically
an attack on William. He took it as such, and again calling together
his forces, Normans and English, led them down to the relief of La
Flèche. Instead, however, of marching straight to the spot, he
crossed the Loir higher up and swept round to the southward
through the territories of Anjou, thus putting the river between
himself and his enemies. The movement naturally drew Fulk back
across the river to defend his own land against the Norman invader.
[524] The two armies drew up facing each other on a wide moor or
heath stretching along the left bank of the Loir between La Flèche
and Le Lude, and overgrown with white reindeer-moss, whence it
took the name of Blanchelande. No battle however took place; some
clergy who were happily at hand stepped in as mediators, and after a
long negotiation peace was arranged. The count of Anjou again
granted the investiture of Maine to Robert of Normandy, and, like his
predecessor, received the young man’s homage to himself as
overlord.[525] Like the treaty of Alençon, the treaty of Blanchelande
was a mere formal compromise; William kept it a dead letter by
steadily refusing to make over Maine to his son, and holding it as
before by the right of his own good sword. A few years later Fulk
succeeded in accomplishing his vengeance upon John of La Flèche
by taking and burning his castle;[526] but the expedition seems to
have been a mere border-raid, and so long as William lived neither
native patriotism nor Angevin meddlesomeness ventured again to
question his supremacy over Maine.

[520] Gesta Amb. Domin. (Marchegay, Comtes), p. 175 et seq.

[521] Acta Pontif. Cenoman. c. 33 (Mabillon, Vet. Anal., p.


308).

[522] Eng. Chron. a. 1074.


[523] See note D at end of chapter.

[524] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p. 533. See


note E at end of chapter.

[525] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p. 533.

[526] Chron. S. Albin. a. 1081 (Marchegay, Eglises, p. 26). See


note E at end of chapter.

But on his death in 1087 the advantage really given to Anjou by


the treaties of Alençon and Blanchelande at last became apparent.
From the moment when Robert came into actual possession of the
fief with which he had been twice invested by an Angevin count, the
Angevin overlordship could no longer be denied or evaded. The
action of the Cenomannians forced their new ruler to throw himself
upon Fulk’s support. Their unquenchable love of freedom caught at
the first ray of hope offered them by Robert’s difficulties in his
Norman duchy and quarrels with his brother the king of England, and
their attitude grew so alarming that in 1089 Robert, lying sick at
Rouen, sent for the count of Anjou and in a personal interview
besought him to use his influence in preventing their threatened
revolt. Fulk consented, on condition that, as the price of his good
offices, Robert should obtain for him the hand of a beautiful Norman
lady, Bertrada of Montfort.[527] Fulk’s domestic life was as shameless
as his public career. He had already one wife dead and two living;
Hermengard of Bourbon, whom he had married in 1070[528] and who
was the mother of his heir,[529] had been abandoned in 1075 without
even the formality of a divorce for Arengard of Châtel-Aillon;[530] and
Arengard was now set aside in her turn to make way for Bertrada.
[531] These scandals had already brought Fulk under a Papal

sentence of excommunication;[532] he met with a further punishment


at the hands of his new bride. Bertrada used him simply as a
stepping-stone to higher advancement; on Whitsun-Eve 1093 she
eloped with King Philip of France.[533]
[527] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p. 681.

[528] Chron. Turon. Magn. a. 1070.

[529] Gesta Cons. (Marchegay, Comtes), p. 140.

[530] According to a charter in Marchegay, Documents inédits


sur l’Anjou, p. 96, Fulk married Arengard on Saturday the feast of
S. Agnes (January 21) 1075—i.e. what we call 1076, as the year
was usually reckoned in Gaul from Easter to Easter; see editor’s
note 4, as above. The Art de vérifier les dates, however (vol. xiii.
p. 62), refers to a document in Dom Huyne’s collection where the
marriage is dated 1087.

[531] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p. 681, seems


to date Bertrada’s marriage about 1089. The Chron. Turon.
Magn. puts it in 1091 (Salmon, Chron. Touraine, vol. i. p. 128);
but a charter in Marchegay, Archives d’Anjou, vol. i. p. 365,
shows that it had already taken place in April 1090.

[532] Gregor. VII. Epp., l. ix. ep. 22. Fulk’s violence to the
archbishop of Tours had also something to do with his
excommunication; see ib. ep. 23; Chron. Turon. Magn. a. 1081
(Salmon, Chron. Touraine, vol. i. p. 126), and Narratio
Controversiæ in Rer. Gall. Scriptt., vol. xii. p. 459. So too had his
imprisonment of his brother; Rer. Gall. Scriptt. as above, p. 664,
note.

[533] Chron. Turon. Magn. a. 1093 (as above, p. 128).

By that time Maine was again in revolt. The leader of the rising
was young Elias of La Flèche, a son of John and Paula; but his place
was soon taken by the veteran Geoffrey of Mayenne, whose
treasons seem to have been forgiven and forgotten, and who now
once more installed Hugh of Este as count at Le Mans. Hugh proved
however utterly unfit for his honourable but dangerous position, and
gladly sold his claims to his cousin Elias.[534] For nearly six years the
Cenomannians were free to rejoice in a ruler of their own blood and
their own spirit. We must go to the historian of his enemies if we
would hear his praises sung;[535] his own people had no need to
praise him in words; for them he was simply the incarnation of
Cenomannian freedom; his bright, warm-hearted, impulsive nature
spoke for itself. The strength as well as the charm of his character
lay in its perfect sincerity; its faults were as undisguised as its
virtues. In the gloomy tale of public wrong and private vice which
makes up the history of the time—the time of Fulk Rechin, Philip I.
and William Rufus—the only figure which shines out bright against
the darkness, except the figure of S. Anselm himself, is that of Count
Elias of Maine.

[534] Acta Pontif. Cenoman. c. 34 (Mabillon, Vet. Anal.), pp.


310–312. Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), pp. 683, 684.

[535] Ord. Vit. (as above), pp. 768, 769.

During these years Anjou interfered with him as little as


Normandy; Fulk was overwhelmed with domestic and ecclesiastical
troubles. His excommunication was at length removed in 1094;[536]
two years later Pope Urban II., on his way to preach the Crusade in
western Gaul, was received by the count at Angers and consecrated
the abbey church of S. Nicolas, now at length brought to completion.
[537] From Angers Urban passed to Tours and Le Mans; and among
the many hearts stirred by his call to take the cross there can have
been few more earnest than that of Elias of Maine. Robert of
Normandy was already gone, leaving his dominions pledged to his
brother the king of England. Elias prepared to follow him; but when
his request to William Rufus for the protection due to a crusader’s
lands during his absence was met by a declaration of the Red King’s
resolve to regain all the territories which had been held by his father,
the count of Maine saw that he must fight out his crusade not in Holy
Land but at home. The struggle had scarcely begun when he was
taken prisoner by Robert of Bellême, and sent in chains to the king
at Rouen.[538] The people of Maine, whose political existence
seemed bound up in their count, were utterly crushed by his loss.
But there was another enemy to be faced. Aremburg, the only child
of Elias, was betrothed to Fulk Rechin’s eldest son, Geoffrey,[539]
whose youthful valour had won him the surname of “Martel the
Second;” Geoffrey hurried to save the heritage of his bride, and Fulk
was no less eager to seize the opportunity of asserting once more
his rights to the overlordship of Maine.[540] The Cenomannians
gladly welcomed the only help that was offered them; and while
Geoffrey reinforced the garrison of Le Mans, Fulk tried to effect a
diversion on the border.[541] But meanwhile Elias had guessed his
design, and frustrated it by making terms with the Norman.[542] If
Maine must needs bow to a foreign yoke, even William Rufus was at
least a better master than Fulk Rechin. To William, therefore, Elias
surrendered his county as the price of his own release;[543] and to
William he offered his services with the trustful frankness of a heart
to which malice was unknown. The offer was refused. Then, from its
very ashes, the spirit of Cenomannian freedom rose up once more,
and for the second time Elias hurled his defiance at the Red King. An
Angevin count in William’s place would probably have flung the bold
speaker straight back into the dungeon whence he had come; the
haughty chivalry of the Norman only bade him begone and do his
worst.[544] In the spring Elias fought his way back to Le Mans, where
the people welcomed him with clamorous delight; William’s
unexpected approach, however, soon compelled him to withdraw;
[545] and Maine had to wait two more years for her deliverance. It
came with the news of the Red King’s death in August 1100. Robert
of Normandy was too indolent, Henry of England too wise, to answer
the appeal for succour made to each in turn by the Norman garrison
of Le Mans; Elias received their submission and sent them home in
peace;[546] and thenceforth the foreign oppressor trod the soil of
Maine no more. When the final struggle for Normandy broke out
between Robert and Henry, Elias, with characteristic good sense,
commended himself to the one overlord whom he saw to be worthy
of his homage.[547] Henry was wise enough loyally to accept the
service and the friendship which Rufus had scorned; and he proved
its value on the field of Tinchebray, where Elias and his
Cenomannians decided the battle in his favour, and thus made him
master of Normandy. On the other hand, the dread of Angevin
tyranny had changed into a glad anticipation of peaceful and equal
union. The long battle of Cenomannian freedom, so often baffled and
so often renewed, was won at last. When next a duke of Normandy
disputed the possession of Maine with a count of Anjou, he disputed
it not with a rival oppressor but with the husband of its countess, the
lawful heir of Elias; and the triumph of Cenomannia received its
fitting crown when Henry’s daughter wedded Aremburg’s son in the
minster of S. Julian at Le Mans.

[536] Letter of the legate, Archbishop Hugh of Lyons, dated S.


Florence of Saumur, S. John Baptist’s day, 1094; Gallia
Christiana, vol. iv., instrum. cols. 10, 11.

[537] Chronn. Rain. Andeg., S. Albin., S. Serg., a. 1095


(Marchegay, Eglises, pp. 14, 27, 140); Chron. S. Maxent. a. 1096
(ib. p. 411). This last is the right year; see the itinerary of Pope
Urban in Gaul, in Rer. Gall. Scriptt., vol. xii. pp. 3 note m, and 65
note d.

[538] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), pp. 769–771.


Acta Pontif. Cenoman. c. 35 (Mabillon, Vet. Anal., p. 313). The
exact date of the capture is April 20, 1098; Chron. S. Albin. ad
ann. (Marchegay, Eglises, p. 28).

[539] Acta Pontif. Cenoman. c. 35 (Mabillon, Vet. Anal., p.


313). Gesta Cons. (Marchegay, Comtes), p. 142.

[540] “Quia capitalis dominus erat.” Ord. Vit. (Duchesne, Hist.


Norm. Scriptt.), p. 772.

[541] Ibid. Acta Pontif. Cenoman., as above.

[542] Acta Pontif. Cenoman. (as above), p. 314.

[543] Ibid. Ord. Vit., as above.

[544] Ord. Vit. (as above), p. 773.

[545] Ib. pp. 774, 775. Acta Pontif. Cenoman., as above.

[546] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), pp. 784, 785.

[547] Ib. p. 822.


The union of Anjou and Maine did not, however, come to pass
exactly as it had been first planned; Aremburg became the wife of an
Angevin count, but he was not Geoffrey Martel the Second. That
marriage, long deferred by reason of the bride’s youth, was
frustrated in the end by the death of the bridegroom. His life had
been far from an easy one. Fulk, prematurely worn out by a life of
vice, had for some years past made over the cares of government to
Geoffrey.[548] Father and son agreed as ill as their namesakes in a
past generation; but this time the fault was not on the young man’s
side. Geoffrey, while spending all his energies in doing his father’s
work, saw himself supplanted in that father’s affection by his little
half-brother, Bertrada’s child. He found a friend in his unhappy uncle,
Geoffrey the Bearded, whose reason had been almost destroyed by
half a lifetime of captivity; and a touching story relates how the
imprisoned count in a lucid interval expressed his admiration for his
nephew’s character, and voluntarily renounced in his favour the
rights which he still persisted in maintaining against Fulk.[549] On the
strength of this renunciation Geoffrey Martel, backed by Pope Urban,
at length extorted his father’s consent to the liberation of the captive.
It was, however, too late to be of much avail; reason and health were
both alike gone, and all that the victim gained by his nephew’s care
was that, when he died shortly after, he at least died a free man.[550]
His bequest availed as little to Geoffrey Martel; in 1103, Fulk openly
announced his intention of disinheriting his valiant son in favour of
Bertrada’s child. A brief struggle, in which Fulk was backed by the
duke of Aquitaine and Geoffrey by Elias, ended in Fulk’s abdication.
For three years Geoffrey ruled well and prosperously,[551] till in May
1106, as he was besieging a rebellious vassal in the castle of Candé
on the Loire, he was struck by a poisoned arrow and died next
morning.[552] The bitter regrets of his people, as they laid him to
sleep beside his great-uncle in the church of S. Nicolas at Angers,
[553] were intensified by a horrible suspicion that his death had been

contrived by Bertrada, and that Fulk himself condoned her crime.[554]


It is doubtful whether her child, who now had to take his brother’s
place, had even grown up among his own people; she had perhaps
carried her baby with her, or persuaded the weak count to let her
have him and bring him up at court; there, at any rate, he was at the
time of Geoffrey’s death. Philip granted him the investiture of Anjou
in Geoffrey’s stead, and commissioned Duke William of Aquitaine,
who happened to be at court, to escort him safe home to his father.
The Poitevin, however, conveyed him away into his own territories,
and there put him in prison. Philip’s threats, Bertrada’s persuasions,
alike proved unavailing, till the boy’s own father purchased his
release by giving up some border-towns to Poitou, and after a year’s
captivity young Fulk at last came home.[555] Two years later, on April
14, 1109, he was left sole count of Anjou by the death of Fulk
Rechin.[556]

[548] Chron. Turon. Magn. a. 1098 (Salmon, Chron. Touraine,


p. 130).

[549] Gesta Cons. (Marchegay, Comtes), p. 141.

[550] Ibid. Chron. Turon. Magn. a. 1098 (Salmon, Chron.


Touraine, p. 128). Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p.
723.

[551] Ord. Vit. (as above), p. 818. Chron. S. Albin. a. 1103–


1105 (Marchegay, Eglises, p. 30).

[552] Ord. Vit. as above. Chronn. Rain. Andeg., S. Albin., S.


Serg., Vindoc., S. Flor. Salm., S. Maxent., a. 1106 (Marchegay,
Eglises, pp. 15, 16, 30, 142, 171, 190, 423). The three first-
named chronicles give the day as May 19, the Chron. S. Maxent.
makes it May 26, and according to M. Marchegay’s note (as
above, p. 171) the obituary of S. Maurice makes it June 1. This,
however, might be owing to an accidental omission of the “xiv.”
(or “vii.”) before Kal. Junii. The Gesta Cons. (Marchegay,
Comtes), p. 142, places the death a year later.

[553] Ord. Vit. and Gesta Cons. as above.

[554] Gesta Cons. as above. Chron. Turon. Magn. a. 1108


(Salmon, Chron. Touraine, p. 130). See also a quotation from Le
Pelletier’s Epitome S. Nicolai, in Rer. Gall. Scriptt., vol. xii. p.
486, note.
[555] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p. 818. Will.
Tyr., l. xiv. c. 1, has a different version, which does not look
authentic.

[556] Chron. Rain. Andeg., S. Albin., Vindoc., S. Flor. Salm. ad


ann. (Marchegay, Eglises, pp. 16, 31, 172, 190). The Chronn. S.
Serg. and S. Maxent. (ib. pp. 143, 424), date it 1108.

“Ill he began; worse he lived; worst of all he ended.”[557] Such is


the verdict of a later Angevin historian upon the man whom we
should have been glad to respect as the father of Angevin history.
Fulk Rechin’s utter worthlessness had well-nigh undone the work of
Geoffrey Martel and Fulk the Black; amid the wreck of the Angevin
power in his hands, the only result of their labours which seemed still
to remain was the mere territorial advantage involved in the
possession of Touraine. Politically, Anjou had sunk far below the
position which she had held in the Black Count’s earliest days; she
had not merely ceased to be a match for the greatest princes of the
realm, she had ceased to be a power in the realm at all. The title of
count of Anjou, for nearly a hundred years a very synonym of energy
and progress, had become identified with weakness and disgrace.
The black cloud of ruin seemed to be settling down over the
marchland, only waiting its appointed time to burst and pour upon
her its torrent of destruction. It proved to be only the dark hour before
the dawn of the brightest day that Anjou had seen since her great
Count Fulk was laid in his grave at Beaulieu—perhaps even since
her good Count Fulk was laid in his grave at Tours.

[557] Hist. Abbr. Com. Andeg. (Marchegay, Comtes), p. 360.

Nearly nine months before the death of Fulk Rechin, Louis VI. had
succeeded his father Philip as king of France.[558] His accession
marks an era in the growth of the French monarchy. It is a turning-
point in the struggle of the feudataries with the Crown, or rather with
each other for control over the Crown, which lay at the root of the
rivalry between Anjou and Blois, and which makes up almost the
whole history of the first three generations of the kingly house
founded by Hugh Capet. The royal authority was a mere name; but
that name was still the centre round which the whole complicated
system of French feudalism revolved; it was the one point of
cohesion among the various and ill-assorted members which made
up the realm of France, in the wider sense which that word was now
beginning to bear. The duke or count of almost any one of the great
fiefs—Normandy, Flanders, Burgundy, Aquitaine—was far more
really powerful and independent than the king, who was nominally
the lord paramount of them all, but practically the tool of each in turn.
In this seemingly ignominious position of the Crown there was,
however, an element of hidden strength which in the end enabled it
to swallow up and outlive all its rivals. The end was as yet far distant;
but the first step towards it was taken when Louis the Fat was
crowned at Reims in August 1109. At the age of thirty-two he
ascended the throne with a fixed determination to secure such an
absolute authority within the immediate domains of the Crown as
should enable him to become the master instead of the servant of
his feudataries.

[558] Hist. Franc. Fragm. (Rer. Gall. Scriptt., vol. xii.), p. 7.

This policy led almost of necessity to a conflict with King Henry of


England, who had now become master of Normandy by his victory at
Tinchebray. Louis appears never to have received Henry’s homage
for the duchy;[559] and it may have been to avoid the necessity of
performing this act of subordination that Henry, as it seems,
refrained from formally assuming the ducal title, at least so long as
his captive brother lived.[560] Whatever may have been his motive,
the fact aptly typifies his political position. Alike in French and
English eyes, he was a king of England ruling Normandy as a
dependency of the English Crown. Such a personage was far more
obnoxious to Louis and his projects than a mere duke of the
Normans, or even a duke of the Normans ruling England as a
dependency of the Norman duchy. On the other hand, Henry, in the
new position given him by his conquest, had every reason to look
with jealousy and suspicion upon the growing power of France. The
uncertain relations between the two kings therefore soon took an
openly hostile turn. In 1110 a quarrel arose between them
concerning the ownership of the great border-fortress of Gisors.
They met near the spot, each at the head of an army; but they parted
again after wasting a day in fruitless recriminations and empty
challenges.[561] Their jealousy was quickened by a dispute, also
connected with the possession of a castle, between Louis and
Henry’s nephew Theobald count of Blois.[562] Uncle and nephew
made common cause against their common enemy; but the strife
had scarcely begun when a further complication destined to be of far
weightier consequence, if not to France at least to England, arose
out of the position and policy of the young count of Anjou.

[559] See Freeman, Norm. Conq., vol. v. p. 193.

[560] Freeman, Norm. Conq., vol. v. p. 180 and note 2.

[561] Suger, Vita Ludov., c. 15 (Rer. Gall. Scriptt., vol. xii. pp.
27, 28).

[562] Ib. c. 18 (pp. 35, 36).

The accession of Fulk V., no less than that of Louis VI., began a
new era for his country. The two princes were in some respects not
unlike each other: each stands out in marked contrast to his
predecessor, and in Fulk’s case the contrast is even more striking
than in that of Louis, for if little good was to be expected of the son of
Philip I., there might well be even less hope of the child of Fulk
Rechin and Bertrada. As a ruler and as a man, however, young Fulk
turned utterly aside from the evil ways of both his parents.[563] Yet he
was an Angevin of the Angevins; physically, he had the ruddy
complexion inherited from the first of his race and name;[564] while in
his restless, adventurous temper, at once impetuous and wary,
daring and discreet, he shows a strong likeness to his great-
grandfather Fulk the Black. But the old fiery spirit breaks out in Fulk
V. only as if to remind us that it is still there, to shew that the demon-
blood of Anjou still flows in his veins, hot as ever indeed, but kept
under subjection to higher influences; the sense of right that only
woke now and then to torture the conscience of the Black Count
seems to be the guiding principle of his great-grandson’s life. The
evil influences which must have surrounded his boyhood, whether it
had been passed in his father’s house, or, as seems more probable,
in the court of Philip and Bertrada, seem, instead of developing the
worse tendencies of his nature, only to have brought out the better
ones into more active working by sheer force of opposition.
Politically, however, there can be no doubt that the peculiar
circumstances of his early life led to important results, by reviving
and strengthening the old ties between Anjou and the Crown which
had somewhat slackened in Fulk Rechin’s days. The most trusted
counsellor of the new king, the devoted supporter and not
unfrequently the instigator of his schemes of reform or of aggression,
was Almeric of Montfort, the brother of Bertrada. She herself, after
persecuting Louis by every means in her power so long as his father
lived, changed her policy as soon as he mounted the throne and
became as useful an ally as she had been a dangerous enemy.
Almeric’s influence, won by his own talents, seems to have been
almost all-powerful with the king; over the count of Anjou, far
younger and utterly inexperienced, natural ties had given a yet more
complete ascendency to him and his sister, Fulk’s own mother. Their
policy was to pledge Anjou irrevocably to the side of the French
crown by forcing it into a quarrel with Henry I.

[563] Gesta Cons. (Marchegay, Comtes), p. 143.

[564] “Vir rufus, sed instar David.” Will. Tyr. l. xiv. c. 1.

The means lay ready to their hands. Aremburg of Maine, once the
plighted bride of Geoffrey Martel, was still unwed; Fulk, by his
mother’s counsel, sought and won her for his wife.[565] Her marriage
crowned the work of Elias. The patriot-count’s mission was fulfilled,
his task was done; and in that very summer he passed to his well-
earned rest.[566] Fulk, as husband of the heiress, thus became count
of Maine, and the immediate consequence was a breach with Henry
on the long-vexed question of the overlordship of the county.
Whether Elias had or had not recognized any right of overlordship in
Fulk Rechin or Geoffrey Martel II. is not clear; he certainly seems to
have done homage to Henry,[567] and their mutual relations as lord
and vassal were highly honourable to both; but it was hardly to be
expected that Fulk, whose predecessors had twice received the
homage of Henry’s elder brother for that very county, should yield up
without a struggle the rights of the count of Anjou. He refused all
submission to Henry, and at once formed a league with the French
Crown in active opposition to the lord of England and Normandy.

[565] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), pp. 785, 818.
Gesta Cons. (Marchegay, Comtes), p. 143. Will. Tyr., l. xiv. c. 1.

[566] Chronn. S. Albin. and S. Serg. a. 1110 (Marchegay,


Eglises, pp. 31, 143). Eng. Chron. a. 1110. Ord. Vit. (Duchesne,
Hist. Norm. Scriptt.), pp. 785, 839.

[567] “Eac thises geares forthferde Elias eorl, the tha Mannie
of tham cynge Heanri geheold, and on cweow.” Eng. Chron. a.
1110. Nobody seems to know what “on cweow” means; Mr.
Thorpe (Eng. Chron., vol. ii. p. 211) suggests that it may stand for
“Angeow.”

The war began in 1111, and the danger was great enough to call
Henry himself over sea in August and keep him on the continent for
nearly two years. The leading part was taken by the count of Anjou,
whose marriage enabled him to add the famous “Cenomannian
swords” to the forces of Touraine and the Angevin March.[568]
Moreover, treason was, as usual, rife among the Norman barons;
and the worst of all the traitors was Robert of Bellême. One after
another the lesser offenders were brought to justice; at last, in
November 1112, Robert himself fell into the hands of his outraged
sovereign, and, to the joy of all men on both sides of the sea, was
flung into a lifelong captivity.[569] Then at last Henry felt secure in
Normandy; the capture of Robert was followed by the surrender of
his fortress of Alençon, and the tide of fortune turned so rapidly that
Fulk and Louis were soon compelled to sue for peace. Early in Lent
1113 Fulk and Henry met at Pierre-Pécoulée near Alençon; the count
submitted to perform the required homage for Maine, and his infant
daughter was betrothed to Henry’s son, the little Ætheling William. In
March the treaty was confirmed by the two kings at Gisors; and as
the first-fruits of their new alliance there was seen the strange
spectacle of a count of Anjou and a count of Blois fighting side by
side to help the lord of Normandy in subduing the rebels who still
held out in the castle of Bellême.[570]

[568] Eng. Chron. a. 1111, 1112.

[569] Eng. Chron. a. 1112. Ord. Vit. (Duchesne, Hist. Norm.


Scriptt.), pp. 841, 858. Will. Malm. Gesta Reg., l. v. c. 398 (Hardy,
p. 626).

[570] Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p. 841.

Henry’s next step was to exact, first from the barons of Normandy
and then from the Great Council of England, a solemn oath of
homage and fealty to his son William as his destined successor.[571]
This ceremony, not unusual in France, but quite without precedent in
England, was doubtless a precaution against the chances of the war
which he foresaw must soon be renewed. This time indeed he was
himself the aggressor; Louis had made no hostile movement, and
Fulk was troubled by a revolt at home, whose exact nature is not
clearly ascertained. The universal tendency of feudal vassals to
rebel against their lord had probably something to do with it; but
there seems also to have been another and a far more interesting
element at work. “There arose a grave dissension between Count
Fulk the Younger and the burghers of Angers.”[572] In this
provokingly brief entry in one of the Angevin chronicles we may
perhaps catch a glimpse of that new spirit of civic freedom which
was just springing into life in northern Europe, and which made some
progress both in France and in England during the reigns of Louis VI.
and Henry I. One would gladly know what were the demands of the
Angevin burghers, and how they were met by the son-in-law of Elias
of Le Mans; but the faint echo of the dispute between count and
citizens is drowned in the roar of the more imposing strife which
soon broke out anew between the rival kings. Its ostensible cause
was now Count Theobald of Blois, whose wrongs were made by his
uncle a ground for marching into France, in company with Theobald
himself and his brother Stephen, in the spring of 1116. Louis
retaliated by a raid upon Normandy; the Norman barons
recommenced their old intrigues;[573] and they were soon furnished
with an excellent pretext. After the battle of Tinchebray, Duke
Robert’s infant son William had been intrusted by his victorious uncle
to the care of his half-sister’s husband, Elias of Saint-Saëns. Elias
presently began to suspect Henry of evil designs against the child; at
once, sacrificing his own possessions to Henry’s wrath, he fled with
his charge and led him throughout all the neighbouring lands,
seeking to stir up sympathy for the fugitive heir of Normandy, till he
found him a shelter at the court of his kinsman Count Baldwin of
Flanders.[574] At last the faithful guardian’s zeal was rewarded by
seeing the cause of his young brother-in-law taken up by both
Baldwin and Louis. In 1117 they leagued themselves together with
the avowed object of avenging Duke Robert and reinstating his son
in the duchy of Normandy; and their league was at once joined by
the count of Anjou.[575]

[571] Eng. Chron. a. 1115. Flor. Worc. (Thorpe), vol. ii. p. 69.
Eadmer, Hist. Nov. (Rule), p. 237.

[572] “Facta est gravis dissensio inter Fulconem comitem


Juniorem et burgenses Andecavenses.” Chron. S. Serg. a. 1116
(Marchegay, Eglises, p. 143). The Chron. S. Albin. a. 1114 (ib. p.
32) has “Guerra burgensium contra comitem”; but M. Marchegay
says in a note that two MSS. read “baronum” for “burgensium.”

[573] See details in Suger, Vita Ludov. c. 21 (Rer. Gall. Scriptt.,


vol. xii. p. 43), and Ord. Vit. (Duchesne, Hist. Norm. Scriptt.), p.
843.
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