Physical Examination of The Heart and Circulation 4th 2009

Physical Examination
of the Heart
and Circulation
Fourth Edition
Joseph K. Perloff, M.D.

Streisand/American Heart Association Professor
of Medicine and Pediatrics, Emeritus
Founding Director, Ahmanson/UCLA Adult Congenital
Heart Disease Center
UCLA School of Medicine
Los Angeles, California
2009
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Notice: The authors and publisher have made every effort to ensure that the patient care recommended
herein, including choice of drugs and drug dosages, is in accord with the accepted standard and practice
at the time of publication. However, since research and regulation constantly change clinical standards,
the reader is urged to check the product information sheet included in the package of each drug, which
includes recommended doses, warnings, and contraindications. Th is is particularly important with new
or infrequently used drugs. Any treatment regimen, particularly one involving medication, involves inherent risk that must be weighed on a case-by-case basis against the benefits anticipated. The reader is
cautioned that the purpose of this book is to inform and enlighten; the information contained herein is
not intended as, and should not be employed as, a substitute for individual diagnosis and treatment.
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To the memory of
PAUL HAMILTON WOOD
from whom I learned the
physical examination of the heart and circulation.
And to those whom I have taught and will teach,

For you have I prepared this book.
In its preparation I have endeavored to be concise,
yet clear and comprehensive. Its name indicates its object;
viz. to give you, in a compact form, a complete view of
what are technically called the physical signs.
Henry I. Bowditch
The Young Stethoscopist, 1848
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Contents
Foreword
vii
Preface
ix
Acknowledgments
xi
Introduction with a Brief Historical Survey
Physical Appearance
The Arterial Pulse
The Jugular and Peripheral Veins
The Movements of the HeartPercussion,

Observation, Palpation ...................................................................... 127
AuscultationThe Audible Language of the Heart
The Chest
The Abdomen
Index
.......................................
.......................................................................... 15
............................................................................. 55
...................................................... 93
.......................... 157
......................................................................................... 225
.................................................................................. 241
251
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Foreword
Specialized laboratory techniques for cardiovascular diagnosis provide a large portion of

the database required to establish a specic anatomical diagnosis of cardiac disease and
to determine the extent of functional impairment of the heart. The development and application of these methods represent one of the triumphs of modem medicine. However,
their appropriate use is to supplement but not to supplant a careful clinical examination,
which remains the cornerstone of the assessment of the patient with known or suspected
cardiovascular disease. There is a temptation in cardiology, as in many other areas of
medicine, to carry out expensive, and occasionally uncomfortable, or even hazardous
procedures to establish a diagnosis when a detailed and thoughtful clinical examination
is sufcient. Obviously, it is undesirable to subject patients to the unnecessary risks,
discomfort, and expenses inherent in many specialized tests when a diagnosis can be
made on the basis of the clinical examination or when management will not be altered
signicantly as a result of these tests.
Intelligent selection of investigative procedures from the ever-increasing array of
tests now available requires far more sophisticated decision making than was necessary
when the choices were limited to electrocardiography and chest roentgenography. The
clinical examination provides the critical information necessary for most of these decisions. With the increasing emphasis on the cost of medical care, it is likely that there
will be a resurgence of interest in the relatively inexpensive and absolutely safe clinical
examination.
Not to be overlooked is the ability to follow patients serially by physical examination. An additional benet is that the actual physical contact (ie, the laying on of hands
by the physician) creates a valued bond with the patient at a time when the patients
encounter with the medical care system is often so impersonal.
Physical Examination of the Heart and Circulation by Joseph K. Perloff, the master
of the physical examination of the heart and circulation of this era, is a true gem. It is
especially important at a time when the physical examination is inadequately emphasized both in education and practice and when many trainees do not elicit or interpret
physical ndings adequately. Physical Examination of the Heart and Circulation should be
required reading for all who practice or train in clinical cardiology.
Eugene Braunwald, MD
Boston, Massachusetts
vii
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Preface
Sophisticated laboratory methods provide contemporary clinicians with remarkable

diagnostic information, but in so doing, risk de-emphasizing the bedside examination
upon which previous generations were much more dependent and therefore much more
adept. There are few areas of clinical cardiology that physical signs do not illuminate.
Lest we feel that these concerns are peculiar to our time, the preface to Sir James
Mackenzies Principles of Diagnosis and Treatment in Heart Affections (1916)* stated:
A great deal of our recent knowledge of heart conditions has been attained by the use of
such mechanical aids as the polygraph and the electrocardiograph. It has been a constant
endeavor on my part to recognize the different conditions which these instruments have
revealed by employing the ordinary bedside methods of examination, and I am concerned
mainly with them in this book.
My purpose in writing this book on the physical examination of the heart and
circulation is to bring to the reader the results of my own experience in employing ordinary bedside methods that beautifully supplement the impressive laboratory techniques
that have done so much to establish the meanings and increase the diagnostic value of
cardiovascular physical signs. I have made every effort to write clearly, while not sparing
the reader the effort of thinking.
Original or early descriptions of cardiovascular physical signs are, more often than
not, impossible to improve upon for accuracy and clarity. I have liberally drawn from
these descriptions, which not only excite admiration for our predecessors, but also serve
to make my book richer by bringing the reader closer to a distinguished past.
Chapter 6, AuscultationThe Audible Language of the Heart, has two novel if
not unique features. First, auscultatory signs that are described in the text are illustrated
by visual recordingsphonocardiogramsthat have long served as the basic tools for
studying these signs and for teaching auscultation. Each phonocardiograms has been
digitized so it appears as on original tracing. This book will be the last to include phonocardiograms because the recording instruments are no longer manufactured. The second
novel feature of Chapter 6 is a dedicated website that features audiovisual sound tracks,
so the reader can hear as with a stethoscope the auscultatory signs that are described in
the text and illustrated in the accompanying phonocardiograms.
*Mackenzie J. Principles of Diagnosis and Treatment in Heart Affections. London: Oxford University Press, 1916.
ix
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Acknowledgments
My largest debt is to the late Dr Paul Hamilton Wood, from whom, more than anyone,
I learned the physical examination of the heart and circulation. To the Fulbright Fellowship and the Institute for International Education I shall always be grateful for making
it possible for me to spend a formative year working closely with Dr Wood and his colleagues at the Institute of Cardiology and the National Heart Hospital, London.
Enthusiastic, receptive, yet critical students, house ofcers, and fellows were a
stimulus to my efforts. I gratefully acknowledge the Ahmanson Foundation Endowment
to the UCLA Adult Congenital Heart Disease Center and the Streisand/American Heart
Association Professorship Endowment for generous support.
Joseph K. Perloff, MD
xi
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Introduction with a Brief

Historical Survey
I hope to demonstrate to you that knowledge essential to the
understanding of the patients complaint can be made out by our
unaided senses, and that articial and mechanical aids can,
in the nature of things, only be accessory aids.1
Sir James Mackenzie
The physical examination of the cardiovascular system includes the heart and circulation
per se, the chest and abdomen, and the physical signs of coexisting noncardiac diseases.
Examination of the heart and circulation includes (1) physical appearance (sometimes
called inspection), (2) the arterial pulse, (3) the jugular venous pulse and peripheral
veins, (4) the location and movements of the heart: percussion, palpation, and observation of the precordium, and (5) auscultation. Examination of the chest (thorax, lungs)
and abdomen frequently reveals signs secondary to or associated with cardiac or vascular
disorders. In infants, children, and young adults, diseases of the heart usually occur in
patients who are otherwise normal. With advancing age, coexisting noncardiac diseases
accrue and modify the cardiovascular physical signs.
Systematic assessment of each physical sign sets the stage for a synthesis of the information so derived. It is axiomatic that emphasis focuses on the relationship of the parts to the
whole, a relationship that ideally results in a harmonious picture devoid of contradictions,
not an assembly of loosely related observations. Maximum information should be extracted
from each physical sign while relating information from one sign to that of another.
No organ system lends itself better to a close association between signs, structure,
and function than the heart and circulation. Laboratory characterization of cardiovascular anatomy and physiology has validated these signs, which in turn permit remarkably
precise pathophysiologic inferences. Excitement, satisfaction, and a feeling of condence
and security are experienced when accurate, practical information is assembled with the
unaided senses apart from a stethoscope, a pocket ashlight, a sphygmomanometer, and
an ophthalmoscope.
My purpose is to describe the physical signs and how they are best elicited. Mechanisms are dealt with chiey when doing so serves this end. Emphasis is placed on the
physical examination rather than on physical diagnosis.
The fabric of the cardiovascular physical examination is woven from threads of the
past. Franciscus de le Boe Sylvius, at the University of Leiden, was one of the most celebrated clinical teachers of the seventeenth century and was the rst champion of bedside
1
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2 Introduction with a Brief Historical Survey
teaching. He would lead his students by the hand to the practice of medicine, taking
them every day to see patients in the public hospital, that they may hear the patients
symptoms and see their physical ndings.2 Two and a half centuries later, Harvey Cushings biography of William Osler (Fig. 11) began with the dedication, To medical
students . . . lest it be forgotten who it was that made it possible for them to work at the
bedside in the wards.3
Each of the ve essential components of the cardiovascular physical examination
is rooted in history. Physical appearance was the subject of the introductory paragraph
of the chapter Preliminary Examination of the Patient in James Mackenzies Diseases
of the Heart4 (Fig. 12):
The attempt to appreciate the patients condition should begin when rst he presents himself before us. On his appearance in the consulting room, his bearing, his
gait, the condition of his respiration, the color of his face, any nervous peculiarity
in his manner of speech and behavior, and so forth, should be noted. If he is in
bed, note the position he assumes, and any change in his color or respiration in
response to such exertions as talking or turning over. By habit, one unconsciously
notices these things.4
The arterial pulse served as the basis for an entire system of diagnostic medicine
circa 2600 b.c. in China with The Yellow Emperors Book of Medicine.5 Nei Ching Su Wen
Figure11 Sir William Osler

(18491919). (Courtesy of the College of
Physicians, Philadelphia.)
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Introduction with a Brief Historical Survey 3
Figure 12 Sir James Mackenzie

(18531925).
is believed to be the oldest medical book extant.5 The text is in the form of a dialogue
between the legendary Huang Ti (The Yellow Emperor, 26962598 b.c.) (Fig. 13) and
his minister Chi Po. The chief means of diagnosis in Nei Ching is the examination of the
arterial pulse. All other methods were secondary. The state of disease was judged by the
volume, strength, or weakness of the pulse and by the regularity or interruption of the
beats. The examination was a time-consuming affair, taking hours and involving palpation in nearly a dozen sites while the pulse rate was timed by the physicians respiratory
excursions. The patient was examined in the early morning before the physician took
food and before the cares of the day distracted him from full concentration. If the patient
were female, the right pulses were palpated rst (Fig. 14) and vice versa.
Despite the signicance attached to the pulse, its origin in the heartbeat was not
remotely considered. It was long in coming before Herophilus (344 b.c.) recognized that the
arterial pulse and the cardiac impulse were synchronous. Herophilus used a water clock to
count the pulse, analyzed rate and rhythm, was inuenced by musical theories, and evolved
an entire rhythmical pulse lore.6 In 1700, Sir John Floyer commissioned an English watchmaker to construct a timepiece with a minute hand that permitted accurate determination
of the rate of the pulse.7 In The Physicians Pulse Watch, Floyer describes the normal and
abnormal arterial pulse, its rate, rhythm, amplitude, forcefulness, and compressibility.
The rst recorded account of the cervical venous pulse was published in 1728 when Lancisi
(Fig. 15) described systolic uctuation of the jugular vein in a patient who at necropsy
had tricuspid regurgitation.8 Rhythmic pulsations of the large veins in the neck were subsequently dened by John Hunter (Fig. 16) in 1794 in his Treatise on the Blood, Inammation,
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Figure 13 Huang Ti, the Yellow

Emperor. (From an eighteenth-century
Japanese scroll.)
and Gun-Shot Wounds.9 The larger veins, near to the heart, have a pulsation which arises
from the contraction of the heart preventing the entrance of blood at that time.9 Almost a
century elapsed before Chauveau and Marey10 published their classic graphic records of the
jugular venous pulse. At the turn of the century, the jugular pulse was shown to have such
striking similarity to waveforms recorded directly from the right atrium that Carl Wiggers
was prompted to write, It became increasingly more obvious to many physiologists that
records of the venous pulse might be of service in the interpretation of dynamic events in
the heart.11 In 1902, Sir James Mackenzie applied this principle at the bedside in his Study
of the Pulse,12 which brought together 20 years of meticulous observation. Mackenzie rmly established the value of examination of the jugular venous pulse and stimulated a lively
interest in its study. Paul Wood (Fig. 17) rekindled this interest in the 1950s.
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Figure 14 If the patient were

female, her right pulses were palpated
rst, as shown here. If the patient were
male, his left pulses were examined
rst. (From Veith I [trans]. Huang Ti
Nei Ching Su Wen: The Yellow Emperors
Book of Medicine. Berkeley: University of
California Press, 1972; reprinted with
permission.)
The practice of precordial palpation was recorded in the Ebers papyrus (Fig. 18) in a
chapter entitled, Knowledge of the Hearts Movement, which physicians can appreciate by
applying their hands or ngers upon the place of the heart.13 Systolic movements imparted
to the precordium are the most visible evidence of the action of the heart and were familiar to
William Harvey (Fig. 19) in the early seventeenth century. The heart is erected and rises
up to a point so that at this time it strikes against the breast and is felt externally.14 In 1857,
Chauveau conrmed Harveys contention that precordial movement observed when the heart
strikes against the breast resulted from ventricular contraction.15 Validation awaited Chauveaus animal experiments done in collaboration with Marey, in which a precordial apex beat
was correlated with intracardiac pressure pulses recorded via a catheter.15
Applying an ear directly to the chest wall was an ancient method of auscultation.
Hippocratic writings circa 400 b.c. described the succussion splash of hydropneumothorax.16 William Harvey, in 1616, referred to the heartbeat as two clacks of a waterbellows, and in De Motu Cordis (1628) Harvey wrote that with each motion of the heart
when there is the delivery of a quantity of blood from the veins to the arteries . . . a pulse
takes place and can be heard within the chest.14 This description leaves no doubt that
Harvey was aware of sounds originating in the beating heart. Robert Hooke was not only
familiar with heart sounds but also foresaw the value of auscultation, stating in his Cutlerian Lectures published in 1705: I have been able to hear very plainly the beating of a
mans heart . . .. Who knows, I say, but that it may be possible to discover the Motions of
the Internal Parts of Bodies by the sound they make.17
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Figure 15 Giovanni Maria

Lancisi (16541720). (From
Castiglioni A. A History of
Medicine. New York: Alfred A.
Knopf, 1947; reprinted with
permission. Iconographic source
the Electa Archive.)
The modern era of cardiac auscultation began in 1816 with Rene Theophile Hyacinthe
Laennec who initially practiced direct auscultation, as illustrated in an eighteenth-century
painting showing him in the Necker Hospital in Paris sitting at the bedside of a patient
with his ear applied to the patients thorax (Fig. 110). Notwithstanding, Laennec was
sensitive to the shortcomings of direct auscultation, writing, As inconvenient for the physician as for the patient, distaste alone renders it almost impractical in the hospital; it cannot even be proposed to most women, and in most of them the volume of the breast is a
physical obstacle to its use.18 The alternative was the stethoscope (Greek stethos the breast
or chest and skopein, to view or examine), the discovery of which is legendary:
In 1816, 1 was consulted by a young woman labouring under general symptoms
of diseased heart, and in whose case percussion and the application of the hand
were of little avail on account on her great degree of fatness. The other method
just mentioned being rendered inadmissible by age and sex of the patient, I happened to recollect a simple and well-known fact of acoustics, and fancied at the
same time, that it might be turned to some use on the present occasion. The fact
I allude to is the augmented impression of sound when conveyed through certain
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Figure 16 John Hunter

(17281793), one of the
greatest gures in English
medical history.
solid bodies as when we hear the scratch of the pin at one end of a piece of wood on
applying our ear to the other. Immediately, on this suggestion, I rolled a quire of
paper into a sort of cylinder and applied one end of it to the region of the heart and
the other to my ear, and was not a little surprised and pleased, to nd that I could
thereby perceive the action of the heart in a manner much more clear and distinct
than I had ever been able to do by the immediate application of the ear. From this
moment, I imagined that the circumstance might furnish means for enabling us
to ascertain the character, not only of the action of the heart, but of every species
of sound produced by the motion of all the thoracic viscera.18
The ridicule and satiric cartoons that greeted Laennecs new device were soon replaced with enthusiasm. The London Times in September 1824, announced, A wonderful instrument called the stethoscope is now in complete vogue in Paris. Physicians
became so attached to the wonderful instrument that the soon-to-come exible binaural stethoscope struggled for recognition. As late as the turn of the century, an article
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Figure 17 Paul Hamilton Wood, MD, OBE

(19071962). Director, Institute of Cardiology,
London. (Courtesy of Dr Arthur Selzer, San
Francisco.)
in the Lancet hotly argued that the double stethoscope should be altogether done away
with.19 At the same time, methods for the graphic recording of auscultatory information
were moving ahead with the investigations of Otto Frank, Carl Wiggers, and Orias and
Braun-Menendez.20 The term phonocardiogram came into use, and Einthoven published an account of the string galvanometer for recording heart sounds.21
Physical signs elicited from the chest are important adjuncts to the cardiovascular
examination and originated in Auenbruggers treatise on percussion:
I here present the Reader with a new sign which I have discovered for detecting
diseases of the chest. This consists in Percussion of the human thorax, whereby,
according to the character of the particular sounds thence elicited, an opinion is
formed of the internal state of that cavity. In making public my discoveries respecting this matter, I have been actuated neither by an itch for writing, nor a
fondness for speculation, but by the desire of submitting to my brethren the fruits
of seven years observation and reection.22
Leopold Auenbrugger (Fig. 111), in his fathers inn, witnessed the practice of percussion of wine barrels to determine the level of their uid content. It later occurred to him
that the same technique might be applied to the examination of the human thorax. In 1761,
a kindly and unassuming junior physician at the Vienna Hospital published his new
inventioninventum novurnfor diagnosing thoracic disease by chest percussion.22 Joseph
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Figure 18 A section of the Ebers papyrus (circa 1550 b.c.) discovered by George Ebers at
Thebes in 1872. (Courtesy of the UCLA Biomedical Library.)
Skoda hailed the discovery as the beginning of modern diagnosis, but Auenbruggers
epochal work lay virtually dormant until Corvisart, the celebrated physician to Napoleon,
published an elaborately annotated 480-page French edition of Auenbruggers unpretentious 95-page book. The stage was set for Laennecs A Treatise on the Diseases of the Chest. In
his chapter on pneumothorax, Laennec recalled the dictum of Hippocrates:
Convinced by these symptoms of the existence of a pneumothorax combined
with a pleuritic effusion, I condently expected that the Hippocratic succussion
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Figure 19 William Harvey

(15781657), one of the greatest gures
in the history of medicine. (Courtesy of
the National Portrait Gallery, London.)
of the chest would let us hear the uctuation of the liquid, and I was not mistaken.18
Richard C. Cabots landmark book Physical Diagnosis (1915) contained three comprehensive chapters on diseases of the lungs and pleural cavity.23
Examination of the abdomen by palpation (Fig. 112) was practiced by the Athenian physician Jason in second century b.c.
Avicenna (9801037), in his Canon of Medicine, described dropsy as cold swellings composed of watery uid.24 Whether Avicenna referred to cardiac ascites is
open to question, but William Witherings account of cure of the dropsy by the foxglove given by a Shropshire gypsy leaves little doubt.25 Nevertheless, well into the
twentieth century, Cabot was less than sanguine about the value of the abdominal
examination:23
Our methods are crude and inexact compared to those applicable to the chest.
Auscultation, despite Canons brilliant foundation studies, is of practically no use.
Inspection is helpful in but few cases. Palpation, our mainstay, is often rendered
almost impossible by thickness, muscular spasm, or ticklishness of the abdominal
walls. Percussion is of great value in some cases, but yields no useful results in the
majority.23
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Figure 110 Laennec

applying his ear to a patients
chestdirect auscultation.
Note the wooden monaural
stethoscope in Laennecs left
hand (arrow added). (Courtesy
of the National Library of
Medicine, Bethesda, MD.)
Figure 111 Leopold Auenbrugger

(17221809), discoverer of percussion
of the thorax. (From Castiglioni A. A
History of Medicine. New York: Alfred A.
Knopf, 1947; reprinted with permission.
Iconographic sourcethe Electa
Archive.)
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Figure 112 Stela (second-century b.c. Greek) showing palpation of the abdomen. (Courtesy
of the British Museum, London.)
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Osler W. The Evolution of Modern Medicine. New Haven, CT: Yale University Press, 1921.
Floyer J. The Physicians Pulse Watch. London: Smith and Walford, 1707.
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11. Wiggers CJ. The Pressure Pulses in the Cardiovascular System. London: Longmans, Green, 1928.
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17. Hooke R. The posthumous works of Robert Hooke, containing his Cutlerian Lectures and
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MD). London: T and G Underwood, Fleet Street, 1824.
19. Sayers HW. The decay of auscultation and the use of the binaural stethoscope. Lancet
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20. Orias O, Braun-Menendez E. The Heart Sounds in Normal and Pathological Conditions. London:
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21. Einthoven W. Die registrierung des menschlichen herztone mittels des sartengalvanometers.
Pugers Arch Physiol. 1907;117:461.
22. Auenbrugger L. Inventum Novum ex Percussione Thoracis Humani. Vienna, 1761 (translated by John Forbes). London: T and G Underwood, Fleet Street, 1824.
23. Cabot RC. Physical Diagnosis, 6th ed. New York: William Wood, 1915.
24. Gruner OC. A Treatise on the Canon of Avicenna. London: Luzac, 1930.
25. Withering W. An Account of the Foxglove and Some of its Medical Uses. Birmingham: M. Swinney,
1785.
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5/19/2009 3:52:05 PM
Physical Appearance
The eye is the chief means whereby the understanding may most fully and
abundantly appreciate the innite works of nature.
Leonardo da Vinci
What the eye seesthe patients general and detailed physical appearanceis the subject of this chapter. In order to see, however, the eye must be trained. The innocent eye,
which should see the world afresh, does not see it at all.1
Certain distinctive physical appearances are associated with certain specic
cardiac diseases, whereas other appearances are caused by cardiac or vascular diseases. General appearance should rst be focused upon, and then detailed appearance
(Table 21). I have selected examples of practical interest. No attempt was made to
be comprehensive.
Systematic assessment of a patients appearance is an integral part of the physical
examination of the heart and circulation. I shall deal in turn with (1) general somatic
features, (2) gestures and gait, and (3) detailed appearance of face, eyes, mouth, hands,
feet, skin, muscles, tendons, thorax, and abdomen.
GENERAL APPEARANCE
General appearance can distinguish at a glance acute from chronic illness, but a patient may look well despite the presence of cardiac or vascular disease. The picture of
certain acute illnesses is well known. Pulmonary edema is characterized by a struggling, frightened, diaphoretic patient, dyspneic while sitting bolt upright. Or witness the patient with an acute myocardial infarctionanxious, ashen, diaphoretic,
reacting to oppressive chest pain with its real and symbolic meanings. The picture of
cardiogenic shock, familiar to us all, was perfectly described in Shakespeares death
of Falstaff:
So he cried out, God, God! three or four times. Now I, to comfort him, bid him
he should not think of God; I hoped that there is no need to trouble himself with
any such thoughts yet. So he bade me lay more clothes on his feet; I put my hand
into the bed and felt them and they were as cold as any stone; I then felt to his
15
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16 Physical Appearance
Table 21 Physical Appearance

General appearance
Gestures and gait
Detailed appearance
Face
Eyesexternal and internal
Mouthexternal and internal
Hands and feet
Skin
Muscles and tendons
Thorax
Abdomen
knees; and they were as cold as any stone, and so upward and upward, all was as
cold as any stone.2
The general appearance of chronic illness is exemplied by the catabolic effects of
congestive heart failurewasted pectoral, shoulder girdle, and arm muscles, edematous
legs, protruding ascitic abdomen, and drawn face. The appearance of the coronary-prone
patient is a stereotypea mesomorphic, balding, hirsute, middle-aged, overweight male
of good appetite whose ngers are stained with nicotine, whose ashtray is lled with the
butts of cigarettes that preceded the one he is smoking, while close by is a briefcase bulging with paperssymbols of deadlines he feels compelled to meet.
The general appearance of thyrotoxicosis is typied by a lean, perspiring, tremulous
individual with quick movements and bright eyes with or without exophthalmos. Hypothyroidism is the antithesislethargic and pallid, with slow movements and coarse features.
A patient may be distinctively tall3 (gigantism) or distinctively short (dwarsm).
Marfan syndrome is an example of a strikingly tall person with excessively long extremities and sparse subcutaneous fat. Gigantism in the neonate is represented by the infant of
the diabetic mother (Fig. 21). The description of James W. Farquhar is apt:
The infants are remarkable not only because, like foetal versions of Shadrach, Meshach
and Abednego, they emerge at least alive from within the ery metabolic furnace of
diabetes mellitus, but because they resemble one another so closely that they might
well be related. They are plump, sleek, liberally coated with vernix caseosa, full-faced
and plethoric. The umbilical cord and the placenta share in the gigantism. During
their rst 24 or more of extrauterine hours, they lie on their backs, bloated and ushed,
their legs exed and abducted, their lightly closed hands on each side of the head, the
abdomen prominent and their respiration sighing. They convey a distinct impression
of having had such a surfeit of both food and uid pressed upon them by an insistent
hostess that they desire only peace so that they may recover from their excesses.4
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Physical Appearance 17
Figure 21 Infant of a diabetic

mother showing typical neonatal
gigantismplump, full-faced,
plethoric, bloated, and ushed.
They lie on their backs, bloated
and ushed, their legs exed and
abducted, their lightly closed
hands on each side of the head, the
abdomen prominent.4
Short stature as represented by the 45/X0 Turner syndrome (Fig. 22A) is characterized by a phenotypic female with webbing of the neck, sexual infantilism (absent or scanty
pubic and axillary hair), wide-set nipples, low hairlines usually concealed by bangs, and
long hair, small chin, and wide carrying angles of the arms.5 The female Turner (45/X0)
predicts the presence of coarctation of the aorta, dilated aortic root, and bicuspid aortic valve.
Noonan syndrome is a Turner phenotype with normal chromosomal composition (46/XX
female, 46/XY male) (Fig. 22B), but dwarsm is not the rule. The cardiac disease is likely
to consist of dysplastic pulmonary valve stenosis or hypertrophic obstructive cardiomyopathy.5 The Ellisvan Creveld syndrome is characterized by dwarsm and polydactyly.5
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Figure 22 A, A 13-year-old girl with 45/X0 Turner syndrome and the typical phenotype
of short stature, webbing of the neck, absence of pubic hair, wide-set nipples, and small chin.
Bangs cover a low anterior hairline. The patient had coarctation of the aorta. B, An 18-year-old
boy with 46/XY Noonan syndrome and typical webbing of the neck. Long hair obscures low
anterior and posterior hairlines. The patient had dysplastic pulmonary valve stenosis and an
atrial septal defect.
Obesity varies in appearance and should be carefully characterized. The

combination of obesity and somnolencethe pickwickian syndromewas so named
by C. Sidney Burwell based upon the description of Charles Dickenss fat boy
(Fig. 23A):
A most violent and startling knocking was heard at the door. The object that
presented itself to the eyes of the astonished clerk was a boya wonderfully fat
boystanding upright on the mat, with his eyes closed as if in sleep. He had
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never seen such a fat boy, and this, coupled with the utter calmness and repose of
his appearance, so very different from what was reasonably to have been expected
of the inictor of such knocks, smote him with wonder. The extraordinary boy
spoke not a word; but he nodded once and seemed to the clerks imagination to
snore feebly.6
Alveolar hypoventilation that accompanies pickwickian obesity results in hypercapnea, somnolence (Fig. 23B), hyoxemia, increased pulmonary vascular resistance, and pulmonary hypertension. By contrast, the obesity of Cushing syndrome
coincides with systemic hypertension. The cushingoid appearance is typied by central obesity with rounding of the face, thick fat pads in the supraclavicular fossae, and
a marked increase in thoraco-abdominal paniculus adiposus. Abdominal obesity can
progress to grotesque proportions while the extremities remain remarkably slender.
Figure 23 A, Charles Dickens Fat Boy: Hes gone to sleep again. Be good enough to pinch
him, sirin the leg, if you please; nothing else wakes him (Pickwick Papers, Chapter IV). B,
An obese 32-year-old man with the pickwickian syndrome photographed by the author as the
patient fell asleep while his history was being taken.
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Gestures and gait can be important features of physical appearance. A clenched st

pressed against the sternum is a time-honored gesture of the oppressive pain of myocardial infarction. The importance of gait was emphasized by James Mackenzie: When
the patient presents for examination, the physician naturally scrutinizes him and makes
a mental note of his gait and how he deports himself generally.7 However, except for
neurologists, physicians seldom routinely observe their patients walk, even though an
abnormal gait may be the rst evidence of a systemic neuromuscular disease with cardiac
involvement. Pseudohypertrophic Duchenne muscular dystrophy, for example, results
in a characteristic slow, clumsy waddling gait caricatured by exaggerated lumbar lordosis and protuberant abdomen (Fig. 24). When such a patient is asked to rise from
a recumbent position, he is apt to use the distinctive gestures originally described by
Gowers in 1888 (Fig. 25). The cardiac involvement in Duchenne dystrophy targets the
posterobasal left ventricular wall.
Figure 24 A, Young boy with classic pseudohypertrophic X-linked Duchenne muscular

dystrophy and exaggerated lumbar lordosis (arrow). B, Striking calf pseudohypertrophy with
shortening of the Achilles tendons (arrows) causing the patient to stand on his toes. Cardiac
disease was characterized by regional dystrophy of the posterobasal left ventricular wall.
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Figure 25 Gowers sign:

Mode of rising from the ground in
pseudohypertrophic paralysis. (From
Gowers WR: Diseases of the Nervous
System. Philadelphia, R Blakiston,
Son & Co, 1888.)
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DETAILED APPEARANCE
For by his face straight shall you know his heart.8
Facial Expression
The face can express anxiety or calm. Anxiety can provoke a variety of cardio-circulatory
disturbances in the absence of organic heart disease, or may be the result of real or imagined fear of cardiac disease. The face is often a barometer of agechronologically appropriate or inappropriate. Premature aging takes one of its most dramatic forms in Werner
syndrome9 (Fig. 26A), a disorder characterized in part by premature graying of the hair,
frontal baldness in males, cataracts, taut skin, and beaking of the nose. Coronary artery
disease and systemic atherosclerosis are strikingly premature.
Figure 26 A, A 34-year-old man with the typical premature aging of Werner syndrome
characterized by graying of the hair, frontal baldness, and a cataract in the left eye. Atrophic skin
is pulled tightly over the bridge of the nose. B, A 10-year-old boy with the HutchinsonGilford
syndrome consisting of progeria (premature aging) with nanism (dwarsm). There is complete
alopecia and tightly drawn atrophic skin. The boy died of myocardial infarction.
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In children, a dramatic variation on this theme is the HutchinsonGilford syndrome (Fig. 26B), with alopecia, senile appearance, premature aging, childhood atherosclerosis, and death from cardiac infarction. Patients with myotonic muscular dystrophy
appear prematurely old, with graying of the hair, frontal baldness or thinning even in
females, cataracts, and an expressionless, myopathic facies (Fig. 27). Abnormalities of
cardiac impulse formation and conduction are typical.
A facial buttery rash with malar depigmentation are features of systemic lupus
erythernatosus. In the carcinoid syndrome, a cardinal facial appearance is a sudden bright
red to violaceous hue accompanied by facial and periorbital edema. During the ush, hypotension, even shock, sometimes occurs. Cardiac involvement usually takes the form of
pulmonary valve stenosis and tricuspid stenosis/ regurgitation.
Facial appearance in hypothyroidism is characterized by dull, coarse features, an enlarged tongue, thickened skin, dry hair that does not maintain a curl, puffy eyelids, and
sparse eyebrows, the outer thirds of which may be absent. In the Hurlers syndrome, gargoylism refers to grotesque facial features recognizable at a glance (Fig. 28A). The skull is
malformed, the supraorbital ridges are prominent, the bridge of the nose is depressed, the
lips are thick, and the teeth are peg-shaped as in a gargoyle (Fig. 28B). Hurlers syndrome
is a form of mucopolysaccharidosis that involves the mitral and aortic valves together with
thickening of the walls and narrowing of the lumina of the coronary arteries.10
Figure 27 A, Expressionless,
myopathic facies, thin frontal
hair and bilateral cataracts in a
woman with myotonic muscular
dystrophy. B, Hair lifted to show
frontal baldness.
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Figure 28 A, Child with typical coarse physiognomy of Hurler syndrome (gargoylism).

Necropsy disclosed thickened mitral leaets and severely narrowed coronary arteries. (Courtesy of
Dr Hines Zellweger, University of Iowa, Iowa City.) B, Gargoyle showing the typical grotesque
bulging eyes, prominent supraorbital ridges, blunt upturned nose, thick lips, and
peg teeth. (Courtesy of Professor Robbert Flick, Department of Fine Arts, University of Southern
California, Los Angeles.)
A number of facial appearances are associated with specic or relatively specic

congenital cardiac or vascular diseases. Figure 29A is an example of Down syndrome with
typical inner epicanthic folds and depressed nasal bridge. Figure 29B is the prole of an
Asian child with Down syndrome, inner epicanthic folds, normal horizontal Asian epicanthic fold above the outer canthus, at nose with depressed nasal bridge, and a characteristically protrubant tongue. Another distinctive facial appearance typies Williams syndrome
that coexists with nonfamilial supravalvular aortic stenosis and pulmonary artery stenosis.
The face is characterized by a large mouth, patulous lips, small chin, baggy cheeks, blunt
upturned nose, wide-set eyes, and malformed teeth (Fig. 210). The fetal alcohol syndrome is a consequence of heavy maternal drinking during gestation. Offspring have short
palpebral ssures, a hypoplastic upper lip with thin vermilion, diminished to absent philtrum, micrognathia, and midfacial growth deciency11 (Fig. 211). Coexisting congenital
cardiac malformations usually take the form of atrial or ventricular septal defect alone or
with pulmonary valve stenosis. The cardiofacial syndrome consists of distinctive unilateral
partial lower facial weakness that appears only when the child cries.12
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Figure 29 A, Down syndrome

with typical inner epicanthic folds
(arrows) and depressed nasal bridge.
B, Prole of a Chinese child with
Down syndrome, inner epicanthic fold
(white arrow), normal horizontal Asian
epicanthic fold above the outer canthus
(black arrow), at nose with depressed
nasal bridge, and a characteristically
protuberant tongue.
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Figure 210 Facial appearance of

Williams syndrome with the typical
small chin, large mouth, patulous
lips, blunt upturned nose, wide-set
eyes, broad forehead, baggy cheeks,
and malformed teeth. The patient was
mentally retarded and had infantile
hypercalcemia, bilateral stenosis
of the pulmonary arteries, and
supravalvular aortic stenosis.
External and Internal Appearance of the Eyes

External examination of the eyes is part of the examination of the face. Some abnormalities are recognizable at a glance (strabismus or conspicuous exophthalmos), while detection of other abnormalities requires careful inspection of lids, lacrimal glands, palpebral
ssures, eyebrows, conjunctivae, sclerae, cornea, iris, and lens.
The bulbus oculi (ocular bulb or eyeball) is normally well contained within its
bony cavity, the orbit. In hyperthyroidism, the appearance of the ocular bulb varies from
symmetric or asymmetric protrusion (exophthalmos) to mild lid retraction and stare.
Slight proptosis and stare in euthyroid patients are occasionally due to chronic elevation of systemic venous pressure. Proptosis in patients with severe tricuspid regurgitation, may be accompanied by systolic anterior movement of the ocular bulb that is best
detected when the examiner observes the eyes with an oblique light while the patient
sits and looks directly forward. Conversely, shrunken eyeballs occur when the catabolic effects of congestive heart failure cause loss of retro-orbital fat and connective tissue.
Nystagmusinvoluntary oscillations of the ocular bulb with lateral gazeis a feature
of Friedreich ataxia.
The eyelids themselves sometimes disclose telltale signs. A common example is xanthalasma, which are circumscribed, yellowish cholesterol-containing plaques.
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Figure 211 Fetal alcohol

syndrome in a 21-month-old
girl. There is a hypoplastic
upper lip, micrognathia, absent
philtrum, and short palpebral
ssure. The cardiac malformation
was ventricular septal defect
with pulmonary valve stenosis.
(Courtesy of Dr David A. Ferry,
Encino, CA.)
Xanthalasma reside near the inner canthus and are best seen when the eyelids are gently
closed. Their presence, especially in young adults, is accompanied by hypercholesterolemia and premature atherosclerotic coronary artery disease. Lid-lag, another ocular
feature of hyperthyroidism (see above), is characterized by sclera visible above the iris
as movement of the upper lid lags behind the eyeball during downward gaze. Ptosis,
often asymmetric, is part of the external ophthalmoplegia and pigmentary retinopathy
of KearnsSayre syndrome (Fig. 212), which is associated with infranodal conduction
abnormalities culminating in complete heart block.13 In sarcoidosis, enlarged lacrimal
glands conspicuously protrude the lateral margins of the upper lids (Fig. 213). Eversion
of the lid permits direct inspection of the enlarged lacrimal glands.14
The conjunctivae are best examined with a pocket ashlight as the lower lid is
retracted downward while the patient looks up. The pallor of anemia or the suffusion of
cyanosis is then apparent. White-centered lesions of infective endocarditis are located on
the conjunctiva of everted lower lids (Fig. 214A). Conjunctivitis with urethritis points
to the diagnosis of Reiters disease. Acute cardiac involvement takes the form of pericarditis and abnormalities in atrioventricular (AV) conduction, while chronic involvement
is represented by AV block and aortic regurgitation.15
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Figure 212 An eighteen-year-old girl with KearnsSayre syndrome and typical asymmetric
ptosis. She also had pigmentary retinopathy. Cardiac involvement took the form of bifascicular
block that required a pacemaker.
The sclera can disclose discoloration as familiar as jaundice, or as unusual as the

blue sclera of osteogenesis imperfecta.16
In young patients, a corneal arcus (Fig. 215) prompts suspicion of hypercholesterolemia and premature coronary artery disease. In Down syndrome, the iris may
reveal distinctive Brusheld spots, a circle of punctate, depigmented dots circumferentially arranged at the periphery (Fig. 216A). Brusheld spots cannot be seen in
patients with darkly pigmented irises. Congenital coloboma or ssures of the iris cause
a change in pupillary shape from circular to oblong, creating the appearance of a cats
eye17 (Fig. 217).
The size, shape, and reaction of the pupils to light and accommodation are diagnostically important. In diabetes mellitus, the pupils are sometimes unequal and nonreactive to light. The distinctive Argyll Robertson pupil, which is small, irregular, and
usually constricts in response to convergence accommodation but not to light, is a feature of neurosyphilis (tabes dorsalis), often accompanied by aortic regurgitation.18
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Figure 213 Young boy with sarcoidosis and typical enlarged lachrymal glands that
caused protrusion of the lateral aspects of the upper lids (arrows). Pulmonary hypertension and
prolonged atrioventricular conduction coexisted.
Figure 214 A, Eversion of the lower lid discloses a typical white-centered conjunctival
lesion (arrow) of infective endocarditis. B, Retinal Roth spot of infective endocarditis with white
center surrounded by hemorrhage (arrow).
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Figure 215 Left corneal arcus (arrow) in a 4-year-old girl with homozygous familial
hypercholesterolemia.
A common abnormal appearance of the lens is the cataract. Premature cataracts

occur in myotonic muscular dystrophy (Fig. 27), in Werner syndrome (Fig. 26A),
and in offspring of mothers with rst-trimester rubella.5 Subluxation of the lens is an
important feature of the Marfan syndrome3 (Fig. 218) and homocystinuria. The unsupported lens imparts a distinctive shimmer to a transverse light beam when lateral motion
of the eye is abruptly halted, an observation best made in a darkened room. In Marfan
syndrome, lens subluxation is typically upward (Fig. 218), whereas in homocystinuria,
downward dislocation is the rule. Homocystinuria is accompanied by systemic arterial
and venous thromboses, myocardial infarction, and pulmonary embolism.
Examination of the internal appearance of the eyeretina, retinal arteries, retinal veins, and optic discrequires an ophthalmoscope, the skilled use of which is a
necessary part of the cardiac and vascular physical examination. The optic fundi provide
visual access to small arteries, arterioles, veins, venules, and capillaries. In hypertensive
retinopathy, permanent or relatively permanent changes consist of increased light reex,
copper wire appearance, arteriovenous nicking, and arteriolar tortuosity with irregular
caliber. Changes that tend to disappear with control of blood pressure include hemorrhages, exudates, cotton wool patches, and papilledema. Less well-known in hypertensive patients is the distinctive appearance of retinal arteries when the hypertension is due
to coarctation of the aorta.5 The retinal arteries show U turns (Fig. 219) but do not
exhibit hypertensive retinopathy.5
Retinal arterial emboli have characteristic appearances that may reveal their sources. Calcic emboli tend to be white, dull, and in close proximity to the disc margin.
Cholesterol emboli (Hollenhorst plaques) are highly refractile.19 Fibrin-platelet emboli
are whitish plugs that are sometimes seen moving through the retinal arteries. In cyanotic congenital heart disease and at high altitude, there is an increase in retinal vascularity
5/19/2009 3:56:11 PM
Figure 216 A, Brusheld spots

consisting of depigmented foci
(arrows) along the outer circumference
of the iris together with sparse,
thin eyelashes in a child with Down
syndrome and an atrioventricular
septal defect. B, Simian crease (arrow)
traversing the palm of a 6-month-old
child with Down syndrome and an
atrioventricular septal defect.
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Figure 217 A, Painting by

Lyonel Feininger, an Americanborn German Expressionist
(photographed by the author).
The distinctive oblong shape of
the pupils creates the appearance
of a cats eye (arrow), suggesting
that the model had congenital
coloboma (ssures) of the irises.
In the original painting, the
cheeks had the reddish blue hue of
cyanotic congenital heart disease,
probably Fallots tetralogy, a
malformation that coexists with
the cats eye syndrome. B, Oblong
pupils of a cats eye (arrows).
and an increase in vascular caliber probably due to vascular endothelial growth factor
elaborated in response to hypoxemia. Exceptionally, papilledema and retinal edema occur in response to low systemic arterial oxygen saturation.
Retinal Roth spots that accompany infective endocarditis have a white, cotton wool
appearance (perivascular collections of lymphocytes in the nerve layer) surrounded by hemorrhage (see Fig. 214B). Bilateral atypical pigmentary retinopathy is a feature of Kearns
Sayre syndrome mentioned earlier.13 Retinal detachment is an occasional feature of the
EhlersDanlos syndrome, in addition to angioid streaks that radiate from the optic discs as
reddish brown or gray lines that are conspicuously wider than the retinal vessels. Angioid
streaks also occur in pseudoxanthoma elasticum, Paget bone disease, and sickle cell anemia.
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Figure 218
syndrome.
Typical upward dislocation of the lenses (arrows) in a young woman with Marfan
External and Internal Appearance of the Mouth

Examination of the mouth includes the lips, mucous membranes, teeth, gums, tongue,
and palate. The color of the lips may disclose the pallor of anemia or the discoloration of
cyanosis. Thick lips are features of Hurlers syndrome (see Fig. 28 mentioned earlier).
Attention has already been drawn to the absent philtrum of the fetal alcohol syndrome
(see Fig. 211).
Mucous membrane lesions are best examined by everting the upper and lower lips,
and by examining the mucosa of the oral cavity with a ashlight. Petechiae of infective endocarditis can be identied. In hereditary hemorrhagic telangiectasia (RenduOslerWeber syndrome), clusters of tiny ruby patches appear on the lips, oral mucous membranes,
palate, and tongue (Fig. 220), and are associated with pulmonary arteriovenous stulae.
These mucous membrane lesions were well described in an annotation from the Lancet:
Every large general hospital is certain to have on its list of frequent attenders a
small group of unfortunate adults who come to the casualty department complaining of recurrent bleeding from the nose, lips or mouth. The blood is seen to stem
from an insignicant leak in the center of a small ruby patch, many of which are
usually to be found gathered here and there on mucous membranes . Although the
ow of blood is seldom vigorous, it may eventually by its persistence, draw some
concern. Its arrest can be infuriatingly difcult. Each ruby patch marks the position of a tiny arteriovenous communication at the capillary level. Whatever the
cause, they can be induced to bleed by the most trivial of injuries.20
An important aspect of the examination of the mouth is the oral hygiene of
teeth and gums in patients with cardiac or vascular lesions that are substrates for
5/19/2009 3:56:21 PM
Figure 219 Retina of a 28-year-old woman with coarctation of the aorta. Arrows identify
typical U-shaped turtousity of a retinal artery. Hypertensive retinopathy was conspicuously absent.
infective endocarditis. Malformations of the teeth are diagnostically important in

Williams syndrome, the nonhereditary form of supravalvular aortic stenosis with pulmonary artery stenosis (see Fig. 210). Peg teeth are common in Hurlers syndrome
(gargoylism) (see Fig. 28). An even more distinctive malformation of the teeth is a
feature of the Ellisvan Creveld syndrome in which abnormal, prematurely erupted
teeth are present at birth, in addition to gingival hypertrophy and multiple frenuls.5
Phenytoin, which is occasionally used as an antiarrhythmic agent, may cause gingival
hyperplasia.
The appearance of the tongue should be judged according to size, texture, position, and surface lesions. A large, protruding tongue is a feature of Down syndrome
(see Fig. 29) and Hurlers syndrome (Fig. 28) mentioned above. An odd variation is
5/19/2009 3:56:23 PM
Figure 220 A 28-year-old man with RenduOslerWeber hereditary hemorrhagic

telangiectasia. Clusters of ruby patches are on his everted lower lip (arrows). Bilateral pulmonary
arteriovenous stulae were present.
retraction of the tongueglossoptosisin the Pierre Robin syndrome. The retraction

may cause upper airway obstruction and pulmonary hypertension.21 Macroglossia is an
important albeit infrequent feature of primary amyloidosis which is accompanied by restrictive cardiomyopathy.
Examination of the hard palate may disclose innocuous torus palatinus, a bony protuberance or ridge found at the junction of the intermaxillary and transverse palatine
sutures. A distinctive high-arched palate is a feature of Mafan syndrome.
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The Hands and Feet

After the face, the hands are the most expressive parts of the human body. A thumb capable of apposing each nger was a major step forward in mammalian evolution. Strictly
speaking, the hand is equipped with four ngers (triphalangeal digits) and one thumb
(a biphalangeal digit). For the purpose of this discussion, the hands and feet will be considered together. Their appearance is assessed in terms of color and texture of the skin,
structure, and the presence of specic lesions.
An abnormality of color is represented by cyanosis, the blue condition from the Greek
kyanos, blue, and osis, condition. Cyanosis accompanied by clubbing (Fig. 221) is a feature
of a right-to-left shunt in cyanotic congenital heart disease. In older adults, digital clubbing may accompany cyanotic cor pulmonale of chronic obstructive lung disease.
Digital clubbing (Fig. 221) differs from an increase in the convexity of otherwise
normal nails.22 Clubbing requires sufcient elevation of the base of the nail to eliminate the
angle with the contiguous soft tissue (Fig. 221). Clubbing therefore consists not only of an
Figure 221 A, Prole of

normal nger. B, Prole of typical
clubbing of cyanotic congenital
heart disease. The dorsum of the
nail is strikingly convex (curved
arrow), and the angle at its base is
absent (vertical arrow).
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exaggeration of the normal convexity of the nail, but an extension of that convexity to include
the base of the nail. Clubbing is best detected by observing the digit in prole (Fig. 221).
The elevated base of the nail has a spongy texture detected by applying light pressure.
Cyanosis and clubbing are diagnostically important not only because of their presence and degree, but also because of their distribution. When equally represented in the
hands and feet, the causative right-to-left shunt is proximal to the brachiocephalic arteries. Conversely, differential cyanosis and clubbing refers to cyanosis and clubbing of the
feet but not the hands. The diagnostic implication of differential cyanosis is a right-to-left
shunt that delivers unoxygenated blood from the pulmonary trunk into the aorta distal
to the left subclavian artery, so the toes are affected but the hands are spared (Fig. 222).
Figure 222 Differential cyanosis in a 28-year-old woman with patent ductus arteriosus,
pulmonary vascular disease, and reversed shunt. The hands were placed on the dorsa of the feet
to compare the ngers and toes. Because the right-to-left shunt was immediately distal to the
left subciavian artery, the spared right hand is acyanotic and the ngers are not clubbed, the left
hand is mildly cyanotic and clubbed (arrows), and the toes are cyanosed and clubbed.
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Patent ductus arteriosus with suprasystemic pulmonary vascular resistance and reversed
shunt is the cause.5 Differential cyanosis and clubbing are best identied when the patient
sits with knees exed and hands placed upon the dorsa of the feet (Fig. 222). Differential cyanosis is highlighted by exercise or immersion of the hands and feet a warm bath.
Exercise increases the right-to-left shunt, and warmth increases skin blood ow.
Normal young females sometimes have peripheral cyanosis, especially of the feet,
because of innocuous vasoconstriction. The feet are conspicuously cooler than the hands.
Diagnostic error can be prevented by warming the hands and feet, an intervention that
abolishes peripheral cyanosis but exaggerates central cyanosis, as just noted.
Clubbing of the digits and hypertrophic osteoarthropathy are responses to platelet-derived growth factor and transforming growth factor , cytokines, and mitogens
derived from the cytoplasm of shunted systemic venous megakaryocytes.
In patients with the protein-losing enteropathy of chronic constrictive pericarditis
or a Fontan operation, discoloration may appear at the distal border of the ngers. Terry nails are characterized by a distal brownish band, with the proximal 80% of nail bed
white22 (Fig. 223). Lindsay nails associated with chronic renal disease are characterized
by red, pink, or brown discoloration occupying approximately half the distal border of
the nail bed.22
In peripheral vascular disease (see Chapter 3), the texture and color of the atrophic
skin of the feet and toes is shiny, tightly drawn, and often interrupted by ischernic ulcers
(Fig. 224). The ischemic foot is pallid when the leg is elevated and red (rubor) when
the leg is dependent.
Raynaud phenomenon, sometimes seen in primary pulmonary hypertension, is characterized by intermittent alterations in color of the ngers, less commonly of the toes.
Figure 223 A brownish band

1- to 2-mm at the distal end
of the nail bed (arrow). Terry
nails is typically associated with
hypoalbuminemia.
5/19/2009 3:56:28 PM
Figure 224 Atrophic, tightly drawn skin, ischemic ulcers (black and white arrows), and
hypoplastic nails (curved white arrow) in patient with peripheral vascular disease associated with
Werner syndrome and premature aging (see Fig. 26A). Note the ischernic loss of the tips of
several toes.
The affected digits initially manifest intense pallor followed by cyanosis. Before restitution of normal color, the digits may develop intense rubor (reactive hyperemia).
The postmyocardial infarction shoulderhand syndrome is characterized by painless
erythema of the palms and ngertips (Fig. 225A). The skin over the dorsa of the hands
subsequently becomes swollen, tense, discolored, and wrinkled (Fig. 225B). The changes may culminate in Dupuytren contractures.23 Pain, stiffness, and limitation of motion
in the shoulder girdle, usually the left, may coexist.23
In progressive systemic sclerosis (scleroderma), which is accompanied by interstitial pulmonary brosis and pulmonary hypertension, the skin of the dorsa of the ngers
is thickened with loss of the ne transverse creases (Fig. 226).
Abnormalities of the hands and feet may be sufciently distinctive to establish
a diagnosis and predict the coexisting cardiac disease. A prime example is Marfan syndrome, with its remarkable appearance of the hands3 (Fig. 227). In osteogenesis imperfecta, another heritable disorder of connective tissue,16 the joints of the hands are
5/19/2009 3:56:29 PM
Figure 225 A, Painless erythema of the

hands and ngertips in a 56-year-old man
with postmyocardial infarction shoulder
hand syndrome. B, Wrinkling of skin of
the dorsum of the hand after a myocardial
infarction.
hyperextensible but the ngers are not elongated (Fig. 228). Jaccouds arthritis (sometimes mistaken for rheumatoid arthritis) is a postrheumatic fever abnormality in which
the deformity can be voluntarily corrected because the cause is subluxation of the joints
rather than erosion and fusion of articular surfaces24 (Fig. 229).
The hands in Down syndrome are characterized by a simian (Latin simia ape) palmar crease, a distal triaxial radius, increased space between the fourth and fth ngers,
and a short fth nger that is curved inward5 (see Fig. 216B). The association of Down
syndrome with atrioventricular septal defect was mentioned earlier. In Hurlers syndrome (see Fig. 28), inward curvature of the fourth and fth ngers results in a clawlike appearance of the hands, which are wider than they are long.10 Broad thumbs and
toes are characteristic of the RubinsteinTaybi syndrome25 in which the coexisting cardiac malformation is usually patent ductus arteriosus.
Structural abnormalities of the hands and feet are sometimes represented by accessory digits or decient digits. The extra digit is almost always an accessory nger as
in Ellisvan Creveld syndrome, which is accompanied by common atrium (absence of
5/19/2009 3:56:30 PM
Figure 226 Hands of a 56-year-old woman with progressive systemic sclerosis (scleroderma).
The skin of the dorsum of the ngers (arrows) is thickened and smooth, with loss of ne
transverse creases.
the atrial septum), as mentioned earlier. Polydactyly of the hands is invariable in Ellis
van Creveld syndrome, but polydactyly of the feet occurs in only 10 percent of patients.
The converse of polydactyly is a reduction in the number of digits, generally loss of the
thumb, as in HoltOram syndrome.26 The thumb may be present but hypoplastic with
an accessory phalanx (triphalangial) that imparts a crooked appearance to the digit and
makes apposition with ngertips difcult. The HoltOram abnormality becomes more
obvious when the palm is supinated (turned up). The most common coexisting cardiac
anomaly is an ostium secundum atrial septal defect.5 Syndactyly is an innocuous variation in digital reduction, an autosomal disorder characterized by extension of interdigital
webbing so that adjacent digits are fused. Syndactyly is the most common congenital
anomaly of the ngers or toes and is of no special diagnostic signicance.
Pes cavus with hammer toe (Fig. 230) is an abnormality of the foot in Friedreich ataxia27 (see earlier). An even more distinctive and diagnostically useful structural
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Figure 227 A, Elongated, hyperextensible ngers of a young woman with Marfan syndrome.
B, Illustration from Marfans original report. (Un cas de dformation congnitale des quatre membres
plus prononce aux extrmits caractrise par l allongement des os avec un certain degr damincissement.
Bull Mm Soc Md Hp Paris 13:220, 1896.)
abnormality is the rocker-bottom appearance of the foot caused by the protruding heel
in trisomy 18, which is usually associated with patent ductus arteriosus or ventricular
septal defect.5
Discrete lesions of the hands and feet may be subtle and unimportant, such as
subungual splinter hemorrhages. Conversely, white-centered (actually yellowish gray)
lesions are important physical signs of infective endocarditis (Fig. 231). Osler nodes
are tender, pea-sized, raised areas on the pads of the ngers or toes (Fig. 231), on the
thenar or hypothenar eminence, or on the soles of the feet. Osler nodes, while uncommon, are relatively specic for infective endocarditis. Not to be mistaken for Osler nodes
are focal, discolored, tender, painful lesions on the tips of the ngers and toes caused by
small emboli from prosthetic cardiac valves, left ventricular mural thrombi, or marantic
endocarditis.
The Skin
Appearance of the skin is important in terms of color, texture, swelling (edema), and focal lesions. Evaluation of small focal lesions benets from use of a magnifying glass or an
ophthalmoscope as a means of magnication.
5/19/2009 3:56:36 PM
Figure 228 Hyperextensible

but otherwise normal ngers in
a young man with osteogenesis
imperfecta and aortic
regurgitation.
Cyanosis, apart from ngers, toes, and mucous membranes (see above), is detected
in areas where the skin is thin, such as the ears, the tip of the nose, and the soles of the
feet in infants. Cardiac implications of jaundice include chronic passive hepatic congestion, hemolysis from microangiopathic anemia of prosthetic cardiac valves, and from
hemolysis following a large pulmonary infarct. Brawny induration of the legs and feet is
a common consequence of the chronic peripheral edema of congestive heart failure. The
bronze pigmentation of hemochromatosis is most prominent on exposed skin surfaces
and is diagnostically important because of coexisting restrictive or dilated cardiomyopathy, which is potentially reversible by phlebotomy.28 Cafe au lait spots (Fig. 232),
freckles (especially axillary), and neurobromas (skin-colored pedunculated tumors and
subcutaneous nodules) are features of von Recklinghausens disease that is accompanied
by pheochromocytoma and hypertrophic cardiomyopathy. Symmetric vitiligo, especially
5/19/2009 3:56:38 PM
Figure 229 A, Hands of

a patient with postrheumatic
fever (Jaccoud) arthritis.
The right hand shows
typical exion subluxation
and u1nar deviation of the
metacarpophalangeal joints
(arrows). In the left hand, the
deformity has been voluntarily
corrected. B, Radiograph of
the hands in Jaccoud arthritis.
Rheumatic heart disease
was manifested by mitral
regurgitation.
of the distal extremities, is an occasional feature of Graves disease. In myxedema (see

earlier), the texture of the skin is coarse, thick, and dry, with brittle, sparse head hair
that doesnt sustain a curl. In EhlersDanlos syndrome (see above), the skin exhibits remarkable hyperextensibility, with a rubber-like response to stretch, and with cigarette
paper scars that result from fragility and poor healing. In pseudoxanthoma elasticum (see
above), the skin of the neck and axillae is reticular and telangiectatic with small tannish
yellow papules that create the texture and appearance of a plucked chicken.
Subcutaneous edema, a time-honored hallmark of congestive heart failure, is
typically pitting and dependent, involving the ankles and feet in the upright position
5/19/2009 3:56:40 PM
Figure 230 Pes cavus with hammer toe (arrows) in a patient with Friedreich ataxia and
hypertrophic cardiomyopathy.
Figure 231 Typical white-centered (actually yellowish gray), nontender palmar lesions (black
arrows) in infective endocarditis. The pea-sized lesion on the pad of the left thumb (black/white
arrow) was a tender Osler node.
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Figure 232 Cafe au lait spot (white arrows), freckling, and cutaneous neurobromas (black arrows)
in a 38-year-old woman with von Recklinghausen disease and hypertrophic cardiomyopathy.
(Fig. 233) and involving the sacrum in the supine position. Facial edema, especially periorbital, occurs in recumbent infants with congestive heart failure unless the baby is put
into an infant seat so its trunk is elevated. Localized nonpitting pretibial edema is related
to hyperthyroidism, rather than to congestive heart failure.
Acne, a form of localized skin lesion, most commonly found on the face, less
commonly on the shoulders or back, incurs the risk of staphylococcic infective endocarditis. Detection sets the stage for prophylactic skin care. An analogous risk results from
biting or picking the ngernails and the periungual skin (onychophagia) which causes
paronychial infection (Fig. 234), staphylococcic bacteremia, and infective endocarditis.
Striated xanthomas (yellowish streaks) along the palmar creases (Fig. 235) are caused by
type III (broad beta) hyperlipoproteinemia, and are associated with coronary artery disease. Xanthomas (soft, yellowish plaques at the inner canthus of the eyelids) were mentioned earlier. Tuberous xanthomas are yellowish, coalescing nodules most commonly
found on the elbows or knees. Eruptive xanthomas are crops of yellow-orange papules
surrounded by erythematous halos, generally on the arms, legs, and buttocks.
In systemic amyloidosis, discrete localized cutaneous lesions may take the form of
subtle, small, translucent, waxy, at-topped nodules. An ophthalmoscope or hand lens is
especially useful in identifying these small lesions, which are ideal for punch biopsy.
Axillary frecklingCrowe signis a useful sign of Von Recklinghausen neurobromatosis (see earlier).29 Large widespread freckling or lentiginosis (leopard syndrome)
5/19/2009 3:56:45 PM
Figure 233 A, Pretibal

digital compression with the
thumb. B, Pitting edema induced
by digital compression.
is sometimes associated with hypertrophic cardiomyopathy, especially when the lentigines are present from the rst year of life.30
Localized linear scars along the course of antecubital veins imply mainline intravenous drug abuse (Fig. 236) with the risk of staphylococcic bacteremia and right-sided
infective endocarditis. A small localized cutaneous scar may be the only visible remnant
5/19/2009 3:56:47 PM
Figure 234 Badly bitten

infected nails, in a 31-year-old
woman with Fallot tetralogy
and pulmonary atresia.
Staphylococcic bacteremia
caused aortic valve infective
endocarditis.
Figure 235 Striated xanthomas (yellowish streaks, arrowheads) along palmar creases in broad
beta-hyperliproteinemia.
5/19/2009 3:56:51 PM
Figure 236 Mainline

scars (arrows) along the course
of arm veins in a 21-year-old
female heroin addict with
pulmonary valve infective
endocarditis.
of the entrance site of the penetrating injury responsible for an acquired systemic arteriovenous stula.
Subcutaneous nodules in acute rheumatic fever tend to reside over bony prominences of the elbows, the dorsa of the hands or feet, and the malleoli or vertebrae. These
nodules vary from pinhead to 1 to 2 cm, and are unattached to the skin so that the integument moves freely over them. In tuberous sclerosis, the cutaneous lesions are yellow
to orange-red nevi varying in size from a few millimeters to a centimeter, symmetrically
distributed on the malar and nasolabial skin. The lesions are also called adenoma sebaceum and are sometimes accompanied by cardiac rhabdomyoma.
Muscles and Tendons

Abnormal appearance of skeletal muscles generally implies a decrease in mass (atrophy,
dystrophy, wasting). A generalized decrease in muscle mass accompanies the catabolic
effects of chronic congestive heart failure. When these catabolic effects occur in infants
and young children, they are accompanied by growth retardation.
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Alternatively, the decrease in muscle mass can be highly selective, reecting specic
phenotypic features of a systemic neuromuscular disease. An example of selective (regional) muscle wasting (dystrophy, atrophy) is myotonic muscular dystrophy (see Fig. 27)
with involvement of facial, temporalis, and sternocleidomastoid muscles, distal forearm
muscles, and dorsiexors of the feet. Cardiac involvement targets specialized conduction
tissues with abnormalities of impulse and conduction, as mentioned earlier.31
The converse of muscle wasting is represented by pseudohypertrophy especially
but not only of the calves, in boys with classic X-linked Duchenne muscular dystrophy
(see Fig. 24B). Cardiac involvement is common and highly specic31 (see above).
As a rule, muscle weakness accompanies a loss of muscle mass, but occasionally
accidity occurs without muscle wasting. An example is the hypotonia of infants with
Down syndrome5 (Fig. 237). The hypotonia decreases or disappears altogether as the
child grows older.
Examination of tendons discloses abnormalities varying from subtle to obvious.
The Achilles tendons should be palpated routinely in adults to detect thickening caused
by tendon xanthomas, which, when large and nodular, are evident at a glance (Fig. 238).
The diagnostic implication is coronary artery disease. Xanthomas attached to dorsal tendons of the hands may not be seen unless the ngers are gently and rhythmically exed,
imparting motion to the xanthomas that are attached to the tendons but not to the skin.
Shortening of Achilles tendons is an important abnormality in boys with Duchenne
muscular dystrophy (see Fig. 24B), causing them to walk on their toes, compromising
an already tenuous balance.
Figure 237 Hypotonic legs and hyperexible hips in a child with Down syndrome. The
bandage is postoperative for atrioventricular septal defect repair.
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HEEL
Figure 238 Large, nodular

Achilles tendon xanthomas
(arrows) in a young adult male
with heterozygous familial
hypercholesterolemia and
premature coronary artery
disease.
The Thorax
The diagnostic value of thoracic appearance lies in its general conguration and in regional abnormalities of bone or soft tissue. Normal and abnormal movements of the
thorax during active respiration are dealt with in Chapter 7.
One of the most common clinical abnormalities of thoracic appearance results
from pulmonary emphysema (chronic obstructive lung disease). Richard C. Cabots description of large-lunged emphysema is a case in point:
The diagnosis can be made by inspection alone. In typical cases, the anteroposterior dimension of the chest is greatly increased, the interspaces are widened, and
the costal angle is blunted, while the angle of Ludwig (formed by the junction of
5/19/2009 3:56:56 PM
the manubrium with the second piece of the sternum) becomes prominent. The
shoulders are high and stooping and the neck is short (see Chapter 7).32
Structural abnormalities of the thoracic spine and/or sternum vary from
marked distortions that are obvious at a glance to subtle abnormalities that reveal themselves only to a pointed search. Kyphoscoliosis, pectus excavatum, and carinatum are
well-known features of Marfan syndrome (see earlier, and see Chapter 7). An innocuous
loss of normal thoracic curvature (straight back) varies from subtle to obvious, and is
best identied with the patient sitting bolt upright (see Chapter 7). The accompanying
decrease in anteroposterior chest dimensions results in physical signs that are sometimes
mistaken for heart diseasea left parasternal systolic impulse and a pulmonary midsystolic murmur, for example. Importantly, this form of straight thoracic spine leaves
the vertebrae mobile, in contrast to ankylosing spondylitis, in which the thorax is characterized by a rigid spine fused in exion, and in which aortic regurgitation is a common feature. Pectus excavatum of moderate degree is easily overlooked in females with
well-developed breasts. Marked pectus excavatum shifts the heart to the left and results
in a parastemal systolic impulse, and a pulmonary midsystolic murmur, signs similar
to those described above in patients with a loss of thoracic kyphosis and a decrease in
anteroposterior chest dimension. Minor degrees of scoliosis are often recognized during
a routine physical examination, but are readily identied in an anteroposterior chest radiograph. The scoliosis is almost always convex to the right. Convexity to the left arouses
suspicion of a systemic neuromuscular disease or poliomyelitis.
Abnormalities of thoracic conguration are relatively frequent in patients with
congenital heart disease, but the hypothesis that these alterations are due to an increase
in right ventricular mass has not withstood scrutiny.33 The usual variety of chest deformity in such patients is anterior asymmetry, especially a left precordial bulge. When
cardiac dyspnea in infants and young children causes chronic repetitive traction on the
diaphragmatic insertions of the rib cage during growth and development, nonrachitic
Harrisons grooves commonly result.
Soft tissue abnormalities of the thorax are diagnostically important, such as the
scar of a previous thoracotomy. A midline sternotomy scar is not likely to be overlooked,
but lateral thoracotomy scars may be missed. A lateral thoracotomy scar together with
ipsilateral absence of the brachial arterial pulse is a feature of a classic BlalockTaussig
shunt. A left thoracotomy scar together with absence of the left brachial pulse is presumptive evidence of a right aortic arch and a left BlalockTaussig shunt.
Abnormalities of the breasts occasionally take the form of unilateral or bilateral
gynecomastia in males receiving digitalis glycosides34 (Fig. 239). Conversely, hypomastia is part of an asthenic habitus in females. In 45/ XO Turner syndrome, widely spaced
nipples are components of the broad shield chest (see Fig. 22A).
Abdomen
For information on the physical appearance of the abdomen, see Chapter 8.
5/19/2009 3:56:59 PM
Figure 239
dose.
Male gynecomastia in response to digitalis glycosides in an average maintenance
REFERENCES
1. Gombrich EH. Meditations on a Hobby Horse. London: Phaidon, 1978.
2. Shakespeare W. King Henry V, Act 11, Scene 111.
3. Milewicz DM. Molecular genetics of Marfan syndrome and Ehlers-Danlos, type IV. Curr Opin
Cardiol. 1998;13:198.
4. Farquhar JW. The child of the diabetic woman. Arch Dis Child. 1958;34:76.
5. Perloff JK. The Clinical Recognition of Congenital Heart Disease, 5th ed. Philadelphia, PA: WB
Saunders, 2003.
6. Burwell CS, Robin ED, Whaley RD, Bickelmann AG. Extreme obesity associated with alveolar hypoventilationA pickwickian syndrome. Am J Med. 1956;21:811.
7. Mackenzie J. Principles of Diagnosis and Treatment in Heart Affections. London: Oxford University Press, 1916.
8. Shakespeare W. King Richard III, Act 111, Scene IV.
9. Perloff JK, Phelps ET. A review of Wemers syndrome, with a report of the second autopsied
case. Ann Intern Med. 1958;48:205.
10. Renteria VG, Ferrans VJ, Roberts WC. The heart in the Hurler syndrome: Gross, histologic
and ultrastructural observations in ve necropsy cases. Am J Cardiol. 1976;38:487.
11. Clarren SK, Smith DW. The fetal alcohol syndrome. N EngI J Med. 1978;298:1063.
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12. Cayler GG, Blumenfeld CM, Anderson RL. Further studies of patients with the cardiofacial
syndrome. Chest. 1971;60:161.
13. Roberts NK, Perloff JK, Kark RAP. Cardiac conduction in the Kearns-Sayre syndrome (a
neuromuscular disorder associated with progressive external ophthalmoplegia and pigmentary retinopathy). Am J Cardiol. 1979;44:1396.
14. Silverman KH, Hutchins GM, Bulkley BH. Cardiac sarcoid: A clinicopalhologic study of 84
unselected patients with systemic sarcoidosis. Circulation. 1978;58:1204.
15. Ruppert GB, Lindsay J, Barth WF. Cardiac conduction abnormalities in Reiters syndrome.
Am J Med. 1982;73:335.
16. Criscitiello MG, Ronan JA, Besterman EM, Schoenwetter W. Cardiovascular abnormalities in
osteogenesis, imperfecta. Circulation. 1965;31:255.
17. Freedom RM, Gerald PS. Congenital heart disease and the cat eye syndrome. Am J Dis
Child. 1973;126:16.
18. Heggtveit HA: Syphilitic aortitis. A clinicopathologic autopsy study of 100 cases, 1950 to
1960. Circulation. 1964;29:346.
19. Hollenhorst JZW. Signicance of bright placques, in the retinal arterioles. JAMA.
1961;178:23.
20. Editorial. Pulmonary arteriovenous stula in hereditary hemorrhagic telangiectasia. Lancet.
1960;1:158.
21. Jeresatz RM, Husyar RJ, Basu S. Pierre Robin syndrome. Am J Dis Child. 1969;117:710.
22. Beaven DW, Brooks SE. A Color Atlas of the Nail in Clinical Diagnosis. Weert, Netherlands:
Wolfe Medical Publications, 1984.
23. Edeiken J. Shoulder-hand syndrome following myocardial infarction with special reference to
prognosis. Circulation. 1957;16:14.
24. Bittl JA, Perloff JK. Chronic post-rheumatic fever arthropathy of Jaccoud. Am Heart J.
1983;105:515.
25. Gellis SS, Feingold M. Rubinstein-Taybi syndrome. Am J Dis Child. 1971;121: 327.
26. Holt M, Oram S. Familial heart disease with skeletal malformation. Br Heart J.
1960;22:236.
27. Child JS, Perloff JK, Bach PM, et al. Cardiac involvement in Friedreichs ataxia. J Am Coll
Cardiol. 1986;7:1370.
28. Dabestani A, Child JS, Henze IN, et al. Primary hemochromatosis: Anatomic and physiologic characteristics of the cardiac ventricles and their responses to phlebotomy. Am J Cardiol.
1984;54:153.
29. Crowe FW. Axillary freckling as a diagnostic aid in neurobromatosis. Ann Intern Med.
1964;61:1142.
30. Somerville J, Bonham-Carter RE. The heart in lentiginosis. Br Heart J. 1972;34:58.
31. Perloff JK. Neurological disorders and heart disease. In: Braunwald E, ed. Heart Disease, 5th
ed. Philadelphia, PA: WB Saunders, 1997: p1865.
32. Cabot RC. Physical Diagnosis. New York: William Wood, 1915.
33. Maxwell GM. Chest deformity in children with congenital heart disease. Am Heart
J.1957:54:368.
34. LeWinn EB. Gynecomastia during digitalis therapy. N Engl J Med.1953:248:316.
5/19/2009 3:57:01 PM
The Arterial Pulse

With careful practice, the trained nger can become a most sensitive
instrument in the examination of the pulse.1
James Mackenzie trained his palpating nger by meticulous documentation with his
polygraph (Fig. 31). The ancient art of feeling the pulse (Fig. 32) can still be applied
with considerable advantage2:
In examining the pulse, our object is to obtain the most complete and exact knowledge attainable and to interpret accurately the facts we observe; the method to be
followed must therefore be carefully described.3
This chapter describes methods of examining the arterial pulse and calls attention
to the clinical information so derived. Examination refers to palpation, observation, and
auscultation of arterial pulses. Certain pulses are examined routinely; others are examined depending upon the clinical circumstances. Palpation in infants routinely includes
the brachial and femoral arteries. In children and young adults, the carotid is palpated
routinely, whereas in still older adults, routine palpation includes the carotids, brachials,
radials, femorals, dorsalis pedis, posterior tibials, and abdominal aorta. Palpation of additional arterial pulses is performed chiey but not exclusively in older adults, and includes
the subclavian, popliteal, u1nar, and digital (ngertip) pulses.
Observation refers to visible arterial pulsations. Certain pulses are readily seen, such
as the carotid pulsations of severe aortic regurgitation, or the serpentine brachial pulse of
Monckeberg sclerosis (see Fig. 33). Others pulses are less obvious, less important, and
are overlooked unless specically sought such as the pulsating dorsalis pedis in an infant
with a large left-to-right shunt through a patent ductus arteriosus.
Auscultation of arterial pulses is based chiey on patient age. In children and young
adults, normal supraclavicular systolic murmurs are common, and are elicited by placing the
bell of the stethoscope over the subclavian arteries in the supraclavicular fossae (see Chapter
6). In older adults, auscultation of the carotids, subclavians, and femoral arteries should be
routine because of the incidence of atherosclerotic obstruction. Auscultation over the spine
between the scapulae is reserved for patients with coarctation of the aorta. Auscultation of
the abdominal aorta and its bifurcation and over the renal arteries is selectively undertaken.
55
5/19/2009 3:59:47 PM
56 The Arterial Pulse
Figure 31 Mackenzies polygraph designed to record a sphygmogram which is a diagrammatic

representation of the variations of pressure within an artery. When the spring of the sphygmograph
(lower right arrow) is so accurately adjusted on an artery that it does not obliterate the artery when
the arterial pressure is at the lowest, and still slightly compresses the artery when the arterial
pressure is at the highest, the spring will oscillate with each variation of pressure within the artery.
This oscillation being communicated to the lever (middle upper arrow) and recorded on the tracing
paper (left lower arrow), gives us a series of wavy lines, which represent the variations of the pressure
within the artery. (Arrows my additions.) (From Mackenzie J: The Study of the Pulse Arterial,
Venous and Hepatic and of the Movements of the Heart. Edinburgh, Young J. Pentland, 1902.)
Figure 32 Franz van Mieris,

The Doctors Visit. (Courtesy
of, Kunsthistorisches Museum,
Vienna.) In female patients,
decorum precluded palpation of
any pulse except the radial.
5/19/2009 3:59:48 PM
The Arterial Pulse 57
Figure 33 The thickened, serpentine brachial artery of Monckebergs sclerosis visible

beneath the skin of the antecubital fossa (arrows). (From Cabot RC: Physical Diagnosis. New
York, William Wood and Co, 1915.)
INFORMATION DERIVED FROM THE ARTERIAL PULSE

The point rst to be noted is the frequencythe number of beats per minutethe regularity or irregularity of the beats as to time, and their equality or inequality in force . . ..
We should naturally wish, in the next place, to estimate the force or strength of the
pulse . . .. An important point to be investigated is the degree of constant pressure prevailing in the arteries . . .. The character of the beat is another matter for study; and brief
as is the period occupied by it, each pulse wave presents a rise, duration, and fall.3
A SYSTEMATIC APPROACH
To avoid oversight, examination of the arterial pulse should be systematic. A consistent
sequence should be employed (Table 31), although the sequence might differ from examiner to examiner.
Blood Pressure
Before the sphygmomanometer was introduced, Mackenzie argued that
the trained nger is as yet the best guide we have in judging the pressure in an
artery. The ngertips become so educated in the course of time, that we readily
appreciate the sensation conveyed in compressing an artery.1
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Table 31 Examination of the Arterial Pulse

1.
2.
3.
4.
5.
6.
Blood pressure
Cardiac rate and rhythm
Waveform
Differential pulsations:
Right/left, upper/lower
Selective diminution, absence, or augmentation
Arterial thrills and murmurs
Structural properties
Systolic arterial pressure can be estimated by the amount of brachial arterial compression required to obliterate the ipsilateral radial pulse palpated by the examiners other hand.
When relatively mild brachial arterial compression obliterates the radial arterial pulse in
adults, the systolic pressure is generally less than 120 mmHg. When considerable compression is required to achieve this end, the systolic pressure generally exceeds 160 mmHg.
Indirect Measurement
Indirect measurement of blood pressure using an occluding pressure cuff and arterial auscultation was one of the earliest quantitative measurements of major importance
employed at the bedside. Potain (18451901) introduced the sphygmomanometer.4 The
occluding cuff was developed almost immediately by Hill and Barnard in England, and
in Italy by Riva-Rocci, a pupil of Potain.4 However, for practical clinical use, a supplement to these two devices was required, namely, a reliable yet simple method for measuring blood pressure at the bedside. A pivotal gure in lling this need was the young
Russian surgeon Nikolai Korotkoff, who wrote in 1905,
Immediately below a completely compressed artery (with obliteration of the lumen) no sounds are heard. As soon as the rst drops of blood escape from under
the site of pressure, we hear a clapping sound very distinctly. This sound is heard
when the compressed artery is released and even before the appearance of pulsation
in the peripheral branches.5
The next step was the binaural stethoscope which facilitated detection of brachial
arterial Korotkoff sounds. The modern binaural stethoscope, and a mercury aneroid, or
digital cuff provide contemporary clinicians with a rened bedside method for accurate
determination of systemic arterial pressure. The stethoscope should be equipped with
a bell and diaphragm. The sphygmomanometers compression cuff, the hand-operated
bulb for ination, and the adjustable valve for cuff deation should be in perfect working order. The inatable bladder must be completely and securely contained within the
sealed inelastic cuff so that pressure is distributed evenly over the area to which the cuff
is applied. Standard portable aneroid and digital manometers should be periodically
recalibrated against a mercury manometer.
5/19/2009 3:59:50 PM
Taking the blood pressure is routine, but errors abound because of faulty technique. In addition to an instrument in perfect working order, correct cuff size is mandatory because an undersized cuff causes falsely high readings and an oversized cuff causes
falsely low readings.6 Cuff size refers to the width and length of the inner inatable
bladder, not to the cloth covering. Selection of appropriate cuff size is determined by the
circumference of the limb to which it is applied, not the age of the patient.6 The width
of the inatable bladder should be approximately 40 percent of the circumference of the
limb, and the length of the bladder within the cuff must completely encircle the extremity without overlapping.
Brachial arterial pressure is best determined in a quiet setting with the patient
comfortably supine and the arms extended and relaxed parallel to and at the approximate
level of the heart. Although upper extremity blood pressure is routinely determined in
the supine position, a sitting position is acceptable in a young child who may be more
relaxed when sitting in the parents lap, or for home blood pressure in adults who while
sitting, should rest the cuffed arm on a table at the approximate level of the heart.
Sufcient time must elapse for the patient to recover from recent activity and to
relax, especially in an outpatient setting. Blood pressure should be taken in both arms
because systolic pressure tends to be somewhat higher in the right arm, as much as
15 mmHg in normal adults. It is useful to palpate the brachial artery during cuff ination to be certain that the ination pressure is 20 to 30 mmHg above the pressure
required to obliterate the brachial pulse. The adjustable screw valve permits controlled,
slow deation of the cuff. Peak systolic pressure is identied by the appearance of Korotkoff sounds for two or more consecutive beats. Continued slow deation determines the
diastolic pressure which is the point at which Korotkoff sounds disappear rather than the
point of mufing, because the disappearance point is closer to the intra-arterial diastolic
pressure. Inappropriately slow cuff deation should be avoided because the accompanying venous congestion decreases the intensity of Korotkoff sounds, so that systolic
pressure is underestimated while diastolic pressure is overestimated. Once the diastolic
pressure is established, the cuff is rapidly deated. At least 1 minute should elapse before blood pressure measurements are repeated. Audibility of brachial arterial Korotkoff
sounds is improved, sometimes appreciably, by having the patient open and close the st
vigorously a dozen or so times while the arm is elevated.
An auscultatory gap occasionally separates initial Korotkoff sounds from subsequent audibility at a lower pressure. The importance of the auscultatory gap is the risk
of misjudging systolic pressure when the cuff is inated to a level within the gap itself.
This error is avoided by inating the cuff well above the level necessary to obliterate the
brachial arterial pulse (see above).
The seemingly outmoded technique of palpating the pulse for estimating arterial pressure occasionally serves a useful purpose in an acute care setting when Korotkoff
sounds are indistinct or inaudible. The approximate peak systolic pressure is the level
at which a brachial pulse is rst palpated when the cuff is slowly deated. The diastolic
pressure is then estimated by detecting a distinctive snapping quality of the palpable
pulse as the cuff is deated further.
5/19/2009 3:59:50 PM
There is a misconception that cuff brachial arterial pressure is inherently inaccurate in patients with obese arms. Error is avoided by selecting a cuff of appropriate size
(ie, width and length of the inatable bladder as recommended above). A cuff of proper
width (40 percent of the limb circumference) should completely encircle the arm and
exert pressure evenly over the enclosed area.6
Blood pressure should be measured beginning at 3 years of age with normal blood
pressure in children judged according to height and weight. Elderly patients may experience a signicant postprandial fall in systolic and diastolic blood pressure. A higher cuff
pressure is required to compress a rigid sclerotic artery in the elderly than to compress
a normally compliant artery at any age. A sclerotic artery of reduced compliance can be
detected if the ipsilateral brachial or radial pulse remains palpable when the blood pressure cuff is inated above systolicspurious systolic hypertension. This observation was
made by William Osler in 1892 before blood pressure was routinely measured in clinical
practice:7
It may be difcult to estimate how much of the hardness and rmness is due
to the tension of the blood within the vessel and how much to the thickening
of the wall. If, for example, when the radial artery is compressed with the index nger, the artery can be felt beyond the point of compression, its walls are
sclerosed.
A potentially useful variation on routine blood pressure is proportional pulse pressure calculated as the difference between systolic and diastolic pressures divided by
the systolic pressure. A proportional pulse pressure 25 percent or less identies left
ventricular failure and cardiac indices of 2.2 L/min/M2 or less in about 90 percent of
patients.
If the only available cuff does not adequately encircle the upper arm, the same cuff
might be tried on the forearm while the bell of the stethoscope is applied to the radial
artery for the detection of Korotkoff sounds (Fig. 34A). This is a satisfactory technique
provided that the forearm is relatively uniform in circumference, but not when a conical forearm prevents an even distribution of pressure over the encircled area. Properly
determined forearm blood pressure is a reasonable approximation of brachial arterial
pressure.
Orthostatic Hypotension
In adults beyond middle age, orthostatic hypotension can be identied by recording

brachial arterial pressure in the supine and upright positionseither with the patient
standing or with legs dangling over the edge of the examining table or bed. A change
in position from supine to upright is normally accompanied by no more than a 5 to
15 mmHg decline in systolic pressure, whereas diastolic pressure tends to rise. These
changes are accompanied by slight reex tachycardia. Symptomatic orthostatic hypotension is a feature of the ShyDrager syndrome, a rare, progressive degenerative disease
of the autonomic nervous system with loss of involuntary control of blood pressure and
heart rate.
5/19/2009 3:59:50 PM
A special and important form of postural (positional) hypotension is provoked by

the left lateral decubitus position.8 To elicit left lateral decubitus hypotension, a cuff is
placed on both arms, and blood pressure recorded in the supine position, bearing in mind
that, in some normal adults, right arm systolic pressure exceeds left arm systolic pressure
(see above). The patient is then asked to turn into the right lateral decubitus position
while blood pressure is taken in the left arm. After a brief return to the supine position,
the patient is asked to turn into the left lateral decubitus position while blood pressure
is recorded from the right arm. Normally, there is no difference in blood pressure from
supine to right or left lateral decubitus position. Left lateral decubitus hypotension includes a fall in both systolic and diastolic pressure, sometimes accompanied by dyspnea,
palpitations, weakness, and light-headedness.
When an infant is quieted with a bottle or pacier, blood pressure can be obtained by the auscultatory method employing a cuff of appropriate size. Alternatively, the ush method can be used. An uninated cuff is applied to the infants elevated forearm, while the limb distal to the cuff is gently massaged to induce blanching.
The cuff is then inated above anticipated systolic pressure while the arm remains
Figure 34 A, If a cuff appropriate for the upper arm is not available, a standard upper arm
cuff can be applied to the forearm as shown here, provided the forearm is relatively cylindrical.
The bell of the stethoscope (arrow) is placed over the radial artery for detection of Karotkoff
sounds. B (see next page), If a cuff appropriate for the leg is not available, a standard upper arm
cuff can be applied to the distal calf as shown here. Korotkoff sounds are elicited by placing
the bell of the stethoscope over the dorsalis, pedis or posterior tibial artery (arrow), the latter
generally providing a better skin seal. Continued
5/19/2009 3:59:50 PM
Figure 34 Continued
elevated and blanched. The arm is then lowered to a horizontal position and the cuff
is slowly deated. The point at which the blanched hand becomes ushed is an estimate of the mean arterial pressure. To perform the ush method two persons are
required, and even then only a mean arterial pressure is secured. Alternatively, a
simple bedside Doppler device can be used by a single observer to record systolic and
diastolic pressures.
In patients with coarctation of the aorta lower extremity blood pressure is obtained
from the popliteal artery with the patient prone. The popliteal artery is identied by
palpation (see Fig. 35A). A large-size cuff is applied to the thigh,6 and inated to a
level just above the brachial arterial systolic pressure. The cuff should be inated slowly
to avoid discomfort, if not pain. Systolic and diastolic pressures are estimated by auscultation with the stethoscope applied in the poplitieal fossa for Korotkoff sounds originating in the popliteal artery. Not uncommonly, only systolic Korotkoff sounds are clearly
heard, but this is not a shortcoming in the assessment of differential blood pressure in
5/19/2009 3:59:52 PM
Figure 35 A, Palpation of the popliteal artery while the patient is prone with knees exed and
muscles relaxed by resting the leg against the examiners shoulder. The midline of the popliteal
fossa is rmly pressed with both thumbs (arrow). B, Alternative method of palpating the popliteal
artery is more convenient but less sensitive. With the patient supine, the knee is exed while the
ngers of both hands are rmly applied to the midline of the popliteal fossa (arrow).
coarctation of the aorta because diagnostic differences in arm and leg pressures are based
upon systolic, not diastolic levels. The auscultatory popliteal systolic pressure is normally
about 10 mmHg higher than the intra-arterial femoral systolic pressure, but the diastolic
pressures are the same.
If the above technique for determining lower extremity blood pressure proves unsatisfactory, the patient can be returned to the supine position and an arm cuff applied
to the lower half of the calf (Fig. 34B). Korotkoff sounds are then sought by placing
the bell of the stethoscope over the dorsalis pedis or for a better skin seal, over the posterior tibial artery after identifying these pulses by palpation. The disadvantages of this
method are that it cannot be used in infants, and Korotkoff sounds are at best inconsistently heard over the dorsalis pedis or posterior tibial arteries in older patients even
when those arteries are palpable. Exercising the limb sometimes increases audibility of
Korotkoff sounds from these two arteries.
Cardiac Rate and Rhythm

The point rst to be noted is the frequencythe number of beats per minutethe
regularity or irregularity of the beats as to time, and their equality or inequality in
force. This is simple and easy.3
Heart rate is usually determined by palpating an arterial pulse, although cardiac auscultation is sometimes employed (see below). Accurate estimates of rate are now taken
for granted, requiring nothing more than a palpable artery and a watch or clock with a
5/19/2009 3:59:55 PM
second hand. However, an appropriate time piece was long in coming as part of the clinicians bedside accoutrements:
I caused a Pulse-Watch to be made which run 60 seconds, and I placed it in a box
to be more easily carried, and by this I now feel pulses.9
Counting the pulse rate should encompass at least 30 seconds, but when the
rhythm is irregular, a full minute provides a more accurate basis. Under certain circumstancesatrial brillation or marked pulsus alternans, for examplethe rate of the
palpable arterial pulse is slower than the ventricular rate, a pulse decit readily identied
by comparing a palpable arterial pulse rate with the heart rate as judged by simultaneous precordial auscultation. It is self evident that normal cardiac rates vary with age,
from person to person, and under different circumstances in the same person. In 1890,
Broadbent wrote:
The average frequency of the pulse in the adult male is 72 beats per minute; in
the female about 80; in the child it is much more frequent, and it gradually loses
in frequency from infancy onwards. There are slight diurnal variations, but independently of any such inuences, the pulse is more frequent in the evening than
in the morning . . . and it would appear from various considerations that during
a long nights sleep the circulation runs down in vigour as well, and not only in
frequency.3
There are no deviations from the normal character of the pulse so easy to recognize as irregularities in rhythm.1 Mackenzie went on to divide cases into two groups, namely, those in which
the duration of systole was regular and those in which systole was variable in duration.
Characterization of arrhythmias based on the arterial pulse is, with important exceptions,
imprecise, but Mackenzies grouping remains a useful point of departure. If the rhythm is
irregular (variable duration of systole), it is necessary to determine whether the irregularity has a pattern. Simple atrial premature beats do not interrupt subsequent cycle lengths,
provided the sinus node recovery time is normal. Conversely, ventricular premature beats
are followed by compensatory pauses. In either case, it is apparent from the pulse that the basic
rhythm is regular. A pronounced sinus arrhythmia sometimes clouds the picture and leads
to the mistaken conclusion that the basic rhythm is irregular. This error can be avoided by
determining the rhythm with the patients breath held in the respiratory mid-position, a
maneuver that abolishes sinus arrhythmia which is coupled to respiration.
Group beating generally means that the basic rhythm is regular but is systematically interrupted by recurrences of premature beats or cyclic absence of a beat. In 1899,
four years before Einthovens string galvanometer, Karel Frederik Wenckebach, using
radial arterial pulse curves (sphygmograms) and a tuning fork for measuring time, described the periodicity that bears his name as an eponym.10 In 1906, employing the newly developed electrocardiograph, Wenckebach demonstrated that PR intervals lengthened before the dropped beat, conrming his previous observations on second degree
atrioventricular block in frogs.10 Complete loss of regular rhythm (beat-to-beat variation
in the duration of systole) is characteristic of atrial brillation. Even so, a slow ventricular
5/19/2009 3:59:58 PM
response in atrial brillation may be accompanied by differences in cycle lengths that are
too subtle to be detected by palpation of the arterial pulse. Multiple ventricular premature beats sometimes disturb the basic rhythm to a degree that precludes condent distinction from atrial brillation. Examination of the jugular venous pulse serves to make
this distinction (see Chapter 4).
The Valsalva maneuver, described in detail in Chapter 6, is mentioned here because the associated changes in heart rate are detectable at the bedside.11 Phase 2, specifically is accompanied by reex tachycardia and a small pulse, while Phase 4 (overshoot)
is accompanied by reex bradycardia. Congestive heart failure results in loss of the reex
tachycardia of Phase 2 and of the reex bradycardia of Phase 4. Accordingly, determination of the pulse rate during Phases 2 and 4 of the Valsalva maneuver is a simple bedside
method that sheds light on left ventricular function.
One of the most important aspects of examination of the arterial pulse is analysis
of waveform. A necessary precondition is an appreciation of the waveform of the normal
arterial pulse in all ages under varying conditions of relaxation and stress.
G
H
F
A
G
B C
I
D
F
M
E
II
G
III
H
Car
IV
D
E
Subcl
H
Bra
I
H M
N
VI
VII
Rad
Fem
Figure 36 Retraced pulse curves

from different arteries showing
modication in contour from the central
pulses (subclavian, Subcl and carotid,
Car) to distal pulses (brachial, radial,
femoral). (Arrows and labels are my
additions.) (From Wiggers CJ: The
Pressure Pulses in the Cardiovascular
System. London, Longmans, Green and
Co, 1928, reprinted with permission.)
5/19/2009 3:59:59 PM
Assessment of waveform begins with selection of the most appropriate pulse for
examination. The basis for judgment depends on the clinical objective, the structural
state or physical properties of the arterial wall, and the patients age. Because a prime
objective is to secure the most accurate representation of the central arterial pulse, it is
well to remember a point made by Carl Wiggers (Fig.36):
By the time the pulse wave reaches the radial artery, friction has modied the
fundamental contour and in addition has wiped out all of the smaller oscillations
which exist in the central pulse.12
The carotid pulse (Fig. 37) provides a relatively close approximation of the waveform of the central aortic pulse and is readily accessible for palpation except in infants.
Before palpating the carotid, however, certain variables must be taken into account, such
as atherosclerotic obstruction in adults, kinking of the right carotid (see below), and
the presence of a thrill or shudder. Alternatively, certain waveforms are more obvious
in peripheral pulses such as pulsus alternans which is best detected in radial and femoral
arteries, and pulsus bisferiens which is best detected in the brachial artery. However,
these exceptions do not reduce the value of information derived from palpation of the
carotid pulse in older children and adults.
The technique of palpation is all-important. It is best to begin the examination of
the waveform of the arterial pulse by palpating the brachial arteries which are readily
accessible from infancy through adulthood. Start with the right brachial pulse (Fig. 38).
Mackenzie emphasized that Ones whole attention should be concentrated upon the observation. Physicians in Ancient China were enjoined to banish all other thoughts from
their minds in order to concentrate on the pulse. Although these directives are excessive
in contemporary context, it still holds that, without care and attention to arterial pulse
waveform, errors are bound to occur.
Routine palpation of the right brachial pulse is best achieved with the thumb of
the examiners right hand as the patients arm lies supinated (Fig. 38A). Alternatively,
the patients elbow can rest in the palm of the examiners right hand, while the free left
hand passively raises and lowers the patients forearm to achieve maximum relaxation
of muscles around the antecubital fossa (Fig. 38B). In infants, gentle restraint of the
right hand or wrist can reduce undesirable arm movement, but forceful restraint must
be avoided (see below).
The ease with which palpation of the brachial pulse is achieved is inuenced by
the thickness and compressibility of surrounding tissues and by the rmness of the bed
upon which the artery rests. Accordingly, a brachial artery is easier to palpate when
it is relatively supercial and rests on a rm support. The pulse is difcult to palpate
in an obese or muscular arm. Pulsatile, tortuous, thick-walled brachial arteries in elderly adults with Monckebergs sclerosis (Fig. 33) may roll away when palpated, but
despite this difculty, the thumb can almost always x the serpentine artery against
its bed.
Once the brachial artery is identied, progressive gentle pressure is exerted by the
thumb until the maximum systolic impact of the pulse is elicited. The examiner should
5/19/2009 3:59:59 PM
Figure 37 Palpation of the carotid pulse. A, The examiner places the right thumb (arrow)
on the right carotid artery. B, The left thumb (arrow) is then applied to the left carotid which is
used to time the contralateral jugular venous pulse.
then vary the pressure ever so slightly while forming a visual image of the components
of the waveform (Fig. 39).
Palpation of the carotid pulse is best achieved with the examiner at the patients
right side. The right thumb is applied to the patients left carotid (Fig. 37A), and the
5/19/2009 3:59:59 PM
Figure 38 A, Palpation of the

right brachial pulse with the thumb
(arrow) while the patients arm lies at
his or her side palm up. B, Palpation
of the right brachial pulse while
the patients elbow is supported
by the palm of the examiners
hand. The thumb is applied to the
antecubital fossa (arrow) while the
patients forearm is passively raised
and lowered to achieve maximum
relaxation of muscles around the
elbow.
left thumb is applied to the patients right carotid (Fig. 37B). This technique permits
application of the thumb without awkward bending of the wrist that decreases sensitivity in the ngertips. It is obvious that simultaneous palpation of both carotids is illadvised, especially in elderly adults. Sequential palpation avoids risk while permitting
accurate comparative assessment. The thumb should gently and slowly exert pressure
on the carotid pulse to elicit the maximal systolic impact as described above. The artery
should be palpated in the lower third of the neck to avoid inadvertent stimulation of the
carotid sinus, especially in elderly adults.
Palpation of the femoral arterial pulse is best achieved with the examiner at the
patients right side. The right thumb is applied to the patients left femoral artery, and
the left thumb is applied to the right femoral artery (Fig. 310A). The examiners right
thumb is used for comparative palpation of the left brachial pulse (Fig. 310B).
5/19/2009 4:00:01 PM
20
Figure 39 A, Normal intra-arterial

brachial pulse showing an ascending
limb, peak, descending limb, and
dicrotic wave. B, Normal indirect radial
pulse recorded by Mackenzie with his
polygraph (see Fig. 31) applied to the
wrist. (From Mackenzie J: The Study of
the Pulse, Arterial, Venous, and Hepatic,
and of the Movements of the Heart.
Edinburgh, Young J. Pentland, 1902.)
The radial pulse was the time-honored site for palpation when females were not to be
disrobed for examination (see Fig. 32). Mackenzie gave impetus to use of the radial pulse
because it was the most convenient site to which he could x his polygraph (see Fig. 31).
However, the modied contour of the radial pulse12 makes it less useful than the more central
brachial and carotid pulses (see Fig. 36), except for detection of pulses alternans (see below).
In infants, palpation of the radial pulse has inherent limitations (James Mackenzie 1902):
The infants radial artery is naturally very small. We are not conscious of its presence,
being unable to differentiate it from the surrounding structures, and we only recognize
its pulse when the nger presses the artery against the bone. This inability to feel the
artery as a distinct structure is due not only to the smallness of the vessel, but to the fact
that very often the padding of subcutaneous fat is relatively great in the very young.1
For palpation of the radial pulse, the patients hand should be supinated. The examiners thumb (Fig. 311A) or the tip of the index nger (Fig. 311B) is then applied.
The index nger is somewhat more sensitive than the thumb, an observation used to
advantage when palpating a relatively small pulse, such as the radial.
Normal Arterial Pulse
Recognition of abnormal waveforms assumes an understanding of the waveform of the

normal arterial pulse (see and Fig. 39) which varies according to physiologic state, patient age, and distance from the aortic root (see Fig. 36).
5/19/2009 4:00:03 PM
Figure 310 Palpation of the femoral pulse. A, The examiners left thumb is applied to the
patients right femoral pulse (arrow), then vice versa. B, With one thumb palpating a femoral
artery, the free thumb is applied to the contralateral brachial artery (arrow) for simultaneous
comparative assessment.
Mackenzies description of the normal arterial pulse still applies:

There is rst an abrupt rise, then a fall, followed by a continuation of the wave at
about the same level. This period is usually described as being divided into two,
the abrupt rise spoken of as the primary or percussion wave, and the latter portion
5/19/2009 4:00:04 PM
Figure 311 Palpation of the radial pulse. The thumb A or the index nger B is applied to
the radial artery (arrows).
as the tidal or predicrotic wave. With the closure of the aortic valve, the aortic
pressure falls rapidly to the bottom of the aortic notch. This fall is interrupted by
a distinct rise in pressure, represented by the dicrotic wave.1
In characterizing the normal arterial pulse from childhood to young adulthood, attention is paid to the ascending limb, the peak, and the descending limb (see Fig. 39).
5/19/2009 4:00:06 PM
Table 32 Abnormal Waveforms

Diminished
Increased
Double peaked
Small, hypokinetic, with or without a delayed, sustained peak

Hyperkinetic with or without a wide pulse pressure
Systolic or systolic/diastolic
With advancing age, reduced arterial distensibility (see section on Blood Pressure) results in a steeper rate of rise, a higher peak, and a more rapid descent. Otherwise, the
ascending limb normally rises to a single, somewhat rounded peak. The descending limb
is less steep, and is interrupted by an incisura (ie, a brief downward displacement associated with closure of the aortic valve). The pulse then rises slightly (dicrotic wave), before
gradually falling throughout diastole. The incisura, the dicrotic wave, and the anacrotic
notch (see Fig. 36) are seldom palpable.
Abnormal Arterial Pulse
Abnormal waveforms of the arterial pulse are designated as diminished (small, weak,
hypokinetic), increased (large, strong, hyperkinetic), and double-peaked (double systolic
peak or systolic/diastolic peaks) (Table 32).
A diminished arterial pulse is sensed as a gentle impact because the rate of rise is
decreased. The peak is relatively distinct but reduced, ill-dened, and sometimes delayed.
A diminished, weak, hypokinetic arterial pulse occurs with depressed left ventricular
function. In severe aortic stenosis, the arterial pulse is also diminished with a slow ascending
3
200
LV
20
20
0
A
20
0
b
Figure 312 A, Panel 1 shows

a normal brachial arterial pulse
for comparison with Panel 2, the
pulse in aortic valve stenosis, that
shows the typical slow rate of rise
and delayed, broad crest. Panel 3
shows simultaneous left ventricular
(LV) and brachial arterial pulses of
aortic stenosis. The lower left arrow
identies a non-palpable anacrotic
notch. B, Anacrotic pulse in a case
of aortic stenosis. (From Mackenzie
J: The Study of the Pulse, Arterial,
Venous, and Hepatic, and of the
Movements of the Heart. Edinburgh,
Young J. Pentland, 1902.)
5/19/2009 4:00:08 PM
200
LV
BA
A
Figure 313 A, Indirect right brachial

arterial pulse and electrocardiogam from a young
male with severe bicuspid aortic stenosis. There
is a characteristic slow rate of rise (rst arrow),
a non-palpable anacrotic notch (second arrow), a
broad crest (curved arrow), and a non-palpable
dicrotic notch (fourth arrow). B, Left ventricular
(LV) and brachial arterial (BA) pulses from an
elderly male with acquired calcic stenosis of
a trileaet aortic valve. The rate of rise of the
brachial arterial pulse is not slow (rst arrow), and
the crest is not broad (second arrow).
0
B
limb (parvus) and an ill-dened late peak (tardus) (Figs. 312A and 313A). Mackenzie
wrote (Fig.312B):
When there is marked narrowing of the aortic orice, the full effect of the ventricular systole upon the arterial column is not at once developed, as the aortic
stenosis offers an increased resistance. Hence, the impact of the pulse wave on the
5/19/2009 4:00:08 PM
nger is not sudden, but feels to push against the nger in a somewhat leisurely
fashion. The tracing in such a case represents a slanting of the stroke with an interruption near the topan anacrotic-pulse tracing.1
An exception is the pulse in elderly patients with calcic aortic stenosis, in whom
decreased systemic arterial compliance (stiffness) accelerates the rate of rise and counters
the sustained peak (Fig. 313B).
A brisk arterial pulse with normal pulse pressure and a single systolic crest characterizes the rapid ejection of severe mitral regurgitation with hyperkinetic left ventricular
contraction (Fig. 314). A wide pulse pressure with double systolic crests (bisferiens) characterizes the rapid ejection of pure severe aortic regurgitation. It is open to question whether the rapid fall of an arterial pulse (Fig. 315A) is sensed by palpation. The distinction
between an increased arterial pulse with or without wide pulse pressure cannot always be
established by palpation, but an attempt can be made by determining the degree of brachial
arterial compression required to obliterate a simultaneously palpated radial pulse. A brisk
arterial pulse with normal pulse pressure requires only normal brachial compression to obliterate the radial pulse. If the pulse pressure is increased, it must then be determined whether
the increase is due to systolic hypertension (older adult) or to systolic hypertension with low
diastolic pressure in aortic regurgitation (Figs. 315A and 15B), or to a large left-to-right
shunt through a patent ductus arteriosus (Fig. 316). When a wide pulse pressure is due to
systolic hypertension of the elderly, the rate of rise of the ascending limb is moderately brisk.
When a wide pulse pressure is due to high systolic and low diastolic pressure of severe aortic
regurgitation, the rate of rise is not only brisk, but markedly so (Figs. 315 and 316).
The Corrigan pulse refers to the visible pulsations of severe aortic regurgitation described by Dominic J. Corrigan in 1832:
When a patient affected by the disease is stripped, the arterial trunks of the
head, neck and superior extremities immediately catch the eye by their singular
A
20
20
Figure 314 A, Normal brachial arterial

pulse for comparison with the brachial pulse
in pure severe mitral regurgitation (B) that
exhibits a brisk rate of rise (arrow) with only
a modest increase in pulse pressure.
5/19/2009 4:00:09 PM
NORMAL
BRISK
BRISK BISFERIENS
20
20
0
20
20
d
B
Figure 315 A, First panel

Normal brachial arterial pulse. Second
panelBrisk arterial pulse with wide
pulse pressure but single brief crest.
Third panelBrisk bisferiens pulse of
pure severe aortic regurgitation with
a rapid rate of rise and two unequal
crests (small vertical arrows). Fourth
panelBrisk bisferiens pulse with
a rapid rate of rise and two equal
crests (small vertical arrows). B, Pulse
of extreme aortic regurgitation.
(From Mackenzie J: The Study of
the Pulse, Arterial, Venous, and
Hepatic, and of the Movements
of the Heart. Edinburgh, Young
J. Pentland, 1902.) C, Toy water
hammer consisting of a sealed glass
tube containing mercury (arrows)
in a vacuum. As the tube is quickly
inverted back and forth, the mercury
falls abruptly from one end to other,
imparting a jolt or impact to the
thumb or ngertip.
5/19/2009 4:00:09 PM
Aorta
FA
20
20
Figure 316 First PanelThe femoral arterial (FA)

pulse in an infant with large patent ductus arteriosus. The
rate of rise is brisk (arrow), the pulse pressure is wide, and
the systolic crest is single. Second PanelThe central aortic
pulse in the same patient is bisferiens (double arrows).
pulsation. From its singular and striking appearance, the name of visible pulsation is
given to this beating of the arteries. It is much more marked in the arteries of the
head and neck in the erect than in the horizontal posture; and a patient suffering
under the disease himself, rst points it out.13
The wide pulse pressure of free aortic regurgitation has been compared to a water
hammer, a term coined in 1844 by Thomas Watson, an English physician. The water
hammer was a popular toy in Victorian England and consisted of a sealed glass tube
containing mercury in a vacuum. Solids and liquids fall at the same rate in a vacuum, so
when the glass tube is quickly inverted, the mercury column falls abruptly from one end
of the tube to the other (see Fig. 315C), imparting an impact or jolt to the ngertip at
the inverted end. The Victorian toy has long since vanished, but the term is still applied
the arterial pulse of pure free aortic regurgitation.
Double-peaked pulses are of two typesthose with two systolic peaks and those
with one systolic and one diastolic peak. The term double-peaked is preferable, because
the two crests are not necessarily identical (see Figs. 315A and 316). By convention, the
double-peaked systolic pulse is designated bisferiens, whereas a paired systolic/diastolic pulse
is designated dicrotic (Fig. 317). The two peaks of a bisferiens pulse are often palpable, but
that is not the case with a dicrotic pulse. However, terms matter less than clarity. It is not
beside the point that, literally translated, dicrotic and bisferiens mean the same thing.
Dicrotic has a Greek root (di, twice, and krotos, beat). Bisferiens is Latin for beat twice.
The term anacrotic is unimportant at the bedside as a designation for systolic double peaking because the anacrotic pulse is seldom palpable even when clearly recorded
(see Figs. 312 and 313A).
Double systolic peaks are most commonly represented by the bisferiens pulse
of pure aortic regurgitation (see Fig. 315A). The two peaks can be equal, or the rst
or second crest can be the larger of the two (see Figs. 315A and 316). The two
5/19/2009 4:00:10 PM
NORMAL
DICROTIC
20
20
0
Figure 317 First panel shows a normal brachial

arterial pulse. Second panel shows a dicrotic pulse
characterized by a single systolic crest (short arrow)
and an amplied dicrotic wave (long arrow).
CAR
Figure 318 A, Direct brachial pulse and B,

indirect carotid pulse (CAR) from two patients
with hypertrophic obstructive cardiomyopathy.
Similar waveforms show brisk rates of rise and
double systolic peaks (bold arrows). Thin arrows
point to low-amplitude dicrotic waves, conrming
the systolic timing of the two preceding crests.
peaks are not only palpable but are sometimes audible as double Korotkoff sounds.
Double systolic peaks of the arterial pulse also occur in hypertrophic obstructive cardiomyopathy, but palpation usually detects only the brisk rise and sharp initial peak
(Fig. 318).
Pulsus alternans, originally described by Traube in 1872,14 refers to alternation of the strength (force or impact) of the pulse sensed by palpation (Fig. 319A) in the
5/19/2009 4:00:11 PM
B.A
PVC
Radial
B
Figure 319 A, Brachial arterial (BA) pulse showing typical pulsus alternans (vertical arrows)
that is exaggerated after a premature ventricular contraction (PVC). There is beat-to-beat
alternation in peak systolic pressures and alternation of the rates of rise of the ascending limbs. B,
Radial pulse showing the rhythmical irregularity (pulsus alternans).1 C, The strong/weak beats
of a bigerninal pulse recorded by Mackenzie must be distinguished from the strong/weak beats
of pulsus alternans as illustrated above. (Arrows my additions) (B and C are from Mackenzie
J: The Study of the Pulse, Arterial, Venous, and Hepatic, and of the Movements of the Heart.
absence of an arrhythmia (Fig. 319B) or of a signicant variation in interval between

beats. Pulsus alternans must be distinguished from the alternating strong/weak beats of
a bigeminal pulse in which the weaker beat is premature (Fig. 319C). Traube drew a
careful distinction between pulsus bigeminus and pulsus alternans.14
Pulsus alternans can also be identied by beat-to-beat differences in the intensity
of Korotkoff sounds (see below). Alternation of a systemic arterial pulse is a sign of depressed left ventricular systolic function. Alternate beats differ from each other in their
peak systolic pressures, but what is sensed by palpation is the alternating rates of rise of
the ascending limbs (Fig. 319A). Alternation is sometimes so marked that the weak
5/19/2009 4:00:11 PM
beat is not perceivedtotal mechanical alternanseffectively halving the cardiac rate as

judged by the arterial pulse.
Alternans tends to increase as the pulse wave moves peripherally. Accordingly, the
radial and femoral pulses are more revealing than the carotids and brachials. Pulsus alternans is best elicited with the thumb applied to a femoral artery or the thumb or nger
applied to a radial artery. The digital compression is gradually increased until the impact
of the pulse is maximal. Slow release of compression discloses a decrease in impact of the
alternating beats. The pulse should be examined for alternation during quiet breathing or
with the breath held comfortably in the respiratory mid-position to avoid respiratory variations in the arterial pulse (see below). When quiet breathing or breath holding is impractical because of supine dyspnea, the radial pulse should be palpated for alternation while the
patient sits with legs hanging over the bedside or examining table, a position that reduces
or eliminates dyspnea, decreases venous return, and tends to exaggerates alternation. Nitroglycerin has the same effect. It is important to anticipate premature ventricular contractions that transiently provoke or exaggerate pulsus alternans, as shown in Figure 319A.
Pulsus alternans can also be detected by sphygmomanometry. The cuff is inated
to above systolic pressure and then is slowly lowered. Auscultation at the brachial artery
initially detects Korotkoff sounds at half the ventricular rate. When the cuff pressure is
lowered further, Korotkoff sounds suddenly double.
Pulsus paradoxus is a term that was introduced into clinical medicine by Adolph
Kussmaul (1873) to describe the marked inspiratory fall in systemic arterial blood pressure
associated with constrictive pericarditis.15 The inspiratory decline is not really paradoxical,
but instead is an exaggeration of the normal inspiratory decrease in systolic pressure. What
Kussmaul referred to, however, was a pulse that dropped excessively hence paradoxically
with inspiration despite the fact that the heart rate and rhythm remained unchanged.
In a healthy adult, normal inspiration results in no more than a 3 to 4 mmHg decline in systolic blood pressure. Even a relatively deep breath seldom causes a decline that
reaches 10 mmHg. Accordingly, the term pulsus paradoxus applies when the inspiratory decrease exceeds 10 mmHg, especially during average respiratory excursions.
Pulsus paradoxus accompanies certain cardiac diseases and certain forms of pulmonary disease. In cardiac disease, a paradoxical pulse is most often associated with
pericardial tamponade, less frequently with chronic constrictive pericarditis which was
the basis for Kussmauls original description (Fig. 320A). Pulsus paradoxus is characterized by an exaggerated fall in systolic and diastolic pressure because of an abnormal inspiratory fall in left ventricular volume. The most common noncardiac cause of
a paradoxical pulse is pulmonary emphysema (Fig. 320B and 20C). A decrease in
lung compliance coupled with airway obstruction causes an excessive fall in systolic
and diastolic pressures, while exhalation is accompanied by an excessive rise in systolic
pressure (Fig. 320B and 20C).
The trunk should be raised to a level that minimizes respiratory effort. The patient is instructed to breathe as regularly and quietly as comfort permits. The examiners thumb is applied to a brachial arterial pulse with just enough pressure to elicit
the maximal systolic impact. Respiratory movements are monitored by glancing at the
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Ins
Ex
Ins
Ex
Ex.
Jn.
Jn
Ex.
Figure 320 A, Direct brachial arterial (BA) tracing in a young adult with pulsus paradoxus
caused by pericardial tamponade. There is an abnormal fall in systolic and diastolic pressures
during inspiration (Ins). (Exexhalation). B, Direct BA pulse in an elderly adult with chronic
obstructive lung disease and emphysema. During inspiration (Ins) there is an exaggerated fall in
systolic and diastolic pressures, while during exhalation (Ex) there is an exaggerated rise in systolic
pressure. C, Radial arterial pulse showing pulsus paradoxus in . . . a case of capillary bronchitis
and catarrhal pneumonia.1 (From Mackenzie J: The Study of the Pulse, Arterial, Venous, and
Hepatic, and of the Movements of the Heart. Edinburgh, Young J. Pentland, 1902.)
patients chest or abdomen as brachial arterial compression is slowly decreased, seeking

the point at which the pulse diminishes or even vanishes altogether during inspiration.
The paradoxical pulse is readily detected with a sphygmomanometer which is best
reserved for clinical settings in which the anticipated paradox is not elicited by palpation.
With the cuff inated above systolic pressure, Korotkoff sounds are sought over the brachial artery while the cuff is deated at a rate of approximately 2 to 3 mmHg per heartbeat. This method permits identication of peak systolic pressure during exhalation. The
cuff is then deated further in order to determine the level at which Korotkoff sounds are
5/19/2009 4:00:12 PM
audible during both exhalation and inhalation. Pulsus paradoxus is considered present
when the peak systolic pressure levels at exhalation and inhalation exceed 16 mmHg.
Differential Pulsations and Selective Absence,

Diminution, or Augmentation
Palpation can be used to grade an arterial pulse from absent to augmented and for comparison
with established norms for age. Palpation also permits comparison of right vs left and upper
vs lower extremity pulses (Figs. 310 and 321). A numerical system employs 0 to 4+ for
grading an arterial pulse with 0 as absent, 1+ as present but diminished, 2+ as normal, 3+ as
moderately increased, and 4+ as markedly increased . Information thus obtained is, in part, an
extension of the preceding sections that dealt with normal and abnormal waveforms.
Palpation is most revealing when a single digit rather than several ngertips is
used to grade and compare arterial pulses. Sensitivity differs from digit to digit, so application of more than one ngertip compromises the delicate control that is desirable
when an artery is palpated. As a rule, the thumb is preferable for palpation (see earlier)
because it can be moved on its metacarpophalangeal hinge without bending the wrist,
thus avoiding a decrease in sensitivity of the ngertips. The thumb is also convenient
for simultaneous or sequential comparison of right and left arterial pulses (Figs. 37 and
321), and for comparison of upper and lower extremity pulses (Fig. 310B).
Contralateral Pulses
Techniques for comparing contralateral pulses are shown in Figure 321. Brachial pulses
are compared by applying a thumb to the right and left antecubital fossae (Fig. 321A).
In infants, the examiner must wait until the arms are voluntarily relaxed. Restraint is
likely to provoke resistance, compromising rather than facilitating the examination. Brachial pulses are compared simultaneously or sequentially.
In elderly adults, the most common cause of diminution or absence of a brachial
pulse is atherosclerotic obstruction. When coarctation of the aorta obstructs the orice
of the left subclavian artery, the left brachial pulse is diminished or absent in addition to
diminished or absent femoral pulses, while the right brachial pulse is increased. When
aortic stenosis is supravalvular, the right brachial pulse is greater than the left because of
amplication of systolic pressure in the former.
Selective diminution of the left brachial pulse in adults, rarely in children, arouses suspicion of a subclavian steal. The suspicion is reinforced if palpation immediately above the left
clavicle nds the ipsilateral subclavian pulse absent or diminished. Asymmetry of brachial
pulses demands that blood pressure be determined in both arms irrespective of age.
The right and left femoral arterial pulses are compared by simultaneous application
of the thumbs. Comparative palpation of the femoral pulses is obligatory in elderly patients in whom asymmetric diminution indicates atherosclerotic obstruction.
Carotid pulses should be routinely compared in adults, especially elderly adults. Prudence demands that comparison of right and left carotids be accomplished sequentially, not
simultaneously (see Fig. 37), a precaution that minimizes the risk of reducing cerebral blood
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Figure 321 Comparison of the right and left brachial arterial pulses in a child A and in an
adult B by simultaneous palpation with the thumbs (arrows).
ow if partially obstructed carotids are compressed simultaneously. Care should be taken to

avoid palpation in the vicinity of the carotid sinus, especially in the elderly (see earlier).
Selective diminution of a carotid pulse is relatively common in elderly adults,
but selective augmentation is unusual at any age. An example of the latter is the kinked
right carotid16 (Fig. 322) which can be mistaken for a pulsating aneurysm. When the
carotid artery becomes too long for the distance it normally occupies, the vessel loops
upon itself, ie, kinks (Fig. 322), a change that occurs almost exclusively in the right carotid, generally but not always in females beyond middle age.16 Comparative palpation
5/19/2009 4:00:13 PM
Figure 322 Schematic illustrations of kinked

right carotid arteries.
of radial pulses in adults is best achieved by simultaneously applying the thumbs while
the patients hands lie comfortably at the side with the palms supinated. Diminution or
selective absence of a radial pulse, particularly in elderly adults, requires assessment of
radial and ulnar ow using Allens test17 (Fig. 323). Patency of the ulnar artery is determined by sequentially compressing the right and left radial arteries while the patient
briskly opens and closes the st a dozen or so times (Fig. 323A, B). Selective arterial
relling is judged by the rate of color return to the opened but not hyperextended palm
(Fig. 323C), while pressure is maintained on the radial artery (Fig. 323D). Prompt
return of normal color or transient reactive rubor of the palms and ngers indicates that
the ulnar artery contributes normally to the circulation of the hand. Persistent pallor
means ulnar occlusion. To assess patency of the radials arteries, the test is repeated while
the right and left ulnar arteries are compressed.
The ngers as well as the palm should be observed during sequential release of
radial and ulnar arteries (Figs. 323C and 323D) because delayed ushing of an individual digit sometimes indicates local arterial obstruction.
The dorsalis pedis and posterior tibial arteries are palpated routinely in adults. A
ngertip is sometimes more convenient and sensitive than the thumb. This is especially so when applying the index or middle nger to the posterior tibials (Fig. 324).
Pulsations in the dorsalis pedis and posterior tibial arteries vary from time to time in
the same subject. Accordingly, diminution or absence during a single examination
does not necessarily imply a persistent reduction. A tablet of sublingual nitroglycerin resolves doubt by rendering a temporarily absent dorsalis pedis or posterior tibial
pulse readily palpable. The posterior tibial pulse is absent in 10 to 15 percent of normal subjects.
5/19/2009 4:00:15 PM
Upper vs Lower Extremity Pulses
Comparison of upper and lower extremity pulses (Fig. 310B) should be routine irrespective
of age. Two methods are advocated. Some clinicians recommend comparison of femoral and
radial arterial pulses, whereas others advocate comparison of femoral and brachial pulses.
The radial and femoral pulse waves are normally sensed as synchronous, so that any femoral delay is considered abnormal. Positioning the patients wrist next to the groin brings
the radial and femoral arteries into proximity, a technique believed to facilitate comparison. My preference is for simultaneous palpation of brachial and femoral arteries which is
accomplished by placing a thumb on each (Fig. 310B). In infants, especially newborns,
Figure 323 Allens test for assessment of ulnar arterial patency. A, Selective occlusion of the
radial pulse with the examiners thumb (arrow). B, The patient rapidly opens and closes the st to
induce blanching as shown in C (black palmar arrow). There is prompt return of color (arrows) to
the opened but not hyperextended hand, while radial compression continues. D, indicating normal
patency of the ulnar artery. Continued
5/19/2009 4:00:15 PM
palpation of the tiny radial pulse is impractical. When using the technique illustrated in
Figure 310B, the examiner must wait for the baby to relax its legs and arms. Restraint is
counterproductive and can render a normal femoral pulse impalpable. When comparing
the brachial and femoral pulses, the trivial normal delay in perceived arrival time of the
femoral pulse (on the order of 15 milliseconds in adults, less in infants and children) is a
norm against which even slight deviations are readily judged. Furthermore, in all except a
minority of patients with coarctation of the aorta, the femoral arterial pulses are distinctly
reduced (Fig. 325) if not absent altogether, so diagnostic differences between upper and
lower extremity pulses are readily apparent. In the occasional patient with mild coarctation, the femoral pulse is palpable, so that meticulous technique and timing are pivotal. In
any event, what the examiner senses as femoral delay in coarctation is not a delay in arrival
of the femoral arterial pulse, but instead a delay in its rate of rise (Fig. 325).
In adults, especially elderly adults, a relative reduction in femoral compared to
brachial arterial pulsations generally means atherosclerotic iliofemoral obstruction.
Asymmetry of right vs left femoral pulse is common.
Figure 323
Continued
5/19/2009 4:00:17 PM
Figure 324 Palpation of

the posterior tibial arterial
pulse with the index nger
(arrow).
Certain arterial pulses are not routinely palpated, but instead are examined only under circumstances that arouse suspicion. When lower extremity peripheral atherosclerotic
arterial disease is suspected, popliteal pulses should be palpated in addition to femorals,
dorsalis pedis, and posterior tibials. Two techniques of popliteal palpation are shown in
Figure 35. The better technique (Fig. 35A) requires a prone position with exed knee
at less than a right angle, and muscles relaxed by resting the exed leg against the shoulder of the examiner who sits or stands at the bedside or examining table. The midline of
140
BRACHIAL
ART.
FEM.
ART.
100
60
20
0
Figure 325 Simultaneous

brachial and femoral arterial pulses
in coarctation of the aorta. The
arrival times are virtually identical
(lower left arrows). The so-called
femoral delay that is perceived by
the examiner reects dissimilarity
in the rates of rise, not in the
arrival times. The femoral rate of
rise is slower than the brachial rate
of rise (upper right arrows).
5/19/2009 4:00:19 PM
the popliteal fossa is rmly palpated with both thumbs (Fig. 35A). An alternative but
less sensitive method of palpating the popliteal artery is with the patient supine and the
knee exed while the examiner rmly applies the ngers of both hands to the midline of
the popliteal fossa as in Figure 35B.
In coarctation of the aorta, intercostal collateral arterial pulsations can sometimes
be palpated in young adults. Normal intercostal arteries are not palpable, but in coarctation, the apex of the axillae provides access to dilated pulsatile intercostal collaterals.
In Chapter 2, brief comment was made on the skin of the feet in peripheral arterial
occlusive disease. Diagnostic changes in color are elicited as follows. Examination begins
with the patient supine. Each leg is passively elevated, a maneuver that intensies pallor
in the ischemic limb, whereas the skin color of a limb with normal arterial circulation
is not affected. It is useful to elevate both legs simultaneously to induce or intensify the
pallor. The patient should then change promptly from supine to sitting with both legs
lowered passively over the side of the bed or examining table. The rate of color return can
be delayed for as long as 60 seconds. Each foot should be compared with the other. When
color returns, continued dependency results in intensication of rubor in the ischemic
foot or in individual ischemic toes.
Digital (ngertip) pulsations are palpated under specic circumstances, such as severe
aortic regurgitation. The patients ngertips are gently but snugly gripped by the ngertips of the examiner (Fig. 326). To be certain that the ngertip pulsations are those
of the patient and not the examiner, the digital pulses can be timed by simultaneously
Figure 326 Upper left portion of the gure shows palpation of the patients ngertips by
the examiners ngertips. Lower right portion of the gure shows simultaneous palpation of the
patients radial pulse (arrow) to provide assurance that the examiner is not sensing his or her own
ngertip pulse.
5/19/2009 4:00:20 PM
palpating the ipsilateral radial artery with the examiners free hand (Fig. 326). The
visual counterpart of increased digital pulsations in severe aortic regurgitation is the
Quincke pulse18 best elicited by trans-illuminating the ngertip with a pocket ashlight
or otoscope applied in a darkened room to the pad of the ngertip opposite the nail. The
examiners free hand encloses the nger to provide a relatively focused eld that highlights the phasic reddening and blanching of the nailbed with each systole and diastole.
Quincke wrote18:
One observes a distinct lightning-like and momentary accentuation of the reddening, so that the manner of the appearance and disappearance of the capillary
pulse is objectively as characteristic a sign of aortic insufciency as the exquisitely
abrupt pulse to the palpating nger.
Thrills and murmurs should be routinely sought over certain arteries, with the
sites varying according to patient age. In normal children and young adults, an innocent
supraclavicular systolic murmur can be sufciently loud to transmit below the clavicles
as a thrill. Auscultation is performed while the patient sits and looks forward with shoulders relaxed and forearms and hands resting on the lap (Fig. 327A). The bell of the
stethoscope is placed in the supraclavicular fossa over the subclavian artery. The shoulders are then hyperextended with the elbows brought back sharply until the shoulder
girdle muscles are taut (Fig. 327B). In response to this maneuver, the innocent supraclavicular systolic murmur diminishes considerably or disappears altogether.
Auscultation over carotid, subclavian, and femoral arteries is obligatory in elderly
adults even if palpation is unrevealing. Carotid and subclavian auscultation is undertaken while the patient is either supine or sitting, with chin pointed straight ahead. The
bell of the stethoscope is applied just rmly enough to achieve a skin seal over each internal carotid artery in its lower, middle, and upper thirds. A carotid arterial murmur
is not necessarily louder on the side on which the pulse is diminished pulse. In fact, the
converse may be the case. The right and left subclavian arteries are then examined by
applying the stethoscope in the supraclavicular fossae. Femoral arterial auscultation requires that the patient lie supine while the bell of the stethoscope is applied sequentially
in the right and left inguinal regions. Each femoral artery is compared to the other, as
the carotids and subclavians were compared. As with the carotid artery, a femoral arterial
murmur is not necessarily louder on the side of a diminished pulse.
Arterial auscultation at unorthodox sites is based on patient age and clinical suspicion. When coarctation of the aorta is suspected, the diaphragm of the stethoscope
should be applied to the posterior thorax over the vertebral column at the estimated level
of the coarctation. In infants, this observation is best made with the patient prone and
the stethoscopic diaphragm applied over the vertebral column between the scapulae. In
older children and adults, auscultation for this purpose is accomplished with the patient
sitting and the shoulders and thorax relaxed. The murmur overlying the coarctation can
be systolic or continuous, depending on the degree of isthmic obstruction.
In elderly adults, auscultation of the abdominal aorta at its bifurcation is useful
especially when palpation of the femoral arteries discloses iliofemoral atherosclerotic
5/19/2009 4:00:21 PM
LEFT NECK
SM
NOTCH
SM
RT. NECK
SM
Figure 327 A, Supraclavicular auscultation begins while the patient is sitting with
shoulders relaxed and forearms resting on the lap. Inset shows the phonocardiogram of a normal
supraclavicular systolic murmur in the left neck, right neck and suprasternal notch. B, When the
patient hyperextends his shoulders by bringing the elbows well behind the back, the murmur
diminishes or disappears altogether.
obstruction. In hypertensive patients, auscultation in the anks over the right and left
kidneys may identify the soft, high-frequency systolic murmur that occasionally accompanies renal artery stenosis (see Chapter 8).
Structural Properties
We recognize the yielding nature of the arterial coats in healthy arteries. In degeneration of the coats, the arterial walls may be universally thickened or contain
bead-like patches of induration as in atheroma, or the artery may have become a
rigid tube, as in calcareous degeneration.1
Structural abnormalities of systemic arteries can be visually evident. The elongated brachial artery of Monckebergs sclerosis can be seen beneath the skin of the antecubital fossa (see
Fig. 33) as each cardiac cycle imparts distinctive movement to the snake-like tortuous
5/19/2009 4:00:21 PM
vessel. When the artery is rolled under the thumb, it imparts the distinctive feel of a
thickened, rm arterial wall as Mackenzie described above. The radial and the dorsalis
pedis pulses are occasionally visible as well as palpable in free aortic regurgitation or with a
large left-to-right shunt through a patent ductus arteriosus. The distinctive tactile and visual properties of a kinked carotid artery (see Fig. 322) can be mistaken for an aneurysm.
Conversely, true aneurysms are sometimes overlooked unless meticulously sought,
such as an abdominal aortic aneurysm in elderly adults, especially hypertensive (see
Chapter 8). Pulsations of a normal abdominal aorta do not extend below the umbilicus,
even in thin patients with relatively accid abdominal walls. When abdominal pulsations extend below the umbilicus, an aortic aneurysm is the presumptive reason. Systolic
murmurs in the vicinity of abdominal aortic aneurysms originate from iliofemoral obstruction rather than from within the aneurysm.
Femoral arterial aneurysms are, as a rule, readily identied because of unilateral
exaggeration of a femoral pulse, especially if that pulse is visible and the contralateral
femoral pulse is not. Small asymptomatic popliteal aneurysms, typically unilateral, are
sometimes discovered incidentally when the popliteal pulse is palpated. The pulsation of
an aneurysm in the popliteal fossa is more apparent when the patient is examined prone
with the knee exed (see Fig. 35A). An obvious popliteal aneurysm can be overlooked
when examination is performed with the patient supine. Diagnosis depends on assessment of the width of the pulsation when the thumbs are rmly applied to the midline of
the popliteal fossa (Fig. 35A).
REFERENCES
1. Mackenzie J. The Study of the Pulse, Arterial, Venous, and Hepatic, and of the Movements of the
2. ORourke MF, Kelly R, Avolio A. The Arterial Pulse. Philadelphia, PA: Lea & Febiger, 1992.
3. Broadbent WH. The Pulse. London: Cassell, 1890.
4. Lewis WH. The evolution of clinical sphygmomanometry. Bull N Y Acad Med. 1941;17:871.
5. Geddes LA, Hoff HE, Badger AS. Introduction of the auscultatory method of measuring
blood pressure including a translation of Korotkoffs original paper. Cardiovasc Res Center Bull
(Baylor). 1966;5:57.
6. Manning DM, Kuchira C, Kaminski J. Miscufng: Inappropriate blood pressure cuff application. Circulation. 1983;68:763.
7. Osler W. Principles and Practice of Medicine. New York: Appleton-Century, 1892.
8. Wood FC, Wolferth CC. Tolerance of certain cardiac patients for various recumbent positions
(trepopnea). Am J Med Sci. 1937;193:354.
9. Floyer J. The Physicians Pulse Watch. London: Smith and Walford, 1707.
10. Upshaw CB, Silverman ME. The Wenckebach phenomenon; a salute and comment on the
centennial of its original description. Ann Intern Med. 1999;130:58.
11. Nishimura RA, Tajik AJ. The Valsalva maneuver revisited. Mayo Clin Proc. 1986;61:211.
12. Wiggers CJ. The Pressure Pulses in the Cardiovascular System. London: Longmans, Green, 1928.
13. Corrigan DJ. On permanent patency of the mouth of the aorta, or inadequacy of the aortic
valve. Edinb Med Surg J. 1832;37:225.
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14. Traube L. A case of pulsus bigeminus. Berl Klin Wochenschr. 1872;9:185. Translated in Willius
FA, Keys TE, eds. Classics of Cardiology. Malabar, FL: Robert E. Krieger, 1983;p 590.
15. Kussmaul A. Euber schweilige mediastinopericarditis and den paradoxen pulse. Klin Wochenschr. 1873;10:433.
16. Metz H, Murray-Leslie RM, Bannister RG. Kinking of the internal carotid artery in relation
to cerebrovascular disease. Lancet. 1961;1:424.
17. Allen EV. Thromboangiitis obliterans: Methods of diagnosis of chronic occlusive arterial lesions distal to the wrist with illustrative cases. Am J Med Sci. 1929;178:237.
18. Quincke H. Observations on capillary and venous pulse. Berl Klin Wochenschr. 1868;5:357.
Translated in Willius FA, Keys TE, eds. Classics of Cardiology. Malabar, FL: Robert E. Krieger,
1983;p 569.
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5/19/2009 4:00:25 PM
The Jugular and

Peripheral Veins
The internal and external jugular veins are sources of anatomic, hemodynamic, and electrophysiologic information within the chambers of the heartthe right atrium and
right ventricle.1 Veins of the extremities and thoracic inlet reect primary, if not intrinsic, venous disease.
THE JUGULAR VEINS

In 1902, James Mackenzie established the jugular venous pulse as an essential part of the
cardiovascular physical examination:
We come now to the study of a subject which gives us far more information of what
is actually going on within the chambers of the heart. In the study of the venous
pulse we have often the direct means of observing the effects of the systole and diastole of the right auricle, and of the systole and diastole of the right ventricle.1
In the 1950s, Paul Wood rekindled interest in the jugular pulse, emphasizing that
Precise analysis of the cervical venous pulse and measurement of the height of each
individual wave with reference to the sternal angle is not only possible at the bedside but highly desirable.2
Information derived from examination of the jugular veins includes (1) waveform and
pressure, (2) anatomic/physiologic inferences, and (3) arrhythmias and conduction defects. The technique described below permits analysis of the jugular veins in most if not
all patients except in infants whose short necks and lack of cooperation make examination impractical, although not impossible.
External and Internal Jugular Veins

The external jugular vein provides estimates of mean right atrial pressure, while the
internal jugular reects right atrial waveform and pressure. The internal jugular is
93
5/19/2009 4:01:59 PM
94 The Jugular and Peripheral Veins
equipped with a bicuspid venous valve at the thoracic inlet, and lies within the carotid
sheath behind the sternocleidomastoid, an important anatomic relationship emphasized
by Mackenzie1 (Fig. 41A). The jugular bulb, a slight dilatation of the internal jugular
vein immediately proximal to the venous valve, lies in a hollow between the two clavicular insertions of the sternocleidomastoid muscle.
Sterno-mastoid
Carotid artery
Subclavian
artery
Jugular bulb
Innominate
artery
Rt. innominate vien
MANUBRIUM STERNI
A
Figure 41 A, Mackenzies illustration showing the relation of the internal jugular vein to the
carotid and subclavian arteries, and to the sterno-mastoid muscle. He identied the valve in the
jugular bulb. (From Mackenzie J: Diseases of the Heart. London, Oxford University Press, 1908.)
B, Sketch illustrating Mackenzies contention that the direct communication of the right internal
jugular through the right innominate vein and superior vena cava in about a straight line renders
it susceptible to the movements from the right heart. REJ, RIJ = right external jugular and
right internal jugular; LEJ, LIJ = left external jugular and left internal jugular; RIV, LIV = right
innominate and left innominate veins; JB = jugular bulb; SVC = superior vena cava; RA = right
atrium; RV = right ventricle. Continued
5/19/2009 4:02:00 PM
95
Phasic pressure imparted to the internal jugular vein accurately reects the right
atrial waveform. Accordingly, more information is derived from examination of the internal jugular pulse than from the external jugular vein, as Mackenzie originally stated
(Fig. 41B):
The movements communicated by the heart to the blood in the veins are usually best observed in the internal jugular veins. The direct communication of the
right internal jugular through the right innominate and superior cava in about a
straight line renders it susceptible to the movements of the right heart.1
The right internal jugular is therefore more important than the left in the physical examination, because it provides a more direct and therefore a more accurate reection of right
atrial mechanical activity, and of right atrial and right ventricular pressurevolume relationships. When pulsations of the internal jugular vein are more prominent on the left
rather than the right side of the neck, the cause is almost always a persistent left superior
LEJ
REJ
LIJ
RIJ
RIV
LIV
JB
SVC
RA
RV
Figure 41 Continued
5/19/2009 4:02:03 PM
vena cava. Pulsations transmitted from the right atrium into the internal jugular vein are
generated when the steady ow of systemic venous return becomes phasic upon reaching the right atrial chamber. The only signicant difference between the waveforms of
the internal jugular vein and the right atrium is the impact of the carotid pulsethe C
waveupon the former (Fig. 42A, B) (see below).
Normal Waveform of the Internal Jugular Vein

Potain described the waveform of the internal jugular vein in 1867,3 and Mackenzie
provided the nomenclature that remains in use with few or no modications (Fig. 42).
Mackenzie designated the two crests as A and V, and went on to write:
There are two rises in the auricular pressure curvea large and a small one, with
of course two falls. The rst rise in pressure immediately precedes the rise in ventricular pressure. It can only be due to the systole of the auricle. Immediately after
the auricle ceases to contract, there is a great fall (x) in the pressure due to the diastole of the auricle. The auriculo-ventricular valves being closed, the blood pouring
into the auricles from the veins, the pressure gradually rises, producing the second
small wave in the curve. This wave is terminated by the opening of the auriculoventricular valves at the beginning of the ventricular diastole. When the pressure becomes lower in the ventricles than in the auricles, the valve opens and the
contained blood passes through, reducing the auricular pressure, and causing the
second fall (y). After this, the pressure slowly rises by the accumulation of blood in
both chambers, until it is suddenly increased by the next auricular systole.1
These remarks need little or no change. The A wave (Fig. 42A) reects right atrial contraction and occurs just before the carotid arterial pulse and the rst heart sound. The X
descent (decline of the A wave) is initiated by right atrial relaxation, and is reinforced as
right ventricular contraction causes descent of the oor of the right atrium. The initial
portion of the descent (atrial relaxation) is sometimes designated X while the remainder
of the descent during right ventricular contraction is designated X. For practical purposes, the designation X is generally used for the entire descent, while not ignoring the
fact that the descent is due sequentially to right atrial diastole followed by descent of the
oor of the right atrium during ventricular systole.
The X descent, which is often the most conspicuous feature of the normal jugular
venous pulse, is interrupted by the C wave (Figs. 42A and 42B), which is the impact
carotid itself. Mackenzie assigned the letter C to this movement, which he correctly ascribed to the carotid pulse. A relatively small C wave is sometimes generated within the
right atrium proper as right ventricular isovolumetric contraction displaces the tricuspid
leaets upward, but this small intra-atrial C wave is overshadowed in the jugular pulse
by the large carotid pulsation with which it coincides.
The V wave (Fig. 42) was so designated by Mackenzie because its ascent begins
during ventricular systole, hence V. The ascending limb reects passive lling of the
right atrium as venous return confronts a closed tricuspid valve. The Y descent represents
5/19/2009 4:02:03 PM
97
Y
JVP
A
Carotid
Rt. Int. Jugular

v
a c
y
x
a
a
v
h
h
RA
y
Figure 42 A, Normal jugular venous pulse (JVP) showing the A wave, the X descent, the C
wave, and the V wave followed by the Y descent. B, James Mackenzies simultaneous tracings
of the carotid pulse and the jugular pulse, showing the exact synchronism of the carotid wave (c)
in the jugular pulse. The designations of the crests and troughs of the jugular pulse as originally
used by Mackenzie are the same as those in tracing A. (From Mackenzie J: The Study of the
Pulse, Arterial, Venous, and Hepatic, and of the Movements of the Heart. Edinburgh, Young J.
Pentland, 1902.) C, Normal right atrial (RA) pressure pulse. The slight rise preceding the a
wave is called the h wave (arrows). The heart rate is slow.
5/19/2009 4:02:03 PM
sudden termination of the V wave as the right ventricle relaxes, the tricuspid valve opens
and the right atrial pressure rapidly falls. The Y descent is normally less conspicuous than
the X descent, and the Y trough is not as deep as the X trough (Fig. 42).
Following the Y trough, right atrial and right ventricular pressures slowly rise
in parallel (diastases), especially when diastole is prolonged by a slow heart rate. A
slight rise preceding the next A wave is called the h wave (Fig. 42C), so designated by
Hirschfelder in 1907.4 The h wave is seldom, if ever, identied in the normal jugular
venous pulse, even when the cardiac rate is slow.
Technique of Examination
Patient Position and Light Source
Proper examination of the jugular venous pulse demands that the patient lie supine on
a bed or examining table that is readily adjustable above the horizontal (Fig. 43). An
electrically controlled adjustment is ideal.
The trunk should be positioned at an angle that corresponds to the maximum visible
oscillations of the right internal jugular vein. Begin with a 30 degree elevation, then lower
or elevate the trunk to achieve the maximum oscillations. If the jugular venous pressure is
low, the trunk is lowered until pulsations become visible. If oscillations of the internal jugular are not visible at 15 degrees above the horizontal, gentle abdominal compression with
the at of the hand increases venous return and transiently reveals the oscillations (see below under Assessment of Jugular Venous Pressure). The higher the central venous pressure,
the greater the required elevation of the trunk above horizontal. If the crests of the jugular
venous oscillations cannot be seen with the patient sitting bolt upright, the legs should be
dangled over the side of the bed or examining table, a maneuver that generally brings into
view the crests of high jugular venous pulsations. If the oscillations still cannot be seen, the
jugular pulse should be examined with the patient standing.
The head should be adjusted from a neutral position slightly upward or downward and to the right (Fig. 43A) by gently moving the chin, but the head should not be
tilted too far upward or turned too far to the left (Fig. 43B), because these maneuvers
tense the right sternocleidomastoid (Fig. 41B) and compress or obliterate the internal
jugular pulse.
The light source such as a small pocket ashlight with a focused beam is mandatory. Illumination should be tangential, ie, across the area under scrutiny (Fig. 43A)
to highlight the shadow cast by the external jugular and the uctuations of the internal
jugular vein. It is best for the examiner to use the left hand to adjust the light source and
the right hand to palpate the left carotid artery for timing purposes (Fig. 43A). The
right hand can also be used to apply the stethoscope to the chest when the jugular pulse
is timed with the heart sounds (see below).
External Jugular Vein
The right external jugular vein may not be visible unless mechanically distended by digital compression at the root of the neck (Fig. 44A). A visible right external jugular vein
5/19/2009 4:02:06 PM
99
Figure 43 A, The trunk is elevated 30 degrees above the horizontal. The head is adjusted
to look forward or slightly to the right to relax the ipsilateral sternocleidomastoid muscle.
The examiners right thumb palpates the left carotid for timing purposes (upper arrow) while a
tangential light (left horizontal arrow) shines across the right lower neck to highlight the crests and
troughs of the jugular pulse. B, Rotating the head to the left tenses the right sternocleidomastoid
(arrow) and compresses or obliterates the jugular pulse. This position is to be avoided.
5/19/2009 4:02:06 PM
Figure 44 A, The external jugular vein distends when compressed just above the clavicle
(arrow). B, The distended vein disappears (arrow) when compression is released.
is a static nonpulsatile column that becomes apparent when it casts a shadow. The external jugular provides an estimate of the mean vena caval and right atrial pressure, which
reect the right ventricular end-diastolic pressure in the absence of tricuspid stenosis.
Before proceeding, there are three caveats. First, in patients with congestive heart
failure, elevation of the trunk above the horizontal serves to decrease venous return and
lower the central venous pressure.5 Second, veno-constriction occasionally obliterates the
external jugular vein despite an increase in mean right atrial pressure. Third, distention of
the external jugular vein does not necessarily indicate that the mean right atrial pressure
is elevated. If the external jugular is not visible because of veno-constriction, examination of the pulsatile internal jugular vein prevents error (see below). If distention of the
external jugular is not caused by an elevated mean right atrial pressure, the following
simple maneuver claries this point. The distended vein is rst emptied by applying
digital pressure to its superior aspect while blood is mechanically expressed by running a
thumb or nger downward along the course of the vessel. The collapsed vein then lies between the two sites of digital compression. If release of the inferior site results in prompt
lling from below, the cause is a high mean right atrial pressure. As the vessel lls from
below, the column of blood occasionally stops at a distinct bulge that represents a competent internal jugular venous valve (Fig. 41). If the external jugular does not ll from
below, the vein is once again mechanically emptied, and the superior site of digital compression is released. Prompt distention of the vein indicates that lling is from above,
which is of no clinical signicance.
5/19/2009 4:02:08 PM
101
Except for these qualications, the crest of the external jugular vein is a convenient
manometer for estimating mean right atrial or central venous pressure. When the trunk
is elevated 30 degrees above horizontal, the crest of the normal right external jugular vein
is seen just above the clavicle. Digital compression at that site impedes ow from above
and elevates the column (Fig. 44A). When compression is released, the column falls out
of sight (Fig. 44B) or is seen just above the clavicle. In any event, the crest of a normal
external jugular vein does not exceed 3 cm above the sternal angle. When the crest of the
external jugular vein cannot be seen at 30 degrees above the horizontal, the trunk should be
elevated until the crest comes into sight. The height is then measured in centimeters above
the sternal angle, as shown in Figure 48 (Assessment of Jugular Venous Pressure).
Internal Jugular Vein

In 1867, Potain recommended timing the internal jugular pulse by precardial palpation
or auscultation of the heart sounds:
I studied them then in this relationship by combining palpation or auscultation of
the precordial region with inspection of the cervical pulsations.3
Mackenzie subsequently employed the carotid artery for timing (see Fig. 42B). The
carotid pulse and the heart sounds, properly applied, achieve the same end; but the carotid is preferable because the physical examination does not have to be interrupted for
auscultatory orientation, which is especially undesirable in patients with complex heart
sounds and murmurs.
The right thumb palpates the left carotid pulse, while the left hand shines a tangential light across the undulations of the right internal jugular vein (see Fig. 43A).
Cervical venous pulsations that are not synchronous with the carotid cannot be arterial,
and therefore must be venous. The A wave and the beginning of the X descent precede
the carotid (C), which is followed by continuation of the X descent to its trough (see
Fig. 42). The V wave commences immediately after the carotid pulse and is followed
by the Y descent, after which a low amplitude h wave is generated but seldom seen even
if diastole is prolonged (Fig. 42C).
Timing of the jugular venous pulse with auscultation requires selection of a precordial site at which the rst and second heart sounds are clearly identied. The stethoscope is positioned with the right hand while the light source is adjusted with the left
hand. The rst heart sound occurs immediately before the carotid pulse. The A wave and
the beginning of the X descent precede the rst heart sound by a space that coincides
with the PR interval (see later). The remainder of the X descent continues beyond the
rst sound. The second heart sound immediately precedes the crest of the V wave and is
followed by the Y descent.
What the Eye Perceives
The normal jugular venous pulse is a sequence of gentle, undulating crests and troughs.6
The descents, especially the X descent, are usually more obvious than the crests (see
5/19/2009 4:02:10 PM
above). A relatively brisk X descent, for example, makes an otherwise subtle A wave
more apparent. The converse is the case with the carotid pulse, which is more obvious in
its ascent than in its decline. Mackenzie recognized these points:
The sudden collapse of the tissues covering the vein is more striking than the protrusion, whereas the carotid pulse is always abrupt and sudden in its protrusion of
the covering tissues, and gradual in its shrinking.1
Effects of Respiration
Mackenzie also observed that

When the steady stream of venous blood approaches the heart, it is subjected to
the intermittent inuences of the respiratory and cardiac actions.1
The jugular venous pulse is usually more obvious during inspiration. A low normal jugular
pulse is sometimes evident only during inspiration. This is so chiey because the descents,
especially the X descent, are brisker during inspiration and are therefore more apparent.
Despite the inspiratory fall in intrathoracic pressure and the accompanying increase in venous return, there is a decline in mean pressure in the right atrium but an
augmentation of right atrial contractile force. This preserves or increases the crest of the
A wave, thus accentuating the initial portion of the X descent as the right atrium relaxes
more rapidly after its vigorous contraction. In addition, the inspiratory augmentation in
right ventricular volume and contractile force results in a brisker descent of the oor of
the right atrium, and accordingly in a brisker descent of the portion of the X descent that
follows the C wave. The Y descent is increased during inspiration because tricuspid ow
during the rapid lling phase is reinforced by the inspiratory fall in right ventricular diastolic pressure. Kussmauls sign (see below) refers to an abnormal response to inspiration,
namely, a rise in right atrial mean and jugular venous pressures.
Jugular Venous Pulse vs Carotid Pulse
The pulse in the internal jugular vein is often mistaken by most experienced observers for beating of the carotids.1
However, the carotid pulse has a single rise and fall, whereas the jugular pulse has two crests
and two troughs. The rise of the carotid is brisker than its descent, whereas jugular venous
descents are brisker than their crests. Inhalation diminishes the carotid pulse, but makes the
jugular pulse more evident. Abdominal compression (see below) has no effect on the carotid,
but transiently improves visibility of the jugular pulse. The carotid artery is normally palpable, whereas the jugular pulse is not. Sitting improves visibility of the carotid pulse, while
the jugular venous pulse drops from sight. Gentle digital compression above the clavicle
obliterates the jugular venous pulse but not the carotid, as Potain recognized:
A light pressure, suitably applied to the lower portion of the neck can impede
them or suppress them entirely, while the pulsations of the carotid persist with all
of their intensity.3
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c v ac v
x
Rt. Int. Jug.

c
x
Liver
v
x
Figure 45 Simultaneous
tracings of the jugular and liver
pulses.1 The major waveforms
are similar in both tracings
except for absence of the carotid
c wave in the hepatic pulse.
(From Mackenzie J: The Study of
the Pulse, Arterial, Venous, and
Hepatic, and of the Movements of
the Heart. Edinburgh, Young J.
Pentland, 1902.)
103
Hepatic Pulse
The right atrial pulse is transmitted via the superior vena cava into the internal jugular
vein (see Fig. 41), and the hepatic pulse (Figs. 45 and 46) is transmitted via the inferior vena cava into the liver.
The relationship between the liver pulse and the jugular pulse is a very intimate
one. In certain cases, waves of blood are sent back into the inferior vena cava, and these
waves distend the liver, and give rise to a pulsatile swelling of the organ. When there
is both a venous and a liver pulse present they are always of the same character, and one
can demonstrate the changes that take place by the liver pulse as well as by the venous
pulse1 (Figs. 45 and 46).
The hepatic pulse is detected by palpation. The palm of the right hand is placed
upon the patients right upper quadrant below the anticipated liver edge. Care should
be taken to avoid bending the wrist, which decreases sensitivity in the ngertips during
contact with the liver edge. A gentle liver pulse is sometimes detectable in normal thin
individuals with accid abdominal walls. When the liver is palpable during normal respiration, the patient is instructed to hold the breath in a respiratory midposition. If the
liver is not palpable, a moderately deep breath is held just long enough to permit accurate palpation of the descended liver edge.
Abdominal Aorta
Liver pulse
v
y
y
x
Figure 46 Simultaneous tracings of the abdominal aorta and of the liver pulse.1 The
waveform of the liver pulse is not altered by the aortic pulsation. (From Mackenzie J: The Study
of the Pulse, Arterial, Venous, and Hepatic, and of the Movements of the Heart. Edinburgh,
Young J. Pentland, 1902.)
5/19/2009 4:02:10 PM
Assessment of Jugular Venous Pressure
Three venous beds are accessible for estimations of pressurethe external jugular vein,
the internal jugular vein, and veins on the dorsa of the hand (see under The Upper Extremities). In assessing the external or internal jugular venous pressure, it is best to avoid
the term jugular venous distention which is imprecise. The rst necessity is to focus
on a reference point and to adjust the patients trunk above the horizontal (see below).
A useful reference against which venous pressure can be measured is the sternal angle
of Louis (Pierre Charles Alexander Louis, 17871872), which has the advantage of easy
identication (Fig. 47). Recent investigations have conrmed Sir Thomas Lewis observation regarding the accuracy and utility of the sternal angle as a reference point.5
The simplest way of judging the height of the external jugular vein and the height of
the A and V waves of the internal jugular is to measure their crests in centimeters above
the sternal angle, as shown in Figure 48. The height of the jugular venous pressure in
centimeters of water is not recommended for contemporary use because it relates to a time
when manometric estimates were employed.
The examiner should focus rst on the nonpulsatile external jugular vein (see above
and Fig. 44) and then on the height of the A and V crests of the internal jugular (see
above and Fig. 42). In analyzing jugular venous pressure, the trunk should be adjusted
above the horizontal to an angle that coincides with the maximum excursions of the right
internal jugular vein (see earlier). The patients head is positioned to avoid compression
of the right internal jugular vein by the sternocleidomastoid muscle (see Figs. 41A and
43). Rotating the head to the left tenses the sternocleidomastoid (Fig. 43B).
The right internal jugular vein permits assessment of the heights of the A and V
crests (Figs. 42 and 43), and the nonpulsatile external jugular permits an approximation of mean right atrial pressure (see Fig. 44). With the trunk elevated 30 degrees
above the horizontal, normal A and V waves undulate just above the clavicle, with the A
wave slightly dominant (see Fig. 42). When related to the sternal angle as a reference,
the crests of the normal A and V waves do not exceed 3 cm above the angle of Louis when
the trunk is 30 degrees above the horizontal.
1st Rib
2nd Rib
Manubrium
Angle of Louis
Body
Figure 47 The sternal angle of Louis

is a well-dened transverse ridge or
junction between the manubrium above
and the body of the sternum below.
5/19/2009 4:02:11 PM
105
Figure 48 Use of a centimeter rule and a tongue depressor to measure the vertical distance
(arrow) above the sternal angle of Louis (see Fig. 47).
In judging the jugular venous pressure, the response to abdominal compression is

useful. The term hepatojugular reux was coined by Rondot in 1898,7 although observations on the response to abdominal compression were published in England a few years
earlier.8 Right upper quadrant pressure generally provokes the most pronounced response,
but neither enlargement nor compression of the liver is required to elicit the response. In
the presence of congestive hepatomegaly, right upper quadrant pressure may be painful.
Central abdominal pressure (Fig. 49A) avoids the tender liver. Accuracy and practicality
recommend the term abdominojugular reux rather than hepatojugular reux.9
The technique of applying abdominal pressure is important. The patient is instructed to relax and breathe as quietly as comfort permits. The palm of the right
hand is gently applied to the center of the abdomen (periumbilical) as illustrated in
Figure 49A. The examiners hand should be comfortably warm, and the contact gentle. When the patient is breathing quietly and has become accustomed to the examiners hand, compression is gradually increased until the desired rise in jugular venous
pressure is observed while the cervical veins are scrutinized with a pocket ashlight
held in the left hand. Rapid pressure provokes reex abdominal tension. Forewarning
the patient is apt to result in anxious anticipation and is best avoided. The objective
5/19/2009 4:02:11 PM
is to minimize inadvertent straining (the Valsalva maneuver) or increased respiratory excursions which interfere with, if not cancel, the desired response. Compression
is maintained for 10 to 15 seconds while the external and internal jugular veins are
monitored.
The normal response to augmented venous return caused by abdominal compression is a transient increase in prominence of the external jugular vein and of the
crests and troughs of the internal jugular (Fig. 49B). Within a few beats, this initial
increase is followed by a fall to control levels as abdominal compression continues. If
the initial rise in jugular venous pressure is not followed by a prompt fall, but instead is
maintained during the entire 10 to 15 seconds of abdominal compression (Fig. 49C),
the cause is likely to be right ventricular failure. However, a sustained response to abdominal compression also occurs with constrictive pericarditis and tricuspid stenosis.
In the presence of emphysema or bronchospastic pulmonary disease, abdominal compression may result in an abnormal rise in jugular venous pressure in the absence of
Figure 49 A, The abdominojugular reux performed with the palm of the hand gently
but rmly applied to the center of the abdomen. B, The normal jugular response to abdominal
compression (arrow) is a modest transient rise in the jugular pulse followed by a prompt fall to or
below baseline level. C, Abnormal jugular venous response to abdominal compression (arrow) is a
prompt obvious rise that is sustained throughout the 10 to 15 seconds of compression. (Modied
from Sochowski RA et al. Clinical and hemodynamic assessment of the hepatojugular reux. Am
J Cardiol 66:1002,1990. Reprinted with permission.) Continued
5/19/2009 4:02:12 PM
107
right ventricular failure, presumably because a sudden increase in intrathoracic pressure

impedes venous return.
Anatomic-Hemodynamic Inferences
Observations of abnormal waveforms of the right internal jugular vein permit gratifyingly precise, anatomic, and hemodynarnic inferences. The A wave, the X descent, the V
wave, the Y descent, and occasionally the h wave all come under scrutiny.
A Wave
In sinus rhythm, the A wave regularly precedes the carotid pulse. If A waves are
present but do not conform to this sequential relationship to the carotid, or if A
waves are absent altogether, a disturbance in rhythm or conduction is the cause (see
below). Giant A waves leap to the eye, towering above and dwarng the other waves
10
0
B
10
0
C
Figure 49 Continued
5/19/2009 4:02:13 PM
of the venous pulse.2 Such a dramatic event has good reasons, as the following story
illustrates:
One afternoon as I was seeing outpatients with Dr. Wood at the National Heart
Hospital, he stood beside an examining table and looked intently at the neck of a young
woman. Woods comments went something like this:
The pulsation in the neck is extraordinarily large. Even from a distance, I see amplication during inspiration, implying that the pulse is venous. Its regularity
implies sinus rhythm. Assuming that this is so, the prominent pulse must be a giant A wave caused by powerful right atrial contraction against a major resistance.
The resistance can only reside at the tricuspid orice (tricuspid stenosis) or within
a thick-walled hypertrophied right ventricle of severe pulmonary stenosis or pulmonary hypertension with intact ventricular septum.2
Wood then leaned forward, palpated the patients left sternal edge, and remarked:
There is no right ventricular impulse and no thrill of pulmonary stenosis. Nor can
I feel a loud pulmonary component of the second heart sound. The A wave, therefore, cannot be due to either pulmonary stenosis or pulmonary hypertension, so
this young woman must have tricuspid stenosis.2
And so she did!
Giant A waves are generated when a forceful right atrium contracts against an appreciable resistance at one of two levelsan obstructed tricuspid orice or within the cavity of
the thick-walled hypertensive right ventricle of severe pulmonary stenosis or pulmonary
hypertension with intact ventricular septum. Wood referred to the giant A wave as the
venous Corrigan,2 indicating that he, like Dominic Corrigan, was referring to the dramatic
visual pulsation in the neck (see Chapter 3).
Increased A waves range from mild at one end of the spectrum to giant at the other
(Fig. 410). At the mild end, the A wave is abrupt and icking rather than elevated. Inspiration or abdominal compression highlights this impression by transiently increasing
venous return and augmenting the X descent.
X Descent
An increase in the initial portion of the X descent represents enhanced right atrial relaxation that follows augmented contraction due to the normal inspiratory increase in venous
return or to the increased contractile force provoked by resistance to right atrial contraction. An increase in the briskness of the second portion of the X descent (descent of the
oor of the right atrium) occurs in response to augmented right ventricular contraction.
An important variation is constrictive pericarditis, in which the conspicuous X descent is
due chiey if not exclusively, to enhanced descent of the oor of the right atrium during
right ventricular systole (Fig. 411).
In the normal heart, the X descent is brisker and deeper than the Y descent
(see Fig. 42). Blunting of the X descent is an early sign of tricuspid regurgitation
5/19/2009 4:02:14 PM
109
20 mmHg
V
X
Y
0
A
Rt. Int. Jug
v
y
Carotid
Figure 410 A, Giant A

wave in an adult with severe
rheumatic tricuspid stenosis.
B, When the auricular wave is
large and stands out clear and
distinct from other elements, it
is evidence of a powerful right
auricle. (Mackenzie J: The Study
of the Pulse, Arterial, Venous, and
Hepatic, and of the Movements of
the Heart. Edinburgh, Young J.
Pentland, 1902.)
which negates the portion of the X descent that coincides with right ventricular systole (Fig. 412).
V Wave and Y Descent
One constantly nds clinical evidence of the ready occurrence of tricuspid incompetence
in the study of the venous pulse.1 In pure tricuspid regurgitation with sinus rhythm, the
5/19/2009 4:02:14 PM
Radial
x
Rt. Int. Jug.
x
E
x
z
A
20
INSPIR.
EXPIR.
x
RV
y
RA
20
EDD
2
0
Figure 411 A, Simultaneous tracings of the radial and jugular pulses, showing a great
depression occurring during the ventricular diastole. From a case of chronic mediastinitis.1
E is the period of ejection (ventricular systole). z is the trough of the y descent. (From
Mackenzie J: The Study of the Pulse, Arterial, Venous, and Hepatic, and of the Movements of
the Heart. Edinburgh, Young J. Pentland, 1902.) B, The right atrial (RA) pulse in constrictive
pericarditis. There is a conspicuous x descent and an even more conspicuous y descent in
addition to an inspiratory increase in the right atrial pressure pulseKussmauls sign. In the
right ventricular (RV) tracing, a steep early diastolic dip (EDD) (arrow) coincides with the y
descent of the right atrial pulse.
5/19/2009 4:02:14 PM
111
Rt. Int. Jug.

v
v
y
Apex beat
A
V
A
RIGHT ATRIUM
ATRIUM
RIGHT
TRICUSPID INSUF.
INSUF
QRS
Figure 412 A, Simultaneous tracings of the jugular pulse and of the apex beat in a patient
during an attack of heart failure.1 Tricuspid regurgitation obliterated the x descent and
increased the height of the v wave. (From Mackenzie J: The Study of the Pulse, Arterial, Venous,
and Hepatic, and of the Movements of the Heart. Edinburgh, Young J. Pentland, 1902.)
B, Right atrial pressure pulse in severe tricuspid regurgitation. The A/C wave is followed by
obliteration of the second portion of the X descent. A tall V wave is followed by a brisk
Y descent. D = diastasis.
5/19/2009 4:02:16 PM
ascent of the V wave is earlier in systole, its crest is higher, and the Y descent is brisker
(Fig. 412). The tall V is sometimes called a systolic venous wave.
The jugular pulse of tricuspid regurgitation in atrial brillation is characterized by an isolated tall, even giant V wave and a rapid Y descent (diastolic collapse)
(Fig. 413).
When the pulsation is due to the ventricular systole, the engorgement of the veins
is usually so great, the arterial pulse so small, and the cardiac mischief so evident,
that the recognition of the venous pulse is comparatively easy.1
In the presence of tricuspid regurgitation with a tall V wave, the valve of the right
internal jugular vein (Fig. 41) becomes incompetent. Disproportionate systolic lling
and expansion of the right internal jugular vein, which is in direct alignment with the
right atrium (see Fig. 41B), results in a right-to-left head bob, best seen when the examiner observes the patient frontally.
A tall V wave with a rapid Y descent indicates that the tricuspid orice is unobstructed. Conversely, a slow Y descent in the presence of a tall V wave is a feature of
obstruction at the tricuspid orice as in rheumatic tricuspid stenosis (Fig. 414). The Y
descent is slow despite the tall V crest because the stenotic tricuspid orice acts as a brake
on the rate of right ventricular lling. The rate of rise of the V wave is not increased (Fig.
414), because the right atrium lls chiey from the venae cavae, indicating that tricuspid regurgitation is mild or absent.
A modest increase in V wave is a subtle sign of a large atrial septal defect. The A
and V waves in the jugular pulse are equal in height when a nonrestrictive atrial septal
defect permits transmission of the left atrial waveform into the right atrium and internal
jugular vein (Fig. 415).
Jugular
v
Liver
Figure 413 In this gure, the venous

and liver pulses of the ventricular type are
given.1 Both pulses show large v waves
and brisk, if not collapsing y descents of
tricuspid regurgitation. (From Mackenzie J:
The Study of the Pulse, Arterial, Venous,
and Hepatic, and of the Movements of the
Heart. Edinburgh, Young J. Pentland,
1902.)
5/19/2009 4:02:18 PM
113
Figure 414 The jugular

venous pulse in severe
rheumatic tricuspid stenosis
with atrial brillation. Despite
a tall V wave (vertical arrow),
the Y descent is slow (slanting
arrow) because obstruction at
the triuspid orice impedes the
rate of ow.
Amplication of A and V Waves
The most common cause of an increase in A and V waves is right ventricular failure.
Both crests are increased, but the A wave remains dominant as long as the tricuspid
valve is competent. The later part of the X descent is less brisk because of diminished right ventricular systolic contribution to its descent. Rarely, right ventricular
failure is associated with A and V waves that alternateright atrial pulsus alternans
(Fig. 416).
Tricuspid regurgitation with pulmonary hypertensive right ventricular failure is
expressed in the jugular venous pulse as an increase in A and V waves with diminished X
descent and a prominent if not collapsing Y trough. Pulmonary hypertension generates
RA
A
2
0
LA
V
Figure 415 Right atrial (RA) and left atrial (LA)

pressure pulses in a nonrestrictive ostium secundurn
atrial septal defect. The A and V waves are equal in
height and resemble a left atrial pressure pulse which is
transmitted into the right atrium.
5/19/2009 4:02:18 PM
V
C
2
0
Figure 416 Striking right atrial

alternans (arrows) in an infant with
severe pulmonary valve stenosis and
right ventricular failure. The A and V
waves summate because of the rapid
heart rate. C = carotid.
the large A wave, while tricuspid regurgitation blunts the X descent and increases the
V crest and Y descent.
Appreciably elevated and equal A and V waves with inconspicuous pulsations
but brisk X and Y descents (see Fig. 411) are best seen with the patient sitting
bolt upright or even standing. Especially conspicuous and most consistent is the
rapid Y descent to which the term diastolic collapse was applied by Friedreich
in 1864.10
In chronic constrictive pericarditis, high nonpulsatile A and V crests are punctuated by rapid X and Y descents that impart a W-shaped pattern to the jugular pulse
(Fig. 411B). Inspiration increases the rate of fall of both the X and Y descents, but
does not signicantly affect the A and V crests except as expressed in Kussmauls
sign,11 a term still applied to an abnormal inspiratory increase in jugular venous pressure. Inspiratory augmentation in venous return results in an abnormal increase in
mean right atrial pressure and in the A and V crests (see Fig. 411B) because the
constricted right ventricle cannot accept the increase in volume without increasing its
lling pressure.
The h wave is briey mentioned here as a matter of completion. In 1907, Alexander G. Gibson wrote (Fig.42C):
In the course of a study of jugular pulses in normal persons, I have noticed that in
those whose pulse rate is slower than the average, a wave between the V wave and
A wave is often to be seen.12
The h wave is also visible when diastasis occurs at a high right atrial pressure and a slow
heart rate. This is so because ow from a high pressure right atrium into a right ventricle with impaired diastolic distensibility results in a prominent Y trough followed by a
steep ascent to a plateau, the onset of which is seen as an h wave.
5/19/2009 4:02:19 PM
115
Hepatic Pulse
The hepatic pulse is cast into a secondary role because of the relative ease and clarity with
which jugular venous pulsations can be seen. Nevertheless,
In many cases the changes in volume of the liver offer a most constructive indication of the condition of the circulation.1
A liver pulse is anticipated when examination of the jugular pulse predicts transmission of an abnormal right atrial waveform into the inferior vena cava and into the liver. The ngertips perceive hepatic movements that coincide with the waveform of the
jugular pulse (see Figs. 45 and 46). Hepatic pulsations are timed more easily when
there is selective amplication of the presystolic or systolic component of the liver pulse.
Mackenzie remarked:
In tricuspid stenosis, when the auricle at rst hypertrophies, the waves sent back
by the auricle are of sufcient strength to cause a marked pulsation in the liver.1
The liver pulse is most dramatic in severe tricuspid regurgitation with hepatomegaly,
because the right ventricle ejects across the incompetent tricuspid valve directly into the
inferior vena cava and hepatic bed (see Fig. 413). Systolic movements of the liver impart
visible motion to the right upper quadrant and the right lower thorax. Severe tricuspid
regurgitation with hepatomegaly not only results in displacement of the liver edge, but
also in systolic expansion of the liver identied by placing the palpating right hand upon
the right upper quadrant while the left hand is applied directly posterior at the margin
of the lower ribs.
Electrophysiologic InferencesArrhythmias and

Conduction Defects
I had been endeavoring to discriminate between the different forms of irregular heart action and it occurred to me to employ the jugular pulse as an aid. By
this means I was able to separate the great majority of irregularities into denite
groups, according to the mechanism of their production.1
Arrhythmias
H. J. L. Marriotts advice in diagnosing cardiac arrhythmias from the electrocardiogram,

cherchez le P, can be applied to the jugular venous pulse cherchez le A.
Electrocardiographic analysis of complex arrhythmias requires identication of atrial
and ventricular activity and their relationship to each other. The A and V waves of the jugular venous pulse provide the clinician with a bedside opportunity to do just this. Occasionally, the A wave is better seen in the jugular pulse than is the P wave in the electrocardiogram.
Arrhythmias recognized in the jugular venous pulse are listed in Table 41.
The slow cardiac rate and regular rhythm of sinus bradycardia are recognized by
the normal, regular sequence of A wave preceding V wave. However, 2:1 sino-atrial
5/19/2009 4:02:19 PM
Table 41 Arrhythmias Recognized in the Jugular Pulse

Sinus bradycardia
Sinus arrhythmia
Ectopic or premature atrial, junctional, or ventricular beats
Ectopic tachycardias or ectopic rhythms (atrial, junctional, ventricular)
Loss of coordinated atrial activity (atrial brillation)
exit block is indistinguishable from sinus bradycardia in the jugular pulse, as in the
electrocardiogram. Sinus arrhythmia is recognized by rate accelerations that coincide
with inspiration and are abolished when the breath is held in the respiratory midposition while the normal A-C-V sequence remains unchanged (Fig. 417). Premature
atrial beats are represented by cycles that begin early but have the normal sequence of
A wave, carotid pulse, and V wave. The changes in cycle length prompted by premature atrial beats are distinguished from the changes in cycle length of sinus arrhythmia
because the latter are abolished during held respiration. In older subjects, premature
atrial beats are sometimes accompanied by pauses because of prolonged sinus reset
times. These pauses should not be mistaken for the compensatory pauses that follow
premature ventricular beats. Error is avoided by observing the jugular pulse in which
the atrial premature beat maintains a normal relationship between the A wave and
carotid pulse.
Cannon wave refers to amplication of the A wave when right atrial contraction coincides with a closed tricuspid valve. In ventricular or junctional premature beats
(Fig. 418), cannon waves are the rule because right atrial systole nds the tricuspid
valve closed by the premature ventricular contraction. Accordingly, cannon waves distinguish ventricular premature beats followed by compensatory pauses from atrial premature beats with a prolonged sinus reset time. With junctional premature beats, cannon
c
v a
v
ac v
E G
E
G
ac v
Figure 417 Simultaneous tracings of the jugular and radial pulses showing agreement in
rhythm of the right auricle and ventricle (waves a and v) with the radial pulse, in the youthful
form of irregularity1 (sinus arrhythmia) E is the ejection period (ventricular systole). (From
the Heart. Edinburgh, Young J. Pentland, 1902.)
5/19/2009 4:02:19 PM
v
a c
a
a
c
o
c v
Car.
a
117
Figure 418 Simultaneous tracings of the jugular and radial pulse. The auricular wave
following a occurs earlier, as if to take on the ventricular rhythm.1 The tracings illustrate
cannon A waves (a) that coincide with premature ventricular beats (o) identied in the radial
pulse. Car = carotid. (From Mackenzie J: The Study of the Pulse, Arterial, Venous, and Hepatic,
and of the Movements of the Heart. Edinburgh, Young J. Pentland, 1902.)
waves occur whether or not the premature beats are accompanied by retrograde atrial
activation (Fig. 419).
Recognition of ectopic tachycardias is, in part, an extension of the comments on
individual ectopic beats. Continuous beat-to-beat cannon A waves in junctional tachycardia (Fig. 420) are examples of the sustained mechanism for generating intermittent
cannon waves of individual junctional premature beats (see Fig. 419). Sustained junctional rhythm with rates above 100 beats per minute is called junctional tachycardia,
and below 100 beats per minute is called junctional rhythm. In atrioventricular nodal
reentrant tachycardia, a discernable A wave precedes each carotid pulse provided that
the rate is not excessive. With rates above 160 beats per minute, the A and V waves
JVP
CANNON
WAVE
Figure 419 Jugular venous pulse (JVP) showing a cannon A wave (horizontal arrow) caused
by retrograde atrial activation (inverted P wave) with a junctional premature beat (rst upper
vertical arrow).
5/19/2009 4:02:19 PM
JVP
C
CANNON
WAVE
Figure 420 Jugular venous pulse (JVP) with a junctional rhythm (1:1 retrograde atrial
activation, inverted P waves) and regular sustained cannon waves. C = carotid.
merge into a single venous crest followed by a single descent. Mackenzies description
is relevant:
With still greater increase of the pulse rate, the ventricular wave v becomes shortened even to such an extent that its rise is blended into that of the auricular wave,
so that only one true venous pulse wave is recognized.1 (Fig. 421)
These summated A and V crests resemble beat-to-beat cannon waves of junctional tachycardia (Fig. 420), the distinction lying chiey in the difference in heart rates. Atrioventricular nodal reentrant tachycardia is usually associated with rates of 160 to 250 beats
per minute, whereas in junctional tachycardia, the rates are slower, generally just above
100 beats per minute. However, in atrioventricular nodal reentrant tachycardia, when atrial
and ventricular activations are simultaneous, or in circus movement tachycardia when ventricular activation immediately precedes atrial activation, atrial contraction is against a
closed tricuspid valve, producing rhythmic cannon waves in the jugular pulse.
Ventricular tachycardia with 1:1 retrograde atrial activation results in beat-to-beat
cannon waves indistinguishable from those of junctional tachycardia. More commonly, however, ventricular tachycardia produces a fundamentally different jugular venous
pulse because atrial activity is independent of ventricular activity (atrioventricular dissociation). Ventricular tachycardia is recognized in the jugular pulse by a regular rhythm and
rapid rate as judged by palpation of the carotid, accompanied by independent A waves at
5/19/2009 4:02:21 PM
Jng.
119
car.
Rad.
Figure 421 Simultaneous tracings of the pulsation in the jugular bulb and in the radial and
carotid pulses during an attack of paroxysmal tachycardia, taken 18 hours from the beginning
of the attack.1 The illustration shows summation of A and V waves into a single venous crest
followed by a single descent. Jug = jugular; car = carotid; Rad = radial. (From Mackenzie J:
The Study of the Pulse, Arterial, Venous, and Hepatic, and of the Movements of the Heart.
a rate slower than the rate of the carotid pulse. Importantly, and distinctively, fortuitous
atrial contraction against a closed tricuspid valve results in intermittent amplication
of right atrial beatscannon A waves. Accordingly, regular tachycardia occurring with
slower independent A waves and intermittent cannon waves is characteristic of ventricular tachycardia. When P waves cannot condently be identied in the electrocardiogram,
this observation is useful in distinguishing ventricular tachycardia from supraventricular
tachycardia with aberrant ventricular conduction.
Atrial utter is represented by coordinated atrial activity at rates of about 300 beats
per minute, and a regular ventricular response at 150 beats per minute (2:1 atrioventricular block). The ease with which utter waves are seen in the jugular venous pulse
(Fig. 422) depends on the functional condition of the right atrium prior to the onset
of utter. When sinus rhythm with large A waves is replaced by atrial utter, the utter
waves are likely to be large as shown in Figure 422. Carotid sinus massage transiently slows the ventricular response, facilitating detection of utter waves in the jugular
pulse. Similarly, when atrial utter occurs with a higher degree atrioventricular block
(generally 4:1), utter waves are easier to identify in the jugular pulse because diastole is
relatively long. Flutter waves amplify in bursts when the right atrium utters against a
closed tricuspid valve (Fig. 422).
Atrial brillation is represented in the jugular pulse by absence of coordinated atrial activity. Loss of A waves in the presence of an irregular rhythm as judged by palpation
of the carotid distinguishes the irregular rhythm of atrial brillation from the irregular
rhythm of multiple premature atrial or ventricular beats in which A waves are present
and often distinctive, as described earlier. Because absent right atrial contraction is necessarily accompanied by absence of relaxation, the initial portion of the X descent is
lacking, so the X trough is relatively inconspicuous.
Conduction defects recognized in the jugular pulse are listed in Table 42. The PR
interval can be estimated by the interval between the A wave and carotid pulse. The
5/19/2009 4:02:22 PM
Figure 422 Jugular venous pulse with prominent utter waves (F) that amplify in bursts
(upper curved arrows) in a case of rheumatic mitral stenosis. The electrocardiogram shows utter
waves (arrows).
practiced eye comes to recognize normal, prolonged, or short A-C (and therefore PR)
intervals. Complete left bundle-branch block slightly prolongs the A-C interval by delaying
left ventricular activation. A corollary of A-C prolongation is Wenckebach periodicity that
is characterized in the jugular pulse by gradual lengthening of A-C intervals, culminating in an A wave that is not followed by a carotid pulse (nonconducted beat). Mobitz I
Wenckebach periods13 differ from Mobitz II atrioventricular block that is represented in
the jugular pulse by A-C intervals that do not vary but are suddenly interrupted by an
isolated A wave that is not followed by a carotid pulse (a nonconducted beat). Interestingly, Wenckebach described the periodicity that bears his name in 1899, which was
prior to the introduction of electrocardiography into clinical practice13 (see Chapter 3). In
two-to-one atrioventricular block, there are two A waves for every carotid pulse (Fig. 423).
The X descent of the blocked (nonconducted) A wave is blunted because only the portion
coinciding with right atrial relaxation is present. The second portion of the X descent is
absent because the blocked A wave is not followed by ventricular systole and descent of
the oor of the right atrium.
Table 42 Conduction Defects Recognized in the Jugular Pulse

PR interval prolongation
Wenckebach periods
Second degree atrioventricular block
Complete heart block
5/19/2009 4:02:22 PM
c
a
121
Figure 423 Tracings of the pulsation in the neck due to a wave, a, in the jugular vein and
the carotid pulse, c, taken at the same time as the radial. There are two auricular waves, a, to one
carotid pulse (2:1 atrioventricular block.) (From Mackenzie J: The Study of the Pulse, Arterial,
Venous, and Hepatic, and of the Movements of the Heart. Edinburgh, Young J. Pentland, 1902.)
Complete atrioventricular block was described by William Stokes (1846) in his Observations on Some Cases of Permanently Slow Pulse.
A new symptom has appeared, a very remarkable pulsation in the right jugular
vein. The number of the reex pulsations is difcult to be established, but they
are more than double the number of the manifest ventricular contractions. About
every third pulsation is very strong and sudden and may be seen at a distance; the
remaining waves are much less distinct and some very minor ones can also be perceived. The appearance of this patients neck is very singular, and the pulsation of
the veins is of a kind which we have never before witnessed.14
In complete heart block, coordinated atrial activity is more rapid than and is dissociated from ventricular activity that arises from a slow, regular, idioventricular focus
(Fig. 424). The long diastoles disclose independent A waves, which are punctuated by
intermittent cannon waves as right atrial contraction fortuitously coincides with right
ventricular systole and a closed tricuspid valve (Fig. 424). Accordingly, complete heart
block is diagnosed in the jugular venous pulse when intermittent cannon A waves occur
with smaller independent A waves at a rate faster than the ventricular bradycardia identied by the carotid pulse (Fig. 424).
VEINS OF THE EXTREMITIES AND THORACIC INLET

Lower Extremities
Physical examination of lower extremity veins seeks chiey to identify varicose veins,
thrombophlebitis (supercial and deep), and signs of chronic venous insufciency. Supercial thrombophlebitis is characterized by a visible and palpable thrombus in a vein just
beneath the skin, hence supercial. Commonest sites are the saphenous veins and their
tributaries. In the acute state, an indurated, palpable tender cord of varying length is
accompanied by a visible red line along the course of the inamed vessel without edema.
As the acute inammation subsides, a palpable nontender cord sometimes persists for
weeks. Thromboplebitis usually destroys venous valves, rendering them incompetent
when the leg is dependent.
5/19/2009 4:02:24 PM
RA
A
A
C
A
Figure 424 Right atrial (RA) pressure pulse in complete heart block. P waves (curved arrows)
in the electrocardiogram are independent of the QRS. The venous waveform shows independent
A waves and intermittent cannon A waves (arrows). C = carotid.
Deep thrombophlebitis typically involves calf veins or iliofemoral veins and may
initially escape attention because physical signs and symptoms are apt to be scanty. It is
therefore important to seek the signs of deep vein thrombophlebitis in clinical settings
that heighten suspicioncongestive heart failure, postpartum, after major surgery, during
protracted debilitating illnesses, and in elderly patients who sit for hours with legs dependent and knees exed. Local calf tenderness is often the earliest sign. With the patient
supine and the knee exed, the relaxed calf muscles are gently compressed against the tibia
(Fig. 425). Gentle compression with the ngertips, is preferable to squeezing the calf, a
maneuver that can elicit pain even in normal subjects. Homans signdorsiexion of the
footis far less useful than careful systematic compression of the calf as just described.
Homans sign is positive in only about 50 percent of patients with calf deep vein thrombophlebitis, and the sign can be elicited in the absence of venous thrombosis in patients
with muscular disorders of the lower extremities. In addition to local tenderness, deep vein
thrombosis is generally accompanied by swelling together with increased skin temperature
and tissue turgor. Iliofemoral venous thrombosis is accompanied by tenderness, pain, edema, skin suffusion, increased skin temperature, and visible supercial venous patterns.
Varicose veins, recognized by Hippocrates 2500 years ago, are the most common
clinical vascular abnormality of the lower extremities. Nevertheless, varicose veins are
5/19/2009 4:02:24 PM
123
Figure 425 With the patient supine and knee exed, the ngertips (arrows) gently compress
the calf muscles against the tibia.
often overlooked during routine physical examination because the legs are not uncovered
and properly examined while the patient is standing.
The word varicose is derived from the Latin varicosus, the adjectival form of varix,
meaning tortuous blood vessel. Varices, the plural of varix, is a term that remains in
general use. Varicose veins, varices, or varicosities vary from cosmetically undesirable but
medically unimportant clusters of small intracutaneous vessels, to the dramatic, serpentine dilatation shown in Figure 426. Gravity distends the vessels, so examination in the
standing position is obligatory (see above).
Hieronymus Fabricus (15371619) described venous valves as extremely delicate little membranes in the lumen of veins, an observation that inuenced William
Harveys study of the circulation of the blood. Incompetence of venous valvessupercial (saphenous) and deep (iliofemoral)sets the stage for chronic venous insufciency,
the signs of which are characteristic. The leg is swollen, and the skin and subcutaneous
tissues of the lower third of the leg and ankle are discolored by brownish stasis pigmentation (Fig. 426). Cellulitis, skin erosion, and ulcerations develop, especially around the
malleoli, more commonly the internal malleoli.
The high systemic venous pressure accompanying right ventricular failure aggravates distention of varicosities. Tricuspid regurgitation, especially when severe, occasionally imparts systolic pulsations to the varicose veins.
5/19/2009 4:02:25 PM
Figure 426 Varicose veins (black arrows) distend when the patient stands. In the ankle and
foot, white arrows identify the swelling and discoloration of chronic venous stasis. (Courtesy of,
Dr. Ronald W. Busuttil, Professor of Surgery, UCLA Medical Center.)
Upper Extremities
Distention of veins of the dorsa of the hands or antecubital fossae without intrinsic venous disease occurs when central venous pressure is appreciably elevated. Dorsal hand
veins have been used to assess central venous pressure. With the patients trunk above
the horizontal and adjusted for comfort, the hand under scrutiny is rst lowered beneath
the sternal angle without exing the elbow until its dorsal veins distend. The arm is then
5/19/2009 4:02:26 PM
125
gradually and passively raised while the dorsal veins are observed as the hand approaches
the level of the sternal angle. Normally, these hand veins empty at that level when the
patients trunk is 30 degrees above the horizontal. Persistent distention indicates elevation of the central venous pressure, the height of which is estimated by the vertical
distance above the angle of Louis at which the dorsal veins visibly collapse.
Transmission of systolic pulsations of severe tricuspid regurgitation into dorsal
hand veins implies incompetence of the valve of the subclavian vein at the thoracic inlet
(Fig. 41) in the presence of high systemic venous pressure.
Intrinsic disease of veins of the arms and hands is uncommon apart from complications of intravenous infusions and injections. The tender, indurated red cord at the
site of a heparin lock is a case in point. Not so innocent are the nontender pigmented
mainline streaks and palpable cords caused by intravenous drug abuse (see Chapter 2,
Fig. 236). The common sites are antecubital fossae, ventral surfaces of the arms, and
dorsa of the hands.
Veins of the Thoracic Inlet

Axillary and subclavian thrombophlebitis are rare but result in a relatively typical array
of physical signs. Axillary vein thrombophlebitis usually occurs in young patients after
trauma to or excessive exertion of the arms. The extremity becomes swollen over a period of hours, and assumes a reddish, cyanotic hue. The skin is warm, the supercial veins
are distended, and there is axillary tenderness. When the subclavian vein is the site of
thrombophlebitis, tenderness is elicited along its course above the clavicle.
Superior vena caval obstructionthe superior vena cava syndromecan be diagnosed
at the bedside.15 The deep jugular veins are bilaterally distended but nonpulsatile. Sudden
superior vena caval obstruction is uncommon and is characterized by dramatic distention of the neck veins together with cyanosis and pronounced edema of the face and eyes.
Chronic obstruction is accompanied by suffusion and cyanosis of the face, neck, and arms,
together with dilated, serpentine vascular collateral channels in the neck, arms and over
the thorax. Edema of the eyes and face is less pronounced than with acute superior vena
caval obstruction.
REFERENCES
1.
2.
3.
4.
5.
Mackenzie J. The Study of the Pulse, Arterial, Venous, and Hepatic, and of the Movements of the Heart.
Edinburgh: Young J. Pentland, 1902.
Wood PW. Diseases of the Heart and Circulation. Philadelphia, PA: JB Lippincott, 1956.
Potain PCE. On the movements and sounds that take place in the jugular veins. Bull Mem
Soc Med Hop(Paris). 1867;4:3. In: Willius FA, Keys TE, eds. Classics of Cardiolog y. 1983;Vol 2:
Malabar, FL: Robert E. Krieger.
Hirschfelder AD. Some variations in the form of the venous pulse. Bull Johns Hopkins Hosp.
1907;18:265.
McGee SR. Physical examination of venous pressure: A critical review. Am Heart J.
1998;136:10.
5/19/2009 4:02:28 PM
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
Wiggers CJ. The Pressure Pulses in the Cardiovascular System. London: Longman, Green, 1928.
Rondot E. Le reux hepato-jugulaire. Gas Hebd Sc Med Bordeaux. 1898;19:569.
Pasteur W. Note on a new physical sign of tricuspid regurgitation. Lancet.1885;2:524.
Sochowski RA, Dubbin JD, Naqvi SZ. Clinical and hemodynamic assessment of the hepatojugular reux. Am J Cardiol. 1990;66:1002.
Friedreich N. Zur diagnose der herzbeutelverwachsungen. Virchows Arch Pathol Anat.
1864;29:296.
Kussmaul A. Uber schwielige mediastino-pericarditis and den paradoxen pulse. Berl Klin
Wochenschr. 1873;10:433.
Gibson AG. The signicance of a hitherto undescribed wave in the jugular pulse. Lancet.
1907;2:1380.
Wenckebach KF. Zur Analyse des unregelmassigen pulses.II Ueber den regelmassig intermitterden Puls. Zeitschr Klin Med. 1899;37:475.
Stokes W. Observations on some cases of permanently slow pulse. Dublin Q J Med Sci.
1846;2:73.
Parish JM, Marschke RF, Dines DE, Lee RE. Etiologic considerations in superior vena cava
syndrome. Mayo Clin Proc. 1981;56:407.
5/19/2009 4:02:28 PM
The Movements of the

HeartPercussion,
Observation, Palpation
Egyptian physicians employed the technique of palpation which was part of the physical examination in ancient Greece and in the Middle Ages (Fig. 51). The Ebers papyrus (1550 b.c.) contained a chapter entitled, Beginning of the Secret of the Physician;
Knowledge of the Hearts Movement and Knowledge of the Heart. William Harveys
De Motu Cordis (1628) dealt with the motions of the heart imparted to the chest wall:
In the rst place, then, when the chest of a living animal is laid open and the capsule that immediately surrounds the heart is slit up or removed, the organ is seen
now to move, now to be at rest.1
Harvey made it clear that the movements of the heart could be identied on the intact
chest wall:
The heart is erected, and rises upward to a point, so that at this time it strikes
against the breast and the pulse is felt externally.1
Laennec in 1819 not only dened the location and size of the apex beat but described
movements conveyed to the chest wall by both the left and right ventricles:
In a healthy person of moderate fullness and whose heart is well proportioned, the
pulsation of this organ is only perceived in the cardiac region, that is, in the space
comprised between the cartilages of the fth and seventh ribs, and under the lower
end of the sternum. The motions of the left cavities of the heart are chiey perceptible in the former position, those of the right cavities in the latter. This is so
much the case that in disease of one side of the heart only, the pulsation in these
two situations gives quite different results. When the sternum is short, the pulsations extend to the epigastrium.2
James Mackenzies The Study of the Pulse (1902) contains a chapter on The Movements of
the Heart in Health and in Disease that represents a landmark in understanding cardiac
motion imparted to the thorax:
127
5/19/2009 4:02:59 PM
128 The Movements of the Heart
Figure 51 From Augustas fteenth

century illustrated manuscript, Regimen
Sanitatis (1482). The medieval physician is
using palpation in the physical examination.
(From Castiglioni A. A History of Medicine.
New York, Alfred A. Knopf, 1947;
reprinted by permission.)
Practically all important precordial movements transmitted by a beating heart can

be palpated and seen by an experienced clinician.3
It is exciting to witness the diagnostic conclusions that can be drawn from these
observations.
Percussion has a place in the physical examination of the heart and circulation,
albeit an abridged place relative to the much older art of palpation. Nevertheless, the
modem art of physical diagnosis began with Auengruggers discovery that uid levels
in wine casks (Fig. 52) could be determined by thumping (see Chapter 7). Referring
specically to the heart, Auenbrugger wrote
Over the space occupied by the heart, the sound loses part of its usual clearness,
and becomes dull. The whole sternum yields as distinct a sound as the sides of the
chest, except in the cardiac region where it is somewhat duller.4
5/19/2009 4:03:00 PM
The Movements of the Heart
129
Figure 52 Leopold Auenbrugger witnessed his fathers practice of percussing wine barrels
to determine the level of their uid contents. The observation led to a new sign which I have
discovered. This consists of the percussion of the human thorax.4 (Burgundian wine barrels
photographed by the author.)
The cardiac examination should begin with percussion, followed by observation and
palpation.
PERCUSSION
The thorax ought to be struck, slowly and gently, with the points of the ngers brought
close together and at the same time extended.4
However, percussion is best achieved using the bony intermediary of the applied
nger, which serves to amplify the response. To elicit the percussion note, the entire
length of the middle nger of one hand is applied rmly to the site of interest while the
dorsum of that digit is struckpercussedby the tip of the arched middle nger of the
free hand using the wrist as the fulcrum (see Chapter 7, Fig. 77).
Information derived from percussion falls into two categories: (1) determination of
visceral situs: heart, stomach, and liver, and (2) less importantly, approximations of the left
and right cardiac borders. The location (situs) of cardiac and hepatic dullness and gastric
tympany must rst be established. Situs solitus with levocardiathe normal positionis
established by percussing gastric tympany on the left and hepatic dullness on the right,
while percussion to the left and right of the sternum identies cardiac dullness on the left (levocardia). If tympany from the stomach is not clearly evident, the patient should inhale and
swallow a few times (aerophagia), a maneuver that generally resolves the problem by making
the air-lled stomach tympanitic. An infant swallows air when sucking an empty bottle.
5/19/2009 4:03:02 PM
Situs inversus with dextrocardia (mirror image) is the reverse of the above, with gastric tympany on the right, hepatic dullness on the left, and cardiac dullness to the right
of the sternum (Fig. 53). Ninety-ve percent of patients with mirror image dextrocardia
have no coexisting congenital heart disease, but unless situs inverus with dextrocardia is
recognized, symptoms accompanying acquired heart disease and accompanying noncardiac disease and can be misleading. In situs inversus with dextrocardia, the pain of angina
pectoris is right precordial with radiation to the right arm. Acute cholecystitis presents
with pain in the left upper quadrant, and the pain of acute appendicitis is in the left lower
quadrant.
Except for identifying visceral situs, percussion competes poorly with precordial
palpation, which with few exceptions, provides all information attained by percussion
and much more. However, percussion is sometimes useful in approximating the location
of the left cardiac border when the apex is not identied by palpation. In the presence
of a large pericardial effusion, cardiac dullness is elicited lateral to the left ventricular
impulse. A very large pericardial effusion causes dullness over the sternum and to the
right of the sternum. A dilated right atrium can cause dullness to the right of the sternum, and a giant left atrium can form the right lower cardiac border and cause dullness
to percussion.
SITUS INVERSUS
WITH DEXTROCARDIA
Right
Left
Desc. co
Desc
AO
Apex
Apex
S
Stomach
A
Liver
Liver
B
Figure 53 A, Schematic illustration and B, chest radiograph of dextrocardia in situs inversus.

Situs inversus of the abdominal viscera is established at the bedside by percussing the stomach (S)
on the right and the liver on the left. Dextrocardia is established by percussing cardiac dullness on
the right.
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131
OBSERVATION AND PALPATION

Topographic Anatomy of the Heart and the
Designation of Precordial Sites
Diagnostic conclusions based on observation and palpation (Table 51) require knowledge of the topographic anatomy of the cardiac and vascular structures that impart movements or vibrations to the chest wall. These sites are best referred to by simple descriptive terms.
The chief topographic areas for routine observation and palpation in patients with
levocardia in situs solitus (normal visceral positions) are the cardiac apex and the sternal
borders (left and right; lower, middle, and upper). The examination is then rened by
focused palpation of individual parasternal interspaces, the subzyphoid area, and the
sternoclavicular junctions.
In the normal heart, the apex is on the left and is occupied by an anatomic left ventricle (Figs. 54 and 55). The anatomic right ventricle is anterior and inferior (Figs. 54
and 55). The inow or sinus portion of the right ventricle underlies the fourth and
fth left intercostal spaces, the outow portion (infundibulum) underlies the third left
interspace, and the main pulmonary artery (pulmonary trunk) lies beneath the second
left interspace (Fig. 55). The border of the right atrium is just lateral to the lower right
sternal edge, and the ascending aorta is convex to the right of the sternum at the level of
the second right interspace (Fig. 55). The left atrium is not border-forming because it is
a posterior structure except for its appendage which underlies the third left interspace.
Methodology and Technique

Precordial palpation at its inception and for centuries thereafter was performed with the
patient standing and facing the physician (Fig. 51). However, examination is currently
performed with the clinician standing or sitting at the right of the bedside or examining
table with the patients he trunk as close to horizontal as comfort permits. Observation,
percussion and palpation begin in the supine position, followed by a partial left lateral
decubitus (Fig. 56). Infants are, as a rule, examined supine but can sometimes be turned
into a partial left lateral decubitus. In adult females, the breasts should be retracted. The
patient can assist when the examiners hands are occupied with palpation and timing
(see below).
Table 51 Information from Observation and Palpation

Systolic movements of the ventricles
Diastolic movements of the ventricles
Systolic movements of the great arteries
Systolic movements of the atria
Palpable heart sounds
Palpable murmurs (thrills)
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RV
S
e
p
t
u
m
S
e
p
LV
LV
m
RV
Figure 54 A, In situ position of the normal heart showing the apical left ventricle (LV)
separated from the anterior right ventricle (RV) by the ventricular septum here shown as the
linear interventricular sulcus. B, Sagittal section of the heart in the same in situ position showing
the relative positions of the right ventricle (RV) and the left ventricle (LV) separated by the
ventricular septum. (From Anderson RF, Becker AE: Cardiac Anatomy. London, Gower Medical
Publishing, 1980. Reprinted with permission. Labels are my additions.)
The palmar surfaces of the handngertips, distal meta-carpals, or the heel

of the handand the amount of pressure applied vary according to what is anticipated
from palpation and according to the precordial site under consideration. Detection of
thrills, ejection sounds, and loud rst and second heart sounds benets from rm pressure of the palmar surface of the distal metacarpals. With this exception, virtually all
other information from palpation is best elicited with the pads of the ngertips which
detect precordial movements and precisely localize them. The heel of the hand applied
NORMAL
A
PA
R.A
R.V.
L.V.
Figure 55 Line drawing of the topographic anatomy

of the normal heart. Arrow points to the interventricular
sulcus. The left ventricle (LV) occupies the apex. The body
of the right ventricle (RV) is anterior, underlying the left
lower sternal border (fourth and fth interspaces). The
infundibulum underlies the left mid-sternal edge (third
interspace), and the main pulmonary artery (PA) underlies
the left second interspace. The aortic root (A) is convex to
the right of the sternum in the second interspace, and the
right atrial border is just lateral the right lower sternal
edge. Compare with Figure 54.
5/19/2009 4:03:11 PM
133
to the left sternal border senses relatively obvious, diffuse systolic movement (see later).
However, impulses in this area, especially when subtle and localized, are best detected
by applying the ngertips between the ribs, as shown in Figure 57. In infants, a single
ngertip sufces (Fig. 58).
Subxiphoid palpation should be routine as recommended by Laennec, because
pulsations extend to the epigastrium.2 In older children and adults, subxiphoid palpation is best achieved by resting the at of the hand on the epigastrium while directing
the tip of the index nger upward and to the left to make contact with the right ventricular impulse as it descends during inspiration (Fig. 59A). In infants, these results are
nicely achieved with the tip of the little nger (Fig. 59B).
The respiratory position is important. Held inspiration in older children and
adults improves detection of the subxiphoid right ventricular impulse and minimizes
mistaking this impulse for the aortic pulsation which is sensed with the palmar surface
of the ngers during held exhalation (Fig. 510). Held exhalation also improves detection
of subtle systolic and diastolic movements of the left ventricle at the apex and the right
Figure 56 Partial left lateral decubitus

position for observation and palpation of the
left ventricle. The ink mark (+ white arrow) is
over the left ventricle, which moves anterior
during systole, while the right ventricle
(medial ink mark minus ) retracts. Retraction
begins at the interventricular sulcus (see
Figs. 54 and 55). The carotid pulse is
palpated for timing purposes as shown in
Figure 512A.
Figure 57 Palpation of the anterior wall

of the right ventricle by applying the tips of
three ngers in the third, fourth, and fth
interspaces at left sternal edge (arrows) during
full held exhalation. Patient is supine with the
trunk elevated 30 degrees. The carotid is used
for timing purposes as shown in Figure 512A.
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Figure 58 Palpation of the anterior

wall of the right ventricle in an infant.
The tip of a nger (arrow) is applied to
the left mid-sternal edge.
Figure 59 A, Subxiphoid palpation of the inferior wall of the right ventricle in an adult. The
tip of the index nger (arrow) is directed upward and to the left, palpating the right ventricle as
it descends during inspiration. B, In infants, subxiphoid palpation is achieved with the tip of the
little nger (arrow).
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135
RV
Ao
Figure 510 Subxiphoid palpation of the inferior wall of the right ventricle (RV) with
the tip of the index nger. The relative position of the abdominal aorta (Ao) is shown by the
vertical arrow.
ventricle at the left sternal edge. Thrills, with few exceptions, are more readily identied during full held exhalation, with the distal metacarpals rmly applied to the area of
interest. More precise localization is then achieved by relatively rm application of the
ngertips at specic sites.
Before beginning systematic palpation, the precordium should be observed for
movements that are obvious at a glance. Subtle movements are enhanced by applying pen marks to the skin (see Fig. 56), and highlighted with the oblique illumination of a pocket ashlight. The examiner should look across the chest tangentially
rather than from above. Parasternal movements are sometimes best seen when the
examiner looks cephalad from the patients feet. Precordial retraction is more readily
seen than palpated, whereas outward displacement is more readily palpated than seen
(Fig 511).
Precordial movements can be timed with the carotid pulse (see Fig. 512) or with the
heart sounds as a reference. In older children and adults, the thumb of the left hand is
applied to the carotid pulse while observing or palpating the precordium with the right
hand (see Fig. 512). Alternatively, the stethoscope can be held in place with the left
hand, freeing the right hand for palpation or observation of precordial movements. It is
sometimes revealing to observe systolic movements imparted to the stethoscope while
monitoring the rst and second heart sounds, a point that recalls Laennecs comment on
the shock or impulse delivered to his wooden stethoscopic cylinder as it was applied
to the cardiac apex.
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LV Systole
S1
S2
Figure 511 Normal apex cardiogram illustrating

left ventricular (LV) presystolic lling (a) in response to
atrial contraction. The LV systolic impulse returns to
baseline before the last third of systole. S1 = rst heart
sound, S2 = second heart sound.
In assessing movements of the heart imparted to the chest wall, it is necessary to

determine the topographic location of a given impulse as well as its timing in the cardiac cycle as early, mid , or late systole, or early, mid, or late diastole; its duration (how
much of the cardiac cycle the impulse occupies); its displacement characteristics (vigor
of movement, amplitude, and contour); and the maximum area occupied by the impulse,
especially the left ventricular.
Figure 512 A, Palpation of the left ventricular impulse by utilizing three ngertips (right
lower arrow). The examiners left thumb is applied to the carotid pulse for timing purposes (upper
arrow). B, More rened analysis of left ventricular systolic movement is achieved by palpation
with one ngertip (lower right arrow). The examiners left thumb continues to palpate the carotid
pulse (upper arrow).
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137
Apart from and in addition to the location (situs) of the heart, stomach, and liver, the position of the heart and the pulsations transmitted to the chest wall are inuenced by body build and thoracic conguration (see Chapter 2). Scoliosis to the right
rotates the heart leftward on its long axis; pectus excavatum shifts the heart to the left;
a decrease in anteroposterior chest dimensions (loss of thoracic kyphosis, saucer-shaped
pectus excavatum) increases contact of the right ventricle and pulmonary trunk with the
anterior chest wall. Ascites or pregnancy elevates the diaphragm and the heart, whereas a
tall, thin habitus has the opposite effect. Eventration of the left hemidiaphragm (usually
in infants) shifts the heart to the right, often dramatically so.
Normal Precordial Movement

Observation and palpation of normal precordial movement assumes an understanding
the characteristics of left and right ventricular impulses. Systolic movements imparted
by the ventricles should be assigned to the ventricle responsible for the impulse. The
imprecise designation point of maximum impulse (PMI) should be replaced by a term
that reects the origin of the impulseleft ventricular, right ventricularor by the
topographic location of the impulse (apical, parasternal, etc.).
The normal neonatal right ventricle imparts systolic movement at the mid to lower left sternal edge and subxiphoid. The impulse is brief, gentle, early systolic, followed
immediately by retraction that occupies the rest of systole. Systolic movement of the
left ventricle is, as a rule, not identied even when the infant is turned into a left lateral
decubitus position.
Elevation of the babys trunk in an infant seat improves detection of the subxiphoid right ventricular impulse as the heart descends. In slightly built patients, and in
the presence of diminished anteroposterior chest dimensions (loss of thoracic kyphosis,
shallow pectus excavatum), a gentle, unsustained right ventricular impulse can be palpated at the mid to lower left sternal edge, but not subxiphoid. The left ventricle outgrows the right during normal development, so in children and adults of average body
build, the only normal precordial impulse is left ventricular.
During left ventricular isometric contraction and early ejection (Fig. 511), the
left ventricle rotates from left to right (clockwise) on its long axis, so a large portion of
the chamber moves toward the chest wall. Mackenzies comment is relevant:
With the onset of ventricular systole a great change takes place in the position
of the left ventricle. The muscle hardens and contracts upon its contents, and at
the same time the heart twists round, so that the hardened apex projects forward,
pressing against the chest wall.3
Interestingly, the physiologic mechanism responsible for the apex beat was long the
subject of controversy. William Harvey correctly attributed the apex beat to ventricular
systole.1 Laennec concluded that Harvey was correct because the rst heart sound was
associated with ventricular systole.2 However, Josef Skoda believed that the apex beat
was a diastolic event, representing recoil after ejection.5
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Chauveau and Marey resolved the problem by catheterizing the heart and correlating intracardiac pressure changes with the onset of the apex beat that represented
contraction of heart muscle against the thorax during ventricular contraction.6 It has
now been proposed that the helical shape of the heart results in twisting that generates
ejection followed by untwisting that generates suction and rapid lling in preparation
for the next beat.7
The normal left ventricular systolic impulse is localized to one interspace, and
occupies an area less than 3 cm in diameter in normal adults. The impulse consists of a
localized, unsustained anterior apical systolic movement with retraction medial to the
interventricular sulcus (Figs. 54 through 56). Medial retraction occurs because the
anterior right ventricle is drawn away from the chest wall during systole. The zone of
medial retraction is relatively localized (see Fig. 56), and does not extend to the left
sternal edge. The horizontal supine position provides a low yield for detecting a normal left ventricular impulse. Accordingly, palpation should begin with the patient in a
partial left lateral decubitus position (Fig. 56) that consistently permits identication
of the left ventricular impulse in virtually all patients in whom that chamber occupies
the apex, especially when palpation is performed during held exhalation. Obesity and
emphysema are exceptions. The left ventricular impulse should initially be sought with
the apposed pads of several ngers (Fig. 512A), shifting the overlying skin in search
of the localized tap which is then palpated with the tips of the ngers (cupping the
hand) and nally, and more precisely, with the tip of a single nger, generally the rst
or second (Fig. 512B). These maneuvers require just enough time and concentration
to attune the examiner and heighten tactile sensitivity. Once anterior ventricular movement is palpated, medial retraction must be established. To achieve this, the palpating
ngertip, without losing skin contact, can be shifted medially, a maneuver that results
in loss of the impulse because medial retraction is not palpated. The ngertip can then
be returned to the palpable impulse while the examiner observes medial retraction by
marking the skin (Fig. 56). A tangential light source (described earlier) adds renement
to detection of an anterior apical impulse with medial retraction, conrming that the
impulse is left ventricular.
When the left ventricular impulse is not palpable in the left lateral decubitus
position despite meticulous search, percussion provides an approximate location of the
left cardiac border. Palpation at that site might then detect the elusive impulse of the
left ventricle.
The location of the left ventricular impulse is by convention, related to the midclavicular line, or to the distance from the left sternal edge, and by the interspace in
which the impulse is palpable. Location should also take into account patient age and
thoracic size and shape. The normal left ventricular impulse in the supine position is
generally localized to the fth intercostal space at or medial to the midclavicular line
(Fig. 512). In infants and in adults with a short, stocky chest, the impulse is often in
the fourth left interspace. In tall, thin patients in whom the heart is in a linear position,
proximity of the left ventricular impulse to the left sternal edge invites the mistaken impression of a right ventricle impulse. Reexamination in the left lateral decubitus
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139
position avoids this error by permitting identication of the telltale retraction medial to
the interventricular sulcus. Although the left lateral decubitus position has the advantage of enhancing palpability of the left ventricle, the location may not accurately reect
left ventricular size. If the impulse remains palpable as the patient returns to the supine
position, the location can be reassessed.
The left ventricular impulse is difcult to identify in the sitting position. In
patients who must be examined while sitting (neuromuscular disease, orthopnea), the
impulse can be related to landmarks described above for the supine position.
Mackenzie argued that in assessing displacement of the left ventricular impulse:
A cardiogram (graphic record) is not nearly so instructive as the physical examination of the apex beat. The position, size and strength of the apex beat can be far
better appreciated by the palpating hand.3
The duration of the left ventricular impulse distinguishes normal from abnormal. A single outward movement normally occurs during isometric contraction and early ejection,
and returns to baseline before the last third of systole (Fig. 511). The three centimeter
area normally occupied by the left ventricular impulse remains unchanged, even in the
left lateral decubitus position.
Anxiety increases the velocity and amplitude of the left ventricular impulse, but
not its duration or area. The relative ease with which a normal but hyperkinetic left
ventricle is palpated invites the mistaken impression that duration and area are also
increased.
Abnormal Systolic Movements of the Left Ventricle

An abnormal left ventricular impulse is characterized by its location (including
ectopic), displacement characteristics, and contour. The impulse of an enlarged left
ventricle is laterally displaced, and usually resides in the sixth rather than the fth
intercostal space. The sixth interspace at the anterior axillary line is at the same horizontal level as the fth interspace at the midclavicular line because ribs slant upward.
Dilatation of the left ventricle tends to displace the apex inferiorly as well as laterally
(Fig. 513).
An ectopic left ventricular impulse (ventricular aneurysm, for example) occupies a
site that is inappropriate for a normally positioned (situs solitus) heart. An ectopic impulse
is most readily recognized when it is above and medial to the expected location of a normal
apical left ventricular impulse. The ectopic segment is often as readily seen as palpated,
and is usually caused by regional dyskinesis of ischemic heart disease. When the dyskinetic or aneurysmal segment occupies the apex, the impulse is indistinguishable from a
dilated left ventricle.
Prolonged duration of a normally located left ventricular impulse is typical of pressure hypertrophy with increased wall thickness but normal internal dimensions. Laennec
wrote:
The more intense the hypertrophia, the longer the time the impulse is perceptible.2
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L.V.
+
Figure 513 Schematic illustration of a left

ventricular (LV) impulse that is displaced laterally and
inferiorly (arrow). When displacement is due to LV
volume overload, a hyperkinetic systolic impulse (+) is
accompanied by exaggerated medial retraction ().
A prolonged left ventricular impulse is maintained into the latter third of systole
approaching the second heart sound, in contrast to the normal impulse illustrated in
Figure 511.
A left ventricular impulse can be abnormal in velocity and amplitude, ranging from
hypokinetic (decreased) to hyperkinetic (increased). A hypokinetic impulse in a patient
of normal body build is a sign of decreased contractility, especially when the impulse is
laterally displaced. When palpation is too medial, the impulse of a hypokinetic, laterally
and inferiorly displaced left ventricle may be missed. Error is prevented by percussing
in the supine position that directs attention to the true lateral cardiac border which may
extend as far as the posterior axillary line.
Low velocity and low amplitude of systolic motion of the left ventricular impulse
are accompanied by low velocity and amplitude of medial retraction, making detection
more difcult. An ectopic left ventricular impulse of increased amplitude and duration
is a feature of post-myocardial infarction dyskinesis or aneurysm (Fig. 514), but may
occur transiently during a bout of angina pectoris. The prolonged systolic impulse of
regional dyskinesis is really paradoxic because it bulges abnormally during mid to
late systole (Fig. 514) at a time when normal anterior systolic movement has ceased
(see Fig. 511).
The maximum area occupied by a normal left ventricular systolic impulse in an
adult of average body build is less than 3 cm in diameter (see earlier), proportionately less in infants and children. An impulse that exceeds 3 cm in adults is evidence of
concentric hypertrophy of systemic hypertension or aortic stenosis, or of the increased
end-diastolic volume of a dilated left ventricle. In the absence of concentric hypertrophy, an increase in the maximum area occupied by the impulse is more reliable evidence of left ventricular enlargement than the location of the impulse relative to the
midclavicular line.
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141
LV
Figure 514 Apex cardiogram showing sustained

dyskinesis and prolonged duration of the left ventricular
(LV) impulse (arrow) in a patient with a transmural
anterior myocardial infarction. The impulse was preceded
by prominent presystolic distention (A). Compare with
Figure 511.
A left ventricular impulse is, as a rule, single. A double systolic impulse is a feature
of hypertrophic obstructive cardiomyopathy (Fig. 515). Identication of this contour
requires precise timing with the carotid pulse (see Fig. 512A) or with the heart sounds.
When the left ventricle occupies the apex but the apex retracts in systole, the cause
is usually chronic constrictive pericarditis.8 Retraction includes the ribs and intercostal spaces, and is usually more pronounced at the apex but may involve most of the left
anterior half of the chest.
Abnormal Systolic Movements of the Right Ventricle

Laennec remarked on an abnormal right ventricular impulse when he applied his stethoscopic cylinder to the precordium:
The contractions of the heart, as explored by the cylinder, gave the same results
nearly, whether the hypertrophia be on the right or the left side; only in the former
case, the shock of the hearts action is greater at the bottom of the sternum.2
James Mackenzie recorded the epigastric impulse of the right ventricle, and distinguished it from the impulse of the abdominal aorta. He wrote (Fig. 510):
At the postmortem examination, a needle pushed through the epigastrium at the
place where the tracing was obtained, was found to have penetrated the right ventricle. The epigastric pulsation due to the abdominal aorta presents quite a different character from that due to a dilated right ventricle.3
For assessment of right ventricular systolic movement, the examiner stands or sits to
the right of the patient who should lie supine with the trunk horizontal or elevated
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LV
Figure 515 Apex cardiogram from a patient with

hypertrophic obstructive cardiomyopathy. A distinctive
left ventricular (LV) triple impulse is caused by presystolic
and double systolic movements (arrows).
30 degrees. In situs solitus, the anatomic right ventricle is anterior and inferior,3 and topographically behind the left sternal edge (Fig. 54). Its inow portion underlies the mid
to lower left sternal edge (fourth and fth intercostal spaces), while its outow portion
(infundibulum) lies behind the third interspace. Accordingly, the area potentially in
contact with the chest wall is greater than the chest wall contact of the left ventricle. The
inferior portion of the right ventricle (Fig. 54) transmits its impulse subxiphoid, which
is accessible to palpation (Figs. 59 and 510). Subxiphoid palpation should be carried
out during held inspiration, whereas palpation of the right ventricle at the left sternal
edge should be carried out during held exhalation.
Age and thoracic conguration signicantly inuence access to the right ventricle. In normal infants, right ventricular contraction generates the precordial impulse
described earlier. In older children and in adults with a slight body build or decreased
anteroposterior chest dimensions (loss of thoracic kyphosis, shallow pectus excavatum),
contact of the right ventricle with the anterior chest wall is increased, producing a brief,
gentle left parasternal impulse. Conversely, an increase in anteroposterior chest dimensions (barrel chest of pulmonary emphysema, see Chapter 7) reduces or abolishes contact
of the right ventricle with the anterior chest wall, so its impulse may not be palpable
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143
even when the chamber is enlarged. Subxiphoid palpation (Figs. 59A and 510) is an
important alternative technique especially when the hyperination of emphysema lowers
the diaphragm and with it the inferior wall of the right ventricle.
Observation plays an important but lesser role than palpation in assessing right
ventricular systolic impulses, while percussion is of little or no value. Two methods of
palpation are recommended, as already briey described. The heel of the hand (distal
metacarpals) can be applied to the left sternal edge during full exhalation, keeping the
ngers elevated while sensing the systolic impulse and observing the motion of the hand
imparted by right ventricular contraction. This technique is relatively insensitive for
detecting subtle systolic movement and does not localize the impulse. A more rened
method employs several ngertips applied simultaneously and in parallel to the third,
fourth, and fth intercostal spaces during held exhalation (see Fig. 57). The left hand
is free for timing with the right carotid pulse, or for applying the stethoscope to the
chest for timing with the rst and second heart sounds. This method not only permits
detection of a gentle right ventricular systolic impulse but localizes the impulse to the
inow portion (fourth and fth intercostal spaces) or to the infundibulum or outow
tract (third interspace). In infants, palpation along the left sternal border is best accomplished with the tip of a single nger during active breathing (see Fig. 58) or during
very brief arrested respiration induced by pinching the nostrils while the infant sucks a
nipple or pacier.
Abnormal anterior movement of the right ventricle during systole is accompanied by retraction in the region of the interventricular sulcus (Fig. 54). An appreciably
enlarged right ventricle displaces the left ventricle from the apex, no longer makes contact with the chest wall, and imparts no precordial impulse (Fig. 516). Right ventricular anterior systolic movement then extends from the left sternal edge to the apex which
retracts (Figs. 516 and 517). Mackenzie recalled these points in admirable detail:
Accepting the usual clinical denition of the apex beat being the lowest and outermost part of the hearts impulse, a totally different form of beat is found when
the right ventricle causes this movement. In certain cases of dilatation of the right
PA.
R.V.
Figure 516 Schematic illustration of an enlarged right

ventricle (RV) that displaces the left ventricle from the
apex. The positive (+) right ventricular systolic impulse
extends to the apex, which retracts (). A dilated main
pulmonary artery (PA) underlies the left second interspace.
5/19/2009 4:04:22 PM
heart, nearly the whole anterior aspect of the heart is composed of the right auricle and ventricle, the left ventricle forming a mere strip of the lateral border. This
portion of the left ventricle is situated so far back that it is covered by the lungs
and does not reach the chest wall. Therefore, the lowest and outermost part of the
heart in contact with the chest wall is the right ventricle. In place of the outward
thrust during systole, as in the apex beat due to the left ventricle, there is drawing
in of the tissues.3
Systolic anterior movement of the right ventricle with lateral retraction can be highlighted by marking the chest wall, as shown in Figure 517. Observation is important in conrming that the right ventricle occupies the apex, because retraction is better seen than
palpated.
Characterization of a right ventricular systolic impulse not only includes timing
and location as described above, but also contour, velocity, amplitude, and duration of
movement. Persistence of the brief, gentle, normal neonatal right ventricular impulse
is a feature of Fallots tetralogy in which the right ventricle continues to function as a
systemic chamber as it does in the fetus and newborn. It is patient age, rather than displacement characteristics that makes the right ventricular impulse abnormal. In Fallots
tetralogy the impulse is conned to the fourth and fth intercostal spaces, and is not present in the third interspace because infundibular pulmonary stenosis assigns the elevated
right ventricular systolic pressure to the body or inow portion of the right ventricle. A
right ventricular impulse that extends to the third interspace means that systolic pressure
is elevated in both the inow and outow portions, as in pulmonary valve stenosis or pulmonary hypertension. Marked to severe elevation of right ventricular systolic pressure
with intact ventricular septum is accompanied by an impulse that is increased in both
amplitude and duration, extends from the fth to the third left intercostal space, and
includes the subxiphoid area.
Figure 517 The medial mark

(+ arrow) is over the right ventricle which
moves anteriorly during systole, while
the apex retracts (lateral mark ). These
movements characterize a right ventricle
that occupies the apex, displacing the left
ventricle and interventricular sulcus.
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145
Volume overload of mild to moderate tricuspid regurgitation generates a right

ventricular systolic impulse characterized by a modest increase in velocity and amplitude, but no increase in duration. At the other end of the spectrum is the tumultuous
right ventricular impulse accompanying the large left-to-right shunt of an uncomplicated ostium secundurn atrial septal defect. Although these left parasternal and subxiphoid
impulses can be dramatic, and apical retraction exaggerated, the duration of the impulses
is increased little if at all.
An abnormal right ventricular systolic impulse must be distinguished from movement imparted to an otherwise normal right ventricle when the chamber is displaced
anteriorly during left ventricular systole. The most common cause is mitral regurgitation (Fig. 518). The left atrium is a posterior chamber, lying behind the heart and
anterior to the rigid vertebral column. An enlarged left atrium moves the heart forward,
so an otherwise normal right ventricle comes into contact with the anterior chest wall.
Mitral regurgitation causes a phasic systolic increase in volume of the enlarged large left
atrium, resulting in phasic systolic anterior movement (Fig. 518). The systolic impulse
is necessarily delayed because the left ventricle must rst contract in order to provide the
regurgitant volume that expands the left atrium and moves the heart forward. Late systolic movement of the impulse is best timed by relating it to the rst heart sound, but
timing is also possible by simultaneously palpating the left ventricle while observing or
palpating the parasternal systolic movement.
LA
RV
Figure 518 Lateral chest

radiograph in a patient with severe
mitral regurgitation and a large
left atrium (LA) that displaces the
right ventricle (RV) anteriorly,
increasing its contact with the
chest wall. Systolic expansion of
the left atrium during regurgitant
ow moves the heart forward with
each left ventricular contraction
(large arrow), rendering the right
ventricle palpable.
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Anterior systolic movement of an inherently normal right ventricle can be caused

by regional wall motion abnormalities of the left ventricle. Dyskinetic motion of the
ventricular septum during angina pectoris displaces the right ventricle and results in a
transient left parasternal impulse that promptly disappears with relief of angina. Postmyocardial infarction dyskinesis of the ventricular septum is analogous, but results in
persistent systolic anterior displacement of the right ventricle. In mitral stenosis, a large
left atrium displaces the right ventricle anteriorly and augments the pulsations of that
chamber associated with pulmonary hypertension.
Biventricular Systolic Movements

A pure left ventricular impulse causes apical systolic anterior movement with medial
retraction (see Fig. 56). A pure right ventricular systolic impulse causes parasternal
anterior movement with lateral retraction (Figs. 516 and 517). When both ventricles
impart systolic movements to the precordium, the apical left ventricular impulse and the
parasternal right ventricular impulse coexist but are separated by a zone of retraction that
represents the plane of the interventricular sulcus (see Figs. 54 and 519).
Mid-Diastolic Movements of Ventricles

Passive lling of the ventricles occurs as atrial pressures rise sufciently to open the mitral
and tricuspid valves. Abnormally rapid atrioventricular ow and/or abnormal diastolic properties of the recipient ventricle impart a brief, distinct mid-diastolic movement
that can be palpated and sometimes seen (Fig. 520). The auscultatory counterpart is an
Figure 519 Biventricular

systolic movements of the
ventricles with anterior
displacement (+) of both right
and left ventricles separated by
a zone of retraction along the
interventricular sulcus (arrow).
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LV
QRS
147
BA
20
0
Figure 520 A, Apex cardiogram in a patient with aortic valve stenosis and left ventricular
failure. Paired arrows identify mid-diastolic and presystolic distention. B, Left ventricular (LV)
and brachial arterial (BA) pulses in the same patient showing the systolic gradient of aortic
stenosis and the mid-diastolic/ presystolic movements (paired arrows) that correspond to the apex
cardiogram in A.
abnormal third heart sound that may be palpated more readily than heard (see Chapter 6).
Normal (physiologic) third heart sounds are, for all practical purposes, not palpable.
Detection of mid-diastolic ventricular movement requires attention to the patients
position, to the phase of respiration, and to the technique of palpation and observation.
If the left ventricle is the focus of attention, the patient should be examined in the left
lateral decubitus position. A mid-diastolic left ventricular impulse that is unnoticed in
the supine position may be obvious in left lateral decubitus.
Once the left ventricle is identied, its impulse should be palpated with the tip of
a single nger (Fig. 512B) while the breath is held in full comfortable exhalation. The
tactile sensation imparted by mid-diastolic movement varies from bare perceptibility
to an obvious impact (Fig. 520). A case in point is chronic severe mitral regurgitation
with rapid mid-diastolic ow into a left ventricle of reduced compliance. The auscultatory counterpart is called a ventricular knock (see Chapter 6). The imparted diastolic movement is most apparent when an X mark is placed over the left ventricular impulse.
Precordial diastolic movement in chronic constrictive pericarditis has been called
the diastolic heartbeat. The movement coincides with rapid early diastolic ow into the
constricted left and right ventricles, and is synchronous with the brisk Y trough in the
right atrial and jugular venous pulse, and the early diastolic dip in the ventricular pressure pulse (see Fig. 411B).
5/19/2009 4:04:37 PM
Let us now focus on right ventricular mid-diastolic impulses. The appropriate position for examination is supine with the thorax horizontal or elevated 30 degrees. The
ngertips are applied one at a time or simultaneously (Figs. 57 and 58) at the left
sternal edge in the fourth and fth interspaces while the breath is held in full but comfortable exhalation. In the older child or adult, subxiphoid palpation (Fig. 59), especially during held inspiration, is sometimes more sensitive for the detection of right
ventricular mid-diastolic movement than is left parasternal palpation. This is so in part
because inspiration augments right ventricular lling and atrioventricular ow. Conditions necessary for generating a mid-diastolic right ventricular impulse are analogous
to those described above for the left ventricle. Chronic severe tricuspid regurgitation,
especially in the presence of reduced right ventricular compliance, is a case in point. The
diastolic heartbeat of chronic constrictive pericarditis is as likely to be palpated over
the right ventricle as over the left.
Presystolic Movements of the Ventricles

Active atrial lling of the ventricles (atrial transport) occurs in presystole (Fig. 521),
and is normally not accompanied by palpable or visible movement of either the left or
right ventricle. However, when the atrial contribution to ventricular lling is augmented
in the presence of aortic stenosis or systemic hypertension in the left heart (Fig. 522A)
or by pulmonary stenosis or pulmonary hypertension in the right heart (Fig. 522B), the
velocity and amplitude of presystolic movement reach thresholds that permit detection
by palpation and sometimes by observation. Mackenzie was aware of distention of the
ventricle by the auricular systole.3
When the left ventricle is the focus of interest, the patient is positioned in a
partial left lateral decubitus position. The left ventricular impulse is palpated with a
single ngertip while the breath is held in full but comfortable exhalation. The ngertip should be applied lightly, because pre-systolic movementas mid-diastolic
Apex Beat
a
Radial
Figure 521 Simultaneous tracings of the apex beat and of the radial pulse, showing the
systolic plateau (E) and the small wave (a) due to the auricular systole. The third beat in the apex
tracing is obliterated by the movement of inspiration.3 (From Mackenzie J: The Study of the
Pulse, Arterial, Venous, and Hepatic, and the Movements of the Heart. Edinburgh, Young J.
Pentland, 1902.)
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149
RV
20
LV
LA
A
V
20
2
A
20
2
0
B
Figure 522 A, Severe aortic valve stenosis with striking presystolic distention (arrow) of
the left ventricle (LV) in response to powerful left atrial (LA) contraction that generates a large
A wave. The V wave is small. B, Primary pulmonary hypertension with striking presystolic
distention (arrow) of the right ventricle (RV).
movementis low frequency and is damped by rm pressure. The tactile sensation

imparted to the ngertip varies from subtle, brief, and indistinct to an obvious impact
immediately preceding the left ventricular systolic impulse (Fig. 522A). The auscultatory counterpart is the fourth heart sound (see Chapter 6); presystolic distention
is often more readily palpated than a fourth sound is heard. In 1876, Potain called
attention to this point:
If one applies the ear to the chest, it affects the tactile sensation more perhaps than
the auditory sense.9
A subtle presystolic impulse can be augmented when the left ventricle is transiently
stressed with isometric exercise (sustained hand grip) (see Chapter 6). An X mark on the
skin over the left ventricular impulse improves visualization of pre-systolic movement
immediately before the major systolic impulse of the left ventricle.
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Right ventricular presystolic distention is best identied in the supine position with
the trunk horizontal or elevated 30 degrees. The ngertips are applied in the fourth and
fth left intercostal spaces during full, held exhalation (see Fig. 57). It is sometimes
better to palpate each interspace separately, especially in infants (see Fig. 58). Subxiphoid palpation during held inspiration may be even more informative, because a right
ventricular presystolic impulse tends to increase during inspiration.
It comes as no surprise that mid-diastolic and presystolic distention of the right or
left ventricle may coexist (see Fig. 520). Identication of these dual impulses is more
readily achieved when the cardiac rate is slow. A rapid rate, especially if the PR interval
is long, results in summation of the two ventricular lling phases and a single, reinforced
diastolic impulse.
Movements of the Atria during Ventricular Systole

Systolic expansion of a dilated left or right atrium in the presence of mitral or tricuspid regurgitation imparts distinctive movements to the chest wall. Anterior movement
caused by systolic expansion of an enlarged left atrium was dealt with earlier (Fig. 518).
A giant left atrium may extend into the right hemithorax. Mitral regurgitation then
causes late systolic movement of the lower right anterior chest, occasionally as far as the
right anterior axillary line. When mitral regurgitation occurs in the presence of an enlarged left atrial appendage, an impulse can be palpated and often seen in the third left
intercostal space where the appendage is border-forming.
The right atrium normally forms the right lower cardiac border. The right lobe of
the liver is just beneath the anterolateral rib cage. In the presence of severe chronic tricuspid regurgitation, the right atrium and liver enlarge appreciably, making broad contact with the anterior and lateral chest walls. Systolic expansion of the large right atrium
together with systolic movement of a large right hepatic lobe cause dramatic late systolic
movement of the entire right lower chest. The right ventricle, even though volumeloaded, causes relatively less impressive anterior movement, so the chest, especially when
viewed from the patients feet, exhibits a striking rocking motion with each ventricular
systole. When tricuspid stenosis occurs with a large, powerfully contracting right atrium,
a presystolic impulse is transmitted to the lower right anterior chest.
Movements of the Great Arteries

The ascending aorta is normally border-forming at the right thoracic inlet, but is palpable only when abnormal in size or position. An ascending aortic aneurysm in the Marfan
syndrome, is an example, causing a systolic impulse in the second, or rst and second
right intercostal spaces near the sternum (Fig. 523). A saccular luetic aneurysm of the
ascending aorta can present similarly or can burrow through the chest wall and present
as a dramatic, visible pulsatile mass (Fig. 524). If an ascending aortic aneurysm is sufciently cephalad as with a dissecting aneurysm, systolic movement can be transmitted to
the right sternoclavicular joint. Stemoclavicular joint pulsations are seldom visible, are generally subtle, and are best sensed by relatively rm pressure with two apposed ngertips
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151
aneurysm
Apex beat
Figure 523 Tracings from a large aneurysm pulsating in the second right intercostal space
and from the apex beat.3 (see Fig. 524). (From Mackenzie J: The Study of the Pulse, Arterial,
Venous, and Hepatic, and of the Movements of the Heart. Edinburgh, Young J. Pentland, 1902.)
which x the joint. Systolic movement of the right sternoclavicular joint is also a sign,
albeit subtle, of an otherwise normal right aortic arch. When a right aortic arch is dilated
as in Fallots tetralogy with pulmonary atresia (Fig. 525), motion is readily imparted
to the right sternoclavicular joint A systolic impulse imparted to the left sternoclavicular
joint occasionally results from distal extension of the transverse portion of a dissecting
Figure 524 Saccular

ascending luetic aortic
aneurysm that burrowed
through the chest wall and
presented as a dramatic, visible
pulsating mass (arrows). (From
Cabot RC: Physical Diagnosis.
New York, William Wood
and Company, 1915. Courtesy
of Dr Sherman M. Mellinkoff,
UCLA Medical Center.)
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Ao
PT
PV
Inf.
RV
Figure 525 Right ventriculogram from a 15 month-old male with Fallots tetralogy.
Proximity of the right aortic arch (three white arrows) to the overlying right sterno-clavicular
junction caused a systolic impulse. The ascending aorta (Ao) was dilated. PT = pulmonary trunk,
PV = pulmonary valve, Inf = infundibulum, RV = right ventricle.
aortic aneurysm. Rarely, late systolic anterior movement of the sternum and contiguous
left parasternal area are caused by a large, pulsatile descending thoracic aortic aneurysm
as it physically moves the heart forward during ventricular systole. If this is suspected,
synchronous late systolic movement should be sought in the posterior thorax to the left of
the vertebral column.
The pulmonary trunk is normally border-forming in the second left interspace (see
Fig. 55). To elicit a systolic impulse imparted by a dilated pulmonary trunk, the patient should be examined supine. The impulse is often better seen than palpated, especially during full held exhalation with the overlying skin marked by an X. Detection
by palpation is best achieved by a gently applied ngertip. Mackenzie recorded systolic
movement imparted by the pulmonary trunk (Fig. 526):
Through the thin chest wall the various movements of the heart could easily be
observed. In the second left interspace there was a marked pulsation. The tracings
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153
Carotid
Pulmonary artery
Figure 526 Simultaneous tracings of the pulses of the carotid and pulmonary artery. (From
the Heart. Edinburgh, Young J. Pentland, 1902.)
of the pulsation, taken at the same time as the carotid pulse, left no doubt as to its
being caused by the pulmonary artery.3
In thin patients, especially with decreased anteroposterior chest dimensions, a normal
pulmonary trunk sometimes transmits a visible and palpable impulse to the second left
interspace. An abnormal impulse becomes evident when the trunk is dilated (pulmonary
hypertensive), or when dilatation is accompanied by an increase in pulsatile excursion
(ostium secundum atrial septal defect), but not when dilatation is accompanied by the
proximal obstruction of pulmonary valve stenosis.
Palpable Heart Sounds

The following remarks deal with sounds that are palpable because of their intensity, not
because they impart movement to the chest wall. These include loud rst and second
heart sounds, ejection sounds, opening snaps, and occasionally tumor plops. Identication by palpation is analogous to the sensing of transmitted murmurs (thrills) (see
below).
The mitral component of the rst heart sound is sometimes palpable by relatively
rm pressure of a ngertip over the left ventricular impulse in the left lateral decubitus
position during held exhalation in thin, slightly built subjects, especially if the PR interval is short and the cardiac rate is rapid. In rheumatic mitral stenosis with a mobile anterior leaet, a loud rst heart sound is readily palpable and may extend to the left sternal
edge and occasionally to the base. An ejection sound accompanying congenital bicuspid
aortic valve stenosis (see Chapter 6) is sometimes palpable, more readily over the left
ventricular impulse than in the second right interspace, and must be distinguished from
a loud rst heart sound. A normal PR interval and a slow heart rate assist in this distinction. Aortic ejection sounds that originate within a dilated aortic root in contrast to
5/19/2009 4:04:50 PM
origin in a bicuspid valve are palpated by moderately rm pressure of a ngertip applied

during held exhalation at the right base over the dilated aorta, or by rmly applying the
distal metacarpals. Pulmonary ejection sounds are palpable in the second left intercostal
space and are sensed during normal exhalation because the sounds diminish or vanish
altogether during inspiration (see Chapter 6). The aortic component of the second heart
sound is palpable in the second right interspace in the presence of systemic hypertension
and when the aortic root is dilated and the pulmonary trunk is small as in Fallots tetralogy with pulmonary atresia, or when the aortic root is anterior to the pulmonary trunk
as in complete transposition of the great arteries.
The pulmonary component of the second heart sound is palpated in the second left
interspace in patients with pulmonary hypertension, although dilatation of the pulmonary trunk with normal pulmonary arterial pressure occasionally renders the pulmonary component palpable. In normal children and adolescents, and in thin subjects
with decreased anteroposterior chest dimensions, a normal pulmonary component of
the second heart sound is occasionally palpated as a gentle tap in the second left intercostal space, and is enhanced when a ngertip is applied with moderate pressure during held exhalation. A very loud pulmonary component transmits widely to the mid
and lower left sternal edge, right base, and apex, especially when the right ventricle
occupies the apex.
The opening snap of mitral stenosis is the most common early diastolic sound amenable to palpation because of intensity per se. The sound is palpable over the left ventricular impulse but when loud, radiates to the lower left sternal edge. A relatively rare
palpable early diastolic sound is the tumor plop (see Chapter 6) which is generated
during abrupt deceleration of a mobile, pedunculated right or left atrial myxoma as the
tumor seats within the tricuspid or mitral orice.
Palpable MurmursThrills
A thrill by denition is a palpable murmur, so the term palpable thrill is redundant. A
thrill should be identied as present or absent but not as palpable or impalpable.
Murmurs that reach or exceed grade IV out of VI are transmitted through the
chest wall as thrills, but frequency composition also affects murmur transmission. Nevertheless, the presence of a thrill implies that a murmur is at least grade IV. The distal
metacarpals are especially useful for the detection of thrills, although ngertips assist in
localization. Thrills are best characterized according to location, direction of radiation,
duration, and timing in the cardiac cycle ie, systolic, diastolic, or continuous: systolic
thrills at the right or left baseaortic valve stenosis or pulmonary valve stenosisare
palpated with the patient supine or still better sitting and leaning forward during full
held exhalation. When a thrill is prominent and widespread, application of the entire
palm of the hand is helpful in sensing the direction of radiation. An aortic stenotic thrill
radiates upward and to the right, and a pulmonary stenotic thrill radiates upward and to
the left. If a thrill is localized, relatively rm application of a ngertip usually sufces for
detection. In adults, application of the metacarpals is helpful.
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155
It is useful to localize the maximum intensity of a left parasternal systolic thrill.

Maximum intensity in the second intercostal space occurs with pulmonary valve stenosis, in the third intercostal space with infundibular pulmonary stenosis, and in the fourth
or fth intercostal space with a restrictive ventricular septal defect. Two or three ngertips
are applied simultaneously in the second, third and fourth, or fourth, fth, and sixth
interspaces, as shown in Figure 57. Sequential lifting and reapplication of the ngertips renes discrimination. In infants, a single ngertip is applied in sequence to each
interspace (Fig. 58). Most systolic thrills are better identied during exhalation, but
the thrill of tricuspid regurgitation is sensed or may appear only during inspiratory amplication of the murmur (see Chapter 6).
An early diastolic left parasternal thrill is more likely to accompany aortic regurgitation, less likely the Graham Steell murmur of high-pressure pulmonary regurgitation which is usually grade III or less. The best technique for eliciting these left
parasternal high-frequency early diastolic thrills is by applying the distal metacarpals
or ngertips at the left sternal edge with the patient rst supine and then sitting and
leaning forward during full held exhalation. When aortic regurgitation is caused by
eversion of a cusp, the pure frequency composition of the diastolic murmur sometimes results in more ready transmission than would be anticipated based upon intensity per se. When the diastolic thrill of aortic regurgitation is better detected at
the right sternal edge, the cause is likely to be an ascending aortic aneurysm, as in
Marfan syndrome.
Systolic and diastolic thrills over the left ventricular impulse are best assessed
during held exhalation with the patient in a partial left lateral decubitus position.
The thrill of mitral regurgitation commonly radiates into the axilla, sometimes to
the left sternal edge, to the base, and even into the neck. Detection of the diastolic or
presystolic thrill of mitral stenosis requires special care. With the patient in a left lateral decubitus position, the left ventricular impulse is identied because the mitral
stenotic thrill is localized to that site. If the left ventricular impulse is inconspicuous,
palpation of the loud rst heart sound assists in identifying the apex. A ngertip is
then applied with gentle to moderate pressure. Equivocal mitral stenotic thrills become evident after a brisk cough that transiently increases the heart rate and mitral
ow (see Chapter 6).
When systole and diastole thrills coexist, a distinction must be made between
two separate thrills and a single continuous thrill. The continuous thrill of patent ductus
arteriosus is a case in point. Maximal intensity is inferior to the left clavicle. The ductus thrill begins in systole, is reinforced before and after the second heart sound, and
proceeds without interruption through the timing of the second heart sound into all
or part of diastole. By contrast, the systolic/diastolic thrills of aortic stenosis/regurgitation are maximal at the right base or mid-left sternal edge, and the systolic and diastolic portions are interrupted. More difcult and sometimes impossible to distinguish
from a continuous thrill is the holosystolic thrill of ventricular septal defect or mitral
regurgitation followed immediately by an early diastolic thrill of aortic regurgitation
(see Chapter 6).
5/19/2009 4:04:51 PM
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
Harvey W. An Anatomical Disquisition on the Motion of the Heart and Blood in Animals.
London. 1628. In: Willius, FA, Keys TE, eds. Classics of Cardiology. Robert E. Krieger, 1983.
Laennec RTH. Treatise on Mediate Auscultation. 1819. (First American edition, Philadelphia,
PA: James Webster, 1823.)
Mackenzie J. The Study of the Pulse, Arterial, Venous, and Hepatic, and of the Movements of the
Auenbrugger L. On Percussion of the Chest. Vienna:1761. (Translated by Forbes J. In: Diseases of
the Chest. Fleet Street, London: T and G Underwood, 1824.
Willius FA, Dry TJ. A History of the Heart and the Circulation. Philadelphia, PA: WB Saunders,
1948.
Chauveau JBA, Marey EJ. Determination graphique des rapports de la pulsation cardiaque
avec les mouvements de loreillette et du ventricule, obtenue au moyen dun appareil enregistreur. C R Soc Biol (Paris). 1861;13:3.
Buckberg G. Guest Editor. Rethinking the cardiac helix. Eur J Cardiothorac Surg. Vol 29, Suppl.1, April 2006.
Boicourt OW, Nagle RE, Mounsey JPD. The clinical signicance of systolic retraction of the
apical impulse. Br Heart J. 1965:27:379.
Potain PC. Concerning the cardiac rhythm called gallop rhythm. Bull. Mem. Soc. Med. Hop.
Paris, 1876. In: Major RH. Classic Descriptions of Disease. 3rd ed. Springeld, IL: Charles C
Thomas, 1948.
5/19/2009 4:04:52 PM
AuscultationThe Audible
Language of the Heart
With each movement of the heart, when there is the delivery of a
quantity of blood from the veins to the arteries,
a pulse takes place and can be heard within the chest.
William Harvey, de Motu Cordis, 1628.
The word auscultation is applied to the examination, made by means of the ear, of
the different sounds which the circulation of the air, the reverberation of the voice,
or the beatings of the heart, produce in the cavity of the chest.1
Auscultation may be mediate or immediate. The application of the naked ear to
the different points of the chest, is called immediate auscultation. It is not only
inconvenient and disagreeable in many cases both to the patient and physician;
but it is besides, far from giving the satisfactory results which it would seem to
promise. These numerous inconveniences prevent us from having recourse to this
method as often as we would wish; but it has now been superseded by another.
I mean the use of the stethoscope, an instrument as simple in its construction,
as it is easy in its application, and which M. Laennec has shown to be so fruitful in results, so advantageous, I will even say indispensable, in the practice of
medicine!1
This testimony to the indispensability of mediate auscultation was written by 21-yearold William Stokes in An Introduction to the Use of the Stethoscope (1825).1 But now it has
been asked whether auscultation should be rehabilitated:
Should it be reserved for the occupational therapy of a dwindling coterie of antiquarians, or should it be promoted more vigorously as a viable part of our diagnostic armamentarium?2
The answer is yesauscultation should be rehabilitated, but
To decipher the auscultatory language of diseases of the heart easily and accurately
is an affair requiring labor and use and docility.3
The phonocardiogram (Fig. 61), which played such a seminal role in dening heart
sounds and murmurs, and which served as an invaluable tool for the teaching of auscultation, has virtually disappeared. The tracings that illustrate this chapter are a rarity not
to be duplicated.
157
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158 AuscultationThe Audible Language of the Heart
Figure 61 High-denition
phonocardiograph consisting
of two Cambridge strings and
two mirror galvanometers.
The recorder was constructed
in the 1950s at the Institute
of Cardiology, National Heart
Hospital, London, and was used
by Dr Aubrey Leatham. Most
of the recordings in Leathams
Auscultation of the Heart and
Phonocardiography (2nd ed.
New York, Churchill
Livingstone, 1975) were made
with this instrument, which is
now housed in the Wellcome
Museum, London.
The stethoscope has superseded the head mirror as the logo of medicine, and has
become more visible than ever, worn draped across the neck or over a shoulder instead
of resting inconspicuously in the pocket of a laboratory coat. Regrettably, the skill with
which the instrument is used tends to be inversely proportional to the prominence of its
display. Is the modem stethoscope that evolved from Laennecs cylinder becoming little
more than a symbolic gesture to a distinguished past? In this chapter, I hope to counter
this trend.
A painting in the Necker Hospital in Paris shows Rene Theophile Hyacinthe Laennec
sitting at the bedside with his ear applied to a patients thorax (see Chapter 1, Fig. 110).
The alternative to direct (immediate) auscultation was a quire of paper and a wooden cylinder that evolved into the binaural stethoscope. Here is Lannecs original description:
In 1816, I was consulted by a young woman laboring under general symptoms of
diseased heart, and in whose case percussion and the application of the hand were
of little avail on account of the great degree of fatness. The other method just mentioned being rendered inadmissible by age and sex of the patient, I happened to
recollect a simple and well-known fact of acoustics, and fancied at the same time,
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159
that it might be turned to some use on the present occasion. The fact I allude to is
the augmented impression of sound when conveyed through certain solid bodies,
as when we hear the scratch of a pin at one end of a piece of wood on applying our
ear to the other. Immediately, on this suggestion, I rolled a quire of paper into a
sort of cylinder and applied one end of it to the region of the heart and the other
to my ear, and was not a little surprised and pleased, to nd that I could thereby
perceive the action of the heart in a manner much more clear and distinct than I
had ever been able to do by the immediate application of the ear. From this moment, I imagined that the circumstance might furnish means for enabling us to
ascertain the character, not only of the action of the heart, but of every species of
sound produced by the motion of all the thoracic viscera.4
Nine years after Laennecs discovery of the stethoscopic cylinder, William Stokes wrote:
We cannot in every case come to an absolutely certain conclusion by means of the
stethoscope, still it is of innite assistance to us, and in the hands of an experienced
observer, will lead to conclusions unattainable without its aid.1
Stokes went on to say:
In the examination of the heart by means of the stethoscope, we must be assured
that the patient is in the calmest possible state; that he shall not have taken any
exercise for some hours previously, nor indulged lately in the use of wine, or other spiritous liquors. He should be examined before his usual time of meals, for in
many patients, the action of the heart is either greatly increased after a meal, or
may become so irregular as to simulate disease.1
These instructions recall the Yellow Emperors Book of Medicine5 in which the arterial
pulse was examined in the early morning before the physician took food and before the
cares of the day distracted him from full concentration (see Chapter 1, Fig. 13).
HEART SOUNDS
Heart sounds are brief, discrete auditory vibrations of varying intensity (loudness), frequency (pitch), and quality (timbre). The rst heart sound identies the onset of ventricular systole, and the second heart sound the onset of diastole. These two auscultatory
events establish a framework within which murmurs and heart sounds can be placed.
Laennec attributed the rst sound to ventricular systole (bruit ventriculaire) and the
second sound to atrial systole (bruit auriculaire).4 In 1832, Joseph Rouanet published his
experiments on the valvular origin of heart sounds,6 conclusions in accord with current
opinion that the rst and second heart sounds originate in cardiac valves, and are generated by tensing of valve membranes rather than collision of cusps.
The four basic heart sounds are the rst, second, third, and fourth (Figs. 62A
and 63A). Each of these sounds can be normal or abnormal. Other heart sounds are
usually abnormal, whereas still others are iatrogenic, ie, produced by prosthetic valves.
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THE BASIC HEART SOUNDS
S1
S2
S3
S4
A
ES
MS
S1
L S
ED MD
LD
S2
Figure 62 A, The basic heart sounds represented by the rst sound (S1), the second sound
(S2), the third sound (S3), and the fourth sound (S4). Each of these sounds can be normal or
abnormal depending on the clinical context. B, Heart sounds within the auditory framework
established by the rst heart sound (S1) and the second heart sound (S2). The additional heart
sounds are designated descriptively as early systolic (ES), midsystolic (MS), late systolic (LS), and
early diastolic (ED), mid-diastolic (MD), and late diastolic (LD) or presystolic.
Heart sounds are assigned simple descriptive designations that identify where in the cardiac cycle a given sound occursearly systolic, midsystolic, late systolic and early diastolic,
mid-diastolic and late diastolic (presystolic) (Fig. 62B and Table 61).
The next step is to infer what a sound so characterized represents (Tables 62
and 63). An early systolic sound might be an ejection sound (aortic or pulmonary) or
an aortic prosthetic sound. Mid/late systolic sounds are typied by the click(s) of mitral
valve prolapse, but occasionally are remnants of pericardial rubs. Early diastolic sounds
are represented by mitral opening snaps, the early third heart sound of constrictive pericarditis, the ventricular knock of mitral regurgitation, the opening of a rigid mitral
prosthesis, or the abrupt seating of a mobile atrial myxoma (tumor plop). Mid-diastolic
sounds are generally third heart sounds or summation sounds (synchronous third and
fourth heart sounds). Late diastolic or presystolic sounds are almost always fourth heart
sounds, rarely pacemaker sounds.
Technique and Principles

The importance of the topographic anatomy of the heart was emphasized by Henry I.
Bowditch in The Young Stethoscopist (1848). Bowditch provided a diagram that
will serve to show the position of the heart, and of its valves with reference to the
sternum and the ribs, during life, when fully distended. It will be well to study
this diagram carefully, in order to get a denite idea of the various parts in which
we should auscult in order to hear most clearly the sounds from the different
valves.7
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S4
S3
S1
161
S2
Y
R.V.
S4
S1
S3
S2
Figure 63 A, Atrial pressure pulse showing the A wave and X descent, and V wave and
Y descent. The fourth heart sound (S4) coincides with the atrial contraction phase of ventricular
lling. The third heart sound (S3) coincides with the Y descent (the phase of rapid ventricular
lling). S1 = rst heart sound; S2 = second heart sound. B, Intracardiac phonocardiogram recorded
from within the right ventricular (RV) cavity. The fourth heart sound (S4) coincides with
presystolic lling of the right ventricle (rst arrow) in response to right atrial contraction. The
third heart sound (S3) coincides with rapid, passive lling of the right ventricle (second arrow).
Table 61 Heart Sounds Within the Framework of the First and

Second Heart Sounds: Descriptive Terminology
Systolic sounds:
Early systolic
Mid systolic
Late systolic
Diastolic sounds:
Early diastolic
Mid diastolic
Late diastolic
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Table 62 Systolic Sounds

Early systolic
Mid/Late systolic
Ejection sounds (aortic or pulmonary)

Prosthetic aortic valve sounds
Mitral clicks
Remnants of pericardial rubs
The topographic areas for cardiac auscultation are designated descriptively as the cardiac apex, left and right sternal borders interspace by interspace, and subxiphoid.
These designations are analogous to those recommended for palpation (see Chapter 5).
Terms such as mitral area, tricuspid area, pulmonary area, and aortic area are avoided
because they assume situs solitus without ventricular inversion and normally related great arteries. Percussion should precede auscultation in order to establish visceral and cardiac
situs, so that the stethoscope can be applied with topographic condence.
Auscultation should begin at the cardiac apex and contiguous lower left sternal edge
(inow), proceeding upward interspace by interspace to the left and right base (outow).
This permits the examiner to think physiologically by using a sequence that conforms to
the direction of blood owinow/outow. It has been recommended that auscultation
begin at the base where the rst and second heart sounds are clearly identied. With few
exceptions, however, timing of the rst heart sound is readily established by simultaneous
palpation of the carotid artery with the thumb of the free left hand (Fig. 64). In addition to
the routine sites described above, auscultation should be conducted at certain nonprecordial
thoracic sites, especially the anterior chest on the opposite side, the axillae, and the back.
Bowditch called attention to signs of cardiac malpositions:
The organs of the body are exactly reversed in their position. . . . inspection shows the
apex of the heart beating to the right of the sternum. Auscultation and percussion prove
Table 63 Diastolic Sounds

Early diastolic:
Opening snaps
Early diastolic sound of constrictive pericardidis
The ventricular knock of mitral regurgitation
Prosthetic mitral valve sound
Tumor plop
Mid-diastolic:
Third heart sound
Summation sound (S3 + S4)
Late diastolic (presystolic):
Fourth heart sound
Pacemaker sound
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163
Figure 64 The bell of the stethoscope applied to the cardiac apex while the patient lies in a
partial left lateral decubitus position. The thumb of the examiners left hand palpates the carotid
artery for timing purposes (arrow).
the same; the sounds being heard at the right side of the sternum, perfectly normal,
and the percussion gives dull sounds on the right of the breast, while the left is clear.7
In situs solitus with a left thoracic heart, the stethoscope is rst applied to the cardiac apex
with the patient in a partial left lateral decubitus position (Fig. 64). Once the rst heart
sound is identied by simultaneous carotid palpation (Fig. 64), auscultation proceeds
by systematic attention to early, mid, and late systole, the second heart sound, then early, mid-, and late diastole (presystole), returning to the rst heart sound (see Fig. 62).
Orderly auscultation should not be distracted by dramatic signs such as a loud murmur,
because less obvious signs will be overlooked.
Pitch or frequency can be assessed within a range from low to moderately high by
applying variable pressure with the stethoscopic bell, reserving the diaphragm for higher
frequencies. A practical sequence is to begin with the stethoscopic bell applied with
varying degrees of pressure at the apex and lower left sternal edge, changing to the diaphragm when the base is reached. Low frequencies are heard when the bell applied just
lightly enough to establish a skin seal. High-frequency events are elicited by rm pressure of the diaphragm.
Respiratory patterns, position, and physical interventions will be dealt with
subsequently.
5/19/2009 4:31:39 PM
First Heart Sound

The initial component of the rst heart sound is most prominent at the cardiac apex
when the apex is occupied by the left ventricle. A second component can be heard at the
lower left sternal edge, less commonly at the apex, and seldom at the base (see below).
The rst component coincides with closure of the mitral valve and abrupt arrest of leaflet motion when the cuspsespecially the larger and more mobile anterior cuspreach
their fully closed position (maximal excursion into the left atrium). The sound is more
a matter of tensing of the valve membranes than of collision of the cusp margins, as
Rouanet originally proposed.6 Calcication renders a valve immobile and hence inaudible. The origin of the second component of the rst heart sound is attributed to closure
of the tricuspid valve based upon an analogous line of reasoning.
Ejection into the great arteries (ascending aorta and pulmonary trunk) is normally
inaudible, although phonocardiograms may record a low-amplitude sound coinciding
with maximal opening excursions of the aortic cusps.
The rst heart sound is characterized according to quality and intensity in addition to the presence and degree of splitting. Because the two major components are
believed to originate in the closing movements of the two atrioventricular valves, the
quality/pitch is similar and is best appreciated with relatively rm pressure of the stethoscopic bell or with the diaphragm. When the rst heart sound is split, its rst component is normally the louder. The softer second component is conned to the apex and
lower left sternal edge. Only the rst component is heard at the base. The intensity of the
rst heart sound, particularly its rst component, depends chiey on the position of the
bellies of the mitral leaets, especially the anterior leaet, at the onset of left ventricular
systole, less on the velocity of ventricular contraction. Accordingly, the initial component of the rst heart sound is loudest when the onset of left ventricular systole nds the
mitral leaets maximally recessed into the ventricular cavity as in mitral stenosis, and
in the presence of a short PR interval, a rapid heart rate, and short cycle lengths in atrial
brillation.
Conversely, the rst heart sound is soft, even inaudible when the onset of left ventricular systole nds the mitral leaets in or near their closed position, as in the presence
of a long PR interval, bradycardia, or long cycle lengths in atrial brillation. In acute
severe aortic regurgitation, the steep rise in left ventricular diastolic pressure exceeds an
elevated left atrial pressure in later diastole, prematurely closing the mitral valve, sometimes before inscription of the P wave. Accordingly, the rst heart sound is attenuated
or absent, an auscultatory sign that stands out because the attenuation occurs despite
tachycardia and a normal PR interval. In complete heart block, the random relationship
between P wave and QRS results in random variability in intensity of the rst heart
soundloud when the PR interval is short, and soft when the PR interval is long (see
Fig. 635A).
Systolic Sounds
Ejection sounds (aortic and pulmonary) are the most common early systolic sounds (see
Fig. 62B), coinciding with timing of the maximum cephalad excursion of the relevant
5/19/2009 4:31:40 PM
165
semilunar valve at its fully opened position, as in bicuspid aortic valve stenosis or dilated aortic root in the left heart, or pulmonary valve stenosis or dilated pulmonary trunk
in the right heart. Ejection sounds are relatively high-frequency, hence the designation
ejection click. The term ejection sound is preferable, however, reserving the term
click for the mid to late systolic sounds of mitral valve prolapse (see below), thus avoiding the awkward term nonejection click for the latter.
Ejection sounds, because of their frequency composition, should be assessed with
the stethoscopic diaphragm or with rm pressure of the bell. The ejection sound of a
congenital bicuspid valve is transmitted into the left ventricular cavity and is heard best
over the left ventricular impulse rather than at the right base (Fig. 65A). An ejection
sound implies that the aortic valve is mobile, because the sound is caused by abrupt
cephalad doming (Fig. 65B,C). In congenital pulmonary valve stenosis, the ejection
sound coincides with abrupt cephalad doming of the mobile pulmonary valve, and is
transmitted to the overlying second left intercostal space (Fig. 66). A distinctive feature of the pulmonary ejection sound is its selective decrease in intensity during normal inspiration (Fig. 66A). That is so because the inspiratory increase in right atrial
contractile force is transmitted into the right ventricle and onto the undersurface of the
mobile stenotic valve, moving its cusps upward before the onset of right ventricular contraction. The result is diminished caphalad excursion of the valve during inspiration,
accounting for the inspiratory decrease in intensity. The source of an ejection sound in
a dilated aortic root or dilated pulmonary trunk is also probably valvular (the timing
is appropriate).
An aortic ejection sound following a rst heart sound at the cardiac apex (see
Fig. 65A) must be distinguished from a split rst heart sound. The quality of the
two sounds is similar if not identical, and both are well heard with the diaphragm of
the stethoscope or rm pressure of the bell. However, a split rst heart sound is characterized by a louder rst component (mitral), whereas a rst heart sound followed
by an aortic ejection sound is represented by a louder second component, as shown in
Figure 65A.
An early systolic sound is generated by a rigid aortic prosthesis but not by a tissue
valve. A ball-in-cage valve sometimes produces a trill of early systolic sounds as the poppet moves upward during left ventricular systole.
Mid to Late Systolic Sounds
The most common mid to late systolic sound(s) are the clicks associated with mitral valve
prolapse (Fig. 67A). The term is appropriate because these sounds are relatively highfrequency and clicking, and are best heard with the diaphragm of the stethoscope or rm
pressure of the bell. The clicks coincide with maximal excursion of the prolapsed leaet(s)
into the left atrium, and are ascribed to abrupt tensing of redundant leaet(s) and elongated chordae tendineae. Variability epitomizes systolic click(s), which from time-to-time
may be present, absent, single, or multiple (Fig. 67A,B), or may be replaced by a cluster
of late systolic crackles. With physical or pharmacologic interventions that reduce left
ventricular volume, such as the Valsalva maneuver, amyl nitrite (Fig. 67C), or a change
5/19/2009 4:31:40 PM
S1
A2
APEX
Figure 65 A, Phonocardiogram over the

left ventricular impulse in a patient with mild
congenital bicuspid aortic stenosis. The aortic
ejection sound (E) is louder than the rst heart
sound (S1). A2 = aortic component of the second
heart sound. B, Transesophageal echocardiogram
from a patient with a functionally normal bicuspid
aortic valve. The diastolic frame shows the linear
closure line (arrows). LA = left atrium; LCA =
left coronary artery. C, Systolic excursion of the
bicuspid leaets. Abrupt cephalad doming produces
the ejection sound. Ao = aorta.
Ao
LA
LA
LCA
in position from supine to sitting to standing (Fig. 68), the click(s) become earlier. Conversely, physical or pharmacologic interventions that increase left ventricular volume, such
as squatting (Fig. 68), sustained hand grip, or infusion of a pressor amine (Fig. 67B),
delay the timing of the click(s). The most practical way to detect mobility of the click(s)
is to examine the patient during the change from squatting to prompt standing.
In 1894, Carl Potain described small, sharp clicking sounds, well localized and
such that one can scarcely attribute them to anything except the tensing of a pericardial adhesion.8 On rare occasions, a pericardial friction rub leaves in its wake mid to late
systolic soundsremnants of rubsthat persist after disappearance of the systolic phase
of the rub.
5/19/2009 4:31:40 PM
167
SM
P2
S1
P2
E
A2
A2
INSP.
EXP.
A
PT
RV
B
Figure 66 A,
Phonocardiograrn (second left
interspace) in a patient with
congenital pulmonary valve
stenosis. The ejection sound (E) is
obvious during exhalation (EXP),
but disappears entirely during
casual inspiration (INSP). The
pulmonary component of the
second heart sound (P2) is soft and
delayed. SM = systolic murmur;
S1 = rst heart sound.
B, Cephalad doming of the
stenotic valve (arrow) produces the
ejection sound. The pulmonary
trunk (PT) is conspicuously
dilated. RV = right ventricle.
Second Heart Sound

Leatham called the second heart sound the key to auscultation of the heart.9 The second
heart sound has two componentsthe rst designated aortic and the second pulmonary. The second sound normally splits into two components during inspiration, and is
single during exhalation, a respiratory variation described by Potain in 1866.10 Splitting
of the second heart sound is most readily identied in the second left intercostal space
because the softer pulmonary component is normally conned to that site, whereas the
louder aortic component is heard at the base, sternal edge, and apex. A2 and P2 are
appropriate terms provided that they apply to the aortic and pulmonary components as
just described and not to the topographic thoracic location in the aortic or pulmonary area.
Inspiratory splitting of the second heart sound is due chiey to a delay in the pulmonary component, less to earlier occurrence of the aortic component (Fig. 69). The
aortic and pulmonary components of the second heart sound coincide with the aortic and
pulmonary arterial dicrotic incisuras. During inspiration, the pulmonary arterial dicrotic incisura moves away from the descending limb of the right ventricular pressure pulse
because of an inspiratory increase in capacitance of the pulmonary vascular bed, thus
delaying the pulmonary component (Fig. 69). Exhalation has the opposite effect.
Earlier inspiratory timing of the aortic component of the second sound is attributed
to a transient reduction in left ventricular volume coupled with unchanging impedance
5/19/2009 4:31:42 PM
LEFT ATRIUM
RIGHT ATRIUM
SM
A S1
A
S1
C
A2
Figure 67 A, Intracardiac phonocardiogram localizing the systolic clicks (C) and late systolic
murmur (SM) of mitral valve prolapse within the left atrium. The clicks (C) and late systolic
murmur (SM) disappeared and the a and v waves declined as the transeptal catheter was
withdrawn from left atrium into right atrium. An atrial sound (A), now termed a fourth heart
sound, was more prominent within the left atrium. (From Ronan JA, Perloff JK, Harvey WP.
Systolic clicks and the late systolic murmur. Intracardiac phonocardiographic evidence of their
mitral valve origin. Am Heart J . 1965;70:319. Reprinted with permission.) B ( facing page),
Phonocardiograms at the cardiac apex with simultaneous brachial arterial (BA) and left atrial
(LA) pressure pulses in a patient with mitral valve prolapse before (control) and after pressor
amine infusion. As resistance to left ventricular discharge increased, the clicks (C) become
multiple and occurred later in systole. The late systolic murmur (SM) increased in parallel with
the increase in left atrial (LA) V wave. BA = brachial artery; M1 = mitral component of the rst
heart sound. C (see p.170), Phonocardiograms at the apex of a patient with mitral valve prolapse
before (control) and after an acute decrease in resistance to left ventricular discharge induced
by amyl nitrite inhalation. The late systolic murmur (SM) was replaced by an early systolic
decrescendo murmur that ends before the aortic component of the second heart sound (A2). The
remaining click (C) occurred earlier in systole. Continued
5/19/2009 4:31:43 PM
CONTROL
169
PRESSOR AMINE
SM
SM
MI
CC A
2
MI
C C C A2
MI C
A2
BA
20
0
LA
Figure 67 Continued
(capacitance) in the systemic vascular bed. Accordingly, normal respiratory variations in

timing are ascribed principally to variations in impedance characteristics (capacitance)
of the pulmonary vascular bed, not to an inspiratory increase in right ventricular volume
as originally believed.9 When the normal increase in capacitance of the pulmonary bed
is lost because of a rise in vascular resistance, inspiratory splitting of the second sound
narrows and, if present at all, reects an increase in right ventricular ejection time and/
or earlier timing of the aortic component.
Splitting of the second heart sound is best assessed with the patient supine or with a
30 degree elevation of the thorax, but reexamination in the sitting position can be useful,
as commented on below. The frequency composition of the two components of the second
sound calls for use of the stethoscopic diaphragm or relatively rm pressure of the bell applied in the second left intercostal space during normal respiration. It is helpful to instruct
older children and adults regarding the rate and depth of respiration by asking them
to breathe in and breathe out. The duration and depth of breathing are established
5/19/2009 4:31:45 PM
SM
APEX
SM
C
C
CONTROL
SM
C
A2
APEX
C
AMYL NITRITE
C
Figure 67 Continued
by the interval elapsed between the instruction to breathe in and the instruction to
breathe out. In infants, the technique for assessing splitting of the second heart sound
differs. Rapid, nonrhythmic breathing together with a rapid heart rate conspire to prevent
matching the splitting with a given phase of respiration. It is best to ignore the respiratory cycle and concentrate on the second heart sound per se. If it can be established with
S1
C S2
SM
Supine
S1
S2
SM
Sitting
S1C
S2
SM
Standing
S1
C S2
M
Squatting
Figure 68 Postural maneuvers that affect the click (s) and late systolic murmur of mitral
valve prolapse. A change from supine to sitting or standing causes the click(s) to become earlier
and the murmur longer, although softer. Conversely, squatting delays the timing of the click,
and the murmur gets shorter but louder. (From Devereux RB, Perloff JK, Reichek N, Josephson
ME.Mitral valve prolapse. Circulation. 1976;54:3. Reprinted with permission.)
5/19/2009 4:31:46 PM
S1
171
S2
EXPIR.
INSPIR.
P
A2 2
Figure 69 During inspiration, the second

heart sound (S2) normally splits into an aortic
(A2) and a pulmonary (P2) component. Splitting
is principally due to inspiratory delay in the
pulmonary component (P2).
condence that the second heart sound is at times single, and at other times split, it is safe
to conclude that the sequence of semilunar valve closure is normal (aortic followed by pulmonary), because reversed or paradoxical splitting (see below) rarely occurs in infants.
Abnormal splitting of the second heart sound falls into three categories: (1) persistently single, (2) persistently split (xed or nonxed), and (3) paradoxically split
(reversed). When the second sound remains single throughout the respiratory cycle, one
component is absent, or the two components remain synchronous. The most common
cause of a single second heart sound is inaudibility of the softer pulmonary component in
older adults with increased anteroposterior chest dimensions. In congenital heart disease,
a single second heart sound can be due to absence of the pulmonary component (pulmonary atresia, severe pulmonary valve stenosis, a dysplastic pulmonary valve), or to the
presence of transposition of the great arteries (inaudible pulmonary component because
of the posterior position of the pulmonary trunk).
A single second heart sound caused by simultaneous occurrence of its two components is a feature of an Eisenmenger ventricular septal defect, in which close if not identical pulmonary and systemic vascular resistances result in aortic and pulmonary arterial
dicrotic incisuras that are virtually simultaneous. A single second heart sound caused by
inaudibility of the aortic component occurs when the aortic valve is atretic or when the
valve is immobilized by calcic or dysplastic leaets.
Both components of the second heart sound are sometimes absent at all precordial sites. This is so in older adults in whom the aortic component is inaudible because
of calcic aortic stenosis, and the pulmonary component is inaudible because of a large
anteroposterior chest dimension.
A single semilunar valve does not necessarily generate a single second heart sound
as perceived on auscultation, and the quadricuspid valve of truncus arteriosus generates
what is perceived as splitting but is due instead to asynchronous closure of the four
unequal cusps. In systemic or pulmonary hypertension (see below), a loud single second
heart sound may be sufciently prolonged and slurred (reduplicated) to encourage a mistaken impression of splitting.
Persistent splitting of the second heart sound means that the two components remain
separate and audible during both phases of respiration. Persistent splitting may be due
to a delay in the pulmonary component, as in complete right bundle-branch block, or
5/19/2009 4:31:49 PM
to early timing of the aortic component as in mitral regurgitation. Inspiratory and expiratory changes in the interval of the split (greater with inspiration, less with expiration)
identify persistent but not xed splitting typical of right bundle-branch block. Persistent
splitting sometimes occurs in healthy children or young adults when they are examined
in the supine position, especially during shallow breathing. Reexamination in the sitting
position prevents error. This simple positional change permits a clearer impression of the
normal respiratory behavior of the second heart sound, especially expiratory synchrony.
Fixed splitting of the second heart sound means that the interval between persistently split aortic and pulmonary components remains unchanged during respiration.
Fixed splitting is a hallmark of uncomplicated ostium secundum atrial septal defect.
The aortic and pulmonary components remain separated during exhalation, and exhibit
little or no change in the degree of splitting during inspiration or during the Valsalva
maneuver (see below). In secundum atrial septal defects, phasic changes in systemic
venous return during respiration are matched by reciprocal changes in volume of the
left-to-right shunt, minimizing respiratory variations in right ventricular lling. The
split is wide because of a delay in the pulmonary component of the second heart sound
due to an increase in pulmonary capacitance that delays the interval between the descending limbs of the pulmonary arterial and right ventricular pressure pulses, and
accordingly delays the pulmonary incisura and the pulmonary component of the second
heart sound. Because the capacitance of the pulmonary bed is already appreciably increased with a secundum atrial septal defect, there can be little or no additional increase
during inspiration and little or no inspiratory delay in the pulmonary component of the
second sound. The result is a xed interval between two widely split components.
Paradoxic splitting of the second heart sound refers to a reversed sequence of semilunar valve closure, with the pulmonary component (P2) preceding the aortic component
(A2). The most common cause is complete left bundle-branch block or a right ventricular
pacemaker, both of which result in initial activation of the right side of the ventricular
septum, and thus in delayed activation of the left ventricle because transseptal depolarization is right-to-left. Paradoxic splitting is recognized on auscultation by a second
sound that separates during exhalation and is single (synchronous) during inspiration.
Inspiratory synchrony is achieved because the two components fuse due to a delay in the
pulmonary component, less to earlier timing of the aortic component.
Assessment of the relative loudness of the two components of the second heart sound
requires comparison of both components heard simultaneously at the same site. The relative softness of the normal pulmonary component accounts for its audibility conned to
the second left interspace, whereas the relative loudness of the normal aortic component
accounts for its audibility at all precordial sites. It should be restated that A2 properly
refers to the aortic component and P2 to the pulmonary component, so that the statement A2 is greater than P2 or vice versa correctly applies only when both components
of the second heart sound are simultaneously compared at the same precordial site. A2
and P2 do not refer to comparison of the second heart sound at the right and left bases.
Similarly, P2 by denition is one soundthe pulmonary componentso the expression
split P2 is a misnomer.
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173
An increase in intensity of the aortic component of the second heart sound is a feature of systemic hypertension. The intensity of the aortic component also increases when
the aorta is closer to the anterior chest wall. Such is the case with aortic root dilatation or
with transposition of the great arteries (aorta anterior to pulmonary trunk), or when an
anterior pulmonary trunk is small or absent, as in pulmonary atresia.
A loud pulmonary component of the second heart sound is a feature of pulmonary hypertension, with loudness enhanced by dilatation of the hypertensive pulmonary
trunk. Graham Steell, in describing the auscultatory signs of pulmonary hypertension,
remarked that
extreme accentuation of the pulmonary second sound is always present, the closure
of the pulmonary semilunar valves being generally perceptible to the hand placed
over the pulmonary area, as a sharp thud.11
An accentuated pulmonary component of the second sound is transmitted to the mid or
lower left sternal edge and, when very loud, throughout the precordium to the apex and
right base (Fig. 610). A loud pulmonary component in the second left interspace may
obscure identication of a closely preceding aortic component. Auscultation at other
2 LICS
S1
A2
P2
APEX
CAR
Figure 610 A loud pulmonary component of the second heart sound (P2) is transmitted from
the second left intercostal space (2LICS) to the apex (arrows). The split between A2 and P2 widens
from the rst cycle (exhalation) to the second cycle (inhalation). CAR-carotid pulse.
5/19/2009 4:31:49 PM
precordial sites serves to identify the transmitted but attenuated pulmonary component
and allows detection of splitting. A moderate increase in loudness of the pulmonary component of the second sound occurs with a decrease in anteroposterior chest dimension
(loss of thoracic kyphosis), and with dilatation of the pulmonary trunk, as with ostium
secundum atrial septal defect.
Early Diastolic Sounds
The aptly named opening snap of rheumatic mitral stenosis is the best known early diastolic sound (Fig. 611 and Table 63). An opening snap indicates mobility of the mitral
valve, or at least its larger anterior leaet, which is the source of the snap (Fig. 611). The
opening snap of mitral stenosis is high-pitched and best detected with the stethoscopic diaphragm or rm pressure of the bell at the lower left sternal edge. The snap is less
well heard at the apex, even when the left ventricle occupies the apex. A loud opening
snap that radiates to the left base invites a mistaken diagnosis of wide splitting of the
second heart sound. However, careful auscultation detects two sounds during exhalation
(synchronous aortic and pulmonary components followed by the opening snap), but three
sounds during inspiration (aortic component and pulmonary component followed by the
opening snap).
The opening snap of tricuspid stenosis is difcult to verify by auscultation, because
mitral stenosis with its snap almost invariably coexists. If the stenotic mitral valve is calcied and immobile, the audible snap becomes tricuspid by default.
The interval between the aortic component of the second heart sound and the
mitral opening snapthe A2OS intervalcan be predicted by auscultation. A short
interval implies a high left atrial pressure, and signicant mitral stenosis. The converse
is not necessarily the case, however, because in older subjects or in the presence of systemic hypertension, tight mitral stenosis can occur with a relatively long A2OS interval
because left ventricular systolic pressure takes longer to descend below left atrial pressure
(high left ventricular systolic pressure in systemic hypertension, abnormally prolonged
rate of fall of the left ventricular pressure pulse in older adults). In atrial brillation, the
A2OS interval varies inversely with cycle length because the higher the left atrial pressure (short cycle length), the earlier the mitral valve opens, and vice versa.
Early diastolic sounds are features of constrictive pericarditis. Dominic Corrigan,
in a presentation before the Pathological Society of Dublin in 1842, commented on a
patient with a very loud bruit de frappement.12 Frapper to knock implies that the bruit
de frappement was a knocking sound in Corrigans patient who had constrictive pericarditis. The term knock has also been applied to an early diastolic sound in pure severe
mitral regurgitation with reduced left ventricular diastolic distensibility. Corrigans
pericardial knock and the ventricular knock of mitral regurgitation are rapid lling sounds that are early and loud because a high-pressure atrium decompresses rapidly
across an unobstructed atrioventricular valve into a recipient ventricle whose compliance is reduced.
An early diastolic sound in pure severe mitral regurgitation occasionally originates
from a mobile anterior leaet that opens rapidly because of a high left atrial V wave and
5/19/2009 4:31:50 PM
175
PM
MDM
S1
S2
S1
O.S.
LV
PSM
MDM
RV
S1
S2
OS
Figure 611 A, Phonocardiogram recorded over the left ventricular impulse in a patient with
pure rheumatic mitral stenosis. An opening snap (OS) is followed by a mid-diastolic murmur
(MDM) that merges into a presystolic murmur (PM) with a crescendo up to a loud rst heart
sound (SI). S2, second heart sound. B, Schematic illustration emphasizing that the loud rst heart
sound (S1), opening snap (OS), mid-diastolic murmur (MDM), and presystolic murmur (PSM) of
mitral stenosis are best heard over the left ventricular (LV) impulse.
a collapsing Y descent. It is difcult if not impossible to distinguish this opening snap

from the ventricular knock of pure mitral regurgitation. The two sounds may coexist.
Early diastolic soundstumor plopsare sometimes caused by mobile atrial myxomas attached to the atrial septum by a long stalk. The plop results from abrupt
5/19/2009 4:31:50 PM
diastolic seating of the myxomatous mass within the right or left atrioventricular orice.
The opening movement of a rigid mitral prosthesis generates an early diastolic sound
which is especially prominent with a ball-in-cage device (StarrEdwards), less so with a
tilting disc prosthesis and absent with tissue valves.
Mid-Diastolic/Late Diastolic (Presystolic) Sounds
In sinus rhythm, each ventricle receives blood during two diastolic lling phases (see
Fig. 63). The rst phase occurs when ventricular diastolic pressure drops sufciently
below atrial diastolic pressure to allow the atrioventricular valves to open, so blood ows
from atrium into ventricle. Flow coincides with the Y descent of the atrial pressure pulse
(see Fig. 63), ie, the rapid lling phase of ventricular diastole that accounts for about
80 percent of normal lling. The rapid lling phase is a complex, active, energy-dependent
process, not a passive event in which inow simply expands the recipient ventricle. The
sound generated during the rapid lling phase is the third heart sound (see Fig. 63).
The second phasediastasisis variable in duration, and is usually accompanied
by less than ve per cent of ventricular lling.
The third phase is in response to atrial systole which accounts for about 15 percent
of normal ventricular lling. The sound generated during the atrial lling phase is the
fourth heart sound (see Fig. 63). Third and fourth heart sounds both occur within the
recipient ventricle when that chamber receives blood. Potain attributed the third heart
sound to sudden cessation of ventricular distention in early diastole, and he attributed
the fourth heart sound to the abruptness with which the dilatation of the ventricle takes
place during the presystolic period which corresponds to contraction of the auricle.13
The presence of third and fourth heart sounds can produce a cadence called gallop
rhythm which is a pathologic designation and therefore inappropriate unless the causative
soundbe it a third or fourth heart soundis abnormal. Potain wrote his classic description of cardiac rhythm called gallop rhythm in 1876.13 The following is his account of
gallop rhythm caused by a fourth heart sound:
The formation of this rhythm of which I wish to speak, is as follows. We distinguish here three sounds, namely: the two normal sounds and an additional sound.
The normal sounds show most frequently their normal characteristics, without
any modication. The rst especially maintains its normal relationship to the apex
heart and to the arterial phase. As to the abnormal sound, it is placed immediately
before it, preceding it sometimes by a very short time; always notably larger, however, than that which separates the two parts of a reduplicated sound.13
Gallop rhythm caused by the addition of a third or fourth heart sound is a triple
rhythm (Fig. 612). The presence of both third and fourth heart sounds is a quadruple rhythm (Fig. 612). When diastole is short or the PR interval long, the third and
fourth heart sounds merge to form a summation sound or a summation gallop rhythm
(Fig. 612).
The presence of these sounds is more important than the cadence they create.
When third or fourth heart sounds coexist with other sounds or murmurs, the gallop
5/19/2009 4:31:52 PM
177
3rd heart soundtriple rhythm
S1
S2
S3
4th heart soundtriple rhythm

S4
S1
S2
3rd + 4th heart soundsquadrupple rhythm
S1
S2
S3
S4
summation soundtriple rhythm
S1
S2
S3
+
S4
MSM
S1
S3
S2
Figure 612 When the rst and second

heart sounds are accompanied by a third
(S3) and/or a fourth heart sound (S4), the
cadence of a triple or quadruple rhythm is
produced. S3 and S4 sometimes summate
(fourth tracing). The lowest tracing is a
phonocardiogram recorded at the apex of a
5-year-old child with a normal third heart
sound (S3) and a trivial vibratory midsystolic
murmur (MSM).
cadence is lost. It is then appropriate to use the term abnormal third or abnormal fourth
heart sound rather than to say that gallop sounds exist without gallop rhythm.
How can one distinguish normal from abnormal third or fourth heart sounds?
Generally by the company they keep rather than by distinctive auscultatory properties of the sounds per se. The abnormal lling sounds that cause gallop rhythms are
not merely exaggerations of normal third and fourth heart sounds at relatively rapid
heart rates, but instead result from the inappropriate presence of the sounds, whose
intensities may, in fact, be soft rather than prominent. Children and young adults
have normal (physiologic) third heart sounds (Fig. 612), but fourth heart sounds are
abnormal. Normal third heart sounds sometimes persist beyond age 40 years, particularly in females. Thereafter, a third heart sound, especially in males, is presumptively
abnormal. Fourth heart sounds are sometimes heard after exercise in healthy adults
5/19/2009 4:31:52 PM
without clinical evidence of heart disease, an observation that prompts the belief, still
debated, that these fourth heart sounds are normal. In any event, there are no auscultatory differences that permit distinction between normal and abnormal third and fourth
heart sounds. Further to the point, normal third or fourth heart sounds can create a
triple rhythm cadence, but the term gallop rhythm is not appropriate because of its
pathologic connotation. The term normal third or normal fourth heart sound should be
used instead.
Third and fourth heart sounds originate in either the left or right ventricle
(Fig. 63B). The fourth heart sound requires active atrial contribution to ventricular
lling, so that fourth heart sounds disappear when coordinated atrial contractions cease,
as in atrial brillation. When the atria and ventricles contract independently, as in complete heart block, fourth heart sounds or summation sounds occur randomly in diastole
because the relationship between the P wave and QRS complex of the electrocardiogram
is random. In light of the fact that third and fourth heart sounds are events of ventricular
lling, obstruction of an atrioventricular orice impedes ventricular inow, and removes
one of the prime preconditions for the generation of these sounds. The presence of a third
or a fourth heart sound therefore implies an unobstructed atrioventricular valve on its
side of origin.
Third and fourth heart sounds, whether normal or abnormal, are soft low-frequency events that require meticulous stethoscopic technique for detection. Potain called
attention to this point:
The sound is dull, much more so than the normal sound. It is a shock, a perceptible elevation, it is scarcely a sound. If one applies the ear to the chest, it affects
the tactile sensation, more perhaps than the auditory sense. If one attempts to hear
it with a exible stethoscope, it lacks only a little, almost always, of disappearing
completely.13
These soft, low-frequency sounds are best heard in a quiet room when the bell of the
stethoscope is applied selectively over the left or right ventricular impulse with just
enough pressure to form a skin seal. Firm pressure of the bell or use of the stethoscopic
diaphragm damps low-frequency vibrations and reduces audibility of third and fourth
heart sounds, or eliminates them altogether. However, these same physical properties
can be used to advantage in distinguishing a split rst heart sound (the two components
of which are preserved or enhanced by the diaphragm or pressure of the bell) from a
fourth heart sound preceding a split rst heart sound (the fourth heart sound is damped
by pressure while the rst heart sound is not) (Fig. 613). This distinction was addressed
by Potain, who asked
Is the rhythm with which we are concerned nothing but a reduplication of the rst
heart sound? I believe this absolutely erroneous and for the following reasons. In
the rst place, the abnormal sound has, in no way, the timbre or usual characteristics of a valvular sound. Finally (and this is the unanswerable argument that makes
unnecessary all other reasons), I have heard, in certain patients, successively and
5/19/2009 4:31:53 PM
179
in the same cardiac revolution, the bruit de gallop itself and a reduplication of
the rst heart sound, I mean that after the dull sound which constitutes the rst
part of the gallop rhythm, one noted clearly a doubled rst sound, a reduplicated
clicking of the usual type.13
Third and fourth heart sounds originating within the left ventricular cavity are best
heard over the left ventricular impulse, especially when the impulse is brought closer
to the chest wall by turning the patient into a partial left lateral decubitus position (see
Fig. 64). Right ventricular third and fourth heart sounds are heard best over the right
ventricular impulse, that is, along the lower left sternal edge or in the subxiphoid region
with the patient supine. The subxiphoid site is especially appropriate in patients with
emphysema.
Audibility of third heart sounds is improved by isotonic exercise. A few sit-ups
may produce the desired augmentation in venous return and acceleration in heart rate
that increase the rate and volume of atrioventricular ow. Venous return can be increased
by passive raising of both legs with the patient supine and recumbent. The heart rate is
also transiently increased by vigorous coughing. Left ventricular fourth heart sounds, especially in patients with ischemic heart disease, can be induced or augmented by increased
resistance to left ventricular discharge in response to sustained handgrip (isometric exercise, see below).
Right ventricular third or fourth heart sounds often respond selectively and distinctively by increasing during inspiration. Auscultation with the bell of the stethoscope
in the subxiphoid region improves the sensitivity of the inspiratory maneuver by avoiding the damping effect of inhalation at the left sternal edge as the anteroposterior chest
dimension increases.
When the heart rate is rapid, atrial contraction coincides with the rapid lling
phase, making it impossible to determine whether an accompanying lling sound is a
third heart sound, a fourth heart sound, or a summation sound (see Fig. 612). Carotid
S4
S1
S2
Figure 613 (Upper tracing)

Schematic illustration comparing a
low-frequency fourth heart sound (S4)
preceding a single rst heart sound,
with a split rst heart sound (S1), the
two components of which are of the
same quality (lower tracing).
5/19/2009 4:31:53 PM
sinus pressure transiently slows the heart rate, so that auscultation can determine where
in diastole a given sound is occurring.
Under what circumstances are abnormal third and fourth heart sounds likely to
occur? Potains response was
The gallop stroke is diastolic and is due to the beginning of sudden tension in the
ventricular wall as a result of the blood ow into the cavity. It is more pronounced
if the wall is not distensible and the failure of distensibility may depend either on a
sclerotic thickening of the heart wall (hypertrophy) or on a decrease in muscular tonicity. Since the wall, by virtue of its own elasticity, is no longer able to resist the inow of blood, it is placed under tension precisely at the moment that this occurs.10
The third heart sound is believed to coincide with sudden arrest of longitudinal expansion of the left ventricular wall during early diastolic lling.14 The majority of abnormal
third heart sounds are the result of altered physical properties of the recipient ventricle
and/or an increase in the rate and volume of atrioventricular ow during the rapid lling
phase of the cardiac cycle.
Abnormal fourth heart sounds can be anticipated when augmented atrial contraction is required to produce presystolic distention of a ventricle (ie, an increase in enddiastolic segment length, so that the ventricle can contract with greater force according
to Starlings law. Typical examples are the left ventricular hypertrophy of aortic stenosis
PS
S2
S1
ACG
ECG
Figure 614
Phonocardiogram (fourth
left intercostal space) with
simultaneous apex cardiogram
(ACG), and electrocardiogram
in a patient with a right
ventricular pacemaker.
The pacemaker sound (PS)
is synchronous with the
stimulus (arrow) shown in the
electrocardiogram (ECG).
5/19/2009 4:31:53 PM
181
or systemic hypertension in the left side of the heart, or the right ventricular hypertrophy
of pulmonary stenosis or pulmonary hypertension in the right side of the heart. Fourth
heart sounds are also common in ischemic heart disease, and are almost universal during
an acute ischemic episode because the atrial booster pump is needed to assist a relatively stiff ischemic left ventricle maintain adequate contractile force.
A pacing catheter in the right ventricular apex may produce a presystolic pacemaker sound that is high-pitched and clicking (Fig. 614) and therefore different in
pitch from a fourth heart sound. The consensus is that the pacemaker sound is extracardiac, resulting from contraction of chest wall muscle following spread of the electrical
impulse from the pacemaker.
MURMURSSYSTOLIC, DIASTOLIC, AND CONTINUOUS

A cardiovascular murmur is a relatively prolonged series of auditory vibrations characterized
by intensity (loudness), frequency (pitch), conguration (shape), quality, duration, direction
of radiation, and timing in the cardiac cycle. Once these features are established by auscultation, the stage is set for diagnostic conclusions that can be drawn from a murmur of a given
description. I shall emphasize the clinical assessment, physiologic mechanisms, and interpretation of murmurs, rather than the physical principles that govern their production.
Intensity or loudness of a murmur is graded from 1 to 6 based upon the 1933 recommendations of Samuel A. Levine.15,16 A grade I murmur is so faint that it is heard only
after several seconds of auscultation. A grade 2 murmur is faint but is heard immediately.
A grade 3 murmur is moderately loud. A grade 4 murmur is loud. A grade 5 murmur is very
loud and can be heard with only the edge of the stethoscope in contact with the skin. A
grade 6 murmur is so loud that it can be heard with the stethoscope just removed from the
chest and not touching the skin.
Frequency or pitch of a murmur varies from high to low. The conguration or shape
of a systolic murmur is characterized as crescendo, decrescendo, crescendo-decrescendo
(diamond-shaped), plateau (even), or variable (uneven) (Fig. 615). Quality can be harsh,
rough, rumbling, scratchy, buzzing, grunting, blowing, musical, whooping, squeaking,
and so forth. Duration varies from short to long, with all gradations in between. A loud
murmur radiates from its site of maximal intensity. The direction of radiation sometimes
provides useful diagnostic information.
There are three basic categories of murmurssystolic, diastolic, and continuous. A
systolic murmur begins with or after the rst heart sound and ends at or before the second
heart sound on its side of origin (Fig. 616). A diastolic murmur begins with or after the
second heart sound and ends before the subsequent rst heart sound (Fig. 617). A continuous murmur begins in systole and continues without interruption through the timing
of the second heart sound into all or part of diastole (Fig. 618).
The following classication of murmurs is based upon timing relative to the rst
and second heart sounds and is in accord with the 1967 recommendations of the Committee on Standardized Terminology of the American College of Cardiology.
5/19/2009 4:31:53 PM
S1
S2
S1
S2
S1
S2
S1
S2
S1
S2
Figure 615 Five basic

shapes or congurations of
systolic murmurs: Acrescendo,
Bdecrescendo, Ccrescendodecrescendo, Dplateau
(even-shaped), and Evariable
(uneven).
Systolic Murmurs
Systolic murmurs are classied according to their time of onset and termination as midsystolic, holosystolic, early systolic, or late systolic (Fig. 616). A midsystolic murmur
begins after the rst heart sound and ends before the second sound. Termination of the
murmur is related to the component of the second heart sound on its side of origin (see
Fig. 616). Midsystolic murmurs originating in the left side of the heart end before the
MIDSYSTOLIC
LEFT SIDED
S1
RIGHT SIDED
A2
S1
A2P2
HOLOSYSTOLIC
LEFT SIDED
S1
RIGHT SIDED
S1
A2
EARLY SYSTOLIC
S1
S2
LATE SYSTOLIC
S1
S2
A2P2
Figure 616 Systolic murmurs

are classied according to their
time of onset and termination as
midsystolic, holosystolic, early systolic,
and late systolic. Termination of the
murmur is related to the relevant
component of the second heart
sound, ie, the aortic component
(A2) for systolic murmurs
originating in the left side of
the heart, and the pulmonary
component (P2) for systolic
murmurs originating in the right
side of the heart.
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183
EARLY DIASTOLIC
LEFT SIDED
S1
RIGHT SIDED
A2
S1
A2 P2
MID DIASTOLIC
S1
S2
LATE DIASTOLIC (PRESYSTOLIC)

LEFT SIDED
S1
S2
RIGHT SIDED
S1
S1
S2
Figure 617 Left- or right-sided diastolic murmurs are classied according to their time of
onset as early diastolic, mid-diastolic, or late diastolic (presystolic).
aortic component of the second sound, and midsystolic murmurs originating in the right
side of the heart, end before the pulmonary component of the second sound. A holosystolic
murmur begins with the rst heart sound, occupies all of systole, and ends with the second heart sound on its side of origin (see Fig. 616). Holosystolic murmurs originating
CONTINOUS
ARTERIAL
AORTO-PULMONARY
S1
S2
MURMURS
S1
HOLOSYSTOLIC-EARLY
VENOUS
S2
S1
DIASTOLIC
SM
S1
S2
MURMUR
DM
S2
Figure 618 Continuous murmurs begin in systole and continue without interruption through the
timing of the second heart sound (S2) into all or part of diastole. Accordingly, continuous murmurs
need not occupy an entire cardiac cycle. The continuous murmurs shown here are aortopulmonary,
arterial, and venous. Note that a holosystolic murmur (SM) followed by a holodiastolic murmur (DM)
is not continuous, but two separate murmurs that occupy all of systole and all of diastole.
5/19/2009 4:31:54 PM
in the left side of the heart should be related to the aortic component of the second sound,
and holosystolic murmurs originating in the right side of the heart should be related to
the pulmonary component of the second sound (see Fig. 616).
The term regurgitant systolic murmur, originally applied to murmurs that
occupied all of systole, has fallen into disuse because regurgitant ow can be accompanied by murmurs that are midsystolic, early systolic, or late systolic. Similarly, the term
ejection systolic murmur originally applied to midsystolic murmurs, has fallen into
disuse because midsystolic murmurs are not necessarily caused by ejection.
Midsystolic Murmurs
Midsystolic murmurs (See Figs. 615 and 616) occur in ve settings: (1) obstruction
to ventricular outow, (2) dilatation of the aortic root or pulmonary trunk, (3) accelerated systolic ow into the aorta or pulmonary trunk, (4) innocent midsystolic murmurs,
including those resulting from morphologic changes in functionally normal semilunar
valves (generally aortic), and (5) some forms of mitral regurgitation. The physiologic
mechanism of outow midsystolic murmurs reects phasic ow across the left or right
ventricular outow tract as originally described by Leatham17 (Fig. 619). Following
isovolumetric contraction and the generation of the rst heart sound, the rise in ventricular pressure opens the aortic and pulmonary valves. Forward ow commences, and the
murmur begins. As ow proceeds, the murmur increases in crescendo; as ow declines,
the murmur decreases in decrescendo, ending before ventricular pressure drops below
central arterial pressure, at which time the aortic and pulmonary valves close, generating
their respective components of the second heart sound (Fig. 619).
GA
S1
S2
Figure 619 Illustration of the

physiologic mechanism responsible
for the conguration of an outow
midsystolic murmur into the aortic
root or pulmonary trunk. Great
arterial (GA) and ventricular (V)
pressure pulses are shown with a
representative phonocardiogram.
The midsystolic murmur begins
after the rst heart sound (S1) as
ventricular pressure exceeds great
arterial pressure. The murmur rises in
crescendo to a peak as ow proceeds,
then declines in decrescendo as ow
declines. The murmur ends before the
second heart sound (S2) as ventricular
pressure falls below the great arterial
pressure.
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185
Aortic valve stenosis is associated with the prototypical midsystolic murmur that can
have an early systolic peak and a short duration, a relatively late peak and a prolonged duration, or all gradations in between. Whether long or short, however, the murmur retains its
symmetric diamond shape, beginning after the rst heart sound or with an ejection sound,
rising to a systolic crest, and declining in decrescendo to end before the aortic component
of the second hart sound (Fig. 616) (midsystolic, left-sided). The typical murmur of aortic
valve stenosis is loudest in the second right intercostal space with radiation upward, to the
right and into the neck because of the high-velocity jet within the aortic root.
An important variation is Gallavardin dissociation that occurs in older adults
with brocalcic changes in previously normal trileaet aortic valves that are either
stenotic (obstruction) or sclerotic (no obstruction). The accompanying murmur in the
second right interspace is harsh, noisy and impure, whereas the murmur over the left
ventricular impulse is pure high-frequency and musical (Fig. 620A,B). The right basal
murmur originates within the ascending aorta because of turbulence caused by the highvelocity jet (Fig. 620A). The musical murmur originates within the left ventricular
cavity (Fig. 620C) and is ascribed to high-frequency periodic vibrations of aortic cusps
that are brocalcic but without commissural fusion (Fig. 620D). These two distinctive
midsystolic murmursthe noisy right basal and the musical apicalwere described by
Louis Gallavardin in 1925,18 and the designation Gallavardin dissociation is still used.
The musical apical midsystolic murmur can be strikingly loud. William Stokes (1855)
reported that such a murmur was heard at a distance of three feet from the chest, and that
this gentleman once observed to me that his entire body was one humming top.19
The pure, high-frequency apical midsystolic murmur of aortic stenosis or sclerosis
must be distinguished from the high-frequency apical murmur of mitral regurgitation, a
distinction that may be difcult or impossible to establish because the two murmurs may
coexist. If the aortic component of the second heart sound is well heard at the base, but
inaudible at the apex, the second sound may be buried in the late systolic vibrations of
an apical holosystolic murmur of mitral regurgitation. However, the aortic valve may be
immobile (calcied), and its closure sound soft or inaudible, so the length and conguration of the apical murmur cannot be timed with the aortic component of the second heart
sound. When premature ventricular contractions are followed by pauses longer than
the dominant cycle length, the apical midsystolic murmur of aortic stenosis or sclerosis
increases in intensity in the long cycle length beat following the premature contraction
(Fig. 621A), whereas the murmur of mitral regurgitation remains relatively unchanged
in intensity (Fig. 621B). The same patterns prevail following longer cycle lengths in
atrial brillation. The validity of these observations assumes that apical aortic and mitral
murmurs do not coexist.
A midsystolic murmur originating in the right ventricular outow tract is represented by the murmur of pulmonary valve stenosis (see Fig. 66A). The murmur begins
after the rst heart sound or with an ejection sound, rises in crescendo to a peak, and
then declines in decrescendo to end before a delayed pulmonary component of the second heart sound (see Figs. 66A and 616) (midsystolic, right-sided). The murmur is
maximal in the second left interspace with radiation upward and to the left, and when
5/19/2009 4:31:56 PM
2 RICS
Aorta
SM
APEX
SM
Impure,
noisy
S2
B
LV
Pure,
musical
Figure 620 A, Illustration of the Gallavardin dissociation associated with brocalcic stenosis
of a trileaet but mobile aortic valve in older adults. The impure, noisy midsystolic murmur at
the right base originates from within the aortic root because of turbulence caused by the highvelocity jet. The pure, musical apical midsystolic murmur originates from periodic high-frequency
vibrations of the mobile brocalcic aortic cusps, and radiates into the left ventricular (LV) cavity.
B, Phonocardiogram illustrating Gallavardin dissociation. The impure, noisy midsystolic murmur
(SM) is recorded at the second right intercostal space (2 RICS), while the pure, musical midsystolic
murmur (SM) is recorded at the apex over the left ventricular impulse. C, Phonocardiogram
from within the left ventricular (LV) cavity recorded the high-frequency musical midsystolic
murmur (SM). The phonocardiogram over the apical left ventricular impulse recorded the musical
midsystolic murmur. D, M-mode echocardiogram of the aortic root (Ao) and left atrium (LA)
from an elderly male with brocalcic stenosis of a trileaet aortic valve. The pure high-frequency
Gallavardin vibrations are well illustrated in the open aortic valve cusps (arrows). Continued
loud, radiates to the suprasternal notch and into the neck, especially the left side of the
neck. The length and conguration of the murmur are useful signs of the degree of pulmonary stenosis. The greater the obstruction, the longer the duration of right ventricular
ejection and the longer the murmur. The relative lengths of right and left ventricular
ejection can be compared by relating the end of the pulmonary stenotic murmur (a rightsided event) to the timing of the aortic component of the second heart sound (a left-sided
event) (see Fig. 66A). A soft, symmetric midsystolic murmur that ends well before
the aortic component is a feature of mild pulmonary stenosis. A loud, asymmetric kiteshaped murmur that peaks in late systole and extends well beyond the aortic component
5/19/2009 4:31:56 PM
187
LV
APEX
LV
Ao
LA
Figure 620 Continued
of the second sound is a feature of severe pulmonary stenosis. There are all gradations in
between (see Figs. 66A and 616).
Short, soft midsystolic murmurs can originate within a dilated aortic root or a dilated pulmonary trunk. Similar midsystolic murmurs are generated into a normal aortic
root or pulmonary trunk during pregnancy, fever, thyrotoxicosis, or anemia because of
rapid ejection. In an uncomplicated ostium secundum atrial septal defect, the midsystolic murmur results from rapid ejection into a dilated pulmonary trunk.
Normal or innocent systolic murmurs are all midsystolic, except for the systolic
mammary soufe (Table 64). The normal vibratory midsystolic murmur described by
George Still (1909)20 is short, buzzing, pure and medium frequency (Fig. 622A). In
characterizing his murmur, Still wrote,
It is heard usually just below the level of the nipple, and about halfway between
the left margin of the sternum and the vertical nipple line; its characteristic feature is a twanging sound very like that made by twanging a piece of tense string.
Whatever may be its origin, I think it is clearly functional, that is to say, not due
to any organic disease either congenital or acquired.20
The mechanism of Stills murmur must account for its conguration (shape), frequency
composition, and thoracic location. The midsystolic conguration is most appropriate
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2RIS
SM
S1
S2
Apex
SM
CAR
PVC
A
SM
CONTROL
SM
PREMAT.
SM
POST-PREMAT.
Figure 621 A, The effect of cycle length on the midsystolic murmur (SM) of aortic
stenosis recorded at the second right interspace (2 RIS) and apex. With a premature ventricular
contraction (PVC), the systolic murmur virtually vanishes. In the following beat after a
compensatory pause, the murmur amplies considerably, both at the second right interspace
and at the apex. CAR, carotid pulse. B, The effect of changes in cycle length on the holosystolic
murmur (SM) of mitral regurgitation recorded at the apex. The intensity of the murmur changes
little if at all when the control beat is compared to the premature beat and to the post-premature
beat that occurs after an increase in cycle length.
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189
Table 64 Normal Murmurs

Systolic murmurs:
Vibratory systolic murmur (Still mumur)
Pulmonary systolic murmur from within the pulmonary trunk
Peripheral pulmonary systolic murmur from within the pulmonary arterial branches
Supraclavicular or brachiocephalic
systolic murmur
Systolic mammary soufe
Aortic systolic murmur from within the aortic root
Continuous murmurs:
Venous hum
Continuous mammary soufe
for an outow murmur. The pure medium frequencytwangingis most appropriate

for periodic vibrations generated in a low-pressure system. The topographic location
between the left margin of the sternum and the vertical nipple line20is most appropriate for origin within the right ventricular cavity. The apical Gallavardin murmur
(see above), which originates in brocalcic but nonfused aortic cusps set into highfrequency vibration during ejection from the high-pressure left ventricle, is transmitted
into the left ventricular cavity and is heard over the left ventricular impulse. By analogy,
Stills murmur, originates in pulmonary valve cusps that are set into low/medium frequency vibration during ejection from the low-pressure right ventricle. The murmur is
transmitted into the right ventricular cavity, and is best heard over the right ventricle.
Interestingly, a catheter across a normal pulmonary valve can tense the cusps and generate a transient pure-frequency midsystolic murmur (Fig. 622C), perhaps analogous to
Stills murmur. Origin of Stills murmur in left ventricular false tendons (Fig. 622B)
is unlikely because the murmur disappears after childhood, while left ventricular false
tendons persist.
A second type of innocent pulmonary midsystolic murmur occurs in children,
adolescents, and young adults, and represents an exaggeration of vibrations generated within the pulmonary trunk during normal ejection. The innocent pulmonary
midsystolic murmur is impure and is best heard in the second left interspace in contrast to the vibratory midsystolic murmur of Still, which is typically heard between
the lower left sternal edge and apex. Normal pulmonary midsystolic murmurs are
also heard in thin patients with diminished anteroposterior chest dimensions. Loss of
thoracic kyphosis shifts the heart forward, increasing the proximity of the pulmonary
trunk to the chest wall, thus increasing audibility of systolic vibrations within the
pulmonary trunk.
The common form of functionally benign midsystolic murmur in older adults is
the aortic sclerotic murmur (see above). The cause of this murmur is brous or brocalcic
thickening of the base of otherwise normal aortic cusps as they insert into the sinuses
5/19/2009 4:32:06 PM
SM
S1
SM
SM
SM
S2
LOWER LSB
A
PT
FT
PA
LV
B
Figure 622 A, Four vibratory midsystolic murmurs (SM) from normal healthy children.
These murmurs described by Still (and so designated) are pure, brief, medium frequency, and
maximal between the apex and lower left sternal border (LSB). The last of the four murmurs was
from a febrile 5-year-old girl. Following defervescence, the murmur decreased in both loudness
and in duration. B, Two-dimensional echocardiogram (apical view) in a 12-year-old boy with a
left ventricular (LV) false tendon (FT, arrow). The false tendon was an incidental nding. The
boy did not have a Still murmur. C, Phonocardiogram from within the pulmonary trunk (PT)
just distal to a normal pulmonary valve. The catheter caused tension of normal pulmonary cusps,
setting them into pure-frequency vibration (arrows).
of Valsalva. As long as the brocalcic thickening is conned to the base of the leaets,
the free edges move well and there is no obstruction. The impure midsystolic murmur in the second right intercostal space results from turbulence within the aortic root,
whereas the pure, high-frequency musical midsystolic murmur at the apex results from
high-frequency vibrations transmitted into the left ventricular cavity from stiffened but
mobile aortic cusps (see Gallavardin dissociation described above).
5/19/2009 4:32:06 PM
191
SM
2RIS
S1
Apex
S2
SM
y
CAR
PVC
Figure 623 Phonocardiograms at the second right interspace (2RIS) and apex from a
patient with a sclerotic aortic valve. A premature ventricular contraction (PVC) is followed by a
compensatory pause and striking amplication of the midsystolic murmur (SM), after which the
murmur alternates in intensity in synchrony with alternation of the carotid (CAR) pulse.
It is important to point out that some forms of mitral regurgitation generate midsystolic murmurs. The physiologic mechanism responsible for the midsystolic murmur
of mitral regurgitation (usually associated with left ventricular wall motion abnormalities of ischemic heart disease) reects early systolic competence of the valve followed by
midsystolic incompetence, then a late systolic decrease in regurgitant ow. In any event,
this is not an ejection murmur despite its conguration.
In elderly patients with depressed left ventricular systolic function, pulsus alternans following a premature ventricular contraction is often accompanied by alternation of
the midsystolic aortic sclerotic murmur (Fig. 623).
An aortic stenotic murmur in patients with normal thoracic conguration is best
heard at the right base (Fig. 624A). In patients with the barrel chest of pulmonary emphysema, this aortic stenotic murmur may be virtually inaudible in any thoracic location,
but clearly heard over the carotids and in the suprastemal notch (Fig. 624B). Cephalad
radiation is reinforced when the jet from a stenotic aortic valve is directed laterally, adheres to the aortic wall, and propagates cephaladthe Coanda effect(Fig. 625), thus
increasing the intensity of the murmur above the clavicles and in the suprasternal notch.
Auscultation in the neck should be routine, especially but not only in elderly patients
with increased anteroposterior chest dimensions (Fig. 624B).
Holosystolic Murmurs
Holosystolic (Greek holos, entire) murmurs (see Figs, 615 and 616) begin with the
rst heart sound and occupy all of systole, going up to the second sound on their side
of origin.16 Holosystolic murmurs are generated by ow from a chamber or vascular bed
whose pressure or resistance throughout systole is higher than the pressure or resistance in
5/19/2009 4:32:07 PM
SM
SM
S1
S1
S2
S2
Figure 624 A, With normal body habitus, the aortic stenotic murmur (SM) is best heard at
the right base. B, With the barrel chest of pulmonary emphysema, the aortic stenotic murmur
(SM) is virtually inaudible in the thoracic locations, but clearly audible over the carotids and in
the suprastemal notch.
the chamber or vascular bed receiving the ow. Holosystolic murmurs in the left side of
the heart are represented by mitral regurgitation, in the right side of the heart by highpressure tricuspid regurgitation, between the ventricles by restrictive ventricular septal
defects, and between the great arteries by an aortopulmonary window or patent ductus
arteriosus when elevated pulmonary vascular resistance eliminates the diastolic shunt
and the diastolic portion of the continuous murmur (see below).
The timing of a holosystolic murmur within the framework of the rst and second heart sounds reects the physiologic and anatomic mechanisms responsible for its
genesis. Figure 626 illustrates the mechanism of the holosystolic murmur of mitral regurgitation or high-pressure tricuspid regurgitation. Ventricular pressure exceeds atrial
pressure from the very onset of systole, so regurgitant ow and murmur begin with the
rst heart sound. The murmur persists up to or slightly beyond the relevant component
of the second heart sound, provided that ventricular pressure at end-systole exceeds atrial
pressure and provided that the atrioventricular valve remains incompetent.
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193
INN
Figure 625 Aortogram illustrating the Coanda effect in a patient with bicuspid aortic
stenosis. (Henri Marie Coanda, a Romanian inventor). The jet is directed laterally (white arrow),
adheres to the lateral aortic wall (curved black arrow), and is carried cephalad toward the orice of
the innominate artery (INN). The Coanda effect is more likely to occur because of the hourglass
narrowing of supravalvular aortic stenosis.
When ow generating the holosystolic murmur of mitral regurgitation is directed

posterolaterally within the left atrial cavity, the murmur radiates into the axilla, toward
the angle of the left scapula, and to the vertebral column, with bone conduction conveying the murmur from the cervical to the lumbar spine (Fig. 627A). When the direction
of the intra-atrial jet is forward and medial toward the atrial septum near the base of the
aorta, the regurgitant murmur radiates to the left sternal edge, to the base, and even into
the neck (Fig. 627B).
5/19/2009 4:32:09 PM
Figure 626 Illustration of great arterial (GA),

ventricular (VENT), and atrial pressure pulses
with phonocardiogram, showing the physiologic
mechanism of holosystolic murmurs commonly
heard in mitral and tricuspid regurgitation.
Ventricular pressure exceeds atrial pressure at the
onset of systole, so regurgitant ow and murmur
commence with the rst heart sound (S1). The
murmur persists up to or slightly beyond the
second heart sound (S2) because regurgitation
persists to the end of systole at which time left
ventricular pressure still exceeds left atrial pressure.
V = atrial v wave.
GA
VENT
V
ATRIUM
S1
S2
The murmur of tricuspid regurgitation is holosystolic when right ventricular systolic pressure is substantially elevated as illustrated in Figure 626. A distinctive and
diagnostically important feature of the murmur of tricuspid regurgitation is its increase
during inspirationCarvallos sign21 (Jos Manuel RiveroCarvallo, National Cardiological Institute, Mexico City). The tricuspid systolic murmur may be audible only
during inspiration. The increase occurs because the inspiratory augmentation in right
SM
SM
CERV.
SPINE
T4-5
SM
T10
SM
LUMBAR
SPINE
II
A
Figure 627 A, Pure severe anterior leaet mitral regurgitation with radiation of the systolic
murmur (SM) to the back with bone conduction from the cervical to the lumbar spine. B, Pure
severe posterior leaet mitral regurgitation with radiation of the systolic murmur (SM) to the base
of the heart (2 LICS, 2 RICS, second left, and second ght intercostal spaces), and into the neck.
The holosystolic murmur (SM) at the apex is followed by wide splitting of the second heart
sound because of premature closure of the aortic valve associated with mitral regurgitation. The
third heart sound (S3) and the prominent but short mid-diastolic murmur (MDM) resulted from
rapid diastolic ow into the left ventricle. The aortic component of the second heart sound (A2)
coincides with the dicrotic notch (DN) of the carotid pulse. Continued
5/19/2009 4:32:12 PM
195
ventricular volume is converted into an increase in the quantity and velocity of regurgitant ow. When the right ventricle fails, this capacity is lost, and so is Carvallos sign.
The murmur of a restrictive ventricular septal defect is holosystolic because left
ventricular systolic pressure and systemic vascular resistance exceed right ventricular
systolic pressure and pulmonary vascular resistance from the onset to the end of systole.
Holosystolic murmurs occur with large aortopulmonary connections (an aortopulmonary window or patent ductus arteriosus) when a rise in pulmonary vascular resistance
abolishes the diastolic portion of the continuous murmur, leaving a murmur that is
holosystolic or nearly so.
SM
SM
MDM
S1
A2 P2
S3
A2
APEX
S1
2 LICS
P2
CAR
D.N.
SM
SM
S1
A2
P2
NECK
2 RICS
Figure 627
Continued
5/19/2009 4:32:13 PM
Early Systolic Murmurs
Early systolic murmurs (see Figs. 615 and 616) have their onset with the rst heart
sound, diminish in decrescendo, and end well before the second heart sound, generally
before or at midsystole.16 Certain types of mitral regurgitation, tricuspid regurgitation,
or ventricular septal defects are examples.
Acute severe mitral regurgitation is accompanied by an early systolic murmur or a decrescendo murmur that diminishes or ends before the second heart sound (Fig. 628A,B).
The physiologic mechanism responsible for a murmur of this conguration is regurgitation into a normal-sized left atrium whose distensibility is limited. A steep rise in left
atrial V wave approaches left ventricular pressure at end-diastole; a late systolic decline
in left ventricular pressure favors this tendency (Fig. 628A,B). The stage is set for regurgitant ow that is maximal in early systole and minimal in late systole. The systolic
murmur parallels this pattern, declining or vanishing before the second heart sound
(Fig. 628).
An early systolic murmur is also a feature tricuspid regurgitation with normal
right ventricular systolic pressure) (Fig. 628A). The regurgitation accompanying tricuspid valve infective endocarditis in drug abusers is a case in point. The mechanisms
responsible for the timing and conguration of these murmurs are analogous to the
mechanisms described in the preceding paragraph and illustrated in Figure 628A. A
tall right atrial V wave reaches normal right ventricular pressure in latter systole, so the
regurgitation and the murmur are chiey, if not exclusively, early systolic and medium or
low-frequency because normal right ventricular systolic pressure generates comparatively low velocity regurgitant ow. This is in contrast to the high-frequency holosystolic
murmur that accompanies tricuspid regurgitation with elevated right ventricular systolic
pressure (see above).
Early systolic murmurs occur with ventricular septal defects under two widely
divergent anatomic and physiologic circumstances. A soft, pure, high-frequency, early
systolic murmur localized to the mid or lower left sternal edge is typical of a very small
ventricular septal defect, because the shunt is conned to early systole (Fig. 629). A
murmur of similar timing and conguration occurs through a nonrestrictive ventricular septal defect when elevated pulmonary vascular resistance decreases or abolishes late
systolic shunting.
Late Systolic Murmurs
Late systolic applies to the murmur (Figs. 615 and 616) of mitral valve prolapse which
begins in mid to late systole and proceeds up to the aortic component of the second heart
sound (see Fig. 67A). One or more mid to late systolic clicks typically introduce the
murmur (see Fig. 67). The responses of the late systolic murmur and clicks of mitral
valve prolapse to postural maneuvers (see earlier discussion) are illustrated in Figure 68.
A decrease in left ventricular volume readily achieved by prompt standing after squatting
(see Fig. 630) and by the Valsalva maneuver, causes the late systolic murmur to lengthen and soften. An increase in left ventricular volume associated with squatting (Fig. 68)
or sustained handgrip causes the murmur to shorten and become louder. Pharmacologic
5/19/2009 4:32:14 PM
197
Figure 628 A, Ventricular

and atrial pressure pulses with
V
phonocardiogram schematically
illustrating the mechanism of the
early systolic murmur of acute severe
mitral regurgitation or low-pressure
A
tricuspid regurgitation. The V
wave reaches ventricular pressure at
end-systole (upper curved arrow), so
regurgitant ow diminishes or ceases.
S1
S2
Accordingly, the murmur is early
S4
systolic decrescendo, paralleling the
A
hemodynamic pattern of regurgitant
ow. The fourth heart sound (S4)
S M
A2 P2
coincides with augmented atrial
contraction that generates the A
S3
wave in the ventricular pressure
S1
V
pulse. B, Phonocardiogram recorded
over the left ventricular impulse of
a patient with acute severe mitral
regurgitation resulting from ruptured
LV
chordae tendineae. An early systolic
decrescendo murmur (SM) diminishes
LA
if not ends before the aortic
component (A2) of the second heart
sound. P2, the pulmonary component,
is loud because of elevated pulmonary
arterial pressure, and is transmitted to
CAR
the apex. S1, rst heart sound; S3, third
heart sound; CAR carotid pulse. The
vertical dotted line times A2 with the
dicrotic notch (DN). C, Schematic left
ventricular (LV) and left atrial (LA)
pressure pulses with phonocardiogram
showing the relationship between the
decrescendo conguration of the early
SM S
systolic murmur and late systolic
DN
S1
2
approximation of the tall left atrial V
wave and the left ventricular pressure
B
C
that declines in latter systole because
forward ow cannot be sustained (curved arrow). Regurgitant ow diminishes or ceases in latter
systole, so the murmur is early systolic and decrescendo, paralleling the hemodynamic pattern of
regurgitant ow as illustrated.
5/19/2009 4:32:14 PM
RV
LSE
RA
SM
LSE
S2
SM
Figure 629 Phonocardiogram from a 4-year-old girl with a small ventricular septal defect,
and a trivial early systolic shunt. A, A soft, pure, high-frequency early systolic decrescendo
murmur (SM) is recorded within the right ventricle (RV) and simultaneously at the lower left
sternal edge (LSE). S2, second heart sound. B, When the intracardiac microphone was withdrawn
into the right atrium (RA), the murmur vanished.
Figure 630 Auscultation while squatting (A), and after promptly standing (B). The right
hand is used for support by holding the edge of the bed or examining table (A arrow).
5/19/2009 4:32:15 PM
199
interventions that alter left ventricular volume (Fig. 67B,C), especially amyl nitrite,
produce analogous results but are less practical at the bedside.
The late systolic murmur of mitral valve prolapse is occasionally converted into an
intermittent, striking late systolic whoop or honk, either spontaneously or in response to
physical maneuvers. The whoop is high-frequency, musical, widely transmitted, and occasionally loud enough to be disconcertingly sensed by the patient. The musical whoop
is thought to arise from mitral leaets and chordae tendineae set into high-frequency
periodic vibration. Here is William Oslers description:
A well-nourished young girl was sent to me in May, 1888 by Dr Buller (the rst
Professor of Ophthalmology at McGill University), who had noticed a remarkable
whistling sound, while examining her eyes. Auscultationas she sits upright in
the chair the heart sounds at the apex and base loud and clear; no murmur. When
she stands, a loud systolic murmur is heard at the apex, high-pitched, somewhat
musical, of maximum intensity in the fth interspace; it varies a good deal, being
loud for three or four beats, then faint for one or two succeeding ones. On removal
of the ear from the chest wall, the murmur can be heard at a distance of several
inches. It disappeared quite suddenly and could not be detected on most careful
examination . . . . The child then suggested that she heard it most frequently when
in the stooping posture; on causing her to lean forward and relax the chest, the
murmur was at once heard, and with greatly increased intensity. It was distinctly
audible at a distant three feet two inches by measurement, and could be heard at
any point on the chest and on the top of the head.22
Systolic Arterial Murmurs
Auscultation at nonprecordial sites detects extracardiac systolic murmurs in systemic

and pulmonary arteries. Systolic arterial murmurs originate in either anatomically normal arteries in the presence of normal or increased ow, or in tortuous or narrowed
arteries. Timing with the rst and second heart sounds is imprecise because extracardiac
murmurs begin at variable distances from the heart. Nevertheless, the arterial murmurs
dealt with here are essentially systolic and tend to have a crescendo-decrescendo conguration that coincides with the rise and fall of pulsatile ow.
A normal supraclavicular systolic arterial murmur is common in children and adolescents (Fig. 631A), and is believed to originate at the aortic arch origins of the brachiocephalic arteries. The conguration is crescendo-decrescendo, the onset abrupt, the
duration brief, and at times the intensity is surprisingly loud with radiation below the
clavicles, inviting a mistaken diagnosis of intrathoracic origin. Normal supraclavicular,
systolic murmurs decrease or vanish in response to hyperextension of the shoulders that
is sufcient to render the shoulder girdle muscles taut (Fig. 631B).
The most common cause of a systolic arterial murmur in older adults is peripheral
vascular disease resulting from narrowing of carotid, subclavian, or iliofemoral arteries.
Auscultation over these arteries should be routine in older adults.
5/19/2009 4:32:20 PM
LEFT NECK
SM
NOTCH
SM
RT. NECK
SM
Figure 631 The phonocardiogram (A inset) recorded a normal supraclavicular systolic

arterial murmur maximal above the clavicles in the left neck, right neck and in the suprasternal
notch. Auscultation is initially carried out (A) while the patient sits with shoulders relaxed and
arms resting in the lap. B, When the elbows are brought well behind the back to hyperextend
the shoulders, the murmur markedly diminishes or disappears.
A variation of arterial narrowing is the compression artifact associated with severe aortic regurgitation. A two-phase systolic/diastolic murmur can be induced over
a femoral artery in severe aortic regurgitation when the artery is compressed with the
bell of the stethoscope. Moderate compression generates a systolic murmur. With further compression, the murmur becomes systolic/diastolic, a sign described in 1861 by
Paul Louis Duroziez, president of the Socit de Mdecine in 1882. The eponym is still
employed.
During late pregnancy, but especially postpartum in lactating women, a systolic
mammary soufe is sometimes heard over the breasts because of increased ow through
normal arteries. The murmur begins well after the rst heart sound because of the interval between left ventricular ejection and arrival of ow at the artery of origin.
Still another type of systolic arterial murmur is heard in the back, and originates
over the site of coarctation of the aortic isthmus. The murmur is elicited by applying
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201
the diaphragm of the stethoscope just to the left of the vertebral column at midthoracic
level between the scapulae. In infants, examination is best performed in the prone position. In older children or adults, the sitting position is satisfactory provided the thoracic
muscles are relaxed.
Transient systolic arterial murmurs are often heard in normal neonates because
of turbulent systolic ow associated with disparity in size and angulation between the
pulmonary trunk and its proximal branches. These normal pulmonary arterial systolic
murmurs disappear with maturation of the pulmonary bed, generally within the rst
few weeks of life. Similar if not identical pulmonary arterial systolic murmurs are heard
in the axillae and back in congenital stenosis of the pulmonary artery and its branches.
Rarely, a pulmonary arterial systolic murmur is caused by luminal narrowing following
a pulmonary embolus.
Diastolic Murmurs
Murmurs in diastole are classied according to their onset as early diastolic, mid-diastolic,
or late diastolic (presystolic16 (see Fig. 617). An early diastolic murmur begins with the
aortic or pulmonary component of the second heart sound depending upon whether the
murmur originates in the left or right side of the heart. A late diastolic or presystolic
murmur begins immediately before the rst heart sound.
Early Diastolic Murmurs
An early diastolic murmur (Fig. 617) originating in the left side of the heart is typical
of aortic regurgitation. The murmur begins with the aortic component of the second
heart sound, ie, as soon as left ventricular pressure falls below the aortic incisura. The
murmur tends to be decrescendo, reecting the decline in volume and rate of regurgitant
ow during the course of diastole. Soft high-frequency early diastolic murmurs are best
detected with rm pressure of the stethoscopic diaphragm while the patient sits and
leans forward in full held exhalation (Fig. 632). In chronic severe aortic regurgitation,
the murmur occasionally begins with a short crescendo; the subsequent decrescendo parallels the rapid decline in aortic root pressure during the course of diastole. In moderate
chronic aortic regurgitation, the aortic diastolic pressure consistently exceeds left ventricular diastolic pressure, so the decrescendo is less obvious, and the murmur is heard
throughout diastole. It is sometimes useful to determine the direction and radiation of
the diastolic murmur of aortic regurgitation by comparative auscultation along the left
and right sternal borders, especially at the level of the third interspace. Selective radiation to the right sternal edge implies aortic root dilatation as in Marfan syndrome. Aortic
regurgitation caused by an everted cusp produces a distinctive musical early diastolic
decrescendo murmur (Fig. 633). An important variation is the murmur of acute severe
aortic regurgitation, which differs importantly from the murmur of chronic severe aortic
regurgitation just described. The duration is relatively short because the rapidly falling
aortic diastolic pressure promptly equilibrates with the steeply rising diastolic pressure
in the poorly compliant left ventricle. The pitch of the murmur is likely to be medium
5/19/2009 4:32:23 PM
Figure 632 The patient leans forward with breath held in full exhalation for detection of the
soft, high-frequency early diastolic murmur of aortic regurgitation or pulmonary hypertensive
pulmonary regurgitation. The stethoscopic diaphragm is pressed rmly against the mid-left
sternal edge (arrow).
and impure because the velocity of regurgitant ow is less rapid than in chronic severe
aortic regurgitation. The pitch may be medium frequency and disarmingly soft in contrast to the conspicuous, long, pure, high-frequency blowing diastolic murmur of chronic
severe aortic regurgitation (see above).
Early diastolic murmurs in the right side of the heart are represented by the Graham Steell murmur of pulmonary hypertensive pulmonary regurgitation. The description by Steell11 (1888) cannot be improved upon:
I wish to plead for the admission among the recognized auscultatory signs of disease of a murmur due to pulmonary regurgitation, such regurgitation occurring
independently of disease or deformity of the valves, and as a result of long-continuing excess of blood pressure in the pulmonary artery. The maximum intensity of
the murmur may be regarded as situated at the sternal end of the third and fourth
intercostal spaces. When the second sound is reduplicated, the murmur proceeds
from its latter part. That such a murmur as I have described does exist, there
can, I think, be no doubt. I am prepared for the objection that the murmur under consideration is only the murmur of a slight amount of aortic regurgitation.
How difcult it is to distinguish between the murmurs of aortic and pulmonary
regurgitation, respectively, by means of auscultation alone, will be admitted.
Writing in 1881, after describing the regurgitant murmur of aortic dilatation,
I referred to the murmur which is the subject of this paper, as follows, I am
5/19/2009 4:32:23 PM
3 LICS
203
EDM
SM
S1
A2
Figure 633 Phonocardiogram in

the third left intercostal space
(3 LICS) records the high-frequency,
musical, decrescendo early diastolic
murmur (EDM) caused by eversion of
an aortic cusp. SI = rst heart sound;
SM = midsystolic murmur; A2 =
aortic component of the second heart
sound.
inclined to believe that a murmur of similar mechanism occurs on the right side
of the heart, when there is much obstruction to the pulmonary circulation, with a
dilated pulmonary artery. My subsequent experience has only served to conrm
the opinion thus cautiously expressed more than 7 years ago though my faith has
from time-to-time been shaken by a case presenting a murmur which I had at
rst imagined to be an example, but which, on further investigation, proved to
be of aortic origin.
A Graham Steell murmur begins with the loud pulmonary component of the second
heart soundWhen the second sound is reduplicated, the murmur proceeds from its
latter partbecause the elevated pressure exerted on the incompetent pulmonary valve
begins at the moment that the right ventricular pressure drops below the pulmonary arterial incisura. The high diastolic pressure generates high-velocity regurgitant ow and a highfrequency murmur that may last throughout diastole. The conguration of the murmur is
decrescendo, although occasionally the amplitude is relatively uniform throughout most if
not all of diastole, and at times the murmur begins with a short crescendo. The auscultatory distinction between the early diastolic murmur of pulmonary hypertensive pulmonary
regurgitation and aortic regurgitation was underscored by Graham Steell (see above). Even
today the distinction is difcult or impossible when the pulmonary murmur is soft and
the systemic arterial pulse is normal. The distinction depends on the clinical setting rather than on auscultation. Squatting and sustained handgrip augment the murmur of aortic
regurgitation (see below), but leave the Graham Steell murmur unchanged.
Mid-Diastolic Murmurs
Mid-diastolic murmurs (Fig. 617) begin at a clear interval after the second heart sound.16
The majority of mid-diastolic murmurs originate across mitral or tricuspid valves during
5/19/2009 4:32:23 PM
the rapid lling phase because of atrioventricular valve obstruction or abnormal patterns
of atrioventricular ow, or across an incompetent pulmonary valve provided that the pulmonary arterial pressure is normal or nearly so. Rarely, a mid-diastolic murmur is due to
ow through an atherosclerotic extramural coronary artery.
The mid-diastolic murmur of mitral stenosis is a useful point of departure. The
murmur is present with sinus rhythm (Fig. 611) or atrial brillation (Fig. 634), and
is characteristically introduced by an opening snap (Fig. 611). With the patient in the
left lateral decubitus position (see Fig. 64), the bell of the stethoscope is placed lightly
against the skin precisely over the left ventricular impulse. The murmur is maximal at
that site because it originates within the left ventricular cavity. In atrial brillation, the
duration of the mid-diastolic murmur is a useful sign of the degree of mitral stenosis, because a murmur that lasts up to the rst heart sound even after long cycle lengths implies
a persistent trans-mitral gradient at the end of diastole (Fig. 634). Soft mid-diastolic
murmurs are augmented when the heart rate and mitral valve ow are transiently increased by brisk voluntary coughs.
The mid-diastolic murmur of tricuspid stenosis with atrial brillation differs from
the mitral mid-diastolic murmur in two important respects: (1) the tricuspid murmur
APEX
S1
DM
SM
DM
S1
S1
A2 S3
A2 S3
OS
OS
SHORT
LONG
LV
LA
V
Y
20
D
SHORT
LONG
Figure 634 Tracings from a patient with rheumatic mitral stenosis, dominant mitral
regurgitation, and atrial brillation. The rst heart sound (S1) varies in intensity with cycle
length. The aortic component of the second heart sound (A2) is followed by a soft opening snap
(OS) and a prominent third heart sound that introduces a mid-diastolic murmur (DM). With a
short cycle length, the murmur proceeds throughout diastole because an end-diastolic gradient
exists between left atrium (LA) and left ventricle (LV) (see lower tracings). With a longer cycle
length, the diastolic murmur ends completely, so the remainder of the diastole is murmur-free,
paralleling equilibration of left atrial and left ventricular diastolic pressures (D diastasis).
5/19/2009 4:32:25 PM
205
selectively increases during inspiration, and (2) the tricuspid murmur is conned to a
relatively localized area along the lower left sternal edge. The inspiratory increase occurs
because inspiration is accompanied by an augmentation in right ventricular volume and
a fall in right ventricular diastolic pressure, a combination that increases the diastolic
gradient and ow rate across the tricuspid valve. The murmur is localized to the lower
left sternal edge because it originates within the inow portion of the right ventricle and
is transmitted to the overlying chest wall.
Mid-diastolic murmurs occur across nonobstructed atrioventricular valves because
of an augmented volume and velocity of ow. Examples in the left side of the heart
include the mid-diastolic ow murmur accompanying pure mitral regurgitation, and
the mid-diastolic ow murmur accompanying a ventricular septal defect with a large
left-to-right shunt. Tricuspid mid-diastolic murmurs result from augmented ow across
nonobstructed tricuspid valves in severe tricuspid regurgitation or with a nonrestrictive
atrial septal defect and a large left-to-right shunt. These mitral or tricuspid mid-diastolic
ow murmurs are typically short and medium pitched, occur with appreciable atrioventricular valve incompetence or large shunts, and are often preceded by third heart sounds,
especially in the presence of mitral or tricuspid regurgitation.
In complete heart block, short, mid-diastolic atrioventricular ow murmurs occur
when atrial contraction coincides with and therefore reinforces the phase of rapid diastolic lling (Fig. 635B). These murmurs result from antegrade ow across atrioventricular valves that are closing as the recipient ventricle is lling. A similar mechanism
has been assigned to the Austin Flint murmur (Fig. 636), as Flint originally proposed23 (see below). In acute severe aortic regurgitation, the Austin Flint murmur is
necessarily conned to mid-diastole because premature mitral valve closure precludes
presystolic ow.
A mid-diastolic murmur is a feature of pulmonary valve regurgitation provided
that the pulmonary arterial pressure is normal or low (Fig. 637A). The cause of the pulmonary regurgitation can be acquired (pulmonary valve infective endocarditis) or congenital. The most common cause of low-pressure pulmonary valve regurgitation, however, is surgical repair of right ventricular outow obstruction. The mid-diastolic murmur
begins at a perceptible interval after the pulmonary component of the second heart sound
and is crescendo-decrescendo, ending well before the subsequent second heart sound.
The physiologic mechanism responsible for the timing of the mid-diastolic murmur of low-pressure pulmonary regurgitation is illustrated in Figure 637B. Diastolic
pressure exerted on the incompetent pulmonary valve at the time of the pulmonary component of the second heart sound is negligible, so regurgitant ow is negligible. As right
ventricular pressure drops below the diastolic pressure in the pulmonary trunk, regurgitation accelerates, and the murmur reaches its maximum intensity (Fig. 637B). Equilibration of pulmonary arterial and right ventricular pressures in late diastolic eliminates
regurgitant ow and abolishes the murmur prior to the next rst heart sound. When
the pulmonary component of the second sound is late, soft, or absent, the gap between
the aortic component and the onset of the pulmonary diastolic murmur is even more
conspicuous.
5/19/2009 4:32:27 PM
SM
S1 S2
R
S1
S2
P
T
A
AM
AM
S1
S2
CONTINUOUS
TRACING
T
P
Figure 635 A, Continuous phonocardiographic recording at the apex with lead 2 of the
electrocardiogram from a patient with congenital complete heart block. The intensity of the rst
heart sound (S1) varies from inaudible (rst cycle) to loud (second and third cycles) according to
the interval between the P waves (arrows) and the QRS complex. B, Phonocardiogram from a
patient with congenital complete heart block, a presystolic atrial murmur (PSM) and a middiastolic atrial murmur (MDM). The timing and amplitude of the atrial murmurs depend on
whether the P wave is presystolic or mid-diastolic (see rhythm strip).
Late Diastolic or Presystolic Murmurs
A late diastolic murmur (Fig. 617) occurs immediately before the rst heart sound, ie,
in presystole. The late diastolic timing coincides with the period of ventricular lling that
follows atrial systole and implies coordinated atrial contraction, generally sinus rhythm.
Late diastolic or presystolic murmurs originate at the mitral or tricuspid orice, usually
because of obstruction but occasionally because of abnormal patterns of presystolic atrioventricular ow.
The most celebrated presystolic murmur accompanies rheumatic mitral stenosis in
sinus rhythm as atrioventricular ow is augmented by an increase in the force of left atrial
contraction (Fig. 611). What is perceived as presystolic accentuation of a mid-diastolic
murmur is occasionally heard in mitral stenosis with atrial brillation, especially during
short cycle lengths, but the timing is actually early systolic, and the mechanism differs
5/19/2009 4:32:27 PM
EDM
SM
SM
207
EDM
LSE
S1
S1
A2
A2
MDM
APEX
ROTID
Figure 636 Phonocardiogram and indirect carotid pulse showing the effect of a decrease
in left ventricular afterload in response to amyl nitrite inhalation in a patient with chronic
severe aortic regurgitation. Control left panel: There is short midsystolic ow murmur (SM). A
prominent high-frequency early diastolic murmur (EDM) begins with the aortic component of
the second heart sound (A2). An Austin Flint mid-diastolic murmur (MDM) is present at the
apex. The carotid pulse is bisferiens. Following inhalation of amyl nitrite, the early diastolic
murmur (EDM) of aortic regurgitation and the aortic component of the second heart sound (A2)
decrease considerably. The apical mid-diastolic murmur vanishes altogether, and the bisferiens
pulse is reduced in amplitude and assumes a single peak (oblique arrow). The intensity of the rst
heart sound (S1) increases because of an accelerated heart rate.
from the true presystolic murmur shown in Figure 611. The technique for eliciting or
reinforcing the presystolic murmur of mitral stenosis is the same as that described above
for the mitral mid-diastolic murmur.
In tricuspid stenosis with sinus rhythm, a late diastolic or presystolic murmur characteristically occurs in the absence of a mid-diastolic murmur (Fig. 638). This is so because the timing of tricuspid diastolic murmurs coincides with the maximal acceleration
of ow and maximal gradient, which are usually negligible until the hypertrophied right
atrium contracts. The presystolic murmur of tricuspid stenosis is crescendo-decrescendo
and relatively discrete, fading toward the rst heart sound (Fig. 638), in contrast to the
5/19/2009 4:32:30 PM
20
PA
RV
DM
S1
S2
DM
0
S1
P2
Figure 637 A, Phonocardiogram of the mid-diastolic murmur (DM) of low-pressure

pulmonary valve regurgitation in a heroin addict with pulmonary valve infective endocarditis.
The murmur begins well after the second sound (S2), is medium frequency and mid-diastolic,
and ends well before the subsequent rst heart sound. B, Pressure pulses and phonocardiogram
illustrating the physiologic mechanism of the mid-diastolic murmur (DM) of low-pressure
pulmonary regurgitation. The pressure exerted against the incompetent pulmonary valve is
low, so the murmur does not begin until well after the right ventricular (RV) and pulmonary
arterial (PA) pressure pulses diverge. The murmur is maximal when the diastolic gradient is
greatest (cross-hatched area). There is an early diastolic dip in the RV pulse. Equilibration of the
pulmonary arterial and right ventricular pressures in later diastole abolishes the regurgitant
gradient so the murmur disappears.
presystolic murmur of mitral stenosis, which tends to rise in crescendo to the rst heart
sound (Fig. 611). However, the most valuable auscultatory sign of tricuspid stenosis
in sinus rhythm is the response to respiration. Inspiration increases right atrial volume,
provoking an increase in right atrial contractile force in the face of a fall in right ventricular end-diastolic pressure. The result is a larger gradient, an increased velocity of
tricuspid ow, and an increase in intensity of the presystolic tricuspid stenotic murmur,
as shown in Figure 638.
Presystolic and mid-diastolic murmurs occasionally occur in patients with a myxoma
of the left or right atrium. These murmurs can resemble the murmurs of mitral or tricuspid
stenosis. The accompanying tumor plop can be mistaken for an opening snap (see above).
In complete heart block, short, crescendo-decrescendo presystolic murmurs are
occasionally heard when atrial contraction fortuitously falls in late diastole (Fig. 635).
However, in complete heart block, the diastolic murmur is usually mid-diastolic (see
above) when atrial contraction coincides with and reinforces the rapid lling phase.
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209
RV
RA
20
A
PSM
PSM
LSE
S1
INS
S2
OS
EXP
Figure 638 Pressure pulses and phonocardiogram illustrating the physiologic mechanism
responsible for the respiratory variation in the presystolic murmur of tricuspid stenosis. During
inhalation, a fall in intrathoracic pressure and an increase in systemic venous return result in
an increase in right atrial (RA) A wave and a decrease in right ventricular (RV) end-diastolic
pressure, so the presystolic murmur (PSM) increases. During exhalation, the right atrial A wave
declines, the right ventricular diastolic pressure increases, the tricuspid gradient is minimal, and
the presystolic murmur all but vanishes.
5/19/2009 4:32:33 PM
The Austin Flint presystolic murmur was described in 1862.23 Flint was one
of Americas most distinguished nineteenth century physicians, and has been called
Americas Laennec.24
The mechanism proposed by Flint was perceptive:
Is this murmur ever produced without any mitral lesions? One would a priori suppose the answer of this question to be in the negative. Clinical observation, however, shows that the question is to be answered in the afrmative. In May, 1860, 1
examined a patient, age 56. At the apex was a presystolic blubbering murmur.23
At necropsy days later:
The aorta was atheromatous and dilated so as to render the valvular segments evidently insufcient. The mitral valve presented nothing abnormal.23
Flint examined a second case the following year and concluded:
In both cases the mitral direct murmur was loud and had that character of sound
which I supposed to be due to vibration of the mitral curtains. In both cases it will
be observed, an aortic regurgitant murmur existed, and aortic insufciency was
found to exist at postmortem. A mitral direct murmur, then, may exist without
mitral contraction and without any mitral lesions, provided there be aortic lesions
involving considerable aortic regurgitation.23
Flint proposed the following mechanism:
Now in cases of considerable aortic insufciency, the left ventricle is rapidly lled
with blood owing back from the aorta as well as from the auricle, before the
auricular contraction takes place. The distention of the ventricle is such that the
mitral curtains are brought into coaptation, and when the auricular contraction
takes place the mitral direct current passing between the curtains throws them
into vibration and gives rise to the characteristic blubbering murmur.23
Current consensus regarding the mechanism of the Austin Flint murmur is in accord
with Flints original proposal. The jet accompanying chronic severe aortic regurgitation
impacts and impinges on the anterior mitral leaet, limiting its opening excursion and
encroaching on the mitral orice, a combination that results in an increase in mitral inow velocity, an increase in vibrations from the anterior mitral leaet, and an increase in
turbulence from the combined effects of aortic regurgitant ow and mitral inow.
Presystolic murmurs tend to be relatively low to medium frequency, so auscultation should be undertaken with just enough pressure of the bell of the stethoscope
to achieve a skin seal. Presystolic murmurs originating across the mitral valve are best
elicited over the left ventricular impulse with the patient in a partial left lateral decubitus position (Fig. 64). Presystolic murmurs across the tricuspid valve are best elicited
with the patient supine while the examiner applies the stethoscope to the lower left
sternal edge, moving the bell in small increments in search of the localized murmur.
The presystolic murmur of tricuspid stenosis may be heard only during inspiration (see
5/19/2009 4:32:36 PM
211
Fig. 638), so the patient should be instructed to breathe rhythmically with a moderate
increase in depth.
Continuous Murmurs
The term continuous applies to murmurs that begin in systole and continue without interruption through the timing of the second heart sound into all or part of diastole
(Fig. 618).16 A holosystolic murmur followed by a holodiastolic murmur occupy both
phases of the cardiac cycle, but represent two murmurs, not a continuous murmur (Fig.
618). Conversely, a murmur that ends before the subsequent rst heart sound is continuous provided the murmur begins in systole and proceeds without interruption through
the timing of the second heart sound (see Fig. 618).
Continuous murmurs are generated by ow from a vascular bed of higher resistance into a vascular bed of lower resistance, without phasic interruption between systole
and diastole. Such murmurs are associated with (1) aortopulmonary connections, (2) arteriovenous connections, (3) disturbances of ow patterns in arteries, and (4) disturbances
of ow patterns in veins (see Fig. 618).
Best known and most celebrated is the continuous murmur of patent ductus arteriosus (Figs. 618 and 639). The murmur characteristically peaks before and after the
second heart sound, and is often soft or absent in late diastole.
In 1847, the London Medical Gazette published the following description:
a murmur accompanying the rst heart sound, prolonged into the second so that there
is no cessation of the murmur before the second sound has already commenced.25
S2
INTRA
CARDIAC
(PUL. ART.)
S1
THORACIC
WALL
(2nd L.I.C.S.)
S1
S2
Figure 639 The classic continuous

murmur of patent ductus arteriosus
simultaneously recorded from within the
main pulmonary artery (PUL ART) and
at the second left intercostal space on the
thoracic wall (2 LICS). The murmur begins
softly and increases in intensity so as to reach
its acme just about, or immediately after the
incidence of the second sound, and from that
point gradually wanes until its termination,
as originally described by Gibson in 1900.26
5/19/2009 4:32:36 PM
The cause of the murmur was correctly attributed to patent ductus arteriosus, and the
term continuous was correctly dened as no cessation of the murmur before the second
sound has already commenced.25
In 1900, George A. Gibson provided a meticulous description of the murmur
(Fig. 639) of patent ductus arteriosus that is still called the Gibson murmur. He wrote:
It persists through the second sound and dies away gradually during the long
pause. The murmur is rough and thrilling. It begins softly and increases in intensity so as to reach its acme just about, or immediately after, the incidence of the
second sound, and from that point gradually wanes until its termination.26
Arteriovenous continuous murmurs can be congenital or acquired, and are associated with
arteriovenous stulae, coronary arterial stulae, anomalous origin of the left coronary
artery from the pulmonary trunk, and communications between a sinus of Valsalva and
the right heart. The conguration, location, and intensity of arteriovenous continuous
murmurs vary considerably. The continuous murmur resulting from a systemic arteriovenous stula was described by the CzechAustrian pathologist Josef Skoda. The English
translation reads:
When a moderately sized artery communicates with a vein, a very loud continuous
murmur usually develops at the point of communication, the strength of which
increases on each pulsation of the artery and is audible over a greater or lesser part
of the surrounding area.27
Acquired systemic arteriovenous stulae are represented by the surgically created forearm connections used for renal dialysis. The continuous murmur of a congenital coronary
arterial stula that enters the right ventricle can be either softer or louder in systole
depending on the degree of compression exerted on the stulous coronary artery by right
ventricular contraction. The continuous murmur of a sinus of Valsalva aneurysm that
ruptures into the right heart does not peak around the second heart sound, but tends to
be louder in either systole or diastole, sometimes creating a to-and-fro impression.
Continuous murmurs can originate in constricted or nonconstricted arteries. In constricted systemic or pulmonary arteries, continuous ow disturbances occur when a signicant
persistent pressure difference exists between the two sides of the narrowed arterial segment. Arterial continuous murmurs arising in constricted arteries are characteristically
louder in systole (see Fig. 618). Atherosclerotic obstruction of carotid or femoral arteries are examples.
Disturbances of ow patterns in normal, nonconstricted arteries sometimes produce
continuous murmurs. The mammary soufe (see above), an innocent murmur heard maximally over lactating breasts during late pregnancy and the puerperium, is typically
continuous, but usually louder in systole. The soufe tends to be more prominent in
the second or third right or left intercostal space. A distinct gap separates the rst heart
sound from the onset of the soufe because of the interval that elapses before blood
ejected from the left ventricle arrives at the artery of origin. The mammary soufe is best
heard with the patient supine, and may vanish altogether in the upright position. Light
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213
pressure with the stethoscope augments the murmur and brings out its continuous features, whereas rm pressure or digital compression peripheral to the site of auscultation
abolishes the murmur.
Continuous murmurs in nonconstricted arteries originate in large systemic-to-pulmonary arterial collaterals in certain types of cyanotic congenital heart disease, especially
Fallots tetralogy with pulmonary atresia. These murmurs are randomly located throughout the thorax, and must be diligently sought.
Continuous venous murmurs are represented by the normal venous hum (Fig. 640)
which is almost universal in healthy children and is frequently present in healthy
young adults, especially during pregnancy. Potain described the venous hum in
1867:
The thrill, which is felt by placing the nger lightly above the clavicle over the
course of the vessel of the neck, is sometimes continuous and frequently intermittent. It is this last case which interests us above all here. A light pressure
exerted above the point of exploration can make it appear or reinforce it, while
a stronger pressure extinguishes it completely, proofs positive that we are concerned with a venous phenomenon and that this thrill does not arise at all from
an artery.28
PRESSURE
Figure 640 Photograph on the left shows the bell of the stethoscope applied to the medial
aspect of the right supraclavicular fossa (arrow). The examiners left hand grasps the chin from
behind and pulls it tautly to the left and upward, stretching the neck. The photograph on the
right shows digital compression of the right internal jugular vein (arrow) that obliterates the
venous hum (vertical arrow insert). The patients head has returned toward a neutral position.
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The venous hum is elicited with the patient sitting (Fig. 640). The stethoscopic bell is applied to the medial aspect of the right supraclavicular fossa, while the
examiners left hand grasps the patients chin from behind and pulls it tautly to the
left and upward (Fig. 640A). The hum disappears when the stretch is removed by
returning the head to a neutral position (Fig. 640B). Occasionally the hum appears
or increases when the chin is simply tilted upward, and at other times it is prominent
without neck maneuvers and irrespective of position. Venous hums in young children can appear when a child turns its head to the left or looks upward. The hum is
abolished by applying pressure to the ipsilateral deep jugular vein with the thumb of
the examiners free hand, as Potain described and as shown in Figure 640. Compression causes instantaneous disappearance of the hum (see phonocardiographic insert,
Fig. 640), which suddenly but transiently intensies as pressure is released. The
term hum does not necessarily describe the quality of these cervical venous murmurs,
which can be rough and noisy, or accompanied by a high-pitched whine. The venous
hum is truly continuous but is characteristically louder in diastole (Fig. 640), as is
the case with venous continuous murmurs in general (see Fig. 618). A loud venous
hum that radiates below the clavicles can be mistaken for an intrathoracic continuous
murmur. Obliteration by digital pressure in the neck abolishes the transmitted hum
and avoids error.
PERICARDIAL RUBS
The pericardial rubaptly called a friction rubresembles the sound produced by
rubbing or scratching sandpaper. Less commonly, indeed rarely, the rub is musical,
resembling the rubbing of a wet nger on a glass surface. Pericardial rubs have three
componentsone during ventricular systole and two during ventricular diastole
the latter coinciding with the rapid lling phase and the presystolic lling phase. A
two-phase rub is usually systolic and presystolic. In atrial brillation, the presystolic
component necessarily disappears. A single-phase rub, which is either systolic or presystolic, cannot be identied as such unless a two- or three-phase rub had previously
been heard.
Pericardial friction rubs originate from the anterior surface of the right ventricle,
and are therefore louder in response to maneuvers that increase right atrial and right
ventricular lling, or that bring the right ventricle closer to the chest wall. With the
patient supine, rm pressure is applied with the stethoscopic diaphragm during full
held exhalation or, more awkwardly, with the patient prone but with the chest lifted
(Fig. 641). The rub is typically louder during inhalation because of the inspiratory increase in venous return to the right atrium and right ventricle. Passive lifting of the legs
with the patient supine transiently increases the rub by the same mechanism. The most
common clinical setting in which pericardial rubs are heard is immediately after open
heart surgery.
5/19/2009 4:32:41 PM
215
Figure 641 A technique for eliciting a pericardial friction rub. The diaphragm of the
stethoscope is rmly applied to the precordium (arrow) while the patient is supported on elbows
and knees.
PHYSICAL MANEUVERS AND

PHARMACOLOGIC INTERVENTIONS
A number of physical maneuvers employed during auscultation have been discussed.
The following remarks reemphasize the importance of these maneuvers and bring them
briey into focus (Tables 65 and 66). Pharmacologic interventions are mentioned, although these are less practical and therefore less important at the bedside.
Changes in position that are useful during auscultation are listed in Table 65. A
partial left lateral decubitus position (see Fig. 64) assists in identifying the left ventricular impulse, which is an important auscultatory landmark. During the act of turning,
the heart rate transiently increases, improving audibility of mid-diastolic and presystolic
murmurs of mitral stenosis. The left lateral decubitus position occasionally induces premature ventricular beats that distinguish an aortic midsystolic murmur at the apex from
the apical murmur of mitral regurgitation (see earlier).
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Table 65 Positions During Auscultation

Left lateral decubitus
Sitting leaning forward
Sitting with legs dangling
Standing/squatting and vice versa
Hyperextension of the shoulders
Stretching of the neck
Passive elevation of the legs
Support of precordium on elbows and knees
Sitting and leaning forward in full held exhalation (Fig. 632) improves audibility of the soft, high-frequency early diastolic murmur of aortic regurgitation, or a soft
Graham Steell murmur. Sitting with legs dangling over the side of the bed or examining
table helps identify normal splitting of the second heart sound when the split fails to fuse
during exhalation in the supine position.
Standing and squatting followed by prompt standing (Figs. 68 and 630) is
achieved with the examining gown securely fastened so the garment doesnt slip off
and compromise the examination. During the squatting/standing maneuver, balance is
important, especially in older adults, who should squat within arms reach of support
from the bed or examining table for support (Fig. 630). The sequence of standing
then squatting followed by prompt standing is useful in assessing the murmurs of
aortic and mitral regurgitation, mitral valve prolapse, and hypertrophic obstructive
cardiomyopathy.
Hyperextension of the shoulders is important in assessing supraclavicular systolic
murmurs (Fig. 631). A venous hum is initiated or reinforced by stretching the neck
upward and to the left as the stethoscopic bell is applied to the medial aspect of the right
supraclavicular fossa (see Fig. 640).
Third heart sounds are augmented by the transient increase in venous return in
response to passive elevation of the legs with the patient supine. The patient must not
to assist in leg raising in order to avoid involuntary straining and a partial Valsalva
maneuver.
Table 66 Other Physical Maneuvers During Auscultation

Respiration
Inhalation, exhalation
Full, held exhalation
Valsalva and Mueller maneuvers
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217
The precordium can be elevated above the bed or examining table by having the
patient rise on elbows and knees (Fig. 641), a maneuver, albeit awkward, that assists in
detecting pericardial friction rubs (see above).
Physical maneuvers other than positional
Normal rhythmic inhalation and exhalation are employed routinely (see Table 66).
Exaggerated respiratory excursions are useful in analyzing splitting of the second heart sound, right-sided third and fourth heart sounds, tricuspid systolic and
diastolic murmurs, and pulmonary ejection sounds. The desired depth and rate
of breathing should be demonstrated. Full held exhalation while the patient sits
and leans forward (Fig. 632) is used to elicit the soft, early diastolic murmur
of aortic regurgitation or pulmonary hypertensive pulmonary regurgitation. The
innocent pulmonary midsystolic murmur associated with decreased anteroposterior chest dimensions (loss of thoracic kyphosis) amplifies when the diaphragm of
the stethoscope is pressed firmly in the second left intercostal space during full
held exhalation.
The Valsalva maneuver (Antonio Maria Valsalva: Italian anatomist, born 1666)
is readily performed at the bedside, and consists of a deep inspiratory effort followed by
forced exhalation against a closed glottis for approximately 10 seconds.29 The maneuver
was described in 1704 as a method for expelling pus from the middle ear by straining
while the mouth and nose were closed. Simulation by the examiner is a simple means of
instructing the patient on how to perform the maneuver. The at of the hand is placed
on the abdomen to provide a force against which the patient can strain, and to provide
an assessment of the degree and duration of the effort.
The normal Valsalva response consists of four phases. Phase I is associated with
a transient rise in systemic blood pressure as straining commences. This phase cannot
be identied at the bedside. Phase 2 is accompanied by a decrease in blood pressure
and pulse pressure, reex sinus tachycardia, and an increase in the intensity of the
murmurs of hypertrophic obstructive cardiomyopathy and mitral valve prolapse.29
Phase 3 begins with cessation of straining, is associated with an abrupt, transient
decrease in blood pressure not perceived at the bedside, and is followed promptly by
Phase 4 which is characterized by an overshoot of systemic arterial pressure and reex
bradycardia.
The increase in venous return and in systemic blood pressure during Phase 4
intensify outow and regurgitant murmurs except the murmur of hypertrophic obstructive cardiomyopathy and the regurgitant murmur of mitral valve prolapse,
both of which decrease as the result of larger left ventricular volume.29 Phase 4 also
identies murmurs that originate in the right side of the heart because right-sided
murmurs promptly return to baseline intensity after release of the Valsalva maneuver in response to an immediate increase in venous return. Conversely, murmurs
originating in the left side of the heart take a longer time to return to baseline after
release of the maneuver because of the time required for systemic venous return to
5/19/2009 4:32:43 PM
traverse the pulmonary circulation. Elderly patients tend to have impaired reex
mechanisms, so the Valsalva maneuver may cause syncope and should be performed
cautiously if at all.29
The Muller maneuver is the converse of the Valsalva, and is less frequently
employed because it is less useful at the bedside. The Muller maneuver is performed for
about 10 seconds as the patient forcibly inhales against a rmly closed nose and mouth.
By exaggerating the inspiratory effort, the Miller maneuver augments the murmur of
tricuspid regurgitation or stenosis, but usefulness is limited.
Isometric exercise (sustained handgrip) is a simple, safe bedside maneuver. Sustained handgrip imposes a pressure load on the left ventricle by increasing systemic
systolic blood pressure which is accompanied by an increase in heart rate and cardiac
output, all of which promptly revert to control levels with cessation of the maneuver.
To achieve the desired effect of isometric exercise, the patient simultaneously squeezes
both sts. But if the ngernails are long, a rm rubber ball or an analogous object can
be compressed. Care should be taken to avoid tensing proximal muscle groups, especially the shoulder girdle. Sustained handgrip is maintained until the patient is told to
desist. The duration depends on whether and when the desired auscultatory response is
elicited. Auscultation should therefore precede, accompany, and follow the maneuver.
Twenty seconds of isometric exercise usually sufce. The response to sustained handgrip
reinforces left ventricular fourth heart sounds and augments the murmurs of mitral and
aortic regurgitation. The click(s) of mitral valve prolapse occur later in systole, while the
late systolic murmur shortens but increases in intensity. The systolic murmur of hypertrophic obstructive cardiomyopathy softens because the increase in afterload increases
left ventricular volume.
Amyl nitrite inhalation occasionally has a place during auscultation. The drug
prompts a fall in systemic vascular resistance and blood pressure and an increase in
heart rate, cardiac output, and ejection velocity. Inhalation is from a broken vial
held close to the nose, preferably under a small cloth or handkerchief. The patient is
instructed to breathe naturally while the arterial pulse is monitored for the rst evidence of reex tachycardia, at the onset of which inhalation is discontinued. The pulse
rate is simpler and easier to monitor than the cuff blood pressure, and the response to
nitrite is easier to monitor during continuous natural breathing than in response to
several deep breaths.
The auscultatory effects of amyl nitrite inhalation are in accord with the
hemodynamic effects just described. An increase in cardiac output and ejection
velocity is accompanied by an increase in intensity of the systolic murmur of aortic stenosis or of isolated pulmonary stenosis (Fig. 642). A decrease in systemic
vascular resistance is accompanied by a decrease in the systolic murmur of mitral
regurgitation (Fig. 643A) and in the diastolic murmur of aortic regurgitation
(Fig. 636). The mid to late systolic clicks and late systolic murmur of mitral valve
prolapse occur earlier because of a reduction in left ventricular volume, but the
murmur becomes softer because of decreased resistance to left ventricular discharge)
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CONTROL
219
AMYL NITRITE
SM
SM
SM
A2 P2
S1
E
RV
RV
PA
PA
20
20
PA
20
20
Figure 642 Phonocardiogram and intracardiac pressure pulses from a 15-year-old patient
with mild pulmonary valve stenosis (control gradient 25 mm Hg). Following amyl nitrite
inhalation, the right ventricular (RV) pressure rose (long oblique arrow), the gradient increased,
and a short, soft midsystolic murmur (SM) became louder and longer. E, pulmonary ejection
sound; PA, pulmonary arterial pulse.
(Fig. 67C). The systolic murmur of hypertrophic cardiomyopathy intensifies because amyl nitrite causes a decrease in left ventricular volume and an increase in
ejection velocity.
Pharmacologic agents that increase left ventricular afterload augment the murmurs
of mitral regurgitation (Fig. 643B) and aortic regurgitation. The late systolic murmur
of mitral valve prolapse becomes louder as regurgitation increases, but the clicks and
murmur occur later in systole (Fig. 67B) because left ventricular internal dimensions
increase. In hypertropic obstructive cardiomyopathy, an increase in resistance to left ventricular discharge reduces the left ventricular-to-aortic gradient and softens the systolic
murmur (Fig. 644) because left ventricular internal dimensions increase. The fourth
heart sound gets louder because the increase in left ventricular afterload prompts an augmentation in left atrial contractile force.
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SM
APEX S
1
S1
S2
Control
CAR.
SM
SM
S2
1719
SEC
S1
SM
S2
S1
S2
2628
SEC
55
SEC
D.N.
A
CONTROL
PRESSOR AMINE
APEX
SM
S1
APEX
SM
S2
S1
S2
V
200
160
120
80
BA
BA
40
0
30
V
C
A
20
10
L.A.
L.A.
0
B
Figure 643 A, Striking decrease in amplitude of the systolic murmur (SM) of mitral regurgitation
in response to a reduction in resistance to left ventricular discharge induced by amyl nitrite inhalation.
At 55 seconds (fourth panel), the amplitude of the murmur had not returned to control level. B,
Striking increase in amplitude of the systolic murmur (SM) of mitral regurgitation in response to an
increase in resistance to left ventricular discharge induced by infusion of a pressor amine. An increase
in systemic systolic pressure was accompanied by an increase in mitral regurgitation, an increase in left
atrial V wave, and an increase in the systolic murmur (SM). LA left atrium.
5/19/2009 4:32:49 PM
221
SM
SM
S4
S4
S1
S2
sin
ten
io
ang
AORTA
Figure 644 The effect of an increase in resistance to left ventricular discharge in a patient
with hypertrophic obstructive cardiomyopathy. The rst panel is a phonocardiogram and
pressure pulse recorded within the ascending aorta just above the aortic valve. There is no
systolic murmur. (S1 S2, rst and second heart sounds.) In the middle panel, recordings are
from within the left ventricular cavity (LV). There is a prominent fourth heart sound (S4) and
a prominent systolic murmur (SM). The third panel illustrates a decrease in intensity of the
intracavity left ventricular systolic murmur (SM, oblique arrow) as resistance to left ventricular
discharge increased in response to an angiotensin infusion The fourth heart sound (S4) recorded
from within the left ventricular cavity increased considerably.
5/19/2009 4:32:51 PM
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Gaz Lond. 1880;2:432.
23. Flint A. On cardiac murmurs. Am J Med Sci. 1862;44:23.
24. Berman P. Austin FlintAmericas Laennec revisited. Arch Intern Med. 1988;148:2053.
25. Williams X. Comment in discussion of case of patent ductus arteriosus with aortic valve disease, coarctation of aorta and infective endocarditis, reported by Babington. Lond Med Gaz.
1847;4:822.
26. Gibson GA. Persistence of the arterial duct and its diagnosis. Edinb Med J. 1900;8:1.
5/19/2009 4:32:54 PM
223
27.
Skoda J. Abhandlung uber Perkussion and Auskultation. Vienna: L. W. Seidl und John. Sechste
Auage, 1864.
28. Potain PC. Des mouvements et de bruits qui se passent dans, les veines jugulaires. Bull Mem
Soc Med Hop.Paris: 1867;4:3.
29. Nishimura RA, Tajik AJ. The Valsalva maneuver revisited. Mayo Clin Proc. 1986;61:211.
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The Chest
The pulmonary circulation was discovered by Michael Servetus (Miguel Servet), who was
born in Villanueva de Sigena in northeast Spain. The date of his birth is disputed (1507
or 1511), but the date of death is beyond doubt. The original draft of Servetus seminal manuscript appeared before 1546, and was published as his Christianismi Restitutio
in 1553.1 Because his books had theological connotations, Servetus was accused by the
Calvinists of heresy. He was arrested in Geneva, and in 1553, was burned at the stake
together with copies of his Restitutio. Servitus was burned slowly to increase his agony.
Michael Servetus wrote:
The heart is the rst organ that lives. The vital spirit is engendered by the mingling of inspired air with the more subtle portion of the blood which the right
ventricle of the heart communicates to the left. This communication, however,
does not take place through the septum, partition or midwall of the heart, as
commonly believed, but by another admirable contrivance, the blood being transmitted from the pulmonary artery to the pulmonary vein, by a lengthened passage
through the lungs, in the course of which it is elaborated and becomes a crimson
colour. Mingled with the inspired air in this passage, and freed from its fuliginous
vapors by the act of expiration, the mixture being now complete in every respect,
the blood becomes a t dwelling-place of the vital spirit.1
Servetus emphasized:
It is in the lungs, consequently, that the mixture of the inspired air with the blood
takes place, and it is in the lungs also, not in the heart, that crimson colour of the
blood is acquired. The vital spirit is at length transfused from the left ventricle of
the heart to the arteries of the body at large.1
With intuitive genius, Servetus proposed:
Within the lungs we nd a new kind of vessels proceeding from the arteries to the
veins. The blood is distributed to those extremely minute vessels or capillary arteries.1
225
5/19/2009 4:33:25 PM
226 The Chest
Servetus Restitutio appeared three quarters of a century before William Harveys De

Motu Cordis et Sanguinis (1628), and a century before Marcello Malpighi published his
discovery of the capillary circulation (De Pulmonibus Observationes Anatomicae, 1661).2
It has been persuasively argued that the story of the circulation was completed by
Malpighi, one of Italys most gifted scientists. Malpighi also established the function
of the uterine placenta, stating in his De Pulmonibus, that the lungs of fetus were at
rest, and that a certain mass called the uterine placenta acted vicariously for the
lungs.
The only skeletal muscles upon which life depends are the respiratory muscles,
especially the diaphragm. Gian Alfonso Borelli (16081679), a teacher of Malpighi,
applied the laws of mechanics, and understood the importance of the diaphragm and
intercostal muscles in respiration and ventilation.
The respiratory system comprises two essential components: (1) the lungs for gas
exchange and (2) a pump that ventilates the lungs.3 The pump consists of rib cage muscles, accessory muscles, abdominal muscles, and the diaphragm.3 The external and internal intercostal, parasternal, interchondral, scalene, and sternocleidomastoid muscles act
directly on the rib cage. The diaphragm has three functionally and anatomically distinct
segments: (1) muscle bers that originate from the costal margin and sternum and insert
into the central tendon; (2) crural muscle bers that originate from the vertebral column
and insert into the central tendon; and (3) the central tendon itself.3 The costal margin
of the diaphragm displaces the rib cage and abdomen while inating the lungs. Contraction of the crural component has no effect on the rib cage because crural bers are not so
attached. Instead, contraction of the crural portions of the diaphragm functions primarily to lower the central tendon and displace the abdominal wall, simultaneously inating
the lungs. If inspiration is performed entirely with rib cage and accessory muscles while
the diaphragm remains relaxed, abdominal pressure falls and the abdominal wall moves
inward rather than outward.
Breathing with intercostal or accessory muscles alone is inefcient, and does not
normally occur. During quiet breathing, the diaphragm is the major component of the
respiratory mechanism. In the supine position, normal respiratory movements are largely abdominal (diaphragmatic). In the upright position during normal quiet breathing,
the diaphragm still predominates, but with a larger contribution from the muscles of
the rib cage. The relative contributions of rib cage vs diaphragmatic/abdominal muscles
is demonstrated by comparing thoracic and abdominal breathing movements when the
at of one hand is placed on the abdomen and the at of the other hand is placed on
the chest. This is a useful means of persuading patients that augmentation of rib cage
(chest) muscles results in the inefcient, deep, sighing inspiratory efforts of anxietyrelated hyperventilation.
It axiomatic that the physical examination of the heart and circulation includes the
chestits appearance, movements, palpation, percussion, and auscultation. Appearance
(see Chapter 2) includes the posterior thoraxscoliosis, kyphosis, kyphoscoliosis, and loss
of thoracic curvature (Fig. 71A)and the anterior thorax (pectus carinatum, Fig. 71B),
pectus excavatum, and the barrel chest (Fig. 72).
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227
Figure 71 A, Absence of thoracic kyphosis (straight back, vertical arrow) in an otherwise

normal young male. B, Marked pectus carinaturn (curved arrow) in a young female with Marfan
syndrome.
RESPIRATORY MOVEMENTS should be assessed when the patient is unaware of the examiners intent. The patient should not be told to breathe normally,
an instruction that is likely to result in a self-conscious change in breathing pattern.
Respiratory movements depend in part on the position assumed to achieve the greatest
comfort while breathing. Assessment should include rib muscles, accessory muscles,
and the diaphragm. In an infant with pulmonary edema, an increase in the work of
breathing is typically manifested by retraction of the supraclavicular fossae and intercostal muscles, and by inspiratory nasal aring. Orthopnea (orthos = straight, pnoia =
breath) implies that sitting upright or semi-upright is the most comfortable position. Trepopnea (trepein = to turn, plus pnoia = breath) refers to a condition in which
breathing is most comfortable when the patient turns into a right or left recumbent
position.
Once the patient is comfortable, the frequency and depth of respiration are observed.
Respiratory frequency is in part age-related. The relatively rapid and somewhat irregular breathing of a normal newborn contrasts with the slower rhythmic breathing of the
normal adult. Respiratory excursions can be abnormally slow (bradypnea) or abnormally
rapid (tachypnea), or may transiently cease altogether (apnea). The depth of a respiratory excursion can be excessive (hyperpnea) or shallow. Hyperpnea can be persistent (the
Kussmaul breathing of metabolic acidosis) or episodic (the intermittent, deep sighing
5/19/2009 4:33:26 PM
228 The Chest
Figure 72 A, Barrel chest due to chronic bronchitis and emphysema.15 (From Cabot RC:
Physical Diagnosis. New York, William Wood and Co., 1915.) B, Barrel chest with striking
increase in anteroposterior chest dimensions, anterior bowing of the sternum, and an increase in
thoracic kyphosis.
excursions of hyperventilation). Inhalation and exhalation may be effortless, or labored

and prolonged. A few examples sufce.
Tachypnea typically announces heart failure in infants, and is accompanied by labored breathing manifested chiey by inspiratory efforts that call into play accessory
muscles that produce subcostal and suprasternal retraction (see above). In adults, the
tachypnea of acute pulmonary edema is accompanied by inspiratory and expiratory gurgling, cough, pink frothy sputum, aring nostrils, and labored use of accessory respiratory muscles (see above). Tachypnea is a common and sometimes insidious sign of
pulmonary embolism.
Periodic breathing takes different forms, among the commonest is the deep, sighing
inspiratory effort of psychophysiologic hyperventilatory dyspnea in otherwise normal
but anxious patients. The deep inspiratory sighs principally utilize rib cage muscles, and
are associated with the sensation of an unfullled, unsatisfying breath (see above). A celebrated type of periodic breathing was described by William Stokes, and subsequently
came to be known as Cheyne-Stokes respiration:
The decline in the length and force of the respirations is as regular and remarkable as their progressive increase. The inspirations become each one less deep than
the preceding, until they are all but imperceptible, and then the state of apparent
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The Chest
229
apnoea occurs. This is at last broken by the faintest possible inspiration; the next
effort is a little stronger, until, so to speak, the paroxysm is at its height, again to
subside by a descending scale.4,5
Figure 73 is a tracing of CheyneStokes respiration recorded by James Mackenzie
on his polygraph.
A colorful report of periodic breathing is C. Sidney Burwells account of what has
come to be known as the pickwickian syndrome.6 Periods of apnea during involuntary sleep
(Fig. 74) alternate with periods of tachypnea that suddenly awaken the patient. Charles
Dickens, a novelist, observed disease with the eye of a clinician; Burwell, a physician,
described illness as a novelist. He reported a 51-year-old obese business executive who
was hospitalized because of hypersomnolence:
The patient was accustomed to playing poker once a week, and on the crucial
occasion he was dealt a hand of three aces and two kings. According to Hoyle,
this hand is called a full house. Because he had dropped off to sleep, he failed
to take advantage of this opportunity. A few days later, he entered the Peter Bent
Brigham Hospital.6
Pulmonary emphysema of chronic obstructive lung disease is accompanied by distinctive
patterns of thoracic movement. The hyperinated lungs (Fig. 72) compromise if not
eliminate the diaphragmatic contribution to breathing, because the crural portions of
both hemidiaphragms are depressed (attened) by the hyperination per se. Accordingly, intercostal and accessory muscles are recruited to assist the ineffectual diaphragm.7
Accessory thoracic respiratory muscles literally lift the sternum with each labored inspiration that coincides with brisk inward movement of the abdomen. Exhalation is forced
and prolonged, often through pursed lips, and is accompanied by tensing of abdominal
muscles and distention of neck veins that briskly collapse during subsequent labored
Fig 5
Respiratory movements
Respiratory movements
Fig 6
Radial pulse
HYPERPNEA
APNEA
Figure 73 Respiratory movements from a case of Cheyne-Stokes respiration.5 (Arrows and

labels are mine.) (From Mackenzie J: Diseases of the Heart. London, Henry Frowde, 1908.)
5/19/2009 4:33:32 PM
230 The Chest
Figure 74 An obese
32-year-old man with the
pickwickian syndrome. The
patient fell asleep while his history
was being taken. (Photographed
by the author.)
inhalations. This distinctive seesaw pattern of thoracic and abdominal motion is best
observed from the side of the bed or examining table with the patient supine. However,
patients with chronic obstructive lung disease often prefer to sit and lean forward with
arms extended.
Broadbent signan inward systolic tugging of the lower dorsal and lateral portions of the left hemithoraxis one of the best known but least useful signs of constrictive pericarditis.
PALPATION
Palpation of the thorax, apart from and in addition to movements imparted by the heart
and great arteries (see Chapter 5), falls into three categories: tactile fremitus, application
of localized pressure, and assessment of inspiratory thoracic excursions.
Fremitus refers to vibrations transmitted to the chest wall by the spoken word
(voice). Vocal fremitus refers to vibrations as the patient repeats ninety-nine or an analogous phrase in a relatively loud, deep voice while the diaphragm of the stethoscope interrogates the chest. Tactile fremitus refers to vibrations transmitted to the chest wall by the
spoken word as the patient repeats ninety-nine or an analogous phrase in a relatively
loud, deep voice while the ngertips or u1nar surface of the hand interrogate the chest.
Voice sounds are conducted through the bronchial tree and lung parenchyma to the
chest wall. Enhanced tactile fremitus identies an increase in parenchymal lung density
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The Chest
231
(consolidation) that increases transmission. Conversely, tactile fremitus is reduced by

obesity (Fig. 74), pleural effusion, pneumothorax, or the hyperinated lungs of emphysema (Fig. 72). Tactile fremitus, is evaluated to the right and left of the midline in the
posterior chest, and is enhanced by a loud deep voice.
Localized pressure elicits noncardiac musculoskeletal chest wall pain. Pressure is
selectively applied to each chondrosternal junction while asking the patient to compare
the left to the right. Musculoskeletal pain thus elicited is typically to the left of the sternum, but may be submammary. The site of tenderness often coincides with the clinical
complaint of localized, sharp chest pain.
The third role of thoracic palpation is to determine the relative degrees of inspiratory
chest excursions. The examiner places the ats of both hands against the patients back with
thumbs parallel to the midline at approximately the level of the tenth rib. The skin beneath
the thumbs is moved toward the midline. The patient is then asked to inhale deeply while
movements of the thumbs away from the midline are observed. Normal movement is symmetric. Asymmetric movement of the thumbs away from the midline signies that the
chest on the side of lesser movement does not expand normally during inhalation.
PERCUSSION AND AUSCULTATION

Thoracic percussion originated with Leopold Auenbrugger (Fig. 75), who observed
his father tapping wine barrels (Fig. 76) to determine their uid level. It occurred to
Auenbrugger that the same technique could be applied to the human thorax:
The method of percussion is founded on the property possessed by the human thorax, in common with most hollow bodies, of giving out certain sounds when struck
in a particular way.8
In 1761, Auenbrugger, an unassuming junior physician at the Vienna Hospital, published his Inventum Novum Ex Percussione Thoracis Humani.8 Josef Skoda heralded the discovery of percussion as the beginning of modern diagnosis, but the epochal work lay
dormant until Corvisart, physician to Napoleon, published an elaborate 480 page French
edition of Auenbruggers unpretentious 95 page book. Now let Auenbrugger speak for
himself:
I here present the reader with a new sign which I have discovered for detecting
diseases of the chest. This consists in percussion of the human thorax, whereby,
according to the character of the particular sounds thence elicited, an opinion is
formed of the internal state of that cavity.
The sound thus elicited from the healthy chest, resembles the sound of a drum
covered with a thick woolen cloth or other envelop. To be able justly to appreciate
the value of the various sounds elicited from the chest in cases of disease, it is necessary to have learned by experience on many subjects, the modication of sound
produced by the habit of the body inasmuch as these various circumstances modify
the sound very considerably. A clear and equal sound solicited from both sides of
5/19/2009 4:33:32 PM
232 The Chest
Figure 75 Leopold
Auenbrugger (17221809).
(Courtesy of Special Collections
Division, Biomedical Library,
UCLA Medical Center.)
Figure 76 Burgundian wine casks. Auenbrugger witnessed his fathers practice of percussing
wine barrels to determine the level of their uid content (see Chapter 5). (Photographed by the
author.)
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The Chest
233
the chest indicates that the air cells of the lungs are free and uncompressed either
by a solid or liquid body.
These varying results depend on the greater or lesser diminution of the volume of
air usually contained in the thorax (lungs); and the cause of which occasions this diminution, whether solid or liquid, produces results analogous to those obtained by striking a cask, for example, in different degrees of emptiness or fullness: the diminution
of sound being proportioned to the diminution of the volume of air contained in it.9
Auenbrugger then sought experimental conrmation:
The effect of effused uids in producing the morbid sound, is at once proved by
the injection of water into the thorax of a dead body; in which case it will be found
that the sound elicited by percussion will be obscure over the portion of the cavity
occupied by the injected liquid.9
Of the method of percussion, Auenbrugger wrote:
The thorax ought to be struck, slowly and gently, with the points of the ngers,
brought close together and at the same time extended. Percussion with the at of
the open hand is also useful, especially on the lateral and posterior parts.8,9
Auenbruggers technique has been superseded by percussion that employs both of the
examiners hands (Fig. 77). The middle nger of the left hand is applied rmly to an
intercostal space while the palm of the other ngers is lifted off the chest. The right
middle nger of the free right hand is used to strikepercussthe distal phalanx of the
left middle nger. The motion of the percussing right middle nger should originate at
the wrist. Posterior thoracic percussion begins between the scapulae and proceeds interspace by interspace downward to the level of the diaphragm, comparing the right and
left sides, as Auenbrugger originally recommended.
The chief objectives of thoracic percussion in cardiac patients are to determine the
presence, degree, and location of pleural effusions, and the relative heights and movements of the hemidiaphragms.9
When water is collected in the cavity of the chest, between the pleura (costalis)
and the lungs, the disease is called dropsy of the chest; and this is said of be of two
kinds, namely, according as the uid occupies one or both sides. This is ascertained
by percussion in the living subject; and is demonstrated by anatomical examination after death.9
Pleural effusions in congestive heart failure are usually bilateral or isolated to the
right, but are seldom conned to the left. Thus, an isolated left pleural effusion is likely
to have a cause other than heart failure.
Diaphragmatic movement is assessed with the patient sitting:
When operating on the back, you are to cause the patient to bend forward, and
draw his shoulders towards the anterior parts of the chest, so as to render the dorsal
region rounded.9
5/19/2009 4:33:33 PM
234 The Chest
Figure 77 Technique of thoracic percussion. A, The middle nger of the left hand (arrow)
is applied rmly to an intercostal space, while the palm is elevated to avoid contact with the
chest. The right middle nger (upper oblique arrow) is poised. B, The tip of the right middle nger
sharply strikes the distal phalanx of the left middle nger (arrow) with motion originating from
the wrist.
The right and left lung bases are then percussed during full held inspiration and full
held expiration. The difference in levels represents the degree of excursion of each
hemidiaphragm. Hyperination of the lungs, as in pulmonary emphysema (see Fig. 72),
is associated with reduced if not absent diaphragmatic movement.
Ewarts singular and most helpful sign10 refers to the posterior pericardial patch
of dullness. When uid is infused into the pericardium, normal resonance is distinctively modied at the left posterior base (Fig 78):
A patch of marked dullness is found at the inner base, extending from the spine
for varying distances outward, usually not quite so far as the scapular (angle) line,
ceasing abruptly with a vertical outer boundary.10
The succession splash of hydropneumothorax was known to Hippocrates circa 400 b.c.11 In
1848, Henry I. Bowditch referred to succession:
If you wish to try it, do as follows. Let a man be seated, and thence seizing him by
both shoulders, shake suddenly and somewhat forcibly the whole trunk. It is very
unsatisfactory in its results, and likewise is troublesome to the patient.12
In 1908, William Osler published Thomas Brownes description of Hippocratic succession
in a Woeman or Mayd in Suffolk who had a splashing and uctuation in her chest.13
5/19/2009 4:33:33 PM
The Chest
235
V. P.
T AZ
Figure 78 Ewart signs. Lower right arrow, The Posterior Pericardial Patch of Dullness
Whenever uid is effused into the pericardium, the normal resonance is modied at the left
posterior base in a most denite way. A patch of marked dullness was found at the left inner
base, extending from the spine for varying distances outwards, usually not quite so far as the
scapular angle, and ceasing abruptly with a vertical outer boundary. Upper left arrow, The
Posterior Pericardial Patch of Tubular Breathing and AegophonyImmediately below or slightly
to the left of the tip of the left scapula, a patch about two inches in diameter presents a wellmarked tubular breathing and aegophony. This sign, although not so important as that of the
patch of dullness, is very commonly, if not always, present in cases of considerable effusion, and
gives valuable conrmation to other signs. (Arrows are mine.) (From Ewart W: Practical aids
in the diagnosis of pericardial effusion in connection with the question as to surgical treatment.
Br Med J March 1896.)
Auscultation
Auscultation of the human thorax by placing an ear directly against the chest long preceded percussion (Fig. 79). Pleural friction rubs and wheezes were probably rst heard
by direct auscultation. However, the major advance was the stethoscope (Fig. 710). In
A Treatise on Diseases of the Chest (1821), Laennec wrote:
The cylinder, applied to the chest of a healthy person who sighs or speaks, produces a sort of vibration, which is more distinct in some places than in others. We
have also examined, by means of the cylinder, the respiration in different parts of
the chest of the healthy person, and found it very distinctively audible in every
point of this cavity which corresponded with the lungs.14
5/19/2009 4:33:37 PM
236 The Chest
Figure 79 Cartoon
satirizing direct auscultation
of the chest. (From McKusick
VA. Cardiovascular Sound in
Health and Disease, Baltimore,
Williams & Wilkins Company,
1958. Reprinted with permission.)
Figure 710 The Laennec

stethoscope (arrow) applied to the
thorax of a child.
Respiratory sounds were among Laennecs major interests and include (1) normal breath
sounds heard during quiet breathing, (2) rales (crackles), (3) wheezes, (4) pleural rubs,
(5) tubular breathing, (6) voice-generated sounds, and (7) the crunch of mediastinal
emphysema.
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The Chest
237
Four types of breath sounds are normally heard during quiet breathing: (1) vesicular, (2) bronchial, (3) bronchovesicular, and (4) tracheal. Soft low frequency vesicular
breath sounds that resemble a gentle rustling or sigh are audible throughout most of the
chest. The inspiratory phase of vesicular breath sounds is longer and more clearly audible
than the expiratory phase that follows without interruption. Vesicular breath sounds are
reduced or absent in the obese (Fig. 74) and in the hyperinated lungs of pulmonary
emphysema (Fig. 72). Bronchial breath sounds, which are normally conned to the manubrium, are loud and high-pitched with a hollow quality, and are usually interrupted
by a pause between the inspiratory and expiratory phases. In normal neonates, breath
sounds are bronchial, and are louder over the periphery of the lungs. Bronchovesicular
breath sounds are intermediate between vesicular and bronchial, as the term implies,
are normally conned to the vicinity of the rst and second intercostal spaces anteriorly or between the scapulae posteriorly, and are usually more obvious on the right. The
inspiratory and expiratory phases of bronchovesicular breath sounds are either continuous or separated only briey, with each phase about the same duration and quality.
Tracheal breath sounds are relatively unimportant, and are not routinely sought.
The time-honored term rale has been replaced in pulmonary terminology by
the term crackle. Rale and crackle are therefore synonymous, with cardiologists preferring rale, and pulmonologists crackle. Rales or crackles are classied as coarse or ne.
The mechanism responsible for their genesis is believed to be the process of bubbling
as gas ows through secretions, with coarse rales or crackles originating in larger airway
secretions, and ne rales or crackles originating in smaller airway secretions (pulmonary
edema).
Wheezes, also referred to as rhonchi, are relatively pure, high-frequency musical
events generated by airow within narrowed bronchi, and are augmented by exhalation,
especially rapid, forced exhalation. Wheezes and rhonchi are the result of the bronchospasm or bronchial swelling of asthma or emphysema. Secretions characterize pulmonary
edema.
The pleural rub was described by Hippocrates as a sound like that made by leather,
a grating sound produced on surfaces, the movements of which are impeded by frictional
resistance.11 Pleural rubs are best heard at the end of inhalation and at the onset of exhalation. The search must be meticulous. Firm pressure of the stethoscopic diaphragm
is applied with the patient in a comfortable sitting position with the elbows away from
the chest wall.
A pleural rub in a cardiac patient is usually the result of a pulmonary embolus
with infarction. Special attention should focus on the lower lobesaxillae and back
which are the usual sites of embolic infarcts.
Tubular breathing is an abnormal breath sound transmitted via patent airways from
a region of parenchymal consolidation. Voice-generated signs include egophony, pectoriloquy, and bronchophony (increased intensity and a nasal quality of the spoken voice heard
through consolidated lungs, e-e is heard as a-a), bronchophony refers to the audible
voice, and pectoriloquy to the whispered voice. The patient repeats in a quiet voice onetwo or ninety-nine or e-e while the examiner listens with the diaphragm of the
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238 The Chest
stethoscope. The patient then repeats in a whispered voice. Voice-generated sounds are
attenuated by transmission through normal air-lled lungs, and have a mufed quality
with indistinct words. Egophony refers to an increased intensity and nasal quality of the spoken
voice heard through consolidated lung. e-e is heard as a-a. Bronchophony and pectoriloquy
indicate that the spoken voice is transmitted with increased intensity and pitch so that
the syllables are distinct and easily recognized. Egophony, bronchophony, and whispered
pectoriloquy are auscultatory manifestations of the same acoustic properties of consolidated lungs, and therefore have the same diagnostic signicance. A common site of consolidation in cardiac patients is the compression atelectasis above a pleural effusion.
The mediastinal crunch (Hamman sign) is a crunching, crackling, or popping sound
generated by breathing movements and cardiac contraction in the presence of mediastinal emphysema. A common setting in which a crunch is detected is immediately after
operation via a midline sternotomy that introduces air into the mediastinum. Air is also
introduced into the mediastinum by chest trauma or cardiopulmonary resuscitation.
Thoracic auscultation occasionally detects a cardiorespiratory murmur which was
known to Laennec, but characterized by Richard Cabot:
Cardiorespiratory murmurs may be produced without any adhesion of the lung to
the pericardium under conditions not currently understood. Such murmurs may
be heard under the left clavicle or below the angle of the left scapula, as well as
near the apex of the heartless often in other parts of the chest. Cardiorespiratory
murmurs may be either systolic or diastolic, but the vast majority of cases are systolic. The area over which they are audible is usually a very limited one. They are
greatly affected by position and by respiration, and are heard most distinctly if not
exclusively during inspiration, especially at the end of that act.15
James Hopes experience with two university students is picturesque:
Both wore very tight waistcoats, preventing the expansion of the lower ribs. During this state of breathing, a bellows murmur existed in both. In both, the murmur ceased entirely when, unbuttoning their waistcoats and waistbands of their
trousers, they breathed with the lungs naturally inated. By alternating the circumstances, the murmur could be created or removed at pleasure. I presume therefore that it proceeded from a cause exterior to the heart.16
The mechanism responsible for the cardiorespiratory murmur remains unclear, but the
location, timing, and relation to respiration are as Cabot described.15
REFERENCES
1.
2.
3.
4.
Servetus M. Christianismi Restitutio. Vienna: Balthasar Arnollet, 1553.

Malpighi M. De Pulmonibus observations anatomicae. Bononiae, 1661. (English translation
by Young J. Proc Roy Soc Med 23:1, 19291930. see previous edition and style accordingly
Roussos C, Macklem PT. The respiratory muscles. N Engl J Med. 1982;307:786.
Stokes W. Diseases of the Heart and Aorta. Dublin, Ireland: Hodges and Smith, 1854.
5/19/2009 4:33:39 PM
The Chest
239
5. Mackenzie J. Diseases of the Heart. London: Henry Frowde, 1908.

6. Burwell CS, Robin ED, Whaley RD, Bicklemann AG. Extreme obesity associated with alveolar hypoventilationA pickwickian syndrome. Am J Med. 1956;21:811.
7. Macklem PT, Macklem DM, DeTroyer A. A model of respiratory muscle mechanics. J Appl
Physiol. 1983;55:547.
8. Auenbrugger L. Inventurn Novum Ex Percussione Thoracis Humani. Vienna: Trattner, 1761.
9. Auenbrugger L. On Percussion of the Chest. Vienna: 1761. Translated by John Forbes. London:
T and G Underwood, 1824.
10. Ewart W. Practical aids in the diagnosis of pericardial effusion in connection with the question as to surgical treatment. Br Med J. 1896;1:717721.
11. The Genuine Works of Hippocrates. Translated from the Greek by Francis Adams. In: Major
RH. Classic Descriptions of Disease. Springeld, IL: Charles C Thomas, 1948.
12. Bowditch HI. The Young Stethoscopist. New York: Samuel S. and William Wood, 1848.
13. Osler W. Sir Thomas Browne. An Alabama Student and Other Biographical Essays. London: Oxford
University Press, 1908.
14. Laennec RTH. A Treatise on the Diseases of the Chest. London: T. and G. Underwood, 1821.
15. Cabot RC. Physical Diagnosis. New York: William Wood, 1915.
16. Hope J. A Treatise on the Diseases of the Heart and Great Vessels. London: John Churchill, 1839.
5/19/2009 4:33:39 PM
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The Abdomen
Abdominal examination in a cardiac patient includes appearance (see Chapter 2), movements (see Chapter 7), percussion, palpation, and auscultation. The abdomen should be
exposed entirely with the patient supine and as close to horizontal as comfort permits. Examination commences from the right side of the bed or examining table. Areas examined
include the upper right and upper left quadrants, the lower right and lower left quadrants,
three central abdominal areasgastric, umbilical, suprapubicand six lateral areas
right and left hypochrondrium, right and left lumbar, and right and left inguinal.
APPEARANCE AND MOVEMENTS

Physical appearance of the abdomen includes contour, striae, and incisional scars. Violaceous
striae in the lower abdominal wall of a hypertensive patient suggest Cushing syndrome
as the cause of hypertension. A right upper quadrant scar in a cyanotic patient suggests
cholecystectomy because of calcium bilirubinate gallstones. The uid of ascites distends
the anks when the patient is supine, and distends the lower abdomen when the patient
stands. An age-related increase in abdominal girth aficts both males and females.
Movements of the abdomen reect the relative contributions of diaphragm vs rib
cage muscles during the process of breathing (see Chapter 7).
PERCUSSION
Percussion establishes situs of the abdominal viscera by identifying the gastric tympany of Traubes space on the left and hepatic dullness on the right in situs solitus, and vice
versa in situs inversus (see Fig. 53). Liver size is estimated by percussing the upper and
lower hepatic borders which are no more than 10 cm apart in the average normal adult.
Percussion extended laterally from the zone of gastric tympany can detect the dullness
imparted by an enlarged spleen (see below).
241
5/19/2009 4:34:07 PM
242 The Abdomen
Percussion for detection of ascites requires special technique. In the at supine

position, uid gravitates to the anks which are dull to percussion, while the tympanitic
center of the abdomen is occupied by air-lled intestine. A line of demarcation separates
ank dullness from the tympanitic center. Once the line of demarcation has been established in the supine position, shifting dullness is elicited as the patient turns into a partial
lateral decubitus position, while the examiner again determines the dull-to-tympanitic
line of demarcation. Ascites causes the demarcation line to shift medially as the patient
turns laterally. A transmitted uid wave is sought in the at supine position. The patient
assists by compressing the center of the abdomen with the u1nar surface of either hand.
The examiner taps one ank and palpates the other ank in anticipation of a uid wave.
PALPATION
Abdominal palpation in a cardiac patient, is concerned chiey with the liver, spleen,
abdominal aorta, and kidneys. Before attempting to palpate a liver edge, its upper
and lower margins should be estimated by percussion as just described. The palm of
right hand of the examiner is placed below the expected inferior hepatic border lateral to the rectus muscle, while the left hand is placed posteriorly diametrically opposite
(Fig. 81A). Flexion of the knees or placement of a pillow under the knees relaxes the
abdominal wall and improves the sensitivity of palpation. The patient inhales slowly but
deeply as the ngertips of the right hand are pressed upward and inward, anticipating
descent of the liver. Care should be taken to palpate gently, because the liver is tender
in congestive hepatomegaly. The liver edge is assessed for consistency, transverse extent
and level below the right costal margin expressed in ngerbreadths or in centimeters.
The right lobe of the liver is more readily palpable than the left.
Horizontal extension of the inferior margin of the liver from the right upper quadrant across the epigastrium represents a transverse liver rather than hepatomegaly,1 and is an
important physical sign of the visceral heterotaxy of left or right isomerism (Fig. 81B).
Careful palpation of the inferior margin of the liver during held inspiration permits
detection of transmitted pulsations from the right atrium via the inferior cava (Fig. 82).
Mackenzie accurately recorded a liver pulse and stated:
When there has been enlargement of the liver, in all my cases of valvular disease, I
could demonstrate that the liver pulsated. In cases with easily demonstrated liver
enlargement and lax abdominal walls, this pulsation may easily be detected. The
hand laid over the enlarged liver is gently heaved up and down.2
The eratic breathing pattern in infants does not lend itself to palpation during inspiration, and the congested neonatal liver is rounded and less distinct than in older children
and adults. Palpation commences once the infant is quiet (Fig. 83). The hand of the
examiner is placed gently on the abdomen, allowing the infant time to adjust to the contact. The right thumb is applied to the right upper quadrant for the liver while the index
nger palpates the left upper quadrant for the spleen.
5/19/2009 4:34:08 PM
The Abdomen
243
Palpation of the spleen in adults requires examination in the supine and right lateral decubitus positions. It is useful to begin by percussion lateral to Traubes space of
gastric tympany. (Named after Ludwig Traube, although it was rst described by a pupil
in 1868.) Dullness over Traubes space heightens suspicion of splenomegaly, although
obliteration can be caused by a full stomach, a left pleural effusion, and enlargement of
the left lobe of the liver.
The examining table or bed should be horizontal and the patient supine with the
physician on the right at a level that permits the right hand to be applied to the abdomen
without exing the wrist, thus avoiding reduction in sensitivity of the ngertips. These
adjustments are best achieved when the examining table is adjustable or when the examiner sits or stands at the bedside. The palm of the right hand is placed below the left costal margin and pressed inward and upward toward the left shoulder, while the left hand
is applied to the left posterior thorax to displace the spleen forward. The patient inhales
deeply and slowly while the ngertips of the right hand anticipate descent of the spleen. If
Figure 81 A, Palpation of the liver. The patient lies supine with knees exed to relax
the abdomen. The at of the examiners right hand (white arrow) is placed on the right upper
quadrant just below the anticipated inferior margin of the liver, while the left hand is placed
diametrically opposite (black arrow). B (see next page), X-ray of chest and abdomen showing the
transverse liver of visceral isomerism. Continued
5/19/2009 4:34:08 PM
244 The Abdomen
the spleen cannot be detected in the supine position, palpation should be repeated in the
right lateral decubitus (Fig. 84), a position that moves the spleen downward and anterior. The right hand is placed beneath the left costal margin and the left hand behind the
posterior thorax, as shown in Figure 84. The examiners right wrist is not exed, thus
improving sensitivity of the ngertips. These maneuvers are repeated while readjusting
the tilt of the patient and the position of the palpating right hand to achieve optimal tactile sensitivity.
A palpable spleen tip is a subtle physical sign that requires diligence and practice to elicit. Palpation should proceed toward the midline, because the spleen enlarges
diagonally from the left hypochondrium toward the umbilicus. The principal settings
in which splenomegaly is anticipated in cardiac patients are congestive heart failure and
infective endocarditis. In the later case, the spleen is likely to be tender, a feature that
calls for a gentle touch. Palpation of the spleen in infants is best achieved with the baby
lying at as the examiner applies the index nger of the right hand to the left upper
Figure 81
Continued
5/19/2009 4:34:10 PM
The Abdomen
Liver
245
v
y
x
A
Jugular
v
v
v
Liver
B
Figure 82 A, Simultaneous tracings of

the liver pulse and the radial arterial pulse.2
The right atrial wave form is reected in the
liver as the a wave, x descent, v wave,
and y descent. B, Jugular venous pulse and
liver pulse of the ventricular type in a patient
with tricuspid regurgitation. The v waves
are tall, and the y descents are brisk if not
collapsing. (From: Mackenzie J. The Study of
the Pulse, Arterial, Venous, and Hepatic, and of
the Movements of the Heart. Edinburgh: Young J.
Pentland, 1902.)
quadrant, as shown in Figure 83. Remember that the spleen tip is often palpable in
normal newborns.
Palpation of the abdominal aorta should be routine, especially in higher risk older
males with systemic hypertension. Dominic Corrigan, whose name is attached to the
Corrigan pulse of aortic regurgitation (see Chapter 3), described the distinctive pulsation of abdominal aortic aneurysm (1853), sometimes referred to as the Corrigan sign.
The patient should lie horizontal and supine with the anterior abdominal wall relaxed as
described above for palpation of the liver.
The normal abdominal aorta is palpable above but not below the umbilicus,
especially in multiparous women with accid abdominal walls, The right hand of
the examiner is applied gently but rmly with gradually increasing pressure above the
5/19/2009 4:34:12 PM
246 The Abdomen
Figure 83 Palpation of liver and

spleen in an infant. The examiners
right thumb is applied to the right
upper quadrant (left arrow) while the
index nger palpates the left upper
quadrant (right arrow). Attention
should be paid to each site, gently
altering pressure rst with the
thumb, then with the nger as the
infant breathes naturally and the
liver and spleen descend during
inspiration.
Figure 84 For palpation of the spleen, the patient turns toward the examiner so that the
left ank is raised. The palm of the right hand (black arrow) is applied to the left upper quadrant
without bending the wrist, while the left hand (white arrow) provides support diametrically
opposite.
5/19/2009 4:34:12 PM
The Abdomen
247
umbilicus, recalling that a normal abdominal aorta can be tender. More important,
however, is palpation of the abdominal aorta below the umbilicus and to the left of
midline. The patient should breathe quietly, utilizing thoracic respiratory muscles
in order to minimize an inspiratory increase in abdominal girth. The ngertips of the
examiners right hand are applied to the left of center just below the umbilicus. Pressure is gently and gradually increased in search of an aortic pulsation. When seeking
to identify the lateral margin of an abdominal aortic aneurysm, the ngertips of the
right hand should attempt to roll the margin of the aorta. Once the margin is identied, bimanual palpation permits an experienced observer to estimate the size of the
aneurysm that can be assessed by observing systolic separation of ngers placed on
either side of the pulsating aorta. Width should not exceed 2.5 cm, allowing for skin
thickness. Remember that an enlarged or an enlarging abdominal aortic aneurysm is
tender if not painful, and when leaking, causes retroperitoneal pain in the low back or
in the posterior aspect of the left ank.
Palpation of the kidneys should be routine in adults, and is obligatory in hypertensive patients. Bimanual palpation is performed in a supine position. For palpation
of the right kidney, the palm of the right hand is applied to the right upper quadrant
with the ngertips just below the costal margin. The left hand is placed behind the
ank diametrically opposite. The patient is instructed to take a gradual deep breath
while the ngertips anticipate the descent of the rounded edge of the lower pole of
the kidney. Because the right kidney is lower than the left, its lower pole is occasionally palpable in normal persons. When palpating the left kidney, care should be taken
to distinguish its lower pole from a palpable spleen. The technique for palpating the
left kidney is similar to that just described for the spleen. The right hand is applied
to the left upper quadrant with ngertips below the left costal margin. The left hand
is applied to the left ank diametrically opposite. When palpating the right or left
kidney, the hands of the examiner should be approximated during deep inhalation; if
the hands are brought together before inspiration, the descent of the kidney is blocked,
and may therefore be missed. These techniques sometimes permit palpation of the
kidney by either the posterior or anterior hand of the examiner. Polycystic kidneys
are readily palpable, and must be approached gently because of their delicate, cystic
surfaces. Huge polycystic kidneys are large enough to be visible through the abdominal wall.
AUSCULTATION
Auscultation is the next step in the abdominal examination. Josef Skoda (1853) recognized the importance of auscultation of the abdomen, to which he devoted a section of
his book, A Treatise on Auscultation and Percussion.3
With the patient supine, the diaphragm of the stethoscope is gently but rmly
applied over the abdominal aorta beginning in the epigastrium, proceeding inferiorly below the umbilicus to the right and left of midline, and then toward the left and
right ileofemoral areas along the courses of the iliac arteries. The degree of stethoscopic
5/19/2009 4:34:13 PM
248 The Abdomen
pressure is adjusted to achieve maximal access to the abdominal aortic wall and its
bifurcation. In the inguinal regions, the bell of the stethoscope is more practical than
the diaphragm.
Renal arterial murmurs are uncommon, but should be sought routinely in hypertensive adults. The examination is best conducted in a quiet room, because renal arterial
murmurs tend to be soft and high frequency. Renal arterial auscultation is undertaken
with the patient sitting with trunk relaxed to minimize interference from tensed muscles. The diaphragm of the stethoscope is applied rmly against the skin of the posterior
ank, rst over one kidney and then over the other. The patient is then reexamined in
the supine position with the diaphragm of the stethoscope applied anteriorly to the right
and left of the abdominal aorta, at levels appropriate for each renal artery. The murmur
of renal artery stenosis is high-frequency systolic. Rarely, the continuous murmur of a
renal arteriovenous stula is detected (Fig. 85).
Another role of auscultation of the abdomen applies to the gravid uterus. In 1853,
Josef Skoda observed that
The sounds of the fetal heart can be heard over the uterus at the sixth month of
pregnancy and become more distinct as the pregnancy advances. Their presence is
a sure sign of the fetus being alive. It is possible, at times, to discover the presence
of twins by the fetal pulse, in those cases where the two hearts do not pulsate with
equal rapidity.3
Skoda also called attention to the placental bruit, but stated that it was not nearly so
valuable a sign in the diagnosis of pregnancy as the sounds of the fetal heart.3
QRS
Figure 85 The continuous murmur of a congenital renal arteriovenous stula in a 50-year-old

woman. The murmur was heard in the ank.
5/19/2009 4:34:13 PM
The Abdomen
249
REFERENCES
1.
2.
3.
Perloff JK. The Clinical Recognition of Congenital Heart Disease, 5th ed. Philadelphia, PA: WB
Saunders, 2003.
Mackenzie J. The Study of the Pulse, Arterial, Venous and Hepatic, and of the Movements of the Heart.
Edinburgh: Young J. Pentland, 1902.
Skoda J. A Treatise on Auscultation and Percussion. London: Highley and Son, 1853.
5/19/2009 4:34:16 PM
5/19/2009 4:34:16 PM
Index
Note: Page numbers in italics indicate illustrations; page numbers followed by (t) refer to tables.
A wave
of atrial pressure pulse, 161
of internal jugular venous pulse, 96, 97,
101, 104
anatomic-hemodynamic inferences from,
107108, 109, 113114, 114
A2, in second heart sound, 172
A2-OS interval, in mitral stenosis, 174
Abdomen
auscultation of, 248249, 249
compression of, and abdominojugular
reux, 102, 105106, 106
movements of, 241
palpation of, 242248, 243248
for aortic aneurysm, 245, 247, 247
for examination of kidneys,
247248, 248
for examination of liver, 242, 243
for examination of spleen, 243245, 246
history of, 10, 10
during pregnancy, 249
percussion of, 241242
physical appearance of, 241
quadrants of, 241
Abdominal aorta
auscultation of, 8889
palpation of, 245, 247, 247
Abdominal aortic aneurysm(s), systolic
murmurs in, 90
Abdominal aortic pulse, and liver pulse, 103
Abdominal muscle(s), function of,
in respiration, 226
Abdominal pain, from aortic aneurysm, 247
Abdominal striae, in Cushing syndrome, 241
Abdominojugular reux, 105, 106
Accessory digit(s), 40
Accessory muscle(s), of respiration, 225

movement of, observation of, 227, 228
Achilles tendon, xanthoma of, 50, 51
Acne, and risk of infective endocarditis, 46
Acoustics, principles of, and development of
stethoscope, 67
Adenoma sebaceum, 49
Afterload, left ventricular, in aortic
regurgitation, amyl nitrite and, 207
pharmacologic agents for increasing, 219
Age, and access to palpation of right ventricle,
142143
and site of arterial pulse examination, 55
Aging, premature, facial appearance in, 22, 23
Allens test, 83, 84
Alveolar hypoventilation, in pickwickian
syndrome, 19
American College of Cardiology,
Committee on Standardized
Terminology of, 181
Americas Laennec, 210
Amine(s), pressor. See Pressor amine(s)
Amyl nitrite, in aortic regurgitation, 207
inhalation of, during auscultation, 218,
219, 220
in mitral valve prolapse, 165
Amyloidosis, macroglossia in, 35
skin lesions in, 46
Anacrotic notch, of arterial pulse, 72, 72
Anacrotic pulse, 72, 76
Anemia, from prosthetic valves, 43
Aneurysm(s). See also under specic site(s)
Angina
ventricular septal dyskinesis from, 146
Angioid streak(s), in Ehlers-Danlos
syndrome, 32
251
Perloff_Index_PTR.indd 251
5/19/2009 4:35:08 PM
252 Index
Angiotensin, in hypertrophic obstructive

cardiomyopathy, 221
Angle of Ludwig (Louis), in emphysema, 51
Ankylosing spondylitis, appearance of thorax
in, 52
Anxiety, and left ventricular impulse, 139
hyperventilation from, 228
Aorta, abdominal, auscultation of, 88, 89
coarctation of. See Coarctation of aorta
Aortic aneurysm(s), abdominal, systolic
murmurs in, 90
ascending, in Marfan syndrome, systolic
impulse from, 150, 151
Aortic cusp, eversion of, diastolic murmur
from, 203
Aortic ejection sound(s), 165, 166
Aortic incompetence, early diastolic murmur
from, 203
Aortic isthmus, coarctation of, systolic arterial
murmur from, 200201
Aortic regurgitation
amyl nitrite in, 207
Corrigan pulse in, 74, 76
diastolic thrill from, 155
digital pulse in, 87, 87, 88
early diastolic murmur in, 201203,
202, 203
intensity of rst heart
sound in, 164, 165
in neurosyphilis, and Argyll Robertson
pupils, 28
in osteogenesis imperfecta, 43
systolic/diastolic thrill from, 155
water hammer pulse in, 75, 76
Aortic root, dilated, in Turner syndrome, 17
in Marfan syndrome, 16
midsystolic murmur in, 187
topographic anatomy of, 132
Aortic sclerotic murmur, 189, 190, 191
Aortic stenosis, bicuspid, ejection sound in,
153, 154, 165, 166
Coanda effect in, 191, 193
diminished arterial
pulse in, 7273, 7374
cycle length and, 185, 188
with emphysema and barrel chest, 191, 192

presystolic left ventricular distention in,
148150, 148
supravalvular, in Williams syndrome, facial
appearance in, 24, 26
right vs. left brachial pulse in, 81
thrills from, 155
Aortic stenosis, brocalcic midsystolic
murmur in, 185, 186187
Aortopulmonary window, holosystolic murmur
in, 195
Apex beat, 137138
Apical dyskinesis, sustained, after myocardial
infarction, 140, 141
Apnea, 227
Appearance. See Physical appearance
Arcus, corneal, 28, 30
Argyll Robertson pupil, 28
Arm(s), obese, and blood pressure
measurement, 60
Arrhythmia(s). See also under specic type(s)
arterial pulse and, 64
jugular venous pulse in, 115119,
116119, 120t
Arterial murmur(s), continuous, 212
systolic, 199201, 200
Arterial pressure, brachial, measurement of,
5960, 61, 62
estimation of, palpation in, 59
Arterial pulse, 5590
alternation of, 7879
carotid. See Carotid arterial pulse
central, accurate representation of, 65, 66
diminished, 7274, 7273
double-peaked, 76, 76, 77
examination of, ancient art of, 55, 56
blood pressure in, 5763, 61, 62.
See also Blood pressure,
measurement of
heart rate in, 6365
heart rhythm in, 6365
historical importance of, 23
sequence for, 57, 58t
sites for, age and, 55
increased, 7476, 7476
information from, 57
palpation of, 6669, 6871
5/19/2009 4:35:08 PM
Index 253
brachial, 6668, 68. See also Brachial

arterial pulse
carotid, 67, 67, 68. See also Carotid arterial
pulse
contralateral, 8183, 82, 8485, 86
femoral, 68, 70. See also Fenzoral arterial
pulse
radial, 69, 71. See also Radial arterial
pulse
right vs. left, 81
selective, 8687, 87, 88
in upper vs. lower extremities, 84, 85, 86
thumb for, 81
physical examination of, 23
synchronicity with cardiac impulse, 3
visible, 55
wave forms of, 6681, 6580
abnormal, 72t
normal, 69, 70, 71, 72
Arteriosclerosis, and blood
pressure measurement, 60
Arteriovenous continuous murmur(s), 212
Arteriovenous stula(s), continuous murmur
from, 212
pulmonary, in Rendu-Osler-Weber
syndrome, 33, 35
renal, continuous murmur from, 249, 249
Artery(ies), structural properties of, 8990
Arthritis, Jaccoudis post-rheumatic
fever, hands in, 44
Ascending aortic aneurysm, in Marfan
syndrome, systolic impulse from,
150, 151
Ascites, and abdominal appearance, 241
percussion of, 242
Ataxia, Friedreich, hammer toes in, 41, 45
nystagmus in, 26
Atherosclerosis, continuous murmurs from, 212
iliofemoral obstruction from, and femoral
arterial pulse, 85
Atrial brillation, fourth heart sound and, 178
jugular venous pulse, 119
mid-diastolic murmur in, 204205, 204
pulse rate in, 64
pulse rhythm in, 6465
rheumatic tricuspid stenosis with, jugular
venous pulse in, 112, 113
tricuspid regurgitation in, V wave of

jugular venous pulse in, 109, 112,
112, 113
Y descent of jugular venous pulse in,
109, 112, 112, 113
Atrial utter, jugular venous pulse in, 119, 120
Atrial movement, during ventricular
systole, 150
Atrial murmur(s), mid-diastolic, 206
presystolic, in complete heart block, 206
Atrial myxoma, presystolic murmur from, 208
tumor plop in, 175
Atrial premature beat(s), jugular venous pulse
in, 116
Atrial pressure pulse, 161
Atrial septal defect, jugular venous pulse in,
112, 113
mid-diastolic murmur in, 205
midsystolic murmur in, 185, 189
ostium secundum, right ventricular impulse
in, 153
second heart sound in, 172
Atrial systole, heart sounds in, 176
Atrial transport, 148, 148
Atrioventricular block, jugular venous pulse
in, 121, 121
Atrioventricular nodal re-entrant tachycardia,
jugular venous pulse in, 117,
118, 119
Auenbrugger, L., 12
on percussion, 89, 128, 129
thoracic, 231234, 232
Augusta, Regimen sanitatis of, 128
Auricular pressure curve, in internal jugular
venous pulse, 96, 97
Auscultation, abdominal, 248249, 249
amyl nitrite inhalation during, 218, 219,
219, 220
as component of physical examination, 1
denition of, 157
direct, Laennecs account of, 67, 11,
158159, 236
during isometric exercise, 218
historical accounts of, 57
immediate, 157
modern era of, 67, 11
of nonprecordial thoracic areas, 162
5/19/2009 4:35:08 PM
254 Index
Auscultation (Continued)
patient position for, 162163, 163
physical maneuvers during, 216t
pitch in, 163
position changes during, 216t
position during, 215216
respiration during, 217
sequence of, 162163
technique of, 160163, 163
thoracic, 235238, 236
history of, 235, 237, 236, 238
information obtained by, 237
in nonprecordial areas, 162
for timing of internal jugular venous
pulse, 101
and topographic anatomy of heart, 162
Auscultatory framework, 159
Auscultatory gap, in blood pressure
measurement, 59
Auscultatory popliteal systolic pressure, in
lower extremity, 63
Austin Flint murmur(s), 205, 207, 210
Avicenna, Canon of Medicine by, 10
Axillary freckling, in neurobromatosis, 46
Axillary thrombophlebitis, 125
Barnard, development of occluding cuff for
blood pressure measurement by, 58
Barrel chest, 226, 227228
with emphysema, midsystolic murmur in,
191, 192
Bicuspid aortic stenosis, Coanda effect in, 193
ejection sound in, 165, 166
Bifascicular block, in Kearns-Sayre syndrome,
28
Bigeminal pulse, vs. pulsus alternans, 78
Binaural stethoscope, controversy over, 7
development of, 58
Bisferiens pulse, double-peaked, 76
in aortic regurgitation, 74, 7576
Biventricular systolic impulses, 146, 146
Bladder, on sphygmomanometer, 59
Blalock-Taussig shunt, thoracotomy
scar from, 52
Blood pressure, during Valsalva maneuver,
217218
measurement of, 5763, 61, 62
auscultatory gap in, 59

brachial arterial, 5960, 61, 62
clinical setting for, 59
cuff deation in, 59
cuff size in, 59
and detection of orthostatic hypotension,
6061
in elderly patient, 60
ush method of, in infants, 61, 62
in forearm, 61
indirect, 5859
Korotkoff sounds in, 59. See also Korotkoff
sound(s)
in lower extremities, 61, 62, 6263
in patient with obese arms, 60
in popliteal artery, 62, 63
position of patient for, 59
proportional pulse pressure in, 60
Borelli, G., on importance of diaphragm, 226
Bowditch, H., on succussion splash, 234
on topographic anatomy of heart, 160
Brachial arterial pressure, measurement of,
5960, 61, 62
Brachial arterial pulse, in aortic valve stenosis,
7274
normal, 72
vs. femoral arterial pulse, 84, 85, 86
right vs. left, 8183, 81
wave form of, 6667, 69
Brachial artery, in Monckebergs sclerosis, 66,
8990
Bradycardia, sinus, jugular venous
pulse in, 115
Bradypnea, 227
Braun-Menendez, E., on use of stethoscope, 8
Breath sound(s), abnormal, 237238
normal, 237
Breathing. See also Respiration
periodic, 228229
tubular, 237238
Broadbent, W., on information from
examination of pulse on
pulse rate, 64
Broadbents sign, 230
Bronchial breath sound(s), 237
Bronchophony, 237, 238
5/19/2009 4:35:08 PM
Index 255
Bronchovesicular breath sound(s), 237

Browne, T., on succussion splash, 234
Brusheld spots, 28, 31
Bulbus oculi, examination of, 26
Bundle-branch block, jugular venous pulse
in, 120
left, second heart sound in, 172
right, second heart sound in, 171172
Burwell, C., on pickwickian syndrome, 1819,
19, 229
Buttery rash, in systemic lupus
erythematosus, 23
C wave, of internal jugular
venous pulse, 96, 97
Cabot, R., on abdominal palpation, 10
on appearance of thorax in emphysema, 51
on cardiorespiratory murmur, 238
Physical Diagnosis by, 10
Caf au lait spots, in neurobromatosis, 43, 46
Calcic aortic stenosis, arterial pulse in, 74
Calf, veins of, examination of, 122, 123
Cannon wave(s), in junctional premature
beats, 116117, 117
in junctional tachycardia, 117118, 117
Canon of Medicine, avicenna, 10
Carcinoid syndrome,
facial appearance in, 23
Cardiac cycle, timing of impulses in, 136
Cardiac impulse, synchronicity with
arterial pulse, 3
Cardiac output, amyl nitrite
inhalation and, 218, 219
Cardiac rate. See Heart rate
Cardiac rhabdomyoma, skin lesions in, 49
Cardiofacial syndrome, 24
Cardiogenic shock, general appearance in,
description of, 15
Cardiomyopathy
hypertrophic, double-peaked arterial pulse
in, 77, 77
left ventricular systolic
impulse from, 141
lentiginosis in, 46
in neurobromatosis, 43
obstructive, double-peaked arterial pulse in,
77, 77
left ventricular discharge in, angiotensin

infusion and, 221
restrictive, in amyloidosis, 35
Cardiorespiratory murmur(s), 238
Carotid arterial murmur, 88
Carotid arterial obstruction, atherosclerotic,
continuous murmurs from, 212
Carotid arterial pulse, as reference for timing
of precordial movements, 135, 136
factors affecting, 65, 66
systolic impulse from, 152
vs. internal jugular venous pulse, 96, 97, 102
Carotid artery, for timing of internal jugular
venous pulse, 101
kinked, 82, 83, 90
Carotid artery stenosis, supraclavicular systolic
arterial murmur from, 199
Carotid sinus, palpation of, avoidance of, 82
Carvallo sign, 194, 195
Cataract(s), 30
Cats eye syndrome, 28, 32
Central arterial pulse, accurate representation
of, 65, 66
Central cyanosis, vs. peripheral cyanosis, 38
Central venous pressure (CVP), estimation of
by examination of dorsal hand veins, 124125
by examination of external jugular vein,
98101, 100
Cervical spine, radiation of holosystolic
murmur to, 193, 194195
Cervical venous pulse, rst account of, 34
Chauveau, J., on jugular venous pulse, 4
on precordial palpation, 5
Chest, physical appearance of, 226
Chest excursion(s), inspiratory, 231
Chest pain, noncardiac, 231
Chest wall, pressure on, in thoracic palpation,
230231
Cheyne-Stokes respiration, 228, 229, 229
Chi Po, dialogue with Huang Ti about
measurement of arterial pulse, 3
Child(ren), innocent murmurs in
midsystolic, 189
supraclavicular systolic arterial, 199, 200
venous hum in, 213214, 213
5/19/2009 4:35:09 PM
256 Index
Christianismi Restitutio, 225

Chronic illness, general appearance in, 16
Chronic obstructive pulmonary disease
(COPD), clubbing in, 36, 36
pulsus paradoxus in, 79, 80
Chronic venous insufciency, 123, 124
Cigarette-paper scar(s), in Ehlers-Danlos
syndrome, 44
Circus movement tachycardia, jugular venous
pulse in, 118
Clavicle, radiation of venous hum below, 214
Click(s), in late systolic murmur, of mitral
valve prolapse, 196, 199, 198
Clubbing, with cyanosis, 37, 38, 3637
Coanda effect, 191, 193
Coarctation of aorta, auscultation of, 88
brachlal arterial pulse in, 85, 86
femoral arterial pulse in, 85, 86
retinopathy in, 30, 34
systolic arterial murmur from, 200
in Turner syndrome, and general appearance,
17, 18
Collateral circulation, systemic-topulmonary,
Coloboma, 28, 32
Committee on Standardized Terminology of
the American College of
Cardiology, 181
Complete atrioventricular block, jugular
venous pulse in, 121
Complete heart block. See Heart block,
complete
Compression artifact, in free aortic
regurgitation, 200
Conduction, cardiac, abnormalities of, in
myotonic muscular dystrophy, 23
Conduction defect(s), jugular venous pulse in,
119121, 120t, 121, 122
Congenital coronary arterial stula(s),
Congestive heart failure (CHF), edema in, 44,
46, 47
general appearance in, 16
Conjunctiva, examination of, 27, 29
Constrictive pericarditis. See Pericarditis,
constrictive
Continuous murmur(s). See Murmur(s),

continuous
Continuous thrill, from patent ductus
arteriosus, 155
Contracture(s), Dupuytren, 39
Cor pulmonale, cyanotic, 36
Corneal arcus, 28, 30
Coronary arterial stula(s), congenital,
Coronary artery disease (CAD), Achilles
tendon xanthoma in, 50, 51
corneal arcus in, 28, 30
in hypothyroidism, 23
Coronary-prone patient, general appearance
of, 16
Corrigan, D., on abdominal aortic
aneurysms, 245
on early diastolic heart sounds, 174
Corrigan pulse, in aortic regurgitation, 74, 76
venous, 108
Corrigan sign, 245
Corvisart, on thoracic percussion, 231
Crackles, 237
Crural ber(s), of diaphragm, 226
Cuff deation, in blood pressure
measurement, 59
Cuff size, in blood pressure measurement, 59
Cushing, H., biography of Osler, 2
Cushing syndrome, abdominal striae in, 241
Cutlerian Lectures, 5
Cyanosis, differential, 3738, 37
peripheral vs. central, 38
with clubbing, 37, 38, 3637
Cyanotic congenital heart disease, retinal veins
in, 30, 32
Cycle length, in mid-diastolic murmurs, 204
da Vinci, L., on physical appearance, 15
De Motu Cordis, 127, 226
account of auscultation in, 5, 157
Decrescendo murmur(s), early diastolic, 201, 203
early systolic, in ventricular septal defect,
196, 198
systolic, in mitral regurgitation, 196, 197
Decubitus position, left lateral, during
auscultation, 215
5/19/2009 4:35:09 PM
Index 257
for auscultation of heart, 163, 163

for palpation of heart, 131, 133, 137
orthostatic hypotension in, 6061
for palpation of mid-diastolic ventricular
movement, 147
Deep thrombophlebitis, 122
Dextrocardia, situs inversus with, 130, 130
Diabetes mellitus, maternal, and neonatal
gigantism, 16, 17
pupils in, 28
Diaphragm, anatomy of, 226
central tendon of, 226
importance of, 226
movement of, observation of, 226
percussion of, 233, 234
Diastasis, 176
Diastolic collapse, of jugular venous pulse, 114
Diastolic heart sound(s), 162t
Diastolic heartbeat, 147
Diastolic murmur(s). See Murmur(s), diastolic
Diastolic thrill(s), 155
Dickens, C., on pickwickian syndrome,
1819, 19, 229
Dicrotic pulse, 76, 77
Dicrotic wave, of arterial pulse, 71
Differential cyanosis, 3738, 37
Digit(s), accessory, 40
clubbing of, 36, 37, 3637
Digital pulse, palpation of, 87, 87, 88
Digitalis, gynecomastia from, 52
Direct auscultation, Laennecs account of, 67,
11, 158159, 236
Diseases of the Heart, 2. See also Mackenzie, J
Dorsalis pedis, palpation of, 83
pulsating, in patent ductus arteriosus, 55
Double systolic left ventricular
impulse, 141, 142
Double-peaked arterial pulse, 76, 77
Down syndrome,
Brusheld spots in, 28, 31
facial appearance in, 24, 25
hands in, 31, 40
hypotonia in, 50, 50
protuberant tongue in, 24, 25, 34
Dropsy, 233
Drug abuse, intravenous, skin lesions from, 47,

49, 125
Duchenne muscular dystrophy, gait in, 20, 20
muscular pseudohypertrophy in, 20, 50
Dupuytren contracture(s), 39
Duroziez, P., on compression artifacts, 200
Dwarsm, progeria with, 22
Dyspnea, psychophysiologic
hyperventilatory, 228
Early diastolic heart sound(s), 160, 162t,
174176, 175
Early diastolic murmur(s), 201203, 202, 203
decrescendo, 201, 203
Early systolic heart sound(s), 160, 162t,
164165, 166, 167
Early systolic murmur(s), 196, 197, 198
Ebers Papyrus, account of precordial palpation
in, 5, 9, 127
Ectopic left ventricular systolic impulse, 139
Ectopic tachycardia, jugular venous pulse in,
117, 117
Edema, in congestive heart failure, 44, 46, 47
Egophony, 238
Ehlers-Danlos syndrome, retinal detachment
in, 32
skin lesions in, 44
Einthoven, on string galvanometer, 8
Eisenmenger ventricular septal defect, single
Ejection sound(s), 165, 166167
palpable, in bicuspid aortic stenosis,
153, 154
from prosthetic valves, 165
Ejection velocity, amyl nitrite inhalation and,
218, 219
Elderly patient(s). See Older adult(s)
Ellis-van Creveld syndrome, accessory
digits in, 4041
malformations of teeth in, 34
Embolism, pulmonary, systolic arterial
murmurs from, 201
Emphysema, barrel chest from, 228
with barrel chest, midsystolic murmur in,
191, 192
pulsus paradoxus in, 79, 80
5/19/2009 4:35:09 PM
258 Index
Emphysema (Continued)
respiration in, 229
thoracic appearance in, 51
Endocarditis, conjunctival lesions in, 27, 29
infective. See Infective endocarditis
marantic, 42
Enteropathy, protein-losing, in constrictive
pericarditis, and Terry nails, 38
Epicanthal folds, in Down syndrome, 25
Eruptive xanthoma, 46
Ewarts sign, 234, 235
Exercise, isometric, auscultation during, 218
isotonic, and audibility of third heart
sound, 179
Exhalation, during palpation of heart, 133,
133, 135
in emphysema, 229
full held, sitting and leaning forward
during, 216
Exophthalmos, in hyperthyroidism, 26
Extracardiac systolic murmur(s), 199, 200
Extrernity(ies), lower. See Lower extremity(ies)
upper. See Upper extremity(ies)
Eye(s). See also under specic parts of eye
examination of, 2633, 2733
ophthalmoscopic, 3033, 34
Eyeball, examination of, 26
Eyelid(s), examination of, 26
Fabricus, H., description of veins by, 123
Facial appearance, 2226, 2226
in carcinoid syndrome, 23
in Down syndrome, 24, 25
in fetal alcohol syndrome, 24, 27
in Hurler syndrome, 23, 24
in hypothyroidism, 23
in myotonic muscular dystrophy, 23, 23
in progeria, 22, 23
in systemic lupus erythematosus, 23
in Werner syndrome, 22, 22
in Williams syndrome, 24, 26
Facial edema, in congestive heart failure, 46
Fallots tetralogy, cats eye syndrome in,
28, 32
right aortic arch in, 151, 152
right ventricular systolic impulse in, 144
False tendon, left ventricular, 189, 190
Farquhar, J., on infants of diabetic mothers,

16, 17
Feet, examination of, 3642, 3739, 45
rocker bottom, in trisomy 18, 42
skin of, in peripheral arterial occlusive
disease, 87
Femoral arterial murmur, 88
Femoral arterial obstruction, atherosclerotic,
Femoral arterial pulse, alternation in, 79
vs. brachial arterial pulse, 84, 85, 86
right vs. left, 81
Femoral artery, aneurysms of, 90
auscultation of, 88
Fetal alcohol syndrome, facial appearance in,
24, 27
Fetal heart, detection of, 249
Fibrin-platelet emboli, in retinal artery, 30
Fibrocalcic aortic stenosis, midsystolic
munnur in, 185, 186
Fingertip(s), transillumination of, for
examination of digital pulse, 87, 88
First heart sound. See Heart sound(s), rst
Fistula(s), arteriovenous, continuous murmurs
from, 212
coronary arterial, continuous murmurs
from, 212
Flank, auscultation of, in hypertension, 89
Flint, A., murmur described by, 205, 207, 210
Floyer, J., Physicians Pulse Watch of, 3
Flush method, of blood pressure
measurement, in infants, 61, 62
Flutter wave(s), in jugular venous
pulse, 119, 120
Fontan operation, and Terry nails, 38, 38
Forem, measurement of blood pressure on,
61, 62
Fourth heart sound. See Heart sound(s), fourth
Frank, O., on use of stethoscope, 8
Freckling, axillary, in neurobromatosis,
4647
Fremitus, 230231
Friction rub, 214, 215
Friedreich ataxia, pes cavus and hammer
toes in, 41, 45
nystagmus in, 26
5/19/2009 4:35:09 PM
Index 259
Gait, and presence of heart disease, 20

in pseudohypertrophic Duchenne muscular
dystrophy, 20, 20
Gallavardin dissociation, 185, 186, 189
Gallop rhythm, 176
Galvanometer, string, 8
Gargoylism, in Hurler syndrome, 23, 24
Gastric tympany, 241
Gesture(s), and presence of heart disease, 20
Gibson, A., on h wave in jugular venous
pulse, 114
Gibson, G., on continuous murmurs, 211, 212
Gigantism, general appearance in, 16
neonatal, 16, 17
Glossoptosis, in Pierre Robin syndrome, 35
Gowers sign, 20, 21
Graham Steell murmur, 155, 202, 203
Graves disease, vitiligo in, 43, 44
Gravid uterus, palpation of, 249
Great artery(ies), systolic movements of,
150153, 151152
Greek physician(s), on palpation of arterial
pulse, 66
Growth retardation, muscle wasting in, 49
Gynecomastia, from digitalis, 52
h wave, in jugular venous pulse,
anatomic-hemodynamic
inferences from, 114
of internal jugular venous pulse, 97, 98
Hamman sign, 238
Hammer toe(s), with pes cavus, 4142, 45
Hand(s), dorsal veins of, examination of, for
estimation of central venous pressure,
124125
position of, for palpation of heart, 132133,
133
for percussion of thorax, 233, 234
Hand vein(s), dorsal, examination of, for
estimation of central venous
pressure, 124125
Handgrip, sustained, auscultation during, 218
Hard palate, examination of, 35
Harrison groove(s), 52
Harvey, W., 10
on auscultation, 5
on left ventricular systolic impulse, 137

on palpation, 127
study of circulation by, 123, 226
Heart. See also under Cardiac entries
examination of, components of, 1
observation in, 131, 133
fetal, detection of, 249
palpation of, 131137, 132136
hand position in, 132133, 133
information obtained from, 131, 131t
patient position for, 131, 133, 137
respiration during, 133, 135
position of, factors affecting, 137
topographic anatomy of, 131, 132
Heart block, complete, fourth heart
sound in, 178
intensity of rst heart sound in, 164
presystolic murmur in, 208
in Kearns-Sayre syndrome, 27
jugular venous pulse in, 121, 121
Heart rate, measurement of, 6365
Valsalva maneuver and, 65
Heart rhythm, measurement of, 365
Heart sound(s), 159181, 160180
auscultation of. See also Auscultation
technique of, 160163, 163
diastolic, 162t
early diastolic, 160, 174176, 175
early systolic, 160, 164165, 166, 167
rst, 160, 164167, 166, 167
rst component of, 164
intensity of, 164
palpation of, 153
quality of, 164
second component of, 164
splitting of, 164
vs. aortic ejection sound, 165
vs. fourth heart sound, 179
timing of, 162, 163
fourth, 160, 161, 176177
abnormal, 180181
frequency composition of, 178179, 179
left ventricular, 179
normal vs. abnormal, 176, 178
5/19/2009 4:35:09 PM
260 Index
Heart sound(s) (Continued)

origin of, 179
right ventricular, 179
late diastolic, 176181, 177, 179, 190
late systolic, 160, 165, 166, 168, 169, 170
mid-diastolic, 176181, 177, 179, 190
midsystolic, 160, 1656, 166, 168, 169, 170
palpable, 153154
presystolic, 176181, 177, 179, 190
second, 160, 167181, 171180
A2 in, 172
aortic component of, 167
auscultation of, 169, 170, 171
xed splitting of, 172
inspiratory splitting of, 167, 169, 171
intensity of, 173, 173
P2 in, 172
paradoxic splitting of, 172173
persistent splitting of, 171172
pulmonary component of, 167
in pulmonary hypertension, palpation
of, 154
in rheumatic mitral stenosis, 174, 175,
175, 176
single, in Eisenmenger ventricular septal
defect, 171
splitting of, classication of, 171
in systemic hypertension,
palpation of, 154
timing of, 167, 169
systolic, 162t
late, 160
terminology related to, 160, 161t
third, 160, 161, 176
abnormal, 180
audibility of, isotonic exercise and, 179
frequency of, 178
left ventricular, 179
normal vs. abnormal, 176, 177, 178
origin of, 178
right ventricular, 179
Hemochromatosis, skin lesions in, 43
Hemolysis, in jaundice, 43
Hepatic pulse, 103, 103
anatomic-heinodynamic inferences from, 115
in tricuspid regurgitation, 112, 115
Hepatojugular reux, 105

Hepatomegaly, congestive, abdominal palpation
in, 242
Hereditary hemorrhagic telangiectasia, lip
lesions in, 33, 35
Herophilus, use of water clock to count the
pulse, 3
Hill, development of occluding cuff for blood
pressure measurement by, 58
Hippocrates, on auscultation, 5
on percussion, 910
on succussion splash, 234
on varicose veins, 122123
Hollenhorst plaque(s), 30
Holosystolic murmur(s). See Murmur(s),
holosystolic
Holosystolic thrill, from ventricular septal
defect, 155
Holt-Oram syndrome, decient digits in, 41
Homans sign, 122
Homocystinuria, lens subluxation in, 30
Honk, late systolic, in mitral valve
prolapse, 199
Hooke, R., Cutlerian Lectures by, 5
Hope, J., on cardiorespiratory murmur, 238
Huang Ti, 4
and Yellow Emperors Book of Medicine, 23
Hunter, J., 7
Treatise on the Blood, Inammation, and GunShot Wounds by, 34
Hurler syndrome, facial appearance in, 23, 24
hands in, 40
Hutchinson-Gilford syndrome, facial
Hydropneumothorax, succussion splash of,
5, 234
Hypercholesterolemia, xanthalasma in, 27
Hyperkinetic left ventricular impulse, 140
Hyperlipoproteinemia, striated xanthoma in,
46, 48
Hypertension, ank auscultation in, 89
in Cushing syndrome, 19
intensity of second heart sound in, 173, 173
pulmonary. See Pulmonary hypertension
renal palpation in, 247248, 248
second heart sound in, palpation of, 154
systolic, increased pulse pressure in, 74
5/19/2009 4:35:09 PM
Index 261
Hypertensive retinopathy, 30, 34

Hyperthyroidism
eyeball in, 26
eyelid in, 27
Hypertrophic cardiomyopathy. See
Cardiomyopathy, hypertrophic
Hyperventilation, 226, 228
Hypokinetic left ventricular impulse, 140
Hypomastia, in mitral valve prolapse, 52
Hypotension, orthostatic, detection of, 6061
Hypothyroidism, facial appearance in, 23
Hypotonia, in Down syndrome, 50, 50
Hypoventilation, alveolar, in
pickwickian syndrome, 19
Iliofemoral artery stenosis, systolic arterial
murmur from, 199
Iliofemoral obstruction, from atherosclerosis,
and femoral arterial pulse, 85
Iliofemoral systolic murmur(s), abdominal
palpation of, 248
Immediate auscultation, 157, 236
Incisura, of arterial pulse, 72
Increased arterial pulse, 7476, 7476
Infant(s), auscultation of second heart sound
in, 170, 171
blood pressure measurement in, ush
method of, 61, 62
palpation of heart in, 133, 134
palpation of liver in, 242, 246
palpation of right ventricular impulse in,
137
palpation of spleen in, 243, 244, 245
respiration in, observation of, 227228
Infective endocarditis, conjunctival lesions in,
27, 29
feet and hands in, 42, 45
risk of, skin lesions and, 42, 45
tricuspid regurgitation in, 196
Inatable bladder, on sphygmomanometer,
5859
Infundibulum, topographic anatomy of, 131, 132
Innocent midsystolic murmur(s), 187, 189t
in children, 187, 189t
Inspection, as component of physical
examination, 1
Inspiration, and intensity of mid-diastolic

murmur, in tricuspid stenosis, 205
audibility of third/fourth heart sounds
during, 179
and internal jugular venous pulse, 102
splitting of second heart sound during,
167, 171
Intercostal muscle(s), breathing with, 226
importance of, 226
Interventricular sulcus, zone of retraction
along, from biventricular systolic
impulse, 146, 146
Intravenous drug abuse, skin lesions from, 47,
49, 125
Introduction to the Use of the
Stethoscope, An, 157
Inventum Novum Ex Percussione
Thoracis Humani, 231
Iris, examination of, 28, 3132
Ischemic heart disease, fourth heart
sound in, 181
ventricular dyskinesis from, 145
Isometric exercise, auscultation during, 218
Isotonic exercise, and audibility of third heart
sound, 179
Jaccoud arthritis, 44
Jason, on abdominal palpation, 10
Jaundice, cardiac complications of, 43
Jugular vein(s), examination of, information
obtained from, 93
external, examination of, 9396, 94,
98101, 100
internal, examination of, 9396, 94
Jugular venous pressure, estimation of,
104107
abdominal compression during examination
of, 105106, 106
patient position for, 104
reference point for, 104, 104105
Jugular venous pulse
anatomichemodynamic
for A wave, 107108, 109,
113114, 114
for h wave, 114
inferences from, 107115, 109114
5/19/2009 4:35:10 PM
262 Index
Jugular venous pulse (Continued)

for V wave, 109, 112, 112, 113,
113114, 114
for X descent, 108, 109, 110, 111
for Y descent, 109112, 112113
electrophysiologic inferences from,
115121, 116120, 116t, 120t
for arrhythmias, 115119,
116119, 120t
for conduction defects, 119121, 120t,
121, 122
light source for, 98
patient position for, 98, 99
external, examination of, 98101, 100
hepatic pulse and, 103, 103
historical account of, 4
internal, respiration and, 102
vs. carotid arterial pulse, 102
wave form of, 9698, 97, 101102
Mackenzies observations of, 93
physical examination of, 1
in rheumatic tricuspid stenosis, with atrial
brillation, 112, 113
visibility of, abdominal compression
and, 102
Junctional premature beat(s), cannon waves in,
116117, 117
Junctional tachycardia, cannon
waves in, 117, 117
Kearns-Sayre syndrome, pigmentary
retinopathy in, 27, 28, 32
ptosis in, 27, 28
Kidney(s), palpation of, 247248, 248
Korotkoff, N., development of blood pressure
measurement by, 58
Korotkoff sound(s), 58, 59, 61, 62
double, 77
in lower extremity, 63
in popliteal artery, 62, 63
Kussmaul, A., on pulsus paradoxus, 79
Kussmaul respiration, 227
Kussmauls sign, 102
in constrictive pericarditis, 110, 114
Kyphoscoliosis, 52
Kyphosis, thoracic, loss of, 226, 227
Lacrimal gland(s), in sarcoidosis, 27, 29

Lactation, and mammary soufe, 187, 200,
212213
Laennec, R., on abnormal right ventricular
systolic impulse, 141
on apex beat, 127, 128, 137
on direct auscultation, 67, 11, 238
on heart sounds, 135
on pneumothorax, 910
on use of stethoscope, 235
Lancisi, G., account of cervical venous pulse, 34
Late diastolic heart sound(s), 176, 176181
Late diastolic murmur(s), 206211, 209. See
also Murmur(s), late diastolic
Late systolic heart sound(s), 160, 162t
Late systolic murmur(s), 196, 198, 199
Leatham, A., on second heart sound, 167
Left atrial appendage, dilated, in mitral
regurgitation, 150
Left atrium, giant, 150
topographic anatomy of, 131
Left bundle-branch block, jugular venous pulse
in, 120
Left lateral decubitus position. See Decubitus
position, left lateral
Left ventricle, displacement of, from abnormal
right ventricular systolic impulse,
143144, 143, 144, 145
false tendon in, 189, 190
hypertrophy of, systolic impulse from, 140
presystolic distention of, in aortic stenosis,
148150, 149
systolic impulse from
abnormal, 139141, 140, 141
displacement of, 139140, 140
velocity and amplitude in, 140
area occupied by, 140
contour of, 141, 142
duration of, 139140
ectopic, 139
hyperkinetic, 140
hypokinetic, 140
location of, 138, 140
normal, 136, 137139
5/19/2009 4:35:10 PM
Index 263
sustained, 141
velocity of, 140
Left ventricular afterload, in aortic
regurgitation, amyl nitrite and, 207
pharmacologic agents increasing, 219
Left ventricular discharge, in hypertrophic
obstructive cardiomyopathy,
angiotensin infusion and, 221
Left ventricular failure, proportional pulse
pressure in, 60
Left ventricular heart sound(s),
third/fourth, 179
Left ventricular hypertrophy, and fourth heart
sound, 180
Left ventricular volume, in mitral valve
prolapse, factors affecting, 169
Leg(s), brawny induration of, 43
elevation of, during auscultation, 216
Lens, examination of, 30, 33
Lentiginosis, in hypertrophic
cardiomyopathy, 46
Leopard syndrome, in hypertrophic
cardiomyopathy, 46
Levocardia, situs solitus with, 129
Lewis, T., on reference point for estimation of
jugular venous pressure, 104
Lid-lag, in hyperthyroidism, 27
Light source, for examination of jugular
venous pulse, 98
Lindsay nail(s), 38
Lip(s), examination of, 33, 35
Liver
palpation of, 242243, 243, 244, 245
in infants, 242, 246
size of, percussion and, 241242
systolic expansion of, 115
Liver pulse, 103, 103
anatomic-hernodynamic inferences from, 115
London Medical Gazette, description of
continuous murmur in, 211212
Louis, P., on reference point for estimation of
jugular venous pressure, 104
Lower extremity(ies), measurement of blood
pressure in, 61, 62
skin of, in peripheral arterial occlusive

disease, 87
vs. upper, palpation of arterial pulses in,
8489, 86
venous pulses in, 121124, 123, 124
Lumbar lordosis, in pseudohypertrophic
Duchenne muscular dystrophy, 20,
20
Lumbar spine, radiation of holosystolic
murmur to, 193, 194195
Lupus. See Systemic lupus erythernatosus (SLE)
Mackenzie, J., 3
on abnormal pulse rhythm, 64
on abnormal right ventricular systolic
impulse, 141, 143
on Cheyne-Stokes respiration, 228, 229,
229
on diminished arterial pulse, 7274
on examination of blood pressure, 5758
on examination of patient, 1
on hepatic pulse, 103, 103
illustration of internal jugular vein by, 94, 95
on jugular venous pulse, 93
on left ventricular systolic impulse, 138
on liver pulse, 115, 242243, 243
on movements of heart, 127128
on normal arterial pulse, 7071
on observation of gait, 20
on palpation of arterial pulse, 66
on palpation of radial pulse, 69
on paroxysmal tachycardia, 119
on physical appearance, 2
on polygraph for recording pulse, 55, 56
Study of the Pulse by, 4, 127
on systolic impulse from pulmonary trunk,
151, 152, 152
on wave form of internal jugular venous
pulse, 96, 97, 101102
Macroglossia, in amyloidosis, 35
Mainline intravenous drug abuse, skin
lesions from, 47, 49, 125
Malar depigmentation, in systemic lupus
erythematosus, 23
Malpighi, on function of placenta, 226
Mammary soufe, 200, 212
Marantic endocarditis, 42
5/19/2009 4:35:10 PM
264 Index
Marey, E., on jugular venous pulse, 4

Marfan syndrome, high arched palate in, 35
ascending aortic aneurysm in, systolic
impulse from, 150, 151
early diastolic aortic murmur in, 201
hands in, 39, 42
lens subluxation in, 30, 33
pectus carinatum in, 227
thoracic abnormalities in, 52
Marriott, H., on jugular venous pulse in
arrhythmias, 115
Mechanical alternans, 7779
Mediastinal crunch, 238
Medieval physician(s), account of palpation by,
127, 128
Mid-diastolic heart sound(s), 176181, 177,
179, 190
Mid-diastolic murmur(s). See Murmur(s),
mid-diastolic
Mid-diastolic ventricular distention, with
presystolic ventricular distention, 150
Mid-diastolic ventricular movement,
146148, 147
Midsystolic heart sound(s), 160, 161t
Midsystolic murmur(s). See Murmur(s),
midsystolic
Mirror image dextrocardia, 130, 130
Mitral leaet(s), position of, and intensity of
rst heart sound, 164
Mitral prosthesis, early diastolic heart sound
from, 176
Mitral regurgitation, arterial pulse in, 74
early systolic murmur in, 196, 197
holosystolic murmur in, 193, 194
radiation of, 193, 194195
midsystolic murmur in, 185, 191
pericardial knock in, 174
right ventricular systolic
impulse in, 145, 145
systolic murmur in, amyl nitrite
inhalation and, 220
systolic thrill from, 155
with dilated left atrial appendage, 150
Mitral stenosis, mid-diastolic murmur in,

204, 204
opening snap in, auscultation of, 174,
175, 175
palpation of, 154
rheumatic, rst heart sound in, 153
mid-diastolic murmur from, 204
presystolic murmur in, 206207
second heart sound in, 174, 175, 175
thrills from, 155
Mitral valve, closure of, and rst heart
sound, 164
Mitral valve prolapse, hypomastia in, 52
late systolic murmur in, 196, 198, 199
systolic clicks from, 165, 166, 168, 169, 170
Mobitz atrioventricular block, jugular venous
pulse in, 120
Mckebergs sclerosis, brachial artery in, 66,
8990
arterial pulse in, 55
Mouth, appearance of, 3335, 35
Mucopolysaccharidosis, facial appearance in,
23, 24
Mucous membrane(s), of mouth, examination
of, 33
Mller maneuver, 218
Murmur(s), 181214, 182213
abdominal aortic, palpation of, 248249, 249
atrial, mid-diastolic, 206
Austin Flint, 205, 207
cardiorespiratory, 238
carotid arterial, 88
characteristics of, 181
continuous, 211214, 211, 213
arterial, 212
arteriovenous, 212
classication of, 181, 183
from coronary arterial stulas, 212
in mammary soufe, 212
in patent ductus arteriosus, 211212, 211
origin of, 211
from renal arteriovenous stula, 249, 249
venous hum from, 213214, 213
diastolic, 201211, 202209
early, 201203, 202, 203
late, 206211, 209
5/19/2009 4:35:10 PM
Index 265
timing of, 206, 207

mid. See Murmur(s), middiastolic
duration of, 181
early diastolic, 201203, 202, 203
early systolic, 196, 197, 198
in ventricular septal defect, 196, 198
femoral arterial, 88
Gallavardin, 185, 186, 189
grading of, 181
holosystolic, 183184, 191195, 192195
in aortopulmonary window, 195
generation of, 191192, 194
in mitral regurgitation, 193, 194
origin of, 183184
in patent ductus arteriosus, 195
radiation of, in mitral regurgitation, 193,
194195
timing of, 192, 194
vs. early systolic, 196
in ventricular septal defect, 195
late diastolic, 206211, 209
late systolic, 196, 198, 199
mid-diastolic, 203205, 204, 206
atrial, 206
in atrial brillation, 204205, 204
in atrial septal defect, 205
in complete heart block, 205, 206
in mitral regurgitation, 205
in mitral stenosis, 204, 204
origin of, 203204
in pulmonary valve regurgitation, 205, 208
in tricuspid regurgitation, 205
in tricuspid stenosis, with atrial
brillation, 204, 205
in ventricular septal defect, 205
midsystolic, alternation of, 191, 191
aortic sclerotic, 189, 190, 191
in aortic stenosis, 185, 191, 192
cycle length and, 185, 188
in dilated aortic root, 187
in dilated pulmonary trunk, 187
in emphysema with barrel chest, 191,
192
in brocalcic aortic stenosis, 185, 186
innocent, 187, 189t
in children, 189
in mitral regurgitation, 185, 191
origin of, 182184
outow, 184, 184
in pulmonary valve stenosis, 185186
amyl nitrite inhalation and, 218, 219
settings occurring in, 184
palpable, 84, 89, 154155. See also Thrill(s)
pitch of, 181
presystolic, 206211, 209
from atrial myxoma, 208
in complete heart block, 206, 208
position for auscultation of, 210
in rheumatic mitral stenosis, 206207
timing of, 206, 207
in tricuspid stenosis, with sinus rhythm,
207, 208, 209
quality of, 181
renal arteial, 248249, 249
Still, 187, 189, 190
systolic, 182201, 183200
in abdominal aortic aneurysms, 90
arterial, 199201, 200
conguration of, 181, 182
decrescendo, in mitral
regurgitation, 196, 197
early, 196, 197, 198
holosystolic. See Murmur(s), holosystolic
iliofemoral, abdominal palpation of, 248
innocent, 187, 189t
late, 196, 198, 199
in mitral regurgitation, amyl nitrite
inhalation and, 220
midsystolic. See Mumzur(s), midsystolic
normal, 187, 189t
regurgitant, 184
supraclavicular, 55, 88, 89
in ventricular septal defect, 196, 198
Muscle(s), examination of, 4951, 5051
Muscular dystrophy
Duchenne, gait in, 20, 20
muscular pseudohypertrophy in, 20, 50
myotonic, facial appearance in, 23, 23
muscle wasting in, 50
Musculoskeletal chest pain, 231
5/19/2009 4:35:10 PM
266 Index
Musical theory, and rhythmical pulse lore, 3

Myocardial infarction, general appearance in, 15
apical dyskinesis after, 140, 141
shoulder-hand syndrome after, 39, 40
ventricular septal dyshnesis from, 146
Myotonic muscular dystrophy, facial
muscle wasting in, 50
Myxedema, shn texture in, 44
Myxoma, atrial, presystolic murmur from, 208
tumor plop in, 175
Nail(s), convexity of, in clubbing, 36, 38
Terry nail(s), 38, 38
Nanism, progeria with, 22
Neck, radiation of holosystolic murmur to,
193, 194195
Necker Hospital, Laennec direct auscultation
in, 67, 11, 158
Nei Ching Su Wen, Yellow Emperors Book of
Medicine, 23
Neonate(s). See also Infant(s)
transient systolic arterial murmurs in, 201
Neurobromatosis, skin lesions in, 43, 46
Neuromuscular disorder(s), scoliosis in, 52
Neurosyphilis, Argyll Robertson pupil in, 28
Nitroglycerin, for enhancement of pedal
pulses, 83
Noonan syndrome, general appearance in, 17, 18
Nystagmus, in Friedreich ataxia, 26
Obesity, general appearance in, 1819, 19
Observation, information from, 131t
Obstructive cardiomyopathy, hypertrophic,
double-peaked pulse in, 77, 77
left ventricular discharge in, angiotensin
infusion and, 221
Ocular bulb, examination of, 26
Older adult(s), aortic sclerotic murmur in,
189, 190, 191
blood pressure measurement in, 60
Valsalva maneuver in, 218
Onychophagia, and risk of infective
endocarditis, 46, 48
Opening snap, and mid-diastolic murmur, 204
in rheumatic mitral stenosis, auscultation
of, 174, 175, 175
palpation of, 154

in tricuspid stenosis, 174
Ophthalmoscopic examination, 3033, 34
Orias, O., on use of stethoscope, 8
Orthopnea, 227
Orthostatic hypotension, detection of, 6061
Osler, W., 2
on blood pressure measurement, 60
Cushings biography of, 2
on late systolic murmur in mitral
valve prolapse, 199
Osler node(s), in infective
Osteogenesis irnperfecta, ngers in, 43
hands in, 3940, 43
sclera in, 28
Ostium secundum atrial septal defect, jugular
venous pulse in
right ventricular impulse in, 145
Outow midsystolic murmur(s), 184, 184
P2, and second heart sound, 172
Pacemaker(s), right ventricular, second heart
sound in, 172
Pacemaker sound, 181
Pagets disease, angioid streaks in, 32
Pain, abdominal, from aortic aneurysm, 247
chest, noncardiac, 231
Palpation
abdominal, 242248, 243248. See also
Abdomen, palpation of
of arterial pulse, 55. See also Arterial pulse,
examination of
history of, 10, 11
for estimation of arterial pressure, 59
of heart. See Heart, palpation of
of heart sounds, 153154
historical accounts of, 127129, 128
precordial, historical accounts of, 5
of thorax, 230231
topographic anatomy and, 131, 132
Paradoxic splitting, of second heart sound,
172
Paradoxical pulse. See Pulsus paradoxus
Paronychial infection(s), and risk of infective
5/19/2009 4:35:11 PM
Index 267
Paroxysmal tachycardia, jugular venous pulse

in, 119
Patent ductus arteriosus, continuous murmur
in, 211212, 211
continuous thrill from, 155
holosystolic murmur in, 195
pulsating dorsalis pedis in, 55
in Rubinstein-Taybi syndrome, 40
with suprasystemic pulmonary vascular
resistance, differential cyanosis and
clubbing in, 38
Pectus carinatum, 226, 227
Pectus excavatum, in Marfan syndrome, 52
Percussion, abdominal, 241242
as component of physical examination, 1
historical accounts of, 89, 128129, 129
information from, 129
in pericardial effusion, 130
principles of, 129130, 130
thoracic, 231234, 232235
history of, 231233, 232
purpose of, 233
Pericardial effusion
percussion in, 130
Pericardial knock, in mitral regurgitation, 174
Pericardial rub(s), 214, 215
Pericardial tamponade, pulsus paradoxus in, 79
Pericarditis
constrictive
amplied A and V waves of jugular
venous pulse in, 114
diastolic heartbeat in, 147
early diastolic heart sound in, 174
jugular venous response to abdominal
compression in, 106
protein-losing enteropathy in, and Terry
nails, 38, 38
pulsus paradoxus in, 79
X descent of jugular venous
pulse in, 108109, 110
in Reiter disease, 27
Pericordium, observation of, 135
Periodic breathing, 228229
Periodicity, Wenckebach, jugular venous pulse
in, 120
Wenckebachs description of, 64
Peripheral arterial occlusive disease,

examination of slun of feet in, 87
Peripheral cyanosis, vs. central cyanosis, 38
Peripheral arterial pulse, wave forms of, 66
Peripheral vascular disease, and supraclavicular
systolic arterial murmur, 199
skin of feet and toes in, 38, 39
Pes cavus, with hammer toe, 4142, 45
Pheochromocytoma, in neurobromatosis, 43
Phonocardiography, 157, 158
development of, 8
in right ventricular cavity, 161
Physical appearance, 1553
of abdomen, 241
of chest, 226
of eyes, 2633, 2733
facial expression in, 2226, 2226
general, 1521, 16t . See also specic illness(es)
in acute illness, 15
in chronic illness, 16
of hands and feet, 3642, 3645
importance of, historic notes of, 2
of mouth, 3335, 35
of muscles, 4951, 5051
of skin, 4249, 4349
of tendons, 4951, 5051
of thorax, 5152, 51, 53
Physical Diagnosis, 10
Physical examination, historical basis of, 210
Physicians Pulse Watch, of Floyer, 3
Pickwickian syndrome, 229, 230
general appearance in, 1819, 19
Pierre Robin syndrome, glossoptosis in, 35
Pigmentary retinopathy, in Kearns-Sayre
syndrome, 27, 28, 32
Pitch, in auscultation, 163
Pitting edema, in congestive heart failure, 44,
46, 47
Placenta, function of, described by
Malpighi, 226
Placental bruit, 249
Plaque(s), Hollenhorst, 30
Pleural effusion, percussion of, 233
Pleural rub, 237
PMI (point of maximum impulse), 137
Pneumothorax, Laennecs account of, 910
Point of maximum impulse (PMI), 137
5/19/2009 4:35:11 PM
268 Index
Polydactyly, 41
Polygraph, for examination of pulse, 55, 56
Popliteal arterial pulse, palpation of, 86, 87
Popliteal artery, aneurysms of, 90
measurement of blood pressure in, 62
Position, and second heart sound, 172
for auscultation, 162163, 163
for blood pressure measurement, 59
changes in, during auscultation, 215, 216t
decubitus. See Decubitus position
for liver palpation, 242243, 243, 244, 245
for palpation of spleen, 243, 244
and venous hum, 214
Posterior tibial artery, palpation of, 83, 86, 86
Posture, and clicks in mitral valve prolapse,
170, 196, 198, 199
Potain, P., introduction of
sphygmomanometer by, 58
on the fourth heart sound, 178179
on gallop rhythm, 178
on splitting of second heart sound, 166
on systolic clicks, 166
on venous hum, 213214
on ventricular presystolic distention, 149
on wave form of internal jugular venous
pulse, 96, 101
PR interval, estimation of, from jugular
venous pulse, 120
Precordial movement, normal, 136, 137139
Precordial movement(s), timing of, carotid
arterial pulse for, 136, 132133
Precordial palpation. See also Heart,
palpation of
Precordial site(s), designations of, 131, 132
Precordium, retraction of, 133, 135
Pregnancy, abdominal palpation during, 249
Premature aging, facial appearance in, 22, 23
Premature atrial beat(s), jugular venous pulse
in, 116
vs. atrial brillation, 119
Premature ventricular beat(s), vs. atrial
brillation, 119
Premature ventricular contraction(s), pulsus
alternans in, 78
Pressor amine(s), and systolic murmur, in
mitral regurgitation, 220
for mitral valve prolapse, 169

Presystolic heart sound(s), 160, 162t,
176181, 177, 179, 190
Presystolic movement(s), ventricular,
148150, 148, 149
Presystolic murmur(s). See Murmur(s),
presystolic
Presystolic thrill(s), 155
Pretibial edema, in congestive heart failure, 46
Progeria, facial appearance in, 22, 23
Progressive systemic sclerosis, nger lesions in,
39, 41
Proportional pulse pressure, 60
Proptosis, in hyperthyroidism, 26
Prosthetic valve(s), anemia from, 43
sounds from, 165
mitral, early diastolic sound from, 176
Protein-losing enteropathy, in constrictive
pericarditis, and Terry nails, 38, 38
Pseudohypertrophic Duchenne muscular
dystrophy, gait in, 20, 20
Pseudohypertrophy, muscular, in Duchenne
muscular dystrophy, 20, 50
Pseudoxanthoma elasticum, angioid streaks
in, 32
skin lesions in, 44
Psychophysiologic hyperventilatory dyspnea,
228
Ptosis, in Kearns-Sayre syndrome, 27, 28
Pulmonary arterial systolic murmur(s),
transient, in neonates, 201
Pulmonary arteriovenous stula(s), in RenduOsler-Weber syndrome, 33, 35
Pulmonary artery, main topographic anatomy
of, 131, 132
Pulmonary artery stenosis, in Williams
syndrome, 34
facial appearance in, 24, 26
Pulmonary circulation, discovery of, 225
Pulmonary edema, general appearance in, 15
in infants, respiration in, 227, 228
tachypnea from, 228
Pulmonary embolism, systolic arterial
murmurs from, 201
Pulmonary hypertension, in sarcoidosis, 27
intensity of second heart sound in, 173, 173
Raynaud phenomenon in, 38, 39
5/19/2009 4:35:11 PM
Index 269
in scleroderma, 39
second heart sound in, palpation of, 154
with right ventricular failure, amplied A
and V waves of jugular venous pulse
in, 113114
Pulmonary regurgitation, hypertensive, early
diastolic murmur from, 202
Pulmonary trunk, dilated, midsystolic
murmur in, 185186
systolic impulse from, 151, 152, 152
Pulmonary valve regurgitation, low pressure,
Pulmonary valve stenosis, ejection sound in,
165, 167
amyl nitrite inhalation and, 218, 219, 219
in Noonan syndrome, 17, 18
thrills from, 155
Pulmonary vascular resistance, suprasystemic,
with patent ductus arteriosus,
differential cyanosis and clubbing
in, 38
Pulse, arterial. See Arterial pulse
bigeminal, vs. pulsus alternans, 78
bisferiens, double-peaked, 76
in aortic regurgitation, 74, 7576
examination of, observation in, 55
grading of, 81
jugular venous. See Jugc~lar venous pulse
palpation of, in Yellow Emperors Book of
Medicine, 5
Pulse decit, 64
Pulse pressure, normal, with brisk arterial
pulse, 74
proportional, 60
wide, with increased arterial pulse, 74, 75
Pulse rate, measurement of, 6465
Pulsus alternans, 66, 7779, 78
pulse rate in, 64
right atrial, in right ventricular failure,
113, 114
Pulsus bisferiens. See Bisferiens pulse
Pulsus paradoxus, 7980, 80
Pupil(s), examination of, 28
Quadricuspid valve, with truncus arteriosus,
Quadruple rhythm, 176, 177

Quincke pulse, 88
Radial arterial pulse, alternation in, 79
vs. femoral arterial pulse, 85
in infants, 69
right vs. left, 8183, 84, 85
Rales, 237
Rash, buttery, in systemic lupus
erythematosus, 23
Raynaud phenomenon, in pulmonary
hypertension, 38, 39
Reux, abdominojugular, 105, 106
Regimen sanitatis, 128
Regurgitant systolic murmur(s), 184
Reiter disease, 27
Renal arterial murmur(s), 248249, 249
Renal arteriovenous stula(s), continuous
murmur from, 248, 249
Rendu-Osler-Weber syndrome,
lip lesions in, 33, 35
Respiration, and internal
jugular venous pulse, 102
Cheyne-Stokes, 228, 229, 229
depth of, 227
during auscultation, 217
during palpation of heart, 133
in emphysema, 229
frequency of, 227
intercostal muscles in, 226
Kussmaul, 227
observation of, 227230, 229, 230
and presystolic murmur, in tricuspid
stenosis, 208
Respiratory system, physiology of, 226
Retinal arterial emboli, etiology of, 30
Retinal detachment, in Ehlers-Danlos
syndrome, 32
Retinopathy, hypertensive, 30
pigmentary, in Kearns-Sayre syndrome,
28, 32
Rhabdomyoma, cardiac,
skin lesions in, 49
Rheumatic fever, Jaccoud arthritis after, 44
subcutaneous nodules in, 49
5/19/2009 4:35:11 PM
270 Index
Rheumatic mitral stenosis, rst heart sound

in, 153
mid-diastolic murmur from, 204
presystolic murmur in, 206, 207
Rhonchi, 237
Rhythmical pulse lore, of Herophilus, 3
Rib cage, in respiration, 226
Right aortic arch, systolic impulse from,
151, 152
Right atrial mean pressure, estimation of,
examination of external jugular vein
for, 102
Right atrial pressure pulse, in complete heart
block, 122
Right atrial pulsus alternans, in right
ventricular failure, 113, 114
Right atrium, systolic expansion of, 150
wave form of, on hepatic palpation, 242,
243, 244
Right bundle-branch block, second heart
sound in, 171172
Right ventricle, hypertrophy of, and fourth
heart sound, 181
mid-diastolic impulse from, 146148
subxiphoid, 135
pericardial rubs originating in, 214
presystolic distention of, 149
systolic impulse from, 137
abnormal, 141146, 143, 144, 145
and left ventricular displacement, 143,
143, 144
in Fallots tetralogy, 151152
in ostium secundum atrial
septal defect, 145
palpation of, examiners position for,
141142
subxiphoid, 143
in tricuspid regurgitation, 145
Right ventricular failure, amplied A and V
waves of jugular venous pulse in,
113, 114
compression in, 105
Right ventricular heart sound(s),
third/fourth, 179
Right ventricular pacemaker, second heart

sound in, 172
Riva-Rocci, development of occluding cuff for
blood pressure measurement by, 58
Rocker bottom foot, in trisomy 18, 42
Rondot, E., on hepatojugular reux, 105
Roth spots, 29, 32
Rouanet, J., on heart sounds, 159
Rub(s), pericardial, 214, 215
Rubella, rst-trimester, and cataracts, 30
Rubinstein-Taybi syndrome, hands and feet
in, 40
Saccular luetic aneurysm, of ascending aorta,
systolic impulse from, 150, 151
Saphenous vein(s), examination of, 121
Sarcoidosis, and enlarged lacrimal glands, 27, 29
Sclera, examination of, 28
Scleroderma, nger lesions in, 39, 41
Sclerotic artery(ies), and blood pressure
measurement, 60
Scoliosis, 52
Second heaxt sound. See Heart sound(s), second
Servetus, M., discovery of pulmonary
circulation by, 225
Sexual infantilism, in Turner syndrome, 17, 18
Shakespeare, on general appearance in acute
illness, 1516
Shifting dullness, in abdominal percussion, 242
Shock, cardiogenic, general appearance in, 15
Short stature, in Turner syndrome, 17, 18
Shoulder(s), hyperextension of, for auscultation
of supraclavicular systolic
murmurs, 216
Shoulder-hand syndrome, 39, 40
Shy-Drager syndrome, orthostatic hypotension
in, 60
Sickle cell disease, angioid streaks in, 32
Simian palmar crease, in Down syndrome, 31, 40
Sinoatrial exit block, jugular venous pulse in,
115116
Sinus arrhythrnia(s), 64
jugular venous pulse in, 116, 117
Sinus bradycardia, jugular venous
pulse in, 115
Sinus of Valsalva, rupture of aneurysm of,
continuous murmur from, 212
5/19/2009 4:35:11 PM
Index 271
Sinus rhythm, with tricuspid stenosis, presystolic

murmur in, 207, 208, 209
Sitting, while leaning forward, during
auscultation, 216
Situs inversus, with dextrocardia, 130, 130
Situs solitus, with levocardia, 129
Skin, examination of, 4249, 4349
of feet and toes, in peripheral vascular disease,
38, 39
Skin lesion(s), and risk of infective endocarditis,
46, 48
in amyloidosis, 46, 48
from cardiac rhabdomyoma, 49
in hemochromatosis, 43
from intravenous drug abuse, 47, 49, 125
Skoda, J., on abdominal auscultation, 248, 249
on apex beat, 137
on continuous murmurs, 212
on detection of fetal heart, 249
on percussion, 89
thoracic, 231
Sphygmogram, 56
Sphygmomanometer, components of, 58
introduction of, 5758
Sphygmomanometry, detection of pulsus
alternans by, 79
detection of pulsus paradoxus by, 79
Spleen, palpation of, 243, 244, 245, 246
Splinter hemorrhage, subungual, 42
Splitting. See Heart sound(s)
Spondylitis, ankylosing, appearance of thorax
in, 52
Standing, after squatting, and systolic clicks in
mitral valve prolapse, 198, 199, 216
Stasis area(s), in varicose veins, 123, 124
Stature, short, in Turner syndrome, 17, 18
Sternal angle of Louis, for estimation of jugular
venous pressure, 104, 104, 105
Sternoclavicular joint, right systolic movement
of, from right aortic arch, 150, 152
Stethoscope
binaural, controversy over, 7
development of, 58
development of, 68, 235, 236, 238
use of, See Auscultation
Still murmur, 187, 189, 190
Stokes, W., on auscultation, 157, 159

on Cheyne-Stokes respiration, 228, 229, 229
on complete atrioventricular block, 121
on midsystolic murmurs, 185
Straight back, in Marfan syndrome, 52
Striated palmar xanthoma, in
hyperlipoproteinemia, 46, 48
String galvanometer, 8
Study of the Pulse, 4, 127
Subclavian artery, auscultation of, 88
Subclavian artery stenosis, systolic arterial
murmur from, 199
Subclavian steal syndrome, right vs. left
brachial pulse in, 81
Subclavian thrombophlebitis, 125
Subcutaneous nodule(s), in active rheumatic
fever, 49
Subungual splinter hemorrhage, 42
Subxiphoid palpation, 133, 134
of mid-diastolic impulse, 147
of right ventricular presystolic impulse, 150
of right ventricular systolic impulse, 143
Succussion splash, of hydropneumothorax,
5, 234
Summation gallop rhythm, 176, 177
Superior vena caval syndrome, 125
Supraclavicular systolic murmur(s), 55,
8889, 89
arterial, in children, 199, 200
auscultation of, position for, 216
Supravalvular aortic stenosis, Coanda effect
in, 193
facial appearance in, 24
Sustained handgrip,
during auscultation, 218
Sylvius, E B., bedside teaching of, 1
Syndactyly, 41
Systemic lupus erythematosus, facial appearance
in, 23
Systemic-to-pulmonary arterial collateral
circulation, continuous murmurs
from, 213
Systolic click(s), from mitral valve prolapse,
165, 166, 168, 169, 170
Systolic heart sound@). See Heart sound(s),
systolic
5/19/2009 4:35:11 PM
272 Index
Systolic hypertension,
increased pulse pressure in, 74
Systolic impulse, biventricular, 145, 146
from great arteries, 150153, 151, 152, 153
left ventricular. See Left ventricle, systolic
impulse from
ventricular origin of, 137
Systolic murmur(s). See Murmur(s), systolic
Systolic pressure, auscultatory, in lower
extremity, 62
Systolic retraction, 141
Systolic thrill(s), 154155
Systolic venous wave, of jugular venous pulse,
anatornichemodynamic correlations
for, 112, 112, 113
Tachycardia, atrioventricular nodal reentrant,
jugular venous pulse in, 118119
ectopic, jugular venous pulse in, 116, 117
ventricular, jugular venous pulse in,
118120
Tachypnea, 228
Tactile fremitus, 230231
Teeth, malformations of, in Williams
syndrome, 26, 34
Telangiectasia, hereditary hemorrhagic, lip
lesions in, 33, 35
Tendon(s), examination of, 4951, 5051
Teny nail(s), 38, 38
Tetralogy of Fallot. See Fallots tetralogy
Third heart sound. See Heart sound(s), third
Thoracic aortic aneurysm, descending, systolic
impulse from, 152
Thoracic inlet vein(s), examination of, 125
Thoracic kyphosis, loss of, 226, 227
Thoracic spine, structural abnormalities of, 52
Thoracotomy scar(s), 52
Thorax
auscultation of, 235238, 236
history of, 235, 236, 237, 238
information obtained by, 238
in nonprecordial areas, 162
conguration of, and access to palpation of
right ventricle, 142
examination of, 5152, 51, 53
palpation of, 230231
percussion of, 231234, 232235
hand position for, 233, 234

history of, 231233, 232
purpose of, 233
Thrill(s), 154155
continuous, 155
diastolic, 155
presystolic, 155
systolic, 154, 155
Thrombophlebitis, axillary, 125
deep, 122
subclavian, 125
Thumb, for palpation of arterial pulse, 81
Thyrotoxicosis, general appearance in, 16
Tongue, examination of, 24, 25, 34, 35
Torus palatinus, 35
Total mechanical alternans, 79
Tracheal breath sound(s), 237
Transverse liver edge, in visceral heterotaxy,
242
Traube, L., on pulsus alternans, 78
Treatise on Diseases of the Chest, A, 9, 235
Treatise on the Blood, Inammation, and Gun-Shot
Wounds, 34
Trepopnea, 227
Tricuspid atresia, cats eye syndrome in,
28, 32
Tricuspid regurgitation, blunting of X
descent of jugular venous pulse in,
108110, 111
in atrial brillation, V wave of jugular
venous pulse in, 112, 112, 113
Y descent of jugular venous pulse in, 112,
112, 113
early systolic murmur in, 196, 197
holosystolic murmur in, 194, 194
vs. early systolic, 196
liver pulse in, 112, 115
right ventricular systolic impulse in, 145
Tricuspid stenosis, A wave of jugular venous
pulse in, 108, 109
with atrial brillation, jugular venous pulse
in, 112, 113
compression in, 106
5/19/2009 4:35:11 PM
Index 273
opening snap in, 174

with sinus rhythm, presystolic murmur in,
207, 208, 209
Tricuspid valve, closure of, and rst heart
sound, 164
Triphalangism, 41
Triple rhythms, 176, 177
Trisomy 18, rocker bottom foot in, 42
Truncus arteriosus, with quadricuspid valve,
Tuberous sclerosis, skin lesions in, 49
Tuberous xanthoma, 46
Tubular breathing, 237
Tumor plop, 154, 160
from atrial myxoma, 175, 208
Turner syndrome, general
Two-to-one atrioventricular block, jugular
venous pulse in, 120, 121
Tympany, gastric, 241
U turns, in retinopathy from coarctation of
aorta, 30, 34
Ulnar artery, palpation of, 83, 84
University of Leiden, Sylvius teaching at, 1
Upper extremity(ies), veins of, 124125
vs. lower, palpation of arterial pulses in,
84, 86
Uterine placenta, function of, described by
Malpighi, 226
Uterus, gravid, palpation of, 249
V wave, in atrial pressure pulse, 161
anatomic-hemodynarnic inferences from,
109113, 112, 113
of jugular venous pulse, amplication of,
anatomichemodynarnic inferences
from, 113114, 114
internal, 97, 98, 101, 104
Valsalva maneuver, 217
and heart rate, 65
and late systolic murmur in mitral valve
prolapse, 196
Valsalva response, 217
Varicose vein(s), 123, 124
Vascular disease, peripheral, skin of feet and
toes in, 38, 39
Veno-constriction, obliteration of external

jugular vein by, 99
Vena cava, superior, obstruction of, 125
Venous Corrigan pulse, 108
Venous hum, continuous murmur from,
213214, 213
Venous insufciency, chronic, 123, 124
Venous pulse, cervical. See Cervical venous
pulse
jugular. See Jugular venous pulse
Ventilation, physiologic pump for, 226
Ventricle(s), atrial lling of, 148, 148
left. See Left ventricle
mid-diastolic movement of, 146148, 147
presystolic movement of, 148150, 148, 149
right. See Right ventricle
Ventricular aneurysm(s), ectopic systolic
impulse from, 139
Ventricular diastole, rapid lling phase of, 176
Ventricular knock, in mitral regurgitation,
147, 174, 175
Ventricular premature beat(s), jugular venous
pulse in, 116117
Ventricular septal defect, early systolic
murmur from, 196, 198
Eisenmenger, single second
heart sound in, 171
holosystolic murmur in, 195
thrills from murmur of, 155
holosystolic, 155
Ventricular septal dyskinesia, after myocardial
infarction, 146
from angina, 146
Ventricular septum, topographic anatomy of,
132
Ventricular tachycardia, jugular venous pulse
in, 118120
Vesicular breath sound(s), 237
Vienna Hospital, use of percussion at, 8
Visceral heterotaxy, transverse liver in, 242
Visceral situs, 241
Vitiligo, in Graves disease, 43, 44
Vocal fremitus, 230
Voice-generated auscultatory sign(s), 237
von Recklinghausen disease, skin lesions in,
43, 46
5/19/2009 4:35:11 PM
274 Index
Waterhammer pulse, in aortic regurgitation,

75, 76
Watson, T., on waterhammer pulse, 76
Wave form(s)
of arterial pulse, 6581, 65, 67
abnormal, 72t
normal, 6972
of brachial arterial pulse, 66, 6970
of internal jugular venous pulse, 9698, 97,
101102
of peripheral arterial pulse, 66
of radial arterial pulse, 66
right atrial, effect on liver palpation, 242, 245
Wenckebach, K., on periodicity, 64
Wenckebach periodicity, jugular venous pulse
in, 120
Werner syndrome, facial appearance in, 22, 22
peripheral vascular disease in, 38, 39
Wheezes, 237
Whispered pectoriloquy, 238
Whoop, late systolic, in mitral valve
prolapse, 199
Wide pulse pressure, with increased arterial
pulse, 74, 75
Wiggers, C., historical account of jugular
venous pulse by, 4
on palpation of arterial pulse, 66
on use of stethoscope, 8
Williams syndrome, facial appearance in, 24, 26

Withering, W., account of dropsy by, 10
Wood, P., 8
on A wave of jugular venous pulse, 107108
on examination of jugular venous pulse, 4,
8, 93
X descent, in atrial pressure pulse, 161
in jugular venous pulse,
anatomichemodynamic inferences
from, 108109, 110, 111
internal, 96, 97, 101
Xanthalasma, 2627
Xanthoma, of Achilles tendon, 50, 51
striated palmar, in hyperlipoproteinemia,
46, 48
Y descent, in atrial pressure pulse, 161
in jugular venous pulse,
anatomichemodynarnic correlations
for, 109111, 112, 113
internal, 97, 98
Yellow Emperor, 4
Yellow Emperors Book of Medicine, 23, 159
Zone of retraction, along
interventricular sulcus, from biventricular
systolic impulse, 146, 146
5/19/2009 4:35:12 PM

Physical Examination of The Heart and Circulation 4th 2009

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Physical Examination

Joseph K. Perloff, M.D.

PEOPLES MEDICAL PUBLISHING HOUSE

Peoples Medical Publishing House

And to those whom I have taught and will teach,

Introduction with a Brief Historical Survey

The Arterial Pulse

The Jugular and Peripheral Veins

The Movements of the HeartPercussion,

AuscultationThe Audible Language of the Heart

Specialized laboratory techniques for cardiovascular diagnosis provide a large portion of

Sophisticated laboratory methods provide contemporary clinicians with remarkable

Introduction with a Brief

2 Introduction with a Brief Historical Survey

Figure11 Sir William Osler

Introduction with a Brief Historical Survey 3

Figure 12 Sir James Mackenzie

4 Introduction with a Brief Historical Survey

Figure 13 Huang Ti, the Yellow

Introduction with a Brief Historical Survey 5

Figure 14 If the patient were

6 Introduction with a Brief Historical Survey

Figure 15 Giovanni Maria

Introduction with a Brief Historical Survey 7

Figure 16 John Hunter

8 Introduction with a Brief Historical Survey

Figure 17 Paul Hamilton Wood, MD, OBE

Introduction with a Brief Historical Survey 9

10 Introduction with a Brief Historical Survey

Figure 19 William Harvey

Introduction with a Brief Historical Survey 11

Figure 110 Laennec

Figure 111 Leopold Auenbrugger

12 Introduction with a Brief Historical Survey

Introduction with a Brief Historical Survey 13

Table 21 Physical Appearance

Figure 21 Infant of a diabetic

Obesity varies in appearance and should be carefully characterized. The

Gestures and gait can be important features of physical appearance. A clenched st

Figure 24 A, Young boy with classic pseudohypertrophic X-linked Duchenne muscular

Figure 25 Gowers sign:

Figure 28 A, Child with typical coarse physiognomy of Hurler syndrome (gargoylism).

A number of facial appearances are associated with specic or relatively specic

Figure 29 A, Down syndrome

Figure 210 Facial appearance of

External and Internal Appearance of the Eyes

Figure 211 Fetal alcohol

The sclera can disclose discoloration as familiar as jaundice, or as unusual as the

A common abnormal appearance of the lens is the cataract. Premature cataracts

Figure 216 A, Brusheld spots

Figure 217 A, Painting by

External and Internal Appearance of the Mouth

infective endocarditis. Malformations of the teeth are diagnostically important in

Figure 220 A 28-year-old man with RenduOslerWeber hereditary hemorrhagic

retraction of the tongueglossoptosisin the Pierre Robin syndrome. The retraction

The Hands and Feet

Figure 221 A, Prole of

Figure 223 A brownish band

Figure 225 A, Painless erythema of the

Figure 228 Hyperextensible

Figure 229 A, Hands of

of the distal extremities, is an occasional feature of Graves disease. In myxedema (see

Figure 233 A, Pretibal