Raju B Soma Ed Clinical Methods in Cardiology PDF

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Foreword
These are exciting times for cardiology! Dramatic breakthroughs in basic research, exciting
results of major clinical trials, and new diagnostic and therapeutic devices have revolutionized
cardiovascular care worldwide. Knowledge and procedures previously available only in large
research centers are now available in local and community hospitals. This rapid diffusion of
information and technology is coming just in the nick of time, as cardiac and vascular disease
is destined to become one of the major public health problems worldwide in this millennium.
One of the unfortunate byproducts of the rapid maturation of many developing countries is
the development of additional cardiac risk factors, and the emergence of a mini-epidemic of
cardiovascular diseases, particularly coronary artery disease.
It is in this milieu that B Soma Raju’s Clinical Methods in Cardiology is so timely and so
appropriate. It addresses two major issues prompted by the rapid dissemination of medical
information, procedures and technology throughout the globe: the need for practitioners to
understand the fundamentals of the history and physical examination, rather than rely blindly
only on technology; and the need to be aware of the unique patient-care issues of different
regions of the globe. This textbook addresses both issues in an outstanding manner. It is a
distillation of Dr Soma Raju’s clinical approach and experience as one of the most respected
cardiologists in India. The book is a private tutorial outlining one master clinician’s approach to
the cardiac history and physical examination. His thesis (with which I agree) is that the clinical
evaluation of the patient forms the foundation upon which the management of the patient is
built. Without such a firm basis, optimal treatment of the patient is not possible.
I have had the pleasure and honor of working with Dr Soma Raju over the last decade on
two collaborative research projects studying the optimal treatment of rheumatic mitral stenosis
that were a joint effort between my institution and his. In that period I have come to cherish my
times in India, and my association with him. He is the best bedside clinical diagnostic cardiologist
I have ever seen, and his enormous wealth of clinical experience is well reflected in Clinical
Methods in Cardiology. I believe that this textbook is destined to become the definitive text from
the subcontinent on the clinical approach to the cardiac patient.
Joshua Wynne
MD
Professor of Medicine
Wayne State University
Detroit, Michigan, USA
Preface
Physical examination and history continue to play
a pivotal role in the evaluation and management of
patients with cardiovascular disease. Currently there
is an increasing tendency to rely on laboratory tests
with the assumption that these methods are more
‘objective’. The following case summary illustrates
this trend.
A 45 year old male hypertensive went for
annual medical examination. The exercise test was
interpreted as ‘strongly positive for myocardial
ischemia’. Coronary angiography was done. During
Fig 1
the angiogram, the left coronary catheter repeatedly
‘damped’ (Fig 1); this was suspected to indicate left
main ostial stenosis particularly on the background
of a ‘strongly positive’ exercise test.
The angiogram was interpreted as ‘consistent’
with left main ostial stenosis though the quality of
the angiographic film was far from satisfactory. The
cardiologist argued that the strongly positive exercise
test explains the angiographic finding and the The
cardiovascular surgeon readily agreed with the
interpretation. Emergency coronary bypass surgery
was advised. The patient was taken aback by the
rapid sequence of events as he had never had any Fig 2
symptoms and was exercising regularly for more than
an hour daily with no difficulty. He was warned of
the danger delaying surgery in this setting and there
was imminent danger to his life. The patient opted
for a discharge from the hospital and sought another
opinion. The review of the angiogram revealed that
the quality of the film was poor and no conclusions
could be drawn from it. As the patient was a
hypertensive, an echocardiogram was done which
showed concentric left ventricular hypertrophy. This
explained his false positive ‘strongly positive’ exercise
test. Angiogram was repeated with a 3.5 Judkin’s left
coronary catheter. There was ‘damping’ of pressure Fig 3
from the coronary catheter as was observed in the earlier investigation. But the angiographer
felt that there was a back flow during the coronary injection which could be easily made out
because of superior angiographic system. A Judkin’s 4 curve left coronary catheter was used to
test the ‘false positive’ or pseudo-damping. There was no damping this time and the angiogram
was interpreted as normal. The 3.5 curve damped because the catheter tip was abutting en face
against the roof of the left main artery. The patient was discharged next day to resume his normal
activities and exercises. He was in excellent health 6 years after the angiogram.
This patient almost had an unnecessary bypass surgery based on ‘objective’ tests. Without
‘subjective’ information, hardly any decision can be made in the care of patients. It should be
realized that objective laboratory tests are not necessarily superior to subjective clinical methods.
The ‘objectivity’ is particularly misleading because of uncritical and almost slavish over-reliance
on anything that is based on sophisticated technology.
In the assessment of stenotic valve disease, cardiac catheterization and hemodynamic
calculation of valve areas is considered the gold standard amongst the presently available
methods. The following table from the study of Defillippo et al illustrates the limitations of
even this method.
Table: Limitations of cardiac catheterization—patients initially diagnosed to have aortic stenosis
Patients were initially thought to have severe aortic stenosis because valve areas were
calculated at low cardiac outputs. Hemodynamic manipulation by dobutamine or valve inspection
proved the initial assessment to be incorrect (Defilippo et al 1995, Am J Cardiol 75: 191–94).
The mistakes in the measurement of intracardiac pressures and cardiac output are common
in the cardiac catheterization laboratories all over the world. Many laboratories do not even have
adequate hemodynamic measurement and recording systems.
The ‘objective tests’ when improperly done without adequate quality control are particularly
less reliable and even dangerously misleading. The decisions for definitive procedures like cardiac
surgery and catheter interventions are made from the ‘objective’ information provided by them.
Medicine deals with human beings who are subjects and not objects on which tests are done and
procedures are carried out.
Though there are books on physical examination of the heart by well-known authors,
I decided to put to print my way of looking at things. I fully realize that there are many ways of
looking at things and hence the need for more of us to communicate by writing. This book is
written with a firm conviction that physical examination of a patient is a way of thinking and not
merely a way of doing. It plays a vital role in decision making: both diagnostic and therapeutic.
I hope this will guide the medical student, the postgraduate, the cardiologist in training, the
practising physician, the medical teacher and the practising cardiologist.
When there is a discrepancy between the ground and the map, the ground is usually right.
Field Marshal Erwin Rommel
The map is the angiogram and the ground is the patient.

Note to the reader
Hippocrates, the first Greek to challenge the notion that
disease was punishment sent from the gods, discovered
the connection between human disease and poor
environmental conditions. Considered to be the father of
medicine, his ability to make accurate clinical observations
led him to the concept of preventive medicine.
THE OATH OF HIPPOCRATES (MODIFIED)

I swear to fulfill to the best of my ability and judgment, this covenant.
I will respect the hard-won scientific gains of those physicians in whose steps I walk, and gladly
share such knowledge as is mine with those who are to follow.
I will apply for the benefit of the sick, all measures which are required, avoiding those twin traps
of overtreatment and therapeutic nihilism.
I will remember that there is art to medicine as well as science, and that warmth, sympathy and
understanding may outweigh the surgeon’s knife or the chemist’s drug.
I will not be ashamed to say “I know not,” nor will I fail to call in my colleagues when the skills
of another are needed for a patient’s recovery.
I will respect the privacy of my patients, for their problems are not disclosed to me that the world
may know. Most especially must I tread with care in matters of life and death. If it is given me to
save a life, all thanks. Bu it may also be within my power to take a life; this awesome responsibility
must be faced with great humbleness and awareness of my own frailty. Above all, I must not play
at being God.
I will remember that I do not treat a fever chart, a cancerous growth, but a sick human being, whose
illness may affect the person’s family and economic stability. My responsibility includes these related
problems, if I am to care adequately for the sick.
I will prevent disease whenever I can, for prevention is preferable to cure.
I will remember that I remain a member of society, with special obligations to all my fellow human
beings, those sound of mind and body as well as the infirm.
If I do not violate this oath, may I enjoy life and art, respected while I live and remembered with
affection thereafter. May I always act so as to preserve the finest traditions of my calling and may
I long experience the joy of healing those who seek my help.
translated by Louis Lasanga (1964) Academic Dean, Tufts University
The following paragraphs are excerpts taken from the Presidential address
of Professor Douglas Zipes at the plenary session of the American College of
Cardiology in March 2002:
The way medicine is practised today raises many questions about where our concerns and our
responsibilities must lie in this world. The questions are many and the answers difficult. But one
answer, particularly for us as physicians, stands out above all the rest. We now know that our
concerns can no longer be limited to a personal agenda, to a regional interest, or to any single corner
of any particular market. We now know that the proper sphere of influence for every responsible
man and woman is this entire fragile sphere called earth. Castes and communities. religious fanatism,
regional parochialism, the and errant politicians fade into the mist of dreams when held up to the
pleading realities affecting our world. It has become blindingly clear that our concerns must encompass
the relief of misery wherever we find it. And that means that we, as physicians and cardiologists,
must expand our vision to include all of humankind.
Our world has been likened to a beautiful book that is of little use to those who cannot read. And
in a similar sense, our knowledge as physicians is a fine and priceless asset whose value is vastly
diminished unless it can be taught, disseminated, and practised throughout the world. In Peru,
Calcutta, and Afghanistan.
I have written about it in one of my president’s pages, and I like to call it a patient in a box. It
is designed to teach physicians at all stages of their careers how to use new medical devices and
perform new procedures.
It will allow trainees to practice new techniques without fear of harming patients. In fact, in the
future a certain number of practice hours logged on a simulator will probably become required before
performing a procedure on a patient.
It will help us to work and train as a team, along with our nurses, technicians, and physician
colleagues. Dealing with rare or infrequent complications, such as cardiac perforation and tamponade,
can be practised many times on the simulator, so that when it actually happens, the cath team can
respond like a crack drill squad.
In the near future, from the first venopuncture that a medical student performs to a complex angioplasty
in the last year of cardiology fellowship training, procedures will be taught in such virtual reality
settings. Perhaps, also in the future, low volume operators will be able to make up for lack of patient
numbers by documented hours spent practising on a simulator.
I submit to you that virtual reality is an unquestionable part of our educational future, and it is
a means through which we can spread knowledge all over the world. It will change forever how we
teach, test, and treat.
We must educate the public of the wrong doings and unethical practices they are subjected to.
What else can we do, as individual clinicians and as a College, to improve the quality of the care
that we deliver? How can we demonstrate that quality to regulatory agencies, third-party payers,
and, most importantly, to our patients and their loved ones?
In searching for an answer to these questions, we must first look to the nature of our relationship
with the society in which we live.
We are social animals with a need to coexist in the company of others, and to interact with them. It
seems to me that the moral glue that binds us together comes in large measure from our accountability
to those others.
For each of us is accountable in some way to someone . . . a husband to his wife, a parent to a child,
a physician to a patient. We know this and live by it.
And in these interactions, we think of ourselves, for the most part, as honorable men and women
with standards that are an unshakable part of our accountability to society. Those standards are
founded on an underlying knowledge of what is right and what is wrong.
And, as physicians, we think of ourselves as knowledgeable and competent professionals with a
distinct understanding of what is right for our patients, and what is not. We know this with complete
confidence. And rarely, if ever, do we find the need to question it.
And, in the most immediate sense, that accountability applies directly to the vulnerable state of the
patients whom we treat.
I like to think that good health is when your body does not talk to you, when it is silent. You are
largely unaware of your body when you are healthy. You don’t consciously think about having an
arm, a head, or a stomach.
But you know very well that you have a back when it aches.
And you know very well that you have a heart when your chest hurts.
It is then that your body talks to you.
We physicians tend to see people when they are most aware of their bodies, when their bodies are
talking to them a lot. Which means that we see them when they are at their most vulnerable.
We see them when they are undressed in every way—physically, emotionally, and spiritually. To see
them so places us in a position of enormous privilege and responsibility.
Because we are all the same when we are naked.
The wise and the foolish.
The mighty and the weak.
The wealthy and the will be gone.
All the same . . . all vulnerable.
And it is this vulnerability that endows the physician with stunning privilege, and an equally
stunning responsibility.
For it is our privilege to shield our patients when they are bare and without defenses.
And to listen to the voice of the patient, not the voice of the disease.
And to clothe them not only with health but also with the ability to thrive once they have left our
care.
And to be their friend, their counselor, their trusted advisor.
These are concerns that apply to every physician in the world. It has nothing to do with national
borders, with ethnicity, or with religious affiliation.
It has everything to do with the framework of humankind that needs our constant support, not just
as physicians but as men and women of sensibility and conscience.
It has everything to do with the achievement and exportation of excellence and it has everything to
do with the Hippocratic Oath, which as a profession we swear.
It has everything to do with putting the patient first, above our own interests.
And we have a great deal to give, a great deal to share with the world.
We must always bear in mind that excellence is elastic. It knows no limits. And it must be
maintained not only by the preservation of the best of the past, but by the brilliance of the future,
by the need to dare, and by the willingness to embrace both innovation and experimentation, and
to stay abreast of these advances.
For excellence is a reflection of spiritual wealth, and the exportation of that wealth is a notion that we
cherish. And to me that notion is what defines the difference between a profession and a calling.
Because a profession is something that you train to do. A profession is something that you can
change; it has an impermanence about it. A profession is something that you are likely to find
routine in later years.
A calling, on the other hand, is something that captures you, entrances and embraces you, and keeps
you enchanted for the rest of your life.
You see, those who have the calling must be healers by conviction, not simply by virtue of a medical
degree.
We become healers when the identifiable purpose of our lives is forever bound up with the relief of
suffering, with the forestalling of death or its embrace when the time has come, and with the creation
of environments where our patients can flourish.
We become healers when the relationship between our patients and us is a covenant of faith, not a
business contract; an article of trust, not simply a fee for services.
We become healers when we come to understand that healing is hard work, for both the patient
and the physician, that the amount of health that we can actually promote is relatively small when
weighed on the scale of human mortality.
And we become healers when we ignore that scale and fight for every inch of health, against the odds,
as if embedded in our fingertips is the ability to create that body that does not talk to you.
These are the sort of healers that our profession cries out for—men and women who are willing to
labor in the trenches.
Who are willing to treat all patients equally.
Who are willing to touch what others see as untouchable.
Who are willing to strive for nothing less than the promise of blood, toil, sweat, and tears in return
for nothing more than the privilege of healing and saving.
To treat each day as if it were your last, and each patient as if he or she were your first.
“We should be ashamed to die until we have won some victory for humanity.”
Saving one life helps save that humanity.
Modified from the Presidential Address of Dr. Douglas Zipes
at American College of Cardiology, March 2002
Abbreviations
ABG Arterial blood gas HOCM Hypertrophic obstructive

ACG Apex cardiogram cardiomyopathy
AF Atrial fibrillation HTN Hypertension
AIDS Acquired immunodeficiency IABP Intra-aortic balloon pump
syndrome ICCU Intensive coronary care unit
AM Acute margin JVP Jugular venous pressure
AMI Acute myocardial infarction L-TGA L-transposition of great arteries
AR Aortic regurgitation LA Left atrium
AS Aortic stenosis LAD Left anterior descending artery
ASD Atrial septal defect LBBB Left bundle branch block
AV Atrioventricular LCA Left coronary artery
BP Blood pressure LCX Left circumflex
CABGS Coronary artery bypass graft LIMA Left internal mammary artery
surgery LLSB Left lower sternal border
CAD Coronary artery disease LMCA Left main coronary artery
CASS Coronary artery surgery study LPSI Left parasternal impulse
CCF Congestive cardiac failure LSB Left sternal border
CCU Coronary care unit LV Left ventricle
CCS Canadian Cardiovascular Society LVEDP Left ventricular end diastolic
CHB Complete heart block pressure
CI Cardiac index LVF Left ventricular failure
CMV Closed mitral valvotomy LVH Left ventricular hypertrophy
CP Constrictive pericarditis LV-RA Left ventricle to right atrium
CT Computerised tomography defect defect
D1 First diagonal MI Myocardial infarction
D2 Second diagonal MR Mitral regurgitation
D-TGA Dextro-transposition of great MRI Magnetic resonance imaging
arteries MS Mitral stenosis
DKA Diabetic ketoacidosis MVO2 Myocardial oxygen consumption
DW Dicrotic wave MVP Mitral valve prolapse
ECG Electrocardiogram MVR Mitral valve replacement
EMF Endomyocardial fibrosis NYHA New York Heart Association
ESM Ejection systolic murmur OM Obtuse marginal
GI Gastrointestinal OMV Open mitral valvotomy
HCM Hypertrophic cardiomyopathy PA Pulmonary artery
PAH Pulmonary arterial hypertension RVF Right ventricular failure
PAW Pulmonary artery wedge RVH Right ventricular hypertrophy
PBMV Percutaneous balloon mitral RVOT Right ventricular outflow tract
valvoplasty S1 First heart sound
PCV Packed cell volume S2 Second heart sound
PCWP Pulmonary capillary wedge S3 Third heart sound
pressure S4 Fourth heart sound
PDA Patent ductus arteriosus SAH Subarachnoid hemorrhage
PD artery Posterior descending artery SAS Specific activity scale
PLVB Posterior left ventricular branch SSS Sick sinus syndrome
PMC Premature mitral closure STK Streptokinase
PMD Papillary muscle dysfunction SVT Supraventricular tachycardia
PND Paroxysmal nocturnal dyspnea TAPVC Total anomalous pulmonary
PPV Positive pressure ventilation venous connection
PR Pulmonary regurgitation TGA Transposition of great arteries
PS Pulmonary stenosis TIA Transient ischemic attack
PTCA Percutaneous transluminal TR Tricuspid regurgitation
coronary angioplasty TS Tricuspid stenosis
PVH Pulmonary venous hypertension TVD Tricuspid valve disease
RA Right atrium VAS Visual analogue scale
RBBB Right bundle branch block VBI Vertebro basilar insufficiency
RCA Right coronary artery VSD Ventricular septal defect
RHD Rheumatic heart disease VT Ventricular tachycardia
RIMA Right internal mammary artery WPW Wolff–Parkinson–White
RV Right ventricle syndrome syndrome
Contents
1. The Science and Art of Medicine 1
2. Patient Presentations 8
3. Cardiovascular Diagnosis 13
4. Functional Categorization of Cardiovascular Disability 21
5. Cardiovascular Dynamics: Basic Considerations 26
6. The Patient’s History 40
7. Evaluation of Chest Pain: Diagnostic and Therapeutic Implications 59
8. Dyspnea 105
9. Syncope 124
10. Palpitation 149
11. Fever in a Patient with Heart Disease 159
12. The Arterial Pulse 176
13. Blood Pressure 206
14. The Jugular Venous Pulse 228
15. The Cardiac Impulse 262
16. Auscultation of the Heart 293
17. The First Heart Sound 297
18. The Second Heart Sound 311
19. The Third Heart Sound 335
20. The Fourth Heart Sound 343
21. Ejection and Non-ejection Clicks 350
22. Heart Murmurs 373
23. Systolic Murmurs 389
24. Diastolic Murmurs 437
25. Continuous Murmurs 477
26. The Pericardial Rub 491
27. Approach to Auscultation 495
Index 498
1 The Science and Art of Medicine
There are qualities beyond pure medical competence that patients need and look for in their physicians.
They want reassurance. They want to be looked after and not just looked over. They want to be
listened to. They want to feel that it makes a difference to the physician.
Norman Cousins
The importance of becoming a doctor is not fully realized by the majority of

students at the time of joining the medical course. Most of us took up medicine
because that was considered the best choice at that time. The students are perplexed
further by the negative attitudes of their own seniors, teachers and the complexity
of the society we live. Having chosen medicine as a profession, the best way to
deal with it is to go all out and not be contented with half hearted efforts at it.
Happiness in life lies in doing something closest to our souls in the best possible
manner. The following paragraph from one of the most respected physicians of
our time emphasizes the scope of medicine in all its dimensions.
No greater opportunity or obligation can fall to the lot of a human being than to become a
physician. In the care of the suffering he needs technical skill, scientific knowledge, and human
understanding. He who uses these with courage, with humility, and with wisdom will provide a
unique service to his fellow man, and will build an enduring edifice of character within himself.
The physician should ask of his destiny no more than this; he should be content with no less.
Tinsely R. Harrison
The limits to medicine are best expressed by Trudeau:

To cure sometimes, to relieve often, to comfort always.
To be able to do this we require to cultivate attitudes that enable us to gain a

broad knowledge of the subject of medicine, technical skills and the wisdom to
use them well. In the dedication to his volume Underwoods, Stevenson wrote:
CLINICAL METHODS IN CARDIOLOGY
There are men and classes of men that stand above the common herd: the soldier, the sailor, and
the shepherd not infrequently; the artist rarely; rarelier still, the clergyman; the physician almost as
a rule. He is the flower (such as it is) of our civilization; and that stage of man is done with, and
only remembered to be marveled at in history, he will be thought to have shared as little as any in
the defects of the period, and most notably exhibited the virtues of the race. Generosity he has, such
as is possible to those who practice an art, never to those who drive a trade; discretion, tested by a
hundred secrets; tact, tried in a thousand embarrassments; and what are more important, Herculean
cheerfulness and courage. So it is that which brings air and cheer into the sick-room, and often
enough, though not as often as he wishes, brings healing.
William Osler maintained that “The practice of medicine is an art, not a

trade; a calling, not a business; a calling in which your heart will be exercised
equally with your head...”
The science of medicine is easily learned in our training. To practice medicine
as an art requires life long commitment and dedication. The practice of any art
requires style. As we practice the art of medicine, develop a style or a manner of
our own, a method by which we deal with our patients, students and colleagues.
The ingredients of an ideal physician involve compassion, gentleness toward
2
patients, a balanced disposition and coolness of mind especially under stress. The
ability to communicate well is particularly important as most of what we do involves
either teaching patients or students.
In his address to the medical students at Harvard Medical School in 1927,
Dr. Peabody said:
The practice of medicine in its broadest sense includes the whole relationship of the physician with
the patient. It is an art based to an increasing extent on the medical sciences but comprising much
that still remains outside the realm of any science. The art of medicine and the science of medicine
are not antagonistic but supplementary to each other. There is no more contradiction between the
science of medicine and the art of medicine than between the science of aeronautics and the art of
flying. Good practice presupposes an understanding of the sciences that contribute to the structure
of modern medicine, but it is obvious that sound professional training should include a much
broader equipment.
The treatment of disease may be entirely impersonal; the care of a patient must be completely
personal. The significance of the intimate personal relationship between physician and patient
cannot be too strongly emphasized, for in an extraordinarily large number of cases both diagnosis
and treatment are directly dependent on it, and failure of the young physician to establish this
relationship accounts for much of his ineffectiveness in the care of patients. What is spoken of as
a clinical picture is not just a photograph of a man sick in bed; it is an impressionistic painting of
the patient surrounded by his home, his work, his relationship, his friends, his joys, sorrows, hopes,
and fears. Thus the physician, who attempts to take care of patient while he neglects those factors
THE SCIENCE AND ART OF MEDICINE
that contribute to the emotional life of his patient, is as unscientific as the investigator who neglects
to control all the conditions that may affect his experiment. The good physician knows his patients
through and through, and his knowledge is bought dearly. Time, sympathy, and understanding
must be lavishly dispensed, but the reward is to be found in that personal bond which forms the
greatest satisfaction of the practice of medicine. One of the essential qualities of the clinician is
interest in humanity, for the secret of the care of the patient is in caring for the patient.
His instruction is even more pertinent today than in 1927. The requisites of a
profession are best summarized by Tuttle and are particularly applicable to medicine.
The professional man is in essence one who provides service. But the service he renders is something
more than that of a laborer, even the skilled laborer. It is a service that wells up from the entire
complex of his personality. True, some specialized and highly developed techniques may be included,
but their mode of expression is given its deepest meaning by the personality of the practitioner. In
a very real sense his professional service cannot be separated from his personal being. He has no
goods to sell, no right price for service, for what is the share of a man’s worth? If he does not
contain the quality of integrity, he is worthless. If he does, he is priceless. The value is either
nothing or it is infinite. So do not set a price on yourself. Do not measure out your professional
services on an apothecary’s scale and say only this for so much. Do not debase yourself by equating
your souls to what they will bring in the market. Do not be a miser, hoarding your talent and
abilities and knowledge either among yourself or in dealing with your clients, patients, flock.
Rather be reckless and spendthrift, pouring out your talent to all to whom it can be of service. 3
Throw it away, waste it, and in the spending it can be of service. Do not keep a watchful eye lest
you slip and give away a little bit of what you might have sold. Do not censor your thoughts to gain
a wider audience. Like love, talent is useful only in its expenditure, and it is never exhausted.
Certain it is that one must eat, so set what price you must, on your service. But never confuse the
performance, which is great, with the compensation, be it money, power, or fame, which is trivial.
All this may be considered too idealistic and impractical by present day
standards and requirements. Everybody is equally concerned about the state of
affairs in medicine today. The best way to deal with this problem appears to be to
take care of one’s own attitudes first. One should avoid being judgmental in dealing
with others but show that right things are still possible, by personal example. Most
of us start as ideal medical students, progress to near ideal postgraduates, good
assistant professors, and finally metamorphose in to that ultimate achievement,
the terrible professor. To maintain these ideals one must constantly struggle.
Systems within which we operate are far from perfect and the personal influence
of the teacher can to some extent compensate for the inadequate academic system.
Cultivate the following qualities and propagate them. Some of the qualities are
elaborated but others are self explanatory.
Qualities of a physician
Enthusiasm
A full personal knowledge of the branch practised/taught
A sense of obligation to teach
The art of detachment
A systematic method
Thoroughness
Honesty
Attitude
Appearance
Humility
Unreserved respect for excellence
The conviction that right things are possible
Certain degree of insensitivity or obtuseness to criticism
Willingness to take another opinion in the best interest of the patient
1. Enthusiasm: One should have deep love for the subject and people. The desire
to teach and care for people, without which all medical knowledge becomes cold
and lifeless. Do not take up a subject that doesn’t interest you for any length of
time. By doing this, you are not only harming yourself but also the patients under
4
your care.
2. A full personal knowledge of the branch taught: Not second hand
information derived from books, but the living experience derived from practical,
well tested experience of a lifetime.
3. A sense of obligation: The feeling which impels a teacher to also be a
contributor, and to add to the stores of medical knowledge from which we so
freely draw to teach and practice medicine.
4. Art of detachment: The faculty of isolating ourselves from the pursuits and
pleasures incident to routine life and an emotional detachment to the diagnoses
we make. In all matters medical, what is right is more important than who is right.
5. Systematic approach: Unless one is a genius, a systematic method is essential
to learn medicine. We must plan each day of ours in such a way that minimum
time is wasted in unnecessary things. What we do daily is going to decide what we
are going to be at the end of a year or two. These few years as a student are going
to make or break your career. The present system of medical education does not
foster competence and conviction in the student or future doctor. By the time the
students finish their course, they are hardly in a position to take care of patients
because they have not spent enough time in the hospital. On many days in a week,
the student neither examines nor even talks to any patient. During their clinical
years, students are not given any clinical responsibilities. In order to learn to deal
with patients they should spend their time taking care of patients as house physicians
or residents do. In the present system, it is not rare that by the time they finish
their medical course, many find it difficult to communicate with patients.
6. Thoroughness: It is essential in all medical matters, be it a preparation for a
talk, examination, or patient evaluation and management.
7. Honesty: The ability to admit a mistake, take another opinion or help when we
are not sure requires courage and conviction on our part. We must conduct
ourselves in an irreproachable manner so that not even the slightest doubt would
be raised about our integrity.
8. Attitude: A doctor should be tolerant and patient. We should avoid judging
people and taking sides because we undertake to take care of everybody irrespective
of their origin or status.
5
9. Appearance: We must pay attention to appearance and behaviour as society
often tends to judge us on this basis. A dignified and cheerful manner is particularly
important in dealing with sick people.
10. The grace of humility: Whatever excellence one achieves in medicine, there
can never be perfection in it. There are always places to go and people to meet
from whom we can learn to do better things. This realization makes us humble
and without this quality, one stands out as an intolerable character.
11. Unreserved respect for excellence: Excellence in any branch of science or
medicine, from whatever person, institution or country it emanates, should be
respected and duly acknowledged. It is true that healthy competition or rivalry
helps in achieving the higher objectives in medicine, but when carried too far, it
becomes counter-productive.
12. Unswerving conviction that good things are possible: In the present
atmosphere of medical practice and medical education, contributed to by the
profession, the politician, the bureaucrat, it is easy to give up all hope of doing
anything extraordinary and to become part of the corrupt system. Only the strong
conviction that right things are still possible and the courage to withstand the
pressures and put up with criticism helps to achieve the desired goals. These ideals
should be maintained in spite of heavy odds in one’s day to day work. The best
time to start learning these attitudes is now when one is a student although it is
never too late even for an older doctor. The attitude towards friends, classmates,
seniors, juniors, patients and their families is an indicator of what one is going to
be. This is the time one must learn to interact with people and patients. It is not
enough to be a good student. One must strive to be a likable person in the college,
hospital, and home. Once cultivated, these habits like bad habits, are contagious.
The best target is the students at various levels who are yet to be spoiled by exposure
to the tricks of the trade of medicine today.
While examining and evaluating patients
Tact, sympathy and understanding are expected of the physician, for the patient is no mere collection
of symptoms, signs, disordered functions, damaged organs, and disturbed emotions. He is human,
fearful and hopeful, seeking relief, help and reassurance. To the physician as to the anthropologist,
nothing human is strange or repulsive. The misanthrope may become a smart diagnostician of
organic disease. But he can scarcely hope to succeed as a physician. The true physician has a
6 Shakespearean breadth of interest in the wise and the foolish, the proud and the humble, the stoic
hero and the whining rogue. He cares for people.
Tinsely R. Harrison
While we do our best we should be prepared to face thanklessness and even

exploitation from some people. A certain degree of obtuseness or insensitivity to
criticism is sometimes necessary in a professional.
Finally, all that is done in medicine is based on the conviction, that human
life is valuable and human beings require to be treated with dignity and respect. As
a doctor if your first reaction to the person is suspicion and hatred, one should
not pursue a career in clinical medicine. Those of us who are religiously oriented
should realize that our religion is medicine and all other religions pale before it.
A good example is the best sermon.
(Anonymous)
With the rapid advances that occurred in the last decade, medicine has become
more remunerative and extremely competitive. The competitive atmosphere
brought out the best in some individuals and institutions leading to superlative
performance. However some institutions and individuals wilted morally under
this pressure and took recourse to devious methods of dealing with the problem.
For them, each patient is a prospect on whom almost all tests and few procedures
can be done. They later call up the referring doctor and tell him or her how much
money can be made on that patient. Unnecessary investigations, surgeries, or
interventions have become commonplace. However the system of fee-splitting is
destroying the soul of medical practice. This practice takes away all the trust that
patients come to us with. This distrust will continue to grow if medicine is debased
with such practices.
The tragedy of life is what dies inside a man while he lives.
7
2 Patient Presentations
Nothing clarifies the issue better than stating the case to someone else.
Sherlock Holmes
The way one presents a patient’s case is an expression of the way of thinking and
perception of the patient’s problem. Presenting the patient’s case is an art that can
be described only partly but can be learned with practice.
8 OUTLINE OF PRESENTATION
There are two varieties of presentations:

1. Short or brief presentations,
2. A complete 7–10 minute presentation.
A good presentation requires sufficient knowledge of the patient and writing
up the patient details. The index card or a note book are best suited for this
purpose. In the initial stage of your career a number of facts may have to be
written, but as your experience increases, you need to write less.
Note the following features (on index card)

1. Patient information : Address, referring doctor with phone number
2. The introductory :
sentence
3. Chief complaint : Note salient points
and duration
4. History of : Relevant negative and positive history, family history, risks
present illness
PATIENT PRESENTATIONS
5. Past medical history : Note active problems

(PMH)
6. Allergies : For drugs, foods, type of reaction
7. Drug therapy : Past, present and response. Alcohol, tobacco
8. Review of systems : Note any positive history
(ROS)
9. Physical exam (PE) : Introductory sentence, vital signs. Only positive findings
10. Lab tests : Positive findings
11. Problem list :
OUTLINE OF BRIEF PRESENTATION

The brief presentation is a 2–3 minute summary for the service round in the
morning. It is intended to orient the members of the team who do not know the
patient at all (or chiefs who come for the round only to have some fun).
1. Introductory :
sentence 9
2. Chief complaint :
3. History of : In a condensed form, summarize the history of the present illness
present illness and duration
4. Drugs :
5. Physical : General condition, good, stable, unstable, drowsy, comatose
examination
Vital signs : Stable, or those that are abnormal
6. Relevant lab : Positive findings
tests
7. Summary : Brief
8. Plan : Of what is to be done next. For example, waiting for discharge
or angiogram.
General principles of brief presentation

1. This is intended to apprise the members of the team and elicit their opinion
of the patient.
2. Any additional information can be provided if asked for.
3. Speak clearly and decisively.
4. Bring out the active problems and also what investigation is awaited. This is
helpful in taking over patients and to cover patients at night. This ensures
continuity of care.
Brief presentation (sample)

This is Mrs. R.S.’s case and is the 4th day of hospitalization. She is a 50-year-old
Hindi speaking housewife with a history of uncontrolled hypertension and diabetes.
She was hospitalized with prolonged chest discomfort typical of acute myocardial
infarction more than 12 hours after the onset of pain. She was taking
Hydrochlorthiazide 25 mg per day and Enalapril 15 mg twice a day. On physical
examination, she is stable with stable vital signs. Pulse: 64/min, regular; respiratory
rate: 20/min; BP:130/90 mmHg; JVP: normal, no cardiac enlargement, LV S4
was heard. Lungs: clear; other systems: Normal.
Lab tests: ECGs showed serial changes of acute inferior MI
Today’s ECG: Normal sinus rhythm, 64/min regular, P-R=0.20 sec and features
of transmural inferior MI without RV infarction lateral extension or true posterior
MI. Other lab tests are normal. X-ray chest is normal.
10 Presently she is on isosorbide dinitrate 10 mg three times a day, aspirin
325 mg/day and diazepam 5 mg twice a day.
Plan: She is waiting to complete the hospital course of 1 week and have an
echocardiogram and functional testing prior to discharge.
FORMAL DETAILED PRESENTATION

1. Patient information: 48-year-old business-man was perfectly well before
14 April etc.
2. Introductory sentence:
3. Chief complaints and duration: In the presentation, unlike write up, avoid
using the patient’s words. Give the description that focuses quickly on the
problem at hand.
4. History of present illness: Present a succinct version of the history of present
illness. Give positive findings from review of systems section. Mention risk
factors and family history.
5. Past medical history: Prior admissions, other active medical problems,
investigations done in the past and their results.
PATIENT PRESENTATIONS
6. Allergies: Drug reactions

7. Medications: All present drugs with their dosage and response to them.
8. Review of other systems: Positive features, pertinent positive symptoms other
than those mentioned during history of present illness.
9. Physical examination: Introductory sentence describing appearance and
condition. (e.g.: patient comfortable, toxic or in respiratory distress, etc.)
Vital signs
Pertinent positive findings
10. Lab tests: Pertinent positive and negative reports if they are significant.
11. Summary: Give a brief 2–3 sentence summary and then pause so that the
discussion is initiated by the consultant.
Case presentation guidelines

1. The routine round is initiated by the case presentation of the previous night’s
admissions. The following aspects are usually discussed.
• Symptoms of the patient, their interpretation, conclusions drawn
• Physical signs, their pathophysiology
• Differential diagnosis 11
• Pathophysiologic mechanisms
• Complications of the disease
• Tests to ask for, their interpretation, sensitivity, specificity
• Drug therapy: Indications, contraindications, side effects, findings from
major trials completed and ongoing
• Future plan
• Natural history of the disease diagnosed
• Indications and results of interventions, findings from major studies.
2. You must feel confident and look confident. When you present a patient
with mitral stenosis, even if others in the room know more about mitral
stenosis, your patients’s mitral stenosis is better known to you.
3. Speed of presentation: Relax and speak as though you are talking to your
friends (on a serious issue).
4. Do not read your presentation.
5. Speak precisely: Do not say the blood pressure is around 120/80 mmHg. Say
the blood pressure is 120/80 mmHg.
6. Speak briefly: The brief presentation is meant to be brief. Even the formal
presentations should be succinct.
7. Omissions/condensations: Describe only the positive and negative findings
relevant to the patient at hand. Purposefully omit the details that are not
relevant to the ‘argument’ you are putting forward.
8. Physical findings: It is common at all levels of clinical experience to have
equivocal physical findings. Present your findings ‘if others disagreed, simply
say, another observer thought differently’.
9. At the end of the history, physical exam and lab data presentations, summarize
the case in two or three sentences. For example, in summary, Mrs. M 58-year-
old with history of hypertension, diabetes and hyperlipidemia, presented with
acute inferior infarction of 4 hours duration and has no contraindication to
thrombolytic therapy.
10. Hospital course: For patients with multiple active problems describe the
hospital course in a problem oriented manner.
11. When you are proven wrong by the bedside : Patients often change histories.
This happens frequently to all of us and one should not feel inadequate or
12 annoyed about it. Consider the implications of the new information made
available.
12. The patient is the centre of importance: It is a good practice to have the
presentations away from the patient’s bedside. If the patient interrupts the
discussion by some questions or information answer those first. Do not use
words like death, severe, irreversible etc., in front of the patient. They are
likely to be misinterpreted and misunderstood.
13. In all matters medical, what is right is more important than who is right.
Do not get emotionally attached to the diagnosis you make.
In order to learn from the experience of an individual patient, you must
read about each of them while they are under your care. Reading about each
patient involves reading and discussing about their symptoms, signs, diagnosis,
differential diagnosis, laboratory tests, the drugs and any interventions when
applicable. This should be done by the end of the day.
3 Cardiovascular Diagnosis
During ward rounds and bedside discussions one may sometimes come across
the resident doctor giving an incomplete diagnosis after a painstaking description
of the history and physical findings. This is a disappointing and annoying sight
for the teacher.
A comprehensive cardiovascular diagnosis is a prerequisite for appropriate
decision-making in patients with heart disease.
Components of cardiac diagnosis
Etiologic
Anatomic defect with severity
Functional derangement with severity
Rhythm and rate
Associated lesions
Complications
Functional categorization
Specific recommendations
Diagnostic
Therapeutic
For example, in a patient with valvular disease (mitral stenosis) the expression
should be:
• Chronic rheumatic heart disease
• Mitral stenosis (severe) calcific, severe subvalvular fusion
• Pulmonary arterial hypertension (severe)
• Right ventricular failure (severe)
• Tricuspid regurgitation functional (severe)
• Atrial fibrillation (ventricular rate=120/min)
• NYHA functional class IV
• No rheumatic activity
• No infective endocarditis.
The importance of each of these features can not be overemphasized. Mild
mitral stenosis does not require any intervention but moderate or tight mitral
stenosis needs surgery. A calcified valve/subvalvular fusion makes the valve
unsuitable for closed mitral valvotomy (CMV), and an open valvotomy (OMV)
may be suitable for milder subvalvular fusion. Mitral valve replacement (MVR)
may be the only choice when the valve is calcific with subvalvular fusion. As the
severity of pulmonary arterial hypertension (PAH) increases, the risk of surgery
also increases.
Right ventricular failure (RVF) and tricuspid regurgitation (TR) have similar
implication and require control with digitalis and diuretics before surgery. Atrial
fibrillation (AF) in a young person with mitral stenosis usually means a tight and
longstanding lesion. It is important to make a note of the ventricular rate in atrial
fibrillation as rapid rates aggravate pulmonary venous hypertension (PVH) and
precipitate pulmonary edema by reduction in diastolic filling time. Digitalis is the
drug of choice to reduce the ventricular rate. Due to the risk of peripheral
14 embolism, anticoagulants are indicated in atrial fibrillation. The risk of surgery is
very high in patients with class IV (NYHA) and is low with class II and III.
CONGENITAL HEART DISEASE
Broadly two categories exist: acyanotic and cyanotic. For example, when a diagnosis
of atrial septal defect is made, the diagnostic expression should be:
Congenital acyanotic heart disease
Left to right shunt
Atrial septal defect (ostium secundum)
Pulmonary to systemic flow ratio of > 2:1
Pulmonary arterial hypertension (mild) hyperkinetic
No congestive cardiac failure
Normal sinus rhythm
Class II (NYHA), no associated defects.
In left to right shunts, the following features should be noted; these are
particularly applicable to ventricular septal defects.
a. Site of the defect
CARDIOVASCULAR DIAGNOSIS
b. Size of the defect

c. Number of defects
d. Shunt pattern : left to right, balanced or right to left
e. Pulmonary to systemic flow ratio (>2:1 or < 2:1)
f. Pulmonary arterial hypertension. presence/absence and severity. Flow
dependent (hyperkinetic) or resistance dependent (fixed)
g. Congestive cardiac failure
h. Associated defects
i. Isolated or part of a complex defect
j. Presence or absence of infective endocarditis, and
k. Height, weight, head circumference and growth percentile.
The NYHA functional categorization is not applicable in children.
CYANOTIC HEART DISEASE
Two forms exist:

increased pulmonary flow, and reduced pulmonary flow. Normal pulmonary flow
is not possible with any cyanotic heart disease. 15
Example:
Congenital cyanotic heart disease,
Diminished pulmonary blood flow,
Tetralogy of Fallot (mild/moderate/severe),
No congestive cardiac failure,
Normal sinus rhythm,
Height, weight, head circumference, growth percentile
Presence or absence of spells, brain abscess, infective endocarditis.
Any increased pulmonary blood flow in cyanotic heart disease, indicates some
form of transposition of great arteries or pulmonary veins (D-TGA or TAPVC)
or an admixture lesion like single ventricle or double outlet right ventricle.
Example:
Congenital cyanotic heart disease,
Increased pulmonary blood flow,
D-transposition of great arteries,
Ventricular septal defect (large),
Congestive cardiac failure,
Pulmonary arterial hypertension (hyperkinetic),

Height, weight, head circumference, growth percentile.
CORONARY ARTERY DISEASE
The common clinical syndromes are:

Chronic stable angina
Acute myocardial infarction
Unstable angina.
Example:
Coronary artery disease
Acute anterior myocardial infarction of 3 hours duration
Past chronic stable angina of 2 years duration
No past myocardial infarction
Normal sinus rhythm, ventricular ectopics <6/min
Hemodynamic subset: left ventricular failure mild
No evidence of acid peptic disease or contraindication to thrombolytic therapy
16 Time from the onset of pain in acute myocardial infarction is important as
interventions to prevent myocardial necrosis are most useful in the first 6 hours.
Previous history of chronic stable angina is indicative of obstructive coronary
disease progressing to acute myocardial infarction and coronary spasm is unlikely.
In the initial evaluation of acute myocardial infarction, spasm needs to be
distinguished from obstructive coronary disease. Rhythm is particularly important,
as most of the deaths in the first few hours of myocardial infarction are due to
arrhythmias. Hemodynamic categorization is essential to intelligent management
of all patients with acute myocardial infarction.
In chronic stable angina the diagnosis should include:
Angiographic right coronary 75% lesion, concentric, short segment
Normal left ventricle function/no regional wall motion abnormality
Chronic stable angina; functional Class III (2 years); no recent change
Mixed angina
No congestive cardiac failure
Normal sinus rhythm 100/min
No previous myocardial infarction
Risks: Hypertension mild, and

Plan: Medical therapy/Suggest angioplasty.
Duration of angina: When it is of more than one year duration the coronary
lesion is usually non-calcific and responds well to percutaneous transluminal
Table 3.1: Hemodynamic subsets of AMI
Subset PA (mean) PAWmmHg CI l/min/m2 Action Remarks
mmHg
1. Normal <15 <12 2.5–3.5 None
2. Hyperdynamic <15 <12 3.0 β-blockers Tachycardia,
HTN
3. Hypotension <15 <9 < 2.7 Volume Reclassify
+ hypovolemia load after PAW is
14–18 mmHg
4. LVF, mild >22 18–22 < 2.5 Diuretic Dyspnea,
Vasodilator Lung rales
5. LVF, severe >25 >22 < 1.8 IABP Lung edema
PPV
6. Cardiogenic >22 >18 < 1.8 IABP 17
shock Dopamine
Dobutamine
Emergent
PTCA/CABGS
PPV = Positive pressure ventilator, IABP = Intraaortic balloon pump.
Table 3.2: Mortality in AMI
Based on clinical examination Based on invasive monitoring
Class Definition GUSTO-I Subset Definition Mortality

Mortality (%)
(%) I Normal hemodynamics
I Rales and S3 absent 5.1 PCWP < 18. CI > 2.2 2
II Rales over <50% of 13.6 II Pulmonary congestion
lung PCWP > 18. CI < 2.2 10
III Rales over >50% of 32.2 III Peripheral hypoperfusion
lung fields (pulmonary PCWP < 18. CI > 2.2 22
edema) IV Pulmonary congestion and
IV Shock 57.8 Peripheral hypoperfusion
PCWP > 18. CI < 2.2 56
coronary angioplasty (PTCA). Beyond an year, calcific lesions with diffuse and
multivessel disease are more likely and are unsuitable for PTCA. With the exception
of left main disease, Canadian Cardiovascular Society class I and II patients do
well with medical therapy and do not need surgery whereas class III and IV patients
are benefited by coronary bypass graft surgery. The classic exertional angina or
fixed threshold angina is due to obstructive coronary disease and responds to
betablockers. In variable threshold angina, dynamic obstruction caused by
vasoconstriction plays an important role in causing myocardial ischemia. The person
may be capable of substantial physical activity at one time, while at another time
minimal activity results in angina. Most of these patients have an underlying fixed
obstruction with superimposed spasm. The term mixed angina is applied to this
group of patients and they are best treated by calcium blockers and betablockers.
Betablockers alone may aggravate spasm. Heart rate has obvious implication in
selecting drug therapy.
PRIMARY MYOCARDIAL DISEASE
18 Is the structural and functional abnormality of heart muscle unrelated to

• Valvular
• Coronary
• Hypertensive
• Pericardial and pulmonary disease?
If the answer is yes, a diagnosis of cardiomyopathy is made. Once the diagnosis
of cardiomyopathy is made, the following questions should be asked.
1. Is it acute or chronic?
2. Is it focal or diffuse?
3. Which clinical syndrome?
a. Congestive (dilated)
b. Restrictive
c. Obliterative
d. Hypertrophy: obstructive or non-obstructive
4. Is there myocardial failure?
5. Is there AV valve regurgitation?
6. Is there an arrhythmia?
7. Are there any identifiable etiologic factors?
8. Functional categorization (NYHA)

Examples:
Cardiomyopathy, chronic diffuse congestive
Biventricular failure
Mitral regurgitation (functional)
Paroxysmal atrial tachycardia
Chronic alcoholism
Class III NYHA
Classification of cardiomyopathies
Specific cardiomyopathies
• Ischemic cardiomyopathy
• Valvular cardiomyopathy
• Hypertensive cardiomyopathy
• Inflammatory cardiomyopathy
Myocarditis
Idiopathic 19
Autoimmune
Infectious
Chagas disease
HIV
Enterovirus
Adenovirus
Cytomegalovirus
Bacterial (endocarditis/myocarditis)
Metabolic
• Endocrine
Thyrotoxicosis
Hypothyroidism
Adrenal cortical insufficiency
Pheochromocytoma
Acromegaly
Diabetes mellitus
• Familial storage disease/infiltration

Hemochromatosis
Glycogen storage disease
Hurler’s syndrome
Refsum’s syndrome
• Neimann–Pick disease
Hand–Schuler–Christian disease
Febry–Anderson disease
Morquito–Ullrich disease
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Arrhythmogenic right ventricularcardiodysplasia
Unclassified cardiomyopathies
20 • Atypical presentation
Fibroelastosis
Non-compacted myocardium
Systolic dysfunction without dilation
Mitochondrial cardiomyopathy
• Mixed presentation
Amyloidosis
Hypertension
4 Functional Categorization of
Cardiovascular Disability
Most diseases have an effect on the functional capacity of the patient. In

cardiovascular disease, the severity of the functional loss is also an important
marker of the prognosis.Often this decides the therapeutic choice. Three methods
are presently used to classify the severity of cardiovascular disease in terms of
functional capacity.
• New York Heart Association functional classification (NYHA)
• Canadian Cardiovascular Society functional classification (CCS)
• Specific Activity Scale of Goldman (SAS)
The NYHA classification is widely used and is applicable to any symptom
that is disabling. The CCS classification is applicable only to angina pectoris and is
currently used in all clinical trials on coronary artery disease. The SAS classification
is more objective but is used less often.
NYHA FUNCTIONAL CLASSIFICATION
Class 1: Patients with cardiac disease but without resulting limitations of physical
activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea
or anginal pain.
Class 2: Patients with cardiac disease resulting in slight limitation of physical
activity. They are comfortable at rest. Ordinary physical activity results in fatigue,
palpitation, dyspnea or anginal pain.
Class 3: Patients with cardiac disease resulting in marked limitation of physical
activity. They are comfortable at rest. Less than ordinary physical activity causes
fatigue, palpitation, dyspnea, or anginal pain.

Class 4: Patients with cardiac disease resulting in inability to carry on any physical
activity without discomfort. Symptoms of cardiac insufficiency or of the anginal
syndrome may be present even at rest. If any physical activity is undertaken,
discomfort increases.
CCS FUNCTIONAL CLASSIFICATION FOR ANGINA
Class 1: Ordinary physical activity, such as walking and climbing stairs, does not
cause angina. Angina with strenuous or rapid or prolonged exertion at work or
recreation.
Class 2: Slight limitation of ordinary activity. Walking or climbing stairs rapidly,
walking uphill, walking or stair climbing after meals, in cold weather, in wind, or
when under emotional stress, or only during the few hours after waking, walking
more than two blocks on level ground and climbing more than one flight of
ordinary stairs at a normal pace and in normal conditions.
22
Class 3: Marked limitation of ordinary physical activity. Walking one or two blocks
on level ground and climbing more than one flight in ordinary conditions.
Class 4: Inability to carry on any physical activity without discomfort. Anginal
syndrome may be present at rest.
SPECIFIC ACTIVITY SCALE (SAS)
The intensity of physical activity can be expressed in metabolic units (MET or

metabolic equivalents of oxygen consumption). The metabolic unit is the ratio of
metabolic rate during exercise to metabolic rate at rest. One metabolic unit
corresponds to energy expenditure of approximately 1 kcal per kg of body weight
per hour, or an oxygen uptake of 3.5 ml per kg per minute.
Class 1: Patients can perform to completion any activity requiring 7 metabolic
equivalents, for example, he can carry 24 lb up eight steps, carry objects that
weigh 80 lb (35 kg), outdoor work like spade soil, recreational activities (jog/walk
5 mph or about 8 kmph)
FUNCTIONAL CATEGORIZATION OF CARDIOVASCULAR DISABILITY

equivalents but cannot and do not perform to completion activities requiring
>7 metabolic equivalents, for example, have sexual intercourse without stopping,
garden or walk at 4 mph (6 kmph) on level ground.
equivalents but cannot and do not perform to completion any activities requiring
>5 metabolic equivalents, for example, shower without stopping, strip and dress
without stopping, walk 2.5 mph (4 kmph)
Class 4: Patients cannot and do not perform to completion activities requiring
>2 metabolic equivalents, cannot carry out activities listed under class 3.
Whatever method is employed, it is good practice to specify the functional
class with therapy or without therapy. Further it should be understood that this
method of evaluation is best suited for certain types of heart disease only and in
situations like arrhythmias, the functional classifications become irrelevant. Also
certain dynamic pathophysiological conditions and non-cardiac illnesses like anemia
may suddenly change the functional class of the patient.
23
NATURE OF WORK
Sedentary work: Sedentary work is defined as ‘lifting maximum 10 lb and

occasionally carrying such articles as books, ledgers, and small tools. Although a
sedentary job usually involves sitting, a certain amount of walking and standing
may be necessary in carrying out duties associated with the job. Jobs are sedentary
if walking and standing are required only occasionally and other sedentary criteria
are met’.
Light work: Light work involves ‘lifting maximum 20 lb with frequent lifting and
carrying of objects weighing up to 10 lb. Even though the weight lifted may be
only a negligible amount, a job is included in this category when it requires walking
or standing to a significant degree, or when it involves sitting most of the time
with a degree of pushing and pulling of arm and or leg controls’.
Medium work: This includes ‘lifting 50 lb maximum with frequent lifting and/or
carrying of objects weighing up to 50 lb’.
Heavy work: This is defined as ‘lifting 100 lb maximum with frequent lifting
and/or carrying of objects weighing up to 50 lb’.
Very heavy work: This involves ‘lifting objects in excess of 100 lb with frequent
lifting and/or carrying of objects weighing 50 lb or more’.
Both men and women who did more than 2 hours of conditioning physical activity a week
and men with a maximal oxygen uptake of at least 2.7 litres per minute, or 34 ml per kg per
minute (10 METS exercise capacity) had less than half the risk of acute myocardial infarction
of the least active or the least fit men.
Table 4.1: Assessing cardiovascular disability
Canadian Cardiovascular Society functional classification Specific Activity Scale
Ordinary physical activity, such as walking Patients can perform to completion any activity
and climbing stairs does not cause angina. requiring ≤ 7 metabolic equivalents, e.g. can
Angina with strenuous or rapid or carry 24 lb up eight steps; carry objects that weigh
prolonged exertion at work or recreation. 80 lb; do outdoor work (shovel snow, spade soil);
and do recreational activities (skiing, basketball,
squash, handball, jog/walk 5 mph).
Slight limitation of ordinary activity. Walking Patients can perform to completion any activity
24 or climbing stairs rapidly, walking uphill, requiring ≤5 metabolic equivalents, e.g., having
walking or stair climbing after meals, in sexual intercourse without stopping, roller-skate,
cold, in wind or when under emotional stress, rake, dance, fox trot, walk at 4 miles per hour on
or only during the few hours after awakening. level ground, but cannot and do not perform to
Walking more than two blocks on the completion activities requiring ≤7 metabolic
level and climbing more than one flight of equivalents.
ordinary stairs at a normal pace and in normal
conditions.
Marked limitation of ordinary physical activity. Patients can perform to completion any activity
Walking blocks on one to two the level and requiring ≤2 metabolic equivalents, e.g., shower
climbing more than one flight in normal without stopping, strip and make bed, clean
conditions. windows, walk 2.5 mph, bowl, play golf, dress
without stopping, but cannot and do not perform
to completion any activities requiring ≤5 metabolic
equivalents.
Inability to perform any physical activity Patients cannot or do not perform to completion
without discomfort. Anginal syndrome activities requiring ≤2 metabolic equivalents.
may be present at rest
Adapted from Goldman L, Cook EF, Loscalzo A. Comparative reproducibility and validity of systems for assessing
cardiovascular functional class: Advantages of a new specific activity scale. Circulation 1981; 64:1227.
FUNCTIONAL CATEGORIZATION OF CARDIOVASCULAR DISABILITY
Table 4.2: NYHA functional classification

Class New York Heart Association functional classification
I Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical
activity does not cause undue fatigue, palpitations, dyspnea, or anginal pain.
II Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable
at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
III Patients with cardiac disease resulting in marked limitation of physical activities. They are comfortable
at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain.
IV Patients with cardiac disease resulting in inability to perform any physical activity without discomfort.
25
5 Cardiovascular Dynamics:
Basic Considerations
It is essential to know intracardiac pressures and flows for a proper understanding

of cardiovascular disease. Often, the student feels that the knowledge of cardiac
hemodynamics is unnecessary for a student and is only meant for specialists.
It must be realized that this is a prerequisite for a proper understanding of the
patient’s symptoms or signs and the results of any laboratory test.
26
SVC RPVs
70% 100%
RA LA
<7mmHg <12mmHg LPVs
IVC
70% 100% 100%
70%
RV LV
25/EDP 7mmHg 120/EDP 12mmHg
70% 100%
MPA Aorta
25/12mmHg 120/80
70% 100%
Fig. 5.1: Depiction of normal intracardiac pressures and oxygen saturation in various cham-
bers
CARDIOVASCULAR DYNAMICS: BASIC CONSIDERATIONS
Normal aortic pressure is 120/80 mmHg. The left ventricular peak systolic
pressure and aortic systolic pressure are equal as there is no pressure difference
across a normal aortic valve and left ventricle; it behaves as a common chamber
in systole. The left ventricular end-diastolic pressure is normally < 12 mmHg. In
diastole when the mitral valve is open, the left ventricle and atrium behave like
a common chamber, and thus the left atrial mean pressure does not normally
exceed 12 mmHg. Pulmonary capillary wedge pressure (< 12 mmHg) reflects
the pressure in pulmonary veins, which are in continuity with left atrium. In the
absence of pulmonary vascular disease, the pulmonary artery diastolic pressure
is equivalent to the capillary wedge pressure. Thus all these five pressures – left
ventricular diastolic, left atrial mean, pulmonary venous, pulmonary capillary wedge
and pulmonary artery diastolic – are equal in the absence of disease.
Thus,
LV diastolic pressure = LA mean pressure = Pulmonary venous pressure
= Pulmonary capillary wedge pressure = Pulmonary artery diastolic pressure =
12 mmHg
Consequently, in routine practice the measurement of pulmonary artery
pressure will give information about the left heart filling pressures. Similarly on 27
the right side, the peak right ventricular pressure is equal to pulmonary artery
systolic pressure, and the right ventricular diastolic pressure is equal to mean right
atrial pressure and the jugular venous pressure. Normal values for hemodynamic
parameters are given in Table 5.1 and Table 5.2.
The oxygen saturation of blood returning from tissues is around 70 per cent
as 5 ml of oxygen per 100 ml blood is normally extracted in the tissues. After
oxygenation in the lungs, the saturation becomes 100 per cent in the left sided
chambers starting with pulmonary veins. As bronchial veins drain into pulmonary
veins, and myocardial veins or thebesian veins drain directly into the left ventricle,
saturation in the left ventricle may not always be 100 per cent but is usually above
95 per cent. Step-up or step-down at any chamber level is indicative of either left
to right or right to left shunt.
CARDIAC OUTPUT
Normal cardiac function is the ability to pump adequate blood, commensurate with
the tissue need, even at maximal exercise without elevation of filling pressures.
Table 5.1: Normal values for hemodynamic parameters and wave patterns
Pressures (mmHg)
Systemic
Peak systolic 100–140
End-diastolic 60–90
Mean (Diastolic
+ 1/3 of pulse pressure)
Left ventricle
End-diastolic 3–12
Left atrium or pulmonary wedge
Mean 3–10
a wave 3–12
v wave 3–12
Pulmonary artery
End diastolic 4–12
Mean 9–18
Right ventricle
28 End diastolic 4–12
Right atrium
Mean 2–7
a wave 3–10
v wave 3–10
Table 5.2: Cardiac output and vascular resistance
Cardiac output 4–8 l/min

Cardiac index 2.6–4.2 l/min
Systemic vascular resistance 700–1600 dynes/sec/cm5
Pulmonary vascular resistance 20–120 dynes/sec/cm5
Oxygen consumption 110–150 ml/min/m2
Arteriovenous oxygen difference 30–50 ml/l
The cardiac output is determined by four major factors: preload, afterload,

contractility and heart rate (Table 5.3).
At any measure of contractility, the extent of muscle fibre shortening varies
directly with preload, and inversely with afterload. The preload is the venous return
and the afterload is the systemic vascular resistance or aortic pressure. Apart
from systemic vascular resistance, afterload is influenced by all the factors that
constitute aortic impedance. Aortic impedance is the ratio of pressure to flow
in the aorta, and is determined by the physical properties of blood and vascular
wall (Table 5.4).
The preload, afterload and contractility are often altered in cardiovascular
disease (Table 5.5).
There are serious limitations in using cardiac output as a measure of cardiac
performance. The cardiac output may remain normal at rest even in heart failure
but may fail to increase with exercise. This is because of alterations in preload
in heart failure.
Ejection fraction
Ejection fraction is a better measure for evaluating systolic emptying of the heart
(Table 5.6).
Ejection fraction (EF) = End-diastolic volume – End-systolic volume
End-diastolic volume
(Normal: 55–80%) 29
Table 5.3: Determinants of cardiac output
Determinant Definition
Preload Load the ventricle has to overcome before it begins contracting
Afterload Load the ventricle has to overcome after it begins contracting
Contractility Intrinsic ability of the heart muscle to contract independent of preload
and afterload
Heart rate The rate at which the heart pumps blood
Table 5.4: Factors influencing aortic impedance
Physical properties of blood Viscosity of blood

Anemia
Polycythemia
Density of blood
Physical properties Diameter of aorta
of vascular wall Viscoelasticity of aorta
Reflected pressure and flow waves
Table 5.5: Alterations in preload, afterload and contractility
Preload Afterload Contractility

Increased in Increased in Increased in
Supine/leg raising Left side Catecholamines
Volume infusion Systemic HTN Tachycardia
Renal failure Aortic stenosis Beta-2 stimulants
Regurgitant lesions Coarctation of aorta
MR/AR Right side
TR/PR PAH
Left to right shunts PS
VSD/PDA/ASD Either side
Hyperkinetic states Polycythemia
Anemia
Decreased in Decreased in Decreased in
Hypovolemia Left side Myocardial ischemia/
Hemorrhage MR infarction
GI loss of fluid Vasodilators Myocarditis
Pregnancy Cardiomyopathy
AV fistula, PDA Drugs (betablockers,
Severe anemia calcium blockers,
Fever disopyramide)
30 Right side
TR
Pulmonary AV fistula
Pulmonary vasodilators
Oxygen
Prostaglandins
Table 5.6: Ventricular volumes
LV end-diastolic volume 72 ± 15 ml/m2

LV end-systolic volume 20 ± 8 ml/m2
Ejection fraction 55–80%
The stroke volume, that is, volume of blood ejected in to aorta per beat (end
diastolic volume – end systolic volume) may be maintained normally in heart
failure by the compensatory increase in ventricular end-diastolic volume. From
a normal end-diastolic volume (say 100 ml) a normal stroke volume (say 60 ml)
ejected is a reflection of normal systolic performance of ventricle with a normal
ejection fraction of 60 per cent. If the cardiac efficiency or ejection fraction
decreases from, say 60% to 30% stroke volume may decrease from 60 ml to 30
ml at an end-diastolic volume of 100 ml. However, the heart compensates by
increasing end-diastolic volume from 100 ml to 200 ml (increase in preload). At
end-diastolic volume of 200 ml, with an ejection fraction of 30% stroke volume
will remain 60 ml. Thus, the heart compensates with increase in end-diastolic
volume in the face of decreased efficiency.
Left ventricular ejection fraction may be characterized as follows. Normal
left ventricular ejection fraction is above 56% (Mild LV dysfunction: 40–50%,
Moderate LV dysfunction: 30–40%, Severe LV dysfunction: < 30%)
Cardiac output = Heart rate x Stroke volume
(Normal: 4–8 L/min)
Cardiac index = Cardiac output / BSA
(Normal: 2.6–4.2 L/min/m2)
Systemic vascular resistance (SVR) = Mean aortic pressure – Mean RA pressure × 80

Cardiac ouput
(Normal: 700-1600 dynes/sec/cm–5.)

Pulmonary vascular resistance (PVR) = Mean PA pressure – Mean RA pressure × 80 31
Pulmonary blood flow (Qp)
(Normal: 20–120 dynes/sec/cm–5.)
CALCULATION OF VALVE AREA
Table 5.7: Valve areas (area in cm2 and area index in cm2/m2)
Normal or Mitral valve Aortic valve Tricuspid valve Pulmonary
abnormal valve
Normal 4–6 2.6–3.5 5.0–10.0 2.0–3.0
Mild stenosis
Area 1.5–2.5 > 1.5 < 5.0 > 1.5
Area index > 0.9
Moderate stenosis
Area 1.0–1.5 1.0–1.5 < 0.8
Area index 0.6–0.9
Severe stenosis
Area < 1.0 < 1.0 < 0.5
Area index 0.4–0.6 < 0.4
The normal function of a valve is to allow free forward flow and prevent any
backward flow. When the valve becomes narrow due to any reason, the flow
across the valve is directly proportional and the transvalvular pressure gradient
is inversely proportional to the valve area. Gorlin and Gorlin have provided the
mathematical formulas for calculating valve area.
Mitral valve area = Diastolic mitral flow
38√ Mean transmitral gradient
Aortic valve area = Systolic aortic flow
45√ Mean transaortic gradient
In pulmonic stenosis, valve area is not often used in actual practice. The
ratio of the peak right ventricular pressure to peak systemic pressure (RV/SA)
is used.
GRADING OF PS: RV/SA PRESSURE RATIO

32
Category RV/SA Gradient
pressure ratio (mmHg)
1. Mild PS < 0.5 < 50
2. Moderate 0.5–0.75 50–75
3. Severe > 0.75 > 75 mmHg
VALVULAR REGURGITATIONS
Regurgitant fraction = Angiographic stroke volume – Fick stroke volume

Angiographic stroke volume
Table 5.8: Correlates of severity of regurgitant lesions: clinical and angiographic correlations
Regurgitant fraction Angiographic severity Clinical severity

1. < 20% + Trivial
2. 20–40% ++ Mild
3. 40–60% +++ Moderate
4. > 60% ++++ Severe
The tricuspid valve area calculated by the Gorlin formula is unreliable and is not
used to assess the severity of tricuspid stenosis. The gradients across the valve
are often used. For a diagnosis of tricuspid stenosis, a minimum gradient of 3
mmHg in diastole is essential. A gradient of 5 mmHg or more suggests significant
stenosis and is generally an indication for surgery.
CORONARY ANATOMY
A basic knowledge of normal coronary anatomy and the blood supply of various
Table 5.9: Coronary arterial division and regional blood supply
Left anterior descending artery (LAD)

Septals Anterior 2/3 of interventricular septum (IVS)
Diagonals Antero-lateral wall of left ventricle
Distal main vessel of LAD Apex
Left circumflex artery (LCX)
Obtuse marginals (OM) Postero-lateral wall of left ventricle
Posterior descending artery (PDA) in 15% Posterior 1/3 of interventricular septum
Right coronary artery (RCA) 33
Right ventricular branches Right ventricular free wall
Acute marginals Right ventricular free wall and sometimes posterior
interventricular septum
Posterior descending artery in 85% Posterior 1/3 of IVS
Posterior left ventricular Posterior left ventricular wall with variable area
of postero-lateral wall
Table 5.10: Segments of myocardium and their blood supply
Structure Usual blood supply Variant

Interventricular septum, LAD RCA (small portions
anterior including the apex),
circumflex (apex)
Interventricular septum, RCA (proximal 2/3) Circumflex, LAD
posterior LAD (distal 1/3) (Distal 2/3)
Anterolateral wall Circumflex, diagonals Ramus intermedius
Posterior wall Circumflex, RCA
Anterolateral papillary muscle LAD and circumflex
Posterior medial papillary muscle RCA Circumflex
Apex LAD RCA, Circumflex
Inferior wall RCA Circumflex, Distal LAD
Fig. 5.2: Anatomy of right coronary artery (RCA)
segments of the heart is essential for understanding the various manifestations

of ischemic heart disease (Table 5.9).
There are two main coronary arteries – the left (LCA) and right (RCA)
34 coronary arteries. The left coronary artery in turn divides into the left anterior
descending (LAD) and the left circumflex (LCX) arteries. The main branches and
the areas supplied by each are given in Tables 5.9 and 5.10.
The right coronary artery arises from the right coronary sinus of the aorta
and is divided into three segments: proximal (from origin to the right ventricular
Fig. 5.3: Branches of the left anterior descending (LAD) artery

(RV) branch); mid (from RV branch to the origin of acute marginal (AM) branch);
and distal (from AM branch to the termination, including the terminal branches,
posterior descending artery (PDA) and posterior left ventricular branch (PLVB)).
When the RCA gives rise to the PDA, it is called dominant. In 15 per cent of cases
the PDA arises from the LCX (Fig. 5.2).
The main trunk of the left coronary artery (LMCA) divides into two main
branches – the left anterior descending and left circumflex artery. The LAD is
demarcated into three segments – proximal (from origin to the major first diagonal
(D1) branch); mid (from D1 to second diagonal (D2)); and distal or apical (the
portion distal to D2, which supplies the apical area). Septal branches (S1, S2 etc.)
arise perpendicularly throughout its length (Fig. 5.3).
The second major division of left coronary artery courses along the
atrioventricular (AV) groove and gives rise to obtuse marginal branches (OMs). The
LCX (Fig. 5.4) is divided into two segments – proximal (the portion proximal to
the origin of first major OM); and distal (the remaining part of LCX distal to OM1).
In 15 per cent of cases, the LCX gives rise to the PDA (left dominant system).
The left ventricle is divided into various segments and can be viewed on
angiography in angulated views (Fig. 5.6). With the right anterior oblique (RAO) 35
view, the anterior and posterior basal, anterolateral, diaphragmatic, and apical
Proximal LAD
Diagonal branch
Circumflex artery
Obtuse marginal
branch
Left main artery
Distal LAD
Fig. 5.4: Anatomy of the left circumflex artery (LCX)

Aortic valve and sinuses

Circumflex artery
Left AV groove
Left main
Left anterior
Inte
Right coronary
rve
artery descending artery
ntri
Crus
cul
Cordus
Right
ar s
Pos
AV groove
ept
teri
m u
or
Posterior
descending artery
Fig. 5.5: Outline of coronary arterial tree in relation to atrioventricular

and interventricular grooves
36
A B
Fig. 5.6: Left ventricular angiogram in systole (A) and diastole (B)
segments can be seen (Fig. 5.7). The anterobasal, anterolateral, and apical segments
are supplied by the LAD; and the posterobasal and diaphragmatic segments are
supplied by the RCA. In some cases, a variable area of the apex is supplied by
the RCA, through its PDA branch.
Fig. 5.7: Segmental division of left ventricle (RAO view)
With the left anterior oblique (LAO) view, the entire anterior septum is well 37
profiled. The posterolateral segment and to a variable extent the apex, is also
seen (Fig. 5.8). The anterior septum and apex are supplied by the LAD and the
posterolateral area is supplied by the LCX.
In conventional angiographic views, some of the segments are not visualized.
However, tomographic (cross-sectional) images can be obtained with two-
dimensional echocardiography or radionuclide methods. In this tomographic
depiction, the basal, mid, distal and apex are depicted from the outer ring to the
innermost ring. The septum is divided into anterior two-thirds, supplied by the
LAD and posterior third, supplied by the PDA; the lateral wall is divided into
anterolateral, supplied by diagonal branches of the LAD, and posterolateral,
supplied by obtuse marginal branches of the LCX. The posterior interventricular
septum and the posterior wall are supplied by the RCA in 85 per cent, and LCX
in 15 per cent of the population.
Coronary arterial lesion assessment

Normally the luminal surface of the coronary artery is smooth and regular. When
there is atherosclerosis, there may be a localized narrowing (stenosis), diffuse
narrowing, ectasia or minor irregularities. All of these lesions may have significance
in relation to future events. A clinically important lesion is defined as stenosis of
at least 50 per cent of the diameter, in a vessel of diameter more than 1.5 mm
as measured by calipers.
Areas of narrowing (stenosis) are assessed based on the degree of narrowing
and are expressed as ‘per cent diameter stenosis’ or ‘per cent area stenosis’. The
common expressions are given below.
Per cent diameter stenosis Per cent area stenosis

25 44
50 75
70 90
75 95
90 99
100 100
38
Fig. 5.8: Segmental division of the left ventricle (LAO view)

Fifty per cent diameter narrowing (75 per cent area) is considered significant,
and 70 per cent diameter narrowing (90 per cent area) is considered critical. When
the vessel is totally occluded, it is considered a 100 per cent block.
The lesions in the coronary artery have been classified into three types
based on the morphological characteristics. These are important in planning the
type of revascularization and prognosticating the outcome following angioplasty
procedures. Table 5.11 gives the classification.
Table 5.11: The American Heart Association/American College of Cardiology Consensus
on the characterization of coronary lesion with reference to suitability for
traditional balloon PTCA
Type A Type B * Type C

Discrete Tubular Diffuse (>2 cm)
Concentric Eccentric —
Accessible Moderate tortuosity Excessive tortuosity
Nonangulated Moderate angulation Extreme angulation
Smooth Irregular —
Little or no calcium Mild calcium — 39
No occlusion Occlusion (<3 months Occlusion (>3 months in duration)
in duration)
Not ostial Ostial —
No major branch indicated Bifurcation Inability to protect a major
side branch
No thrombus Thrombus Degenerated vein grafts
* Ellis et al suggested modification to stratify type B lesions into type B1 (one type B characteristic) and
type B2 (more than one type B characteristic) lesions.
6 The Patient’s History

It is the province of knowledge to speak and it is the privilege of wisdom to listen.
Oliver Wendell Holmes
The patient’s version of the disease is the most important source of information.
It directs both the extent of physical examination and the sequence of diagnostic
testing. The process of history taking is not mere collection of information. It is at
40 this period that the physician and the patient assess each other. The doctor is
obviously eager to reach a diagnosis and to plan the investigation of the patient.
The patient, in a subtle and passive manner, will also judge the physician by his
appearance and manner. It is at this stage that the ‘faith and trust at first encounter’
develop. If the doctor does not conduct himself well, the initial interview is summed
up as ‘distrust at first sight’. The doctor’s dress should be clean and dignified.
Wearing sports shoes and colourful clothes gives an appearance of casualness and
indifference. Also, blank and vacant looks or indulgence in some other activity
will lessen the patient’s faith. The physician should never appear to be in a great
hurry especially during the first encounter.
The interview should take all these patient’s concerns and fears into
consideration. The history is the source of maximum information related to any
illness. It is vitally important to note the patient’s main concerns and address
them, as the patient is more interested in them than any other smart diagnosis the
physician may make. Careful and thoughtful history taking establishes a bond
with the patient that may be vital later in securing the patient’s acceptance of
hospitalization for intensive diagnostic work-up and therapeutic intervention. Some
general guidelines are useful.
THE PATIENT’S HISTORY
Table 6.1: The patient’s concerns

Anxiety and fear.
Do I really need all these tests and procedures?
Do I have the disease?
Possible death and disability.
Will I be able to afford the cost of investigation/treatment? Will they do everything that is necessary
and nothing that is unnecessary?
Unnecessary investigation and treatment are common today.
Outcome of procedures.
Complications of procedures.
Long queues in the hospitals (for treatment, medication, investigation).
Mistakes in diagnosis and treatment are not rare.
Should I take a second opinion? Doctors get upset if patients ask for another opinion.
Do I need all these medicines?
What happens if I stop medication?
The doctor didn’t spend enough time with me. Has he thought deeply enough about my illness?
I am rich and important. Will they overinvestigate and treat?
Does he really care about what happens to me?
Table 6.2: Patient interview

Patient interview: guidelines to the doctor 41
The patient is the most important person in the room.
Introduce yourself to the patient and the family.
There should be no interruptions during the interview or in the physical examination that follows it.
Telephone calls, and interruptions by hospital staff entering and leaving the room should be avoided.
The patient should have privacy during the interview. Find out who else the patient wants in the room
during the examination.
The patient should not be interrupted while he talks.
Do not give an appearance of jumping to conclusions during the initial evaluation even if things appear
obvious.
In eliciting family history of sudden death, use tact and caution when a close family member died at the
same age as the patient.
Avoid being judgmental when patients mention habits of smoking or alcoholism.
Do not look disinterested and bored; instead individualize patient evaluations.
Never appear to be in a hurry; appear relaxed.
Dress in a sober and dignified way.
One should go out of the way to give an appearance of respecting the patient
as an individual. But these appearances cannot be feigned for long, unless one
genuinely respects people who come for help. The patient and the family should
be given separate interviews at least once, to have a complete picture of the illness.
The doctor should introduce himself to the patient and the family. This is
particularly applicable to the ward round. Often the patient and the family do not
know the name of the doctors even after discharge from the hospital.
CASE RECORD
The case format that is frequently used is described below.

Patient’s name: Hospital No: i) Name and
Address/telephone number: Hospital No: The
Age: Sex: importance of
Height: Weight: properly identifying
Body Mass Index: the patient cannot be
Presenting complaint: overemphasized. In
Patient’s immediate concerns: busy hospitals and
Accompanying symptoms: laboratories,
History of risk factors: mistakes related to
Hypertension
Diabetes mellitus
patient identity are
42
Smoking more common than
Hyperlipidemia is realized. Since
Family history of CAD
Past CAD
more than one
System review:
patient may have the
Associated disorders of importance:
same name, the
Peptic ulcer hospital number
Bronchial asthma/COPD should be routinely
Drug history: used.
Drug allergies:
Work details:
ii) The importance
Dietary history:
of height, weight,
Description of a typical daily and body mass index:
weekly routine of the patient: The height of the
Conclusions drawn from history: individual has
Patient’s perception of illness: significance in
Previous tests done and results: certain cardio-
Details of previous treatment and response: vascular disorders
Concerns of the family: (for example,
Marfan’s syndrome). Tall and lean individuals have a proclivity to have mitral
valve prolapse.
iii) The importance of age and congenital heart disease: Congenital heart
disease is likely until 3 years of age. Rheumatic heart disease is unlikely before the
third year. The commonest cyanotic heart disease at birth is D-transposition of
great arteries (Table 6.4). After 2 years of age, the commonest cyanotic heart
disease is tetralogy of Fallot. Rheumatic heart disease is most common between
10 and 30 years of age. After 40 years, coronary artery disease is more common.
Age of onset of heart failure and cyanosis give valuable clues to underlying heart
defect in congenital heart disease.
Table 6.3: Definitions of age related terms
Newborn First week of life
Neonate First month of life
Infancy First year
Childhood 1–16 years
Adolescence or teenage 13–18 years
Adulthood Beyond 18 years
43
Middle age 50–60 years
Old age 65–75 years
Very old age (octogenarian) More than 75 years
Table 6.4: Clues to identify underlying cyanotic congenital heart disease from age
Age of onset of cyanosis Possible diagnosis
At birth D-TGA
Admixture lesions
TAPVC
Single ventricle
DORV
Truncus arteriosus
Tricuspid atresia
Tetralogy of Fallot
After first month Tetralogy of Fallot
After 2 years Eisenmenger syndrome due to VSD
After 10 years Eisenmenger syndrome due to VSD
After 20 years Eisenmenger syndrome due to ASD
Onset of heart failure gives a useful clue to the diagnosis of underlying

cardiovascular disorder. This is particularly valuable in the pediatric age group (Table 6.5).
Table 6.5: Clues to the diagnosis of heart failure from age in congenital heart disease
Age of onset of CHF Possible diagnosis
On the first day of life Neonatal heart muscle dysfunction
Asphyxia
Transient myocardial ischemia
Sepsis
Hypoglycemia
Hypocalcemia
Neonatal hematological abnormalities
Anemia
Hyperviscosity syndrome
Neonatal structural abnormalities
Congenital tricuspid regurgitation
Congenital pulmonic regurgitation
Systemic arteriovenous fistula
Neonatal heart rate abnormalities
Supraventricular tachycardia
44 Congenital complete heart block
Neonatal myocarditis
First week of life Structural abnormalities
Critical aortic stenosis
Coarctation of the aorta
Interrupted aortic arch
Hypoplastic left heart syndrome
TAPVC
Critical pulmonic stenosis
PDA (premature infants)
Heart muscle dysfunction as above (asphyxia is less likely)
Heart rate abnormalities as above
Renal abnormalities
Renal failure
Systemic hypertension
Endocrine disorders
Neonatal hyperthyroidism
Adrenal insufficiency
First 2 months of life Structural abnormalities
Aortic level shunt (PDA, truncus, AP window)
Ventricular level shunt (VSD, AV canal, single ventricle)
Left sided obstructive lesions as above
Atrial level shunt (ASD, non-obstructed TAPVD)
Age of onset of CHF Possible diagnosis

Anomalous left coronary arising from
pulmonary artery
Pulmonary abnormalities/chronic hypoxia
(right heart failure)
Central nervous system hypoventilation
Upper airway obstruction
‘Bronchopulmonary dysplasia’
Heart muscle abnormalities
Cardiomyopathy/endocardial fibroelastosis
Myocarditis
Pompe’s disease
Renal and endocrine disorders
Hypothyroidism
As a univariate feature, age at onset of symptoms as a powerful factor in the

diagnosis of congenital heart disease is illustrated in the following case summary.
Case summary
A 9-year-old girl presented with history of dyspnea. After a physical examination, two-
dimensional echo and pulse wave Doppler evaluation, she was diagnosed to have ostium 45
secundum atrial septal defect with left to right shunt and moderate pulmonary arterial
hypertension. She was scheduled for surgical closure of ASD two days later.
A day before surgery the patient was presented by a student for a bedside discussion.
The student made a clinical diagnosis of ASD but clearly brought out the fact that the
child had symptoms of heart failure at the age of 1 month and gradually improved in the
next one year. Surgery was postponed and cardiac catheterization and angiography
confirmed the diagnosis of atrial septal defect and large ventricular septal defect with
hyperkinetic pulmonary arterial hypertension. Obviously the diagnosis of VSD was missed
on initial echo evaluation and diligent history taking pointed to this; the mistake was
rectified.
Age is a guiding clue not only in the diagnosis as outlined above but also in
the management of cardiovascular disease. The age of the child is a very important
variable in the management of the ventricular septal defect, which is the commonest
of congenital defects.
Age plays a very important role in diagnosing ventricular septal
defect (Table 6.6). Spontaneous closure of ventricular septal defect most commonly
occurs by 2 years of age but may occur later and is reported in adults. If a new
murmur appears after 6 months of age, ventricular septal defect is unlikely.
Table 6.6: Age of child and ventricular septal defect

Age of detection of murmur
Murmur < 18 hrs of life Almost never due to isolated VSD
Murmur detected 2–6 weeks VSD is most likely
2nd or 3rd day (prior to discharge Small VSD with a very rapid decline
from newborn nursery) in PVR; almost never due to isolated
small VSD
Later than 4th month Delayed appearance of murmur means
delayed fall in PVR and may suggest
large VSD
Some other lesion is likely
Murmur may have been overlooked in
the previous examination or the child
was not examined
Later than 6 months VSD is unlikely
Onset of heart failure
3rd to 4th month Most common
Earlier than 1st month Prematurity, Some other lesion is likely
Timing of surgery Indication for surgery
< 12 months Uncontrolled CCF
> 12 months Qp/Qs > 2:1
46
Long term result
Surgery before 2 yrs Normal PVR on long term follow up
Surgery after 2 yrs Less predictable fall in PVR
Patients with large ventricular septal defect and pulmonary arterial hypertension
due to vascular disease who are inoperable, deteriorate by the second or third
decade of life, and most of them may die before the age of 40 years.
iv) Age and valvular heart disease: Mitral stenosis occurring below 17 years of
age is called juvenile mitral stenosis. Above 35 years of age, all patients with valvular
heart disease require coronary arteriography before they are considered for valve
surgery by open heart operation. In any patient with valvular heart disease who is
above 35 years of age, if the symptoms are atypical or disproportionately high for
the degree of valvular defect, coronary artery disease should be excluded. In patients
with valvular aortic stenosis above 40 years of age, almost all male patients have
calcified aortic valves. In elderly patients requiring valve replacement, a bioprosthetic
valve rather than an ordinary prosthetic valve is the choice.
Prognosis in coronary artery disease is significantly influenced by age. The
major studies in coronary artery disease highlighted this. In patients above 80
years, mortality with open heart surgery is as high as 25 per cent. In the CASS
(Coronary Artery Surgery Study) registry data of patients with left main coronary
artery stenosis, older patients benefited more with coronary artery bypass grafting
(CABG) than with medical therapy. The results are summarized in Table 6.7.
Thus magnitude of the survival gains associated with coronary artery bypass
surgery increase with age above 50 years, but again decrease as the age
exceeds 75 years. Recent studies showed that thrombolysis in acute myocardial
infarction is not only safe but also reduces mortality significantly even in the elderly.
Older age is generally considered an incremental risk factor for premature death
within 5 years after the coronary artery bypass surgery operation. Patients aged
40–50 years have a 5 year survival of 91 per cent compared to those above 50 years,
whose survival is about 81 per cent.
v) Sex and coronary artery disease: Coronary artery disease is rare in
premenopausal women. Apart from coronary artery disease, the sex of the patient
has important implications in the diagnosis and management of heart disease.
Women differ from men in the clinical presentation and the pattern of disease.
False positive exercise tests are more common in women. In the CASS registry, 47
39 per cent of women and 11 per cent of men had normal coronary angiograms.
This is despite a typical history of angina and a positive exercise electrocardiogram.
Several studies indicate that the morbidity and mortality of coronary artery
disease occur 10 years later in women than in men. But once they develop
myocardial infarction, women have higher mortality during the first 30 days after
myocardial infarction. This interesting set of observations is frequently quoted.
A recent review of English literature from 1966 to 1994 by Vaccarino et al analyzed
the reasons for this apparent paradox in women with coronary artery disease.
Table 6.7: Age and coronary bypass surgery
Age 4 year survival with 4 year survival Percentage gain
medical therapy with CABG
< 50 yrs 68% 95% 40%
> 65 yrs 51% 82% 61%
65–69 yrs 67% 81% 22%
70–74 yrs 51% 77% 51%
>75 yrs 56% 75% 34%
Much of the increased early mortality after myocardial infarction in women is

explained by the older age, and the more unfavourable risk characteristics of the
women. In the long run, when the differences in age and other risk factors are
controlled, women tend to have an equal survival.
vi) Drug history: In the initial interview, it is important to enquire into the nature
of treatment or drugs the patient is receiving as it has implications in the diagnosis
and management (Table 6.8). A detailed account of drug therapy is of help in
proper management of patients with heart disease. These features include the
name, dosage, duration of therapy, and compliance with therapy.
Table 6.8: Importance of drug history
Drugs can cause, mask, modify, aggravate, abolish or cure a disease or
physical symptoms and signs.
Drugs can induce cardiovascular disease.
Implications in selection of drugs in the light of previous drug therapy.
Drugs may have to be stopped or modified before certain
cardiovascular procedures.
48
Public relation component to the specialist: Check the prescription
made by the referring doctor carefully before replacing it.
Drugs taken on the day of examination could have a bearing on the
symptoms or test results.
Get specific information about the drug, such as:

Nature of drug
Dosage/spacing
Response to therapy
Improvement
Deterioration
Side effects/toxicity
Duration of therapy
Drug compliance
Drug intake on the day of consultation
Drug monitoring
Both the pharmacological and trade name should be known. Inappropriate

dosage and improper spacing of drugs may be responsible for inadequate response
to drugs.
Response to drugs is used as a valuable diagnostic clue in clinical medicine
(Table 6.9). The response to the earlier medication helps in the diagnosis and in
planning future treatment. For example, improvement with diuretics and digoxin
makes heart failure the most likely cause for dyspnea. On the other hand,
improvement with bronchodilators suggests bronchial asthma. Angina pectoris
responds promptly to sublingual nitroglycerine.
The fever and joint pain of acute rheumatic fever responds promptly to aspirin
distinguishing it from rheumatoid arthritis. The chest pain of acute benign
pericarditis responds to steroids. Following acute myocardial infarction, chest pain
may be due to postinfarction angina or due to pericarditis. Prompt response to
steroids suggests pericarditis as the cause of pain. Prompt response to nitrates
suggests angina.
Not only improvement, but also deterioration gives valuable clues to the
underlying disorder (Table 6.10). The deterioration of patients with pericardial
tamponade and constrictive pericarditis with diuretics is well known. Conditions 49
with diastolic dysfunction like hypertrophic cardiomyopathy also deteriorate with
the volume depletion of diuretic therapy.
In the management of any specific cardiac defect, one must always elicit the
history of drugs which aggravate the underlying disorder. Significant or dramatic
improvement occurs when these drugs are discontinued. Sometimes drugs
themselves may be responsible for inducing cardiovascular disease (Table 6.11).
Table 6.9: Response to drug(s): diagnostic clues
Drug and response Most likely diagnosis
Chest pain responds to sublingual Angina pectoris
nitrate/nitroglycerine
Dyspnoea responds to diuretics and digoxin Heart failure
Acute polyarthritis responds to aspirin Acute rheumatic fever
Acute chest pain responds to steroids Acute pericarditis of acute
myocardial infarction,
idiopathic benign pericarditis
Table 6.10: Drugs aggravating cardiovascular disease

Disease Drug responsible Mechanism(s)
CAD Hydralazine Reflex sinus tachycardia
Angina or MI increases MVO2
Nifedipine As above
Dipyridamole Coronary steal
Aspirin Anemia due to GI bleed
Ergot preparations Coronary spasm
Valvular disease
MS Vasodilators Reflex tachycardia with
reduced diastolic filling
time
AS Vasodilators Hypotension, syncope
AR, MR Vasopressors SVR, hypertension
aggravation of lesion
Systemic hypertension As above (Bronchodilators
like ephedrine, sympatho-
mimetic in nasal decon-
gestants, cold medications, SVR, systemic
cough syrups) hypertension
50 Steroids Salt and water retention
NSAIDs
Tricyclic antidepressants
Excessive use of potent Reflex vasoconstriction
diuretics
Antidiabetic agents Adrenergic excess of
hypoglycemia
Betablockers Hypertension in
pheochromocytoma due
to selective alpha
stimulation
Congestive heart failure Calcium blockers Myocardial depression
Disopyramide
Steroids Salt and water retention
NSAIDs
Cardiovascular drugs affecting other systems: Drugs could affect systems other
than the one that is targeted. A list of cardiovascular drugs that could affect other
systems is given in Table 6.12. It is a useful practice to rule out a drug-induced
disorder whenever a patient develops new or unusual phenomena (symptoms,
signs or a laboratory test abnormality).
Table 6.11: Drug induced cardiovascular disease

Disease Causative drugs
1. Systemic hypertension Sympathomimetic drugs
Ephedrine and related drugs
Nasal decongestants
Cold medications
Cough syrups
Steroids
NSAIDs
Estrogens
Contraceptive pills
Hormone therapy to treat menorrhagia
Excessive sodium intake
2. Cardiomyopathy a) Direct acting
Alcohol
Bleomycin
Adriamycin
Phenothiazine
Emetine hydrochloride
Paracetamol
Cyclophosphamide
51
Reserpine
Catecholamines
Corticosteroids
Lithium
Chloroquine
Cocaine
Methysergide
b) Hypersensitivity
Methyl dopa
Penicillin
Sulfonamides
Tetracyclines
Phenindione
Phenylbutazone
Antituberculous drugs
3. Pulmonary arterial Aminorex fumarate
hypertension Monocrotaline or other pyrrolizidine
(alkaloids)
Oral contraceptives
Phenformin
Disease Causative drugs

4. Hyperlipidemia Betablockers
Diuretics
Alcohol
Oral contraceptives
5. Acute myocardial Ergot preparations
infarction Cocaine
6. Prolonged QT Quinidine
Procainamide
Amiodarone
Disopyramide
Sotalol
Phenothiazines
Tricyclic antidepressants (amitryptaline)
Non-sedative antihistamines
(terfenedine, astemazole)
Drugs enhancing the effects of antihistamines
(antimalarials, erythromycin, ketoconazole),
liquid protein diets
7. Valvular heart disease Fenfluramine
52
Table 6.12: Common side effects of some of the drugs used for heart disease
Disorder Drugs
Dry cough ACE inhibitors
Acid peptic disease Aspirin
Reserpine
Hyperkalemia Potassium sparing diuretics
Angiotensin-converting enzyme inhibitors
Betablockers
Hypokalemia Diuretics
Systemic lupus Hydralazine
erythematosus Procainamide
Pulmonary fibrosis Amiodarone
Bronchial asthma Betablockers
Hepatic dysfunction Amiodarone
Isoniazid for tuberculous pericarditis
Osteoporosis Prolonged heparin use
Embryopathy Warfarin sodium during pregnancy as anticoagulant
Neutropenia Ticlopidine
Table 6.13: Drugs masking cardiovascular disease

Condition Drugsmodifying
Systemic hypertension Antihypertensive therapy
Coarctation of aorta Antihypertensive therapy
Congestive heart failure Decongestive therapy
Tricuspid stenosis Diuretics
Mitral stenosis Diuretics, betablockers
MVP Betablockers
HCM Betablockers
Aortic regurgitation Vasodilator therapy
Table 6.14: Drug withdrawal crises in cardiology
Withdrawndrug Consequence
Antihypertensive drugs (particularly clonidine) Hypertensive crisis
Betablockers in CAD Unstable angina or acute MI
Calcium blockers in CAD Unstable angina or acute MI
Diuretics Heart failure or pulmonary edema
53
Betablockers in tetralogy of Fallot Hypoxic spells
Oral anticoagulants for prosthetic valves Thrombotic occlusion of the prosthetic valve
Aspirin following PTCA Risk of abrupt closure
Heparin following PTCA Risk of abrupt closure
Heparin or oral anticoagulants following
intracoronary stenting Acute stent thrombosis
Aspirin in unstable angina with severe
coronary disease prior to bypass surgery Acute myocardial infarction
Drugs masking cardiovascular disease: Hypertension or coarctation of the aorta

can be masked by antihypertensive drug therapy (Table 6.13). The physical signs
in tricuspid stenosis like prominent a wave and elevated JVP may be modified by
diuretic therapy. The mid-diastolic murmur of mild mitral stenosis may be
obliterated by the bradycardia induced by betablockers. Betablockers may also
mask any signs of mitral valve prolapse.
Drugs and coronary artery disease: In the functional evaluation of patients with
angina, it is important to check whether the angina is in the presence or absence
of drug therapy. Patients who are meeting a new doctor have a habit of stopping
Table 6.15: Drugs and other factors that alter the anticoagulant response to warfarin
Prolongs prothrombin time Reduces prothrombin time
Pharmacokinetic
Increases warfarin levels Decreases warfarin levels
Phenylbutazone* Cholestyramine*
Sulfinpyrazone* Barbiturates*
Metronidazole* Rifampicin*
Cotrimoxazole* Carbamazepine*
Erythromycin* Griseofulvin*
Fluconazole* Dextropropoxyphene†
Miconazole*
Nafcillin
Cimetidine*
Omeprazole*
Amiodarone*
Disulfiram†
Pharmacodynamic‡
Clofibrate* High vitamin K intake* (certain vegetables,
nutritional supplements)
Low vitamin K intake*
Malabsorption
54 Liver disease
Hypermetabolic states
Coagulopathies
Mechanism not established
Isoniazid* Chlordiazepoxide*
Propafenone* Sucralfate*
Propranolol* Dicloxacillin†
Piroxicam*
Acetaminophen†
Anabolic steroids†
Aspirin†
Chloral hydrate†
Ciprofloxacin†
Itraconazole†
Quinidine†
Phenytoin†
Simvastatin†
Tamoxifen†
Tetracyclines†
Influenza vaccine†
†
* Highly probable interaction Probable interaction
‡
No effect on warfarin levels.
the drugs they were on like betablockers, diuretics or antihypertensives. This may
precipitate a critical state.
Patients undergoing coronary bypass surgery (CABG) are often already taking
betablockers or calcium channel blockers which have to be continued before
surgery. Sudden withdrawal may precipitate unstable angina or myocardial infarction
(Table 6.14). Digoxin is usually stopped 36 hours before operation.
Drugs and valvular heart disease: Diuretics mask congestive heart failure and the
fourth or third heart sound may be diminished or absent. In tricuspid stenosis, the
jugular venous signs and the tricuspid diastolic murmur may decrease or disappear.
Even at cardiac catheterization, tricuspid stenosis may be underestimated or may
be missed as a result of excessive diuretic therapy. It is for this reason, that all
patients with rheumatic heart disease should have their diuretics stopped prior to
cardiac catheterization, unless essential. In patients fully digitalized, the diagnosis
of atrial fibrillation may be missed as the heart may be normal and relatively regular.
In patients on digitalis, the diagnosis of atrial fibrillation may be missed unless one
exercises the patient to bring out the rapid and irregular rates. Almost all the
patients after prosthetic valve insertion are on oral anticoagulant therapy for life. 55
Drugs prescribed by the referring doctor: When the patient is prescribed certain
drugs, one must make a careful note of all the drugs with the trade names. The
specialist should not change the drugs (this includes the trade names) unless
essential. Inadequate attention to this is likely to induce misunderstandings between
the specialist and the referring doctor. The patient is likely to feel that the original
drugs were wrongly prescribed by the referring doctor.
Drugs on the day of consultation: Many patients have the habit of stopping the
drugs before visiting a new doctor. Most argue that when they go to the new
doctor, the drugs will be changed anyway. When patients are asked to come for
the next visit after one month, they interpret it as having to take the drugs only for
one month. Some patients believe that they are under unnecessary medication
and stop the drugs to see the effect on blood pressure. If the patient’s blood
pressure is normal on the day of consultation the patient concludes that he may
not need drugs for his hypertension and the high blood pressure is ‘cured’. Typically,
a patient with systemic hypertension may not take the drugs on the day he visits
the doctor. The blood pressure will naturally be high and the doctor obligingly
steps up the dosage of antihypertensive agents. This may result in postural

hypotension or even frank syncope. The physician finds it puzzling as the blood
pressures are high. He may consider another cause for syncope and extensive and
costly diagnostic work-up is unnecessarily resorted to.
INCREMENTAL RISK FACTORS
Information from the history, independent of stress testing may be of value in

predicting ischemic events. Clinical variables predicting future ischemic events
are:
• Angina prior to infarction
• History of symptomatic hypertension
• Diabetes mellitus
• Peripheral vascular disease
• Anterior Q wave first MI
• Heart failure on admission
Patients with 5 or 6 of these variables had a one year reinfarction rate of 23
56
per cent compared with 4 per cent in those with none or one of these factors, 5.5
per cent with two of these factors, 8 per cent with three of these factors, and 15
per cent with four of these factors. The ability to predict recurrent myocardial
infarction is of importance since it has been shown that recurrent myocardial
infarction is one of the most important predictors of subsequent death after
infarction.
Incremental risk factors in cardiac surgery

The multiple variables that interact with one another to influence the results of
cardiac surgery are called incremental risk factors. Awareness of these factors is
useful in decision making in individual patients. Risk assessment of a patient with
coronary artery disease, likely to undergo coronary artery bypass graft surgery is
given below as an example.
The incremental risk factors for hospital death in CABG are:
• Age > 60 years
• Frank diabetes mellitus
• Systemic hypertension
• Severity of angina
• Grade of dyspnea
• Female sex
• Unstable angina
• Emergency operation
• Skill of the surgeon
The value of considering this information is that even at the stage of history
taking, the risk of interventions like cardiac surgery can be predicted. All the
information listed is obtainable from history.
It is useful to follow a checklist in history taking. Table 6.16 gives the list of
symptoms to be checked. Though using a checklist gives an appearance of
artificiality with regard to history taking, it is better to be thorough. A methodical
approach to history taking without a checklist comes only after years of practice.
Even then, the senior physician is actually using a mental checklist. The junior
student should not hesitate to use the checklists till he has gained enough experience
to use a mental one.
Table 6.16: Cardiovascular history checklist
57
Coronary artery Valvular Congenital Cardiomyopathy Prosthetic valves
disease heart disease heart disease
Risk factors Fever Consanguinity Family history Age
Family history Sore throat Cyanosis Drug history Sex
Hypertension Arthralgia/ Spells Alcohol Pregnancy plan
Diabetes arthritis Dyspnea Respiratory type illness Bleeding tendency
Smoking Dyspnea Syncope Dyspnea Food intake
Hyperlipidemia Palpitation Edema Syncope Vitamins (K)
Female hormones Syncope Chest pain Diarrhea
Chest pain Edema Systemic disorder Antibiotics
Dyspnea Chest pain Aspirin/analgesics
Palpitation Prophylactic Prothrombin time
Syncope Penicillin Peripheral embolism
Weakness Fever
Dyspnea
Syncope
Edema
Valve noise
The best thing one can say about history is that there can never be enough of it.
“Opportunity is often lost because we are broadcasting when we should be tuning in.”
Anonymous
CONTROVERSIES AND PERSONAL PERSPECTIVE
It is clear that increasingly, taking a thorough history has become less of a priority
for most doctors. First, there is less time available for physician-patient direct
contact as a result of the demands placed on a physician’s time. Frequently, a
physician extender or nurse obtains part or all of the history to reduce the time
burden on the doctor. Under the putative heading of ‘efficiency’, the time and
importance given to detailed, thorough interview has been markedly reduced.
Second, with advances in technology, history taking and physical examination
have been partially supplanted by rapid use of bedside tools such as the 2-D
echocardiogram, treadmill or dobutamine thallium test, Holter recording or even
diagnostic angiography or electrophysiologic study.
This development is unfortunate. The history is the most important way to
58 create a patient-physician bond and is precious and irreplaceable. The task should
not be delegated to a physician extender, ideally, except for such perfunctory aspects
as the medication and dose, risk factors, and minor details. It is absolutely essential
to directly query the patient in depth for the principal symptoms such as chest
discomfort, loss of consciousness, or dyspnea. Only in this way will there be the
optimal accuracy and relationship building that are critical to treatment. Also,
imprudent use of advanced diagnostic technology is not only expensive but can
uncover findings that, while accurate, have no bearing on the patient’s symptoms.
The detailed history will preempt or properly guide the use of more refined
diagnostic tests. The history is the most cost-effective tool that one can use to
soundly lay the foundation of patient evaluation.
Although history taking has lost the pride of place in a diagnostic work-up in
the past decade, it will be increasingly relied on in the future due to its relatively
low cost and pivotal importance in guiding more diagnostic and therapeutic decision
making.
7 Evaluation of Chest Pain:
Diagnostic and Therapeutic
Implications
There is a disorder of the breast marked with strong and peculiar symptoms, considerable for the
kind of danger belonging to it, and not extremely rare, which deserves to be mentioned more at
length. The seat of it, and sense of strangling, and anxiety with which it is attended, may make it
not improperly called angina pectoris … Those who are afflicted with it are seized while they are
walking and more particularly when they walk soon after eating with painful and most disagreeable
sensations in the breast which seem as if it would take their life away, if it were to increase or to
continue. The moment they stand still all this uneasiness vanishes.
William Heberden
This masterly description of effort angina by William Heberden over two hundred
years ago has not been improved upon. Chest pain is the most common clinical
expression of coronary artery disease. The interpretation of chest pain to this day
remains the most important method of recognizing coronary artery disease. There
are however many reasons for failure to recognize coronary artery disease from
its symptomatic expressions. Myocardial infarction is unrecognized in 12 per cent
and unaccompanied by chest pain in 25 per cent of patients. The more recent and
realistic description of the problem is by Harrison and Reeves.
Discomfort in the chest whether actually painful or not, is usually due to a relatively innocent or a
potentially grave disorder. Unfortunately there is no parallelism between the severity of the disease
and the gravity of its cause.
Case summary
A 39-year-old airline engineer presented with substernal chest discomfort related to food.
Each episode lasted 5–10 minutes and was relieved by belching. He was a chronic smoker
and had a history of acid peptic symptoms in the past. He was admitted in CCU for
observation. Physical examination was unremarkable and the serial ECGs were normal.
The cardiac enzyme levels were normal. The pain was considered atypical for myocardial
ischemia by the treating cardiologist but he was prescribed diltiazem, nitrates and H2
antagonists. During the two days of hospital stay he had two brief episodes of burning
chest discomfort partially relieved by nitrates. He was discharged after 2 days of hospital
stay and was advised to come back for an exercise test after 1 week. Three days after
discharge, he developed substernal pain and collapsed. He was ‘brought dead’ to the
emergency room. He is survived by a 32-year-old wife and a 7-year-old son suffering
from severe rheumatic mitral regurgitation.
The factors related to the patient, the physician, medical education, medical
literature and other issues conspire together in this distressingly common failure
to recognize myocardial ischemia or infarction. Pain is a warning signal. The reaction
to a warning is a matter of attitude of the person, affordability, and the culture of
the society we live in. The patient should first have pain and feel the need for
immediate medical help. When the pain is at unusual sites or is mild and vague,
the patient tends to neglect it altogether and may never reach a physician. Even
when they reach a medical care facility, there is no guarantee that all that needs to
60
be done will be done. The professional inadequacy of the doctors is easily
understood if one looks at their training. Neither medical students nor postgraduates
are trained properly in the clinical evaluation of patients with coronary artery
disease (CAD), as patients with coronary artery disease are not ‘examination cases’.
APPROACH TO A PATIENT WITH CHEST PAIN
A patient with acute chest pain needs a systematic approach that combines the
diagnostic considerations and therapeutic options. The table below gives the
suggested approach.
If cardiac, is it due to
• Myocardial ischemia?
• Pericarditis?
• Aortic dissection?
• Acute pulmonary embolism?
• Mitral valve prolapse?
• Hypertrophy disorders of myocardium?
EVALUATION OF CHEST PAIN: DIAGNOSTIC AND THERAPEUTIC IMPLICATIONS
If due to myocardial ischemia, is it due to

• Hypertrophy disorders of myocardium?
• Coronary artery disease?
If due to CAD is it
• Acute myocardial infarction?
• Unstable angina?
• Chronic stable angina?
• Vasospastic angina?
• ‘Mixed angina’?
If non-cardiac, is it
• Esophageal?
• Gastroesophageal reflux?
• Nutcracker esophagus/esophageal spasm
• Following vomiting?
• Musculoskeletal?
• Costochondritis (Tietz’s syndrome)
• Increased muscle tension?
• Osteoarthritis of cervical/dorsal spine? 61
• Tumors of breast?
• Hyperventilation/psychiatric?
• Panic disorder?
• Depression?
• Somatization disorder?
• Acute peptic ulcer syndrome?
• Acute pancreatitis?
• Acute cholecystitis?
Causes of chest pain

Chest pain may be due to extrathoracic and thoracic structures like tissues of the
neck, or thoracic wall, thoracic muscles, cervicodorsal spine, costochondral
junctions, breasts, sensory nerves, spinal cord; intrathoracic structures like aorta,
pulmonary artery, bronchopulmonary tree, pleura, mediastinum, esophagus and
diaphragm; subdiaphragmatic organs like stomach, duodenum, pancreas, and gall
bladder and liver.
Structures responsible for chest pain are:

A. Intrathoracic
Heart
Aorta
Pulmonary artery
Pleura
Mediastinum
Bronchopulmonary tree
Esophagus
Diaphragm
B. Extrathoracic
Skin and subcutaneous tissue of thorax
Soft tissues of the neck
Cervical spine/dorsal spine
Costochondral junctions
62
Breasts
Sensory nerves
Spinal cord
C. Subdiaphragmatic
Duodenum
Stomach
Gall bladder
Liver
Pancreas
Spleen
Non-organic
If the physician has a complete knowledge of the varied clinical manifestations of

each these disorders, he will easily be able to differentiate each type of pain from
the other. Certain features of the pain help distinguish cardiac from musculoskeletal
causes of pain as listed in Table 7.1.
MYOCARDIAL ISCHEMIA
EVALUATION OF CHEST PAIN DUE TO MYOCARDIAL ISCHEMIA

Doubt is not a pleasant condition, but certainty is absurd.
Voltaire
Appropriate management of a patient presenting with chest pain needs a systematic

approach as outlined (Table 7.1). The central theme is to be overcautious in the
approach to the problem. As no single feature in chest pain is diagnostic, integration
of all the available data helps in the diagnosis. Given a subset of clinical presentation,
the probability changes significantly by the associated risk factors for coronary
artery disease. A risk factor may be defined as any habit or trait that can be used to
predict the probability of developing that disease in an individual. It is a causative
agent or condition that can be used to predict an individual’s probability of
developing disease.
The risk factors for coronary artery disease are:
• Family history of premature coronary artery disease 63
• Tobacco smoking
• Elevated plasma cholesterol
• Ageing
Table 7.1: Features of cardiac pain
Feature Cardiac, if Non-cardiac, if
Location Diffuse, substernal with Localized, left inframammary
radiation
Quality Dull, deep, aching, Shooting, sharp, cutting
pressing
Intensity Mild to moderate with Rapidly fluctuating
gradual fluctuation
Duration Minutes or hours Seconds or fluctuating
Precipitated by Effort, emotion, cold Posture, respiration
Relieved by Brief rest and Lengthy rest and most other
nitroglycerine measures
• Male sex
• Obesity
The prior probability of coronary artery disease is high in patients with one
or more of these risk factors. The characteristic features of chest pain must be
interpreted in the light of the prior probability that a person of a given age and
sex, with a particular past medical history would have such a cause of chest
discomfort. For example, if a 50-year-old man with coronary risk factors like
smoking, hypertension and diabetes mellitus presents with even atypical chest
discomfort, coronary artery disease should be considered. On the other hand, if a
25-year-old woman with no risk factors or use of oral hormones comes with
typical chest discomfort seemingly suggestive of angina, coronary artery disease is
unlikely.
Before we explain the value and limitation of each of the features that help
evaluate chest pain, we need to define certain terms.
The history and mechanism of various clinical subsets of angina
64 Effort stable angina: Angina usually occurring at a predictable level of exercise, relieved
gradually with cessation of exercise (mechanism:disproportionate increase in
myocardial oxygen requirements, demand ischemia).
Unstable angina: Rest angina; new onset of accelerated angina; rapidly progressive
worsening stable angina with or without changes in character, severity, or duration
(mechanism:recurrent nonocclusive coronary artery thrombi; supply ischemia).
Postinfarction angina: Recurrence of angina at rest or during activity within 30 days
of infarction (mechanism:similar to primary unstable angina).
Vasospastic or Prinzmetal angina: Rest angina only, or rest angina and angina only at a
very high level of exercise; history of ‘cyclical angina’; often due to focal spasm of
the epicardial coronary arteries. There may be history of Raynaud’s phenomenon
or migraine.
Mixed angina: Variable exercise threshold (mechanism:combined demand and supply
ischemia).
Postprandial angina: Angina precipitated by meals (mechanism:supply ischemia).
Nocturnal angina
• Occurring within 1–2 hours after assuming recumbent position (mechanism:
demand ischemia).
• Occurring after going to sleep, usually in the early morning hours (mechanism:
supply ischemia).
Walk-through angina: Angina occurring at the beginning of exercise and resolving
despite continuing same level of exercise (mechanism:supply ischemia).
Linked angina: Angina occurring with esophageal reflux, gall bladder, or other
visceral disease.
Syndrome X or microvascular angina: History is similar to that of effort stable angina.
(Diagnosis can be made only after coronary angiography which demonstrates
normal epicardial coronary arteries; mechanism not certain; impaired coronary
vasodilatory reserve is a possibility).
Atypical chest pain syndrome: Chest pain of variable character, duration and location;
localized or diffuse; not precipitated or influenced by physical activity (not due to
myocardial ischemia; the mechanism of pain is unknown; decreased pain threshold
and anxiety may be associated).
Pathophysiology of discomfort due to myocardial ischemia 65
Ischemic myocardium releases adenosine, bradykinin, histamine and serotonin.

Acidosis and elevated potassium may trigger release of these substances. The
sensory end plates of the cardiac sympathetic nervous system are stimulated by
these substances. The endplates are the receptors of a network of unmyelinated
fibres that lie between cardiac muscle fibres. They are also found around coronary
vessels. They form the cardiac plexus and ascend to the sympathetic ganglia. The
endplates transmit the pain impulses to the corresponding spinal ganglia, through
the spinal cord to the thalamus and the cerebral cortex. The discomfort is referred
to the peripheral dermatomes that supply afferent nerves to the same segment of
the spinal cord as the heart. A common pool of secondary neurons can be
stimulated by somatic and visceral afferent impulses. When the visceral stimuli are
excessive, the surrounding intermediate neurons that are receptors for somatic
impulses may be excited, resulting in discomfort in the cutaneous location. This is
called the phenomenon of irradiation of impulses. The connections to the brachial
plexus and cervical nerve roots explain the pain in the medial aspect of the arm
and neck, respectively.
There is a wide variation in pain perception in myocardial ischemia. The

autonomic denervation in diabetes may explain the frequent occurrence of silent
ischemia (ischemia without pain) in diabetic patients. Patients with silent ischemia
may have altered central modulation of pain perception. Patients with silent ischemia
have a higher dental pain threshold, and the intensity of pain is less even when the
threshold is reached. Studies have shown that the angina is less likely if the exercise
induced endorphin levels are high.
A systematic evaluation of chest pain should take into account the following
factors (Table 7.1):
Onset: A dramatic or crushing type of pain is a feature of acute aortic dissection.
The pain is most severe at the time of onset but gradually decreases in severity over
a period of time. On the other hand, the pain of acute myocardial infarction is
sudden in onset, continues in severity for 1–6 hours and subsides, or may wax and
wane. The waxing and waning pain correlates with subtotal occlusion of infarct
related artery by a thrombus with superimposed spasm, spontaneous recanalization,
reocclusion, or recruitment of collateral. The discomfort of angina is usually gradual
66
in onset. Acute coronary syndromes (a spectrum encompassing unstable angina,
non-QMI and acute MI) tend to occur most commonly in the early morning hours
or at the time of waking up in the morning. The pathophysiological mechanisms
underlying this circadian periodicity for acute coronary syndromes are listed below:
• Increased plasma catecholamines
• Increased cortisol
Table 7.2: Factors in evaluation of chest pain
Onset/time of occurrence
Duration/time to treatment
Site
Radiation
Character
Severity
Relation to physiological act
Relief with rest and drugs
Accompanying symptoms:
Symptoms related to loss of contracting
myocardium and conducting tissue
Symptoms of autonomic excess
Sympathetic excess
Parasympathetic excess
• Increased blood pressure and heart rate

• Increased platelet aggregation
• Increased tissue plasminogen activity
• Increased fibrinolytic inhibitor (PAI-I)
Site and radiation: The commonest site of ischemic pain is substernal and a similar
area over the back with radiation to the left arm. The left arm radiation is because the
same nerves supply the arm and the heart. The site of pain is variable and can occur
anywhere, from the upper abdomen to the lower jaw and can occur on either side of
chest and may radiate to the right or left arm, to the neck or jaw. In patients with a
pre-existing chronic disorder, the site of referral is usually to the site of previous pain.
The discomfort seldom extends above the jaw or below the umbilicus.
The primary pain may be altogether absent with the site of referral as the
only site of pain. For example, patients with peptic ulcer have their pain of acute
myocardial infarction referred to the epigastrium.
Case summary
A 56-year-old practising cardiologist started having pain in the neck and back variably
related to exertion. He had symptoms attributable to cervical spondylosis for the past 10 67
years. He interpreted the recent symptoms to the same disorder and ignored the symptom.
When the pain became more frequent, he started using analgesics and cervical collar. He
had frequent pain on exertion and also at rest with occasional nocturnal pain for 2 months.
He drove about 300 km himself to attend his daughter’s marriage and drove back. His
symptoms progressively worsened and he sought an orthopedic consultation. The
orthopedic surgeon noticed edema of both lower limbs and suggested an ECG and
consultation with a cardiologist. The ECG revealed extensive anterior myocardial infarction
of uncertain age and ischemia in other territories. He was hospitalized and was found to
have congestive heart failure and recurrent angina. In view of recurrent angina and episodic
pulmonary edema, an intra-aortic balloon pump was inserted. His condition improved in
the next few days but angina recurred the moment intra-aortic balloon was discontinued.
Coronary angiogram revealed severe triple vessel disease and severe left ventricular
dysfunction with an ejection fraction of 25 per cent. An emergency surgery was planned,
but he had an arrest before he was shifted to the operating table. Attempts at emergency
revascularization were unsuccessful. He expired.
This case summary illustrates the treacherous deception of the presenting

symptoms of coronary artery disease. Even a cardiologist who deals with this
disorder all the time is deceived into believing for several weeks that it was cervical
spondylosis.
Table 7.3: Typical sites of pain due to myocardial ischemia

Common Uncommon
Substernal Elbow
Back (interscapular) Hand
Jaw Right side of chest
Throat Right arm
Left arm Head
All over anterior chest
Both shoulders
Both arms
Upper abdomen
As the site of pain is variable and can be atypical in location, mistakes in

diagnosis are common (Table 7.4).
The terms typical and atypical angina are often used in clinical practice.
Substernal location, precipitation by exertion and relief by nitroglycerine were
68 required for the diagnosis of definite angina in the coronary artery surgery study
(CASS), and this is considered typical angina. Table 7.5 summarizes the features
of typical and atypical angina.
Table 7.4: Typical sites for pain due to myocardial ischemia
Site of pain Mistaken for

Upper abdomen Acid peptic disease
Neck pain Cervical spondylosis
Back pain Muskuloskeletal pain
Jaw pain Dental pain
Throat pain Throat problem
Right sided chest pain Non-cardiac problem
Left arm pain Spondylosis
Right arm pain Spondylosis
Bilateral shoulder/arm pain Spondylosis
Substernal pain Esophagitis/acid peptic disease
Anterior chest pain Esophagitis/acid peptic disease
Table 7.5: Characteristics of typical and atypical angina

Typical angina Atypical angina
Substernal Location in the left chest, abdomen,
back, or arm in the absence of mid
chest pain
Heavy, squeezing, or burning Sharp, fleeting
Precipitated by exertion or Repeated or very prolonged
emotion Unrelated to exercise
Prompt relief by rest or Not relieved by rest or nitroglycerine
nitroglycerine Relieved by antacids
Shortness of breath or palpitations
without chest pain
Duration of pain: If the duration of pain is less than a minute, the pain is unlikely
to be of cardiac origin. In classic stable angina, the pain usually lasts 3–5 minutes,
generally does not exceed 15 minutes and almost never lasts beyond 30 minutes.
In chronic stable angina, the duration of pain in a given patient is constant. Any
change in the duration of pain should be considered suggestive of progression of
the disease to either unstable angina or acute myocardial infarction. Angina induced 69
by emotion usually lasts longer and may be misinterpreted as change in chronic
stable angina. Prolonged pain by definition means pain lasting longer than 30
minutes and usually suggests unstable angina or acute myocardial infarction.
Persistent or continuous pain for many days or weeks is obviously not consistent
with pain of myocardial ischemia or infarction.
Two aspects of the duration are important: the time from the onset of pain to
hospitalization, and the duration for which the pain lasts. In an evolving myocardial
infarction, if the pain is less than 6 hours in duration, interventions to recanalize
the occluded coronary artery are applicable. The recanalization rates with
streptokinase in the first hour are 75 per cent and are only 40 per cent in the sixth
hour. Significant reduction in mortality occurs if the patient reaches the hospital
early and thrombolytic therapy is given (Table 7.6).
The crucial importance of the time factor in the setting of myocardial infarction
should be stressed at all relevant professional and public fora.
In a very useful study, Cox and associates have shown that patients with
acute myocardial infarction who are otherwise eligible for thrombolytic therapy,
have a high likelihood of developing an infarct even if they are free from chest pain
Table 7.6: Importance of early thrombolytic therapy in acute myocardial infarction

Time from onset Reduction in mortality
< 1 hr 47%
< 3 hrs 23%
3–6 hrs 17%
6–9 hrs 11%
before lytic therapy is begun. Lytic therapy appears to be safe in this group of
patients as in those with continuing chest pain; also subsequent left ventricular
function is better. Thus, it is reasonable to consider thrombolytic therapy for patients
with ST elevation and ischemic chest pain of less than 4 hours duration who
become free of chest pain with nitrates, morphine or betablockers.
Character of pain: The pain is usually described as heaviness, constricting or
choking. However the character is highly variable and should not be relied upon.
Burning pain is common and could be confused with acid peptic disease. A diffuse
burning pain all over the anterior chest, is highly suggestive of acute myocardial
70 ischemia. A significant number of patients come with a ‘difficult to describe’ type
of discomfort. This non-specific and vague feeling is particularly associated with
myocardial ischemia. The terms commonly used by people vary from country to
country and in the same country from place to place. The student and practitioner
should be aware of these descriptions in the community in which they practise
medicine.
The terms commonly used to describe the chest discomfort of myocardial
ischemia are:
• Heaviness
• Squeezing
• Gripping
• Compression
• Burning
• Gas
• Acidity
• Uneasiness
• Uncomfortable feeling
Severity of pain: The severity of pain is highly variable and is an unreliable feature
in the evaluation of chest pain. It is understandable when we know that the pain
of myocardial ischemia or infarction varies from absence of pain to extremely
severe pain. In many patients, the pain is so mild that they fail to seek medical
opinion. The classic descriptions of pain of myocardial infarction as one of the
most severe pains next only to the pain of acute pancreatitis, perforated peptic
ulcer and aortic dissection is true only in a minority of patients. Narins et al in a
prospective study evaluated the relationship between pain tolerance and several
clinical variables and ischemic test variable including stress thallium scintigraphy.
Patients with high pain threshold had less angina prior to the index coronary
event but more inducible ischemia after the event. There was no difference in
cardiac event rates (death or non-fatal myocardial infarction) between the low and
high pain threshold groups. Patients with high pain threshold are usually younger.
Aggravating and relieving factors

Relation to a physiological act: In the evaluation of pain anywhere in the body,
this feature is the most valuable. For example, the pain of peptic ulcer is related to
food and movement of the body part aggravating the musculoskeletal pain. The 71
pain of classic angina is related to exertion and is relieved by rest. Unlike
musculoskeletal pain, where the pain starts flush with the beginning of exercise,
the pain of angina starts some time after the exercise and subsides some time after
the cessation of exercise. In other words there is always a lag period between the
beginning of exercise to the onset of pain, and cessation of exercise to relief of
angina. Pain that starts a few minutes or hours after the cessation of exercise is
also not due to angina. Apart from exercise, other factors can precipitate angina
like exposure to cold or hot weather, food, bending forward, dreams, and emotions.
Myocardial oxygen consumption depends upon the following determinants:
• Heart rate
• Blood pressure
• Myocardial contractility
• Wall tension
All the above factors precipitate myocardial ischemia either by increase in
demand or by decrease in supply of coronary flow. Chauhan et al in a study
demonstrated angina pectoris precipitated by acid stimulation of esophagus in
Table 7.7: Precipitating factors for angina

Factor Mechanism
Exercise Heart rate, blood pressure
Emotion Excessive catecholamines
Heart rate
Blood pressure
Cold environment Vasoconstriction
Blood pressure
Coronary vasoconstriction with diminished
coronary reserve
Hot environment Vasodilatation
Reflex tachycardia
Cardiac output
Food Splanchnic vasodilatation
Cardiac output
Reflux esophagitis Linked angina due to acid stimulation
Dreams Emotion
Precipitation of arrhythmia
Supine position Increased venous return
72 Increased end-diastolic volume of ventricles
Increased wall tension
Bending forward ? Reflex coronary vasoconstriction
? Compression of epicardial coronaries
Fever especially with chills Vasodilatation and reflex tachycardia
and rigors Chills and rigors are similar to muscular
exercise
Straining at stool or Like Valsalva straining phase
micturition Fall in central aortic pressure
Reflex tachycardia
patients with angiographically proven coronary artery disease. Acid stimulation of

esophagus failed to elicit angina in a group of patients with heart transplantation,
proving the neural reflex mechanism. As this angina is related closely to esophageal
stimulation by acid, this is termed as linked angina. Marchant et al studied the
effects of cold weather in patients with angina pectoris. They showed that exposure
of patients to cold weather causes peripheral vasoconstriction and an increase in
blood pressure, particularly at submaximal exercise level. In spite of rise in blood
pressure, increase in myocardial oxygen consumption may not occur if the heart
rate is reduced by the baroreceptor mechanism.
Table 7.8: Clinical situations where drugs can precipitate angina

Clinical state(s) Mechanism
Bronchial asthma
Sympathomimetics Tachycardia
Ephedrine Hypertension
Alpha-2 stimulants (Salbutamol) Cardiac output
Myocardial contractility
Steroids
Salt and water retention
Hypertension Cardiac output
Nasal allergy
Decongestants/sympathomimetics Hypertension, tachycardia
Hydralazine Sinus tachycardia
Nifedipine Sinus tachycardia
Coronary steal phenomenon
Hypotension
Diabetes mellitus
Insulin and oral drugs Hypoglycemia
Tachycardia
Hypertension with adrenergic excess 73
Nifedipine Reflex tachycardia
Coronary steal
Nitrates/nitroglycerine Mitral valve prolapse or hypertrophic
cardiomyopathy mistaken for CAD
Aspirin Anemia due to GI bleed

Hypothyroidism
Thyroxine Excessive dosage
Tachycardia
Cardiac output
Joint disease
NSAIDs Fluid and salt retention
Steroids Hypertension
Anemia due to GI bleeding
Peptic ulcer
Parasympatholytics Tachycardia
Antacids Interfere with absorption of anti-
anginal agents
Depression/chronic pain
Tricyclic anti-depressants Ventricular arrhythmias
Hypertension
In patients with abnormal baroreceptor function, the reduction in heart rate

may not occur in response to cold induced increase in blood pressure. The rate
pressure product increases resulting in ischemia at lower work load. This mechanism
explains the variability in clinical behavior between ‘cold tolerant’ and ‘cold
intolerant’ patients with angina. The baroreceptor function is abnormal in cold
intolerant patients.
The accompanying chills and rigors in fever act like muscular exercise and
may precipitate a myocardial infarction in a patient with significant angina or
unstable angina.
Certain drugs can precipitate or aggravate the existing angina by increasing
the heart rate, blood pressure or cardiac output (Table 7.8).
The patient with angina and another systemic disorder is best helped by a
comprehensive approach taking into consideration the interaction between two
diseases and the drug therapy. Especially important fact is that anemia often
aggravates angina.
Angina is relieved by rest, sublingual nitroglycerine and sitting or standing
(Table 7.9). In some patients angina is relieved by belching. Both sublingual
74 nitroglycerine and sitting reduce venous return or preload. Additionally,
nitroglycerine decreases aortic pressure (afterload). Relief with nitroglycerine should
be prompt (2 minutes) for it to suggest the diagnosis of angina. Relief occurs with
Table 7.9: Angina pectoris: relieving factors
Factor Mechanism
Rest Heart rate
Blood pressure
MVO2
Sublingual nitroglycerine Venous return (preload)
Blood pressure
MVO2
Sitting/standing Venous return (preload)
MVO2
Belching Reflex?
Mechanism not clear
Walking through Exercise induced peripheral
vasodilatation
Coronary vasodilatation?
Recruitment of collaterals?
a mean time of 1.9 minutes with sublingual nitroglycerine but takes 2.9 minutes
(chewable) and 3.4 minutes (sublingual) with isosorbide dinitrate (Sorbitrate). Relief
occurring much later should suggest some other diagnosis. Relief with nitroglycerine
may occur in esophageal spasm, gall bladder colic or any smooth muscle spasm.
The tablets should be fresh, unexposed to light, should be chewed to powder and
then kept under the moist tongue. In contrast to the exertional pain of classic
angina pectoris, pain at rest is a feature of acute myocardial infarction and unstable
angina. The pain of vasospastic angina also occurs at rest, usually at night.
The presence of rest pain means that there is absolute reduction in coronary
flow and not relative increase in myocardial oxygen requirements (Table 7.10).
The term mixed angina is applied when in a patient with exertional angina (or
fixed angina due to fixed obstruction), occasional pain occurs at rest, particularly
at night or early morning. This has therapeutic significance as a combination of
betablockers and calcium blockers is effective.
Occasionally, in patient with ‘mixed’ angina, vasospastic angina may be
precipitated by betablockers. Addition of calcium blockers relieves it. Angina
induced by emotion usually lasts longer than exertional angina and may be mistaken
for unstable angina. Nocturnal angina is generally suggestive of associated left 75
ventricular failure but also occurs in a variety of other conditions.
Accompanying symptoms: The accompanying symptoms are those related to
the abnormally contracting myocardium and the conducting tissue.
Table 7.10: Mechanisms of rest pain
Cause Mechanism
Acute myocardial infarction Occlusive thrombus superimposed
over a preexisting coronary stenosis
Unstable angina Atherosclerotic plaque rupture
Thrombus
Platelet aggregates
Vasospastic angina Coronary vasospasm
(Prinzmetal angina)
Mixed angina Fixed obstruction with superimposed spasm
Emotion induced angina Catechol excess
Tachycardia
Hypertension
a) Dyspnea: Shortness of breath occurs either as an anginal equivalent or as a

manifestation of left ventricular failure. This symptom suggests a large area of
myocardium at risk and these patients require early evaluation and revascularization.
When shortness of breath is the presenting feature in a patient with no pulmonary
disease, and normal left ventricular systolic function, one should consider the
possibility of angina pectoris or diastolic dysfunction.
b) Syncope: Transient loss of consciousness may occur either due to the low cardiac
output due to loss of contracting myocardium, or arrhythmia. Vasospastic angina
or Printzmetal angina may present with syncope of unexplained origin without
chest pain. Though chest pain with syncope is often an indicator of coronary
artery disease, alternative diagnostic possibilities should be considered (Table 7.11).
Recurrent syncope due to chronic stable angina is distinctly uncommon and a
single episode suggests an acute coronary syndrome, usually inferior wall myocardial
infarction.
Due to the area of overlap, upper gastrointestinal disorders and acute
pancreatitis are often mistaken for coronary artery disease.
c) Vomiting: Vomiting may accompany chest pain or may even be the presenting
76 feature in myocardial infarction (Table 7.12). It is more likely to occur in the
setting of acute inferior infarction due to excessive para-
sympathetic excess.Vomiting may also be the dominant feature in myocardial
Table 7.11: Causes of chest pain with syncope
Condition Mechanism
Acute myocardial infarction Large area of myocardium at risk
Arrhythmias
Vasospastic angina Arrhythmias (VT/VF)
Angina pectoris Large area of myocardium at risk
Arrhythmia
Acute pulmonary embolism Obstruction to circulation
Pericardial tamponade Cardiac compression
Tension pneumothorax Cardiorespiratory embarrassment
Pleural hemorrhage Cardiorespiratory embarrassment
Upper gastrointestinal bleeding Loss of blood
Acute pancreatitis Hypovolemia due to chemical peritonitis
Severe pain
Table 7.12: Causes of vomiting in acute myocardial infarction

Cause Distinguishing feature
Acute inferior MI Other symptoms of parasympathetic
excess like bradycardia
Drug induced Morphine, aspirin, rarely nitrates
Cardiac rupture Bradycardia, weakness, urge to pass stool
Pericarditis type of pain
rupture occurring as a complication of acute myocardial infarction. Aspirin and

morphine given in acute myocardial infarction may also be responsible for vomiting.
Vomiting may also be a feature of acute right heart failure due to right ventricular
infarction.
The esophagitis following vomiting often simulates the chest discomfort of
acute coronary syndromes, and a mistaken diagnosis of coronary artery disease is
often made.
d) Symptoms of autonomic excess: The symptoms related to excessive autonomic
discharge are common in acute myocardial infarction and unstable angina but are
uncommon with chronic stable angina (Table 7.13). 77
These symptoms of autonomic excess are suggestive of visceral origin to
pain in contrast to somatic pain. They are not diagnostic of myocardial ischemia
or infarction. In the absence of chest pain, one more of these symptoms may be
the only indicators of myocardial ischemia or infarction.
Painless myocardial infarction or ischemia: A third of myocardial infarctions
are unrecognized; these include completely asymptomatic (silent) events and those
with atypical symptoms. The patient or the physician (when contacted) do
notentertain the diagnosis of acute myocardial infarction.
Table 7.13: Symptoms and signs of autonomic excess
Sympathetic excess Parasympathetic excess

Sweating Weakness
Anxiety Nausea
Fear Vomiting
Palpitation (tachycardia) Bradycardia
Hypertension Hypotension
The causes of painless MI could be:

• In diabetic patients due to autonomic neuropathy
• In elderly patients with dementia or cerebrovascular disease
• Under general anesthesia
• In pulmonary edema when dyspnea is the dominant feature
• ? Betablocker therapy
• A quarter of patients do not have pain
• Failure on part of the patient/doctor to recognize the symptoms
Patients with diabetes are prone to silent myocardial infarction and silent
exertional ischemia. Though the exact mechanism is unclear, it may reflect an
impairment of the sensory innervation of the heart. Gamini et al studied anginal
perceptual threshold in 32 diabetic patients and 36 non-diabetic control patients,
all of whom had typical exertional angina. Anginal perceptual threshold was defined
as the time from onset of 0.1 mV ST depression to the onset of chest pain during
treadmill stress electrocardiography. Anginal perceptual threshold is delayed in
the diabetic group compared to the controls.
78 When myocardial infarction is painless, the only clue can be the presence of
one of the associated symptoms. Unexplained dyspnea, palpitation, syncope, or
any of those symptoms listed above either in combination or in isolation should
make one suspect myocardial infarction or ischemia. When myocardial infarction
develops during anesthesia, unexplained hypotension, hypertension, tachycardia
or bradycardia or ventricular arrhythmia may be the only clue. In a recent study
Theisen et al observed that patients with unrecognised AMI showed greater
‘alexithymia’ or deficient psychological awareness and a greater belief that chance
or fate determines their health. In India, religious beliefs, belief in alternative systems
of medicine and economic factors also may play varying roles.
It is presently recognized that 60–80 per cent of ischemic episodes are
asymptomatic. These silent ischemic episodes can be prolonged up to 40 minutes
(Table 7.14).
Total ischemic burden is defined as the total duration of ischemia in minutes
for 24 hours with or without symptoms. A total of more than 60 minutes connotes
a poor prognosis. It has been proved that total ischemic burden is a better predictor
of prognosis than symptoms alone.
Table 7.14: Classification of silent myocardial ischemia

Type Clinical subset
Type I Silent ischemia in asymptomatic patients
(detected by exercise screening)
Type II Asymptomatic post-myocardial infarction
patients
Type III In symptomatic stable or unstable angina
Symptoms due to associated disorders: In the management of patients with

coronary artery disease, the presence of associated disorders has significant
implications (Table 7.15).
Table 7.15: Significance of symptoms of associated disorders
Condition Significance
Acid peptic disease Difficulties in evaluation of pain
Mistakes in diagnosis between acid peptic disease
and clinical expressions of CAD are common
Contraindication to thrombolytic therapy or
anticoagulants and aspirin 79
Bronchial asthma Mistakes in differential diagnosis with left
ventricular failure (LVF)
Betablockers contraindicated
Allergic reactions to STK and contrast are more likely
Hypertension Contraindication to thrombolytic therapy
(> 110 mmHg, Indication for aggressive management of hypertension
diastolic) during acute MI
Obstructive uropathy The acute stress of MI, atropine, vasodilators and
diuretics may precipitate acute retention of urine
During interventions like PTCA, need for an
indwelling Foley’s catheter may arise
Recent cerebrovascular May be a contraindication to thrombolytic therapy
accident
Diabetes mellitus Hypoglycemia may precipitate or simulate
angina/left ventricular failure.
Contrast induced renal failure is more likely
Renal failure Choice and dosage of medication may need change
Use of non-ionic contrast may be appropriate
for angiographic procedures. Precautions need to be taken.
A thorough knowledge of the presenting manifestations of disorders

producing pain in the chest is essential for a proper evaluation of each patient. A
brief description of each of these entities is given below.
ANGINA PECTORIS
The typical characteristics of angina pectoris are shown in Table 7.16.
Table 7.16: Characteristics of angina pectoris
Feature Description
Location Substernal and a similar area over back
Left shoulder and arm
Interscapular area on either side
Both shoulders
Any where between upper abdomen to lower jaw
Lower cervical or upper thoracic spine
Lower jaw
Only right shoulder or arm
Quality Pressure like sensation or heaviness
80 Constriction around chest or larynx or trachea
Burning
Tightness
Shortness of breath
Suffocating feeling
Uneasiness
Difficult to describe feeling
Deep aching
Duration 0.5–30 minutes
Precipitating and Exercise
relieving factors Food
Emotion
Cold/hot environment
Sexual intercourse
Relief with nitroglycerine
Relief with rest
Relief with upright posture
Radiation Medial aspect of left arm
Left shoulder
Jaw
Occasionally right arm
Feature Description
Physical findings Heart rate and blood pressure
during angina Prominent a wave in JVP due to right ventricular
ischemia
Palpable precardial impulse due to dyskinesia
S4
S3 in case of left ventricular failure (LVF)
Mitral regurgitation due to papillary muscle
dysfunction
Crepitations over lung bases due to LVF.
ECG Normal or ST segment depression or T wave
inversion
Exercise testing Exercise induced ST depression, fall in blood
pressure, and wall motion abnormalities
Coronary arteriography Fixed obstruction >75% in one vessel or >50%
lesion in more than one vessel
Table 7.17: Functional classification of angina pectoris: (Canadian Cardiovascular Society +

Goldman’s specific activity scale)
Class I Ordinary physical activity such as walking and climbing stairs does 81
not cause angina. Angina with strenuous or rapid or prolonged
exertion at work or recreation.
Can perform any activity requiring 7 METs
Class II Slight limitation of ordinary physical activity, walking or climbing
stairs rapidly, walking uphill, walking or stair climbing after meals in
cold in wind, or when under emotional stress or only during the
few hours after awakening. Climbing more than one flight of ordinary
stairs at a normal pace in normal conditions. Ordinary walking for
less than two blocks on the level or climbing one flight of stairs
does not cause angina.
Can perform any activity requiring 5 METs, but cannot perform to
completion any activity requiring 7 METs
Class III Marked limitation of ordinary physical activity, walking less than
two blocks on level ground and climbing one flight in normal
conditions.
Can perform any activity requiring 2 METs, but cannot perform to
completion any activity requiring 5 METs
Class IV Inability to carry on any activity without discomfort, anginal
syndrome may be present at rest but must be brief (if longer than
15 minutes, it is called unstable angina)
Cannot perform any activity requiring 2 METs
NOCTURNAL ANGINA
Chest pain awakening the person from sleep or occurring at night at rest is called
nocturnal angina. The wider meaning of nocturnal chest pain extends to that of
pain occurring at night. Nocturnal pain at rest implies sudden and severe
decompensation of the supply and demand balance of myocardial perfusion. In
the absence of occult and extreme increases in demand, such as accelerated
hypertension or severe anemia, nocturnal pain refers to sudden loss of myocardial
perfusion (that is, occlusive coronary artery disease) of any type.
The causes of nocturnal angina could be:
• Acute coronary syndromes
• Associated left ventricular failure
• Vasospastic angina
• Left main coronary artery disease
• Mixed angina
• Betablockers precipitating vasospasm
• Nocturnal angina with dreams due to propranolol
82 • Angina in severe aortic regurgitation
• Accelerated hypertension
• Inadequate spacing of drug therapy
• Nocturnal angina of sleep apnea
Vasospastic angina usually occurs at night or in the early hours of the morning
since coronary vascular tone is highest at this time. In patients with mixed angina,
the exertional angina responds to betablockers but the rest angina due to vasospasm
continues or may get aggravated. This responds promptly to the addition of calcium
blockers. Angina is less common in aortic regurgitation and often occurs at rest or
nocturnally. The bradycardia of sleep increases aortic regurgitation, decreases the
aortic diastolic pressure and increases the left ventricular diastolic pressure. As a
result, the coronary perfusion pressure decreases, precipitating angina. The
hypoxemia of sleep apnea may induce nocturnal angina. In the study by Franklin
et al sleep apnea was present in 9 of 10 patients with nocturnal angina pectoris.
POSTPRANDIAL ANGINA
Postprandial angina is defined as angina occurring within 30 minutes of a meal
and repeatedly reproducible by the same stimulus. The common patterns are
postprandial angina at rest, postprandial exertional, and isolated postprandial angina.
Postprandial angina pectoris is a well known symptom and was recognized
by Heberden in 1772 and William Osler in 1897. The mechanism of postprandial
angina is unclear. Postprandial redistribution of blood flow away from coronary
circulation when it occurs at rest is likely. Redistribution to the gut and exercising
muscles is likely in postprandial exertional angina. However, animal experiments
in dogs and studies in human volunteers failed to support this idea. Other possible
mechanisms suggested are coronary vasoconstriction secondary to postprandial
gastric and esophageal dilation or gastric receptor stimulation, increased
postprandial myocardial oxygen consumption (increased demand), increased
postprandial cardiac output, postprandial lipid induced decrease in myocardial
oxygen transport, and possible role of vasoactive intestinal peptide in modulating
the cardiac response to food intake. A recent study by Berlinerblau et al suggested
postprandial angina as a marker for severe coronary artery disease, and is often
associated with unstable angina. It is often associated with left main or severe
triple vessel disease.
83
UNSTABLE ANGINA
Unstable angina is defined as absence of ECG and enzymatic evidence of acute

MI, crescendo angina on a preexisting chronic stable angina, angina at rest and on
minimal exertion or angina pectoris of new onset (less than 1 month). It is also
known as preinfarction angina, crescendo angina, acute coronary insufficiency or
intermediate coronary syndrome.
As unstable angina comprises of a heterogeneous subset of conditions, the
following classification is suggested by Braunwald. The severity, the clinical
circumstance, and the presence or absence of ECG changes, and the therapy
received and response to it were taken into consideration. The bases of the
classification (Table 7.18) are the following factors:
• Severity of clinical manifestations
• Clinical circumstances
• Presence or absence of transient ECG changes
• Nature of therapy, and the response to it.
Table 7.18: Classification of unstable angina

Severity
Class I New onset, severe or accelerated angina
Patients with angina of < 2 months
Increase in severity, frequency, precipitated by lesser exertion.
No rest pain in the last 2 months.
Class II Angina at rest, subacute
Patients with one or more episodes of angina at rest during the preceding
month but not within the preceding 48 hours.
Class III Angina at rest, acute
Patients with one or more episodes at rest within the preceding 48
hours.
Clinical circumstances
Class A Secondary unstable angina
A clearly defined condition extrinsic to the coronary vascular bed that
has intensified myocardial ischemia.
Anemia often due to gastrointestinal bleeding related to aspirin
Fever
Infection
Hypotension
84 Tachyarrhythmia
Thyrotoxicosis
Hypoxemia due to respiratory failure
Class B Primary unstable angina
Class C Postinfarction unstable angina < 2 weeks of myocardial infarction
Treatment Intensity of treatment
1 No treatment or minimal treatment
2 Occurring in presence of standard therapy for chronic stable angina
(conventional doses of oral betablockers or nitrates.)
3 Occurring despite maximally tolerated doses of all three categories of
oral therapy, including intravenous nitroglycerine.
Unpredictability is the hallmark of unstable angina. It is important to recognize

unstable angina because of the disabling nature of symptoms and the possibility
of it ending in acute myocardial infarction.
The National Heart, Lung and Blood Institute published practice guidelines
which defined unstable angina:
Unstable Angina is defined as having three possible presentations:
• Symptoms of angina at rest (usually prolonged >20 minutes).
• New onset (<2 months) exertional angina of at least Canadian

Cardiovascular society Classification (CCSC) Class III in severity.
• Recent (<2 months) acceleration of angina as reflected by an increase in
severity by at least one CCSC Class to CCSC Class III.
In most, but not all, of these patients symptoms will be caused by significant
coronary artery disease. Unstable angina has to be viewed as part of the spectrum
of acute coronary syndrome. Variant angina, non-Q wave myocardial infraction,
and post-MI (>24 hours) angina are part of the spectrum of unstable angina.
ACUTE MYOCARDIAL INFARCTION
APPROACH TO A PATIENT WITH ACUTE CHEST PAIN

Both unstable angina and acute myocardial infarction require hospitalization and
management. Before considering any interventions in acute coronary syndromes,
rule out acute abdominal disorders simulating them. Pain in the chest is the
commonest symptomatic expression of coronary artery disease (which is the
commonest cause of death in adult population). A physician who is not proficient 85
in evaluating it, is at a serious disadvantage in his practice and himself becomes an
additional risk to the patient. Unfortunately, the present curricula of undergraduate
and postgraduate education fosters this incompetence further.
Clinical features of acute myocardial infarction are given in Table 7.19.
Table 7.19: Coronary artery disease: acute myocardial infarction
Feature Description
Precipitating factors No precipitating factor in 50% of patients
Heavy exertion
Modest exertion
Surgical procedure
Sleep 8%
Emotional stress 18% (increase in life change units)
Within a few hours after heavy physical exercise
Physical exertion under emotional stress or fatigue
Drug withdrawal (betablockers, nitroglycerine in munitions
workers)
Ergot preparations as for migraine
Respiratory infections
Acute pulmonary embolism
Feature Description
Hypoxemia due to any cause
Hypoglycemia
Vasospasm
Tachycardia due to any cause
Fever
Time of the day Early morning hours due to
(Circadian rhythm) Catecholamines
Cortisol
Platelet aggregability
(Exceptions to circadian periodicity
Patients receiving aspirin and betablockers)
Prodromal symptoms 20–60% of patients have prodrome of angina 1–4 weeks
prior to MI
Nature of pain at Acute gradually increasing in severity, may wax and
onset wane
Location/radiation Retrosternal and a similar area over the back
Spreads to either side of chest anteriorly more to left
Ulnar aspect of the left arm with numbness in the wrist,
hand and even fingers
86 May radiate to shoulders, upper limbs, neck, jaw and
interscapular region
Rarely the pain may begin in the epigastrium
Duration Prolonged > 30 minutes to many hours
Severity of pain Variable (often severe, occasionally intolerable or mild)
Character Heaviness, squeezing, choking, constricting, crushing, boring,
stabbing, knifelike, burning, ‘palpitation’
In patients with past angina the pain is similar to angina but
is longer and severe
Relieving factors Usually not relieved by nitroglycerine
May be relieved fully or partially if spasm is the dominant or
associated feature
Analgesics (morphine) may relieve it
Thrombolytic agents may relieve it by recanalizing occluded
vessel
Congestive heart failure de novo or worsening of existing
failure
Atypical presentations Like classic angina pectoris
Atypical location of pain
Central nervous system manifestations
Embolic stroke
Feature Description
Transient ischemic attack due to low cardiac output with
underlying cerebrovascular disease
Apprehension and nervousness
Psychiatric manifestations
Syncope
Extreme weakness
Acute indigestion
Peripheral embolism
Physical signs Tachycardia or bradycardia
Hypertension or hypotension
JVP elevated with CCF or RV infarction
Palpable dyskinesia over precordium
S4 or S3
Mitral regurgitation
VSD
Angiographic Thrombotic occlusion of one of the major
correlation epicardial artery with a preexisting stenosis
Rapid identification and treatment of acute MI

If you cannot make a diagnosis, make a decision. 87
Chester M. Jones
It is important to identify acute MI as early as possible (Table 7.20).

Table 7.20: Approach to a patient with acute chest pain: differential diagnosis
If non-cardiac, rule out Acute peptic ulcer syndromes
Esophageal spasm/esophagitis
Acute pancreatitis
Acute cholecystitis
Acute tension pneumothorax
If cardiac, is it due to Coronary artery disease?
Pericarditis?
Acute pulmonary embolism?
Aortic dissection?
Mitral valve prolapse?
Hypertrophic disorders?
Severe aortic stenosis?
Hypertrophic cardiomyopathy ?
If due to CAD is it Acute myocardial infarction?
due to Unstable angina?
Chronic stable angina?
Vasospastic angina?
Mixed angina?
If due to chronic What is the functional category?
stable angina Is there occasional rest pain suggesting mixed angina?
Is there recent change in angina suggesting unstable angina?
How many hours elapsed after the onset of pain?
If due to acute MI What is the extent of myocardium at risk?
Even if the diagnosis is uncertain, routine drug therapy (nitrates, betablockers,

calcium blockers, antiplatelet agents) should not be delayed. The decision to
discontinue the drugs can be taken after serial observation and follow-up stress
test. Medical literature is full of information on how to handle patients with acute
chest pain. Guidelines regarding admission and management into coronary care
units are also provided based upon these studies Table 7.21 presents a possible
approach to the management of such a patient.
One must realize that absence of proof is not proof of absence.
Table 7.21: Approach to management of a patient with acute chest pain
Category Proposed action
88
Acute chest pain Do not waste time
typical for acute First things first.
ischemic syndromes Check vital signs
with abnormal ECG Insert IV line
Monitor rhythm
Bradycardia and hypotension: IV atropine/pacing
Irregular pulse: monitor rhythm and appropriate treatment
If the ECG shows evolving MI, make arrangements for
thrombolysis or angioplasty.
Pain as above but no Manage as above but withhold thrombolysis
objective evidence Administer heparin, aspirin, nitroglycerine, nitrates,
betablockers if no contraindication exists
Pain atypical but CAD Hospitalize but not necessarily in CCU / TRIAGE Unit
can not be ruled out Look for enzyme elevation including troponin and CPK–
with confidence MB.
Drug therapy as above but the physician should use judgment
and individualize
Chest pain clearly Rule out
non-cardiac Acute peptic ulcer syndromes
Esophageal spasm or esophagitis
Acute pancreatitis
Acute cholecystitis
Patient does not need hospitalization if the above conditions
are ruled out
CHEST PAIN AND CORONARY ANGIOGRAPHY/ANGIOPLASTY
Chest pain is a common adverse event during diagnostic coronary arteriography.

The incidence of severe angina is reduced by use of low osmolality contrast media.
A recent study by Mathai et al showed angina related to type of contrast agent
used but not to hemodynamic effects produced by the contrast.
The chest pain during coronary angioplasty is principally due to two
mechanisms. One is related to myocardial ischemia during balloon inflation and
the other related to mechanical stretch of the vessel wall itself. Fabrizio and
associates showed that during coronary angioplasty, the cardiac pain experienced
by patients is caused in part by stretching of the vessel wall. If the stretching is
maintained at a constant level during repeated coronary occlusions, the cardiac
pain is entirely predicted by the severity of myocardial ischemia and does not
appear to be directly modulated by the mechanisms responsible for the ischemic
preconditioning. Cardiac pain can be caused by chemical, thermal, and mechanical
stimuli and the cardiac sensory receptors are polymodal. The presence of chest
pain during angioplasty is an indication that the myocardium supplied by the vessel
is viable. 89
The causes of chest pain due to coronary angioplasty are:
During angioplasty
Myocardial ischemia
Balloon inflation
Mere presence of wire/balloon across a tight lesion
Coronary spasm
Damping of the main artery by guiding catheter
Distal embolization
Vessel wall stretch
Pericardial pain due to perforation of vessel
Immediatelyfollowingangioplasty
Vessel closure
Coronary spasm
Non-cardiac pain
PERICARDITIS
The characteristics of pain due to pericarditis are given in Table 7.22. As pericarditis
is usually due to some other systemic disorder, there is often evidence of systemic
infection like tuberculosis, septicemia, malignancy, or myocardial infarction. It is
important to recognize the associated pericarditis in acute myocardial infarction.
ACUTE PULMONARY EMBOLISM
The characteristics of the chest pain of acute pulmonary embolism are:

• Pleuritis type of pain in the axilla or interscapular region
• Central substernal pain like that of myocardial ischemia
• Dyspnea is the main symptom
• Central cyanosis may be present
• Sinus tachycardia is present
• Hypotension with elevated JVP and clear lungs
Sudden onset dyspnea in a patient with predisposing factors favours the
90 diagnosis. Sinus tachycardia is always present and bradycardia rules out the diagnosis.
Table 7.22: Features of pericarditis
Site Substernal, on either parasternal region
Posterior or anterior cervical region
Either trapezius or either shoulder, usually left
Epigastrium or upper abdomen
Radiation to arm or forearm is rare
Character and severity Sharp or dull ache
Pain may be very severe or mild
Pain may be absent
Aggravating factors Respiration
Turning to side
Lying on the back
Relieving factors Sitting and leaning forward
Steroids/analgesics
Associated features Pericarditis is almost always secondary to some other
systemic disorder or spread from other sites
Pericardial rub
Fever
Signs of effusion/tamponade
Cyanosis though useful, is difficult to make out. The chest x-ray and ECG are
often normal.
AORTIC DISSECTION
Acute aortic dissection though rare is often mistaken for the pain of acute
myocardial infarction or unstable angina. Common features are:
• Sudden or dramatic onset of pain with gradual waning
• The pain is often ripping, tearing or stabbing
• Can simulate the pain of acute MI or unstable angina but is more
commonly felt over the back
• Radiates to the neck, shoulders, abdomen or lower limbs if those arteries
are involved in the process of dissection
• Features of acute myocardial infarction if the coronaries are involved in
the dissecting process
• The murmur of AR if the aortic valve is involved
• Asymmetry or absence of arterial pulses
91
• Predisposing conditions like systemic hypertension, Marfan’s syndrome
Aortic dissection can be confused for acute ischemic syndromes because of
the similarity of pain and the frequently associated ST-T alterations of longstanding
severe hypertension. It is important to differentiate between the two disorders
because anticoagulant or thrombolytic therapy may be dangerous dissecting with
Table 7.23: Pain of aortic dissection: correlations

Location of pain Site of dissection
Dominant anterior Proximal dissection (DeBakey’s
thoracic pain Types I, II)
Dominant interscapular Distal dissection (90%) (DeBakey’s
pain Type III)
Both anterior and Proximal and distal dissection
posterior pain
Absence of Distal dissection is highly unlikely
interscapular pain
Pain in the neck, jaw, Dissection involving ascending
teeth, throat aorta and arch
a hematoma of the aorta.

The location of pain may correlate with the site of dissection (Table 7.23).
Aortic dissection should be ‘looked for’ in any patient with chest pain with any of
the following presenting features (Table 7.24).
Table 7.24: Aortic dissection: possible presenting features
Presenting feature Mistaken for Mechanism
Acute chest pain Acute MI Aortic tear
Unstable angina
Acute interscapular or Musculoskeletal pain Aortic tear involving the
low back pain Acute disc prolapse descending thoracic or
abdominal aorta
Asymmetry of arterial Embolic occlusion Dissection involving branches
pulses of aorta
Aortic regurgitation (50% Acute AR Dilatation of aortic root
of proximal dissections) and annulus by dissection
Asymmetrical dissecting
hematoma pressing on one
of the leaflets
92 Tear of annular support for
leaflets or leaflets
Pericardial type of pain Pericarditis
with rub or effusion or Hemorrhaged cardiac
tamponade tamponade (malignancy) Dissection into pericardium
Neurological deficit Acute stroke TIA Proximal or distal dissection
Acute paraplegia involving various arteries
Acute peripheral
neuropathy
Acute MI by ECG Acute MI alone Dissection involving
coronaries
Acute abdominal Acute abdominal Dissection of
pain/Ileus emergency abdominal aorta
Mesenteric occlusion
Renal infarction
Severe hypertension, Hypertensive Renal infarction
altered sensorium encephalopathy Renal failure
Fever Fever of obscure Resolving hematoma
origin
Mediastinal widening Mediastinal mass Widened aortic shadow
In all patients presenting with acute chest pain, check for peripheral pulses to
rule out dissection of aorta. When a patient appears to be in shock but has
hypertension and has pain both above and below the umbilicus, aortic dissection
should be suspected. Aggressive control of hypertension and appropriately timed
surgery can be life saving. Unlike in acute ischemic syndromes, anticoagulants or
thrombolytic agents are contraindicated in this condition.
MITRAL VALVE PROLAPSE

Mitral valve prolapse (MVP) is relatively common and may present with chest
pain.
• Chest pain may suggest myocardial ischemia but is often atypical
• Patient is usually young, tall and lean
• Non-ejection click(s)/late systolic murmur on auscultation
• ECG shows ST, T alterations in inferior and lateral leads
• Exercise ECG may be falsely positive
• Echocardiography is diagnostic
• Carries a favourable prognosis in contrast to coronary artery disease. 93
Mitral valve prolapse should be distinguished from coronary artery disease.
MVP generally carries an excellent prognosis in comparison to coronary artery
disease. The mistake is compounded by the abnormal looking ECG, and false
positive exercise test. Nitrates which are commonly used in coronary artery disease
may aggravate the symptoms in mitral valve prolapse due to reduction in heart
size.
NON-CARDIAC CAUSES OF CHEST PAIN
Esophageal pain
Pain of esophageal origin accounts for 10–25 per cent of acute chest pains admitted
to emergency rooms to rule out acute myocardial infarction. Of all the causes of
non-cardiac pain, esophageal pain simulates anginal pain most closely. The features
of esophageal pain are listed below.
• Provocation by swallowing
• Oral regurgitation of liquid
• Retrosternal pain without lateral extension
• Relief by antacids
• Pain provoked by stooping
• Inconsistent relationship to exercise
• Frequent episodes of spontaneous pain
• Nocturnal pain
• Periods of prolonged remission
• Delayed response to nitroglycerine
• Accompanying symptoms (nausea, vomiting, swallowing difficulty, acid
eructations)
The pain of esophageal origin shares some of the features of angina making
the distinction difficult.
• Precipitated by exercise, emotion and food
• Pain radiating to left arm
• Relief by nitrates
• Nocturnal pain
Added to the above confusion, esophageal pain may precipitate myocardial
94
ischemia in a patient with coexistent coronary artery disease. The association of
the pain with swallowing, stooping forward, and oral regurgitation, and relief with
antacids, will help in the differential diagnosis. These symptoms in patients less
than 50 years favour an esophageal cause for the pain. As esophageal pain carries
a benign prognosis, it should not be labelled angina. It is equally important to
reach a positive diagnosis of esophageal pain before giving a benign prognosis as
it is dangerous to miss the diagnosis of significant coronary artery disease.
When a woman presents with chronic chest pain, it is not enough to make a
diagnosis of ‘non-cardiac chest pain’. Rule out carcinoma of breast by asking for a
mammographic examination. Delay in diagnosis of non-cardiovascular causes of
chest pain may prove fatal in certain situations.
Case summary
A 45-year-old married lady presented with chest pain of 6 months duration. The pain was
left sided and was variably related to exertion. The resting ECG and exercise ECG were
normal. The echocardiogram was within normal limits. She had mild hypertension which
was controlled with atenolol 50 mg per day. Her chest pain responded to alprazolam and
antidepressants. She was seen by three cardiologists and one physician within a period of
9 months for hypertension and occasional chest discomfort. Nine months later, she had
fever with chills, redness and mild swelling of the left breast. A mammographic evaluation
revealed a small discrete mass in the left breast. Aspiration cytology was suggestive of
ductal carcinoma of breast with mild axillary extension. A radical mastectomy was done.
The term ‘atypical chest pain’ is often used when one or more features are
atypical for angina. While symptoms may be due to myocardial ischemia, this
description also includes chest pain with low probability of angina or non-cardiac
chest pain. The term atypical chest pain does not rule out angina pectoris or
myocardial infarction.
Chest pain of undetermined etiology

About 10–30 per cent of patients with chest pain suggestive of coronary artery
disease are found to have normal or near normal coronaries. These patients were
often labelled as having Prinzmetal angina (vasospastic angina), microvascular
angina (small vessel disease), esophageal spasm or more commonly, syndrome X.
The term syndrome X was used by Kemp in 1973, to denote the uncertainty of
the etiology. Though there are differences of opinion about the pathophysiology
of this syndrome, there is universal agreement that the long term survival of patients
with chest pain syndromes associated with normal coronary arteries is excellent. 95
The survival is not influenced by an ischemic response in ECG during exercise
testing. The term microvascular angina was proposed by Cannon and Epstein in
1985, for this group of patients. These patients are suspected to have hypersensitivity
of coronary microcirculation to vasoconstrictor stimuli with an associated limitation
of microvascular vasodilator capacity. Dysfunction of the small intramural
prearteriolar arteries may be site of abnormality. The demonstration of coexisting
abnormal forearm hyperemic responses to ischemia, esophageal motility, and
bronchoconstrictor responses to methacholine inhalation suggest a generalized
disorder of vascular and other smooth muscle function. The demonstration of
coronary microvascular dysfunction in patients with systemic hypertension who
had chest pain, absent LVH and normal coronaries supports the concept. Some
of these patients are shown to develop deterioration in left ventricular function in
time. The common features in patients who have chest pain but have normal
coronary vessels are:
• Hypersensitivity of coronary microcirculation to vasoconstrictor stimuli
• Limited vasodilator capacity
• Abnormal forearm hyperemic response to ischemia

• Esophageal motility disorder
• Bronchoconstrictor response to methacholine inhalation
• Ischemic exercise ECG response in some patients
• Deterioration of left ventricular function over time in some patients
• Exercise induced LBBB which over a period of time develops LBBB even at
low heart rates.
In the last twenty years, investigation has not established any specific cause.
As more information is obtained, the syndrome has become more confusing. For
example, esophageal manometry when used in these patients sometimes revealed
an abnormality, thereby converting a manometric abnormality into a ‘disease’.
To many physicians and cardiologists, the absence of significant coronary
artery disease in angiogram excludes the heart as a potential cause of pain. If these
patients have relief with coronary vasodilators, it is important to continue the
same. There are many case examples when these patients have developed acute
myocardial infarction, when the coronary vasodilators were stopped abruptly. The
96
patients with chest pain of psychological origin suffer as much or sometimes more
than the patients with organic disease. Despite reassurance, many patients continue
to have chest pain, receive drugs, frequent hospitalization, and diagnostic testing
including cardiac catheterization. Adequate explanation and reassurance would
be helpful. The patient’s fears are best allayed by listening to him carefully and
sympathetically.
EVALUATION AND MANAGEMENT OF PATIENTS WITH NON-ACUTE CHEST PAIN

In the management of patients with coronary artery disease, it is vital to estimate
the severity of disease, for planning diagnostic studies and therapeutic approaches.
A recent study by Pryor and his colleagues from Durham, North Carolina, clearly
demonstrated the ability of simple history to predict the likelihood of severity of
coronary artery disease. They studied the clinical characteristics of 6,435 consecutive
patients that were most important in estimating the likelihood of severe disease. A
list of these features is given below.
The ability of each characteristic to predict the likelihood of severity of disease
increased with the presence of another characteristic. For example, in a patient
with typical chest pain, long duration of symptoms predicted severe disease more
accurately. The presence of hypertension, diabetes, and smoking were more
important predictors in women. Diabetes mellitus provides more prognostic
information about women patients than any of the other traditional risk factors.
In women presenting with chest pain, diabetes is the only risk factor that
distinguishes those with angiographically verified coronary artery disease from
those without it.
The clinical characteristics predicting severe CAD are:
• Age
• Gender
• Risk factors: Smoking, hypercholesterolemia, hypertension, diabetes mellitus
• Symptoms
• Pain type: Typical, atypical, non-anginal
• Duration of chest pain
• Pain frequency
• Accompanying dyspnea/syncope
• Evidence of myocardial damage
97
Congestive heart failure symptoms
ST-T wave changes
Ventricular gallop
Cardiac enlargement
• Premature ventricular complexes
• History of myocardial infarction
• Q waves on electrocardiogram
• Digitalis use
• Diuretic use
• Rales
• Heart murmur
• Left ventricular hypertrophy
• Conduction abnormalities
• Peripheral or cerebrovascular disease
The determinants of coronary artery disease in women with chest pain are:
Major
Typical angina pectoris
Postmenopausal status without hormone replacement

Diabetes mellitus
Peripheral vascular disease
Intermediate
Hypertension
Smoking
Lipoprotein abnormalities
HDL cholesterol levels
Table 7.25: Coronary artery disease: evaluation
Symptom Implication(s)
Angina at rest within Absolute contraindication to exercise testing
the preceding week. Calcium blockers should be given in addition to other
antianginal agents, as vasospasm plays a dominant role in
rest pain
As the intracoronary thrombus is common in unstable
angina, prior treatment with heparin and antiplatelet agents
like abciximab, clopidogrel will facilitate better outcome.
Direct coronary angiogram without exercise testing may be
98
indicated and may be more cost-effective
Surgical standby is needed even for coronary angiogram
Facility to support the circulation by IABP is
preferable
Angina Class III or Contraindication to exercise testing/angiogram is
more indicated straightaway
IABP/surgical standby is mandatory as the patient may start
deteriorating after angiogram
Non-ionic contrast is used preferably to avoid hemodynamic
side effects of ionic contrast
The number of injections should be limited
The first few views in coronary angiogram should be directed
to rule out left main coronary artery disease
Chest pain associated Right heart catheterization is mandatory in all patients
with shortness of who present with dyspnea, to estimate pulmonary
breath/syncope or arterial wedge pressures
hypotension
History of TIA, Avoid the inadvertent entry of guide wire or catheter
carotid bruit in neck vessels to avoid plaque disruption and
embolism
Minor
Age > 65 years
Obesity (especially central)
Sedentary lifestyle
Family history of coronary artery disease
Other risk factors for CAD (psychosocial, hemostat)
Tables 7.25 and 7.26 describe the value of symptoms in planning diagnostic
studies in patients with coronary artery disease and in making decisions in coronary
artery disease after coronary arteriography.
Even a single episode of rest pain within the preceding week should be
considered a contraindication to exercise testing. Exercise can precipitate serious
arrhythmias or even acute myocardial infarction in this setting.
Table 7.26: Treatment implications after coronary arteriography
Symptoms Decision
Angina Class I Medical therapy is the choice
Chronic stable angina No difference in survival between medical and
99
Class II surgical choices
Mildly +ve or –ve
stress test (Exercise capacity
> 7 METS)
Angina Class III–IV
3 vessel disease with Excellent surgical outcome
normal LV function 5 years survival 92% with surgery
Medical therapy 74% survival
3 vessel disease with Surgery definitely indicated
LV dysfunction Surgery 82% survival
Medical 52% survival
Asymptomatic post-MI CABGS does not prevent recurrent MI (CASS)
patient
Left main obstruction > 50%, Surgery indicated as sudden death is common
asymptomatic without CABGS
Surgery prolongs life
Asymptomatic patient with Revascularization is not indicated as errors in
50% lesion of one or interpretation are common in lesions of 40–70%
more coronary arteries The native disease progresses rapidly after surgery
PRACTICE IMPLICATIONS
In a patient with acute chest pain, do not waste valuable time by waiting for
an ECG to be done or going through all the details of family history. A ‘first
things first’ approach is mandatory here. Check vital signs (pulse rate and
blood pressure) even before asking for an ECG. If there is bradycardia and
hypotension, intravenous atropine can be life saving.
If the diagnosis of acute anterior myocardial infarction is obvious, start giving
soluble aspirin and thrombolytic therapy without delay if no contraindication
exists.
If a patient has diffuse anterior chest pain for the first time in his life, take it
seriously because it is almost always due to myocardial ischemia.
When anyone comes to the emergency room at 3 AM in the night, always
admit such a patient for observation even if you are clearly convinced that
the pain is non-cardiac. This is for two reasons: one that the patient may not
be telling you everything and you are not at your best at this time of the night.
Always be impressed by the veracity of nocturnal symptoms such as headache,
100 dyspnea, diarrhea, and chest pain – if they are serious enough to awaken the
person from sleep, they constitute the most sincere physiological testimony
and must be respected.
A normal electrocardiogram in the presence of clinical syndrome of acute
coronary ischemia does not rule out any acute ischemic syndrome or
myocardial infarction. It is such a patient who can be helped most by the
presently available methods.
Continuing pain in acute myocardial infarction may mean continuing ischemia
and calls for urgent intervention.
It is unwise and dangerous to do an exercise test in a patient with history of
rest anginal pain in the preceding week. Exercise test can be disastrous in this
situation.
Case summary
A 60-year-old retired accountant consulted a cardiologist for exertional chest discomfort
of 15 days duration and discomfort at rest of two days duration. The rest pain lasted 10–
15 minutes and was typical of myocardial ischemia. He was known to have systemic
hypertension for 20 years and diabetes mellitus for 15 years. The cardiologist did an
exercise test during which the patient developed severe substernal discomfort along with
ECG changes suggestive of severe myocardial ischemia. The pain was partially relieved
by sublingual nitroglycerine and he was advised to undergo coronary arteriography early
and was sent home to take rest with a prescription of standard antianginal drugs and
aspirin. The pain lasted for several hours but no electrocardiogram was done for next 2
days. Two days later he went to another hospital for recurrence of pain of 15 minutes
duration and was hospitalized. The ECG showed anterior myocardial infarction of
uncertain duration. After a 3 day course of intravenous heparin, he was subjected to
coronary arteriography. This revealed total occlusion of left anterior descending and 70
per cent lesion of proximal right coronary artery. The left ventriculogram revealed severe
hypokinesia of anterolateral wall with moderate dysfunction.
If your patient is asymptomatic but is advised bypass surgery or angioplasty

ask for another opinion. The only exception is left main obstruction of more than
50 per cent.
Case summary
A 40-year-old businessman underwent a routine ‘heart check’ facilitated by a health card
of medical insurance. Many tests were done including an echocardiogram and treadmill
exercise test. The echocardiogram reported mitral valve prolapse and the computer printout
of the treadmill test read ‘Exercise test positive for myocardial ischemia; coronary
101
arteriography must be considered’. As he was covered by insurance, coronary arteriography
was performed and was interpreted as showing 50% narrowing of the right coronary
artery and 50% narrowing of the circumflex artery with normal left ventricular function.
He was referred to the cardiac surgeon who advised a prophylactic bypass operation. The
patient who never had any symptom, without any clinical evaluation, found himself
recovering from the operation, nursing a median sternotomy scar. He returned to work
after 3 months but it took him another 3 months before he could resume his normal
activities fully. The following year he underwent another routine check up. The treadmill
test reported ‘Exercise test strongly positive for myocardial ischemia; suggest coronary
arteriography’.
This is a fictitious case summary, but could easily be real, as in some institutions,
the overall philosophy exemplified is being followed. It is presented as an example
of cardiology at its worst. Automation, gadgetry, assembly-line medicine and
overreliance on laboratory findings may become substitutes for clinical judgment
if the limitation of the methods we use is not realized (modified from Selzer).
Evaluation and management of patients with chest pain is too important to
be left to cardiologists and cardiac surgeons alone. The medical curricula
should be modified to educate the medical student. Unfortunately, the Medical
Council of India which is the apex body formulating policies in medical

education maintains that a medical student should not be exposed to the
specialties during their student years. In real life, the level of general practice
in any community is linked to proper education of medical students.
The answer to the commercial practices of specialists lies in the general
practitioner and practising physicians closely participating in decision making
and management of their patients. They must update their knowledge from
time to time by attending continuing medical education programmes and
should work with an institution for a few weeks each year.
If the cardiologist or cardiac surgeon points out a lesion in the angiogram,
but you cannot see it, in all probability it is not present. Ask for another
opinion.
After a bypass surgery or angioplasty if the patient has pain similar to what
was present before the procedure, it is always angina. The cardiac surgeons
and cardiologists usually ascribe it to a musculoskeletal cause.
It is a good practice to see the angiogram of your patient before decisions are
made for them. This is the best way of learning to evaluate coronary
102 angiograms.
Learning to interpret a coronary angiogram is easier than interpreting chest
pain. Most cardiologists and cardiovascular surgeons are only as intelligent as
you are.
If the patient’s chest pain is atypical for myocardial ischemia, a positive exercise
test does not necessarily establish that it is of ischemic origin. False positive
exercise tests are common.
The diagonal earlobe sign is completely useless in predicting the presence,
absence or even severity of coronary artery disease. Many elderly individuals
have it as an incidental sign.
It is helpful to choose a working diagnosis and commit it to paper. Do not
give a diagnosis as ‘chest pain for evaluation’; specify ‘myocardial infarction’,
‘unstable angina’, or ‘rule out unstable angina’ or ‘rule out acute myocardial
infarction’. You do not need to be right, but you do need to allow for timely
action. This serves to fix in the mind the signal observations, the criteria, for
which the patient is being observed so closely and which will trigger decisive
action. This is all the more important when the costs of inaction may exceed
those of early action.
When the electrocardiographic and clinical criteria suggest an evolving

myocardial infarction of less than 12 hours duration, thrombolytic therapy
should be given even if the chest pain is absent or subsides with nitroglycerine
or morphine.
Overreliance on stress thallium scintigraphy is a frequent source of error in
decision making in coronary artery disease. It should not be used as a semifinal
test before coronary angiography. When the chest discomfort is suggestive
of myocardial ischemia, a negative thallium scintigraphy does not rule out
the need for coronary arteriography if the patient has more than one risk
factor for coronary artery disease. There is a common misconception among
physicians and cardiologists that a negative thallium scintigraphy rules out
the need for a coronary arteriography. This is wrong. The latitude with which
thalliums are done and interpreted is highly variable from country to country
and institution to institution. To rely on this test from the reported sensitivity
and specificity of existing literature can be misleading.
Case summary
A 48-year-old physician consulted a cardiologist in November 1994 for palpitation and 103
occasional episodes of chest discomfort variably related to exertion. He himself noted
irregularity of pulse and was hospitalized for his arrhythmia. Earlier, in 1989, he was
diagnosed to have angina pectoris and was receiving nitrates, aspirin, diltiazem and
betablockers. An exercise ECG done at that time was positive for myocardial ischemia.
He was a diabetic for 15 years with a family history of coronary artery disease. This time
a stress thallium was done and was interpreted as negative for inducible ischemia. His
symptoms and arrhythmia were considered related to overwork and exhaustion and he
was advised to stop all medication.
Two months later, he woke up from sleep with severe anterior chest pain which was
unrelieved by antacids. He was taken to a gastroenterologist and an upper GI endoscopy
was done which was normal. As the pain continued even after 10 hours, the
gastroenterologist felt that an ECG should be taken. The ECG revealed acute anterior
myocardial infarction of several hours duration. As pain was continuing, 1.5 million units
of intravenous urokinase was given. Coronary angiogram done before discharge showed
a total occlusion of left anterior descending artery before the first septal with collaterals
from the right coronary artery. Other coronaries were normal. Left ventricular systolic
function was severely impaired and had an ejection fraction of 35 per cent.
In eight publications since 1983 involving over 4000 patients, the diagnostic
sensitivity and specificity of thallium stress testing averaged 86 and 54 per cent
respectively. If corrected for referral bias, the specificity increases to 68 per cent
and the sensitivity falls to 70 per cent. In symptom free individuals with risk factors,
the diagnostic specificity is much lower, about 40 per cent or less.
LIMITATIONS OF CORONARY ANGIOGRAM

All symptomatic post-MI patients should directly have an angiogram. Non-invasive
tests cannot help determine the need for angiogram.
It is widely believed that coronary arteriography is the gold standard test for
the diagnosis of coronary artery disease. This is incorrect because coronary
arteriography also has significant limitations.
Case summary
A 56-year-old executive was admitted in hospital with acute anterior chest pain typical of
myocardial ischemia. The pain lasted for 20 minutes but the ECG, and serial myocardial
enzymes were within normal limits. He was known to have systemic hypertension and
diabetes mellitus for 5 years and never smoked. As the pain was typical, coronary
arteriography was done and was interpreted as showing 25% lesion of proximal left anterior
descending coronary artery. The other coronaries were normal with normal left ventricular
104 function. He was told to ignore the symptoms and resume work. A week after discharge
from the hospital, he sought another opinion with reconfirmation of the same findings.
Fifteen days later, he was admitted with evolving anterior myocardial infarction which failed
to respond to sublingual and intravenous nitroglycerine. He was given 1.5 million units of
intravenous streptokinase with prompt relief of pain and resolution of ECG changes.
A repeat angiogram showed a 40% lesion in the proximal left anterior

descending coronary artery with normal left ventricular function. This patient’s
story illustrates the limitations of coronary angiography.
A major limitation of the conventional angiographic assessment of coronary
artery disease is that it disregards plaque morphology and it relies only on plaque
stenosis. This purely anatomic-geometric approach is still standard practice despite
evidence that coronary arteries are not passive conduits and a complex angiographic
morphology is the marker of more profound endothelial damage. Plaque
morphology is of recognized pathophysiological, clinical, and prognostic relevance
but is ignored in clinical practice. Also currently it cannot be evaluated satisfactorily.
In all matters clinical, distrust everything and everybody, including yourself.
8 Dyspnea
Dyspnea is difficult and uncomfortable breathing. It occurs in a variety of situations.
It is the commonest symptom of cardiac disease. Some of the common terms and
their definitions are given below in Table 8.1.
Table 8.1: Definitions of terms
Dyspnea Uncomfortable breathing
Tachypnea Rapid breathing
Hyperpnea Increased ventilation due to increased metabolic needs
Hyperventilation Ventilation in excess of metabolic needs
Orthopnea Dyspnea related to flat position
Platypnea Dyspnea related to upright position
Trepopnea Dyspnea related to lateral position
The causes of dyspnea are

• Cardiac
• Pulmonary
• Anemia
• Obesity
• Hysterical/psychogenic
• Malingering
• Physical deconditioning
In practice, cardiac and pulmonary causes are the most common. Pulmonary
venous hypertension (PVH) is the basis for dyspnea in most cardiac disorders. In
pulmonary venous hypertension, transudation of fluid from intravascular to
extravascular space occurs when the pressures in the capillaries exceed 25 mmHg.
This results in greater stiffness of the lungs, increase in the work of breathing and
increased resistance to airflow. The ventilator drive is increased due to stimulation
of stretch receptors in lung vessels and interstitium. The hypoxemia and metabolic
acidosis increase the ventilator drive.
The mechanisms of cardiac dyspnea are
• Increased mechanical work of breathing
Decreased compliance of lungs
Increased blood volume in the lungs
Increased vascular pressure in the lungs
Decreased air volume
Interstitial edema in the lungs
Increased airway resistance
Bronchiolar compression
Airway edema
• Increased ventilator drive
Hypoxemia
Ventilation-perfusion mismatch
106
Acidosis
Increased PaCO2
Increased lactic acid
• Fatigue of respiratory muscles
• Decreased cardiac output
EVALUATION
For proper management of the patient with dyspnea, the following checklist of
questions is useful in practice.
• Is it dyspnea, or a condition simulating it?
• If dyspnea, is it of cardiac or pulmonary cause?
• If cardiac, what is the grade of dyspnea?
• Is there paroxysmal nocturnal dyspnea and orthopnea?
• What is the duration of the symptoms?
• What is the time interval between the onset of dyspnea and edema?
• Is the patient receiving drugs; if so what is the response?
• What are the associated symptoms?
DYSPNEA
Some patients with coronary artery disease present with ‘shortness of breath’
instead of chest discomfort. This should be interpreted as an anginal equivalent.
In contrast to true dyspnea, these patients on careful questioning admit to the fact
that they have to stop walking for a while for relief of dyspnea. If a 50-year-old
patient with a background of diabetes, hypertension and smoking presents for the
first time in life with ‘dyspnea’ with a normal cardio-respiratory system, angina
pectoris should be ruled out by proper testing. Depression with sighing and fatigue
is common and may be mistaken for dyspnea.
The rapid and deep breathing of metabolic acidosis is recognized by lack of
sustaining evidence of left ventricular failure and alteration in the sensorium that
often accompanies metabolic acidosis. Even slight drowsiness is an important
clue because left ventricular failure does not produce alteration in sensorium unless
there is severe hypoxia or hypotension. Most patients with acute pulmonary edema
are anxious and alert. Drowsiness supervenes only when they are severely hypoxic
or hypotensive.
Conditions simulating dyspnea are
• Dyspnea as anginal equivalent
107
• Acidotic breathing (Kussmaul’s breathing): Diabetic ketoacidosis,
renal failure
• Hyperventilation
• Anxiety/hysteria
• Malingering
• Acute pulmonary embolism
• Central neurogenic hyperventilation
• Drug induced dyspnea: Salicylates, methyl xanthine derivatives,
beta adrenergic agonists, progesterone
• Pregnancy
• Fever
• Septicemia
• Depressive illness
• Sleep apnea
• Protracted cough
Drowsiness in left ventricular failure has diagnostic implications (discussed
above) as well as therapeutic significance. Traditionally, patients with left ventricular
failure and pulmonary edema are given morphine to alleviate the anxiety and reduce
the work of breathing. Though morphine is the ‘drug of choice’ in this setting, in
the special subset of patients with pulmonary edema and drowsiness, morphine
depresses the respiratory centre further and induces respiratory arrest. In this
situation, morphine should be given only when the facility for mechanical ventilation
is readily available.
The causes of dyspnea with drowsiness are:
With the rapid deep breathing (Kussmaul’s) of metabolic acidosis
Renal failure
Diabetic ketoacidosis
Methyl alcohol poisoning
With dyspnea of left ventricular failure
Associated metabolic encephalopathy
Hypoglycemia
Renal failure
Hyponatremia
108
Associated severe hypoxia/hypotension preterminally
Drug induced (morphine)
Withcentralnervoussysteminvolvement
Central neurogenic hyperventilation
Hypertensive encephalopathy
Central neurogenic pulmonary edema
Embolic stroke
Aspiration pneumonia in any unconscious patient
Occasionally the condition responsible for drowsiness may trigger left
ventricular failure and the causative disorder may go unnoticed. The following
case summary illustrates this.
Case summary
A 68-year-old male was admitted to the emergency ward with acute pulmonary edema.
He was known to have hypertension, diabetes and coronary artery disease, anterior
myocardial infarction with left ventricular dysfunction. He was on therapy with nifedipine,
enalapril, oral nitrates, and oral hypoglycemic agents. At admission, pulse rate was
124/minute, regular, BP 180/110 mmHg. Lungs showed bilateral coarse rales consistent
DYSPNEA
with pulmonary edema. Auscultation of the heart was unrewarding due to noisy respiratory
sounds. He was given intravenous furosemide and intravenous nitroglycerine with mild
relief of pulmonary edema. Samples were sent for routine biochemical investigations but
the reports were not immediately received. As the patient was found to be drowsy,
hypoglycemia or cerebrovascular accident were considered. The blood sugar was 28 mg%.
He was given intravenous glucose and recovered promptly.
Drowsiness often goes unobserved in many clinical settings. Even when

noticed, it is explained away as being drug induced. The adrenergic excess of
hypoglycemia can precipitate left ventricular failure by aggravating myocardial
ischemia and systemic hypertension. The symptoms of left ventricular failure may
precede or dominate the symptoms of neuroglycopenia (altered sensorium).
Once dyspnea is distinguished from conditions simulating it, differentiate
whether it is cardiac or pulmonary.
Features in dyspnea suggesting pulmonary cause:

Cough with expectoration
Wheezing
May not be related to exertion 109
Fever
Pleural type of pain
Loss of weight
Seasonal variation
Progressive increase over many years
Prompt response to bronchodilators
Prompt response to oxygen
Deep cyanosis in adults
Absence of heart disease by physical examination or investigation.
In elderly patients with systemic hypertension, known to have coronary artery
disease and chronic obstructive pulmonary disease it may be difficult to pinpoint
the cause.
Features in dyspnea suggesting cardiac cause:

Paroxysmal nocturnal dyspnea and orthopnea
Associated symptoms of heart disease
Expectoration of brown, frothy sputum
Rapid progression of symptom

Little or no cyanosis with severe dyspnea
Response to diuretics and digoxin
Evidence of heart disease by physical examination and investigation
Cheyne–Stokes breathing
In some situations it is difficult to distinguish between cardiac and pulmonary
dyspnea on the basis of the clinical examination. Investigations like ECG, X-ray,
echocardiogram, pulmonary function tests and arterial blood gases may be needed.
DURATION AND ONSET OF SYMPTOMS

It is important to know the total duration and the time of onset of symptoms of
right heart failure. If the duration of dyspnea is longer than 5 years particularly
with paroxysmal nocturnal dyspnea and orthopnea, mitral stenosis is the most
likely diagnosis. Other disorders like aortic valve disease and coronary artery disease
are less likely as most of these patients do not survive longer than 3 years after the
onset of heart failure. The time interval between dyspnea and symptoms of right
110 ventricular failure is longer in mitral stenosis than in the other causes of left heart
failure. In mitral stenosis the right ventricle fails under high pressures of pulmonary
artery. This is because it hypertrophies due to the slowly developing pulmonary
arterial hypertension in mitral stenosis. In other disorders like aortic valve disease
or myocardial infarction, the pulmonary venous and arterial pressures are suddenly
elevated with the development of left ventricular failure on a right ventricle which
was unprepared by prior hypertrophy. In chronic aortic regurgitation, if the duration
of dyspnea is more than 18 months, the outcome of surgery is poor.
MEASUREMENT OR GRADING OF DYSPNEA

The degree of disability by dyspnea can be graded semi-objectively. In dyspnea
due to pulmonary venous hypertension (PVH), the degree of dyspnea correlates
with severity of pulmonary venous hypertension.
The visual analogue scale (VAS) can also be used for grading dyspnea. The
VAS is a vertical line of 100 mm with the bottom labelled ‘no breathlessness’ and
the top ‘greatest breathlessness’. Similarly, the Borg category scale can be used
which ranges from 0–10.
DYSPNEA
Table 8.2: Grading for dyspnea

Grade Degree of exertion PVP (mmHg) at rest
Grade 1 Severe unaccustomed exercise <12 (normal)
Grade 2 Moderate exertion 12–18
Grade 3 Mild exertion 19–24
Grade 4 Dyspnea at rest >25
10 Greatest breathlessness
0 No breathlessness
VISUAL ANALOGUE SCALE (VAS)

A patient may be shown this chart and explained that greatest breathlessness
corresponds to 10 and no breathlessness to 0. Then he may be asked to point out
to where his breathlessness would fit in. This will be a useful way of assessing his 111
breathlessness.
A patient with paroxysmal nocturnal dyspnea is graded as having grade 3
dyspnea even if the patient is not dyspneic on mild exertion. Orthopnea is obviously
ranked as grade 4. Whatever the grade, drug therapy with diuretics and digoxin
should be mentioned. The presence of paroxysmal nocturnal dyspnea and
orthopnea strongly suggest pulmonary venous hypertension as the underlying
cause of dyspnea.
Paroxysmal nocturnal dyspnea (PND)

The patient wakes up 2–3 hours after going to sleep with shortness of breath and
cough, sits up on the bed or stands and opens the window as if hungry for air.
Usually the dyspnea subsides spontaneously but sometimes may progress to frank
pulmonary edema. Paroxysmal nocturnal dyspnea is related to interstitial pulmonary
edema. The most important mechanism of paroxysmal nocturnal dyspnea appears
to be absorption of edema fluid from the interstitial compartments of the lower
limbs in a supine position with increase in venous return to the right heart. When
the right ventricular output exceeds that of the left ventricular emptying, pulmonary
edema occurs. More than one of the following mechanisms may be responsible:
• Absorption of edema fluid with increase in right ventricular output
overfilling the lungs
• Diminished sympathetic drive of sleep decreasing LV contractility
• Sleep induced dreams with attendant increase in emotional activity
• Nocturnal arrhythmias
• Sleep apnea (central neurogenic hypoventilation)
Once the right ventricle fails, paroxysmal nocturnal dyspnea usually disappears
and gives way to easy fatiguability, a reflection of low cardiac output. Paroxysmal
nocturnal dyspnea is not always diagnostic of left heart failure as nocturnal episodes
of dyspnea occur in a variety of conditions.
Conditions simulating PND are:
• Nocturnal episodes of asthma
• Nocturnal episodes of recurrent minute pulmonary emboli
• Sleep apnea with arousal
• Cheyne-Stokes respiration
112
• Postnasal discharge with attendant severe cough
• Anxiety with hyperventilation
• Nocturnal angina with dyspnea as anginal equivalent
• Obesity
• Nocturnal aspiration in gastroesophageal reflux disease.
The patient with bronchial asthma is younger, with a history of similar illness
earlier in life. Recurrent episodes of dyspnea with clear lungs in any patient with
unexplained pulmonary arterial hypertension, should suggest the possibility of
recurrent pulmonary emboli.
Orthopnea
This refers to increase in dyspnea in supine posture and relief by sitting upor
upright posture. This is related to increased venous return in supine position with
increase in right ventricular output, further increasing the pulmonary venous
congestion. Though orthopnea is generally suggestive of left heart failure, it may
also occur in chronic obstructive lung disease or any condition with large ascites
encroaching on the lung volume. The causes could be:
• Left heart failure
DYSPNEA
• Chronic obstructive pulmonary disease

• Any condition with significant ascites
• Constrictive pericarditis
• Any severe right ventricular failure
• Bilateral diaphragmatic paralysis
There is a mechanical advantage to breathing in the upright posture compared
to the supine position. For this reason, in all situations with respiratory distress,
many patients feel more comfortable sitting up.
Table 8.3: Drugs aggravating or relieving dyspnea
Betablockers
Aggravate Bronchospasm
Ventricular failure
Depression
Relieve Anxiety
Angina pectoris (anginal equivalent)
Bronchodilators
Aggravate Anxiety (salbutamol)
Arrhythmia related dyspnea 113
Mitral stenosis (tachycardia)
Angina pectoris (tachycardia)
Relieve Bronchospasm
Nitrates
Aggravate Angina of HOCM, MVP
(anginal equivalent)
Relieve Ventricular failure
Digoxin
Aggravate Angina or dyspnea in HOCM
Relieve Mitral stenosis with atrial fibrillation
Ventricular failure
Diuretics
Aggravate Pericardial disease
Obstructive pulmonary disease
Diastolic dysfunction
Relieve Left heart failure
Renal failure
Steroids
Aggravate Heart failure
Renal failure
Relieve Bronchospasm
Response to drugs: Dyspnea should be graded keeping the drug therapy in mind,
as drugs like diuretics significantly influence pulmonary venous pressure and may
even normalize it (Table 8.3). Grading of dyspnea has a direct bearing on functional
categorization by NYHA. The patient’s prognosis may be wrongly categorized if
the influence of drug therapy is not considered. Almost all the studies on valvular
heart disease use NYHA functional classification. Both relief and aggravation of
dyspnea give valuable clues to the underlying mechanisms or causes of dyspnea.
As drug therapy can widely influence many disorders, careful drug history
and the sequence of progression or regression of symptoms give useful clues.
CHEYNE–STOKES BREATHING
The chemoreceptors controlling ventilation are effected by oxygen and carbon

dioxide tensions in the blood. In a normal circulation, the transfer of information
is prompt with a normal circulation time. In heart failure and in cerebrovascular
disease, prolonged circulation time and abnormal neural control can produce
Cheyne–Stokes breathing.
114 The various mechanisms are:
• Heart failure
• Prolonged circulation time
• ↑CO2 sensitivity due to pulmonary congestion
• ↑CO2 sensitivity due to arterial hypoxemia
• Decreased O2 and CO2 storage in lungs
• Associated cerebrovascular disease
• Neurologic disease
↑CO2 sensitivity (cortical/brainstem disease)
↓CO2 sensitivity with O2 dependence
↑CO2 threshold
Loss of wakefulness drive
↓Cerebral blood flow response due to changes in CO2
If cerebrovascular accident is excluded, Cheyne–Stokes breathing is diagnostic
of left ventricular failure.
DYSPNEA
DYSPNEA IN VARIOUS CLINICAL STATES
CORONARY ARTERY DISEASE

Dyspnea is often an anginal equivalent implying that all patients with unexplained
dyspnea require evaluation for coronary artery disease. Dyspnea in association
with chest discomfort usually means a significant area of myocardium is at risk,
and is an indication for more aggressive interventions in the acute coronary
syndromes.
Left ventricular failure in myocardial infarction generally means a loss of
25 per cent or more of myocardium and the ejection fraction is usually less than
40 per cent. Though other signs of left ventricular failure like third heart sound
are helpful, dyspnea is the most sensitive feature. If the patient has dyspnea with
ejection fraction of more than 40 per cent, conditions listed below should be
suspected.
• Anginal equivalent
• Left ventricular failure due to
Ischemia
115
Infarction
Ventricular aneurysm
Ventricular septal defect
Arrhythmias
Pulmonary embolism
• Betablocker induced bronchospasm
• Associated chronic obstructive airway disease
• Extreme weakness of physical deconditioning due to prolonged bed
rest
• Associated metabolic abnormality either simulating or aggravating
left ventricular failure
• Renal failure
• Diabetic ketoacidosis
• Lactic acidosis
Dyspnea is more common in anterior myocardial infarction than in inferior
myocardial infarction because of the larger area of myocardium involved in the
former. Dyspnea in a patient with inferior myocardial infarction means an associated

lateral or true posterior myocardial infarction, mitral regurgitation, ventricular septal
defect, old anterior myocardial infarction, associated ischemia of anterior wall, or
some other disorder. In patients with diabetes mellitus the site and size of infarction
on the ECG may not correlate with the degree of left ventricular dysfunction.
The causes of dyspnea in inferior myocardial infarction are:
• Inferior myocardial infarction + lateral myocardial infarction/true
posterior myocardial infarction
• Old anterior myocardial infarction
• Ischemia of left coronary territory
• Mitral regurgitation
• Ventricular septal defect
• Inferior myocardial infarction in a diabetic patient
• Pulmonary embolism
• Pulmonary embolism mistaken for inferior myocardial infarction
• Diabetes mellitus with cardiomyopathy
116
Once dyspnea of heart failure occurs after myocardial infarction, the 4 year
survival rate is only 50 per cent in contrast to patients who have 80 per cent
survival without heart failure and more than 50 per cent ejection fraction (CASS
study).
VALVULAR HEART DISEASE
Mitral stenosis
Dyspnea is the initial and most important symptom of mitral stenosis in contrast
to other lesions where it is a late manifestation. Dyspnea occurs from the beginning
of the disease because pulmonary venous hypertension is an intrinsic part of any
significant mitral valve obstruction. This is unlike aortic valve disease where
pulmonary venous hypertension occurs late in the disease with the onset of left
ventricular failure. Unlike aortic valve disease, patients with mitral stenosis live
beyond 5 years after the onset of dyspnea. Once dyspnea occurs in aortic valve
disease, survival beyond 3 years is unusual since once left ventricular dysfunction
occurs, there is rapid deterioration. As a general rule, if a patient has dyspnea with
paroxysmal nocturnal dyspnea for more than 5 years, mitral stenosis is most likely
DYSPNEA
to be present and aortic valve disease is unlikely. Dyspnea in mitral stenosis is

related to alterations in lung function secondary to pulmonary venous hypertension
(PVH). As the severity of pulmonary venous hypertension increases, all aspects of
lung function deteriorate.
The alterations in lung function that take place in mitral stenosis are:
• Decreased vital capacity
• Decreased forced expiratory flow rates and volumes
• Decreased maximum breathing capacity
• Decreased dynamic compliance
• Decreased arterial oxygen tension
• Increased airway resistance
• Increased alveolar-arterial gradient for oxygen
These features correlate well with the increase in pulmonary arterial pressure
and vascular resistance. Features of right heart failure appear many years after the
onset of symptoms of left heart failure in mitral stenosis. The hypertrophied right
ventricle is capable of working despite pulmonary arterial hypertension for many
years. In lesions beyond the mitral valve, symptoms of right heart failure closely 117
follow that of left heart failure as the non-hypertrophied right ventricle is not
capable of working under significant pressure overload and fails at lower pulmonary
arterial pressures. After the first episode of rheumatic fever, there is always a latent
period of at least 3 years before dyspnea appears in mitral stenosis as mitral stenosis
takes time to develop.
The severity of dyspnea has prognostic implications in mitral stenosis
(Table 8.4). In mitral stenosis, it takes 3–5 years for dyspnea to progress from
functional class II to functional class IV. Only 15 per cent of patients of class IV
survive 5 years after the diagnosis. In the absence of significant dyspnea, paroxysmal
Table 8.4: Degree of dyspnea: effect on survival in mitral stenosis
NYHA functional class 10 year survival
Class I 85%
Class II 50%
Class III 20%
Class IV None
nocturnal dyspnea or orthopnea, if a patient with mitral stenosis has features of

right heart failure, associated tricuspid stenosis should be suspected. Only 2 per
cent of patients with severe mitral stenosis and pulmonary arterial hypertension
present with right ventricular failure straightaway without ever having had severe
dyspnea or paroxysmal nocturnal dyspnea.
Aortic stenosis
Angina, syncope and dyspnea are the three cardinal symptoms of aortic stenosis.
Dyspnea is the most menacing of the three symptoms. The average survival after
the onset of dyspnea is only 1.5 years but is 2–3 years with syncope and angina. If
the duration of dyspnea is longer than 5 years in aortic stenosis, an associated
mitral valve disease should be suspected. Dyspnea in a patient with ‘mild aortic
stenosis’ may suggest underlying mitral valve disease, coronary artery disease or
hypertrophic cardiomyopathy. In hypertrophic cardiomyopathy, the symptoms have
no correlation to the presence, absence or the degree of outflow obstruction. The
fundamental mechanism of dyspnea in hypertrophic cardiomyopathy is diastolic
dysfunction related to the restriction to ventricular filling leading to pulmonary
118 venous hypertension.
The causes of dyspnea in mild aortic stenosis are:
• Hypertrophic cardiomyopathy
• Coronary artery disease
• Associated mitral valve disease
• Unrelated disorder (pulmonary)
Though dyspnea is often a symptomatic expression of left ventricular systolic
dysfunction in aortic stenosis, it may be due to diastolic dysfunction of severe left
ventricular hypertrophy. The exertional angina of aortic stenosis may be mistaken
for dyspnea.
Palpitation is usually the first symptom in mitral regurgitation and dyspnea follows
it. Dyspnea in mitral regurgitation is usually due to left ventricular failure, but may
also be due to elevated left atrial pressures related to severe mitral regurgitation
into a non-dilated, non-compliant left atrium. Unlike mitral stenosis, dyspnea is a
later symptom in mitral regurgitation. Tachycardia increases the frequency of v
waves in left atrium and pulmonary veins increasing the mean pulmonary venous
DYSPNEA
pressure. The mechanisms of pulmonary venous hypertension in MR are:

• Left ventricular failure
• Severe mitral regurgitation with non-compliant LA
• Tachycardia (more v waves)
• Associated MS
Sudden onset of dyspnea in a patient with mitral regurgitation may suggest
recurrence of rheumatic activity, infective endocarditis, chordal rupture or the
onset of atrial fibrillation. The causes of rapid progression of dyspnea in mitral
regurgitation are:
• Infective endocarditis
• Recurrence of rheumatic activity
• Chordal rupture
• Onset of atrial fibrillation
• Onset or progression of coronary artery disease
Appropriate timing of surgery for mitral regurgitation is important and most
of the presently available investigations have serious limitations.The onset of
dyspnea is the most important event that suggests the beginnings of ventricular 119
dysfunction. Dyspnea of NYHA functional class II is presently considered an
indication for surgery. The duration of dyspnea is important because if the symptom
has been present for less than one year the surgical outcome is good. On the other
hand, if the duration of dyspnea is more than 2 years, significant deterioration in
left ventricle function is likely with a poor surgical outcome. If the duration of
dyspnea is more than 5 years with obvious biventricular failure, many of these
patients have poor left ventricular function and are at a very high risk for surgery.
Evaluation must be based on:
• Onset
• Grade/functional class
• Duration of the symptom
• Diuretics/digoxin
As the onset of dyspnea triggers the decision for surgery in mitral regurgitation,
it is important not to give diuretics and digoxin to these patients with minimal or
no symptoms. When a diuretic or digoxin is given, the decision for surgery is
already made. As diuretics and digoxin mask the beginnings of dyspnea, advanced
left ventricular dysfunction may exist without being symptomatic. Objective testing
of functional class and serial echocardiographic evaluations are helpful.
Aortic regurgitation
Dyspnea occurs very late in the course of aortic regurgitation and is suggestive
of left ventricular failure. If dyspnea occurs early in the clinical course of aortic
regurgitation, one must consider associated mitral valve disease or acute aortic
regurgitation, acute on chronic aortic regurgitation or associated diseases. The
symptom is not only late to appear but is slow in progressing. Rapid progression
of dyspnea in aortic regurgitation should elicit the possibility of infective
endocarditis, retroversion of the aortic cusp, or the onset of systemic hypertension.
The causes could be:
• Recurrence of rheumatic activity
• Retroversion of the aortic cusp
• Aortic dissection
• Onset of systemic hypertension.
120 • Associated coronary artery disease
Dyspnea of class II, III or IV should be considered an indication for surgery
in aortic regurgitation if other causes of dyspnea are ruled out. Left ventricular
dysfunction may exist in aortic regurgitation without dyspnea due to a compliant
left ventricle. If the duration of dyspnea is less than 2 years, the outcome of surgery
is good. Some patients with aortic regurgitation, feel better with walking than at
rest. This is related to exertional increase in heart rate decreasing the amount of
aortic regurgitation, and fall in peripheral vascular resistance, which also reduces
the degree of aortic regurgitation. However, once left ventricular failure occurs,
exertion always aggravates dyspnea.
PULMONARY EMBOLISM
Dyspnea is the most common and consistent symptom of acute pulmonary

embolism. Usually it is of sudden onset with acute presentation. However, recurrent
pulmonary emboli can result in pulmonary arterial hypertension which may cause
exertional dyspnea. The severity of the symptoms depend upon the extent of the
pulmonary arterial tree involved.
DYSPNEA
The electrocardiographic patterns of pulmonary embolism may be mistaken

for inferior myocardial infarction plus true posterior myocardial infarction due to
the Q waves in L III, and taller R in V1.
RIGHT HEART FAILURE
Though significant dyspnea is generally considered a feature of left heart failure,

right heart failure also produces dyspnea. Gibbs et al clearly showed the lack of
correlation between pulmonary artery (capillary) pressure and dyspnea. It is now
generally accepted that the mechanism of breathlessness is too complex to be
explained by alterations in pulmonary capillary pressures alone. Respiratory muscle
dysfunction plays an important role. Sullivan et al demonstrated that an abnormal
increase in physiologic dead space per breath is the primary mechanism of
breathlessness in heart failure. They hypothesized that ventilation-perfusion
mismatch due to an abnormally low cardiac output is responsible. As right
ventricular dysfunction reduces the pulmonary perfusion, the pulmonary arterial
pressures or (indirectly the capillary pressures) fall. In any case, right ventricular
dysfunction appears to be an important determinant of dyspnea but fails to produce 121
paroxysmal nocturnal dyspnea or orthopnea.
ARTERIAL BLOOD GAS (ABG) ANALYSIS
In present day critical care practice it is essential to know how to interpret arterial
blood gases. Arterial blood gas analysis not only aids in diagnosis, but is also
useful in guiding subsequent therapy. Normal values are given below:
pH: 7.38–7.44
PO2: 80–100 mmHg
PCO2: 35–45 mmHg
HCO3: 21–28 meq/l
SaO2: 97–100%
Interpretation of arterial blood gases is extremely useful in the evaluation of
unexplained acute dyspnea. The common patterns in various conditions are given
in Table 8.5.
At times the interpretation may be compounded by a combination of disorders.
Table 8.5: ABG analysis in various disorders with dyspnea

pH PO2 PCO2 HCO3 RR
Acute pulmonary edema →↓ ↓ to ↓↓↓ →↓ ↓ to ↓↓↓ ↑↑
Cardiogenic shock ↓↓↓ ↓↓ ↓↓ ↓↓↓ ↑↑
Acute pulmonary embolism →↓ ↓↓ ↓↓ →↓ ↑↑
Cardiac shunt (R-L) →↓ ↓↓ → → →↑
Hypoventilation
neural ↓ ↓↓ ↑↑↑ →↑ ↓
neuromuscular ↓ ↓↓ ↑↑↑ →↑ ↑
Hyperventilation
neurogenic ↑ → ↓↓↓ → ↑↑↑
DKA ↓↓ → ↓↓ ↓↓↓ ↑↑
For example, pulmonary edema in association with chronic obstructive airway

disease will result in greater hypoxia with normal or elevated carbon dioxide tension
due to associated hypoventilation. Similarly, if carbon dioxide tension is normal or
elevated in association with pulmonary edema, the cause of hypoventilation, such
122 as oversedation with morphine and diazepam or a central nervous system disorder,
Table 8.6: Indications for arterial blood gas estimation
Severe breathlessness
Pulmonary edema
Respiratory failure due to any cause
Severe pneumonia
Suspected pulmonary embolism
Severe bronchial asthma
Metabolic encephalopathy
Poisoning
Acidotic states
Uremia
Metabolic acidosis of any cause
Alcohol intoxication
Electrolyte imbalance
Hypokalemia
Hyperkalemia
Shock of any cause
DYSPNEA
needs to be investigated. Commonly, acute cardiac illness may precipitate diabetic

ketoacidosis in a diabetic, thereby adding another factor in the interpretation of
arterial blood gas analysis.
Apart from its role in diagnosis, arterial blood gas analysis is useful in making
decisions about artificial ventilation and also in monitoring progress.
Though dyspnea is often identified with cardiac or pulmonary disease, a variety
of medical disorders manifest or resemble dyspnea. Intelligent discrimination of
one from the other greatly assists patient management and limits unnecessary
laboratory testing.
Aspiration pneumonia as a cause of dyspnea is often missed.
In all patients with ‘unexplained’ dyspnea, arterial blood gases (ABGs) should
be obtained. It is not rare for metabolic acidosis to be mistaken for dyspnea
due to cardiac or pulmonary disease.
Drowsiness or altered sensorium in a dyspneic patient should alert the clinician
to the possibility of associated metabolic disorder (hypoglycemia, metabolic
123
acidosis, drug induced) or cerebrovascular accident.
Surprisingly, dyspnea as a symptom or as a physical sign may be missed.
Pulmonary venous hypertension is not equivalent to dyspnea.
Acute respiratory failure may be missed when weakness is the presenting
symptom and dyspnea may not be obvious.
9 Syncope
Syncope is a sudden, transient loss of consciousness. It may be due to a trivial
vasovagal episode or due to a life threatening arrhythmia. Unless proved otherwise
syncope should be considered as an aborted sudden death. This dual significance
makes it an important symptom to evaluate carefully. As the potentially serious
causes are usually cardiac, the cardiologist or the physician is usually consulted.
While syncope is transient loss of consciousness, near syncope or pre-syncope
is near loss of consciousness by lesser degrees of the same cause producing syncope.
124 Patients use a variety of terms to describe this symptom, which can be misleading.
The common descriptions are faint, blackout, spell, swoon and giddiness.
Syncope occurs either due to fall in cerebral blood flow or reduction in energy
substrates to the brain. The mechanisms are:
Reduction in cerebral blood flow
Fall in central aortic pressure (<60 mmHg, mean)
Elevation in cerebrovascular resistance or intracranial pressure
Reduction of energy substrates
Hypoxia (PO2<60 mmHg)
Hypoglycemia
When the mean aortic pressure falls to below 60 mmHg in a normal person,
cerebral perfusion falls significantly and syncope occurs. The blood sugar values
are usually less than 40 mg% when syncope occurs due to hypoglycemia. The
arterial PO2 is usually less than 60 mmHg (saturation 80 per cent) before syncope
occurs due to hypoxia. These values are applicable when a singular factor is
operative. When more than one factor is operative, even lesser degree of
abnormality can result in syncope (for example, hypoglycemia in a 70-year-old
with cerebrovascular disease).
SYNCOPE
Causes of syncope
Syncope could be due to vasovagal/psychogenic, cardiovascular, metabolic
encephalopathy/drug related, and central nervous system disorders. Sometimes
no attributable cause may be found. Table 9.1 shows the various categories and
the relative frequency of each in the combined results from the three major
prospective studies.
The numbers are a summation of the prospective studies on syncope. The
largest single cause is surprisingly ‘unknown cause’. This information is valuable
in the diagnostic testing and advice to the patients with syncope.
VASOVAGAL/PSYCHOGENIC SYNCOPE
The vasovagal syncope is the most common form of syncope accounting for half
of all the causes of syncope. It is also known as neurocardiogenic syncope. It
could be triggered by:
• Acute severe pain due to any cause
• An unpleasant or distressing sight
• Prolonged standing 125
• Fasting state
• Crowded, suffocating, uncomfortable surroundings
• Micturition
• Defecation
• Swallowing
• Laughing
• Carotid sinus hypersensitivity
• During cardiac catheterization/pressure over groin
Table 9.1: Incidence of major categories of syncope
Diagnosis No. of patients Percentage
Vasovagal/psychogenic 203 37
Cardiac 75 13
CNS 26 5
Metabolic/drugs 16 3
Unknown 230 43
Total 550
• Postural hypotension
• Hyperventilation
• Psychogenic factors
Since a syncope may be associated with certain special situations like sudden
severe pain, grief, humiliation or anger, death of a loved one, sight of blood, and
so on, it led to the use of the term ‘situational syncope’. It occurs more commonly
in hot humid environments.
The typical vasovagal episode has two phases. In the first phase a steady fall
in arterial pressure occurs with or without increase in heart rate. In the second
phase, a sudden fall in heart rate occurs, resulting in an abrupt fall in arterial
pressure. Atropine prevents the fall in heart rate but the vasodilatation during the
first phase may be enough to cause hypotension and loss of consciousness. Blood
flow to skeletal muscles increases but that of brain, kidney and mesenteric
circulation decreases.
The typical vasovagal episode is described in Table 9.2.
Table 9.2: Features of a vasovagal syncope
126
Position Usually standing or sitting but may occur in supine position
(as during cardiac catheterization)
Prodrome Few seconds to minutes
Weakness, light-headedness, sweating, nausea, yawning, pallor
or the sensation of impending doom
Urge to pass urine or motion
The event Loss of consciousness, with a fall to the ground or may just
slump to one side while sitting
Pallor, sweating, dilated pupils
Pulse is slow or of low volume
Urinary incontinence may occur
Total duration is most often less than a minute, rarely
2–5 minutes
Post event Awakens with a feeling of dizziness and nausea, sweating,
and the urge to defecate
Orients to surroundings within seconds after gaining
consciousness
Total duration of episode 5–10 minutes
If tries to stand up immediately, may again fall
SYNCOPE
The commonest form of vasovagal syncope is usually benign and is self

limiting. The vasovagal episodes that occur during cardiac catheterization are
generally related to the anxiety and fear, and pain related to groin puncture and
pressure. These episodes are often promptly recognized as almost all these patients
are closely monitored. They promptly respond to atropine and fluid load.
Unrecognized, the hypotension of vasovagal episode may prove fatal in patients
with severe obstructive coronary disease or in patients with limited cardiac reserve.
Rock concert syncope

Lempert and Bauer recently described this entity of mass fainting among rock
concert audiences. The faints were classified as hyperventilation or panic attacks.
In the majority, anxiety is provoked when they felt squeezed, choked, and trapped
in the middle of the crowd whereas others start hyperventilating when they are
overcome by emotion. A combination of syncope provoking factors were identified.
These are sleeplessness during the previous night, fasting from early in the morning,
when they first line up, long period of standing in the arena, and hyperventilation.
Rock concert syncope provoking factors causing cerebral vasoconstriction
and Valsalva-like pressure induced either by screaming or reflexly by external 127
compression of the thorax by the pushing masses. Valsalva maneuver impairs
venous return to the heart and consequently reduces cardiac output. The authors
gave a few guidelines to prevent this syncope, summarized as follows: sleep, eat,
sit, keep cool, and stay out of the crowd.
SYNCOPE IN CARDIOVASCULAR DISORDERS
Though cardiovascular disease is often suspected as the first etiological possibility,

these disorders are responsible for only 13 per cent of cases of syncope. In
cardiovascular causes of syncope, arrhythmias account for nearly 80 per cent of
cases. The various causes of syncope in cardiovascular disorders are listed in
Table 9.3.
Arrhythmias produce syncope when the heart rate is too high or too low, to
sustain cardiac output and arterial pressure. The commonest arrhythmia producing
syncope is ventricular tachycardia.
Table 9.3: Causes of syncope in cardiovascular disorders

Arrhythmias
Bradyarrhythmias Sinus bradycardia
Acute ischemic syndromes
Sick sinus syndrome
Hyperkalemia
Acute intracranial hypertension
Complete heart block
Congenital
Acquired
Drug induced
Degenerative disease
Hyperkalemia
Diphtheritic myocarditis
Tachyarrhythmias Supraventricular
Ventricular
Conditions predisposing Myocardial ischemia
to arrhythmias Ventricular aneurysm
Structural defects with chamber enlargements
Mitral valve disease
128 Atrial septal defect
Ebstein’s anomaly of tricuspid valve
Heart failure
Hypokalemia
Hyperkalemia
Prolonged QT syndromes
Pre-excitation syndromes
Renal failure
Severe emotion
Carotid sinus hypersensitivity
Intramyocardial tumours
Structural defects Severe aortic stenosis
Cardiac tamponade
Primary pulmonary arterial hypertension
Mitral stenosis
Severe pulmonary stenosis
Atrial myxoma
Acute myocarditis
Tetralogy of Fallot (severe)
Eisenmenger syndrome
SYNCOPE
Ventricular tachycardia (VT)

This arrhythmia accounts for about 40 per cent of cardiovascular causes of syncope.
In elderly patients beyond 70 years, this is the most common diagnosis and accounts
for 25 per cent of all episodes of syncope. Almost all patients with ventricular
tachycardia have underlying heart disease. Most of the patients have no prodromal
symptoms. A brief episode of dizziness or light headedness may be experienced.
A preceding history of palpitation may occur. As a rule, most of these patients
lose consciousness within a few seconds and a history of several minutes of warning
symptoms generally suggests a vasovagal syncope. The diagnosis of ventricular
tachycardia is often established during the initial evaluation of the patient either
by the 12-lead ECG or monitoring.
Long QT syndrome
Prolongation of QT interval occurs due to a variety of causes and predisposes to
a peculiar form of ventricular tachycardia called torsade de pointes.
Idiopathic long QT syndrome is common. There are bizzarre morphologies
of the T waves. Syncope or cardiac arrest may occur under physical or emotional
stress. These patients are often misdiagnosed as having epilepsy. The majority of 129
patients have their first syncope before the age of 20 years. If left untreated, mortality
is high due to torsade de pointes degenerating into ventricular fibrillation.
Antiadrenergic interventions by either betablockers or left cardiac sympathetic
denervation are very effective in ventricular fibrillation and sudden death. With
treatment, the 5 year mortality is below 4 per cent. Untreated, mortality is 20 per
cent within the first year after the syncope and is 50 per cent within 10 years. The
diagnosis would not be missed, provided one interprets the ECG carefully in a
case of syncope evaluation.
Supraventricular tachycardia (SVT)

Syncope is less common with this arrhythmia in comparison to ventricular
tachycardia and accounts for 8 per cent of all the causes of syncope of cardiovascular
origin. Presence of certain factors predisposes to syncope:
• Underlying heart disease/failure
• Aortic stenosis
• Pulmonic stenosis
• Restrictive cardiomyopathy
• Rate of SVT (>200/min)
• Underlying pre-excitation
• Age (advanced age)
• Standing position at the time of onset of SVT
The underlying heart disease has to be severe to produce syncope with
supraventricular tachycardia. When the rates are exceedingly high, as in pre-
excitation, diastolic filling is impaired and the cardiac output and the arterial pressure
fall to below the critical level. Advanced age, with associated cerebrovascular disease,
may predispose to syncope even with a slight fall in arterial pressure. Paradoxically,
younger individuals with better AV nodal conduction and more ventricular rates
may be more susceptible to syncope than the elderly with slow AV nodal
conduction.
Bradyarrhythmia
Bradyarrhythmias and advanced AV blocks account for about 31 per cent of all
the cardiovascular causes of syncope; complete heart block and sick sinus syndrome
130 (SSS) account for the majority of cases. More than one mechanism may be
responsible for syncope in sick sinus syndrome.
• Severe sinus bradycardia
• Complete heart block
• Sinus arrest either spontaneous or due to post SVT pause.
• SVT/AF with rapid ventricular rates
• SVT/AF degenerating into VT/VF
• Verapamil or betablocker therapy
Following the relief of a sudden onset palpitation if the patient has syncope,
sick sinus syndrome should be suspected. It is important to rule out sick sinus
syndrome in all patients presenting with supraventricular tachycardia because
verapamil given for supraventricular tachycardia can aggravate bradyarrhythmia
and may result in a fatal asystole. In any supraventricular tachycardia with heart
rate less than 200 per minute but recurrent syncope and a normal heart, suspect
sick sinus syndrome.

Syncope is rare in patients with congenital complete heart block (CHB) as the
SYNCOPE
ventricular rates are usually adequate. Most of the patients with syncope due to
complete heart block have some form of conduction defect. The ECG features at
the time of admission are:
• RBBB + Left anterior hemiblock
• Alternating bundle branch block
• RBBB with first degree AV block
• LBBB with first degree AV block
• Fascicular blocks with Mobitz II AV block
In syncope due to complete heart block, prodromal symptoms are often
absent. Unconsciousness supervenes within 5 seconds in standing position or
within 15 seconds in recumbent position. Bowel or bladder incontinence with fits
may occur and a diagnosis of seizure disorder is often made initially. In a patient
with syncope, if the ECG shows one of the changes mentioned above, complete
heart block as a cause of syncope should be considered. In a study by Dhingra et
al, 200 patients with chronic bifascicular block were studied; syncope occurred in
30 patients (15 per cent). In 5 of them complete heart block was documented. A
pacemaker was needed in only 6 of the 30 patients (20 per cent). The majority of 131
patients had syncope due to ventricular arrhythmia or unknown cause. This
illustrates the need to use caution and judgment in evaluation of patients with
syncope and a seemingly abnormal ECG.
To a quick question give a slow answer.
Italian proverb
RENAL FAILURE PRESENTING WITH BRADYCARDIA AND SYNCOPE

Renal failure is generally not considered a diagnostic possibility in patients
presenting with syncope. The mechanisms of syncope in renal failure are:
• Hyperkalemia (bradycardia)
• Drug induced bradycardia (atenolol)
• Postural hypotension (drug induced)
• Hypertensive encephalopathy
• Pericardial tamponade
• Gastrointestinal bleeding
• Hypermagnesemia (magnesium containing antacids)
The first two categories deserve special mention as they are often missed in
practice.
Case summary
A 50-year-old housewife was admitted for evaluation of syncope and was detected to
have complete heart block. She was referred for a permanent pacemaker implantation by
a cardiologist. Initial evaluation revealed her to be in complete heart block with a ventricular
rate of 35 per minute and a narrow QRS complex. The blood pressure was 120/80 mmHg.
A temporary pacemaker was inserted with a view to implant a permanent one selectively.
Serum electrolytes including potassium were reported as normal. Another routine sample
of serum electrolytes showed serum potassium of 7 meq. The creatinine was 9 mg%. She
was hemodialysed with regression of complete heart block and improvement of renal
parameters and was discharged home without a pacemaker.
This patient illustrates the need to obtain serum electrolyte levels as a routine
in all patients presenting with arrhythmia and the need to recheck the values more
than once if the clinical features warrant it. In this patient, the tall T-waves were a
possible clue. Even if this was missed, the drowsy patient with well maintained
132
blood pressure is a pointer to a metabolic encephalopathy like abnormal glycemic
state or renal failure. Elevated creatinine value was a clue to the underlying
hyperkalemia. If the laboratory error was not rechecked this patient would have
had a fatal outcome.
Case summary
A 61-year-old retired police officer started having recurrent syncope at rest and on exertion.
He was referred for bradycardia and heart failure. He was known to have hypertension
and diabetes mellitus. His serum creatinine was found to be 2.4 mg% six months prior to
admission. He was given atenolol 50 mg per day along with glybenclamide for diabetes.
Evaluation at presentation revealed complete heart block with a ventricular rate of 40/
min, mild left ventricular failure and serum creatinine of 3 mg%. He improved with
restoration of sinus rhythm after 4 days of withholding atenolol.
This case illustrates the danger of prescribing atenolol in patients with renal
failure. Even routine doses accumulate and cause life threatening bradycardia.
This is such a common occurrence that the authors recommend routinely checking
serum creatinine levels again whenever there is unexpected bradycardia with
atenolol.
SYNCOPE
NON-ARRHYTHMIC CARDIOVASCULAR CAUSES OF SYNCOPE
AORTIC STENOSIS (AS)

Among valvular lesions, aortic stenosis is the commonest defect responsible for
syncope. In three prospective studies of 550 patients with syncope only 6 (1.09%)
had aortic stenosis. In aortic stenosis, syncope is generally suggestive of severe
obstruction or arrhythmia. The causes could be
• Exertional syncope due to severe aortic stenosis
• Arrhythmias
• Supraventricular
• Ventricular
• Bradyarrhythmias
• Associated coronary artery disease
• Unrelated to AS
Exercise induced syncope is one of the three principal symptoms of aortic
stenosis and occurs in two stages. The first stage is heralded by sudden fall in
blood pressure, pallor, inattention and light headedness. This is followed by loss 133
of consciousness. The ECG during this stage is normal. If the episode lasts more
than a few seconds, the second stage may supervene. Most of the features of the
second stage are secondary to severely reduced coronary blood flow.
First stage (20–40 seconds)
Sudden fall in blood pressure
Pallor
Light headedness
Inattention
Unconsciousness
Sinus rhythm
Reduced intensity of heart sounds
Second stage
Cyanosis
Absent pulse and heart sounds
Apnea
Twitching of body or seizure
Bladder or bowel incontinence

Abnormal ECG
Sinus tachycardia
Ventricular tachycardia
Ventricular fibrillation
Atrial fibrillation
AV block
Asystole
Mechanisms of exertional syncope in aortic stenosis

The normal cardiovascular response to exercise is characterized by fall in systemic
vascular resistance with increase in cardiac output so that the central aortic pressure
is maintained. When a patient with severe aortic stenosis exercises, the exertional
fall in systemic vascular resistance is not counteracted by a rise in cardiac output.
As a result, the blood pressure falls and syncope occurs. The reflexes (Bezold–
Jarisch reflex) from the left ventricle under increasing pressure of exercise may
also play a role. Normally, the leg exercise is accompanied by a reflex
134 vasoconstriction in the forearm. When a patient with severe aortic stenosis exercises,
the high intraventricular pressures reflexly inhibit forearm vasoconstriction and a
precipitous fall in arterial pressure occurs.
The mechanisms are:
• Fall of systemic vascular resistance (vasodilation in skeletal muscles)
• Failure of forearm vasoconstriction during leg exercise (ventricular
Bezold–Jarisch reflex)
• Cardiac output fails to rise due to severe fixed obstruction
Once syncope occurs in aortic stenosis, most of the patients do not survive
longer than 3 years. After the severity of aortic stenosis is assessed by echo-Doppler
studies, cardiac catheterization should be done to confirm it and surgery should
be offered as early as possible. If syncope is not accompanied by angina or dyspnea,
or there is a discrepancy between the clinical examination, ECG, and echo-Doppler,
cardiac catheterization should be performed to estimate the severity of stenosis. If
aortic stenosis is found to be non-severe, some other cause for syncope is likely,
such as coronary artery disease, hypertrophic cardiomyopathy, or arrhythmic, non-
cardiac cause.
SYNCOPE
Exercise thallium or coronary arteriogram help in detecting coronary artery

disease. In hypertrophic cardiomyopathy, syncope occurs independent of the
severity of outflow obstruction, and is related to restriction to ventricular filling or
arrhythmias.
CORONARY ARTERY DISEASE (CAD)
Though traditional teaching focuses on aortic stenosis as an important cause of
syncope, coronary artery disease probably is the commonest cause of syncope in
middle aged and elderly patients. Multiple mechanisms are responsible for syncope
in coronary artery disease. The causes are:
Arrhythmias
Bradyarrhythmias
Tachyarrhythmias
Large area of myocardium at risk
Acute ischemia
Parasympathetic excess
Acute inferior MI 135
Druginduced
Vasodilators (nitrates, nifedipine, morphine)
Volume depletion (diuretics)
Arrhythmias (dopamine, isoproterenol, digoxin, antiarrhythmic agents,
proarrhythmia).
Onset of acute mechanical complications
Ventricular rupture
Cardiac tamponade
Postinfarct pericarditis (thrombolysis, anticoagulants)
Perforation by pacemaker wire
During coronary angioplasty
Postural hypotension after prolonged bed rest
Vasospastic angina (ventricular arrhythmia is common)
During and after coronary arteriography
Syncope with chest pain suggestive of myocardial ischemia usually suggests a

polymorphic ventricular tachycardia or ventricular fibrillation or large area of
myocardium at risk resulting in hypotension and is an indication for aggressive
investigation and management. In the early hours of acute myocardial infarction,
syncope with a history of fall should make one look for evidence of injury to the
head or blunt trauma to abdomen as thrombolysis may precipitate serious
hemorrhage in these patients.
Case summary
A 34-year-old hypertensive engineer presented with chest pain of 2 hours duration and
the ECG revealed an evolving inferior myocardial infarction with sinus rhythm. Prior to
hospitalization, he had syncope once. There were no obvious signs of external injury to
the head or any other site. Pulse was 70/min and BP 150/100 mmHg. The rest of the
physical examination was unremarkable. Intravenous streptokinase 1.5 million units was
given. Two hours after thrombolysis, he became drowsy and later became unconscious.
Bogginess and hematoma appeared over the left frontoparietal region of the scalp. A CT
scan revealed diffuse intracerebral hemorrhage and he died 24 hours later.
136 This patient illustrates the need to be cautious in patients with a history of
syncope before instituting thrombolytic therapy. On careful analysis, this patient
probably should have had a thorough examination to rule out head injury and
should not have received thrombolysis directly as the infarction was inferior with
a small area of myocardium at risk and the patient was a hypertensive. The evidence
of external injury to the head was obviously missed.
Nitrate syncope
Sublingual nitrate can produce syncope by sudden reduction of venous return due
to venodilation and is often counteracted by reflex tachycardia (Table 9.4).
Concomitant therapy with diuretics, vasodilators and betablockers increases the
tendency for syncope. A new onset of nitrate syncope in a patient with chronic
stable angina may mean progression of the disease to unstable angina or evolving
myocardial infarction. Such a history should be used as a clue for prompt
hospitalization and management.
The indication for temporary pacing should be more liberal when the patient
with acute MI presents with syncope.
SYNCOPE
Table 9.4: Factors predisposing to ‘nitrate syncope’

Factor Mechanism
Progression to unstable angina/ Unrelieved ischemia
acute MI Additional area of ischemia
Bradycardia (inferior MI)
Diuretics Hypovolemia with venodilation
Vasodilators Additional vasodilatation
Betablockers Prevents reflex tachycardia

Prolonged standing Venous pooling
OTHER LESIONS CAUSING SYNCOPE

Apart from aortic stenosis, any severe obstruction to circulation may cause syncope.
Syncope is not uncommon in severe primary pulmonary arterial hypertension. It
can be the presenting feature of acute pulmonary embolism. Syncope is rare in
mitral stenosis even when it is severe. Recurrent syncope in a patient with mitral
stenosis should suggest a left atrial myxoma as a cause of mitral obstruction. Rarely, 137
paroxysmal atrial arrhythmias, severe pulmonary arterial hypertension, acute
pulmonary or cerebral embolism may cause syncope in mitral stenosis. Associated
aortic stenosis may also be the cause of syncope.
Ball valve thrombus though very rare, is more easily detected now with
echocardiography. The patient may present with syncope or shock and can be
relieved of the obstruction by elevation of the foot end of the bed.
Syncope in mitral stenosis: The causes could be:
• Untreated critical disease
• Left atrial myxoma
• Paroxysmal atrial arrhythmias
• Severe pulmonary arterial hypertension
• Cerebral embolism
• Pulmonary embolism
• Ball valve thrombus
• Associated aortic stenosis
• Cardiac tamponade during balloon mitral valvuloplasty
Systemic hypertension and syncope: Syncope in a patient with hypertension

should suggest postural hypotension due to drugs (methyl dopa), hypertensive
encephalopathy, pheochromocytoma or cerebrovascular accident. The causes could
be due to:
• Postural hypotension
• Drug induced (methyl dopa)
• Acute intermittent porphyria
• Hypertensive encephalopathy
• Pheochromocytoma
• Intracranial hemorrhage (cerebellar)
Syncope during and following cardiac catheterization: Hypotension can occur
during or after the procedure. The commonest cause remains vasovagal. The typical
patient is anxious, and is either not informed or is too well informed about the
procedure. Syncope often occurs at the time of groin punctures. This should be
suspected when the patient becomes restless, starts yawning and may vomit. The
fall in blood pressure may not be noticed until later as the arterial sheath is not yet
138
inserted. They respond promptly to atropine if given early. Though vasovagal
episodes are self limiting and respond easily to atropine in the majority of patients,
in rare cases it can be fatal. A fatal outcome is more likely in a patient with underlying
severe cardiac disorder (left main disease, severe triple vessel disease, or severe
aortic stenosis, primary pulmonary arterial hypertension or severe congestive heart
failure). I know of a patient who had normal coronary arteries and normal
intracardiac pressures who died later in the ward of a vasovagal episode which
was not recognized early. Proper hydration of the patient would prevent many
episodes of vasovagal syncope.
Once hypotension occurs in patients with left main disease, coronary perfusion
falls leading to myocardial ischemia and further hypotension, which prevents any
recovery. An episode of vasovagal attack may be disastrous in this setting. The
pain associated with groin compression during sheath removal may result in vagal
episodes. In post-PTCA patients, femoral sheaths should be removed under the
surveillance of trained personnel. Prophylactic intravenous atropine prevents the
vagal episodes. Adequate sedation and analgesia are important. The patients should
be monitored for their rhythm and blood pressure during the removal and
immediately afterward.
SYNCOPE
Vasovagal episode of cardiac catheterization/PTCA

The setting
Anxious, fearful patient
During femoral punctures
During sheath removal
Potentially serious in
Left main coronary disease
Severe triple vessel disease
Severe AS
Severe pulmonary arterial hypertension
Post-PTCA (abrupt vessel closure)
Prophylactic measures
Adequate explanation to the patient regarding the procedure.
The atmosphere of the catheterization lab and the attitude of staff.
Intravenous atropine in anxious bradycardiac patients particularly prior to sheath removal.
Adequate hydration and appropriate sedation.
NEUROLOGICAL DISORDERS WITH SYNCOPE
Any episode of syncope is most commonly believed to be and is confused with 139
epilepsy. This is more likely when the classic signs and symptoms are not obvious.
Other neurological disorders that may mimic syncope are:
• Epilepsy
• Akinetic seizures in adults
• Petit mal seizures in adolescents/children
• Partial complex seizures
• Generalized tonic clonic seizures
• Narcolepsy/cataplexy
• Transient ischemic attacks (posterior territory)
• Loss of consciousness
• Drop attacks
• Subarachnoid hemorrhage
• Basilar artery migraine
• Bulbar syncope
Complex partial seizures are often mistaken for syncope. In one study, 25 per
cent of this type of seizures arising from temporal and deep frontal structures
presented with staring spells and loss of consciousness without other signs of
seizure disorder. Visceral symptoms like abdominal discomfort, nausea and
vomiting occur in 40 per cent of patients. Symptoms of sympathetic excess such
as anxiety, fear, sensation of impending doom, flushing, tachycardia and
hypertension are common. An erroneous diagnosis of vasovagal syncope or
cardiovascular disorder causing syncope is often made. Complex partial seizures
may mimic angina, cardiac arrhythmia or pheochromocytoma. In a recent study
almost half of the patients were shown to have an arrhythmia during the seizure.
Drop attacks are probably caused by brainstem ischemia. Consciousness is retained
during the episode. Basilar artery migraine is possibly caused by vasospasm of the
posterior cerebral circulation. The accompanying typical migrainous symptoms
help in the differentiation. Bulbar syncope is caused by any brainstem lesion
(tumours, previous infarcts, amyotrophic lateral sclerosis, syringobulbia) that
regulate heart rate and vasomotor functions. Unconsciousness of psychogenic
origin is common and usually occurs in the presence of an audience. The person
never hurts himself when falling and the accompanying pallor, flushing and other
autonomic disturbances are absent.
140 It is difficult to differentiate a syncope from a seizure (Table 9.5). An abrupt
loss of consciousness, aura, and prolonged period of amnesia favour a diagnosis
of seizure.
Table 9.5: Differentiation of syncope from seizure
Features favouring seizure Features common to both
Aura Blackout or loss of vision
Abrupt loss of consciousness Giddiness
Sensory hallucinations Nausea
Deja vu experiences Sweating
Emotional states Weakness
Confusional states Yawning
Motor automatism Sighing
Prolonged amnesia Pallor
History of alcohol withdrawal, head trauma,
cerebrovascular accident
Recurrent syncope in young healthy person
Known malignancy (potential for secondaries in brain)
SYNCOPE
Carotid disease: Unilateral carotid disease is accompanied by symptoms of

hemispheric ischemia. Bilateral carotid stenosis (as in Takayasu’s arteritis) can result
in exertional syncope like aortic stenosis. In elderly patients who frequently have
an ejection systolic murmur due to aortic valve sclerosis, this can be mistaken for
aortic stenosis. However, the murmur being better audible in the carotids than
over the precordium or aortic area is a helpful indicator.
Vertebrobasilar insufficiency (VBI): Syncope due to this entity is more common
in patients of age 65 years and older. Associated diplopia, ataxia, dysarthria and
sensorimotor disturbances are common. Though atherosclerosis is the commonest
underlying cause, cervical spondylosis, subclavian steal syndrome, and congenital
anomalies of cervical vertebrae may be responsible. The bony abnormality can
obstruct blood flow.
Subarachnoid hemorrhage (SAH): Sudden loss of consciousness or syncope
can occur in subarachnoid hemorrhage due to sudden rise of intracranial pressure
with recovery of sensorium either fully or partially. Preceding severe headache
though common, is not often remembered by the patient, due to retrograde
amnesia. Hypertension and bradycardia are common. The ECG may show ST-T 141
alterations which can mimic unstable angina, subendocardial infarction or anterior
myocardial infarction. Arrhythmias can also occur. Careful evaluation often reveals
slight alteration in sensorium, neck rigidity or other neurological signs. A CT scan
should be asked for in case of doubt.
Case summary
A 60-year-old hypertensive man, was admitted for evaluation of syncope. He was fully
conscious at admission to ICCU. Pulse: 66/minute; BP:170/110 mmHg; S4 was audible.
ECG showed LVH with strain and deep symmetrical T wave inversions with ST
depressions all over the chest leads. A diagnosis of acute ‘silent’ subendocardial infarction
was made. He was given aspirin and intravenous heparin. After 24 hours he was frankly
unconscious and developed a full blown clinical picture of subarachnoid hemorrhage
confirmed by CT scan. He died a month later.
This patient illustrates how subarachnoid hemorrhage can mimic acute

coronary syndromes. This entity deserves special mention for more than one reason.
Firstly, it is not generally realized that subarachnoid hemorrhage is capable of
transient loss of consciousness with recovery, only to recur later. Secondly, patients
with undiagnosed syncope often go to an intensive coronary care unit or a

cardiologist. Thirdly, subarachnoid hemorrhage mimics acute ischemic syndromes
by the ECG changes that it can produce. Finally, antiplatelet agents, anticoagulants
or thrombolytic therapy given in this setting can be disastrous.
Common reasons for mistakes in diagnosis or treatment are:
• The presumption that syncope is almost always cardiovascular in
origin
• Lack of knowledge that syncope occurs in SAH
• Most patients with syncope go to coronary care units or cardiologists
• The ECG changes (ST depressions, deep T wave inversion)
occurring in SAH mimic acute ischemic syndromes
• The esophageal pain that follows vomiting mimics the chest pain
of myocardial ischemia
• Present tendency for a lower threshold to prescribe antiplatelets,
anticoagulants, and thrombolytic agents
Case summary
142 A 55-year-old businessman presented with chest pain and vomiting 3 hours prior to
admission. The blood pressure was 170/100 mmHg and the pulse 70/minute. The rest
of the physical examination was ‘unremarkable’. The ECG showed features suggestive of
acute subendocardial infarction and he was prescribed aspirin, heparin nitroglycerine and
diltiazem. He complained of severe headache while in the CCU (this was attributed to
nitrates). Four hours after admission, he became drowsy and a diagnosis of subarachnoid
hemorrhage was confirmed on CT scan. Luckily this patient survived all this and was
discharged without neurological deficit. On careful questioning, the patient admitted to
having had a headache first followed by vomiting. The chest pain followed three vomitings.
Syncope in intracerebral hemorrhage: In intracerebral hemorrhage, syncope

can occur but some alteration in sensorium is a rule and the diagnosis is easier.
Cerebellar hemorrhage often presents as syncope and the associated severe
hypertension and ECG changes may be misleading.
Brain tumours presenting with syncope: Tumours of the third ventricle (colloid
cysts), those involving the foramen of Monro, and both frontal lobes can present
with recurrent syncope without any definitive evidence of seizure activity. Posterior
fossa tumours or malformations may present with loss of consciousness during
episodes of coughing or sneezing related to cerebellar tonsillar herniation. This
SYNCOPE
entity may be dismissed as cough syncope and the dangerous underlying condition
may be missed. Rarely, brainstem tumours can present as postural hypotension.
Peripheral neuropathies presenting with syncope: Many peripheral
neuropathies with associated autonomic neuropathy can cause postural hypotension
and syncope. Other causes are:
• Diabetic neuropathy
• Alcoholism
• Guillain-Barre syndrome
• Amyloidosis
• Familial dysautonomia
• Drug induced
• Vincristine
• Cisplatinum
• Acute neuralgias with pain eliciting vagal reflex
• Glossopharyngeal neuralgia
• Trigeminal neuralgia
Shy–Drager syndrome (primary autonomic insufficiency and parkinsonism) 143
can also present with syncope.
Metabolic and drug induced syncope: The most common of these is
hypoglycemia induced by insulin or oral drugs; rarely insulinoma may be
responsible. Alcoholics lose consciousness due to central nervous system effects
of alcohol but the autonomic neuropathy may also be responsible.
In actual practice, postural hypotension is most likely when a vasodilator is
combined with a diuretic in the initial prescription. Other causes are:
• Alcohol intoxication
• Porphyria
• Drug induced postural hypotension
Methyl dopa
Diuretics
Vasodilators
Nitrates
Prazosin hydrochloride
ACE inhibitors
Calcium blockers
Nifedipine
Gastrointestinal and abdominal causes of syncope: Internal hemorrhage is

the most important cause in this group of disorders. Other intra-abdominal causes
are:
• Upper GI bleeding
• Exaggerated vagal reflex
• Vomiting
• Micturition syncope
• Endoscopy
• Barium enema (visceral distension)
• Any acute severe abdominal pain
• Acute perforation of a viscus
• Blunt trauma to abdomen with
Rupture of spleen
Rupture of liver
• Acute pancreatitis
• Liver abscess bursting into pericardium/pleura
144
Upper gastrointestinal bleed presenting as syncope is often missed. The
obvious evidence of bleeding by hematemesis and melena may be altogether absent.
As much as 500 ml of blood can be sequestered in the gastrointestinal tract without
either of these signs apparent. Abdominal pain may be absent, or it may be difficult
to distinguish upper abdominal pain from lower chest pain. The use of aspirin,
heparin and thrombolytic agents can be dangerous.
Case summary
A 60-year-old businessman had palpitation, syncope and chest discomfort. He went to
the emergency room 30 minutes after the episode. There was no pallor. The blood pressure
was 150/100 mmHg and pulse wa: 120/min. There was no abdominal tenderness. The
ECG showed sinus tachycardia with ST segment depression and T wave inversion in
inferior and lateral chest leads. A diagnosis of unstable angina was made and he was given
aspirin, heparin, nifedepine and betablockers. Four hours after admission, the BP fell to
90 mmHg, with a pulse rate of 120/min. The BP came up to 120/80 mmHg with fluid
load, but started falling again. At this stage, he vomited 200 ml of altered blood. Ryle’s
tube aspiration revealed 500 ml of fresh blood. Blood transfusion, antacids and ranitidine
were given. Endoscopy confirmed an actively bleeding peptic ulcer. He was managed
conservatively and was discharged home 2 weeks later. Six weeks after discharge, the
exercise test was found to be normal.
SYNCOPE
Table 9.6: Syncope of GI bleeding: misleading features

Feature Mechanism
Syncope Transient hypotension due to sudden loss of
blood counteracted by sinus tachycardia,
peripheral vasoconstriction.
Postsyncopal hypertension Reactive hypertension due to adrenergic
excess
Lack of hematemesis/malena 500 ml of blood can be sequestered in GI
tract without external evidence of bleeding
Lack of abdominal pain Bleeding into gastrointestinal tract is usually
painless
Chest discomfort Esophagitis
ECG signs of ST depression, Hypotension/tachycardia may trigger
T wave inversion myocardial ischemia with associated CAD
in older patient
Associated left ventricular hypertrophy
of hypertension
Acute gastrointestinal bleeding presenting with syncope is often mistaken

for a cardiovascular disorder. That the hypotension can be transient (due to 145
gastrointestinal bleeding) is often not realized (Table 9.6).
When the clinical picture is not typical in acute ischemic syndromes, one
should defer the use of aspirin and heparin, until a Ryles tube aspiration is negative
for gastrointestinal bleed. Rectal examination may help to detect the condition.
Unknown cause: After initial evaluation, as many as 42 per cent of patients may
fall under this category. Though recurrent syncope is rare in this group, one year
mortality is as much as 6 per cent in them. In elderly patients, the prognosis must
still be guarded as many of them tend to have transient ischemic attacks or
cerebrovascular accidents later. Incidence of sudden death may be 5 per cent or
higher in the elderly age group. In all elderly patients with syncope of unknown
origin, a possible cardiac or neurological cause should be sought by careful
evaluation and follow up.
APPROACH TO A PATIENT WITH SYNCOPE
History and physical examination help to diagnose 75 per cent of patients with
syncope.
Table 9.7: Important aspects in the history of a patient with syncope

Feature Significance
Clinical background
Diabetic patient Hypoglycemia
Cerebrovascular accident
Transient ischemic attack
Postural hypotension due to autonomic
neuropathy
Hypertension Postural hypotension (drugs)
Encephalopathy
Intracranial hemorrhage
Transient ischemic attack
Alcoholism Intoxication
Autonomic neuropathy
CAD Arrhythmias
Mechanical complication
Drugs
146 Postoperative or prolonged rest Pulmonary embolism
Postural hypotension
Peptic ulcer Gastrointestinal bleeding
Acute perforation
The deaf patient Prolonged QT syndrome
Painful/unpleasant event/sight Vasovagal
History of fall or head injury Subdural hematoma
Related to a physiological act
Exertional syncope Left ventricular outflow obstruction; Bilateral
carotid stenosis (Takayasu’s arteritis)
Syncope with upper limb exercise Subclavian steal syndrome
Syncope with cough Cough syncope
Syncope with micturition Micturition syncope
Syncope with neck turning Carotid sinus hypersensitivity
Careful physical examination gives valuable clues in some patients with syncope.
In general, if the patient with syncope is young, and the features are suggestive
of vasovagal syncope, tilt test may be done, he/she should be reassured and
SYNCOPE
Table 9.8: Important aspects of physical examination

Feature Could indicate
Drowsiness/altered Hypoglycemia
sensorium Central nervous disorder
Pulse rate Vasovagal
Arrhythmia
Blood pressure Postural hypotension
Hypertension
Reactive hypertension following a fall
Tongue (bruise, bleeding) Epilepsy
Head injury Subdural hematoma
Carotid bruit Transient ischemic attack
Heart
S4, murmurs Aortic stenosis, or other valvular lesions
Non-ejection click Mitral valve prolapse
Irregular rhythm Arrhythmia
Pericardial rub Cardiac tamponade
Leg veins/calf muscles Deep vein thrombosis with pulmonary embolism
Rectal examination/stool Occult gastrointestinal bleeding 147
heme test
Neurological examination Neurological cause
Provocative maneuvers Tests to bring out vagal instability
Carotid sinus massage
Hyperventilation
Valsalva maneuver
Ocular compression
Table 9.9: Diagnostic testing in syncope

Test Mechanism
Blood sugar Hypoglycemia
Hemoglobin, PCV Low level indicates bleeding
Serum potassium Arrhythmias due to high or low levels
Serum bicarbonate Low level suggests seizure occurred
Blood gases Hypoxia indicates pulmonary embolism
Cardiac enzymes Myocardial infarction
Electrocardiogram (2–8 % yield) Arrhythmia
Myocardial infarction
Test Mechanism
Unstable angina
Vasospastic angina
Hyperkalemia
Hypokalemia
Pre-excitation
Prolonged QT interval
Cardiac tamponade
Holter monitoring (2% yield) Arrhythmia
Echocardiogram (1.3% yield) Valvular disease
Pulmonary hypertension
Intracardiac tumours
Cardiac tamponade
LV dysfunction
Wall motion abnormalities
Tilt test Indicated to confirm a diagnosis of vasovagal
syncope
148 Usually no underlying heart disease
Electrophysiological study Low yield if done in all patients
VT, VF, Syncopal SVT or AF may be induced
Useful in assessing sinus node function and
Conduction system
Neurologic testing (EEG, CT, MRI) Low yield
extensive diagnostic testing is not indicated. On the other hand, the syncope of
‘unknown cause’ in an elderly patient requires thorough evaluation and if the
cause is not clear at the end, careful follow up is indicated. These patients have a
6 per cent one year mortality either due to cardiovascular or cerebrovascular cause.
The patient and the family should be educated about the warning signals of heart
disease and stroke. Invasive electrophysiologic testing may be indicated in this
subset of patients.
10 Palpitation
If we had keen vision and feeling of all ordinary human life, it would be like hearing the grass grow,
or the squirrel’s heart beat, and we should die of that roar which lies on the other side of silence.
George Eliot
Palpitation is the uncomfortable awareness of the heart beat, and is usually related
to an alteration in heart rate, rhythm or augmentation of contraction. Though it is
classically suggestive of an arrhythmia, it occurs in a wide variety of disorders of
cardiac and non-cardiac origin. Due to the commonness, and the dual significance
of a life threatening arrhythmia on the one hand, and a trivial anxiety on the other,
it requires a careful evaluation. Palpitation occurs due to a forceful cardiac
contraction, or an abnormality of heart rhythm. Forceful heart contraction occurs
in volume overloads due to excessive preload or all conditions with adrenergic
excess. An arrhythmia produces palpitation either when the rate is too high, too
low or is irregular.
Evaluation
A systematic approach to this symptom is useful in patient evaluation.
• Is it palpitation or some other symptom simulating it?
• Did it precede or follow the knowledge of heart disease?
• Is it persistent or paroxysmal?
• What is the nature of palpitation?
• What are the associated symptoms?
• Is there an extra cardiac cause for palpitation?
• Is the patient taking any drugs that produce arrhythmias?
The chest discomfort of myocardial ischemia and dyspnea can be confused
for palpitation. Some patients use these three terms to describe whatever happens
from the upper abdomen to the lower jaw. When palpitation follows the knowledge
of heart disease, it is more likely to be psychogenic. Multiplicity of symptoms and
the setting under which it occurs make situational anxiety more likely.
Some serious disorders which can present as palpitation are:
• Arrhythmias
• Coronary artery disease: Angina, acute myocardial infarction
• Valvular heart disease
• High output states
• Internal hemorrhage (sinus tachycardia)
• Acute pancreatitis (sinus tachycardia)
• Acute pulmonary embolism (sinus tachycardia/dyspnea)
Paroxysmal palpitation is suggestive of an arrhythmia. Persistent palpitation
is suggestive of a volume load like aortic regurgitation or a persistent arrhythmia
like atrial fibrillation. Even in these situations, palpitation may not be experienced
at rest but may manifest on exertion. If the palpitation is paroxysmal, and an
150
arrhythmia is likely further enquiries are necessary.
The clinical setting in which palpitation occurs gives clues to the nature and
seriousness of the arrhythmia (Table 10.1). Knowledge of preexisting heart disease
like mitral valve disease or Ebstein’s anomaly of tricuspid valve suggests
supraventricular arrhythmias. A pre-existing WPW syndrome suggests a re-entrant
supraventricular arrhythmia. Digoxin is generally contraindicated in this situation,
particularly with atrial fibrillation.
Causes of palpitations
Cardiovascular
Regurgitant lesions (aortic, mitral and tricuspid regurgitation)
Left to right shunts
Hyperkinetic heart syndrome
Prosthetic heart valves
Electronic pacemaker
Arteriovenous fistula
Aortic aneurysm
Arrhythmias
Rapid regular (paroxysmal atrial tachycardia)
PALPITATION
Rapid irregular (atrial fibrillation)

Bradyarrhythmias (complete heart block)
Normal rate but irregular (ventricular ectopics)
Non-cardiac
Hyperkinetic circulatory states
Anemia
Fever
Thyrotoxicosis
Anxiety
Hypoglycemia
Pheochromocytoma
Drugs
Sympathomimetic drugs
Vasodilators
Digitalis
Diaphragmatic flutter
Migraine 151
Table 10.1: Clues to arrhythmia in the clinical setting

Setting Clues
Coronary artery disease Ventricular arrhythmias
Conduction disturbances
Heart failure Digitoxicity
Hypokalemia of diuretics
Mitral valve prolapse Ventricular or atrial arrhythmias
Deafness Prolonged Q-T
Ventricular arrhythmias
Antiarrhythmic drugs Proarrhythmia
Prolonged Q-T
Diuretics Hypokalemia
Ventricular dysfunction
A patient with depression Prolonged Q-T
on tricyclic antidepressants Ventricular arrhythmias
Thyrotoxicosis Atrial fibrillation with rapid
ventricular response
Setting Clues
Pre-excitation Re-entrant SVT
AF with wide QRS/rapid rates
Mitral valve disease Atrial fibrillation
Diabetic patient Hypoglycemia
Bronchial asthma Drug induced sinus or
supraventricular tachycardia
Systemic hypertension Vasodilators
Pheochromocytoma
Nature of palpitation
The nature of palpitation may give clues as to the nature of the arrhythmia
(Table. 10.2). The associated symptoms are related to the disorder responsible for
palpitation or to the arrhythmia (Table 10.3). Syncope is the most important
symptom to enquire after as it may indicate a serious underlying arrhythmia or a
large area of myocardium at risk since palpitation and chest discomfort may be
confused with each other. Syncope in association with palpitation should be
152 considered a danger signal. If recent, the patient should be hospitalized and
Table 10.2: Diagnostic clues to nature of palpitation
Nature of palpitation Clue
Missing of a beat Premature ventricular contraction
Thump in the chest
Fullness in the neck
Rapid regular palpitation Sinus tachycardia
Supraventricular tachycardia
Rapid irregular palpitation Atrial fibrillation
Atrial flutter with varying block
Atrial tachycardia with varying block
Sudden palpitation with The tachycardia-bradycardia of sick
sudden cessation or asystole sinus syndrome
followed by syncope
Rapid pulsations in the neck Supraventricular tachycardia
Giddiness/syncope Bradyarrhythmia
PALPITATION
evaluated. If it happened some time ago, the patient can be investigated on an out
patient basis.
Dyspnea with palpitation may mean that an arrhythmia is responsible for
heart failure, if palpitation preceded dyspnea. If palpitation followed dyspnea, it
may mean heart failure precipitating arrhythmia or acute episode of asthma with
atrial arrhythmias due to respiratory insufficiency, or acute pulmonary embolism
with atrial arrhythmias. When dyspnea accompanies palpitation, intrinsic heart
disease is likely. As dyspnea can be an anginal equivalent, underlying coronary
artery disease remains a possibility.
Palpitation with dyspnea in patients with coronary artery disease usually
indicates ventricular arrhythmia, and poor ventricular function and sudden death
is common. Such patients require hospitalization and monitoring before
antiarrhythmic drugs are administered.
Table 10.3: Associated symptoms in palpitation
Symptom Significance
Syncope Low cardiac output during arrhythmia
Hypoglycemia 153
Pheochromocytoma
Dyspnea Heart failure due to arrhythmia
Myocardial ischemia/infarction with LVF
Acute episode of severe asthma with
respiratory insufficiency
Chest pain Arrhythmogenic myocardial ischemia
(chest discomfort follows palpitation)
Angina or infarction with arrhythmia
(chest discomfort precedes palpitation)
Polyuria following Paroxysmal atrial tachycardia
palpitation Paroxysmal atrial fibrillation
Sweating Anxiety
Arrhythmia with hypotension
Angina/myocardial infarction
Hypoglycemia
Diarrhea Thyrotoxicosis
Irritable bowel syndrome
Hypokalemia induced arrhythmia
Chest pain following palpitation is due to arrhythmia precipitating angina. If

chest pain precedes palpitation, myocardial ischemia precipitating arrhythmia is
likely. Both brady- and tachyarrhythmias can cause angina: bradyarrhythmias by the
mechanism of hypotension and increase in ventricular diastolic pressure which
reduces the coronary perfusion pressure and tachyarrhythmias by increasing the
myocardial oxygen demands and the often associated hypotension.
The mechanisms of angina in arrhythmias are
Tachyarrhythmias
Increased heart rate increasing myocardial oxygen consumption
Less diastolic time
Hypotension (coronary perfusion)
Elevated ventricular diastolic pressure (coronary perfusion pressure)
Bradyarrhythmias
Hypotension (coronary perfusion)
Elevated ventricular diastolic pressure
It is often not realized that a bradyarrhythmia can present as angina and can
154
also be the presenting manifestation occasionally in sick sinus syndrome.
Paroxysmal atrial tachycardia or atrial fibrillation are often associated with
polyuria during and immediately after the episode of tachycardia. This is possibly
mediated by atrial natriuretic hormone released from the atria.
PALPITATION IN VARIOUS DISORDERS
PALPITATION IN NORMAL PEOPLE

Palpitation occurs in otherwise normal people with exercise, emotional excitability
and the daily anxieties.
Many lamentable effects of this fear causeth in men, as to be red, pale, tremble, sweat; it makes
sudden cold and heat to come all over the body, palpitation of the heart, syncope, etc. It amazeth
many men that are to speak or show themselves in public assemblies, or before some great personages.
Robert Burton in The Anatomy of Melancholy
Palpitation is a very common feature of anxiety states. The multiplicity of

symptoms and the precipitating factors help in identifying it. In acute anxiety
states, palpitation may be the dominant but transient symptom and is usually relieved
PALPITATION
spontaneously or with reassurance. The chronic form of anxiety is relatively resistant

to therapy and is called by various names such as
• Da Costa syndrome
• Soldier’s heart
• Effort syndrome
• Neurocirculatory asthenia
• Functional cardiovascular disease
• Irritable heart
The signs and symptoms are often indistinguishable from other hyperkinetic
circulatory states.
Symptoms and signs of palpitations in anxiety states

Symptoms
Palpitation
Shortness of breath (deep sighing respiration)
Chest pain or tightness
Weakness
Insomnia 155
Giddiness
Signs
Sinus tachycardia
High pulse pressure
Excessive sweating
Hyperventilation
Hyperkinetic apical impulse
Hyperkinetic parasternal impulse
Ejection murmurs across right or left ventricular outflow tract
Non-specific ECG abnormalities (ST-T alterations, voltage LVH in thin people)
The chronic nature of the disorder, deep sighing type of respiration, and
atypical type of pain of coronary artery disease distinguish this disorder from the
diseases it so commonly simulates. This diagnosis should be made only after
carefully excluding a variety disorders. The conditions mistakenly labelled as anxiety
disorders are:
• Anemia
• Thyrotoxicosis
• Mitral valve prolapse
• Coronary artery disease
• Hyperkinetic heart syndrome
• Rabies
• Episodic asthma
• Hypoglycemia in diabetic patients
• Insulinoma with recurrent hypoglycemia
• Pancreatic carcinoma
• Hepatic cirrhosis
• Drug addiction with periods of withdrawal
• Chronic low-grade fever as in pulmonary tuberculosis
• Drug use
Smoking
Coffee
Sympathomimetic drugs
156 Alcohol
Thyroid medication
The conditions listed above should be carefully ruled out before labeling
somebody as having palpitation.
Choose your specialist and you choose your disease
Anonymous
PALPITATION IN VALVULAR HEART DISEASE

Palpitation is often the initial and most dominant symptom in mitral and aortic
regurgitation. Even if palpitation is significant, surgical intervention is almost never
indicated due to this symptom. Dyspnea is often the basis for decision making.
Palpitation is rare in aortic stenosis. In mitral stenosis, palpitation occurs late in
the disease with the onset of atrial fibrillation. In the initial stages of the disease,
the arrhythmia tends to be paroxysmal and later becomes persistent. Once
established, palpitation may be experienced only on exertion. Recurrent
supraventricular tachycardia or atrial fibrillation may precipitate pulmonary edema
in patients with mitral stenosis.
PALPITATION
Typically palpitation precedes dyspnea in such situations.

• Look for mitral stenosis in all patients with ‘unexplained’ atrial
fibrillation
• Indicates chronic severe mitral stenosis in young patients
• Increased incidence of peripheral embolism
• Indication for long term oral anticoagulation
• Indication for transesophageal echocardiography to rule out left atrial
thrombus
• Indication for relief of mitral stenosis
• Atrial fibrillation in elderly patients may occur even with mild mitral
stenosis
• Paroxysmal palpitation explains ‘unexplained’ peripheral embolism
with sinus rhythm or recurrent pulmonary edema
If atrial fibrillation occurs in a young patient with mild mitral stenosis, some
other associated cause should be looked for.
The causes of atrial fibrillation in a young patient with mild mitral stenosis
are: 157
• Associated atrial septal defect
• Thyrotoxicosis
• Pre-excitation
• Recurrent pulmonary embolism
• Sick sinus syndrome
Inappropriate sinus tachycardia and palpitation is common in many patients
with mild to moderate mitral stenosis with exercise. They respond well to
betablockers, and intervention can be postponed for months to years.
PALPITATION IN CONGENITAL HEART DISEASE

The equivalent of palpitation in infancy and childhood is increased precordial
motion noted by the parent. This, as a sign or symptom, may be the presenting
feature in ventricular septal defect and patent ductus arteriosus in early childhood,
but occurs later in life in atrial septal defect. Palpitation is uncommon in Tetralogy
of Fallot or conditions with similar physiology. Palpitation as a dominant symptom
in cyanotic heart disease should suggest Ebstein’s anomaly of tricuspid valve as
they are predisposed to recurrent atrial arrhythmias due to large right atrium. In
cyanotic heart disease with increased pulmonary blood flow, palpitations may occur.
Atrial arrhythmias are common after Mustard operation of redirecting the venous
blood in transposition of great arteries.
PALPITATION IN SYSTEMIC HYPERTENSION

Recurrent palpitation and sweating in a patient with paroxysmal hypertension
should suggest the possibility of pheochromocytoma. More commonly, palpitation
in patients with hypertension is related to drug therapy with vasodilators or the
mere knowledge of hypertension.
Causes
• Isolated use of vasodilators
Palpitation as anginal equivalent
Arrhythmias
• Hypokalemia causing arrhythmia
158 Diuretic induced
Primary aldosteronism
• Psychogenic: after the knowledge of hypertension
Palpitation may be an anginal equivalent, and careful evaluation in high risk
patients by detailed history and objective testing will be helpful.
All palpitations are not arrhythmias and many arrhythmias do not palpitate.
11 Fever in a Patient with
Heart Disease
Fever is a characteristic sign of infection. The majority of patients who present

with fever have viral or bacterial infections. Fever in a patient with cardiovascular
disease has different connotations and should be treated with concern and respect.
Fever in this setting may indicate serious infection of the heart as infective
endocarditis or pericarditis. It may also be responsible for aggravation of existing
disorder due to increased demands on the heart. Some of the terms commonly
used in this context are defined in Table 11.1.
Table 11.1: Definitions of terms commonly used in relation to fever
Normal body temperature Oral: Usually 37 ºC (98. 6 ºF)

Rectal: 0.6 ºC higher
The normal temperature varies with time of the day, and between
individuals (range 36.4 – 37.2 ºC, or 97.5 – 98.9 ºF)
Diurnal variation Lowest in the early morning
Highest in the late afternoon or early evening (4.00–8.00 PM)
Variation may be as much as 0.5 ºC (1.0 ºF)
Diurnal variation is consistent for each person
Lack of diurnal variation may suggest factitious fever or
hypothalamic disorder
Fever Oral temperature > 37. 2 ºC (99 ºF) in the morning
and > 37.7 ºC (100 ºF) in the evening
Chills and rigors At the onset of fever an abrupt increase in core temperature
occurs by means of vigorous muscle contractions called
rigors, associated with cutaneous vasoconstriction and
piloerection, called chills.
Lethal temperature Less than 26 ºC (78.8 ºF) or more than 43 ºC (109.4 ºF),
Upper lethal limit Temperatures above 41 ºC (105.8 ºF)
DISORDERS ASSOCIATED WITH FEVER
That infections declare themselves with fever is a common knowledge, but a variety
of non-infectious disorders may be accompanied by fever.
The clinician taking care of patients with cardiovascular disease should be
aware of all the mechanisms responsible for this important and commonly occurring
symptom, so that it may be managed appropriately (Table 11.2).
PATTERNS OF FEVER
INTERMITTENT (HECTIC OR SEPTIC) FEVERS

These are characterized by wide fluctuations in temperature with the temperature
returning to normal at least once during any 24 hour period.
Causes
• Malaria
• Pyogenic abscess
160 • Bacteremia
• Irregular use of antipyretics
• Miliary tuberculosis
DOUBLE FEVER SPIKE IN A SINGLE DAY
Causes
• Gonococcal endocarditis
• Miliary tuberculosis
• Kala azar
VARIANTS OF INTERMITTENT FEVER

a. Alternate day fever: Causes could be Plasmodium vivax, steroid withdrawal
fevers (alternate day dosage schedules)
b. Fever spike every third day: Cause could be Plasmodium malaria infection.
FEVER IN A PATIENT WITH HEART DISEASE
Table 11.2: Some causes of fever

Infections Bacterial
Viral
Rickettsial
Chlamydial
Parasites particularly protozoal
Fungal
Vascular Inflammation
Phlebitis, arteritis
Thrombosis
Infarction (myocardial, pulmonary, cerebral)
Immune mechanisms Connective tissue disorders
Drug reactions
All immunological reactions
Acquired immunodeficiency syndrome
(AIDS)
Neoplastic disorders Hematopoietic
Lymphoreticular
Hypernephroma
Carcinoma of pancreas
Cancer lung 161
Hepatoma
Bone tumours
Complications of malignancy
Disseminated metastasis
Obstruction, stasis, infection
Granulomatous disorders Sarcoidosis
Granulomatous hepatitis
Inflammatory bowel disease Ulcerative colitis
Crohn’s disease
Others (acute pancreatitis, hepatitis)
Mechanical trauma Trauma
Surgery
Hemolysis, myolysis Hemolytic anemia
Rhabdomyolysis
Acute metabolic disorders Gout
Porphyria
Thyrotoxicosis
Pheochromocytoma
Fabry’s disease
SUSTAINED FEVER (CONTINUOUS FEVER)

There is moderately sustained elevation of temperature with minimal fluctuations.
Causes
• Typhoid fever
• Pneumococcal pneumonia
• Brucellosis
• Tularemia
• Psittacosis
• Rickettsial infections
REMITTENT FEVER
The fluctuations in temperature are less dramatic than in intermittent fever and
the temperature does not return to normal
Causes
• Acute viral respiratory infections
162
• Plasmodium falciparum malaria
• Mycoplasma pneumonia
RELAPSING (RECURRENT) FEVER

Periods of fever and normal temperature alternate cyclically. During febrile
episodes, the fever may follow any pattern.
Causes
• Lymphomas
• Rat bite fever
• Berylliosis
• Dengue fever
The catabolic response may impose serious hemodynamic burden on the
cardiovascular system. A normal cardiovascular system responds to this challenge
without any adverse effects. However, an abnormal cardiovascular system responds
variably (Table 11.3).
Table 11.3: Metabolic changes associated with fever and their significance in cardiac patient
Metabolic change Clinical significance
Metabolic rate increases by 12% with The net metabolic effect is catabolism. If
each degree centigrade increase in the need for calories and amino acids is
temperature not met, body wasting ensues.
Heart rate increases by 15 beats/ Can precipitate heart failure
minute per degree centigrade increase
in temperature May be responsible for unstable angina or
myocardial infarction
Expected increase may not occur in patients
with sick sinus syndrome, complete heart
block and patients receiving calcium or
betablocker therapy
Expected increase may not occur with
typhoid fever, central nervous system
infections with intracranial hypertension
Increased insensible water loss of Hypovolemia may lead to hypotension
300–500 ml/m2/1 ºC/day. Influenced in diastolic dysfunction, patients on
by degree of fever, hyperventilation, diuretics, vasodilators or nitrates for
humidity, and ambient temperature angina
The above drugs may have to be reduced in 163
dosage or withdrawn temporarily
Electrolyte depletion Hypokalemia may induce arrhythmias
Hyperventilation early in course of May induce respiratory alkalosis
febrile illness with consequent Respiratory alkalosis early and metabolic
respiratory alkalosis acidosis late in the clinical course of
septic shock
Hyperventilation may be mistaken for LVF
or acute pulmonary embolism
Pathogenesis
The principal mechanisms of fever in heart disease are infection, tissue necrosis,
resolution of a thrombus, hemolysis, or autoimmune phenomenon (Table 11.4).
FEVER IN PATIENTS WITH INFECTIVE ENDOCARDITIS
Fever is the most common presenting symptom and occurs in 85 per cent of
patients with infective endocarditis. Chills and sweats are noted in 50 per cent of
patients. Though fever is the most common symptom, it may be absent in some
patients and some other symptom may dominate the clinical presentation.
Table 11.4: Causes and mechanisms of fever in cardiovascular disease

Causes Mechanism(s)
Infective endocarditis Infection
Immunological mechanisms
Drug induced fever
Intravenous lines/phlebitis
Metastatic abscesses
Pericarditis Infection
Non-infectious
Drug induced (antituberculous)
Rheumatic fever Immunological response to streptococcal infection
Acute myocardial infarction Necrosis of myocardium
Thrombolytic therapy (STK)
Thrombophlebitis at venous access sites
Pacemaker lead related phlebitis/infection
Post-myocardial infarction Dressler’s syndrome
Pulmonary embolism Thrombus resolution
Thrombolytic therapy
Septic pulmonary emboli
Phlebitis/infection at venous access sites
164 Aortic dissection Resorption of hematoma
Systemic hypertension Aortitis
Systemic vasculitis
Connective tissue disorders
Pheochromocytoma
Drug induced (hydralazine)
Acute glomerulonephritis
Acute pyelonephritis
Left atrial myxoma Tumour factors
Immunologic response
Drug fever Drugs used in cardiac patients
Streptokinase
Atropine
Dilantin
Heparin
Hydralazine
Meperidine
Procainamide
Quinidine
Salicylates
Isoniazid
Streptomycin
P-aminosalicylic acid
Presenting manifestations of infective endocarditis features

• Fever (85%)
• Weakness, malaise (12–94%)
• Chills, sweats (50%)
• Dyspnea, chest pain, cough (17–42%)
• Skin lesions (25%)
• Headache (50%)
• Onset of hemiparesis (10–20%)
• Personality changes, psychosis (30%)
• Altered sensorium (30%)
• Arthralgia, myalgia (30%)
• Back pain (37%)
• Anorexia, weight loss (15–75%)
Documented fever occurs in 90 per cent of patients but may be absent in a
certain subset of patients.
Causes of absence of fever

• Age (elderly patient) 165
• Congestive heart failure
• Renal failure
• Severe sepsis
• Prior antibiotic therapy
• Fungal endocarditis
As fever is identified as an essential feature for the diagnosis of infective
endocarditis, in the absence of it, the diagnosis may be missed completely. Fever
may go unrecognized by some patients but manifests itself as a vague feeling of
uneasiness, feverishness, body pain, weakness, loss Fever equivalents
of appetite or other constitutional symptoms. These Weakness and malaise
symptoms should be considered as fever equivalents. Arthralgia/body pain
Any of the above symptoms should arouse the Headache
Loss of appetite
suspicion of elevated temperature and it should be
Sweating
checked. Insomnia
With appropriate antibiotic therapy, most of the Uneasiness
patients with endocarditis become afebrile and Feverishness
cultures are negative by the end of first week. Some patients respond more slowly.
However, emboli, petechiae, and other peripheral manifestations may occur weeks
after starting curative therapy. Heart failure due to valvular damage can occur
much later, even years after appropriate therapy. Some patients continue to be
febrile in spite of antibiotic therapy; this may be due to inappropriate antibiotic
choice but other causes should be checked for:
• Phlebitis, intravenous access sites
• Intramuscular injections
• Drug fever
• Metastatic abscess
• Myocardial or ring abscess
• Rheumatic fever as the cause of fever
• Some other unrelated infection (for example, tuberculosis)
• Superinfection from intravenous catheters. Superinfection of the valve
or vegetation by bacteremia or fungemia may occur. It is for this reason
that intravenous catheters should be avoided or changed every 48 hours.
166
FEVER AND POLYARTHRITIS OF RHEUMATIC FEVER
Polyarthritis with fever is the presenting manifestation of acute rheumatic fever,

which is the most common form of acquired heart disease in children and
adolescents. However a variety of disorders present similarly and require to be
differentiated from acute rheumatic fever.
Differential diagnosis
The causes are given in Table 11.5. It is important to consider these conditions, in
the differential diagnosis for a patient presenting with polyarthritis and fever
(Table 11.6).
RHEUMATIC FEVER
Cardiac involvement dominates the clinical picture in rheumatic fever in children
and the arthritis may be less prominent or may be absent. In adults, arthritis is the
dominant feature with mild or no carditis. The arthritis is usually abrupt with
fever and a third of patients have no recollection of a sore throat. Classic migratory
pattern though characteristic is not diagnostic of rheumatic fever and occurs in
Table 11.5: Causes of polyarthritis and fever

Features Confirmatory
Septic arthritis Synovial fluid and blood culture
Bacterial endocarditis Blood cultures, Echocardiogram
Lyme disease Serologic studies
Mycobacterial and fungal arthritis Culture or biopsy
Viral arthritis Serologic studies
Postinfectious or reactive arthritis Culture or serologic studies
Enteric infection Blood culture
Urogenital infection (Reiter’s syndrome) Clinical findings
Rheumatic fever Clinical findings
Inflammatory bowel disease Biopsy
Rheumatoid arthritis and Still’s disease Serologic studies
Systemic rheumatic illnesses
Systemic vasculitis
Systemic lupus erythematosus
Crystal induced arthritis Polarizing microscopy of
synovial fluid or tophus
Gout and pseudogout
Mucocutaneous disorders Biopsy or clinical findings
Dermatomyositis
Behcet’s disease 167
Henoch–Schönlein purpura
Kawasaki’s disease
Erythema nodosusm
Erythema multiforme
Pyoderma gangrenosum
Pustular psoriasis
Other diseases
Cancers
Sarcoidosis
Familial Mediterranean fever
other conditions also. Even the rapidly additive large joint involvement is shared
by other forms of reactive arthritis. Without aspirin or steroids, fever usually
fluctuates without returning to normal for a week or more. Demonstration of
recent group A streptococcal infection by serologic studies or throat culture and
dramatic response to salicylates supports the diagnosis.
Polyarthritis, fever and bacterial endocarditis

Contrary to expectations, musculoskeletal symptoms are very frequent (44%) in
bacterial endocarditis. Arthralgia and low back pain are the most common. Arthritis
Table 11.6: Polyarthritis and fever: diagnostic possibilities derived from discriminating features
Symptom or sign Diagnostic possibilities
Migratory arthritis Rheumatic fever
Gonococcemia
Meningococcemia
Viral arthritis
Acute leukemia
Whipple’s disease
Fever preceding arthritis Bacterial endocarditis
Viral arthritis
Reactive arthritis
Still’s disease
Lyme disease
Temperature >40 ºC Bacterial arthritis
Still’s disease
Pain disproportionately greater than Rheumatic fever
effusion Acute leukemia
Familial Mediterranean fever
168 AIDS
Effusion disproportionately greater Tuberculous arthritis
than pain Bacterial endocarditis
Inflammatory bowel disease
Giant cell arteritis
Lyme disease
Morning stiffness Rheumatoid arthritis
Polymyalgia rheumatica
Still’s disease
Any viral and reactive arthritis
Episodic recurrences Still’s disease
Crystal induced arthritis
Inflammatory bowel disease
Whipple’s disease
Mediterranean fever
Lyme disease
Symmetric small joint synovitis Rhematoid arthritis
Viral arthritis
Symptom or sign Diagnostic possibilities

Positive test for rheumatoid factor Rheumatoid arthritis
Viral arthritis
Tuberculous arthritis
Bacterial endocarditis
Sarcoidosis
Systemic vasculitis
Leukocytosis (>15,000/mm3) Bacterial arthritis
Bacterial endocarditis
Still’s disease
Systemic vasculitis
Acute leukemia
Leukopenia Systemic lupus erythematosus
Viral arthritis
or joint swelling involving one to three joints occur in 14 per cent of patients.
Synovial fluid cultures are usually negative. Rheumatoid factor may be positive in
about a third of patients. Arthralgia or arthritis should not be used to differentiate
rheumatic fever from infective endocarditis. 169
APPROACH TO A PATIENT WITH FEVER AND HEART DISEASE
Fever in a patient with structural heart disease

Fever in patients with structural heart defects should always suggest the possibility
of infective endocarditis unless proved otherwise. All patients presenting with
fever in this background should be investigated for infective endocarditis. This
rule should be rigorously applied whether the fever is of one hour, one day, one
week or one month duration. The investigation of choice is properly taken blood
cultures. It is not a common practice to ask for blood cultures until the fever is
prolonged. This is obviously incorrect and blood cultures should be drawn even
on the first day of fever in a patient with structural heart defect. The most serious
complications like peripheral embolism and heart failure are related to the duration
of fever and delayed institution of antibiotic therapy.
Blood cultures
To minimize the risk of contamination, proper method should be followed. Skin
contaminants like coagulase negative staphylococci, and diphtheroids may be
misleading. In prosthetic valve endocarditis, even contaminants from the skin may
be blood borne and pathogenic.
Techniques:
• Hands should be washed.
• Obtain appropriate media, 2 per cent tincture of iodine, or Betadine, alcohol
swabs, tourniquet, disposable plastic syringe and two needles.
• Remove the caps from the culture bottles and using friction, swab the stopper
twice with alcohol.
• Select the antecubital site and prepare a circular area with a radius of about 2
inches. Starting at the puncture site, scrub the area with Betadine, using a
circular motion with overlapping strokes and working towards the periphery.
Repeat the procedure twice. (Use 70 per cent isopropyl alcohol to clean the
area for two minutes if the patient is allergic to iodine and Betadine).
• For better recognition of the puncture site, clean the Betadine with alcohol
swabs. Follow the same ‘clean to dirty’ circular motion.
• With a 10 ml syringe, puncture the vein carefully. Avoid touching the needle
170
or prepared skin site. To palpate the vein use a sterile glove.
• Remove the needle from the vein. Avoid touching the needle outside the
prepared area.
• Aseptically remove the needle from the syringe and put on the other sterile
needle. Transfer not more than 5 ml into each bottle.
• Carefully label the blood culture slip with the date and exact time the culture
was drawn. This information is important in interpretation of data later.
Due of low density of most bacteremias, 5 ml samples for adults and 1–5 ml
samples for children are commonly recommended. The 1:10 to 1:20 dilution of
blood upon inoculation into the culture media usually suffices to reduce intrinsic
serum antibacterial activity and reduce the concentration of antibacterial substances
to subinhibitory levels.
POST-OPERATIVE FEVER
Fever is common until 5 days after cardiac surgery and is the normal response to
tissue disruption and cardiopulmonary bypass. Elevated interleukins may be
responsible. Rarely, this normal fever may persist for up to 2 weeks or longer.
Chills are uncommon but may occur. This rise in temperature should be
conservatively managed and unnecessary testing should be avoided.
On the other hand, hyperthermia occurring 6–36 hours after open heart
operations is usually not due to infection but due to the hypermetabolic state
following cardiopulmonary bypass. This hyperthermia is associated with low cardiac
output and diminished skin blood flow, which impairs heat loss. This should be
considered an emergency and the condition may respond to peritoneal dialysis
with cold dialysate. This condition is unrelated to ‘malignant hyperthermia’.
Postoperative wound complications though less common these days, still occur
occasionally. Mediastinitis and sternal wound dehiscence are common causes. The
risk factors for postoperative wound infection are:
• Prolonged operative time
• Retrosternal hematoma
• Inaccurate sternal closure
• Obesity
• Diabetes
• Bilateral internal mammary dissection
• Male sex (shaving the chest) 171
• Prolonged postoperative ventilation
• Corticosteroids
• Surgical team and the operative setting (operative time, tissue handling,
general ambience)
Unusual fever and malaise, sternal tenderness and persistent severe central
chest pain unrelieved by analgesics suggest the possibility of a sternotomy infection.
External evidence of inflammation or redness of the skin may be absent. CT scan
of the chest may be diagnostic.
FEVER IN PATIENTS WITH CORONARY ARTERY DISEASE

Fever is common in patients with acute myocardial infarction and is related to
tissue necrosis. It occurs within 24–48 hours of infarction. The body temperature
begins to rise within 4 hours after the onset of infarction. Fever usually subsides
by seventh day of infarction. Chills and rigors do not occur and the temperature
rarely exceeds 102 ºF. Fever may also be related to other factors in acute myocardial
infarction, like pericarditis, Dressler’s syndrome or after thrombolysis, especially
with streptokinase.
As fever increases the myocardial oxygen demands, it is poorly tolerated by

patients with severe coronary artery disease. Significant elevation of temperature
may precipitate unstable angina or even acute myocardial infarction. In patients
with severe left ventricular dysfunction, congestive heart failure may be precipitated
or aggravated. It is for this reason that infection or fever in these patients should
be promptly controlled with antipyretics and suitable antibiotics if appropriate.
The vasodilatation, loss of water and electrolytes through excessive sweating may
induce hypotension, which may be aggravated by nitrates and other antianginal
drugs.
The commonest causes of fever in patients hospitalized with acute coronary
syndromes are intravenous fluids and indwelling catheters. Adequate antiseptic
techniques and changing the lines after 48 hours reduces this complication.
A FEBRILE PATIENT
As pericarditis and infective endocarditis are easily amenable to therapy when
recognized early, all patients presenting with fever should be examined to rule out
these disorders (Table 11.7). It is not a common clinical habit to look for a pericardial
172
rub or a heart murmur in all patients presenting with fever. Looking for a pericardial
rub in a patient with fever involves careful auscultation over the left sternal border
at the 3rd and 4th spaces, by pressing the diaphragm during either phase of respiration.
One must particularly look for the early diastolic murmur of aortic regurgitation
or the soft systolic murmur of mild mitral regurgitation.
Looking for the murmur of aortic regurgitation involves listening with the
diaphragm of the stethoscope pressed close to the chest wall, making the patient
sit, lean forward, while holding the breath in expiration. Looking for the murmur
of mitral regurgitation involves, not only auscultating in the supine position but
also doing so in the standing position, to bring out the murmur of mitral valve
prolapse.
Congenital bicuspid aortic valve is the commonest congenital anomaly and
occurs in 2 per cent of all live births. A bicuspid aortic valve predisposes to infective
endocarditis particularly when associated with aortic regurgitation. Takayasu’s
arteritis is a systemic disease which may present with fever, night sweats, malaise,
arthralgias, anorexia and weight loss. These systemic manifestations may precede
arterial involvement by months. The disorder most often affects young females. A
Table 11.7: Cardiovascular signs to be looked for in the febrile patient

Disorder Sign Maneuver/laboratory test
Pericarditis Pericardial rub Left sternal border (3rd, 4th spaces)
Diaphragm pressed to chest wall
During inspiration (or expiration)
Sitting, leaning forward
Infective Early diastolic murmur Along left sternal border, aortic area,
endocarditis of AR apex
Diaphragm pressed to chest wall
Sitting, leaning forward, held expiration
Pansystolic murmur of At the apex
MR Diaphragm of stethoscope
Standing for the murmur of MVP
Ejection click of At the aortic area, left sternal border,
congenital bicuspid apex
aortic valve With the diaphragm of stethoscope
Mistaken for loud S1 best heard at
the aortic area
Also mistaken as split S1 best heard at
the aortic area
Acute myocarditis Disproportionate sinus 173
tachycardia
Cardiac enlargement Auscultate
Ventricular gallop with the bell lightly applied
May be palpable
Takayasu's arteritis Asymmetry of peripheral Palpation of all peripheral pulses
pulses
Bruit over neck vessels, Look for a bruit over neck,
interscapular area, abdomen abdomen, interscapular areas
Temporal arteritis Headache
Palpable temporal artery Palpation of temporal region
Mucocutaneous Cervical adenopathy ECG evidence of myocardial
lymph node syndrome Erythema of skin ischemia or infarction
(Kawasaki’s disease) Erythema of mucous Coronary artery aneurysms
membranes made out by echocardiography
Desquamation of skin and coronary angiogram
and finger tips
Pericardial rub due to
pericarditis
Signs of myocarditis
Signs of myocardial
ischemia or infarction
Disorder Sign Maneuver/laboratory test

Recurrent pulmonary Fever may dominate the Ventilation perfusion lung scan
emboli clinical picture Pulmonary angiogram
Dyspnea may not be
prominent
Sinus tachycardia is
common
Phlebitis Intravenous line sites
Redness, pain, swelling
decrease or absence of arterial pulses, bruit over the neck, chest, or abdomen, or
blood pressure difference between the upper and lower limbs in any young woman
presenting with fever of obscure origin is suggestive of Takayasu’s arteritis.
Kawasaki’s disease is an acute febrile multisystem disease in children. The affected
children have non-suppurative cervical adenitis failing to respond to antibiotics,
edema, conjunctival congestion, erythema, of oral cavity, lips, and palms, and
desquamation of the skin and finger tips. Coronary vasculitis is the cause for
myocardial ischemia and infarction. Echocardiography and coronary angiography
174 reveal coronary artery aneurysms. Recurrent minute pulmonary emboli may present
with fever as the dominant manifestation and the commonly expected dyspnea
may not be impressive. Ventilation perfusion lung scan and pulmonary angiogram
may be confirmatory.
In any patient with fever, whether it is the first hour, first day or first week,
look for a heart murmur. If you don’t do this, an opportunity to detect infective
endocarditis at an early stage is missed.
Looking for a heart murmur means truly looking for it by careful auscultation
at rest and with various maneuvers.
Surprisingly, a significant number of patients with infective endocarditis fail
to mention fever unless queried by the doctor. This is because the fever is
either low-grade or is attenuated by antibiotics.
Arthralgias and even arthritis does not distinguish rheumatic fever from
infective endocarditis.
Musculoskeletal symptoms are common in infective endocarditis.
In a patient with structural heart disease, any fever has to be viewed with
suspicion to rule out infective endocarditis from the beginning.
Nowadays, the most common presenting feature of infective endocarditis is
recurrent fever due to indiscriminate use of antibiotics. All patients with
valvular and congenital heart disease should be educated regarding this.
Fig. 11.1: Vegetation on aortic valve as seen in transesophageal echocardiography
175
12 The Arterial Pulse

The arterial pulse reflects the performance of the left ventricle and the response
of the vascular system to left ventricular ejection. The palpable arterial pulse is the
pressure pulse transmitted along the arterial system as with each systole, blood is
ejected by the left ventricle into the proximal aorta. The normal arterial pulse
consists of an ascending limb, the peak, and the descending limb. The pulse wave
is transmitted along the aorta to the periphery at a speed of 5 m/sec but the
intraluminal blood travels much slower, at only 40–50 cm/sec. The main
176 determinants of the morphology of arterial pulse are outlined in the Table 12.1.
With a normal stroke volume, the normal upstroke of the arterial pulse occurs.
When the stroke volume increases, the upstroke is sharper and the peak is higher,
resulting in a larger pulse volume. The reduction in the stroke volume has the
opposite influence. As the velocity of ejection increases, the upstroke is sharper,
and the peak is reached earlier. When the velocity of left ventricular ejection
decreases with reduced contractility, the upstroke is less sharp and the peak is
Table 12.1: Determinants of arterial pulse
Left ventricle Stroke volume
Left ventricular contractility
Velocity of left ventricular ejection
Aortic valve Normal
Stenotic
Regurgitation
Combined stenosis and regurgitation
Arterial system Compliance or distensibility
Peripheral vascular resistance
Aortic run off
THE ARTERIAL PULSE
reached later. With a regurgitant aortic valve, the descending limb of the arterial
pulse is steeper and the attendant increase in stroke volume results in a sharper
upstroke with a higher peak, giving rise to the collapsing pulse of aortic regurgitation.
In aortic stenosis, the arterial system is filled slowly, resulting in the slow rising
upstroke and a delayed peak.
NORMAL ARTERIAL PULSE
The normal arterial pulse consists of the upstroke, the peak and the descending
limb. The upstroke comes out with the first sound and the peak is reached well
before the second heart sound. In the central arterial pulse, the peak of the arterial
pulse consists of an initial percussion wave, and a smaller and later-occurring tidal
wave. The percussion wave is due to the initial left ventricular ejection, and the
tidal wave is due to aortic recoil or a reflected wave from the periphery.
The normal arterial pulse consists of a rapid upstroke (percussion wave, P)
and a second wave in systole, called the tidal (T) wave. The end of systole is
indicated by the sharp dicrotic notch, which is followed by a dicrotic wave. These
wave forms are better recorded in the central arteries. The dicrotic notch and 177
dicrotic wave are not clearly discernable towards the periphery.
ECG
EKG
S1 S2
PHONO P
T
DW
CAROTID
Fig. 12.1: Normal arterial pulse

P: Percussion wave, T: Tidal wave, DW: Dicrotic wave
Technique of palpating the pulse

The carotid artery is the most suitable for evaluating the character of the arterial
pulse, because it is near the aortic valve. If the carotid artery is not available, the
brachial artery is the next choice. A more peripheral pulse like radial artery is
suitable when attempting to appreciate a collapsing pulse or a dicrotic pulse since
these waves are exaggerated as the pulse wave is transmitted to the periphery. The
paradoxic pulse is best appreciated at the femoral artery as the patients with cardiac
tamponade usually have low pulse volume, and severely elevated jugular venous
pressure, which interferes with palpation of the carotid pulse. To palpate the carotid
pulse, the patient should be lying supine, with the neck slightly turned to the side
of palpation to relax the sternomastoid muscle. The carotid artery is felt by using
two or three fingers (the middle three fingers), along the lateral border of the
trachea. By simultaneous auscultation and palpation, the upstroke of the carotid
pulse appears as an abrupt outward movement along with the first heart sound
and the peak is reached well before the second heart sound. A systematic approach
to the arterial system requires looking for the following features.
178 Evaluation
• Rate and rhythm
• Volume, tension
• Character
• Vessel wall
• Peripheral pulses
• Grade the palpability
• Brachiofemoral and brachio-brachial delay
• Bruit over the artery
• Palpation of the abdominal aorta
• Ocular fundi
• Allen’s test
Rate and rhythm: The arterial pulse is often the inaugural part of the physical
examination, and one often forms the initial impressions regarding the patient’s
illness at this stage. The pulse rate should be counted for at least half a minute to
be reliable. The normal range of pulse rate is 60–90/min. Pulse rates above 140/min
cannot be reliably counted. In infants, the rates are higher, and can reach 160/min.
THE ARTERIAL PULSE
The causes of rapid regular pulse (more than 90/minute) could be:
• Sinus tachycardia
• Supraventricular tachycardia
• Paroxysmal atrial tachycardia
• Junction tachycardia
• Atrial tachycardia with fixed block
• Atrial flutter with fixed block
• Ventricular tachycardia
The causes of sinus tachycardia could be:
• Anxiety
• Visit to the doctor
Long waiting period
Doctor’s personality and attitude
• Emotion
• Fever
• Septicemia with or without fever
• Pregnancy 179
• Vasodilator drugs
• Soon after consuming food or beverages.
The causes of slow pulse (less than 60/minute) could be:
• Sinus bradycardia
• Heart block of 2:1 or 3:1
• Bigeminal rhythm with impalpable premature beat
• Pulsus alternans with the weak beat impalpable
The causes of sinus bradycardia could be:
Physiological
Normal variant
Athletes
Neonates
During sleep
Vagaloveractivity
Vasovagal episodes
Acute inferior myocardial infarction
Any visceral pain

Sick sinus syndrome
Intracranial hypertension
Myxedema
Hypothermia
Mediastinal tumours
Obstructive jaundice
Convalescence from infections
Depression
During reperfusion after thrombolytic therapy
Drugs
Betablockers
Digoxin
Some calcium blockers (verapamil, diltiazem)
Clonidine
Lithium
Amiodarone
180
One must consider whether the rate is appropriate or inappropriate for the
clinical circumstance. For example, a patient with fever should have sinus
tachycardia. If the expected tachycardia fails to occur in a patient with fever one
must consider various possibilities.
The causes of normal or slow pulse rate with fever (relative bradycardia)
could be:
• Typhoid fever
• Viral infections
• Hemorrhagic fevers
• Lassa fever
• Lymphocytic choriomeningitis
• Intracranial infection with intracranial hypertension
• Meningitis
• Brain abscess
• Encephalitis
• Fever in a patient with
Bradyarrhythmia
Drug induced bradycardia
THE ARTERIAL PULSE
The causes of rapid irregular pulse could be:

• Atrial fibrillation
• Atrial flutter with varying block
• Atrial tachycardia with varying block
• Frequent atrial and ventricular ectopy
An irregularly irregular pulse suggests the possibility of atrial fibrillation. If
the irregularity is predictable, as in frequent premature ventricular contractions, it
is called a regularly irregular pulse. Slight respiratory alteration in pulse rate is
common in children and is called sinus arrhythmia. It is of two forms, the respiratory
form where the rate increases during inspiration and decreases during expiration,
and the non-respiratory sinus arrhythmia characterized by phasic variation in heart
rates unrelated to respiratory cycle, and is often suggestive of digitoxicity.
The importance of the pulse rate is increasingly recognized by the recent
information that the pulse rate is a major correlate of blood pressure. Rapid heart
rates may predict the development of sustained hypertension in subjects with
normal or borderline elevated blood pressures. Sinus tachycardia is associated
with increased risk of cardiovascular death. Also sinus tachycardia is the single 181
most important long term prognostic factor following acute myocardial infarction.
Pulse volume: The amplitude of excursion of the pulse is used to assess the
volume of pulse and generally correlates with the stroke volume. In elderly patients
with rigid atherosclerotic aorta and in systemic hypertension, the pulse volume is
high due to non-distensible arterial system (Table 12.2). In these settings, the pulse
volume is not a true reflector of stroke volume.
Table 12.2: Causes and mechanisms of high pulse volume
Cause Mechanism
Elderly Atherosclerotic non-distensible arterial system
Emotional excitability, anxiety Stroke volume
High cardiac output states like Stroke volume
anemia, thyrotoxicosis Low diastolic pressure
Conditions with aortic run off Low diastolic pressure
Stroke volume
Hyperkinetic heart syndrome Stroke volume
Systemic resistance
Systemic hypertension Non-distensible arterial system
In a typical patient with systemic hypertension, the rise in systolic pressure is

not in proportion to the elevation in diastolic pressure.
The causes of low pulse volume could be:
• Shock
• Low cardiac output
• Myocardial disease
• Valvular disease
• Pericardial disease
• Acute hypertension as in eclampsia of pregnancy
• Hypovolemia
Character of the pulse

Normal arterial pulse: The normal arterial pulse consists of an abrupt upstroke
coming up with the first sound, and a peak which occurs well before the second
sound. This is best appreciated in the carotid pulse by simultaneous auscultation
and palpation.
The best way to become proficient in the technique of pulse evaluation is to
182 practice this in otherwise normal people or by palpating one’s own carotid.
Collapsing pulse or water hammer pulse: The collapsing pulse refers to the
rapid descent in the arterial pulse and is accompanied by a sharp upstroke and a
high volume. The collapsing pulse occurs in all situations where there is run off of
blood from the aorta or the arterial system. Aortic regurgitation is the most
important cause of a collapsing pulse. The collapse is related to the back flow into
left ventricle, and the reflex vasodilatation mediated by the carotid baroreceptors
secondary to the large stroke volume. In other words, the arterial system in aortic
regurgitation behaves as if it is open at both ends in diastole, unlike the normal,
which is open only at the arteriolar end of the circulation. This sign is best
appreciated at the radial pulse, with the palmar side of the wrist held in the
examiner’s hand, and the arm elevated above the shoulder. This may be related to
the artery being more in line with the central aorta allowing direct systolic ejection
and diastolic backward flow. All the peripheral signs of aortic regurgitation are
related to this collapsing pulse.
It is not essential to elicit all these signs in a patient with aortic regurgitation.
Hill’s sign is particularly important, because it allows estimation of severity of
THE ARTERIAL PULSE
aortic regurgitation and correlates well with angiographic severity of aortic

regurgitation. The collapsing pulse is not specific for aortic regurgitation and occurs
in a variety of conditions.
Table 12.3: Peripheral signs of aortic regurgitation
Sign Description Mechanism/Significance
Hill’s sign Systolic BP in lower limb Phenomenon of recruitment of
higher by more than 20 mmHg reflected waves
< 20: Trivial AR/Normal
20–40: Mild AR
40–60: Moderate AR
> 60: Severe AR
Duroziez’s double To and fro murmur over the Forward murmur due to
murmur femoral artery increased stroke volume
Backward murmur due to
arterial recoil and backflow
Always indicates severe AR
Very large SV, low diastolic
pressure
Pistol shot femorals Audible sound during systole Moderate to severe AR 183
coinciding with upstroke of FA
de Musset’s sign To and fro motion of the head Large stroke volume
synchronous with systole and Severe AR
diastole
Quincke’s sign Advancing and retreating flush Arteriolar dilatation
with each cardiac cycle by light Severe AR
pressure over nail bed, mucous
membranes of mouth
Traube’s sign Booming systolic and diastolic As for Duroziez’s murmur
sounds over FA
Muller’s sign Pulsations in the uvula As above
Gerhardt’s sign Pulsations in the enlarged As above
spleen
Rosenbach’s sign Pulsations in the liver As above
Ladolfi’s sign Change in pupil size with
each cardiac cycle
Pulsations of retinal Appearance and disappearance Severe AR
vessels of blood column with cardiac
cycle
The causes of a collapsing pulse could be:

Pregnancy
Fever
Anemia
Thyrotoxicosis
Beriberi
Paget’s disease of bone
Hyperkinetic heart syndrome
Cirrhosis of liver
Drug induced vasodilatation
Conditions with aortic run-off
Patent ductus arteriosus
Aortopulmonary window
Rupture of sinuses of Valsalva into right heart chambers
Arteriovenous fistula
184 Systemic to pulmonary artery shunt in cyanotic heart disease with
reduced pulmonary flow
In all the above states, a collapsing pulse generally means a severe lesion.
Slow rising pulse of aortic stenosis (anacrotic pulse, pulsus tardus)

In all forms of fixed obstruction to left ventricular outflow, the upstroke of the
arterial pulse is slow, and the peak is delayed nearer to the second sound. This is
best appreciated by simultaneous auscultation of the heart and palpation of the
carotid pulse.
Fig. 12.2: Slow rising pulse in aortic stenosis

THE ARTERIAL PULSE
Slow rising pulse: The correlate of this type of pulse in aortic stenosis is, a gradient
of at least 70 mmHg across the aortic valve or a severe aortic stenosis (Fig. 12.2).
At extremes of age, this sign may be absent, as in children with rapid velocity of
circulation and elderly with non-distensible arterial system. For the same reason,
elderly patients with significant AS may have coexistent systolic hypertension.
These patients belong to a subset with not only a dynamic left ventricle but also a
markedly non-compliant arterial system. The delay and the slow rise may not be
appreciable once heart failure sets in, when only the low volume pulse may be
appreciated. If the pulse is normal in the setting of aortic stenosis, one should
consider various possibilities.
Pulsus parvus et tardus (slow rising small pulse): This is typically present in a
patient with severe aortic stenosis. The upstroke of the pulse is very slow-rising
and the pulse volume tends to be low due to elevated systemic vascular resistance.
In dynamic obstruction, as in hypertrophic obstructive cardiomyopathy, despite
severe left ventricular outflow tract obstruction, the pulse tends to be brisk.
The causes of normal arterial pulse with aortic stenosis could be:
• Mild aortic stenosis or conditions simulating aortic stenosis (for example 185
MR)
• Associated AR
• Hypertrophic obstructive cardiomyopathy
• Supravalvular aortic stenosis (normal right arm pulse)
• Associated coarctation of aorta
• Associated mitral stenosis
• Extremes of age: children and elderly
In severe aortic stenosis, the slow rising pulse with a delayed peak, the long
ejection systolic murmur with late peaking and the sustained apical impulse go
hand in hand.
Bisferiens pulse: In the bisferiens pulse both the percussion and tidal waves are
appreciable; it occurs in a variety of conditions.
• Severe aortic regurgitation (Fig. 12.4)
• Aortic stenosis and regurgitation
• Hypertrophic obstructive cardiomyopathy (Fig. 12.3)
• Hyperkinetic circulatory states
• Muscular exercise
ECG
ESM PA
S1
PHONO
2 LICS
PHONO
APEX S4 P
T
CAROTID
Fig. 12.3: Bisferiens pulse in HOCM

Bisferiens pulse in hypertrophic obstructive cardiomyopathy (HOCM): Typically, in HOCM, the pulse is bisferiens, that is,
both the percussion and tidal waves are well appreciated. Characteristically, the percussion wave is prominent in HOCM.
ECG
186 T
P
CAROTID
Fig. 12.4: Bisferiens pulse in severe AR

Bisferiens pulse in severe aortic regurgitation: In severe AR, the character of the pulse is bisferiens.
Unlike in HOCM, in AR both the tidal and percussion waves are prominent. More often, the bisferiens pulse is seen,
when there is associated mild aortic stenosis.
Mechanisms of bisferiens pulse: Normally the percussion wave is felt but not the
tidal wave. The tidal wave is due to the elastic recoil of the aorta and the reflection
wave from the periphery. In all situations where the initial percussion wave is
exaggerated, the tidal wave is also prominent. This mechanism is applicable in
severe aortic regurgitation and other hyperkinetic circulatory states. In combined
aortic stenosis and aortic regurgitation, the stenotic component permits a jet. Lateral
to the velocity jet, there occurs a fall in pressure (Bernoulli phenomenon). This
results in a dip or inward movement in the pulse with a secondary outward
movement or tidal wave. In hypertrophic cardiomyopathy, the initial part of left
ventricular ejection is normal or more rapid than normal, resulting in a rapid
THE ARTERIAL PULSE
upstroke. As obstruction to outflow starts later in systole, due to thickening of

interventricular septum and systolic anterior motion of the anterior leaflet of the
mitral valve, a sudden interruption to left ventricular ejection occurs resulting in a
dip in the pressure pulse followed by the slow rising pulse wave like ordinary
aortic stenosis. In effect, the arterial pulse of idiopathic hypertrophic subaortic
stenosis behaves partly like aortic regurgitation (the initial sharp component) and
aortic stenosis (the later slow rising wave).
Technique of palpating for bisferiens pulse: This is usually best appreciated on the
carotid but the prominent systolic thrill over the carotid (the carotid shudder) may
mask the features. A more distal pulse like the brachial or the radial may be suitable.
One should use a graduated pressure to be able to appreciate the two waves.
Alternatively completely obliterate the pulse, and gradually release it, and at one
point the two waves are appreciable.
Dicrotic pulse: The dicrotic pulse occurs when the dicrotic wave is exaggerated.
The dicrotic wave is possibly related to the reflection wave from the periphery.
When the reflection wave travels slowly, and gets added to the original wave, an
additional dicrotic wave is appreciable (Fig. 12.6). On the other hand, when the 187
reflection wave travels rapidly and meets the original wave well in advance, it is
lost in it.
When the arterial system is rigid and non-distensible as in systemic
hypertension, the dicrotic pulse is never present (Fig. 12.5). The dicrotic pulse is
commonly seen in low cardiac output states like cardiomyopathy, myocarditis,
cardiac tamponade or after aortic valve replacement for aortic regurgitation. In
the above states with a low cardiac output and the underfilled arterial system, the
reflection wave travels slowly to be appreciated as an additional wave. Dicrotic
pulse is commonly seen in typhoid fever and is possibly related to the circulating
vasculotoxins.
Fig. 12.5: Pulse wave and reflected wave in elastic aorta (left) and stiff aorta (right)
ECG
DW
CAROTID
Fig. 12.6: Dicrotic wave (DW)
ECG
188
Fig. 12.7: Augmented wave (AW) with IABP usage
The causes of a dicrotic pulse are:

• Typhoid fever or any fever with vasodilatation
• Any condition with low cardiac output
• Cardiomyopathy
• Myocarditis
• Cardiac tamponade
• Hypovolemia
• During intra-aortic balloon pumping
The dicrotic pulse is distinguished from the bisferiens pulse by the second
wave occurring after the second heart sound. Simultaneous auscultation is helpful.
The bisferiens pulse is generally best felt over the carotid but the dicrotic pulse is
most often appreciated over the radial pulse. It is better appreciated during
THE ARTERIAL PULSE
inspiration or inhalation of amyl nitrite. The dicrotic pulse is unusual when the
systolic pressure exceeds 130 mmHg, or in a person beyond 50 years of age.
Dicrotic pulse during intra-aortic balloon pumping (IABP): With the increasing
use of IABP in various clinical settings, the dicrotic pulse is more often recorded
(Fig. 12.7). In this setting, the prominent dicrotic wave is the augmented wave
resulting from diastolic flow occlusion in the descending aorta due to the inflation
of the balloon.
Bigeminal pulse: The bigeminal pulse is due to the bigeminal rhythm. Alternating
beats are strong and weak (Fig. 12.8). However, unlike pulsus alternans, these
beats do not occur regularly. This is commonly seen with ventricular bigeminy.
The weak beat is prematurely close to the previous normal beat and the weak beat
is followed by a long pause. The stronger beat correlates with preceding longer
diastole due to post-extrasystolic pause resulting in greater left ventricular end
diastolic volume. The bigeminal pulse is often accompanied by auscultatory
bigeminy. Sometimes the weak contraction may be able to close the mitral valve
producing the first heart sound but unable to open the aortic valve to produce the
second sound. In the latter case it may be mistaken for a third heart sound. When 189
the premature beat is very low in volume or is not felt, the pulse rate counted may
be half of the heart rate and a mistaken diagnosis of bradycardia is often made.
The premature beat is often accompanied by a cannon wave in the neck veins.
Post-extrasystolic pulse: Normally, the post-extrasystolic pulse shows an increase
in volume, due to the long pause and more diastolic filling. More importantly, the
extrasystolic potentiation of ventricular contraction also contributes to this. This
normal pattern is seen in all forms of fixed obstruction to the left ventricular
outflow. In hypertrophic obstructive cardiomyopathy, the extrasystolic potentiation
increases the obstruction, and decreases the pulse volume of the post-extrasystolic
pulse (Fig. 12.9). Lack of rise of post-extrasystolic beat by 10 mm Hg or actual fall
in pulse is called Brockenbrough sign and is the surest sign of a dynamic obstruction
to left ventricular outflow (Table 12.4). Even failure of the pulse volume to rise
should be considered a positive sign but this may also be seen in severe ventricular
dysfunction or constrictive pericarditis.
Pulsus alternans: This is characterized by a regular sinus rhythm with alternate
beats strong and weak due to alternation in contraction of the heart (Fig. 12.10).
ECG VPC VPC
CAROTID
Fig. 12.8: Bigeminal pulse
ECG
CAROTID
190 NORMAL
RISE
CAROTID
HOCM FALL
Fig. 12.9: Postectopic behaviour of pulse

Normal compared to HOCM. Note the absence of post-extrasystolic potentiation in HOCM
The equivalent of this by sphygmomanometry is alternation of the intensity of

Korotkoff sounds.
It was first described by Traube in 1872. It is often a sign of severe myocardial
depression and is related to more and less number of contractile elements
participating in each contraction alternately. Pulsus alternans is most commonly
seen in aortic stenosis with heart failure but also occurs in any condition with
THE ARTERIAL PULSE
severe ventricular dysfunction. Alternans can be total, when left ventricular systolic
pressure generated is less than the aortic diastolic pressure when the left ventricle
fails to open the aortic valve. When it occurs on both sides of the heart (right
andleft ventricles), it is called concordant. When it involves only the right or the left
ventricle, it is called discordant. In aortic stenosis, the strong and weak beats are
appreciated as variation in the intensity of the murmur alternately. When the weak
beat is too weak to be palpable, only auscultatory alternans is appreciable. Aortic
regurgitation, systemic hypertension and reducing the venous return by head tilting
or nitroglycerine usually exaggerate pulsus alternans and assist in its detection.
Premature ventricular contractions, rapid atrial pacing, inferior vena caval occlusion,
myocardial ischemia and intracoronary injection of contrast during coronary
arteriography are known to induce alternans.
Table 12.4: Causes of positive Brockenbrough sign
Cause Mechanism
Hypertrophic obstructive Post-extrasystolic potentiation of
cardiomyopathy dynamic LV outflow obstruction
Constrictive pericarditis Failure to fill the ventricle more even 191
after longer diastole due to constriction
Severe ventricular dysfunction Failure to augment contraction in
due to any cause spite of more preload
Extremely severe aortic stenosis Same as above
at any site
ECG
CAROTID
Fig. 12.10: Pulsus alternans

Definitions
1. Pulsus alternans: Regular alternation of strong and weak pulse in the absence
of respiratory or cycle length alteration.
2. Total alternans: When the weak contraction fails to open the aortic valve,
alternans pulsus may be absent.
3. Independent alternans: Pure alternans of either right or left ventricles alone.
4. Concordant alternans: Simultaneous alternans of right and left ventricles.
5. Discordant alternans: Alternating alternans of right and left ventricles.
6. Compound alternans: Further alternation of the weaker beats superimposed
on the routine alternans.
Pulsus alternans is easier to detect by sphygmomanometer (Fig. 12.11) but
when the aortic pressure shows alternans by more than 20 mmHg, it can be detected
by palpation of the peripheral pulse. Pulsus alternans is usually accompanied by
alternation in the intensity of Korotkoff sounds. Electrical alternans is an
independent phenomenon and has no relationship to pulsus alternans.
The causes of pulsus alternans could be:
• Severe aortic stenosis
192
• Severe pulmonic stenosis
• Dilated cardiomyopathy
• Myocarditis
• Severe aortic regurgitation with left ventricular failure especially after
aortic valve replacement
Fig. 12.11: Pulsus alternans as noted in blood pressure

THE ARTERIAL PULSE

• Severe coronary artery disease
• Any cause for ventricular dysfunction
• Briefly during or after supraventricular tachycardia
• Severe systemic hypertension
• Transient right ventricular outflow occlusion during balloon dilatation
of pulmonary stenosis
• Normal hearts (rare)
Pulsus alternans is accompanied by alternating intensity of heart sounds and
or S3 gallop.
The precise mechanism of this phenomenon is not known. It may primarily
be due to decreased myocardial contractility of alternate beats with relatively less
effect produced by changes in preload, afterload or diastolic relaxation. Decreased
contractility is attributed to deletion of a number of myocardial elements with
alternate beats. Intracellular calcium cycling involving the sarcoplasmic reticulum
leading to localized electromechanical dissociation. Alterations in diastolic volume
or relaxation may also play a role. 193
Pulsus alternans is best appreciated by light pressure and the patient holding
the breath in mid expiration. This limits respiratory influence on pulse volume.
Pulsus alternans is augmented by maneuvers, which decrease venous return, such
as standing or administration of nitroglycerine.
Compound pulsus alternans: Sometimes, an additional alternation involving only the
weak beats can occur in association with the usual alternation of weak and strong
beats, and is known as compound pulsus alternans.
Pulsus alternans may disappear with improvement in ventricular function or
administration of digitalis. It may also disappear with progressive deterioration of
ventricular function. It is for this reason, that a new appearance or disappearance
of this sign should be viewed with concern.
Pulsus paradoxus: Normally there is an inspiratory fall and expiratory rise in
systolic pressure related to the alteration in the stroke volume of the left ventricle.
In pulsus paradoxus there is an exaggerated fall in systolic arterial pressure with
inspiration. The normal inspiratory fall in systolic pressure is usually less
than 8 mmHg. Any exaggeration from this is called pulsus paradoxus (Fig. 12.12).
It can occur in any condition with an exaggerated respiratory act, as in a severe

attack of asthma or in any other form of obstruction to the airways.
The causes of pulsus paradoxus could be:
Normal
Pregnancy
Exaggerated inspiration voluntarily (student paradoxus)
Extreme obesity
Severe obstruction to airways
Acute severe bronchial asthma
Severe emphysema
Upper airway obstruction
Pericardialtamponade
Tense pericardial effusion
Severe constrictive pericarditis
Effusive constrictive pericarditis
Hypovolemic shock
Massive pulmonary embolism
194
Fig. 12.12: Pulsus paradoxus: Note the exaggerated fall in blood pressure with inspiration
Table 12.5: Cause and mechanism of absence of paradoxus in cardiac tamponade
Cause Mechanism
Atrial septal defect Equal filling of ventricles in either phase of respiration
Ventricular septal defect Free communication between ventricles prevents
differential filling
Aortic regurgitation Filling of LV is maintained irrespective of respiration
THE ARTERIAL PULSE
In cardiac tamponade, the right and left ventricles are equally compressed by
the tense pericardial effusion. Normally the inspiratory increase in venous return
is accommodated by the easily distensible right ventricle. In cardiac tamponade,
the increased venous return to the RV cannot be accommodated as in normal
situations and the RV distension occurs at the expense of left ventricle resulting in
reduced left ventricle end diastolic volume and stroke volume. The evidence can
be seen in the echocardiogram as increase in RV dimension, displacement of
interventricular septum toward left ventricle and reduction in the left ventricle
dimension during inspiration. The opposite of all this occurs in expiration.
The femoral pulse is most convenient for appreciating a paradoxic pulse
because most patients with paradoxic pulse (cardiac tamponade, constrictive
pericarditis and obstructive pulmonary disease) have neck edema, and the carotid
pulse is therefore difficult to palpate. In obstructive pulmonary disease, the
accessory activity of the neck muscles interferes with carotid palpation. The patient
should be breathing normally, and it is a wrong practice to ask the patient to take
a deep breath. Otherwise normal people can have a paradoxus with deep breathing.
To measure the pulsus paradoxus the sphygmomanometer cuff is inflated to above
the level of systolic pressure and is deflated very slowly (2 mmHg/beat). The level 195
at which the first Korotkoff sounds are heard is marked. Initially the sounds are
intermittently heard during expiration, and are inaudible during inspiration. As
the cuff is deflated slowly, the sounds are heard continuously at one point in both
phases of respiration. The difference between the point of intermittent audibility
of sounds to the point of continuous audibility gives the degree of paradoxus. By
definition, it should be above 10 mmHg. Any value above 15 mmHg is called
significant paradoxus. When the paradoxus is extreme, the pulse may disappear only
to reappear during expiration, in which case, a mistaken diagnosis of atrial
fibrillation, or some other arrhythmia is often made. However on auscultation,
the heart is regular. This seeming irregularity of the arterial pulse but regular beating
of heart sounds, was considered paradoxical by Kussmaul, who originally described
this pulse and named it thus. The principal determinant of pulsus paradoxus is
reduced filling of the left ventricle during inspiration in relation to the right ventricle.
Any condition which permits equal filling of both ventricles (shunt lesions), or
more filling of left ventricle (aortic regurgitation) prevents paradoxus from occurring
(Table 12.5).
Table 12.6: Causes and mechanisms of reversed pulsus paradoxus

Cause Mechanism
Positive pressure breathing Intrathoracic pressure is higher in inspiration
with artificial ventilators and lower in expiration
Isorhythmic AV dissociation The atrial activity precedes ventricular activity
during inspiration and follows it during expiration.
The atrial contribution during inspiration
increases stroke volume and the lack of it
during expiration decreases it
Hypertrophic obstructive Mechanism not known
cardiomyopathy
Reversed pulsus paradoxus: Inspiratory increase and an expiratory decrease

may occur during positive pressure breathing of artificial ventilation, as the
intrathoracic pressure is high during inspiration and low during expiration (the
reverse of normal). In this setting if cardiac tamponade occurs an expiratory fall is
seen and this is the reverse of routine pulsus paradoxus. Similar manifestation
may be seen during isorhythmic AV dissociation when the P wave precedes the
196 QRS during inspiration and marches into the QRS during expiration. Reversed
pulsus paradoxus is also described in hypertrophic cardiomyopathy but the
mechanism is not clear (Table 12.6).
The peripheral pulses

Palpation of the peripheral pulses is helpful in the diagnosis of peripheral vascular
disease, coarctation of the aorta, aortic dissection and embolic manifestations of
atrial fibrillation or infective endocarditis, Takayasu’s arteritis and some vasculitis
syndromes. The following system of expressing the results in a tabular form is
helpful. All the accessible arteries should be palpated bilaterally including the
abdominal aorta. Auscultation for a bruit should be looked for over the femorals,
ilio-femorals, abdominal aorta, renal arteries, celiac trunk or superior mesenteric
artery and the carotids.
Recording of normal peripheral pulses

Artery Carotid Brachial Radial Femoral Popliteal Posterior Dorsalis
tibial pedis
Right +++ +++ +++ +++ +++ +++ +++
Left +++ +++ +++ +++ +++ +++ +++
THE ARTERIAL PULSE
Table 12.7: Grading of arterial pulse

Finding Grade
Impalpable 0
Feeble +
Palpable but diminished compared to the other side ++
Normal +++
High volume or bounding pulse ++++
Additionally, the presence or absence of bruit and the palpability of abdominal

aorta should be commented. The dorsalis pedis and posterior tibial arteries are
impalpable in 2 per cent of normal people due to their anomalous course.
Bruit over an artery
In general the more severe the obstruction, the higher the frequency and length
of the bruit (Table 12.8). Additionally the skull, the liver and any other site which
was injured, operated or punctured should be auscultated for any evidence of
arteriovenous fistula. In a child with unexplained congestive heart failure the skull
should be auscultated for an intracranial AV fistula. 197
Table 12.8: Bruit over an artery
Severity of obstruction Nature of bruit

Less obstruction Short systolic bruit
More obstruction Continuous bruit
High pitched
No bruit
Table 12.9: Sites of auscultation for arterial bruit
Artery involved Site of bruit

Internal/external carotid Anterior neck
Subclavian Supraclavicular
Axillary Infraclavicular
Thoracic aorta Left interscapular
Abdominal aorta Epigastrium
Celiac Epigastrium
Renal Upper abdominal quadrants, lumbar
Aorto-iliac bifurcation Umbilicus
Common femoral Inguinal
Superficial femoral Femoral triangles, anteromedial thighs
Popliteal Popliteal fossa
Table 12.10: Normal time delay for pulse wave propagation

Carotid 30 msec
Brachial 60 msec
Radial 80 msec
Femoral 75 msec
Brachiofemoral delay
The brachiofemoral delay rather than radiofemoral delay appears to be more
sensitive in the diagnosis of coarctation as there is already a delay of 15 milliseconds
from the brachial to femorals in normals. Any further delay is easily detected
(Table 12.10).
Unless the delay is more than 20 msec it is not appreciable clinically. Blood
pressure measurement is a more sensitive indicator of coarctation of aorta than
brachiofemoral delay. A radio-radial or brachio-brachial delay is suggestive of
vascular obstruction anywhere from the innominate artery on the right or subclavian
artery on the left to the site of palpation.
In patients presenting with intermittent claudication but palpable peripheral
198 pulses, evaluation is incomplete unless the patient is exercised and the pulses sought
for by palpation, auscultation for a bruit, and also measurement of blood pressure.
Since atherosclerotic vascular disease tends to be generalized, it is a good
clinical practice to examine peripheral pulse thoroughly in all patients with coronary
artery disease.
Allen test
Negative result Positive result
Fig. 12.13: Allen test to demonstrate the presence of ulnar artery

THE ARTERIAL PULSE
Evaluation of the patency of the radial and ulnar arteries supplying the hand is a
pre-requisite for using the radial artery either for cardiac catheterization or as an
arterial conduit for coronary bypass surgery. This test is intended to test the patency
of the ulnar artery to maintain the circulation to the hand if the radial artery is
occluded as a result of the procedure or harvested for a graft.
The result of the Allen test is considered normal when after compression of
both ulnar and radial arteries, the hand colour returns to normal within 10 seconds
after release of the radial artery.
THE ARTERIAL PULSE IN VARIOUS CLINICAL STATES
ARTERIAL PULSE IN A PATIENT WITH SHOCK

The pulse rate is usually rapid in shock. Disproportionate tachycardia should elicit
the possibility of acute myocardial infarction, myocarditis, septic shock or an
arrhythmia (Table 12.11).
The causes of an inappropriately rapid pulse rate could be:
• Acute myocardial infarction 199
• Myocarditis
• Septic shock
• Tachyarrhythmia
A normal or diminished pulse rate in the setting of shock may suggest a
Table 12.11: The arterial pulse in shock
Characteristic feature in pulse Cause of shock
Rapid, low volume Cardiogenic shock
Hypovolemic shock
Septic shock
Paradoxic pulse Pericardial tamponade
Tension pneumothorax
Acute large pleural effusion
Irregular pulse Refer to atrial fibrillation
Pulse rate half of heart rate in ECG ‘AFORMED’* phenomenon as in
supraventricular tachycardias
*AFORMED = Alternate failure of response mechanical to electrical depolarization
vasovagal shock, complete heart block or drug induced bradycardia and

hypotension. The causes of normal or diminished pulse rate could be:
• Drug induced
• Betablockers
• Calcium blockers
• Hypotension in patients with autonomic neuropathy
• Idiopathic
• Shy–Drager’s
• Under anesthesia
• Vasovagal
• Intracranial surgery
An irregular pulse in shock should suggest an arrhythmia like atrial fibrillation.
An impression of irregularity is often created in patients with cardiac tamponade and
paradoxic pulse but cardiac auscultation dispels the doubt. The causes could be:
200
• Acute myocardial infarction
• Mitral stenosis
• Thyrotoxic crisis
• Acute cardiac tamponade
• Atrial fibrillation in WPW syndrome (rapid ventricular rate)
The paradoxic pulse of cardiac tamponade may be mistaken for atrial
fibrillation.
Careful evaluation of the arterial pulse usually reveals the cause of shock in
many situations. The characteristic features and causes are given in Table 12.11.
As can be seen, careful evaluation of the arterial pulse gives valuable clues
regarding the etiology of shock.
ARTERIAL PULSE IN VALVULAR HEART DISEASE

The nature of arterial pulse in aortic stenosis and aortic regurgitation has already
been discussed.
THE ARTERIAL PULSE
Arterial pulse in mitral stenosis

The arterial pulse in mitral stenosis is altered by the following variables.
• Rhythm
• Severity of mitral stenosis
• Associated
Aortic valve disease
Anemia
• Age of the patient
• Presence or absence of systemic embolism
The irregularly irregular pulse of atrial fibrillation usually means severe mitral
stenosis except in elderly patients, when AF can occur even with mild mitral stenosis.
If the arterial pulse is regular in a patient with established atrial fibrillation on
digitalis therapy, digitoxicity with AV nodal rhythm should be considered.
Asymmetry or absence of peripheral pulses should particularly be checked for in
all patients with mitral stenosis as evidence of systemic embolism. All patients
with mitral stenosis and systemic embolism should have a transesophageal
201
echocardiography to rule out left atrial thrombus as it is a contraindication to
closed mitral commissurotomy or balloon dilatation. If peripheral embolism occurs
with sinus rhythm, left atrial myxoma should be considered. In mild or moderate
mitral stenosis, the pulse volume is normal. The typical low volume pulse occurs
with severe mitral stenosis, severe PAH and right ventricular failure. Pulse volume
can also be low with associated aortic stenosis or TS. High volume pulse in mitral
stenosis occurs with associated aortic regurgitation, anemia or systemic
hypertension. Rarely, a sharp carotid pulse may be simulated by severe tricuspid
regurgitation with high RV pressures and peripherally transmitted venous pulse.
Arterial pulse in mitral regurgitation

The manifestations in the arterial pulse in mitral regurgitation depend on the
following factors:
• Severity of mitral regurgitation
• Left ventricular function
• Etiology of mitral regurgitation
• Rhythm
• Associated aortic valve disease
Table 12.12: The arterial pulse in mitral regurgitation

Characteristic pulse Significance
Normal volume collapsing pulse Severe MR with good LV function
Bisferiens pulse MR in association with HOCM
Attenuation of post-extrasystolic pulse
(Brockenbrough sign)
Slow rising pulse AS mistaken for MR
Functional MR with AS
Pulsus alternans Secondary MR with cardiomyopathy
or myocarditis
Irregularly irregular pulse of AF Rheumatic MR
Slow but regular pulse L-TGA with left AV valve regurgitation
Asymmetry of pulses Infective endocarditis with systemic embolism
Severe mitral regurgitation with good left ventricular function results in normal
volume collapsing pulse (Table 12.12). This is due to rapid ejection by the left
ventricle with an advantage of lesser afterload and more preload.
With the onset of left ventricular dysfunction, the pulse loses its collapsing
202
character. Atrial fibrillation in a young person with mitral regurgitation usually
means rheumatic mitral regurgitation. Bisferiens pulse in mitral regurgitation should
bring in the possibility of hypertrophic obstructive cardiomyopathy where mitral
regurgitation is part and parcel of the lesion, or mitral regurgitation associated
with aortic stenosis and aortic regurgitation.
Arterial pulse in congenital cyanotic heart disease

The arterial pulse may give a clue about the underlying lesion in this setting.
Tetralogy or tetralogy-like lesions with right to left shunts, have normal or mildly
increased pulse volume. Low volume pulses are a feature of severe defects like
hypoplastic left heart syndrome or any of the conditions with heart failure. High
volume or collapsing pulse occurs in some of these disorders (Table 12.13).
The ductus, bronchopulmonary collaterals and systemic to pulmonary artery
shunt often are responsible for the aortic run off in most of these disorders. In
tetralogy of Fallot, the left arm pulse is absent after left subclavian artery to
pulmonary artery shunt.
THE ARTERIAL PULSE
Table 12.13: Causes and mechanisms of collapsing pulse in cyanotic heart disease
Condition Mechanism(s)
Truncus arteriosus Truncal run off into pulmonary artery
Truncal insufficiency
Pulmonary atresia Bronchopulmonary collaterals
Tetralogy of Fallot Bronchopulmonary collaterals
Associated ductus
After systemic to pulmonary artery shunt
Associated aortic regurgitation
ARTERIAL PULSE IN CORONARY ARTERY DISEASE

Evaluation of the arterial pulse in coronary artery disease has more practical
utilitythan in any other cardiovascular disease. The findings of the arterial pulse
help in the differential diagnosis, diagnostic testing strategies, selection and dosage
of drug therapy, access to invasive testing and interventions, as well as the surgical
approach.
During acute coronary syndromes the pulse rate is usually increased but may
decrease if the right coronary or the circumflex arteries are the culprits. The pulse 203
rate is often used as a guide to select drugs in coronary artery disease. When the
resting pulse rate is less than 60 per minute, betablockers are usually contraindicated
and are never given if the pulse rate is less than 50/minute. Betablockers are the
choice when the resting pulse rate is normal or higher. Amlodepin or nifedipine
can be given safely in patients with a slow pulse rate.
Arterial pulse in a patient with acute chest pain

In patients with chest pain as a presenting feature, the arterial pulse gives valuable
information of use in the diagnosis and decision making (Table 12.14).
In view of the above mentioned reasons, the peripheral pulses in patients
with CAD should be carefully evaluated.
In conclusion, examination of the arterial pulse is often the inaugural part of
the physical examination. It is at this time the doctor touches the patient physically
first time. The advantage of starting the examination from the dorsalis pedis pulses
is that one can avoid missing palpating the peripheral pulses.
Table 12.14: The significance of the arterial pulse in a patient with chest pain
Feature of arterial pulse Significance
Slow rising pulse Severe fixed AS with angina
Bisferiens pulse Hypertrophic cardiomyopathy
AS with AR
Paradoxic pulse Pericardial tamponade
High volume or collapsing pulse Severe AR of any cause (especially, syphilis)
Anemia precipitating or aggravating angina
Aortic dissection with AR
Asymmetry of pulses Aortic dissection
Acute MI with embolism
Aortic valve disease with infective endocarditis
Femoral bruit/diminished pulses Peripheral vascular disease
in lower limbs Vascular access for catheterization/ angiography
from upper limb
Patient unsuitable for IABP or PCPS
Associated claudication may mask angina
Betablockers may aggravate claudication
204 Carotid bruit/diminished Carotid evaluation along with coronary arteriography
carotid pulse History of stroke or TIA increase the risk of stroke
during CABGS
Carotid surgery may have to be combined with CABGS
Diminished or absent left or Left subclavian arterial obstruction is a
right upper limb pulses contraindication to LIMA/RIMA grafting in CABGS
Poor graft flow in LIMA/RIMA
The most common error in evaluation of arterial pulse is missing to palpate

the peripheral pulses.
When the patient presents with intermittent claudication with palpable
peripheral arterial pulse, peripheral arterial disease is not ruled out unless
pulses are evaluated after exercising the patient. Peripheral pulse has to be
examined by palpation, auscultation and measurement of blood pressure both
at rest and after exertion.
Improper recording of pulse rate is more common than is realized.
Always look for pulsus paradoxus in all patients with hypotension or shock.
THE ARTERIAL PULSE
If the left arm pulsus are impalpable, left internal mammary (LIMA) grafting
may be contraindicated.
Chronotropic incompetence is defined as a slow resting pulse that fails to
accelerate normally with exercise. When it is not due to betablockade, it
indicates sick sinus syndrome.
Sinus node deceleration, defined as initial increase followed by subsequent
decrease in heart rate during continued exercise, is a marker of right coronary
artery disease.
205
13 Blood Pressure
Blood pressure is the product of cardiac output and peripheral vascular resistance
and is a reflection of the performance of the heart and responsiveness of the
vascular system. Elevation of arterial pressure as a physical sign is unique because
the very elevation of it suggests the diagnosis of systemic hypertension, which is
one of the most common cardiovascular disorder in adult population. Systemic
hypertension is a major risk factor for coronary arterial disease, cerebrovascular
206 disease and renovascular disease.
Blood pressure is expressed as mmHg or kPa
(1 mmHg = 0.13332 kPa; 1 kPa = 7.5006 mmHg).
The factors that determine arterial pressure are:
• Cardiac output
• Systemic vascular resistance
• Compliance of the vascular system
• Competence of the aortic valve
• Isolation of the arterial from venous system by the arterioles
Blood pressure in the arteries is the product of cardiac output and systemic vascular
resistance.
Measurement of blood pressure

Among the various methods available for measuring blood pressure the auscultatory
technique is the most commonly used. The other methods are:
Non-invasive methods (indirect)
Palpation
BLOOD PRESSURE
Auscultation
Flush
Ultrasound Doppler
Oscillometric
Invasive method (direct)
Intra-arterial
Non-invasive methods: Prior to any discussion on blood pressure recording it is
essential to understand the nature of Korotkoff sounds and the requirements for
the cuff used to measure blood pressure.
Korotkoff sounds are the sounds audible over the artery when a compressing
cuff is gradually released. The vibrations produced by the flow of blood at different
levels of release of cuff produce these sounds. There are five phases of Korotkoff
sounds (Table 13.1).
The sphygmomanometer
The pneumatic cuff permits controlled occlusion of the underlying artery when
inflated. A mercury or aneroid manometer is connected to a rubber bladder encased
in a non-distensible outer cuff. The bladder length should be at least 75 per cent 207
Table 13.1: Korotkoff sounds

Phase Description Comment
Phase I Onset of auditory sound At peak systolic pressure
Clear tapping sound
Phase II Onset of swishing sound or murmur Onset 10–15 mmHg lower from
peak systolic pressure
Phase III A louder murmur-like sound Auscultatory silent gap occurs
when phase II sounds are fainter
or not heard
15–20 mmHg below phase II
Phase IV Sudden muffling of sounds Occurs 5–10 mmHg above the
true diastolic pressure.
Represents diastolic pressure in
severe aortic regurgitation (AR)
and hyperkinetic states
Phase V Disappearance of sounds Represents true diastolic
pressure except in severe AR and
hyperkinetic states
Table 13.2: Suggested sphygmomanometer cuff size in centimeters (modified from AHA)
Patient subset Armcircumference Bladder width Bladder length

(mid-arm) (cm) (cm) (cm)
Newborn 2.5–4.0 5–10
Infant 6–8 12–13.5
Child 13–20 9–10 17–19
Small adult 17–26 11–12 19–22
Standard adult 24–33 12–13 22–24
Large adult 33–42 15–17 32–33
Thigh 42–50 18–20 35–42
of the arm circumference. The cuff should be long enough to be wrapped around
the arm (Table 13.2).
The cuff width should be at least 20 per cent larger than the arm diameter.
The cuff for the thigh should be at least 15 cm in width and twice that in length.
Methods of measuring blood pressure

1. Palpation: The palpatory method allows a quick assessment of the systolic
208 pressure though the systolic pressure estimated is about 10 mmHg lower than the
intra-arterial or auscultatory method. Sometimes, in infants and young children
this may be the only method possible. The diastolic pressure cannot be measured
by this method. The systolic pressure estimated by this method is used as a guide
to inflate the cuff above systolic pressure.
2. Auscultatory method: The cuff should be quickly inflated to 20 mmHg above
peak systolic pressure estimated by palpatory method. The deflation should be
slower. The deflation rate can be at the rate of 2–3 mmHg per second. The first
appearance of Korotkoff sounds represents the systolic pressure and the point of
disappearance is taken for diastolic pressure. In situations where the Korotkoff
sounds are heard to the level of zero, the level of muffling should be taken as the
diastolic pressure but a note should be made of this feature. For example, in a
patient with severe AR, the BP should be expressed as 150/40–0 mmHg, indicating
that muffling occurred at 40 mmHg but the sounds continue to be audible until
zero. If more than one measurement is made, the cuff should be fully deflated and
the arm emptied of venous blood before the next measurement. Venous pooling
can muffle or drown out the Korotkoff sounds.
3. Doppler method: With the ultrasonic transducer placed over the artery, the
BLOOD PRESSURE
cuff pressure is deflated slowly as in the auscultatory method. An audible signal is

appreciable over the artery when the cuff pressure is lower than the intravascular
pressure. The sound signal disappears when the cuff pressure drops below the
diastolic pressure. This method is very accurate for the estimation of systolic
pressure but the diastolic pressure cannot be measured accurately.
4. Oscillometric method: This method permits estimation of systolic, diastolic
and mean arterial pressures as well as the heart rates digitally. Recordings can be
automatically repeated when required. Technical artifacts are common and the
mean pressure is most accurate with this method. The systolic and diastolic
pressures can be calculated from the mean pressure.
5. Flush technique: The principle of this method is similar to that of cuff
application in the other methods. The limb is elevated, and an elastic bandage is
applied from the finger tips or toes proximally to eliminate blood from the skin
capillaries and veins to blanch the distal forearm and hand or lower leg and foot.
With the bandage still applied, the BP cuff is inflated at least 20–30 mmHg above
the expected systolic pressure. With the BP cuff inflated, the bandage is removed.
The distal limb should now be blanched white. The cuff is deflated by 2–3 mmHg 209
per second, and the pressure at which the first blush appears in the limb is taken
as the blood pressure. The reading obtained is closer to mean arterial pressure
than to peak systolic pressure. This method is most useful in infants with suspected
coarctation of the aorta. In the presence of severe coarctation, this may be the
only method possible, short of direct intravascular measurement.
Patient factors: The patient should be relaxed and shouldn’t have taken
medications which increase pressure. On the first visit, BP should be measured in
all the four limbs in adults and at least in one upper limb and one lower limb in
children. The other guidelines are listed in Table 13.3.
One of the methods of avoiding anxiety related rise in pressure is to apply
the cuff at the beginning of physical examination, and measure the BP at the end
of examination by which time the patient is accustomed to the idea of having a
cuff tied around the arm.
Right arm and left arm pressures: Normally, the difference between the right and
left upper limb pressures may be up to 10 mmHg. A significant pressure difference
may occur in a variety of clinical situations and are listed in Table 13.4.
Table 13.3: Guidelines for measuring blood pressure

Patient factors Patient relaxed
Quiet, comfortable room
No coffee or smoking prior to
measurement
Avoidance of drugs which elevate pressure
(nasal decongestants, cough syrups
containing ephedrine, tricyclic
antidepressants)
Full and correct information of the dosage
and nature of antihypertensive therapy
Posture
First visit Supine + Standing
Revisit with drugs Supine + Standing + Sitting
Follow up visit Sitting
Any visit with postural symptoms Supine + Sitting + Standing
Technical Appropriate cuff size encircling and covering
two-thirds of the arm
Mercury manometer is the choice
Aneroid electronic equipment require
calibration from time to time.
210 For infants and children use appropriate sized
cuff
Which limb to use? All 4 limbs in the first visit in adults, one upper
and one lower in children
In the first visit take pressure in both arms;
Followup: use the arm with the higher
pressure
When to take pressure? Don’t take pressure the moment the patient
enters the room
Apply the cuff at the beginning of physical
examination and take pressure at the end
Attitude and manner Do not be in a hurry
Make the patient feel as comfortable as
possible
How many readings? At least two recordings in first visit
If the readings vary by more than 5 mmHg,
take additional readings until two are close
For a diagnosis of hypertension at least 3 sets
of readings at least a week apart are needed.
How to measure pressure? Inflate the cuff quickly to a pressure of
20 mmHg above systolic guided by radial
pulse
BLOOD PRESSURE
The rate of deflation to be 2–3 mmHg/sec

Disappearance of sounds (Phase V) is taken
for diastolic pressure in adults
Muffling (Phase IV) is taken as diastolic
pressure in children
Inaudible Korotkoff sounds Elevate the arm, open and close the fist for
4–6 times to empty the arm of pooled blood,
and rapidly inflate the cuff
Table 13.4: Conditions under which there may be disparity in pressures between two arms
Condition Mechanism
Normal variation Orientation of origin of right arm and left arm arteries
Right arm pressure is usually higher by 10mmHg
Arterial occlusion Cardiogenic embolism
Atherosclerosis
Takayasu’s arteritis
Subclavian steal syndrome
Coarctation of aorta Left subclavian arising from coarct segment
Aberrant right subclavian artery distal to coarct
segment
211
Dissecting aneurysm of aorta Involvement of right innominate or left subclavian
arteries
Thoracic outlet syndrome Arterial compression
Supravalvular aortic stenosis Jet of aortic ejection directed to right innominate
artery
Normal fluctuations in pressure
between two readings
When measuring pressure most doctors have a tendency to use the figures
that are most ‘popular’. For example, 120/80 mmHg is the most popular normal
pressure and is often the figure most often recorded. As the upper limit of normal
is 140/90 mmHg, any reading slightly above this is often mentioned as lower than
this to ‘avoid’ the diagnosis of hypertension.
Common errors
• Failure to measure blood pressure
• Failure to enter the correct reading in the case record even after measurement
• Inflating and deflating the cuff too rapidly
• Failure to concentrate on the mercury column while deflating

• Defective BP apparatus
• Reliance on electronic apparatus
• Cuff applied too loosely
• Inappropriate size of the cuff
• Failure to recognize ‘auscultatory silent gap’
• Absence of Korotkoff sounds due to venous congestion
• Failure to keep the arm and BP apparatus at the level of the heart
• Measuring pressure as soon as the patient enters the room
The commonest error in measurement of blood pressure is surprisingly not
measuring it at all. All patients who enter a hospital or a doctor’s office should
have their blood pressure measured irrespective of their symptoms. By not
measuring blood pressure, the commonest cardiovascular disease in adults, systemic
hypertension, is missed.
ALTERATIONS IN BLOOD PRESSURE

212
SYSTEMIC HYPERTENSION
Systemic hypertension is a risk factor for coronary, cerebral and renovascular
disease. Careful control of pressure reduces the vascular complications. The
diagnosis of this common and potentially life-threatening disease is missed if blood
pressure is not measured and classified accurately (Table 13.5).
Table 13.5: Classification of blood pressure for adults (18 years and older)
Category Systolic Diastolic
Normal <130 <85
High normal 130–139 85–89
Hypertension
Stage 1 (mild) 140–159 90–99
Stage 2 (moderate) 160–179 100–109
Stage 3 (severe) 180–209 110–119
Stage4 (very severe) >210 >120
BLOOD PRESSURE
POSTURAL HYPOTENSION
In a normal person, the arterial pressure is maintained within physiological limits
in all positions. With a change in position from supine to standing, there is a slight
fall in systolic pressure not exceeding 5 mmHg, and the diastolic pressure remains
constant or may rise slightly. These changes revert to normal levels within 3–5
minutes in normal individuals. This is made possible by the increase in systemic
vascular resistance and heart rate. The integrity of the autonomic nervous system
is essential to bring about these changes.
Postural hypotension is defined as a fall of 20 mmHg or more in systolic pressure, or
10 mmHg or more in diastolic pressure in upright posture. If the patient is symptomatic, even a
marginal decrease should be considered significant.
Symptoms
• Light headedness
• Dizziness
• Blurring or loss of vision
• Extreme weakness
213
• Syncope
Technique of measurement
• Supine BP and heart rate after the patient is supine for at least 5 minutes
• Standing BP immediately, and at 2–5 minutes
Table 13.6: Cardiovascular alterations in upright posture
Alteration Mechanisms
Increased heart rate Diminished venous return
Sinus tachycardia Fall in stroke volume
Fall in cardiac output
Lesser distention of carotid stretch receptors
Less reflex inhibition from carotid
baroreceptor on the vasomotor centre in
the brain stem
Blood pressure
Systolic Fall of less than 5 mmHg
Diastolic Constant or rise of less than 5 mmHg
• Continue to measure BP upto 10 minutes if postural hypotension is

suspected
The clinical diagnosis should take into consideration not only the blood
pressure changes but also the symptoms. The commonest cause of postural
hypotension in clinical practice is that induced by antihypertensive medication.
Hypovolemia remains another common cause. An intact autonomic nervous system
is essential for maintenance of arterial pressure in general, and particularly in an
upright position.
Causes
A. Drugs
Antihypertensive
Centrally acting: Methyl dopa, clonidine
Adrenergic blockers: Guanethidine
Alpha blockers: Phenoxybenzamine, labetalol
Vasodilators: Prazosin, hydralazine
ACE inhibitors
214 Diuretics
Calcium channel blockers: Nifedipine
Antianginal agents: Nitrates/nitroglycerine
Antidepressants: Tricyclic antidepressants, monoamine oxidase inhibitors
Tranquilizers/Sedatives: Barbiturates, phenothiazines
Selective neurotoxic drugs: Alcohol
B. Hypovolemia
Diuretics
Dehydration due to any cause
Hemorrhage
Excessive perspiration
Overdialysis
Idiopathic hypovolemia
C. Endocrine disorders
Addison’s disease
Hypoaldosteronism
BLOOD PRESSURE
Pheochromocytoma
Renovascular hypertension
D. Vascular insufficiency
Varicose veins
Absent venous valves
Arteriovenous malformations
E. Vasodilator excess
Mastocytosis (histamine, prostaglandin D2)
Hyperbradykinenism (bradykinin)
Carcinoid (bradykinin)
Hypermagnesemia
F. Autonomic neuropathy
Primary
Primary autonomic failure (Bradbury Eggleston syndrome)
Shy–Drager syndrome
Autonomic failure with Parkinson’s disease
215
Riley–Day syndrome (familial dysautonomia)
Baroreflex failure
Acute pandysautonomia
Secondaryautonomicneuropathies
Diabetes, alcoholism, amyloid
Autoimmune disorders
Guillain–Barre syndrome
Acute/subacute dysautonomia
Mixed connective tissue disease
Rheumatoid arthritis
Eaton–Lambert syndrome
Carcinomatous autonomic neuropathy
Porphyria, Fabry’s disease, Tangier’s disease
B12 deficiency
Hereditary sensory neuropathies
CNS infections
Syphilis, Chagas’ disease, herpes zoster, HIV infection, botulism
Spinal cord lesions
Familial hyperbradykininism
Cerebral/mid-brain lesions: Vascular lesions or tumours involving
hypothalamus and mid-brain (craniopharyngioma), multiple sclerosis,
Wernicke’s encephalopathy, Adie’s syndrome
Spinal cord lesions
Advanced age
Dopamine hydroxylase deficiency
Renal failure
Elderly patients are particularly susceptible to volume depletion and adverse
effects of drugs because of associated cerebrovascular disease, decreased
baroreceptor sensitivity, decreased muscle tone and increased renal sodium loss.
The diagnosis of postural hypotension is missed if blood pressure is not measured
in standing position. One must look for this sign in certain clinical situations:
216
• All patients on antihypertensive medication on follow up
• All patients on vasodilator therapy for heart failure
• All patients with syncope or near syncope
• Patients presenting with chronic fatigue or weakness
• Patients diagnosed to have depression
• Hypovolemia due to any cause
• Hemorrhage either external or internal
Postural hypotension is an early sign of hypovolemia due to any cause before
frank hypotension supervenes.
HYPOTENSION AND SHOCK

When the systolic blood pressure is less than 90 mmHg, hypotension is said to
exist. Shock is a clinical syndrome with hypotension as an important but not
essential part of the clinical picture. The traditional definition of shock as equivalent
to low arterial pressure, and excessive focus on arterial pressure, results in many
cases in misdiagnosis and mismanagement of patients with shock.
Shock is a syndrome, a constellation of symptoms and signs that are subjective
BLOOD PRESSURE
and imprecise. A low arterial pressure is only one of the signs of shock.
Hypotension, though common, is not essential for a diagnosis of shock.
Signs and symptoms

• Hypotension or normotension
• Pallor
• Cold, clammy skin
• Tachycardia
• Altered mental status
• Oliguria
Though hypotension is common, normal blood pressure or even hypertension
can occur in the initial stages of shock. Fall in pressure can be precipitous in such
situations. In the presence of shock, or low perfusion states, indirect measurement
of pressure by the cuff method is imprecise and can be misleading. With extreme
vasoconstriction of shock, the central aortic pressure is often higher (by as much
as 40 mmHg) than peripheral arterial pressure.
Routine cuff method is unreliable and can be misleading in this setting. Though
direct invasive pressure monitoring is superior to indirect methods (Table 13.7), 217
errors can occur even with the direct method due to improper techniques or
instrumentation.
Hypotension is often a danger signal suggesting a serious inadequacy of the
circulatory system. Prompt recognition and management is the key to successful
Table 13.7: Unreliability of indirect pressure recording in shock
Cause Mechanism
Adrenergic vasoconstriction Gradient of pressure between central aorta
and peripheral arteries (upto 40 mmHg)
Reduction in stroke volume, Diminished or absent Korotkoff sounds
increased vascular resistance
Indications for direct intra-arterial pressure monitoring

• Shock
• Nitroprusside infusion
• Hypertensive crises
• Acute mitral regurgitation
Indications for measuring blood pressure immediately in hospitalized patients

• Restlessness
• Drowsiness
• Excessive sweating
• Weakness
• Unexplained tachycardia or bradycardia
• Respiratory distress
• Elderly patients exposed to any hypotensive medication
• Identification of high–risk patients and monitoring them frequently
outcome in this setting. Though blood pressure is measured routinely in all patients
coming to the outpatient or emergency room, this is not often the case with patients
who are already hospitalized. For a variety of reasons, onset of hypotension is not
promptly recognized in hospitalized patients. The box above summarizes the
situations where blood pressure should be measured immediately in hospitalized
patients.
The common story is that the nurse when called to see a restless patient in the night gives a
sedative (diazepam) without informing the doctor. The doctor in turn when called does the same
218 only to realize several hours later that the beginning of hypotension was missed.
The moment hypotension is detected, one should look for causative factors.
The clues to the diagnosis often come from the history and the rest of the physical
examination. The importance of clinical examination is often not realized in patients
with shock.
Clinical evaluation
In patients with trauma and loss of blood, the clinical signs may help estimate the
volume of blood lost (Table 13.8).
State of consciousness Restlessness, anxiety,
Skin Temperature, moistness, color and turgor, rash
Mucous membranes Colour and moistness
Nail beds Colour and capillary filling
Peripheral veins Collapsed or distended
Jugular venous pulse Collapsed or distended
Pulse Rate and rhythm
Respiration Rate and depth
Urine Hourly output
BLOOD PRESSURE
Table 13.8: Clinical correlates in hemorrhagic shock

Vital sign <15%* 15–30%* 30–40%* >40%*
Heart rate <100 >100 >120 >140
Systolic BP Normal Normal Decreased Decreased
Pulse pressure Normal/ Decreased Decreased Decreased/
increased absent
Capillary refill Normal Delayed Delayed/ Absent
absent
Respiratory rate 14–20 20–30 30–40 40–50
CNS, mental state Anxious More anxious Anxious/ Confused/
confused lethargic
* Blood loss as volume percentage
Table 13.9: Causes of shock and clues to the diagnosis

Cause Clues to diagnosis
Hypovolemic shock
Diarrhea, vomiting, hemorrhage, Sinus tachycardia
Diuretics Cold extremities 219
No elevation of jugular venous pressure
No ventricular gallop
Cardiogenic shock
Myocardial infarction, Sinus tachycardia
acute myocarditis Cold extremities
Elevated jugular venous pressure
Ventricular gallop
Crepitations at lung bases
Arrhythmia Heart rates too high or too low or impalpable
Abnormal wave pattern in jugular venous
pressure
Obstructive shock
Acute pulmonary embolism Dyspnea is the rule
Sinus tachycardia
Cold extremities
Dry lungs
Right ventricular S3/S4
Compressive shock
Pericardial tamponade History of infection or trauma
Tension pneumothorax Sinus tachycardia
Bilateral large pleural effusions Tachypnoea
Cold extremities
Cause Clues to diagnosis

Pulsus paradoxus
No gallop
Dry lungs
Distributive shock Sinus tachycardia
Septic shock Warm extremities
Fever may be present
Evidence of infection
Anaphylactic shock
Drugs, radiologic contrast History of drug allergy/bronchial asthma/
Bee sting, Poison ivy skin allergy
Evidence of exposure to a drug/agent
Bronchospasm
Skin rash/itch/angioedema
Sinus tachycardia
Drug induced
Antihypertensive agents Warm extremities
Calcium blockers Sinus tachycardia
Betablockers Bradycardia with betablockers or calcium
220 blockers
Nitrates Warm extremities
Phenothiazines Other systemic effects of drug
Barbiturates (suicidal intent)
Endocrine shock
Addison’s disease Long term steroid use/acute stress
Panhypopituitarism pallor
Pheochromocytoma (adrenaline Paroxysmal hypotension with signs of
secreting) adrenergic excess
Vasovagal shock Sinus bradycardia
Hypotension
In the majority of patients, the diagnostic clues as to the cause of shock are
often available from the clinical examination (Table 13.9).
As the outcome is often dependent on the measures taken in the initial few
minutes or hours, a practical ‘first things first’ approach is useful. As anaphylactic
shock is rapidly fatal and responds to adrenaline and steroids promptly if given in
time, never waste time on detailed evaluations if there is any element of doubt.
Apply the same rule to the adrenal crisis, which responds dramatically to intravenous
steroid.
BLOOD PRESSURE
Table 13.10: Initial approach to a patient with shock

Step Approach
Rule out conditions simulating Confirm the presence of shock
shock Rule out peripheral vascular disease with
diminished pulses
Treat conditions which are rapidly Rule out vasovagal shock
fatal but respond dramatically to (if in doubt give atropine and volume infusion)
specific therapy Rule out anaphylactic shock
(If in doubt, give adrenaline and steroid IV)
Rule out addisonian crisis
(If in doubt give steroid IV)
Rule out cardiac tamponade
(If in doubt, insert a needle into the
pericardium)
Rule out tension pneumothorax
(If in doubt, insert a needle into the pleural
cavity)
Always consider septic shock in the
differential diagnosis even in afebrile
patient
Take care of volume Infuse fluid if in doubt, as hypovolemia is a 221
common cause of shock, even in
cardiovascular disorders
Take care of ventilation Ensure adequate ventilation
This combined diagnostic and therapeutic approach is ideally suited to a

condition like shock because, any delay can cause irreversible damage to vital
organs.
Clinical recognition and management of anaphylactic shock
• Sudden unexpected tachycardia (increase of >20 beats/minute) or hypotension >30 mmHg
fall in pressure, especially if a drug has been given within the preceding 10 minutes.
• Skin rash, angioedema and bronchospasm are confirmatory
• Stop further administration of the drug
• Airway maintenance with 100% oxygen, if the patient is not ventilated, use mask ventilation
• The first drug of choice is epinephrine 2.5 ml 1:10,000 dilution every 5–10 minutes
• Start maintenance infusion 1–20 μg/kg body weight
• Inject 200 mg of hydrocortisone intravenously
• Volume expansion: rapidly infuse 2–10 litres of crystalloid. Appropriate venous access may
be necessary
• Intravenous antihistamine (H1 and H2) may be given if the reaction persists
• Give bicarbonate early based on acid-base balance
Some of these criteria are particularly helpful in recognizing the disorder

during anesthesia, cardiac catheterization, postoperative state, cerebrovascular
accidents or in patients under sedation. To confirm the diagnosis, plasma histamine
levels are helpful. A sample of 2–5 cc blood is collected in an EDTA tube and
kept on ice immediately. The plasma is then separated and stored at –70 ºC, to be
assayed later. The plasma tryptase is an enzyme released during mast cell
degranulation. The levels of this enzyme persist for many hours and can be
estimated serially over a 24 hour period. In initial studies of 30 severe reactions,
levels of 1–2 ng/ml tryptase were associated with significant hypotension.
In the cardiac catheterization laboratory, the best way to treat these patients
is to be aware that these reactions are possible due to iodine containing contrast
agents. The high-risk patient can be identified if he has a history of allergies.
Betablocker therapy appears to increase the tendency for anaphylaxis. Pre-treatment
with steroids diminishes the risk. All catheterization laboratories should keep pre-
diluted and preloaded injections of adrenaline each morning before the procedures
are started (to save time should the need arise). Routine femoral venous sheath is
particularly valuable as a reliable access in case of shock to administer large volume
222 of fluid.
PULSUS PARADOXUS
Pulsus paradoxus is best elicited with the sphygmomanometer. It is an exaggeration
of normal fall in systolic pressure in inspiration. The patient is asked to breath
normally. The cuff is inflated to above the level of systolic pressure and is deflated
very slowly (2–3 mmHg/sec). The point at which the Korotkoff sounds are
intermittently heard is noted. By further deflation, the sounds are continuously
audible during both inspiration and expiration. The difference between the two
points is measured as the degree of paradoxus. In normal people the inspiratory
fall in pressure is not more than 8 mmHg. Any exaggeration above this value is
considered a positive sign.
Causes
Normal
• Pregnancy
• Exaggerated voluntary inspiration (student paradoxus)
• Extreme obesity
BLOOD PRESSURE
Severe obstruction to airways

• Acute severe bronchial asthma
• Severe emphysema
• Upper airway obstruction
Pericardial disease
• Cardiac tamponade
• Effusive constrictive pericarditis
• Severe constrictive pericarditis
• Shock
• Hypovolemia
Sphygmomanometric paradoxus is not only a more sensitive sign than pulsus paradoxus,
but also permits quantification of the degree of paradoxus in mmHg. This sign
should be looked for in all clinical syndromes with any of the presenting features
given below:
• Whenever palpable paradoxus is suspected
• In all patients with pericardial effusion
• Constrictive pericarditis 223
• Unexplained heart failure
• ‘Heart failure’ without S3
• Acute episode of asthma
• All patients with shock
• ‘Unexplained’ liver enlargement/Right hypochondriac pain
• All patients with syncope
• All patients with history of trauma (hemopericardium)
When the Korotkoff sounds are feeble, the clue to the beginning of sounds
or systolic pressure is oscillation of the mercury column with each pulse.
Blood pressure alternans (pulsus alternans)

This is characterized by a regular sinus rhythm with alternate strong and weak
beats. It is often a sign of myocardial dysfunction and is related to alternating
more and fewer contractile elements participating in each contraction. Alternans
is most commonly seen in severe aortic stenosis with left ventricular dysfunction,
but also occurs with any condition with severe ventricular dysfunction. Alternans
can be total, involving both sides of the heart, or partial, involving only the right
or left ventricle. In aortic stenosis, the strong and weak beats are appreciated as
variation in the intensity of systolic murmur alternatively. When the weak beat is
too weak to be palpable, only auscultatory alternans is appreciable. Aortic
regurgitation, systemic hypertension and reducing the venous return by head tilting
or nitroglycerine usually exaggerate pulsus alternans and assist in its detection.
Pulsus alternans is easier to detect by sphygmomanometer than by palpation of
the arterial pulse. Palpable alternans over the peripheral pulse is detectable only
when the aortic pressure alternates by more than 20 mmHg. The Korotkoff sounds
alternate in their intensity with alternating beats. Electrical alternans is an
independent phenomenon and has no relationship to pulsus alternans.
Causes of blood pressure alternans
• Dilated cardiomyopathy
• Myocarditis
• Severe AR with left ventricular failure especially after aortic valve
replacement
224 • Any cause for ventricular dysfunction
The purpose of describing this physical sign in the chapter on blood pressure
is that alternans of blood pressure is a more sensitive sign than palpable pulsus
alternans. One must look for this sign in all patients with aortic stenosis and heart failure while
measuring blood pressure.
BLOOD PRESSURE IN AORTIC REGURGITATION

In aortic regurgitation, the diastolic pressure falls and the systolic pressure increases
as the severity of regurgitation increases. As a result, the pulse pressure increases.
When the pulse pressure is above 70 mmHg, severe aortic regurgitation is likely.
Diastolic pressure above 70 mmHg is unlikely in moderate to severe aortic
regurgitation. The systolic pressure is often normal in children with severe aortic
regurgitation but is commonly elevated in older patients with aortic regurgitation.
Though the systolic pressure does not correlate well with the degree of aortic
regurgitation in elderly patients, in younger patients elevated systolic pressure is
often indicative of significant aortic regurgitation. Significant systolic hypertension
in aortic regurgitation is a feature in elderly patients with rigid arterial system,
associated systemic hypertension or coarctation of aorta.
BLOOD PRESSURE
The systolic blood pressure in AR correlates with left ventricular end-diastolic

volume. The higher the systolic blood pressure, the larger the end-diastolic volume.
In a recent study by Pirwitz et al, the higher PSP/ESV ratio is found to be a
reliable predictor of symptomatic improvement after valve replacement.
If the systolic pressure is above 170 mmHg, in a patient with aortic
regurgitation, associated aortic stenosis of significance is unlikely. Similarly, if the
diastolic pressure in aortic regurgitation is 40 mmHg or less, severe free aortic
regurgitation is likely and usually rules out associated AS of any significance.
Accurate measurement of blood pressure in severe aortic regurgitation may be
difficult due to the fact that the pistol shot sounds may be audible over the brachial
arteries and gives an impression of very high systolic pressures nearing 300 mmHg.
The Korotkoff sounds may be audible until zero giving an impression of zero
level of diastolic pressure. However, the diastolic pressure is never zero in any
degree of aortic regurgitation. The onset of Korotkoff sounds at systolic pressure
is recognized by their sharper quality in comparison to the pistol shot sounds.
Though the Korotkoff sounds are audible to the level of zero, the onset of muffling
occurs around 40 mmHg and should be taken as diastolic pressure. The BP in
severe aortic regurgitation is typically expressed as 130/40–0 mmHg, and implies 225
that though the sounds are audible up to 0 mmHg, muffling occurred at 40 mmHg.
By the mechanisms described above, the systolic pressure is overestimated and
the diastolic pressure is underestimated in severe aortic regurgitation. Normalization
of diastolic pressure with fall in pulse pressure can occur in aortic regurgitation
with the onset of left ventricular failure.
Normally, the lower limb systolic pressure is 10–20 mmHg higher than the
upper limb pressure. In aortic regurgitation and other conditions with aortic run-
off, the lower limb pressure increases to above 20 mmHg. This increase in systolic
pressure in the lower limb above 20 mmHg is called Hill’s sign. The more the
severity of aortic regurgitation, the more the systolic pressure in the lower limbs.
The degree of abnormality or positivity of Hill’s sign correlates well with the
angiographic severity of aortic regurgitation.
Brachio-femoral or brachio-brachial delay is a less sensitive sign than blood
pressure measurement in the limbs. The blood pressure should be measured in all
the limbs in all the patients with aortic regurgitation because Hill’s sign permits
estimation of severity but any asymmetry of pressure gives a clue to the underlying
coarctation of aorta or aortic dissection. An equal systolic pressure in upper and
Table 13.11: Angiographic correlations of Hill’s sign in aortic regurgitation (AR)

Lower limb systolic pressure Evaluation of AR
< 20 mmHg Normal or
Trivial or mild AR
Angiographic 1+ AR
Associated coarctation
20–40 mmHg Angiographic 2+ AR
40–60 mmHg Angiographic 3+ AR
> 60 mmHg Angiographic 4+ AR
Table 13.12: Situations in which sphygmomanometer cuff is used as a venous tourniquet

Indication Method and mechanism
Acute pulmonary edema Cuff inflated around three limbs
Reduction in venous return
Inflation pressure to less than diastolic or
70–80 mmHg
Rotate the cuff between the limbs
To bring out the murmur of AR Cuff inflated around both lower limbs
226
Increase in systemic vascular resistance
lower limbs may still suggest coarctation of aorta especially in the presence of
significant aortic regurgitation.
BLOOD PRESSURE IN ACUTE MYOCARDIAL INFARCTION

A systolic blood pressure of less than 100 mmHg, at admission carries an
unfavourable prognosis in acute MI. Uncontrolled severe hypertension is a
contraindication to thrombolytic therapy in acute MI. Acute myocardial infarction
with systemic hypertension is associated with low hospital mortality even without
thrombolytic therapy.
OTHER USES OF THE SPHYGMOMANOMETER
Venous tourniquet
The sphygmomanometer cuff can be used to reduce venous return in certain
conditions. The cuff is tied around both thighs and one of the arms and is inflated
BLOOD PRESSURE
to just below the level of diastolic pressure or 80 mmHg. The cuffs are kept inflated
for about 15 minutes at a time and rotated through the other arm. This method is
of value in treating acute pulmonary edema by reducing the venous return (Table
13.12).
Diagnosis of thrombocytopenia (Hess sign)

This test is intended to assess the capillary fragility. The cuff is tied around the
arm and is inflated to a pressure midway between the systolic and diastolic pressures
for 5 minutes. The number of petechiae appearing in an area of 2.5 cm2 on the
inner aspect of the arm, are counted. More than twenty petechiae are considered
abnormal.
Blood pressure should be measured in all patients who visit a doctor.

Systemic hypertension is the commonest chronic cardiovascular disorder and
can be missed if the BP is not measured.
‘Sphygmomanometric paradoxus’ is a more sensitive sign than pulsus 227
paradoxus. Make it a habit to look for cardiac tamponade while measuring
blood pressure.
A normal blood pressure or even hypertension does not rule out shock
syndrome or pericardial tamponade.
Improper recording of blood pressure is more common than realized.
Pressure is the force per area unit. Expressed as mmHg or kPa (kilo Pascal).
KPa is not commonly used, except by some examiners.
kPa = 7.5006 mmHg; 1 mmHg = 0.13332 kPa.
A normal blood pressure or even severe hypertension does not rule out cardiac
tamponade. Cardiac tamponade manifests in a wide clinical spectrum.
Even when the blood pressure has been recorded earlier by somebody else,
always re-record the blood pressure as a routine. Unreliable recording of
blood pressure is more common than is realized. It happens at all levels of
training.
When you measured the blood pressure and found it elevated, you made a very important
cardiovascular diagnosis.
14 The Jugular Venous Pulse

The normal arterial pulse reflects the performance of the left ventricle and is easily
available for evaluation. The filling pattern of the left ventricle is unavailable, as
we do not have access to the intrathoracic pulmonary veins. The performance of
the right ventricle is not available externally by pulmonary arterial pulse, but the
filling pattern is readily available through the jugular veins. The student, as well
as the physician, is often confused as to the method of measuring the level and
recognizing the wave pattern in the jugular venous pulse (JVP). In this chapter,
228 we intend to clarify certain concepts basic to the understanding of jugular venous
pulse (Tables 14.1; 14.2).
Table 14.1: Information derived from the jugular venous pulse
Information Clue in jugular venous pulse

Level of right atrial pressure Level of jugular venous pressure
Right ventricular filling pressure (RVF)
Central venous pressure
Obstruction to superior vena cava Elevated jugular venous pressure with absent pulsations
Pattern of RV filling or RA emptying y descent
Rapid filling (RVF, TR, CP) Rapid y descent
Slow filling (TS) Slow y descent
Little or no filling (tamponade) Obliterated y descent
Resistance to pre-systolic RA emptying Prominent a wave
(TS, non-compliant RV)
Hyperkinetic circulatory state Venous hum
(Anemia, thyrotoxicosis)
Sequence of atrioventricular contraction Analysis of rhythm
(AV dissociation, CHB, junctional rhythm)
(RVF: right ventricular failure, TR: tricuspid regurgitation, CP: constrictive pericarditis, TS: tricuspid
stenosis, AV: atrioventricular, CHB: complete heart block)
THE JUGULAR VENOUS PULSE
Table 14.2: Relation of atrial pressure to waves in JVP
Waves in JVP Atrial pressure Mechanism

a wave •• Atrial contraction
x descent • Atrial relaxation; descent of AV
septum
v wave • Atrial filling
y descent • RV filling/atrial emptying
The normal jugular venous pulse (Figs. 14.1; 14.2) consists of an a wave,
x descent, c wave, v wave and the y descent.
Normal jugular venous pattern

The positive wave just preceding the carotid upstroke and corresponding to the
P wave on ECG results from atrial systole. This is an a wave. A small positive
deflection may be recorded and is due to tensing of the tricuspid valve at the
onset of systole. Sometimes it is considered to be due to the transmitted carotid
pulse. The x descent is due to the descent of the tricuspid valve during ventricular
emptying in systole. The subsequent positive wave, the v wave, is due to the venous
return to the atrium. With the opening of the tricuspid valve in early diastole there 229
is sudden flow of blood from atrium into the ventricle resulting in the y descent.
Any obstruction in superior vena cava will obliterate these wave forms.
Fig. 14.1: Time relationship of wave pattern of JVP with other cardiac events
A C
V
Fig. 14.2: Normal jugular venous pattern
The c wave is not appreciated by the bedside easily and is related to the
transmitted carotid pulse when recorded in the neck, and due to tricuspid valve
closure when recorded in the right atrium.
230 Table 14.3: Differentiating arterial and venous pulsations in the neck
Feature Venous pulsations Arterial pulsations

Site Laterally located, superficial More medial, deeper and
and widespread localized
Changes with respiration, Alters with all these No alterations
position and increased maneuvers
abdominal pressure
Number of pulsations Multiple Single pulsations
Level Definite upper level is No definite upper level
visible
Visibility and palpability Better visible than palpable Better palpable than visible,
and is easy to obliterate difficult to obliterate
(though in severe TR with
high RV pressure, considerable
pressure is needed to obliterate
the v wave needed)
Ascents and descents The descents are equally The ascent or upstroke is
impressive or more impressive impressive, the descent or
downstroke is unimpressive
Associated features PAH, PS, TR, RVH, RV failure AR, hyperkinetic states
As a first step, one must differentiate arterial pulsations from venous

pulsations in the neck (Table 14.3).
In general, if the pulsations in the neck are prominent and none of the
peripheral arterial pulses are impressive, venous pulsations are likely.
EVALUATION
The following features have to be noted in the jugular venous pulse for optimal
clinical information:
1. Level
2. Wave pattern
3. Respiratory variation in level and wave pattern
4. Hepatojugular reflux
5. Venous hum
6. Liver size and pulsations.
Level
Any measurement requires a point to start with and a point to end at. The starting
point or the venous pressure is the centre of the right atrium. This is called the 231
phlebostatic axis. The upper level of the venous column in the neck is the end
point of venous pressure. By its intrathoracic location, the centre of the right
atrium is not available for any direct measurement.
Fig. 14.3: Technique of measurement of jugular venous pressure

(Height of JVP=Height of venous column of sternal angle (SA) + 5 cm)
In an adult with anatomically normal chest, the sternal angle or angle of

Louis is found to be 5 cm above the centre of the right atrium.
Technique of measurement of jugular venous pressure (Fig. 14.3): The jugular
venous pressure (JVP) corresponds to the vertical height of the venous column
from the centre of right atrium. Since the angle of Louis has a fixed relationship
with the centre of right atrium, this landmark is used for measurement. The vertical
height of the venous column can be measured either in the sitting position, if it is
elevated, or in a semi-reclining position. In supine position, the upper level of the venous
column is usually not seen, but the wave forms are best seen in this position.
As the sternal angle is readily available, all measurements of jugular venous
pulse can be made starting from that point; adding 5 cm gives the total right atrial
pressure. The sternal angle is available in all positions of the body. However,
the upper level of the venous column is not available either in sitting or supine
positions. In normal persons, in sitting position it is below the clavicle, and
therefore cannot be seen. In supine position, the whole column moves beyond
the angle of the jaw into the intracranial cavity and cannot be reached. (Since the
232 whole column becomes horizontal, vertical height cannot be measured). To bring
up the venous column from below the clavicle in the sitting patient, the patient is
positioned at an approximate angle of 45 degrees on the bed. The angle should
be subtended between the trunk and the bed, not at the neck. The neck and trunk
should be in the same line. There is nothing sacrosanct about this angle as any
angulation which permits viewing of the upper level of the venous column is
appropriate. Two horizontal lines are drawn, one from the sternal angle and the
other from the upper level of the venous column (in relation to the floor), and
the vertical measurement between these lines is noted. If the venous column is
seen above the upper border of the clavicle in sitting or standing position, direct
vertical measurement from the sternal angle can be made and no horizontal line
need be drawn. The jugular venous pressure is expressed as the number of cm
above the sternal angle. The total pressure in the right atrium is obtained by adding
5 cm to it. Normal measurement does not exceed 4 cm above the sternal angle,
hence it is hardly seen above the clavicle. By way of conversion, 1.3 cm column
of water or blood is equal to 1 mmHg. Normal right atrial mean pressure does
not exceed 7 mmHg (or 9 cm of jugular venous pressure by blood).
Normally the height of a and v waves is clearly seen and measured. Usual
bedside assessment of JVP does not clearly indicate the mean pressure of the
right atrium and only an approximation can be made.
The easiest way to detect an elevated JVP is to ask the patient to sit or stand,
and if the venous column cannot be seen above the upper border of the clavicle,
the JVP is not elevated. The internal jugular vein, between the two heads of the
sternomastoid, should be used for measurements and the external jugular veins
should be used only when they are pulsatile. The jugular venous pressure may be
elevated when there is elevation of right ventricular end diastolic pressure, tricuspid
stenosis, superior vena cava obstruction, compressive pericardial disorders or
circulatory overload as in renal failure.
Causes of elevated JVP: The causes of elevated jugular venous pressure are:
• Superior vena cava obstruction
• Right ventricular failure due to any cause
• Tricuspid stenosis/regurgitation
• Pericardial compression (constriction/tamponade)
• Circulatory overload
• Renal failure 233
• Excessive fluid administration
• Atrial septal defect with mitral valve disease
Except in the setting of superior vena cava obstruction, all conditions
producing elevated jugular venous pressure give rise to pulsations in neck veins.
Rarely, in situations where jugular venous pressure is markedly elevated without
associated tricuspid regurgitation, pulsations may be absent. Though superior
vena cava obstruction is the most common cause of pulseless elevation of
jugular venous pressure, cardiac tamponade and severe constrictive pericarditis
may occasionally present in the same way. The causes of elevated JVP with little
or no pulsations are:
No pulsations
• When external jugular veins are used
• Superior vena cava obstruction
Little or no pulsations
• Acute severe cardiac tamponade
• Severe constrictive pericarditis
In the clinical settings described above, there may be two problems:

1. The venous pulsations may be difficult to discern,
2. The elevation of jugular venous pressure may be missed for the same reason.
Wave pattern
The normal jugular venous pulse consists of two positive waves or ascents and
two negative waves or descents. The best way to identify them would be to
simultaneously auscultate and observe the wave pattern. Position the patient in
such a way that the wave pattern is clearly seen. If the JVP is elevated, check
pulse in the sitting position. If there is no rise in JVP, inclination of about 45
degrees brings out the venous column and wave pattern. Though the a wave in
the jugular venous pulse occurs before the first heart sound, in actual appreciation
by the bedside, the a wave appears to occur along with S1. This is due to the
time delay between atrial contraction and transmission of the wave into the neck
and also the intrinsic delays with left and right sided events. In fact, if the a wave
appears to occur well before S1, the P-R interval is prolonged as in first degree
heart block. The descent that follows S1 is x descent and v wave coincides with
234 S2. The y descent follows the S2. In individual patients either the ascents or the
descents are impressive. One can use either the wave or the descent to identify the
pattern. As an example if the y descent is detectable the wave that precedes this
must be the v wave and the wave that precedes the x descent must be the a wave.
In the normal jugular venous pulse, the a wave (due to active atrial contraction)
is sharper and more prominent than the v wave (due to passive atrial filling). One
must practice looking at the jugular venous pulses of as many normal people as
possible to attain proficiency. The y descent is more prominent than the x descent
in normal people.
Abnormalities of a wave
These are either absence of a wave or exaggerated a waves. Absence of a wave is
a feature in atrial fibrillation as there is no effective atrial contraction. Absence
of a wave also occurs in sinus rhythm immediately after electrical conversion of
AF to sinus rhythm as a temporary phenomenon till mechanical activity of the
atrium is restored.
In the presence of sinus rhythm with the normal sequence of atrial and
ventricular contraction, a prominent a wave occurs when the tricuspid valve is
obstructed as in tricuspid stenosis, or when the right atrium contracts against a
ECG
PHONO
S4 S1
S2 S4 S1
A V A
X X
Y
JUGULAR
Fig. 14.4: JVP – prominent ‘A’ wave
non-compliant right ventricle as in a severe concentric right ventricular hypertrophy

(Fig 14.4). Concentric hypertrophy of right ventricle occurs in either significant
pulmonic stenosis or pulmonary arterial hypertension. In the absence of pulmonic
stenosis or pulmonary arterial hypertension, it may be due to right ventricle
cardiomyopathy or severe septal hypertrophy as in asymmetric septal hypertrophy. 235
Acute reduction in right ventricle compliance may also occur as in right ventricle
infarction in association with inferior myocardial infarction. In the presence of
severe aortic regurgitation and a collapsing arterial pulse, the transmitted c wave
may be sharp and may simulate a prominent a wave.
When the sequence of atrial and ventricular contraction is disturbed as in
atrioventricular dissociation due to any cause (such as, complete heart block,
classic AV dissociation or ventricular tachycardia), the atrium may contract against
closed tricuspid valve. Normally, the main force of atrial systole is expended in
distending the ventricle and part of the atrial energy is wasted away into the neck
veins as a wave. (The main purpose of the atrium is filling the ventricle and not
production of an a wave!) In situations where the tricuspid valve is closed at the
time of atrial contraction, all the atrial energy is ‘wasted’ away into the neck veins
as a very prominent a wave and is called the cannon wave. In all the conditions with
A-V dissociation the P-R interval varies unexpectedly and irregular cannon waves
occur. But when the atrium and ventricle are simultaneously activated by a focus
in the A-V junction as in junctional rhythm, a regular cannon wave occurs. When
the P-R is longer than 0.21 seconds, (first degree heart block), the a wave can be
appreciated well in advance of first sound.
The causes of a prominent a wave are resistance to right atrial emptying at tricuspid
and right ventricle level.
• Tricuspid level
Tricuspid stenosis
Right atrial tumours
• Right ventricular level: Severe concentric right ventricular hypertrophy
due to
Severe pulmonary hypertension with intact interventricular septum
Right ventricular cardiomyopathy
Asymmetric septal hypertrophy as in hypertrophic cardiomyopathy
Severe aortic stenosis with septal hypertrophy as part of symmetric
left ventricular hypertrophy
Acute tricuspid regurgitation
The causes of cannon waves are:
Regular cannon waves (Fig. 14.5)
236 • Junctional rhythm
• Ventricular tachycardia 1:1 retrograde conduction
• Isorhythmic AV dissociation
Fig. 14.5: JVP – regular cannon a waves: Regular cannon waves (C) are seen with junctional
rhythm with 1:1 retrograde atrial activation (P’)
ECG
Fig. 14.6: JVP – irregular cannon a waves: Irregular cannon waves associated with complete
heart block. Corresponding first heart sound (S1) is louder due to short P-R interval
Irregular cannon waves (Fig. 14.6)

• Ventricular tachycardia 237
• Ventricular ectopy
• Ventricular pacing
• Classic AV dissociation
The causes of absent a waves are:
• Atrial fibrillation
• Post-DC conversion of atrial fibrillation
• Sinoventricular conduction in hyperkalemia
The situations in which a single wave occurs are:
• Heart rates above 120/minute
• Severe tricuspid regurgitation with obliteration of x descent
• Chronic tricuspid regurgitation
• Acute tricuspid regurgitation
When the heart rates are beyond 120/minute, a and v waves merge together to
produce a single wave and the details of wave pattern are difficult to discern. The
a and v will also be difficult differentiate one from each other when the x descent
is obliterated as in early v wave of severe chronic tricuspid regurgitation or in
acute tricuspid regurgitation due to infective endocarditis. In the latter situation

the heart rates are often beyond 120/min.
Abnormalities of x descent
Normally during x descent, the atrial pressure is falling due to relaxation of the
atrium and also descent of the atrioventricular septum. If for some reason the
atrial pressure fails to fall, the x descent gets obliterated (Table 14.4). If there is
no atrial contraction, there is generally no x descent, as in atrial fibrillation. As the
descent of atrioventricular septum also contributes to x descent, occasionally an
x descent may be seen or recorded in spite of atrial fibrillation. This is more likely
in patients with constrictive pericarditis dominantly involving the atrioventricular
groove. The x descent may be obliterated in tricuspid regurgitation. The influencing
factors are severity of tricuspid regurgitation, size of the right atrium and whether
the tricuspid regurgitation is acute or chronic. The more severe the tricuspid
regurgitation, the smaller the RA, the earlier the v wave obliterates the x descent.
In acute tricuspid regurgitation, in addition to the above features there is sinus
tachycardia above 120/minute, merging the a wave with the v wave. An exaggerated
238 x descent may be seen in constrictive pericarditis.
Abnormalities of v wave
The v wave reflects the filling pattern of the right atrium and depends on the
venous return through the venae cavae. If there is any exaggerated filling of
right atrium as in all conditions where the venous pressure is high (such as, right
ventricle failure or constrictive pericarditis) or when there is more than one source
for the right atrium to fill, as in tricuspid regurgitation from the right ventricle,
ASD from the left atrium and ASD with mitral regurgitation when the left atrial
systolic v wave is transmitted into the right atrium and neck veins, then the v wave
will be prominent.
Table 14.4: Abnormal x descent
Absent x descent Atrial fibrillation

Severe chronic tricuspid
regurgitation
Acute tricuspid regurgitation
Constrictive pericarditis
Prominent x descent Cardiac tamponade
Fig. 14.7: Ventricularisation of v wave with obliteration of x descent due to

severe tricuspid regurgitation
The most prominent v waves occur in tricuspid regurgitation with a surging

and expansile wave in the neck. The prominent v wave in the neck is accompanied
by a systolic impulse over the liver. The presence, absence and amplitude of the
v wave depends on the severity of tricuspid regurgitation, and the size of the
right atrium. A mild tricuspid regurgitation may exist without any significant
change in right atrial pressure and thereby no v wave may occur. Significant
tricuspid regurgitation may occur into a large accommodative right atrium without 239
much alteration in right atrial pressure (Fig. 14.7). Lesser degrees of tricuspid
regurgitation may produce significant rise in right atrial pressure and prominent
v wave when the right atrium is relatively small and non-accommodative. With
high right ventricle pressure and severe tricuspid regurgitation, the systolic right
ventricle pressures may be transmitted across the peripheral veins and may produce
unusual phenomena like pulsatile exophthalmos with each v wave and palpable
venous pulse simulating a collapsing pulse at the brachial or femoral pulses. In
such states the v wave may measure as much as 60 mmHg and is difficult to
obliterate in the neck.
Table 14.5: Abnormal v waves
Prominent v wave Right ventricular failure

Tricuspid regurgitation
Atrial septal defect
Atrial septal defect with mitral regurgitation
Ventricular septal defect of left ventricle to right atrial
communication (Gerbode’s defect)
Diminished v wave Hypovolemia
Venodilators (nitrates)
Abnormalities of y descent
During y descent the atrial pressures are falling and the ventricular pressure is rising.
All abnormalities related to atrial emptying or ventricular filling should naturally
influence the y descent (Table 14.6). The y descent is more rapid than normal in all
conditions where the preceding v wave is prominent as in tricuspid regurgitation,
heart failure or constrictive pericarditis (Fig. 14.8). A slower y descent occurs in
tricuspid stenosis due to the difficulty in atrial emptying. The y descent is reduced
or absent in pericardial tamponade as the high intrapericardial pressure does not
allow ventricular filling. The auscultatory equivalent of a rapid y descent in the
neck is a right sided third heart sound, of the slow y descent the tricuspid diastolic
murmur and of no y descent, absent third heart sound in spite of elevated jugular
venous pressure as in pericardial tamponade. The slow y descent of tricuspid
stenosis is not easily detected by the bedside, as this is a difficult sign to quantify.
In patients with elevated JVP and prominent v wave often the most impressive
feature in the JVP is the rapid y descent. An unimpressive y descent in the face of
elevated jugular venous pressure is suggestive of slow y descent (Fig. 14.9).
240
ECG
Fig. 14.8: JVP – constrictive pericarditis. JVP wave pattern showing prominent x and
y descents. Both a and v wave are prominent, and are equal in height.
ECG
Fig. 14.9: JVP – tricuspid stenosis. JVP wave pattern showing prominent a waves
and slow y descent. 241
Venous hum
The normal flow of blood across normal veins in the neck is noiseless. However,
when there is increased velocity of flow (hyperkinetic states such as thyrotoxicosis)
or diminished viscosity of blood (as in anemia) there occurs a continuous bruit
over the neck veins. This is called venous hum (Fig. 14.10). In the supine position,
with the veins distended there is little or no turbulence, and therefore no hum
is heard.
Table 14.6: Abnormal y descent
Rapid y descent All causes of prominent v wave

(Correlates with RV S3) Right ventricular failure
Atrial septal defect with mitral regurgitation
Ventricular septal defect of LV to RA type
Slow y descent Tricuspid stenosis
(Absent S3) Pericardial tamponade (y descent may be absent)
Tension pneumothorax
Fig. 14.10: Continuous murmur of venous hum
In a sitting patient with the bell of the stethoscope lightly applied at the
base of the neck between the two heads of the sternomastoid, the venous hum
can be heard as a continuous murmur. The hum disappears by interrupting the
venous flow (by pressure above the stethoscope). The venous hum is normally
heard in the majority of children and also during pregnancy. The presence of a
venous hum in adults, is generally abnormal. It occurs in hyperkinetic circulatory
states like anemia or thyrotoxicosis. It also occurs in intra cranial or head and
neck arteriovenous fistulas. If a venous hum is heard in an adult in the absence
of anemia, one should check for thyrotoxicosis. In a child with congestive heart
failure and a high volume arterial pulse, look for a bruit over the head and a venous
242 hum in the neck to rule out an intracranial arteriovenous fistula.
The causes could be physiological or pathological (Table 14.7).
An audible venous hum in the presence of congestive heart failure should
suggest the possibility of hyperkinetic state like severe anemia or thyrotoxicosis
with heart failure. Intra cranial arteriovenous fistula is a rare but important cause
of heart failure in infancy. A cervical venous hum with high volume arterial pulse
and bruit over the skull suggest the diagnosis.
Table 14.7: Causes of venous hum
Physiological Children
Pregnancy
Normal adults (rarely)
Pathological Hyperkinetic states
Anemia
Thyrotoxicosis
Beriberi
Intracranial arteriovenous fistula
Compression of jugular vein by fascia, or
bony structures in the neck
Respiratory variation
Normally during inspiration venous return to the right side of the heart increases.
However, this is accommodated by the inspiratory decrease in pulmonary vascular
impedance. As a result the pulmonary artery, right ventricle and right atrial
pressures fall in spite of increased venous return. During expiration the lungs are
squeezed of their air and the pulmonary circulation is compressed by the thoracic
cage increasing the pulmonary impedance and pressures. As a result the venous
column rises during expiration and falls during inspiration. In conditions where the
increase in venous return of inspiration cannot be translated as more pulmonary
filling, inspiratory filling of neck veins occurs. This is called Kussmaul’s sign and
occurs in constrictive pericarditis, restrictive cardiomyopathy, tricuspid stenosis, or
severe right ventricular failure itself. In many of these patients the venous column
is beyond the angle of the jaw and is not easily available. In these conditions with
inspiration, the wave pattern appears exaggerated while there is no obvious and
discernible change in venous pressure as it is already very high. Conversely with
expiration the venous wave undulations appear diminished.
Hepatojugular reflux 243

When the venous return is increased to the right ventricle, it readily accommodates
it and translates it as more output into the lungs and there is only a transient rise in
pressure. Abdominal compression increases venous return further and results in
only a transient rise in jugular venous pressure with the right ventricle emptying
the veins in the next few beats. In the presence of right ventricular dysfunction,
abdominal compression results in a longer duration of pressure rise (Fig. 14.11).
Fig. 14.11: Increase in RA pressure with abdominal compression: hepatojugular reflux

As a guideline a 10 second abdominal compression results in rise in JVP that

lasts less than 10 seconds; if it persists for more than 15 seconds it is suggestive of
right ventricle dysfunction. It may be the earliest sign to appear in right ventricle
dysfunction, occult constrictive pericarditis or tricuspid stenosis. Recent studies
demonstrated a good correlation between positive abdomino-jugular reflux and
increased pulmonary capillary wedge pressures (Fig. 14.12).
Liver pulsations
The liver should be considered an extension of the right atrial cavity. It generally
reflects the jugular venous pressure rise by enlargement, and jugular venous
pulsations like a, v waves and rapid y descent are easily evident over the liver. Due
to the further delay of events from the RA to the liver, the pre-systolic wave or
a wave seem to appear immediately after the first heart sound, and the systolic
wave or v wave slightly later, after the second heart sound. The y descent in the
neck and rapid outward filling of the right ventricle in the parasternal region (third
heart sound) coincide with inward movement of the liver. In an infant, the liver
is the only guide to the recognition of elevated right atrial pressure as the JVP is
244 difficult to delineate.
JVP IN SPECIFIC DISEASES

1. Jugular venous pulse in superior vena cava obstruction: In superior vena cava
obstruction, the level is elevated usually above the angle of the jaw and the
Fig. 14.12: Correlation between abdominal compression and pulmonary wedge pressure
pulsations are absent. The liver is not enlarged. A severely elevated jugular venous
pressure without pulsations is often missed, unless one carefully looks for it. The
associated edema of the neck makes it more difficult to elicit this sign.
2. Jugular venous pulse in tricuspid stenosis: In tricuspid stenosis, the findings
depend upon the severity of tricuspid stenosis, the rhythm, the volume status of
the patient (diuretic therapy) and associated lesions (Table 14.8).
Elevated jugular venous pressure in a patient with mitral stenosis, with no
significant dyspnea or PND, could indicate associated tricuspid stenosis.
3. Jugular venous pulse in tricuspid regurgitation: The jugular venous pulse
appearance in tricuspid regurgitation depends on the severity of tricuspid
Table 14.8: JVP in tricuspid stenosis
Level Elevated or normal Obstruction to tricuspid valve.

The level of JVP is a reflection of
the severity of TS and the volume
status. The level may be normal in
mild TS or even with moderate TS
on diuretics.
Wave pattern 245
a wave Prominent and can reach as Obstruction to pre-systolic atrial
high as 30 mmHg equaling emptying due to tricuspid stenosis.
RV systolic pressure Longstanding TS elicits right
(giant a wave) atrial hypertrophy and dilatation
increasing the force of contraction
against narrow tricuspid valve. Most
of the atrial energy is wasted away
into the neck veins. Pre-systolic
hepatic impulse is common.
x descent Normal and consistent with Obliterated only when atrial
large a wave fibrillation develops late in the
disease
v wave Normal and consistent with Filling of obstructed RA will
the degree of JVP elevation result in larger v wave than
normal, but is always less than
a wave. Once AF sets in, v wave may
be the only positive wave
y descent Slow y descent Obstruction to right atrial
emptying. Rapid y descent excludes
TS, but this sign is unreliable in
actual practice
Table 14.9: Jugular venous pulse in tricuspid regurgitation
Feature Findings Mechanisms/significance

Level Normal or elevated Right ventricular failure
Wave pattern
a wave Prominent with PAH or acute Severe PAH with non-compliant
organic TR. a wave may RV
merge with v wave with
severe tricuspid regurgitation
x descent Preserved with milder or Obliteration of x descent occurs
chronic TR or larger RA with severe TR or smaller RA or
Obliterated with severe TR acute TR
and smaller RA or acute TR
v wave Can be very prominent or Large v wave with severe TR,
normal Smaller RA and acute TR. Small
or no v wave with milder TR,
larger RA or chronic TR
y descent Steep and impressive Rapid filling of RV
Slow with associated TS Slower filling of RV
h wave Can be prominent, can be Occurs after the rapid filling wave
mistaken for a wave in RV and may be reflected into RA
246
regurgitation, the size of right atrium, the systolic pressure in right ventricle, and
the mode of onset of tricuspid regurgitation (acute or chronic) (Table 14.9).
The more severe abnormalities are seen with more severe tricuspid
regurgitation, smaller right atrium, and higher right ventricle systolic pressure.
The H wave can be mistaken for an a wave, and may be the source for
confusion in patients with atrial fibrillation.
4. Jugular venous pulse in pulmonic stenosis: The findings depend on the severity
of pulmonic stenosis, the presence or absence of right ventricular failure, and the
associated lesions (Table 14.10).
Pure pulmonic stenosis is often mistaken for small ventricular septal defect
and tetralogy of Fallot. The jugular venous pulse is of help in this setting. If
jugular venous pressure is elevated and the a wave is prominent; it rules out small
ventricular septal defect and tetralogy.
5. Jugular venous pulse in mitral stenosis: The JVP in mitral stenosis depends
on the severity of mitral stenosis, degree of pulmonary arterial hypertension,
associated organic tricuspid valve disease, diuretic therapy, rhythm (atrial fibrillation
or sinus rhythm) and the presence or absence of right ventricular failure. Mild
mitral stenosis with no pulmonary arterial hypertension and sinus rhythm will
show normal jugular venous pressure (Table 14.11).
Table 14.10: Jugular venous pulse in pulmonary stenosis
Features Findings Mechanisms/significance

Level Normal or elevated with right Elevated JVP usually means
ventricular failure RV systolic dysfunction
Wave pattern
a wave Prominent with severe PS Elevated JVP favours intact
can be ‘jumping’ ventricular septum,
tetralogy is unlikely.
x descent Normal, or may be obliterated Hypertrophied, small cavities,
with severe TR non-compliant right ventricle
v wave Normal, may be increased with Severe TR results in early
Right ventricular failure filling of RA
y descent Normal, or rapid with right Increased atrial filling
ventricular failure or TR
Table 14.11 Jugular venous pulse in mitral stenosis 247

Features Findings Mechanisms/significance
Level Normal or elevated Elevated with
Right ventricular failure
Associated organic tricuspid disease
Associated atrial septal defect
(Lutembacher syndrome)
Wave pattern
a wave Normal or prominent Prominent a wave with
Tight mitral stenosis with severe PAH
Associated TS
Associated ASD
x descent Normal or obliterated Absent with
Atrial fibrillation
Severe TR
v wave Normal or prominent Prominent with
TR
y descent Normal or rapid or slow Rapid with right ventricular
failure, TR
Slow with associated TS
The most impressive of jugular venous pulse features are seen with severe
mitral stenosis, severe pulmonary arterial hypertension, severe functional tricuspid
regurgitation and right ventricular failure. The v wave in some patients can be
so prominent that it is mistaken for an arterial pulse. Rarely, the v wave can be
transmitted to the more peripheral pulses veins like femoral veins. The earlobe
may move with each v wave and pulsatile exophthalmos may be seen in some
patients with severe tricuspid regurgitation.
6. Jugular venous pulse in mitral regurgitation: The jugular venous pressure in
mitral regurgitation depends on the presence or absence of pulmonary arterial
hypertension, size of the left atrium, right ventricular failure, cause of mitral
regurgitation, rhythm of the heart, associated organic tricuspid valve disease or
Table 14.12: Jugular venous pulse in mitral regurgitation
Feature Finding Mechanism/significance

Level Normal or Elevated JVP with
elevated PAH and right ventricular failure
Associated ASD
Organic TVD
248 RV infarct in mitral regurgitation of CAD
Secondary MR with myocardial dysfunction
of cardiomyopathy/CAD
Wave pattern
a wave Normal or Prominent a wave with
prominent Severe pulmonary hypertension with
mitral regurgitation
Severe PAH with TR mistaken for mitral
regurgitation
Mitral regurgitation in association with
HOCM
Inferior MI, mitral regurgitation due to PMD
and associated right ventricular infarction
x descent Normal or May be obliterated with mitral
obliterated regurgitation associated with ASD
v wave Normal or Prominent with
prominent Pulmonary hypertension and right
ventricular failure
Associated tricuspid regurgitation
y descent Normal or Associated atrial septal defect
prominent Rapid y descent with any of the above
conditions
ASD. For a particular degree of mitral regurgitation, the size of the left atrium
influences the degree of pulmonary venous hypertension, which in turn is the
mediator for pulmonary arterial hypertension and the consequent right ventricular
failure (Table 14.12).
In the most common form of mitral regurgitation (rheumatic mitral
regurgitation), prominent a wave in the neck veins are always associated with
either severe pulmonary arterial hypertension, or organic tricuspid stenosis. In
mitral regurgitation associated with hypertrophic obstructive cardiomyopathy, and
papillary muscle dysfunction of inferior myocardial infarction with associated
right ventricular infarction, the a wave may be prominent without accompanying
pulmonary arterial hypertension. Though the severity of mitral regurgitation
has no direct influence on JVP, the degree of pulmonary arterial hypertension
influences it. The degree of pulmonary arterial hypertension is in turn related to
the severity of mitral regurgitation and the size of the left atrium. A smaller left
atrium even with a moderate mitral regurgitation, results in significant pulmonary
venous and arterial hypertension leading to right ventricular failure.
7. Jugular venous pulse in aortic stenosis: The jugular venous pulse in aortic stenosis
depends on the severity of aortic stenosis, presence or absence of right ventricular 249
failure, associated mitral valve disease with pulmonary arterial hypertension or
organic tricuspid valve disease.
Table 14.13: JVP in aortic stenosis
Feature Finding Mechanism/significance

Level Normal or Elevated with
elevated RVF secondary to LVF
Associated mitral stenosis, PAH and RVF
Associated organic tricuspid valve disease
Wave pattern
a wave May be prominent Prominent with
HOCM with or without associated RVOT
obstruction
Any severe AS
Associated mitral stenosis + PAH
Associated TS
x descent, v wave and Normal May be abnormal with RVF, TR,
y descent coexisting TS
The elevated jugular venous pressure in aortic stenosis usually occurs late in
the disease and carries a poor prognosis. Prominent a wave can occur in isolated
AS without any pulmonary arterial hypertension due to severe septal hypertrophy
decreasing right ventricular compliance as interventricular septum is shared by
both ventricles. In ‘fixed’ obstruction, a prominent a wave always indicates severe
aortic stenosis in the absence of associated lesions. If the a wave is prominent
with ‘mild aortic stenosis’, consider hypertrophic cardiomyopathy, associated mitral
stenosis with pulmonary arterial hypertension, or associated tricuspid stenosis. Late
in the disease with severe right ventricular failure and elevated JVP, the severity
of AS may be underestimated.
8. Jugular venous pulse in aortic regurgitation: The jugular venous pressure
in aortic regurgitation depends on the severity, presence or absence of right
ventricular failure, associated lesions at the mitral or tricuspid valve and the cause
of aortic regurgitation (Table 14.14). The commonest error in actual practice is
to mistake the c wave of carotid artifact as prominent a wave.
9. Jugular venous pulse in atrial septal defect: The determinants of jugular
venous pressure in atrial septal defect are pulmonary arterial hypertension,
250 associated left sided disease, pulmonic stenosis, right ventricular function, and the
Table 14.14: Jugular venous pulse in aortic regurgitation
Feature Significance/mechanism
Level Normal or elevated
Elevated with
RVF secondary to LVF
Associated tricuspid valve disease
Bernheim’s syndrome
Aneurysm of ascending aorta
Dissection of ascending aorta
Aortic regurgitation with CRF and fluid load
Wave pattern
a wave Normal, rarely prominent
Prominent with
Associated TS
Associated mitral stenosis and PAH
Prominent c wave due to carotid pulse simulating
a wave
x descent, v wave, y descent Depend on presence of RVF and associated lesions
Venous hum May be mistaken for the murmur of AR
cardiac rhythm. Usually a wave and the v wave tend to be equal in height but in
some patients the v may be slightly more prominent. Similarly expected slight fall
in venous pressure with inspiration may not be obvious due to phasic alterations
in left to right shunt.
Evaluation of jugular venous pulse in atrial septal defect gives important
clues as to the presence or absence of one these conditions (Table 14.15).
Table 14.15: Jugular venous pulse in atrial septal defect (ASD)
Feature Finding/significance
Level Usually normal
Elevated Mitral valve disease (Lutembacher syndrome)
Left ventricular failure ofany cause
Severe PAH with RVF
RVF due to volume load
Underlying TAPVC
Wave pattern
a wave Normal
Prominent with
Associated mitral stenosis
PAH 251
PS
x descent Normal
v wave Prominent due to overfilling of RA from venae cavae
and LA
PAH with TR
Associated mitral regurgitation
y descent Prominent with any of the above
Fig. 14.13: JVP in ASD; note the prominent v wave

In an isolated secundum atrial septal defect without pulmonary arterial

hypertension, the jugular venous pulse as a rule is not elevated and the v wave is
slightly prominent (Fig. 14.13). If the jugular venous pressure is elevated in atrial
septal defect with continuing left to right shunt, one should consider associated
mitral valve disease.
10. Jugular venous pulse in ventricular septal defect: In small to moderate ventricular
septal defects, the jugular venous pressure is normal. In large ventricular septal
defect with heart failure in infancy, the jugular venous pressure may be elevated.
In spite of severe pulmonary arterial hypertension, the a wave is generally not
prominent. In an infant, the jugular venous pulse is not easy to evaluate and the
liver size and pulsations are of use. In a patient with a long systolic murmur, the
presence of a prominent a wave supports the possibility of pulmonic stenosis
over ventricular septal defect (Table 14.16).
Elevated jugular venous pressure or congestive heart failure in ventricular
septal defect is a feature of large ventricular septal defect in infancy and is rare
in older children. If the jugular venous pressure is elevated in an older child or
adolescent, left ventricle to right atrial defect or tricuspid regurgitation due to
252 cleft leaflet (part of AV canal defect), or due to infective endocarditis should be
considered.
Table 14.16: Jugular venous pulse in ventricular septal defect (VSD)
Feature Finding /significance

Level Normal with small VSD
Elevated Large VSD with CCF in infancy
VSD with MR/TR as in AV canal defects
LV to RA communication (Gerbode’s defect)
Associated large PDA, severe AR
Wave pattern
a wave Normal
Prominent with
Severe PS mistaken for VSD
Restrictive VSD with severe PS
x descent Normal
Obliterated with TR, LV to RA defect
v wave Normal
Prominent with CCF, TR, LV to RA defect
y descent Normal
Prominent with v wave prominence
Table 14.17: Jugular venous pulse in Eisenmenger syndrome
ASD VSD PDA

Level may be elevated Usually normal May be elevated
a wave normal; absent with AF Normal May be prominent
v wave prominent with CCF or TR Normal, CCF and As in ASD
TR rare
11. Jugular venous pulse in Eisenmenger syndrome: The jugular venous pulse in
Eisenmenger syndrome gives clues to the underlying defect (Table 14.17).
In primary pulmonary arterial hypertension with right to left shunt at atrial
level, the a wave is usually prominent and the JVP is often elevated by the time
cyanosis appears. In atrial septal defect and ventricular septal defect, the a wave
is not prominent in spite of severe pulmonary arterial hypertension due to the
underlying defects permitting easy right atrial decompression. In ventricular
septal defect with Eisenmenger syndrome, elevated JVP is rare unlike the other
two defects.
12. Jugular venous pulse in congenital cyanotic heart disease: Evaluation of
jugular venous pulse gives valuable clues to the underlying defect in this set of 253
disorders (Table 14.18). Tetralogy of Fallot, or lesions with similar physiology
(non-restrictive ventricular septal defect with significant pulmonic stenosis) have
unremarkable jugular venous pulse with normal level and wave pattern.
Elevated jugular venous pressure in cyanotic heart disease usually means
either an intact ventricular septum or increased pulmonary flow or both. Rarely the
Table 14.18: Jugular venous pulse in cyanotic heart disease
TOF or TOF-like PS with intact IVS Tricuspid atresia Transposition of
physiology + Right to left atrial arteries or veins
shunt with high
pulmonary flow
(TGA, TAPVC)
Level is normal Usually elevated Elevated with Usually elevated
restrictive ASD
Wave pattern
a wave normal Prominent Prominent May be prominent
v wave normal Normal Normal Normal
y descents vary by Prominent with TR Prominent with Prominent with
the waves MR CCF or TR
Table 14.19: Causes of elevated jugular venous pressure in tetralogy of Fallot
Cause Mechanism
Anemia Volume load
Systemic hypertension Non-compliant ventricles
Biventricular failure
Infective endocarditis Aortic regurgitation
Anemia
Renal failure
Aortic regurgitation Volume load
Cardiomyopathy Ventricular dysfunction
Bronchopulmonary collaterals Volume load
Increased pulmonary flow
After systemic to pulmonary shunt Volume load
Increased pulmonary flow
Associated PDA Volume load
Adult tetralogy Myocardial dysfunction
254 jugular venous pressure may be elevated in tetralogy of Fallot due to an associated
abnormality (Table 14.19).
The wave pattern as mentioned earlier is normal in tetralogy of Fallot.
However, the a wave may be prominent in adult tetralogy, tetralogy of Fallot with
restrictive ventricular septal defect, systemic hypertension, or cardiomyopathy.
The causes of a prominent a wave in tetralogy of Fallot are:
• Adult tetralogy
• Restrictive ventricular septal defect
• Cardiomyopathy
As a general rule, some other disorder should be considered when an a wave
is prominent. Consider the following conditions when there is a prominent a wave
in cyanotic heart disease:
• Tricuspid atresia
• Pulmonic stenosis with intact ventricular septum and right to left atrial
shunt
• Total anomalous venous connection
• Pulmonary atresia with intact ventricular septum

• Adult tetralogy
• TOF with systematic hypertension
• TOF with restrictive VSD
• TOF with cardiomyopathy
In infants, the pulsations of the liver are more often used than the jugular
venous pulse and the a wave appears to occur along with or immediately after
the first heart sound.
The venous hum is uncommon in congenital cyanotic heart disease. When
present, it should raise the possibility of total anomalous pulmonary venous
connection into the superior vena cava, severe anemia or hepatic cirrhosis with
multiple microvascular pulmonary arteriovenous fistulae.
13. Jugular venous pulse in cardiomyopathies: The jugular venous pulse in
cardiomyopathies depends on whether the cardiomyopathy is dilated or restrictive
(Table 14.20).
It is often mistakenly believed that dilated or congestive cardiomyopathy
always has congestive heart failure or elevated jugular venous pressure. Congestive 255
cardiomyopathy can exist with or without congestive heart failure or elevated
jugular venous pressure. In obliterative cardiomyopathy, the a wave is often
prominent and is lost after the onset of atrial fibrillation. With severe tricuspid
regurgitation, the v wave assumes prominence. Selective prominence of either
a or v waves distinguish cardiomyopathies from constrictive pericarditis.
14. Jugular venous pulse in pericardial disease: The jugular venous pulse in
pericardial disease depends on the clinical syndrome. In pericardial effusion
without
Table 14.20: Jugular venous pulse in cardiomyopathy
Feature Dilated CM Restrictive Obliterative (EMF)

Level Normal/elevated Normal/elevated Usually elevated
Wave pattern
a wave Normal Prominent Prominent
v wave Normal/prominent Normal Prominent (TR)
x descent Normal Normal May be obliterated with
TR
y descent Normal/prominent Normal Prominent
Table 14.21: Jugular venous pulse in pericardial tamponade
Feature Finding Mechanism

Level Marked elevation Cardiac compression due to high
usually above angle of intrapericardiac pressure
jaw
Wave pattern
a wave Never prominent The atrial compression prevents
exaggerated atrial contraction
x descent Normally preserved Fall in atrial pressure due to ventricular
contraction producing descent of
atrioventricular septum
v wave Normal Atrial filling is preserved
y descent Obliterated or absent Ventricular compression due to high
intrapericardiac pressure prevents rapid
ventricular filling
Kussmaul’s sign May be present Additional venous return not admissible
due to cardiac compression
cardiac compression, the JVP is not elevated. A mere elevation of JVP is not
256
suggestive of cardiac tamponade. In cardiac tamponade, the JVP is elevated
usually above the angle of the jaw. The a and v waves are equal and the y descent
is obliterated or absent. The x descent is more prominent.
The jugular venous pressure as a rule, is grossly elevated in cardiac tamponade.
However, in low pressure cardiac tamponade, it may not be elevated due to
accompanying hypovolemia. As pericardial tamponade is not considered as a diagnosis
in the absence of elevated jugular venous pressure, one must be aware of situations
when cardiac tamponade occurs without elevated jugular venous pressure.
The causes of cardiac tamponade without elevated jugular venous pressure
(low pressure tamponade) are given in Table 14.22.
As a general rule, over a stable preexisting pericardial effusion, hypovolemia
precipitates tamponade in the above situations.
Though cardiac tamponade and constrictive pericarditis are pericardial
disorders, the jugular venous pressure is different in both these conditions, and
gives clues to differential diagnosis (Table 14.23).
The most impressive sign in jugular venous pulse in constriction is rapid
y descent with equal a and v waves. If there is a very prominent a wave or v wave,
constriction is unlikely; check for another diagnosis.
Table 14.22: Causes of low pressure tamponade
Cause Mechanism
Peri-operative tamponade Fall in venous pressure due to
venodilatation of anaesthesia, blood
loss
Postoperative tamponade Hypovolemia
During hemodialysis Hypovolemia, bleeding into
pericardium due to heparinization
Pericardial tamponade with multiple Blood loss
trauma
Selective left ventricular tamponade and Isolated compression of left
after cardiac surgery ventricle by hematoma, etc.
Diuretic therapy Hypovolemia
Table 14.23: Jugular venous pulse in constrictive pericarditis
Feature Finding Mechanism

Level Elevated, the severity of Variable degree of cardiac
elevation is related to the compression, the mildest form being 257
severity of constriction occult constriction
where the disorder is evident only after
fluid load rapidly
Wave pattern
a wave Never prominent Atrial constriction does not permit
exaggerated atrial contraction
x descent May be normal or Constriction around the AV groove
exaggerated results in excessive descent of the
AV septum
v wave Normal, usually equal to Venous return to right atrium unaffected
a wave
y descent Rapid or steep Rapid ventricular filling due to active
ventricular relaxation encouraged by spring
like pericardium. The rapid y descent
coincides with diastolic outward movement
of the precordium and pericardial knock
Kussmaul’s sign Positive Additional venous return of inspiration
is not accommodated by RV due to rigid
shield of constriction
Table 14.24: Elevated jugular venous pressure with shock
Cause Mechanism
Heart failure Ventricular or valvular dysfunction
Cardiac tamponade Cardiac compression
Right ventricular infarction Right ventricular failure
Inadequate filling of left ventricle
Acute pulmonary embolism Obstruction to pulmonary circulation
Tension pneumothorax Cardiorespiratory embarrassment
Massive pleural effusion especially bilateral Cardiorespiratory embarrassment
15. Jugular venous pulse in shock: The findings in jugular venous pulse are often
the first clue to the differential diagnosis of shock (Table 14.24). Though a
cardiogenic cause is the most likely when the jugular venous pressure is elevated,
other non-cardiac conditions can present similarly.
In actual practice, tension pneumothorax and pleural effusion are often not
considered in the differential diagnosis of shock.
16. Jugular venous pulse in arrhythmias: In the interpretation of cardiac rhythm,
258
the sequence of atrial to ventricular activity is of primary importance. The a and
v waves in jugular venous pulse correlate with the P wave and the QRS complex
in the electrocardiogram. The normal sinus rhythm is characterized by sequential
a and v waves. The a wave occurring along with the first sound is a reflection of
normal PR interval. The number of a waves and v waves is equal. Any disturbance
in this relationship is suggestive of a different rhythm. Cardiac rhythm can be
recognised by the sequence of atrial to ventricular activity, the rate, the presence
or absence of cannon waves and the correlation with auscultatory and arterial
pulse features. The value of these features are given in Table 14.25.
In a rapid regular tachycardia with wide QRS complexes, the diagnosis could
be either ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with
aberration. The presence of irregular cannon waves is virtually diagnostic of VT
rather than SVT. The patient should be positioned slightly propped up to bring
out the venous waves. Holding breath also helps in appreciation of cannon waves.
A recent study by Garratt et al showed that the variability in JVP and first heart
sound were highly sensitive and specific signs of ventriculoatrial dissociation
during tachycardia. Unlike the first heart sound and JVP, the arterial pulse was
not of much value in the diagnosis.
Table 14.25: Jugular venous pulse in arrhythmias
Rhythm A to V sequence Cannon waves Correlations

Sinus rhythm a precedes v regularly Absent S1: Constant
a occurs along with S1 S4: Regular
First degree heart a precedes v regularly Absent S1: Diminished
block a wave occurs before S1 Rarely regular cannon S4: S4-S1 interval
or even well before waves occur with long
extreme prolongation
of PR, with P wave
falling on the
preceding T wave
Wenckebach’s Gradual lengthening of Absent S1: Progressive
phenomenon A-V interval, ends with diminution in
a wave that is not intensity
followed by v or S1 with pause
Mobitz type II block Constant A-V interval, Absent Constant S1
suddenly a is not followed by
followed by v. sudden pause
2:1 ratio between
a waves and S1
Second degree AV Two a waves for one Absent. May be Constant S1
259
block v wave or S1 present if the
non-conducted P
wave falls on the
preceding T wave.
Cannon waves are 2:1.
Complete heart Variable A-V interval Present, irregular S1: Variable
block More a waves than May be absent with S4: Variable
v waves or S1 associated AF Arterial pulse
volume may vary
Junctional rhythm a occurs after S1 Regular S1: Constant
Ventricular Variable relationship Irregular S1: Variable
tachycardia Regular with retrograde Regular with constant with
atrial activation retrograde atrial retrograde atrial
conduction conduction
Arterial pulse may
vary in volume
Atrial tachycardia a to v sequence normal Absent S1: Constant
Arterial pulse
constant in
volume
DIAGNOSTIC CLUES IN PRACTICE
When checking the JVP there is nothing sacrosanct about the 45 degree
angle. The only thing about jugular venous pulse many people remember
after leaving medical school is this 45 degrees and nothing else.
Nobody’s jugular venous pulse can be measured in the supine position.
The easiest way to detect a raised jugular venous pressure is to make the
patient sit or stand and if the venous column cannot be seen above the upper
border of the clavicle, the jugular venous pressure is not elevated.
The first heart sound coincides with the a wave, and the second heart sound
with the v wave. The x descent follows the first heart sound and the y descent
follows the second heart sound.
Elevated jugular venous pressure with no history of significant dyspnea,
paroxysmal nocturnal dyspnea or orthopnea generally indicates pure right
heart failure.
In a patient with mitral stenosis, elevated jugular venous pressure, edema of
face or feet without dyspnea, PND, or orthopnea indicates associated tricuspid
260
stenosis.
Prominent a wave, slow y descent, no right ventricular impulse, no palpable
P2 indicates tricuspid stenosis.
Elevated jugular venous pressure rapid y descent, diastolic outward moment
of the whole precordium coinciding with the y descent and pericardial knock
indicates constrictive pericarditis.
Elevated jugular venous pressure but no y descent or third heart sound,
indicates pericardial tamponade.
Elevated jugular venous pressure in an atrial septal defect with large left to
right shunt (tricuspid mid-diastolic murmur) generally indicates associated
mitral valve disease.
Prominent a wave, normal y descent, sustained right ventricular impulse
palpable S4 and pulmonary arterial pulsations and P2 indicates severe pulmonary
arterial hypertension. The last two components are substituted by a systolic thrill
in the pulmonary area in pulmonic stenosis.
Elevated jugular venous pressure but no cyanosis in a patient with severe
pulmonary arterial hypertension rules out Eisenmenger syndrome. By the
time they have right heart failure, severe pulmonary arterial hypertension,
they always have cyanosis in Eisenmenger syndrome.

‘Pulseless elevation’ in level of JVP is often missed.
With extreme elevation of jugular venous pressure as in pericardial tamponade
or severe constrictive pericarditis, the very elevation of jugular venous
pressure may be missed due to unimpressive venous pulsations.
Venous hum is a valuable clinical clue to the presence of hyperkinetic
circulatory disease in adults.
Venous hum in a cyanotic patient points to the diagnosis of hepatic cirrhosis
with multiple microvascular pulmonary arteriovenous fistulae.
In a febrile patient with small or moderate VSD, elevated JVP usually indicates
infective endocarditis of tricuspid valve with TR.
An elevated JVP of more than 7 cm or a prominent abdominojugular test
have a sensitivity, specificity and predictive accuracy of about 80 per cent
for elevated pulmonary wedge pressure.
How to express findings in jugular venous pulse

If the jugular venous pulse is normal, it may be expressed as follows:
JVP, level is normal, wave pattern is normal, hepatojugular reflux is negative, 261
Kussmaul’s sign is negative and there is no venous hum.
If the jugular venous pulse is abnormal, it may be expressed as follows:

JVP, level is 8 cm above sternal angle, a wave is prominent, v is normal, y descent is
rapid. Kussmaul’s sign is negative and there is no venous hum.
15 The Cardiac Impulse

The apical impulse is the outermost, lowest point of maximal cardiac impulse. It
is formed by the region of the left ventricle adjacent to interventricular septum.
With each contraction, all the walls of the left ventricle move inward reducing the
ventricular size, except the region of the apex which rotates and moves outward
lifting the chest wall over it. The normal apical impulse comes out along with the
first sound and stays on as an outward movement as long as the ventricle ejects
blood into the aorta. The outward movement retracts from the palpating finger
262 well before the second heart sound by two-thirds of systole. The duration of
outward thrust is a reflection of the duration of left ventricular ejection. The
passive diastolic filling of the ventricle is not appreciable over the chest wall, though
it is at this time that the whole ventricular cavity is expanding to fill itself. Only
when the ventricle fills abnormally, a diastolic event is palpable. The right ventricular
events underlying the parasternal area are not palpable unless the right ventricle is
enlarged or the chest wall is very thin.
The apical impulse is usually in the 5th left intercostal space inside or at the
mid-clavicular line. It may be in the 4th intercostal space in children. In thin and
tall individuals, the impulse may be more distal (6th space) and medial. In obese
people with elevated diaphragm, the impulse may be displaced laterally. Normally
it is within 10 cm of the mid-sternal line or 8 cm from the left sternal edge. The
normal impulse does not exceed 2.0–2.5 cm in diameter and is never felt in more
than one intercostal space. The amplitude of excursion of the impulse is greater in
thin persons as a normal variant. The normal impulse is only a gentle tap but no
objective measurements are available. Clearly exaggerated amplitude of excursion
is easily made out. The amplitude of excursion of the impulse is exaggerated in
volume loaded and hyperkinetic circulatory states but the duration of the impulse
THE CARDIAC IMPULSE
Table 15.1: Normal cardiac impulse

Feature Description
Site of impulse Fifth space, at or inside mid clavicular line,
10 cm or less from mid-sternal line
Size of impulse Less than one and half rib spaces or not more
than 2–3 cm
Amplitude of excursion No objective measurement available
Comparison to the experience of normal
Duration of impulse Less than 50% of systole
Palpable sounds and murmurs No sound or murmur is palpable over a
normal apical impulse
Retraction of apical impulse The events at apex may not represent left
ventricle
is normal. In the majority of adults, the impulse is difficult to palpate. Therefore,

a clearly palpable cardiac impulse in a thick chested adult generally indicates cardiac
enlargement.
RECORDING THE PRECORDIAL IMPULSE 263
The normal apexcardiogram consists of a broad systolic upstroke (Fig. 15.1). The
rapid filling wave (rfw) corresponds to the third heart sound. There is a small a
wave corresponding to atrial contraction. In situations where fourth heart sound
is heard, the height of the a wave increases. Point o corresponds to opening of the
mitral valve.
ECG
S1 S2 S3
PHONO e
a
sf
rf
ACG
o
Fig. 15.1: Normal apexcardiogram
S1: first heart sound, S2: second heart sound, S3: third hear sound, ACG: apexcardiogram,
ECG: electrocardiogram, Phono: phonocardiogram, a :atrial contraction,
o: opening of mitral valve, rf: rapid filling wave, sf: slow filling wave.
Table 15.2: Information obtainable from precordial palpation

Information Observation
Ventricular enlargement RV or LV enlargement
(lateralization of heart lesion)
If ventricle is enlarged, Volume load or
Pressure load
Abnormalities of systolic emptying Sustained impulse (pressure load)
Systolic thrill across ventricular outflow
Abnormalities of diastolic filling of the Palpable third sound
ventricles Palpable fourth sound
Diastolic thrill at apex/tricuspid area
Ventricular dysfunction Dilatation
Sustained impulse
State of great vessels Palpable vessel + palpable sound
(dilatation + high pressure)
Impalpable vessel + thrill
(Outflow obstruction)
Mediastinal shift due to lung disease Displacement of apical impulse
Dextrocardia To determine which side the heart is located
264
Left ventricular enlargement could be due to

• Volume load
• Pressure load
• Combined volume and pressure load
• Coronary artery disease with
• Cardiomyopathy or Myocarditis
Hyperkinetic apical impulse (or forcible impulse)

In volume overload states due to increase in preload and decrease in afterload the
extent of myocardial fibre shortening is increased. The apical impulse is then
exaggerated in its amplitude of excursion. This type of impulse is characteristic of
volume overload states like aortic regurgitation, mitral regurgitation and all other
hyperkinetic states (Fig. 15.2). The duration of the impulse is the same as that of
the normal impulse. There is no objective method of measuring the amplitude of
excursion of the impulse.
THE CARDIAC IMPULSE
PHONO
ACG
ECG
Fig. 15.2: Hyperdynamic apical impulse with rapid filling wave in MR
Sustained apical impulse

When the impulse stays on as an outward movement after the 50 per cent of
systole or nearer to the second heart sound, it is called a sustained impulse. The
duration of the impulse is a reflection of the duration of the left ventricular ejection 265
(Fig. 15.3).
It is best appreciated by simultaneous auscultation and palpation. Pressure
overload of the left ventricle as in severe aortic stenosis or longstanding severe
systemic hypertension are usually responsible for a sustained impulse.
Table 15.4: Causes of volume overload to the left ventricle
Mechanism Disease
Valvular regurgitations Mitral regurgitation
Left to right shunts (post-tricuspid) Ventricular septal defect
Systemic to pulmonary artery shunt
(Blalock–Waterston)
Hyperkinetic circulatory states Anemia
Thyrotoxicosis
Pregnancy
Beri-beri
PHONO
ACG
ECG
Fig. 15.3: Sustained apical impulse in aortic stenosis
266 Severe volume overload, severe left ventricular dysfunction due to any
condition or a dyskinetic impulse as in coronary artery disease, may also produce
a sustained impulse. With severe left ventricular enlargement the normal elliptical
left ventricle becomes spherical. This may result in a sustained impulse even up to
the second heart sound.
Systolic retraction of apical impulse

As the apex is formed by the interventricular septum adjacent to the left ventricle,
the motion of the interventricular septum naturally influences the apical impulse.
The normal interventricular septum behaves as if it is a part of the left ventricle
and the normal outward apical impulse in systole occurs. In conditions with right
ventricular volume load as in atrial septal defect, tricuspid regurgitation or
pulmonary regurgitation the interventricular septum behaves as if it is a part of
the right ventricle and this anterior motion of the interventricular septum is called
paradoxic septal motion in the echocardiogram. When the interventricular septum
moves along with the right ventricle anteriorly, the apex retracts in systole and
moves out in diastole. This apical retraction is the palpable equivalent of paradoxic
septal motion in the echocardiogram.
THE CARDIAC IMPULSE
ECG S2 K
S1 S1 S2 K
PHONO OM
ACG
SYSTOLIC RETRACTION
Fig. 15.4: Apexcardiogram of constrictive pericarditis

S1: first heart sound, S2: second heart sound, K: pericardial knock,
OM: opening of mitral valve.
The most prominent event in constrictive pericarditis is the rapid ventricular

filling. This is appreciated all over the precordium, including the apex. It coincides
with the pericardial knock on auscultation and the rapid y descent in the jugular
venous pulse (Fig. 15.4).
On simultaneous auscultation and palpation, the impulse comes out following
the second heart sound and moves in following the first heart sound. Unless
267
carefully looked for, this is often mistaken for systolic impulse and some other
diagnosis is considered. This most prominent impulse is seen and felt over the left
parasternal area.
In the presence of apical retraction any significant left ventricular enlargement
is unlikely.
Location of the apical impulse in left ventricular enlargement

In concentric hypertrophy of pressure-loaded states the impulse is not displaced
significantly and may stay the same place, that is, the 5th space. In moderate to
severe volume-loaded states, the impulse is always displaced downwards and
outwards. Apical displacement may be due to non-cardiac disease. In such a case
the impulse is neither hyperkinetic nor sustained. An enlarged left ventricle produces
a larger impulse that is more than 2 cm or more than one rib space. But if the
chest wall is thick or deformed or with obstructive lung disease the impulse may
not be palpable in spite of enlargement of the left ventricle. In other words, in
these situations even if the impulse is just palpable it may indicate enlargement.
A very large left ventricle may in rare cases, produce a left parasternal impulse.
Localized versus diffuse apical impulse

The term diffuse apical impulse is applicable to the situation when severe right
ventricular enlargement results in the right ventricle forming the apex with the
point of maximal impulse at the parasternal area. The apical impulse in this situation
is diffuse and non-localizable. The severe left ventricular enlargement in chronic
severe AR or MR or heart failure produce a larger apical impulse but is still localized
by definition. This impulse should not be termed diffuse.
Table 15.5: Major types and causes of apical impulse
Type of impulse Cause

Tapping impulse Normal impulse with loud S1
Mitral stenosis
Hyperkinetic or forcible impulse Hyperkinetic states
Anemia
Thyrotoxicosis
Pregnancy
Regurgitant lesions
268 Aortic regurgitation
Sustained impulse Pressure loads
Aortic stenosis
Severe volume loads
Severe aortic regurgitation
Severe MR with left atrial lift
LV aneurysm
Apical infarct or aneurysm
Severe LV dysfunction
Severe LV dysfunction due to any
cause with low ejection fraction
Cardiomyopathy (dilated)
Myocarditis
Systolic retraction Constrictive pericarditis
RV volume load
Pulmonary regurgitation
THE CARDIAC IMPULSE
Left ventricular wall motion abnormalities in coronary artery disease

Normally except the region of the apex, all the other walls of the left ventricle
move inwards to generate pressure inside the chamber. When any of these regions
is ischemic or infarcted or thinned and fibrotic, a systolic outward lift may occur
in the region between the apex and the left parasternal area (ectopic area). If the
region of the apex is involved, a larger and longer impulse may occur simulating a
pressure overload. This palpable dyskinesia may occur during ischemia or infarction.
If in a patient with chest pain, the impulse appears along with pain but disappears
after the subsidence of pain it is diagnostic of myocardial ischemia which must be
causing the chest pain. When recognized, its clinical significance cannot be
overemphasized. Palpable dyskinetic segment over precordium during angina has
more diagnostic value than an exercise test or coronary angiogram, as a coronary
angiogram can only reveal an anatomical obstruction but fails to predict whether
the patient’s chest pain is related to the lesion at hand. In adults (over 40 years),
the cardiac impulse is generally difficult to palpate. In these patients, any such
palpable impulse should not be ignored.
Palpable diastolic events at the apex 269

Palpable third heart sound: Normally the diastolic filling of the ventricle during
the rapid filling phase and pre-systole are not visible or palpable. When the rapid
filling of the ventricle is exaggerated, it results in an abrupt and prominent diastolic
wave following the second heart sound and can be seen and palpated. It is normally
appreciable in childhood and pregnancy but in adults this generally indicates either
a volume-loaded state (mitral regurgitation/aortic regurgitation), hyperkinetic state
(anemia) or ventricular failure (Table 15.6). The most prominent rapid filling wave
Table 15.6: Palpable rapid filling wave (third heart sound)
Apex (left ventricle) Parasternal area (right ventricle)

Physiological
Children
Pregnancy
Pathological
Left ventricular failure Right ventricular failure
Mitral regurgitation Severe tricuspid regurgitation
Hyperkinetic states Pericardial knock
Anemia
Thyrotoxicosis
Table 15.7: Palpable a wave (pre-systolic impulse)

Apex (left ventricle) Parasternal area (right ventricle)
Hypertrophic cardiomyopathy Severe pulmonary hypertension of any cause
Aortic stenosis Pulmonic stenosis (severe)
Coronary artery disease, acute or chronic Cardiomyopathy
Acute aortic regurgitation Right ventricular infarction
Acute mitral regurgitation Acute tricuspid regurgitation
(third heart sound) is appreciated in severe mitral regurgitation and constrictive

pericarditis. In constrictive pericarditis the only outward impulse may be this rapid
filling wave; it coincides with the pericardial knock or the third heart sound with
systolic retraction of the whole precordium.
Pre-systolic impulse
The pre-systolic atrial contraction distending the ventricle is never palpable in
health but may become palpable when the ventricle is non-compliant due to
hypertrophy or ischemia (Table 15.7). It is appreciated as an initial hesitant
270 movement of the apex before the bold, sweeping systolic impulse. The anatomical
correlate of this is a ventricle with severe hypertrophy and a small cavity (concentric
hypertrophy). The hemodynamic correlate of a palpable fourth heart sound is an
LV end-diastolic pressure of 15–18 mmHg (normal less than 12). Severe concentric
hypertrophy of the left ventricle occurs in severe aortic stenosis, severe systemic
hypertension and hypertrophic cardiomyopathy. In coronary artery disease either
during ischemia or an acute phase of infarction, a palpable fourth heart sound can
occur due to diastolic dysfunction leading to a non-compliant ventricle. In angina
pectoris this may appear with pain and may disappear along with subsidence of
pain. When the apical impulse is palpable, the fourth heart sound is usually palpable
as in aortic stenosis, hypertension and hypertrophic cardiomyopathy. However,
when the apical impulse is not palpable, as in the majority of patients with acute
myocardial infarction, the fourth heart sound is often not palpable, though heard.
The belief that the fourth heart sound is better palpated than heard, is based upon
the low frequency components of the sound, but this is applicable only when the
left ventricular impulse is available for palpation, as in aortic stenosis, hypertrophic
cardiomyopathy or hypertension. When the impulse is not palpable as in coronary
artery disease, the fourth heart sound is better heard than palpable. The most
THE CARDIAC IMPULSE
prominent palpable fourth heart sound occurs with hypertrophic cardiomyopathy.

Whenever the fourth heart sound or third heart sound are palpable, an AV valve
stenosis on that side of the heart is unlikely, as neither the pre-systolic impulse nor
the rapid filling of the ventricle are possible with mitral or tricuspid stenosis.
Prolonged diastolic vibrations at apex (left ventricular inflow)

This is suggestive of mitral stenosis and reflects the turbulence to flow during
ventricular filling. It is also known as a diastolic thrill. As this thrill is localized to the
apex, enough care should be taken to locate the apex and graduated pressure
should be used to appreciate the thrill. In mitral stenosis a palpable diastolic thrill
generally means a mobile non-calcific valve. When the right ventricle is enlarged
due to severe pulmonary arterial hypertension and comes to occupy the apex, the
diastolic thrill may not be appreciable. The diastolic thrill at the apex may occur in
severe rheumatic mitral regurgitation due to the mid-diastolic murmur associated
with it, as there is always some degree of anatomical narrowing of the valve in
rheumatic heart disease. The associated third heart sound differentiates this from
mitral stenosis, as a third heart sound is unlikely in the presence of mitral stenosis.
In non-rheumatic mitral regurgitation a diastolic thrill does not occur. 271
Left ventricular outflow palpation

A systolic impulse in the aortic area is never normal and indicates a dilated aorta
or ascending aortic aneurysm. The systolic thrill indicates aortic stenosis. A systolic
thrill only in the carotids but no thrill over the precordium, is suggestive of
supravalvular aortic stenosis.
Right ventricular enlargement

The right ventricle lies under the left lower sternum and any enlargement in the
ventricle is most evident there. The normal right ventricle is not palpable except
in very thin persons or children, where a brief outward movement followed by
retraction is a feature. Right ventricular enlargement is maximal at the 4th or 5th
interspace at the left sternal border and directly beneath the lower sternum.
Hyperkinetic left parasternal impulse

This occurs in pure volume overload conditions like atrial septal defect of organic
tricuspid regurgitation with normal right ventricular pressures. The amplitude of
the lift is increased but not the duration.
Sustained parasternal lift

This occurs in pressure overload states as in pulmonic stenosis or pulmonary
arterial hypertension.
Combined hyperkinetic and sustained lift

This can occur in atrial septal defect with pulmonary arterial hypertension, or
pulmonary arterial hypertension with tricuspid or pulmonary regurgitation.
Grading of parasternal lift: The parasternal lift is often graded according to the
amplitude of lift. This grading does not take the duration of the lift into
consideration.
Grade 1: Mild lift made out after careful observation or looking at the chest
from a tangential view. May require to use a pencil, or scale to be kept
along the parasternal region. May be normal
Grade 2: An obvious lift easily made out
Grade 3: A very prominent lift
The presence of a parasternal bulge should be commented upon along with
272 the grading. As the grading takes into account only the amplitude of excursion,
the duration of the lift should be commented upon additionally (for example, left
parasternal lift Grade 2/3, not sustained).
Left parasternal lift of mitral regurgitation (or left atrial lift)

In severe mitral regurgitation, there is a left parasternal lift; it does not indicate
right ventricular enlargement. The systolic rise in pressure in the left atrium,
produces an expansile impulse (large v wave). Part of the left ventricular pressure
is transmitted into the left atrium expanding it. The left atrium is bound by the
spine posteriorly and any posterior expansion is limited. This results in anterior
expansion and displacement of the anterior structures towards the chest wall (the
right ventricle, right atrium, pulmonary artery), producing the parasternal lift. This
lift is late systolic as it takes time for the left ventricle to fill the left atrium and
expand it. It is also more diffuse than the right ventricular impulse. The late onset,
diffuseness of the impulse and absence of signs of pulmonary arterial hypertension
distinguish this lift from that of right ventricular enlargement. This left atrial lift
indicates severe mitral regurgitation with a non-compliant, less dilated left atrium.
THE CARDIAC IMPULSE
Diastolic events over right ventricle

The third heart sound and fourth heart sound may be palpable over the parasternal
region and they increase on inspiration and decrease during expiration. The jugular
venous pulse counterpart of the third heart sound is rapid y descent, and that of
the fourth heart sound is a prominent a wave.
Palpation of right ventricular outflow (infundibulum of right ventricle and

main pulmonary artery): The normal pulmonary artery may be palpable in thin
chested persons. A palpable pulmonary artery and pulmonary component of the
second heart sound generally indicates pulmonary arterial hypertension. A palpable
pulmonary artery with no palpable second sound (pulmonary component) may
mean large flow into pulmonary artery without rise in pressures as in left to right
shunts. A systolic thrill in the pulmonary area with no palpable pulmonary artery
or pulmonary sound associated with a sustained parasternal lift, indicates pulmonic
stenosis.
Right ventricular inflow: The diastolic thrill at the left 4th or 5th space, increasing
on inspiration indicates tricuspid stenosis. The jugular venous pulse should be 273
viewed as part of the right ventricular inflow as it gives valuable clues to the filling
patterns of the right ventricle (y descent/and a wave). A rapid y descent correlates
with palpable third heart sound, and a slow y descent with the diastolic thrill of
tricuspid stenosis. A raised jugular venous pressure, no y descent and no palpable
third heart sound indicates cardiac tamponade. The prominent a wave in the jugular
venous pulse correlates with a palpable fourth heart sound.
Right sternoclavicular joint pulsations

Pulsations of the sternoclavicular joint may be appreciated in a right sided aortic
arch, as in tetralogy of Fallot or acute aortic dissection. In tetralogy of Fallot, the
Blalock-Taussig anastomosis is performed on the side opposite the aortic arch,
while a modified shunt is performed on the same side as the aortic arch. A right
aortic arch is a contraindication to the descending aorta to the left pulmonary
artery shunt since the bronchus is interposed between the pulmonary artery and
the aorta.
TECHNIQUE OF PRECORDIAL EXAMINATION

The patient should be supine or at 45 degrees elevation. Each of us must identify
the part of our hand that is most sensitive for detecting thrills or palpable sounds.
Once the apical impulse is located, graduated pressure of the hand or fingers is
helpful in appreciating a thrill or palpable sound. High frequency events such as
first heart sound and second heart sound are best felt by firm pressure. Low
frequency events such as third heart sound and fourth heart sound are best felt by
light palpation. The patient can be asked to hold the breath in expiration when the
heart moves closer to the chest wall. The left lateral position can be used to check
the presence or absence of an apical impulse, for palpable thrills or sounds. To
assess the site, size, amplitude and duration, the supine position is the best.
The clinical features may alter in people with chest wall deformities.
Causes of non-palpable apical impulse
• Obesity
• Muscular chest wall
• Barrel chest
274 • Emphysema
• Coronary artery disease with decreased apical motion
• Pleural or pericardial effusion
• Age above 40
• Heart is in a different site (?dextrocardia)
CHARACTERISTICS OF PRECORDIAL MOTION IN VARIOUS CARDIAC ABNORMALITIES
The cardiac impulse in various disorders gives valuable clues to the underlying
lesion, its severity, associated lesions and complications.
Cardiac impulse in mitral stenosis
The factors influencing the cardiac impulse in mitral stenosis are:
• Severity of mitral stenosis
• Presence and severity of pulmonary arterial hypertension
• Right ventricular failure and functional TR
Associated factors
• Mitral regurgitation
• Aortic valve disease
THE CARDIAC IMPULSE
• Tricuspid valve disease

• Atrial septal defect
Complications
• Calcification of mitral valve
• Rhythm
The typical impulse in mitral stenosis is related to the right ventricular
hypertrophy secondary to pulmonary arterial hypertension and the lack of left
ventricular enlargement. Classic features of the cardiac impulse in mitral stenosis
are:
• The apical impulse is diffuse and is formed by the right ventricle
• Diastolic thrill at apex
• Sustained left parasternal impulse
• Palpable pulmonary arterial pulsations
• Palpable pulmonary sound
Any alteration in the above features or absence of expected features are of
importance in mitral stenosis. 275
As mentioned in Table 15.8, the most prominent of parasternal impulses is
seen when mitral stenosis is complicated by pulmonary arterial hypertension and
tricuspid regurgitation, or is associated with atrial septal defect (Lutembacher
syndrome).
The impulse is influenced by the cause, severity, complications and associated
lesions in mitral regurgitation. Classic features of the cardiac impulse in this
condition are:
• The apical impulse is localized, displaced downwards and outwards
• Hyperkinetic character
• Palpable third heart sound at apex
• Systolic thrill at apex (uncommon)
• Late systolic, diffuse left parasternal left atrial lift
• Palpable pulmonary arterial pulsations and pulmonary sound with
pulmonary arterial hypertension
Any deviation from the above features is of importance in the setting of
mitral regurgitation.
Table 15.8: Cardiac impulse in mitral stenosis

Feature Alterations/significance
Apical impulse Site Normal with mild mitral stenosis
Lateral displacement in moderate to severe mitral stenosis
Diastolic thrill Is common with moderate to severe mitral stenosis
Absent with
Extremes of obstruction
Mild obstruction with little or no turbulence
Severe MS with severe PAH, RVF and TR with low
cardiac output
Indicates a relatively mobile mitral valve, severe
calcification is unlikely
Diffuse impulse RV forming the apex in moderate to severe mitral
stenosis
Localized impulse Mild mitral stenosis
Associated
Anemia
276 Thyrotoxicosis
Associated CAD
Rheumatic myocarditis
Left parasternal impulse (LPSI) Mild mitral stenosis
Normal Moderate mitral stenosis and PAH in adults with
thick chest wall
Associated tricuspid stenosis
Sustained parasternal impulse Indicates moderate or severe mitral stenosis with PAH
(> Gr 2/3)
Sustained + hyperkinetic Mitral stenosis + PAH
LPSI (Gr 3/3) Tricuspid regurgitation
Associated atrial septal defect
Palpable pre-systolic impulse Severe PAH with concentric RVH, non-compliant RV
(RV S4) along left sternal border Correlates with pronounced a wave in JVP
Rules out associated tricuspid stenosis
Palpable rapid filling wave Right ventricular failure
(RV S3) along LSB Correlates with rapid y descent
Palpable P2/Pulmonary artery Pulmonary arterial hypertension
Systolic thrill Associated atrial septal defect (Lutembacher
syndrome)
THE CARDIAC IMPULSE
Table 15.9: Significance of cardiac impulse in mitral regurgitation

Apical impulse
Site
Normal Mild mitral regurgitation
AS mistaken for mitral regurgitation
Downward displacement Moderate to severe mitral regurgitation
Character
Hyperkinetic Moderate to severe mitral regurgitation
Sustained impulse AS mistaken for mitral regurgitation
Mitral regurgitation secondary to coronary artery disease
HOCM
Congestive cardiomyopathy
Severe mitral regurgitation with LV dysfunction
Systolic thrill Less common
May occur with moderate to severe mitral regurgitation
Chordal rupture
Rule out AS or VSD simulating mitral regurgitation
Diastolic thrill Associated mitral stenosis
Indicates severe rheumatic mitral regurgitation in the
absence of mitral stenosis 277
Palpable S3 Mitral regurgitation is more likely than AS
Indicates moderate mitral regurgitation in adults
Rules out associated mitral stenosis
Palpable S4 AS may have been mistaken for MR
Rules out rheumatic mitral regurgitation
Mitral regurgitation in association with
HOCM
Late, diffuse parasternal lift Left atrial lift with severe mitral regurgitation
Early LLSB lift RVH due to pulmonary arterial hypertension
In acute mitral regurgitation, the murmur of MR may be faint or absent and

the only clue to the underlying MR is unexplained hyperkinesia of the apical impulse.
Cardiac impulse in aortic stenosis

The cardiac impulse in aortic stenosis depends on the severity, nature, associated
lesions and complications of aortic stenosis. The classic cardiac impulse in aortic
stenosis is located in the 5th space without displacement, and is of sustained duration
Table 15.10: Cardiac impulse in aortic stenosis

Normal Mild aortic stenosis
Aortic valve sclerosis
May occur even with severe aortic stenosis
Displaced downward and outward Mitral regurgitation mistaken for aortic stenosis
AS complicated by CCF
Associated
patent ductus arteriosus
ventricular septal defect
Sustained impulse Moderate to severe aortic stenosis
Mild aortic stenosis with associated
Severe aortic regurgitation
Large patent ductus arteriosus
Systolic thrill at
Aortic area (Right 2nd space) Favours organic AS in the presence of severe AR
278 Carotids (Right) Can occur in functional AS with severe aortic
regurgitation
Left sternal border May favour sub-valvular obstruction
Apex May simulate mitral regurgitation
May be the only site of thrill in calcific AS in elderly with
severe emphysema
Carotids only Supravalvular aortic stenosis
Carotid stenosis
Palpable S4 Favours aortic stenosis over mitral regurgitation
Absence of this sign makes HOCM unlikely
Indicates severe obstruction
Palpable S3 Rules out associated mitral stenosis
Mitral regurgitation mistaken for aortic stenosis
Aortic stenosis complicated by LVF
Associated mitral regurgitation, PDA or VSD
(Fig. 15.3); the fourth heart sound may be palpable. A systolic thrill is felt over the
left sternal border, aortic area and carotid artery.
Any deviation from this classic impulse may mean either an associated lesion
or a complication of aortic stenosis. In the majority of patients even with severe
THE CARDIAC IMPULSE
aortic stenosis, the cardiac impulse is normally located due to concentric left
ventricular hypertrophy without much dilatation of the cavity. Once the impulse is
significantly displaced, an associated disorder enumerated above should be
considered.
Cardiac impulse in aortic regurgitation

The determinants of the nature of the impulse are the severity and the presence of
associated disorders. The classic features are:
• The impulse is displaced outward and downward
Table 15.11: Significance of the cardiac impulse in aortic regurgitation
Location
Normal Mild aortic regurgitation
Displaced downward and outward Moderate to severe aortic regurgitation
Mild aortic regurgitation with associated mitral regurgitation
coarctation
patent ductus arteriosus 279
Hyperkinetic impulse Suggests moderate to severe aortic regurgitation
Mild aortic regurgitation with associated
mitral regurgitation
patent ductus arteriosus
Palpable S3 Suggestive of
Left ventricular failure
Palpable S4 Acute aortic regurgitation
Associated hypertension
Aortic regurgitation with acute aortic dissection
Diastolic thrill Rare
Suggests retroversion of aortic cusps as in aortic root disease
Systolic thrill Is often mistaken for systolic thrill
nd
Right 2 space Associated aortic stenosis
nd
Right 2 space and carotids Functional aortic stenosis in severe aortic regurgitation
Only carotids Aortic regurgitation in association with Takayasu’s arteritis
Left sternal border only Subaortic obstruction
Associated ventricular septal defect
• Hyperkinetic or forcible in nature

• Pulsations of ascending aorta may be palpable at right 2nd space
• Systolic thrill may be palpable over the carotids
• No additional sounds are palpable
Any alteration from the above or any additional sign is of significance in the
setting of aortic regurgitation (Table 15.11).
In pure severe aortic regurgitation, a systolic thrill over the carotids is common
and does not indicate associated aortic stenosis. The systolic thrill along the left
sternal border should be carefully interpreted in the setting of aortic regurgitation.
The systolic thrill along the left sternal border with accompanying thrill at right 2nd
space and carotid is suggestive of valvular aortic stenosis. A similar thrill at the
lower sternal border without associated thrill at right 2nd space and carotid may
indicate either subaortic stenosis or ventricular septal defect.
Cardiac impulse in congenital acyanotic heart disease

Evaluation of the precordial impulse is of great value in the assessment of this
group of disorders.
280
Pulmonic stenosis
The classic features are:
• Apical impulse is diffuse
• Left parasternal impulse Grade 2/3
• Sustained
• Systolic thrill at pulmonary area
• Impalpable pulmonary artery
• Palpable pre-systolic impulse at LSB
Any deviation from these classic features is of significance in the recognition of
pulmonary stenosis. Very often, even in severe pulmonic stenosis, the left
parasternal impulse is unimpressive as it is a pure pressure load to the right ventricle
(Table 15.12).

The atrial septal defect is the purest example of volume load to the right ventricle.
• The apical impulse is diffuse formed by RV with systolic retraction
THE CARDIAC IMPULSE
Table 15.12: Significance of cardiac impulse in pulmonic stenosis

Apical impulse
Diffuse RV may form the apex
Localized Ventricular septal defect or AS mistaken for PS
As a variant in pulmonic stenosis(rare)
Systolic retraction Atrial septal defect mistaken for pulmonic stenosis
Associated TR
Left parasternal impulse
Grade 1–2/3 Consistent with pulmonic stenosis
Grade 3/3 Unlikely to be pure pulmonic stenosis
Associated atrial septal defect or TR likely
Sustained impulse Moderate to severe pulmonic stenosis
Palpable S4 Indicates severe pulmonic stenosis
Favours pulmonic stenosis with intact ventricular
septum
Palpable S3 Favours intact atrial septum
Associated RV failure
Systolic thrill
Pulmonary area Valvular pulmonic stenosis
281
Left 2nd space Infundibular pulmonic stenosis
rd th
Left 3 or 4 space Infundibular pulmonic stenosis
Infraclavicular/laterally to Supravalvular pulmonic stenosis
pulmonary area
Diastolic thrill Associated pulmonary incompetence as in
Dysplastic valve of Noonan’s syndrome
Infective endocarditis
Absent pulmonary valve with annular stenosis
• Hyperkinetic left parasternal impulse Grade 2/3

• Palpable pulmonary arterial pulsations at left 2nd space
• P2 may be palpable
• Systolic thrill at pulmonary area in 25 per cent of cases
Any variation from the above features may signify an associated disorder or
a complicating feature (Table 15.13).

In ventricular septal defect, the left ventricle is volume loaded and the right ventricle
Table 15.13: Significance of cardiac impulse in atrial septal defect

Apical impulse
Diffuse RV enlargement forming apex
Localized LV enlargement due to associated
mitral regurgitation as in MVP/RHD or AV canal defects
VSD mistaken for atrial septal defect or associated VSD
Systolic retraction RV volume load
Left parasternal impulse Suggests left to right shunt > 1.5:1
Hyperkinetic 2/3 Consistent with RV volume load due to atrial septal
defect
Sustained impulse Atrial septal defect with pulmonary arterial
hypertension
Atrial septal defect with pulmonic stenosis
Atrial septal defect with mitral valve disease
Palpable S4 Primary PAH simulating atrial septal defect is likely
Palpable S3 RV failure
Diastolic thrill Ebstein’s anomaly is more likely than atrial septal
282 defect
Pulmonary area
Pulsations of PA Favours atrial septal defect over pulmonic stenosis
Palpable P2 May occur due to large shunt or pulmonary arterial
hypertension
Systolic thrill Various possibilities exist
Pulmonic stenosis is more likely than atrial septal defect
Associated pulmonic stenosis with atrial septal defect
Associated mitral valve disease (Lutembacher syndrome)
Ostium primum atrial septal defect
Some of atrial septal defects , 25% may have this sign without
associated disease; suggests large shunt
is both volume-and pressure-loaded.

• Apical impulse localized and hyperkinetic
• Left parasternal impulse is hyperkinetic and sustained
• Systolic thrill anywhere along the left sternal border
• Pulsations of PA at pulmonary area
• P2 may be palpable
THE CARDIAC IMPULSE
Each of these features can be modified by the size, location, associated defects
and complications of ventricular septal defect.
Other determinants are
• Site of defect
• Location of the defect
• Complications: pulmonary arterial hypertension
• Congestive cardiac failure
Table 15.14: Significance of cardiac impulse in ventricular septal defect
Apical impulse
Normal Small ventricular septal defect
Localized, Hyperkinetic Moderate to large ventricular septal defect
Continuing left to right shunt
Sustained impulse AS mistaken for ventricular septal defect
Associated coarctation
Associated AS
Diffuse RV forming apex as in atrial septal defect
283
Hyperkinetic Moderate ventricular septal defect without PAH
Hyperkinetic and sustained Moderate or large defect with PAH
Combined apical + left parasternal Ventricular septal defect with left to right shunt
impulse
Isolated left parasternal impulse VSD with PAH with little or no left to right shunt
Isolated hyperkinetic apex MR mistaken for ventricular septal defect
Small VSD with significant aortic regurgitation
Palpable pulmonary arterial Favours VSD over pulmonic stenosis
pulsations Significant left to right shunt or PAH
Palpable pulmonary sound Suggests PAH and rules out pulmonic stenosis
Systolic thrill
Left sternal border Consistent with ventricular septal defect
Pulmonary area Supracristal ventricular septal defect
Right sternal border LV to RA communication (Gerbode’s defect)
Palpable third heart sound Heart failure
Palpable fourth heart sound VSD is unlikely; pulmonic stenosis is more likely
PAH with TR is also likely
Table 15.15: Significance of cardiac impulse in patent ductus arteriosus

Apical impulse
Normal Small ductus
Venous hum mistaken for patent ductus arteriosus
Displaced downward and Moderate to large ductus with significant left to right
Hyperkinetic shunt
Sustained impulse Very large ductus with large shunt and associated
aortic stenosis
coarctation of aorta
systemic hypertension
Normal No pulmonary arterial hypertension
Small ductus
Sustained with hyperkinetic apical Hyperkinetic pulmonary arterial hypertension due to
impulse large pulmonary flow
Sustained with diffuse apical ‘Fixed’ pulmonary arterial hypertension due to
impulse increased pulmonary vascular resistance
Sustained and hyperkinetic with ‘Fixed’ pulmonary arterial hypertension with
284 diffuse apical impulse pulmonary or tricuspid incompetence or both
Thrill at pulmonary area
Continuous Consistent with ductus
Systolic only Ductus with pulmonary arterial hypertension
Diastolic only Rules out patent ductus arteriosus with left to right
shunt
Severe pulmonary arterial hypertension with
pulmonary incompetence
Thrill at other sites
Left sternal border Ventricular septal defect or aortic stenosis
Aortic area Aortic stenosis
Suprasternal notch Consistent with ductus
Favours ductus over ventricular septal defect
Palpable pulmonary arterial Implies moderate to large ductus
pulsations and palpable pulmonary Pulmonary arterial hypertension
sound
• Associated defects:aortic regurgitation, pulmonic stenosis, patent ductus

arteriosus
• Coarctation of aorta
THE CARDIAC IMPULSE
Table 15.14 gives the significance of any deviation from the classic pattern
expected in ventricular septal defect.
With isolated parasternal impulse without an accompanying left ventricular
enlargement, ventricular septal defect is highly unlikely.

The left ventricle is volume-loaded and the right ventricle is excluded from the
shunt in patent ductus arteriosus. The determinants of the impulse are the size of
the ductus, the degree of pulmonary arterial hypertension and the presence or
absence of associated lesions.
• Apical impulse is localized and displaced downward and outward
• Hyperkinetic apical impulse
• Continuous or dominantly systolic thrill at pulmonary area
• Pulmonary arterial pulsations may be palpable
• Pulmonary sound may be palpable
• Pulsations over suprasternal notch
Any alteration in any of these features is of significance in the assessment of 285
patients with patent ductus arteriosus (Table 15.15).
A continuous thrill at the pulmonary area with left ventricular enlargement
and collapsing pulse is virtually diagnostic of patent ductus arteriosus. The only
other condition that produces a continuous thrill at this site is the peripheral
pulmonary stenosis. The isolated right ventricular enlargement distinguishes the
two conditions.
Cardiac impulse in congenital cyanotic heart disease

Cyanosis in congenital heart disease is due to right to left shunt, abnormal origin
of great vessels or admixture of blood in one of the four chambers. Careful
evaluation of cardiac impulse gives clues to the underlying mechanism in the
majority of patients. The first question one asks in congenital cyanotic heart disease
is whether there is a cyanotic heart disease at all in this patient. If present, is it due
to diminished pulmonary flow or increased pulmonary flow.
Evaluation
Evaluation of the cardiac impulse gives clues in some of the above situations.
The classic cardiac impulse in some of the common cyanotic heart diseases is
described below.
Tetralogy of Fallot
• Absence of cardiac enlargement
• Apical impulse is normal or unimpressive
• Left parasternal impulse < Grade 2/3
Is it CHD or a condition Conditions simulating congenital cyanotic heart disease
simulating it? Methemoglobinemia: congenital or acquired
Primary pulmonary hypertension with right to left atrial shunt
Chronic cor pulmonale
If it is CHD, is it due to Decreased pulmonary flow conditions
increased pulmonary Tetralogy of Fallot
flow or to diminished All conditions with tetralogy like physiology
pulmonary flow? DORV with pulmonic stenosis
TGA with ventricular septal defect and pulmonic stenosis
Single ventricle with pulmonic stenosis
Increased pulmonary flow conditions
286 Transposition of great vessels
TAPVC
DORV
Truncus arteriosus
Single ventricle
Table 15.16: Evaluation of the cardiac impulse in congenital heart disease

Clues and features Increased pulmonary flow Decreased pulmonary flow
Clues from cardiac Cardiac enlargement Absence of cardiac enlargement
impulse Biventricular enlargement Parasternal impulse < Grade 2/3
Systolic thrill at lower left Systolic thrill at pulmonary area
sternal border (ventricular Impalpable pulmonary artery
septal defect)
Palpable third heart sound
Palpable pulmonary artery
Palpable pulmonary sound
Accompanying features Presence of heart failure Absence of heart failure
Elevated jugular venous pressure Normal level of jugular venous pulse
Presence of third sound Absence of third heart sound
Presence of mid-diastolic Absence of diastolic murmurs
murmurs at AV valves at AV valves
THE CARDIAC IMPULSE
• No pulsations in pulmonary area

• Usually no systolic thrill at pulmonary area
The cardiac impulse in tetralogy of Fallot can be almost normal and
unimpressive (Table 15.17).
The differential diagnosis of congenital heart disease is best approached by
considering ventricular enlargement (Table 15.18). Usually the right ventricle is
the enlarged ventricle in congenital heart disease; left ventricular or biventricular
enlargement is less common.
Table 15.17: Significance of cardiac impulse in tetralogy of Fallot
Apical impulse
Normal Consistent with tetralogy of Fallot
Unimpressive or impalpable As above
Localized, hyperkinetic Pink tetralogy with left to right shunt or ventricular
septal defect
Associated aortic regurgitation with tetralogy of Fallot
Left parasternal impulse 287
Normal or < Grade 2/3 impulse Consistent with tetralogy of Fallot
More than Grade 2/3 Tetralogy of Fallot is unlikely
Pulmonary stenosis with intact ventricular septum and
atrial right to left shunt is likely
Systolic thrill
With mild cyanosis Milder tetralogy
With deep cyanosis Tetralogy is unlikely
Conditions with obligatory ventricular septal defect
likely
tricuspid atresia
double outlet right ventricle
With no cyanosis Pink tetralogy or VSD mistaken for tetralogy of Fallot
Systolic and diastolic thrill at
pulmonary area Pulmonary regurgitation with absent pulmonary valve
Continuous thrill Associated patent ductus arteriosus
Palpable fourth heart sound Tetralogy of Fallot is unlikely
Pure pulmonic stenosis with right to left atrial shunt
is likely
Pulsations at left 2nd space Though unusual may occur due to outflow pulsations
Table 15.18: Ventricular enlargement in cyanotic heart disease

Conditionswith Conditionswith Conditionswith Conditions with no
RVH LVH BVH ventricularenlargement
TOF Tricuspid atresia DORV without PS Pulmonary AV fistula
TGA, VSD+PS Pulmonary atresia TGA, VSD without PS SVC or IVC
DORV with PS with intact IVS draining to LA
TAPVC Hypoplastic RV Truncus arteriosus
Trilogy of Fallot ASD Pulmonary atresia
with bronchial
collaterals or PDA
Tetralogy of Fallot with
PDA
after shunt
Cardiac impulse in coronary artery disease

Most physicians do not care to palpate the precordium when evaluating patients
with coronary artery disease (CAD) as the cardiac impulse is often normal in the
majority of patients. However, when it is carefully evaluated, it gives valuable clues
in a significant number of patients. The determinants of the impulse are the clinical
288
subset, presence or absence of angina during examination, extent of coronary
artery involvement, presence or absence of myocardial infarction, the duration of
infarction, presence or absence of mitral regurgitation or ventricular septal defect,
and the associated disorders like systemic hypertension (Table 15.19).
The area of the precordium over the third, fourth and fifth interspace to the
left of the sternum and apex is called the ectopic area. In the initial evaluation of
patients presenting with angina pectoris, one should rule out conditions producing
angina as a secondary manifestation. These are hypertrophic cardiomyopathy, mitral
Table 15.19: Significance of the cardiac impulse in coronary artery disease
Clinical subset Findings
Chronic stable angina The impulse is most commonly normal
During the episode of angina
Palpable fourth heart sound
Palpable dyskinesia (ectopic impulse)
Acute myocardial infarction Palpable fourth heart sound
Palpable dyskinesia
Systolic thrill at apex in mitral regurgitation due to PMD
Systolic thrill at left sternal border in VSD
THE CARDIAC IMPULSE
valve prolapse, severe systemic hypertension, cardiomyopathy and/or severe

pulmonary hypertension (thromboembolic or primary).
The majority of patients with coronary artery disease are above 40 years of
age and have a thick chest wall making it difficult to palpate the cardiac impulse.
When the cardiac impulse is easily palpable in this group of people, cardiac
enlargement is most likely. It is for this reason that any easily discernible impulse
has diagnostic significance in this age group. Palpable fourth heart sound and
dyskinesia appearing during the episode of pain and disappearing later with the
subsidence of pain, is virtually diagnostic of ischemic origin of pain.
Cardiac impulse in pericardial disease

a) Pericardial effusion: The most common feature in moderate to large pericardial
effusions is increase in cardiac dullness with impalpable cardiac impulse. If the
cardiac impulse is well felt in the presence of large effusion, associated intracardiac
defect with cardiac enlargement is likely. Significant pericardial effusion can co-
exist with intracardiac defect in acute rheumatic fever with pancarditis,
endomyocardial fibrosis, acute myopericarditis, and uremic pericarditis. In uremic
pericarditis due to chronic renal failure, underlying cardiac enlargement due to 289
preexisting systemic hypertension is common.
b) Chronic constrictive pericarditis: The cardiac impulse is impalpable in the majority
of adults with this disease. In younger patients with thin chest wall the impulse is
often palpable and can be prominent. On careful examination the impulse will be
found to be retracting in systole with a prominent diastolic outward movement.
The impulse reflects the pathophysiology of constrictive pericarditis, namely the
very rapid ventricular filling coinciding with pericardial knock and a rapid y descent
Table 15.20: Cardiac impulse in conditions simulating coronary artery disease
Condition Cardiac impulse

Hypertrophic cardiomyopathy Left ventricular hypertrophy
Palpable fourth sound
Systemic hypertension As above
Mitral valve prolapse Systolic thrill of mitral regurgitation
Bifid apical impulse
Hyperkinetic left ventricular impulse
Severe pulmonary arterial Left parasternal impulse, sustained
hypertension Palpable PA and P2
in the neck veins. This diastolic outward impulse is often mistaken for systolic,
and some other diagnosis is considered. It is best detected by simultaneously
palpating the parasternal impulse, and auscultating the pulmonary area. The impulse
occurs following the second heart sound. Timing with carotid impulse is often
misleading particularly with rapid heart rates. It is important to look for this sign
because other conditions simulating constriction very rarely produce this sign.
Cardiac impulse in cardiomyopathy

The cardiac impulse in cardiomyopathy gives clues as to the nature of
cardiomyopathy (Table 15.21). In congestive cardiomyopathy, systolic dysfunction
with exaggeration of rapid ventricular filling is the central feature.
In restrictive cardiomyopathy the systolic function is normal. There is
restriction to ventricular filling, calling for exaggerated atrial contraction trying to
distend a non-compliant ventricle, resulting in fourth heart sound or pre-systolic
impulse. In hypertrophic cardiomyopathy, not only is the restriction to ventricular
filling a fundamental problem but a varying degree of obstruction to left ventricular
outflow may also occur. As cardiomyopathy is always a diagnosis of exclusion,
290 certain features in the cardiac impulse help to rule out conditions that simulate
cardiomyopathy.
Features unusual for a diagnosis of cardiomyopathy are:
• Signs of significant pulmonary arterial hypertension
Parasternal impulse > Grade 2/3
Palpable pulmonary arterial pulsations
Palpable pulmonary sound
Table 15.21: Features of cardiac impulse in cardiomyopathy
Feature Congestive Restrictive Hypertrophic

Apical impulse
Location Displaced Normal Normal
Diffuse bulge Common No May occur
Palpable S4 No Common Common
Palpable S3 Common May occur May occur
Systolic thrill No No May occur with LV
outflow obstruction
THE CARDIAC IMPULSE
• Systolic or diastolic thrill anywhere over the precordium

• Impalpable third or fourth heart sound even with careful palpation
• Systolic retraction of cardiac impulse
With careful palpation a third heart sound or fourth heart sound can be felt
in cardiomyopathies. Absence of this sign makes the diagnosis suspect. As
constrictive pericarditis simulates restrictive cardiomyopathy so closely, a systolic
retraction of the impulse should be looked for in all patients when either diagnosis
is considered. The diagnosis of cardiomyopathy is unlikely when a systolic or
diastolic thrill is palpable. The exceptions to this are rare but may occur with
hypertrophic obstructive cardiomyopathy (systolic thrill), or endomyocardial fibrosis
with severe mitral or tricuspid regurgitation (systolic or diastolic thrill).
In HOCM, there will be a triple impulse due to prominent a wave and bifid
systolic wave. The notch in systole represents the onset of obstruction (Fig. 15.5).
PHONO 291
ACG
ECG
Fig. 15.5: Apexcardiogram in hypertrophic obstructive cardiomyopathy (HOCM)

S1: first heart sound, S2: second heart sound, S4: fourth heart sound, SM: systolic murmur,
A: atrial contraction, ACG: apexcardiogram, ECG: electrocardiogram, Phono: phonocardiogram
The most basic information you can get out of cardiac impulse is whether
the heart is on the right side or left side. Your search is incomplete till you
turn the patient to the left side to locate the impulse; if it cannot be found,
look for it on the right side. This simple measure could save you the humiliation
of missing a case of dextrocardia.
If the cardiac enlargement (left ventricular or right ventricular) is unexpected,
or is out of proportion to the severity of lesion, look for a chest deformity.
When you make a diagnosis of mitral stenosis, go out of the way to look for
the diastolic thrill at apex. If a student fails to detect it but the examiner
palpates thrill, the implications are unspeakable.
In the presence of extreme enlargement of one ventricle, mild enlargement
of the other ventricle is difficult to detect.
One has to identify the ventricular chamber that has hypertrophied.
Very rarely, even experienced physicians and cardiologists mistake enlargement
of one ventricle for the other. I have mistaken myocarditis for primary
292 pulmonary arterial hypertension, hypertrophic cardiomyopathy for right
ventricular hypertrophy, and the right ventricular hypertrophy in severe
pulmonic stenosis for left ventricular hypertrophy.
It is often said that the fourth heart sound is better palpable than audible.
This however depends whether you are good in palpation or auscultation or
both. Palpation is better when the cardiac impulse is palpable. With a loud
murmur of aortic stenosis masking the fourth heart sound, palpation is
superior to auscultation.
When the electrocardiogram shows a pattern of LVH, but no LVH is detected
on palpation and echocardiogram, apical cardiomyopathy is likely. The
transesophageal echocardiography helps to confirm the diagnosis.
As mistakes are common in the evaluation of cardiac impulse, examiners
should try not to be too harsh in judging students. What looks typical and
easy may not be so from the point of view of a student facing an examination.
(This should be borne in mind by examiners who pretend infallibility.)
16 Auscultation of the Heart
In the naked light, ten thousand people, may be more – people talking without speaking, people
hearing without listening...
Paul Simon in Sound of Silence
When the stage of auscultation is reached, valuable information has already been
obtained from history and physical examination. Though we routinely try to hear
any sound or murmur, we often try to check for conditions guided by the
information already available. Looking for the mid-diastolic murmur of mitral
stenosis in a patient presenting with dyspnea, paroxysmal nocturnal dyspnea and
orthopnea is an example. On the other hand, one tries to hear a ventricular gallop
or third heart sound if the left ventricular impulse is prominent, for evidence of
left ventricular failure. This clinical skill or faculty of ‘looking for things’ on
auscultation distinguishes a good clinician from an average one.
For a proper understanding of auscultatory findings, it is important to
understand certain commonly used terms.
Frequency is sometimes referred to as pitch. Frequency is an objective
expression of the number of vibrations per second; pitch is the subjective
description of frequency. Intensity and loudness are the same as intensity is
expressed as decibels and loudness is the subjective expression of the same.
High frequency sounds or murmurs

High frequency sounds are usually described as soft, blowing, musical or cooing.
High frequency sounds (400 cps) are sharp and clicky as in the two components
of second heart sound, ejection clicks and non-ejection clicks. The murmurs of
mitral regurgitation, aortic regurgitation and tricuspid regurgitation are often of
Table 16.1: What to ‘look’ for auscultation

Guiding clue What to look for
Dyspnea, PND, orthopnoea
With no LV enlargement Mid-diastolic murmur of MS
With LV enlargement Third or fourth heart sound
Chest pain, palpitation in a Non-ejection click, late systolic murmur of mitral
young patient valve prolapse
Febrile patient Heart murmur, particularly early diastolic murmur
of AR by keeping the patient in sitting, lean-forward
position, with held expiration, and diaphragm of
stethoscope well pressed to the chest wall
soft systolic murmur of MR
ejection click of bicuspid aortic valve
Fever with asymmetry of As above
arterial pulses
Fever with or without chest Pericardial rub
pain
Acute chest pain with Early diastolic murmur of AR complicating aortic
asymmetry of arterial pulses dissection
294 Paradoxic pulse, elevated JVP, Pericardial rub, absence of third heart sound
slow y descent, impalpable suggestive of cardiac tamponade
cardiac impulse
Terms used in the study of sound or auscultation

Acoustics is the science of sound and its effects on people.
Beats are periodic variations in the loudness of sound. Beats are heard when two tones of
slightly different frequencies are sounded at the same time.
Decibel is the unit used to measure the intensity of a sound. A 3,000 Hertz tone of about
zero decibels is the weakest sound that the normal human ear can hear.
Frequency of sound waves refers to the number of compressions or rarefactions produced
by a vibrating object each second.
Pitch is the degree of ‘highness’ or ‘lowness’ of a sound as perceived by the listener. It is
the subjective expression of frequency.
Hertz is the unit used to measure frequency. One Hertz equals one cycle (vibration) per
second.
Intensity of a sound is related to the amount of energy flowing in the sound waves.
Sound quality, also called timber, is a characteristic of musical sounds. Sound quality
distinguishes between notes of the same frequency and intensity produced by different
musical instruments.
Ultrasound is sound with frequencies above the range of human hearing.
Infrasound is sound with frequencies below the range of human hearing.
AUSCULTATION OF THE HEART
High
frequency
Medium
frequency
Low
frequency
Fig. 16.1: Diagrammatic representation of frequencies
high frequency. The high pitched sounds, or murmurs are best appreciated with
the diaphragm of the stethoscope and are widely conducted. Thrills are uncommon
with these murmurs. They are often produced when the pressure difference is
high.
Low frequency sounds or murmurs

Low frequency sounds are usually described as rough, rumbling, dull and thud.
Low frequency sounds (60–200 cps) are dull (for example, the first heart sound,
third heart sound and fourth heart sound). The murmurs of mitral stenosis and 295
tricuspid stenosis are low pitched. All low frequency sounds and murmurs are
best appreciated with the bell of the stethoscope applied lightly over the chest.
Low pitched murmurs and sounds have less number of vibrations per second, but
have increased amplitude of vibrations. For this reason they are often palpable
(third heart sound/fourth heart sound) or have thrills (mitral stenosis/tricuspid
stenosis). Low pitched murmurs usually suggest low pressure difference between
the two chambers in the heart (left atrium to left ventricle as in mitral stenosis, or
right atrium to right ventricle as in tricuspid stenosis). The murmurs of aortic
stenosis, pulmonic stenosis and ventricular septal defect are often described as
harsh in quality. A harsh murmur has a combination of frequencies and the low
frequency component is localized to the site of best audibility but the high frequency
component is widely transmitted. This is most common with the murmur of aortic
stenosis where the rough component of the murmur is best heard at the aortic
area but the high frequency soft component is transmitted to the apex and is often
confused for mitral regurgitation.
Table 16.2: High frequency and low frequency events

Frequency Description Examples
High frequency Sounds Sounds
(about 400 cps) Sharp Aortic and pulmonary
Clicky Ejection clicks
Opening snap
First heart sound in MS
Non-ejection clicks
Pericardial knock
Murmurs Murmurs
Soft EDM of AR/PR
Blowing MR
Cooing Functional TR
Musical
Low frequency Sounds Sounds
(60–200 cps) Dull Third heart sound
Thud Fourth heart sound
Pericardial knock
Murmurs Murmurs
Rough MDM of MS/TS
296 Rumbling Austin Flint murmur
Flow murmurs at AV valves
PR with normal PA pressures
Mixed frequency Sounds Sounds
(combination of Not as sharp as second First heart sound
high and low heart sound or as dull
frequencies) as third heart sound
Murmurs Murmurs
Rough AS
Harsh PS
VSD
17 The First Heart Sound
The first heart sound is produced by the closure and after vibrations at the mitral
and tricuspid valves. The mitral component occurs first followed by the tricuspid
component. Additionally, the myocardial and vascular components contribute to
it. Heart sounds and murmurs are due to the following mechanisms:
• Valvular
• Myocardial
• Vascular
• Vibration of the cardiohemic system
Though the above mechanisms are universally applicable to the genesis of
all heart sounds and murmurs, for clinical purposes it is useful to consider individual
sounds and the mechanism of production.
INTENSITY OF FIRST HEART SOUND

Intensity is determined by:
• Structural integrity of the mitral valve
• Position of the AV valve at the time of ventricular contraction
• Integrity of isovolumic systole
• Heart rate
• P-R interval
• Myocardial contractility
Structural integrity of mitral valve

The various components of the mitral valve make up the mitral valve apparatus
(Fig. 17.1).
Fig. 17.1: Components of the mitral valve apparatus
The mitral valve apparatus consists of:

• Leaflets/commissures
• Chordae
• Papillary muscles
298 • Left ventricle
• Mitral annulus
The normal mitral valve has thin pliable leaflets, which are capable of
producing a normal first heart sound. A calcified immobile valve results in
diminished or absent first heart sound. Loss of leaflet tissue (as in infective
endocarditis) will have a similar effect.
Position of AV valve during ventricular contraction

The normal mitral valve is in a semi-closed position by the end of the diastole as
the leaflets float up in the left ventricle that is almost completely filled. The
ventricular contraction closes it further, producing the normal first heart sound.
When the mitral valve is open, or cannot semi-close by the end of the diastole, a
loud first sound occurs as in mitral stenosis. In mitral stenosis, the mitral valve is
kept open in the later phase of the diastole due to high pressure in the left atrium
(Fig. 17.2). This is because, the excursion of the valve is increased and the mitral
valve closes late and at a higher pressure of the left ventricle, due to left atrial
hypertension. In atrial septal defect, the tricuspid component of the first heart
sound is increased due to large tricuspid flow keeping the valve open. Hyperkinetic
THE FIRST HEART SOUND
circulatory states and left to right shunts also increase flow across the mitral valve
to accentuate the first heart sound. A short P-R interval keeps the mitral valve
wide open when the next ventricular contraction begins and also produces a loud
first heart sound. Paradoxically, if the mitral valve is closed prematurely the first
heart sound is diminished or absent.
Pressure wave forms of left ventricle and left atrium are represented to indicate
the end-diastolic gradient at the onset of systole that keeps the mitral valve in
open position, thus increasing the amount of excursion the valve has to undergo
before it closes. This results in the loud first heart sound. Conversely a soft first
heart sound is generated when the mitral valve closes prematurely. Normally, the
mitral valve closes at the onset of systole as LV pressure exceeds LA pressure.
However, in acute aortic regurgitation or chronic aortic regurgitation with left
ventricle dysfunction, the left ventricular diastolic pressure exceeds the left atrial
pressure before the onset of systole, resulting in premature closure of the mitral
valve. This is very well appreciated in the M-mode echocardiogram.
The causes for premature closure of the mitral valve could be:
• Acute severe AR
• Chronic severe aortic regurgitation with LV dysfunction 299
• Prolonged PR interval
The mechanism is shown in (Fig. 17.3).
Fig. 17.2: Mechanism of loud first heart sound in mitral stenosis

Fig. 17.3: Mechanism of premature closure of mitral valve in aortic regurgitation
Integrity of isovolumic systole

300
Normally, during the phase of isovolumic systole, the ventricle contracts like a
closed chamber, due to integrity of the ventricular muscle, mitral valve and the
aortic valve. During this phase the pressure rises steeply and the rate of rise of
pressure (dp/dt) is maximum. When isovolumic systole is lost or abbreviated due
to any cause (Fig. 17.4), the rate of rise of left ventricle pressure (dp/dt) falls
steeply resulting in decreased velocity of closure of the mitral valve. The first heart
sound is diminished or absent when isometric contraction is compromised as in
severe mitral regurgitation, aortic regurgitation or in ventricular aneurysm. In mitral
regurgitation, ventricular aneurysm with dyskinesia, the isovolumic systole is lost
(as shown in Fig. 17.4), whereas, in aortic regurgitation, it is abbreviated due to
very low diastolic pressure of aorta. However, in ventricular septal defect, in spite
of loss of isovolumic systole the first sound is not diminished as often and is
possibly related to the two ventricles behaving like a common chamber.
The causes of loss of isovolumic systole are:
• Severe mitral regurgitation
• Severe aortic regurgitation
• Large ventricular septal defect
• Ventricular aneurysm
Normal Mitral regurgitation
Fig. 17.4: Loss of isovolumic systole

301
Normally, the mitral valve closes at the onset of systole as left ventricle pressure
exceeds LA pressure (Fig. 17.4). However, in acute aortic regurgitation or chronic
aortic regurgitation with left ventricle dysfunction, the left ventricular diastolic
pressure exceeds the left atrial pressure before the onset of systole, resulting in
premature closure of the mitral valve. This is very well appreciated in the M-mode
echocardiogram.
Heart rate
Tachycardia accentuates first heart sound by shortening the P-R interval, increase
in contractility, and a wide open valve due to an abbreviated diastole. Bradycardia
has the opposite influence.
P-R interval
The short P-R interval increases first heart sound by the mechanism of wide open
valve as the atrial contraction occurs in tandem with ventricular contraction.
A prolonged P-R interval results in diminished first heart sound due to premature
closure of the mitral leaflet.
ECG
Fig. 17.5: Relationship of P-R interval to the intensity of first heart sound – intracardiac
pressure mechanics
302 The P-R interval influences the intensity of the first heart sound due to the
relationship of atrial contraction to the onset of systole (Fig. 17.5). When the
P-R is short, closely occurring atrial contraction keeps the mitral valve open at the
onset of systole, thereby increasing first heart sound intensity.
Myocardial contractility
Increase in myocardial contractility increases the first heart sound; diminished
contractility has a negative influence.
The causes of increased myocardial contractility could be:
• Exercise
• Emotional excitability
• Hypoglycemia
• Thyrotoxicosis
• Drugs: sympathomimetics, β2 stimulants
The causes of diminished myocardial contractility could be:
• Myocardial ischemia or infarction
• Myocarditis
• Cardiomyopathy
• Ventricular dysfunction due to any cause
• Drug induced myocardial depression
• Betablockers, verapamil, diltiazem, disopyramide
The normal first heart sound is a relatively prolonged, low frequency sound
having two components, and is best heard at the apex. The split of the first heart
sound is heard only at the tricuspid area, as the tricuspid component is heard only
at this site.
EVALUATION OF FIRST HEART SOUND

The first heart sound has to be evaluated along the following parameters:
• Intensity
Normal
Accentuated
Diminished
Constancy or variability
• Split 303
For example, when the first sound is normal it is expressed as follows: ‘The
first sound is normal in intensity, split is normal and is constant in intensity’. The
split of the first heart sound does not have the same significance as that of second
heart sound and is heard in only 40 per cent of normal individuals.
Intensity
Normally, the first heart sound should be loudest at the apex and the second heart
sound should be louder at the base. If the first heart sound is equal to, or higher in
intensity than the second heart sound at the base, the first heart sound is considered
accentuated (Table 17.1). Diminution of the first heart sound is based on subjective
evaluation (Table 17.2). Further the concept of ‘normal’ is itself relative. As this
evaluation is subjective, mild alterations in intensity should not be used to rule in
or rule out a disorder. With a normal heart rate and P-R interval, if the first heart
sound is loud one should consider mitral stenosis.
Variable intensity
The normal first heart sound is constant in intensity because most of the
determinants of the intensity of first heart sound are constant over a period of
Table 17.1: Causes and mechanisms of loud first heart sound

Causes Mechanisms
Exercise Tachycardia
Shortened P-R interval
Increased myocardial contractility
Increased flow across AV valves
Emotional excitability As above
Catecholamines
Mitral stenosis Wide open mitral valve at end diastole
Delayed mitral valve closure
Mitral closure at higher left ventricle pressure
Thickened but mobile mitral leaflets
Hyperkinetic circulatory states Increased AV valve flow
Tachycardia
Atrial septal defect Increased tricuspid flow
Sinus tachycardia Shortened diastole
Wide open mitral valve
304 (Treppe phenomenon)
Short P-R interval
Short P-R interval Wide open AV valves
time. Certain features like valve anatomy cannot vary, but others like heart rate,
P-R interval, position of the AV valve by the end of diastole, and force of ventricular
contraction can vary. In eliciting constancy or variability in the intensity of first
heart sound, the patient should be asked to hold breath to avoid respiratory
alteration in the intensity of first heart sound.
The causes could be:
• Atrial fibrillation
• Ventricular tachycardia
• Classic atrioventricular dissociation (isorhythmic AV dissociation)
• Atrial flutter with varying block
• Atrial tachycardia with varying block
• Multifocal atrial tachycardia
• Frequent atrial and ventricular ectopy
Table 17.2: Causes and mechanisms of diminished first sound

Cause Mechanisms
Sinus bradycardia Long diastolic filling allows premature closure of
AV valve
Due to reverse of Treppe phenomenon there can be
diminished contractility in sinus bradycardia leading
to diminished first sound
Prolonged P-R interval Premature mitral valve closure
Severe mitral regurgitation Loss of isovolumic systole
Failure of leaflets to close
Fibrosis shortening and diminished mobility of valve
Chronic severe AR Loss of isovolumic systole
Premature closure of MV (rare)
Acute severe AR Premature closure of MV (common)
Loss of isovolumic systole
Ventricular aneurysm Loss of isovolumic systole
Diminished ventricular contractility
Acute myocardial infarction Diminished ventricular contractility
Prolonged PR interval
LBBB 305
Myocarditis Loss of contractility
Cardiomyopathy As above and under myocardial infarction
Calcific MS Immobile mitral valve
Left bundle branch block Asynchronous ventricular activation
Betablocker therapy Depressed ventricular function
Bradycardia
In atrial fibrillation variation in diastolic cycle lengths results in variable position

of the AV valve by the end of the diastole (Fig. 17.6); the force of ventricular
contraction is also variable due to the differing diastolic volumes of the ventricle.
In complete heart block, ventricular tachycardia and classic AV dissociation,
variability in first sound due to the variability of the P-R interval. In mitral stenosis,
in spite of atrial fibrillation, the first heart sound may not vary significantly due to
a very loud first heart sound. The valve is generally kept open irrespective of the
diastolic cycle lengths due to high left atrial pressures.
ECG
Fig. 17.6: Mechanism of varying intensity of first heart sound in atrial fibrillation
306
ECG
Fig. 17.7: Mechanism of varying first heart sound in complete heart block
In complete heart block, due to dissociation of atrial and ventricular activation,

the atria and ventricles contract independently. When the atria contract just before
the ventricular contraction, the first heart sound tends to be loud (Fig. 17.7).
Similarly, if the atria contract much before ventricular activation, the first heart
sound tends to be softer.
Similar to complete heart block, there may be atrioventricular dissociation in
junctional tachycardia resulting in varying intensity of first heart sound (Fig. 17.8).
Varying diastolic intervals result in differing force of ventricular contraction,
which also determines the intensity of first heart sound (Fig. 17.9). The
atrioventricular dissociation also contributes to the varying first heart sound.
ECG
307
Fig. 17.8: Mechanism of varying intensity of first heart sound in AV dissociation
ECG
Fig. 17.9: Mechanism of varying intensity in atrial flutter with variable block
Mechanism and significance of varying first sound in ventricular tachycardia

Variation in S1 intensity, irregular cannon waves in jugular venous pulse, and
variation in arterial pressure are well known signs of ventricular tachycardia. In a
recent study, Garratt et al analyzed systematically the value of physical signs in the
bedside diagnosis of ventricular tachycardia. It has been shown that variable
intensity of S1 and jugular venous pulse are highly specific and sensitive in the
diagnosis of ventriculoatrial dissociation during ventricular tachycardia. The
variability of arterial pulse volume was not very helpful.
First heart sound split

The causes of a wide split first sound could be:
• Right bundle branch block
• Ebstein’s anomaly of tricuspid valve
FIRST HEART SOUND IN VARIOUS CLINICAL STATES
308 MITRAL STENOSIS

The loud first heart sound in mitral stenosis calls attention to the possible presence
of mitral stenosis, as this sign is the easiest to detect. The mid-diastolic murmur
and opening snap are not as easily detectable. With calcification or severe
subvalvular fusion the sound is reduced or altogether absent. The intensity of first
heart sound is no guide to the severity of mitral stenosis but may help in assessing
the pliability.
Mechanism of loud first heart sound

The mechanisms of a loud first heart sound in mitral stenosis are:
• Open mitral valve at end diastole
• Delayed closure of mitral valve
• Mitral valve closure at higher pressure of left ventricle
• Thickened but mobile mitral valve
The thickened leaflets and high pressure in the left atrium are the central
features.
Causes of soft first heart sound

The causes of normal or diminished first heart sound in mitral stenosis are:
• Heavily calcified mitral valve
• Severe subvalvular fusion
• Associated mitral regurgitation
• Associated severe aortic regurgitation
• Masked left ventricular events due to severe right ventricular hypertrophy
The aortic ejection click is often mistaken for a loud first heart sound. When
the first heart sound is louder at the base than the apex, an ejection click is likely.
MITRAL REGURGITATION
The first sound is diminished or absent in mitral regurgitation depending on the
severity of mitral regurgitation. In mild mitral regurgitation, the first heart sound
is normal but is diminished or absent in moderate to severe mitral regurgitation.
The loss of isovolumic systole and lack of leaflet apposition may be responsible
for reduction in the intensity of the first heart sound.
309
Mechanism
The mechanisms of reduced first heart sound in mitral regurgitation are:
• Loss of isovolumic systole
• Fibrosis and shortening of leaflets
• Failure of leaflets to close
• Myocardial dysfunction as in secondary mitral regurgitation
Causes of loud first heart sound

If the first heart sound is loud, mitral regurgitation is unlikely and one of the
following conditions is likely:
• Loud ejection click of AS mistaken for first heart sound
• Severe TR of silent mitral stenosis, mistaken for mitral regurgitation
• Associated mitral stenosis
• Mitral regurgitation of MVP
• Rheumatic mitral regurgitation with well preserved anterior leaflet
When aortic stenosis is mistaken for mitral regurgitation, the accompanying
ejection click will be mistaken for a loud first heart sound. In mitral valve prolapse
when the prolapse occurs early the click simulates a loud first sound. In some
children with rheumatic mitral regurgitation, the first heart sound is loud with a
well preserved anterior leaflet. This has implications in management as these valves
are amenable to repair of the valve and mitral valve replacement can be avoided.
The first heart sound is diminished out of proportion to the severity of mitral
regurgitation in papillary muscle dysfunction of coronary artery disease and
functional mitral regurgitation of cardiomyopathy.
The causes of milder mitral regurgitation with diminished first heart sound are:
• Mitral regurgitation in coronary artery disease
• Papillary muscle dysfunction
• Severe ventricular dysfunction
• Accompanying first degree AV block
• Left bundle branch block
• Secondary mitral regurgitation in cardiomyopathies
The basic underlying mechanism in all the above conditions is severe left
310
ventricular dysfunction which by itself decreases the intensity of S1.
Loud S1 with normal heart rate and P-R interval could be indicative of mitral
stenosis.
The intensity of S1 has no correlation to the severity of mitral stenosis.
A loud S1 does not rule out calcified mitral valve.
Variable intensity of S1 is a very reliable sign of ventricular tachycardia and is
helpful in distinguishing it from supraventricular tachycardia with aberration.
This sign is more useful than some of the electrocardiographic signs.
18 The Second Heart Sound
The second heart sound is due to closure and vibrations of the semilunar valves.
The aortic component is louder and earlier than the pulmonary component. The
aortic sound is louder due to the higher pressure in the aorta. The aortic sound
occurs earlier and the pulmonic sound later, because of the pressures the valves
face and the ejection properties of the two ventricles. The pressures in the aorta
are higher and the left ventricular ejection is finished earlier. Additionally, the
hangout interval plays an important role.
Hangout interval
By the end of ventricular ejection, the ventricular pressures start falling and are
lower than the arterial pressures.
ECG S1 A2 P2
PHONO
EXP
INSP
CAROTID
MPA
HANGOUT INTERVAL
RV 65 msec
Fig. 18.1: Pressure wave form depiction of hangout interval on the right side
The semilunar valve is expected to close at the point of crossover of pressures

(the point where the ventricular pressure falls lower than the arterial pressure).
However, in reality, the semilunar valve closure does not occur at the time of
crossover of pressures but slightly later. This time interval from the crossover of
pressures to the actual occurrence of sound is called the hangout interval (Fig. 18.1).
The hangout interval is related to the pressures in the artery, distensibility and the
elastic recoil of the arterial system. Due to higher pressure and less distensibility,
the hangout interval on the aortic side is approximately 30 msec compared to
80 msec on the pulmonary side. The factors influencing hangout intervals are:
• Pressure beyond the valve
• Dilatation of the artery
• Distensibility of the arterial system
• Vascular impedance
• Phase of respiration
In reality, all these factors are interrelated. Inspiration, by stretching the
pulmonary vasculature, increases the hangout interval of pulmonary circulation.
312
EVALUATION OF SECOND HEART SOUND
The features used for evaluating the second heart sound are the split and the
intensity of the two components.
SPLIT
Normal split
The normal second heart sound is split into two components during inspiration
and is single during expiration (Fig. 18.2). During inspiration, we not only inspire
air into the lungs, but also draw in blood into the thorax, secondary to a fall in
intrathoracic pressure.
This inspiratory increase in venous return increases the stroke volume of the
right ventricle prolonging RV ejection. This postpones the pulmonic sound to a
later time in the cardiac cycle. The inspiratory decrease in venous return to the left
ventricle reduces the left ventricular stroke volume and shortens the left ventricular
ejection. This advances the aortic sound to an earlier time in cardiac cycle.
THE SECOND HEART SOUND
Fig. 18.2: Normal splitting of S2 with respiration
Abnormal split
Two features describe the characteristics of second heart sound splitting: the width,
and the movement with respiration. The determinants of a normal split are:
• Pressure difference between the two circulations
• Different ejection properties of the two ventricles
• Difference in the hangout interval in the aorta and pulmonary artery
• The right and left sided venous returns separated by the interatrial septum
• Ability of respiration to alter the above factors
313
• The simultaneous onset of electrical impulse to either ventricle
The possible abnormalities are:
• No split or single second heart sound
• Wide split variable
• Wide split fixed
• Reversed or paradoxic split
The single second heart sound: The single second sound by definition means
absence of an audible split in either phase of respiration.
Fig. 18.3: Definitions of splitting of second heart sound (S2): normal split, reversed split in
LBBB, wide split in RBBB
Table 18.1: Mechanisms of single second sound

Mechanism Disease
Only one semilunar valve is present Truncus arteriosus
One of the semilunar valves is atretic Pulmonary atresia
Aortic atresia
Posterior location of pulmonary valve Transposition of great vessels
Severe stenosis of one semilunar valve AS or PS, with or without calcification
Extreme loudness of one of the sounds Single loud P2 in extreme PAH
In severe pulmonary arterial hypertension, the pulmonic sound is extremely

loud and masks the preceding aortic sound by the phenomenon of retrograde
masking.
To recognize a single second heart sound one must auscultate carefully in
either phase of respiration, supine position with passive leg raising, during the
post-release phase of Valsalva, and tilting the patient upside down (in case of
infants). Normally the second heart sound split is audible only in the pulmonary
area unless the pulmonic sound is accentuated.
314
The detection of a single second heart sound is of diagnostic and prognostic
significance in various clinical settings.
The single second sound is due to
• Normal variant as in elderly people
• Congenital heart disease
• Acyanotic
• Severe AS especially calcific
• Severe PS
• Ventricular septal defect with PAH
Wide split second sound: The wide split by definition means an audible split in
expiration. This definition is qualitative and not quantitative. Theoretically, a wide
split can occur whenever the pulmonic sound occurs later or the aortic sound
occurs earlier (Fig. 18.4).
The normal A2-P2 interval ranges between 20 and 50 msec in inspiration. It
varies by >20 msec with expiration. When the split is more than 50 msec it is
easily appreciated as a wide split. Normally, the split is not detectable in standing
position, in expiration as the split is < 15 msec, which cannot be heard by the
Fig. 18.4: Wide splitting of second heart sound
human ear. Clinically, the split is defined as wide, if it is heard well in standing
position, in expiration.
The pulmonic sound can occur later when there is a delay in the onset of
electrical impulse to the RV or prolongation of right ventricular ejection (Table 18.2).
The aortic sound may occur earlier than normal when the left ventricular ejection
is finished earlier (than normal).
Table 18.2: Mechanisms and causes of wide split second heart sound 315
Mechanisms Causes
Prolonged RV ejection Moderate to severe PS
Severe pulmonary arterial hypertension
ASD (large RV stroke volume)
Severe right ventricular failure
Delayed electrical impulse to RV RBBB
LV pacing (epicardial pacing)
LV ectopy
Increase in hangout interval Normal variant
Idiopathic dilatation of pulmonary artery
ASD
Postoperative ASD
Pulmonic stenosis with post-stenotic dilatation
Earlier completion of LV ejection Severe mitral regurgitation
Extreme delay in aortic sound Reversed wide split
Impaired diastolic filling Restrictive cardiomyopathy
Hypertrophic disorders of myocardium
Fig. 18.5: Wide split

S2: in severe valvular pulmonary stenosis E: ejection click, SM: systolic murmur, A2: aortic
component of second sound, P2: pulmonic component of second sound, DN: dicrotic notch.
316
SUPINE
STANDING
Fig. 18.6: Normal spilt that is audible in supine position disappears in standing position
In conditions with diastolic dysfunction, a change in filling pressure evokes a

smaller change in cardiac dimension. This results in lesser alteration in systolic
performance with respiration causing ‘fixed’ or near fixed split of second heart
sound.
Some of the conditions mentioned above are associated with a ‘wide and
fixed split’. The split is considered as ‘fixed’ if the two components fail to move
with respiration. The normal second heart sound split varies because of the ability
of respirations to vary the venous return to either side of the heart
The variability of the second heart sound split could be due to:
• The two atria separated by interatrial septum
• Ability of respirations to alter venous return to either side of heart
• A competent non-failing right ventricle capable of increasing the output
by the increase in stroke volume
Once the reasons for the variability of the split is known, the mechanisms of
a ‘fixed’ split are easy to understand.
Causes of wide and ‘fixed’ split Mechanisms of ‘fixed’ split
317
Atrial septal defect Defect in the interatrial septum allowing free
communication between the two atria
All the causes of wide split with Right ventricle failing to increase the stroke
associated severe right ventricular failure volume from the increased venous return
Recognizing a wide and ‘fixed’ split: An audible expiratory split during standing
always means a wide split. Some normal children have an expiratory split in supine
position. In case of any doubt, the persistence of the split during the straining
phase of Valsalva can be looked for.
Reversed split: The reversed split by definition means an inaudible split during
inspiration and an audible split during expiration. A reversed split may occur due
to delayed occurrence of aortic sound or an early pulmonic sound. The mechanisms
of delayed occurrence of aortic sound may be electrical or mechanical. Earlier
than normal occurrence of pulmonic sound is generally due to an electrical
mechanism (Table 18.3).
Normally, the aortic sound precedes the pulmonic sound in both the phases
of respiration. When the pulmonic sound precedes aortic sound it is called a reversed
split. If the reversal is confined to expiration, it is called partial reversed split. Clinically,
Table 18.3: Mechanisms and causes of reversed splitting of second heart sound
Mechanisms Causes
Delayed electrical activation of LV LBBB
RV pacing
RV ectopy
Prolonged LV mechanical systole Severe AS
Severe systemic hypertension
During an episode of angina
Cardiomyopathy
Severe AR
Large patent ductus arteriosus
Increase of hangout interval on the Aneurysm of ascending aorta
aortic side Post-stenotic dilatation in AS
Early pulmonic closure Early electrical activation of RV as in type B
WPW syndrome. In WPW syndrome,
reversed split occurs only when there is
significant pre-excitation.
Severe tricuspid regurgitation
318
the reversed split is recognized by a wider split in expiration and often can be
mistaken for a wide normal split.
Clinical recognition of reversed split: Based on the degree of delay in A2, the
spectrum of reversed split varies from a single second heart sound to a frankly
audible paradoxical split (Fig 18.7). When the split is audible in expiration and not
in inspiration, it is fairly easy to recognize the reversed split.
Fig. 18.7: Paradoxical splitting of second sound, left bundle branch block depicted on right side
Fig. 18.8: Reversed splitting of second heart sound
The spectrum of reversed split is:

• A single second heart sound
• Incomplete reversed split
• Complete reversed split
• Reversed wide split variable
• Reversed wide split ‘fixed’ 319
In actual practice the reversed split is often confused for a wide and variable
split or a wide and fixed split. This is because in inspiration the split may narrow
or may remain the same when there is a left ventricular dysfunction in association
with aortic stenosis or left bundle branch block. The best way to appreciate the
reversed split is to trace the two components of the second heart sound away
from the pulmonic area to the apex. Normally only the earlier of the two
components (aortic sound) is traced to the apex and the last component is not
heard away from the pulmonary area. When the ‘later’ of the two components is
traceable to the apex a reversed split is likely.
INTENSITY
After evaluation of the split, the intensity of the two components of second heart
sound should be stated. As the mechanism of the closure of the atrioventricular
valves are different from that of the semilunar valves, the aortic sound and pulmonic
sound are influenced differently from S1. The intensity is influenced by:
• Pressure beyond the valve
• Flow across the valve

• Size of the vessel beyond the valve
• Stenosis of the valve
• Regurgitation of the valve
When the pressure beyond the valve is elevated, as in systemic or pulmonary
hypertension, the corresponding second sound is increased. When the flow across
the pulmonic valve is increased as in left to right shunts, the pulmonic component
is accentuated. The flow across the aortic valve is increased in hyperkinetic states
and aortic regurgitation. Dilatation of the vessel beyond the valve as seen in
pulmonary hypertension, left to right shunts and idiopathic dilatation of the
pulmonary artery also increases the pulmonic sound. The aortic component is
similarly affected when the ascending aorta is dilated as in aneurysm of the
ascending aorta. Stenosis of the semilunar valve with attendant restriction of valve
mobility, reduces the intensity of the corresponding second heart sound.
Whether the aortic sound is accentuated or diminished in aortic regurgitation,
depends on the mechanism of the regurgitation (Table 18.4). In aortic regurgitation
320
due to aortic root disease, as in syphilis or ankylosing spondylitis, the aortic sound
is usually accentuated. In aortic regurgitation due to aortic valve disease, as in
rheumatic heart disease, the aortic sound is diminished or absent due to a fibrous
and immobile valve. The aortic sound is often sharper than normal in congenital
bicuspid aortic valve as long as the valve is not significantly stenosed.
When the pulmonic sound is extremely loud and banging as in severe
pulmonary arterial hypertension, the preceding aortic sound cannot be heard due
to retrograde masking (Tables 18.5 and 18.6).
Table 18.4: Causes and mechanism of accentuated aortic sound
Causes Mechanisms
Systemic hypertension Elevated pressure beyond the valve
Dilated ascending aorta
Aneurysm of ascending aorta Dilatation of vessel
Aortic regurgitation Aortic root disease
Well preserved leaflet mobility
Increased flow across the valve
Dilated ascending aorta
Congenital bicuspid aortic valve Thickened but mobile aortic leaflets
Table 18.5: Loud pulmonic sound

Causes Mechanisms
Normal in infants and children Higher pulmonary arterial pressure
Adults with chest deformity or Proximity of PA to the stethoscope
thin chests
Pulmonary arterial hypertension Higher closing pressure of valve
Dilated PA
Left to right shunts Increased flow across the valve with
exaggerated valve excursion
Dilated PA
PAH
Hyperkinetic circulatory states Increased flow across the valve with
exaggerated valve excursion
Dilated PA
Table 18.6: Diminished pulmonic sound

Causes Mechanisms
Diminished
Normal in elderly
321
Thick chested adults
Pulmonary stenosis Diminished valve excursion
Dysplastic valve
Absent
Tetralogy of Fallot Severe pulmonic stenosis
Transposition of great arteries Pulmonary artery posteriorly located
Truncus arteriosus Pulmonary valve is absent
Pulmonary atresia
Absent pulmonary valve
Clinical evaluation
Normally, in the pulmonary area both components of the second heart sound are
audible and the aortic component is louder. The pulmonic component is localized
to the pulmonary area and the aortic component is widely audible in other areas.
Even in the pulmonary area, the aortic component is louder than the pulmonary
component. The pulmonic sound is considered accentuated if it is equal to the
aortic sound in the pulmonary area. Accentuation of pulmonic sound is graded as
mild (if it is equal to the aortic sound), moderate (if it exceeds aortic sound) and
severe (if it is extremely loud and banging). It is also expressed, respectively, as
(+), (++) and (+++).
Table 18.7: Grading and correlations of pulmonic sound intensity

Grading of pulmonic sound Basis Correlation to PA pressure
Normal Pulmonic sound less than A2 Normal PA pressures
Systolic <30
Mean 20
Mild or + Pulmonic sound equal to A2 Mild PAH
Systolic 30–35
Mean 20–30
Moderate or ++ Louder than A2 Moderate PAH
Systolic 40–75;
Mean 30–50
Severe or +++ Very loud/banging Severe PAH
Systolic >75
Mean >50
In mild pulmonary hypertension (PAH), the pulmonic sound is equal in

intensity to the aortic sound; in moderate pulmonary hypertension, the pulmonic
sound is louder than the aortic sound; and in severe pulmonary hypertension, the
322 pulmonic sound is very loud and banging. Other variables like chest wall thickness
or emphysema, might influence the correlations.
When the aortic sound is diminished as in aortic stenosis the audibility of the
pulmonic sound away from the pulmonary area, is helpful in its evaluation. The
grading of intensity of pulmonic sound as mild, moderate and severe is helpful as
it correlates well with similar degrees of pulmonary arterial hypertension.
Exceptions to this are patients with thin chest wall, chest deformities and children
(where the pulmonic sound can be loud as a normal variant). The intensity of the
pulmonic sound is underestimated in patients with thick chest wall, emphysema
with chronic cor pulmonale and some patients with primary pulmonary
hypertension and severe heart failure.
NORMAL VERSUS ABNORMAL HEART
In children and adolescents, systolic murmurs along the left sternal border and
pulmonary area are common. The differential diagnosis often involves an innocent
systolic murmur, straight back syndrome, atrial septal defect, or pulmonic stenosis.
If the second sound split is normal, the first two possibilities are likely.
Fig. 18.9: Innocent systolic murmur, physiological S3, normal split of S2
323
Fig. 18.10: Innocent systolic murmur in a child
The innocent systolic murmur in children is often accompanied by a physiological

third sound as shown in Figs. 18.9 and 18.10.
CONGENITAL HEART DISEASE
ATRIAL SEPTAL DEFECT

The second heart sound is wide and fixed. The pulmonic sound may be loud in
atrial septal defect (ASD) even in the absence of pulmonary arterial hypertension
due to increased flow across the pulmonic valve with a dilated pulmonary artery
(Fig. 18.11).
If the split varies with respiration in an atrial septal defect, either an ASD
is unlikely or is too small, or partial anomalous pulmonary venous drainage is
present. Even after the advent of Eisenmenger syndrome, the wide split continues
to be heard in atrial septal defect (Fig. 18.12).
Fig. 18.11: Phonocardiogram in a patient with artial septal defect
324
Fig. 18.12: Second heart sound in atrial septal defect
Typically, the split is wide and fixed with accentuated pulmonic sound, which
becomes intensifies with pulmonary hypertension. When Eisenmenger syndrome
develops, the split is still wide and fixed with a banging pulmonic sound. ASD
associated with pulmonic stenosis results in further widening of the split with
diminution in pulmonic sound intensity. The split can be mobile if there is a
restrictive atrial septal defect.
VENTRICULAR SEPTAL DEFECT

In small ventricular septal defect (VSD), the split is normal with a normal intensity
of pulmonic sound. In moderate ventricular septal defect with left to right shunt,
the split is normal with moderate accentuation of pulmonic sound. In a large

ventricular septal defect with left to right shunt the split is close or single. Once
pulmonary arterial hypertension develops with a balanced or right to left shunt
(Eisenmenger syndrome) the second sound is single as a rule. If the second heart
sound is wide split in a patient with ventricular septal defect, an AV canal ventricular
septal defect or associated atrial septal defect should be considered. Once the
stage of Eisenmenger syndrome is reached, the second sound is single. A wide
split second sound in an Eisenmenger ventricular septal defect indicates an
underlying AV canal ventricular septal defect. Pulmonic sound is diminished with
associated pulmonic stenosis (TOF physiology).
The aortic component of the second heart sound is usually normal in
ventricular septal defect. An unusually loud A2 in VSD should indicate the
possibility of the existence of a condition other than a simple VSD.
Table 18.8: Second heart sound in various subsets of ventricular septal defect
VSD subset Second heart sound split Mechanism
Small VSD Normal Normal PA pressures
P2 normal Normal hangout interval 325
Moderate VSD Normal or wide split Moderate PAH
P2 moderate intensity
Large VSD Close split or single S2 PA pressures near systemic range
P2 severe in intensity
AV canal VSD Wide split Associated RBBB, ASD or MR
Identical pressures
Eisenmenger VSD Single S2 as loud P2 Equalization of hangout interval in both
circulations
VSD as a part of a Single loud A2 Pulmonary stenosis
complex defect like Posteriorly located PA
TOF, TGA, or
DORV
VSD with coarctation Loud A2 Systemic hypertension
of aorta, unruptured Dilated aortic sinus
or ruptured sinus of Thickened but mobile valve
Valsalva, bicuspid
aortic valve
Diagnostic implications of loud A2 in VSD

• Associated coarctation of aorta
• PDA mistaken for VSD when the diastolic component of the continuous
murmur is inaudible or absent
• Bicuspid aortic valve
• Transposition of great vessels with VSD
• Unruptured or ruptured sinus of Valsalva with VSD
• Associated aortic regurgitation
Coexistence of any of the above conditions with VSD modifies the
management of a patient with VSD (Table 18.8).
PATENT DUCTUS ARTERIOSUS

The second heart sound is normally split in patent ductus arteriosus of different
sizes and remains so even after the development of severe PAH with Eisenmenger
syndrome. The split is usually difficult to hear due to the continuous murmur
326 covering the second heart sound (Fig. 18.13).
PULMONIC STENOSIS
The second heart sound is normally split in mild pulmonic stenosis. Once post-
stenotic dilatation occurs, the split can be wide and variable. In moderate and
Fig. 18.13: Second sound in patent ductus arteriosus

severe pulmonic stenosis, the second heart sound is wide and variably split with a
diminished pulmonic sound. The pulmonic sound can be absent in a severe
pulmonic stenosis. In the absence of post-stenotic dilatation, the degree of wide
split correlates with the severity of pulmonic stenosis (Fig. 18.14). A small ventricular
septal defect is often a differential diagnosis for a moderate or severe pulmonic
stenosis; the nature of the second heart sound split is helpful in diagnosis. A single
second heart sound in a pulmonic stenosis should suggest the possibility of
tetralogy of Fallot, dysplastic pulmonary valve or severe pulmonic stenosis itself.
BICUSPID AORTIC VALVE AND AORTIC STENOSIS

In congenital bicuspid aortic valve in the absence of stenosis or regurgitation, the
second sound is split normally and the aortic sound is normal or mildly accentuated
due to thickening of the valve. In moderate to severe aortic stenosis, the second
sound is single or reversed split due to prolongation of left ventricular ejection.
When the second heart sound split is reversed in aortic stenosis, the gradient
across the aortic valve is usually more than 70 mmHg.
The second heart sound is normal in mild aortic stenosis (Fig. 18.15).
327
The aortic sound may be sometimes accentuated with bicuspid valve. An unusually
accentuated aortic sound in a child should raise the suspicion of associated
coarctation.
Fig. 18.14: Second sound in pulmonic stenosis of varying severity

Fig. 18.15: Second heart sound in aortic stenosis (AS)
COARCTATION OF AORTA
The second heart sound is normally split and the aortic sound is accentuated. The
accentuation has diagnostic significance in the sense that blood pressures are not
328 routinely recorded in children and the loud aortic sound calls attention to the
possible presence of hypertension or coarctation.
Case summary
A two-year-old boy was seen by a pediatrician who suspected a heart murmur and referred
him to a cardiologist. After clinical and echocardiographic evaluation, a diagnosis of
hypertrophic non-obstructive cardiomyopathy was made and he was referred for further
evaluation. An ejection systolic murmur Grade 3/6 was heard along the left sternal border;
the ECG showed left ventricular hypertrophy with strain consistent with hypertrophic
cardiomyopathy. A repeat echocardiogram was interpreted as consistent with hypertrophic
non-obstructive cardiomyopathy. On a review examination the aortic sound was found
to be unusually loud for a child and blood pressures were recorded in both upper and
lower limbs which was diagnostic of coarctation.
CONGENITAL CYANOTIC HEART DISEASE

The second heart sound is central in the evaluation of cyanotic heart disease. With
rare exceptions, it is invariably abnormal in this setting (Table 18.9).
The important features of evaluation are:
Presence or absence of split
• Site of best audibility
• If split, normal or wide split

If single
• The site of best audibility
• Intensity
The causes of a wide split second sound in cyanotic heart disease are:
• Total anomalous pulmonary connection
• Single atrium
• ASD at fossa ovalis with preferential drainage into left atrium
• ASD with Eisenmenger syndrome
• PS with intact ventricular septum and right to left atrial shunt
• Primary PAH with right ventricular failure and right to left atrial shunt
Table 18.9: Single second heart sound in cyanotic heart disease

Condition Site of best audibility Mechanisms
TOF Single loud A2 Absent P2 due to PS
LLSB Loud A2 due to dilated, dextroposed aorta. 329
Best audibility at LLSB because of normally
related aorta
D-TGA Single loud A2 Single S2 due to inaudible P2 due
Left second space to posteriorly placed PA. Left second space
audibility due to superiorly located aorta
L-TGA Single loud A2 best Single S2 due to inaudible P2 due to
heard at left second space posteriorly placed PA. Left second space
audibility
Split may be audible at due to superiorly located aorta.
right second space Split audible at right second space due to PA
placed to the right of aorta
DORV As in D-TGA As in D-TGA
Single ventricle As in D-TGA As in D-TGA
Tricuspid atresia Single loud A2 at LSB, Absent P2 due to PS
apex Normally located aortic valve
Truncus arteriosus Single loud truncal Single because only one semilunar valve
valve closure at LSB, present
apex Loud due to dilated truncal root
Normally located truncal valve
Table 18.10 Second heart sound in Eisenmenger syndrome

Condition Nature of split
ASD Wide and fixed
VSD Single loud P2
PDA Close split with normal inspiratory split
VSD of AV canal type Wide and fixed
TGA, single ventricle, DORV Single second sound
TAPVC Wide and fixed
The commonest of cyanotic heart diseases, tetralogy and transposition have

a single second heart sound. A normally split second sound is extremely uncommon
in cyanotic heart disease and it is a good practice to recheck the physical sign. The
causes could be:
• The patient may not be cyanotic
• The second sound may not be split
• If cyanosis is real, consider methemoglobinemia
• Pulmonary arteriovenous fistula
330 • Vena caval drainage into left atrium
The Eisenmenger syndrome is often considered the end stage of all left to
right shunts. But there is recent evidence to suggest that some forms of this
syndrome are still operable with a favourable outcome. Evaluation of the second
heart sound in a patient with Eisenmenger syndrome gives a clue to the underlying
defect (Table 18.10).
VALVULAR HEART DISEASE
MITRAL STENOSIS
The second heart sound is normally split in mild to moderate mitral stenosis
(MS), and is close split or is single in severe mitral stenosis with severe pulmonary
hypertension. The intensity of pulmonic sound correlates well with the severity of
pulmonary hypertension. The second heart sound opening snap, is often mistaken
for a wide split second sound in mitral stenosis. The fact that the first component
is louder is a clue that one is dealing with second heart sound and opening snap.
In mitral stenosis with pulmonary hypertension, in the combination A2-P2, the

last of the two components is louder. When the second sound is wide split in
mitral stenosis, an associated atrial septal defect should be considered. Among all
valvular lesions, mitral stenosis produces PAH most commonly and consistently.
For this reason, if the pulmonic sound is very loud in aortic valve disease, underlying
mitral stenosis is likely.
The second heart sound in mitral regurgitation (MR) gives clues as to the cause,
severity and complications of MR. The nature of split is a clue to the severity and
cause of mitral regurgitation. The intensity of pulmonic sound is a clue to the
complications of MR. The second heart sound in MR when combined with other
features gives valuable information in assessment (Table 18.11). One of the
common errors is to mistake the third heart sound at the apex as second sound in
moderate to severe mitral regurgitation.
AORTIC REGURGITATION
331
The second heart sound in aortic regurgitation varies depending on the cause, left
ventricular function and the associated lesions. The second heart sound is split in
the majority of patients with mild, moderate and even severe aortic regurgitation.
In severe aortic regurgitation, particularly in association with left ventricular failure
the second heart sound may be single or reversed split. The intensity of the aortic
sound in aortic regurgitation depends on the cause of the regurgitation. In aortic
regurgitation due to aortic root disease, the aortic sound is accentuated; in
regurgitation due to valve affection, the aortic sound is diminished or absent. The
pulmonic sound can be loud in aortic regurgitation after the onset of left ventricular
failure. However, a very loud pulmonic sound in the setting of aortic regurgitation
generally means an associated mitral valve disease. Aortic valve disease producing
loud aortic sound is unusual but occurs with aortic regurgitation in association
with ventricular septal defect and tetralogy of Fallot. Though the list of causes is
long for loud aortic sound with aortic regurgitation, they are all uncommon causes
for aortic regurgitation. The commonest cause for aortic regurgitation remains
rheumatic.
Table 18.11: Second sound in mitral regurgitation

Second sound MR subset
Normal split Mild to moderate MR
Wide and variable split Severe MR
Associated RBBB
Wide and fixed split Severe MR with heart failure
Associated ASD
MR as part of AV canal defect
Reversed split MR associated with HOCM
Functional MR in severe AS with LVF
MR in coronary artery disease
Functional MR in cardiomyopathy
Single second heart sound MR in association with L-TGA
Functional MR in severe calcific AS with LVF
All causes of reversed split
Normal intensity of P2 with severe MR The syndrome of severe MR with giant LA with
normal LA, PV, and PA pressures
Loud P2 with moderate MR The subset of less severe MR with smaller LA with
high LA, PV and PA pressures
332
Causes of loud aortic sound in aortic regurgitation (aortic root disease)

Syphilis
Marfan’s syndrome
Annuloectasia of aortic root
Rheumatoid arthritis
Reiter’s syndrome
Aortic dissection
Functional aortic regurgitation in severe systemic hypertension
Loud A2 with aortic valve disease (prolapse of the leaflet(s))
Ventricular septal defect with aortic regurgitation
Tetralogy of Fallot with aortic regurgitation
Diminished A2 in aortic regurgitation (aortic valve disease)
Rheumatic heart disease
In association with aortic stenosis
THROMBOEMBOLIC PULMONARY ARTERIAL HYPERTENSION

In the earlier stages of the disease, the only evidence is a mild accentuation of
pulmonic sound with a normal split. As the disease advances, the pulmonic sound
becomes louder and the split is narrower or single. In advanced stages of the
disease with right ventricular dysfunction, the split may be wide and fixed. As the
disease is asymptomatic in the early stages, and the chances for reversal are higher
at this stage, early detection becomes particularly more important. The earliest
evidence remains a chance detection of an accentuated pulmonic sound with a
narrow split or no split. In general, the pulmonic sound is unimpressive in the
early and sometimes even later stages of thromboembolic pulmonary arterial
hypertension. Normal intensity of pulmonic sound does not rule out pulmonary
hypertension in this setting. For this reason, all patients with recurrent dyspnea,
should have a careful echo Doppler evaluation to estimate pulmonary arterial
pressures. The threshold to investigate them further by catheterization and
angiography should be low.
SECOND SOUND IN A PATIENT WITH SHOCK

333
If carefully looked for, the second heart sound gives clues to the cause of shock
(Fig. 18.16). In non-cardiac causes of shock due to hypovolemia, the second heart
Fig. 18.16: Second sound in various shock states

Table 18.12: Second heart sound in shock

Condition producing shock Second heart sound
Hypovolemic shock Normal split
Pulmonic sound diminished
Cardiogenic shock Split reversed/normal or single
Pulmonic sound accentuated
Right ventricular infarction Normal split or wide split
Pulmonic sound diminished or normal
Cardiac tamponade Normal split
Pulmonic sound normal
Acute pulmonary embolism Wide split or normal split
Pulmonic sound accentuated or normal
Tension pneumothorax Normal or wide split
Pulmonic sound normal or accentuated
sound is normally split and both the aortic sound and pulmonic sound are normal
or diminished. In cardiogenic shock as in acute myocardial infarction or myocarditis,
the pulmonic sound is accentuated due to the attendant pulmonary hypertension.
334 In shock due to right ventricular infarction, the pulmonic sound is normal or
diminished. In pericardial tamponade the pulmonic sound is normal with a normal
split. In acute pulmonary embolism, the second heart sound may be wide split
with a loud pulmonic sound. However, in many patients, the pulmonic sound may
not be loud due to acute severe right ventricular dysfunction (Table 18.12).
Thus the evaluation of second sound is of immense value in the assessment
of the majority of heart lesions. With a normal split second heart sound and normal
intensity of both components, no significant heart disease is likely to be present.
Even if heart disease exists with a normal second heart sound, there is no precipitate
need for invasive investigation or surgical intervention. For that matter if the second
heart sound is normal in split with normal intensity of both components, congenital
heart disease is unlikely.
19 The Third Heart Sound
The third heart sound, also called a ventricular gallop or protodiastolic gallop,
follows the second heart sound during rapid ventricular filling.
MECHANISMS
Though various mechanisms are proposed for the genesis of third sound (Table
19.1, Fig. 19.1), the most consistent feature remains rapid ventricular filling. The
proposed mechanisms are valvular, ventricular and the impact of the left ventricle
on the chest wall. More than one mechanism may be responsible.
Table 19.1: Mechanisms of third heart sound
Valvular
Ventricular
Left ventricular chest wall interaction
Sudden limitation in the long axis filling
Movement of the ventricle
With the opening of the mitral valve, there is a sudden rush of blood from
the left atrium to the left ventricle, which is halted abruptly in situations where
early compliance of the LV chamber is decreased. Thus, S3 corresponds to the
peak of rapid filling wave (RF) seen in an apexcardiogram. The normal A2-S3
interval in LV varies between 120 and 160 msec. In pathological states, the third
heart sound is of early onset and is loud.
Whatever the mechanism, a sudden inherent limitation in the long axis filling
movement of the left ventricle is consistently observed. The third heart sound
occurs in all situations where there is rapid filling of the ventricle, and can happen
ECG
Fig. 19.1: Mechanism of third heart sound (S3).

S1: first heart sound, A2: aortic closure sound, P2: pulmonic closure sound, S3: third heart sound,
MVO: mitral valve opening, AVC: aortic valve closure, RF: rapid filling of ventricle
on either side of the heart. In the presence of AV valve stenosis no third heart
sound is possible, as rapid filling of the ventricle is impossible in this setting.
336 Table 19.2: Causes of third heart sound
Category Causes
Physiological Children
Young adults (<40 years)
Pregnancy
Pathological Ventricular failure (RV or LV)
Non-heart failure causes
Hyperkinetic circulatory state
Anemia
Thyrotoxicosis
Beri-beri
Volume overload
AV valve regurgitation
MR/TR
Semilunar valve regurgitation
AR/PR
ASD/VSD/PDA
S3 like sounds Pericardial knock
Tumour sound as in left atrial myxoma
THE THIRD HEART SOUND
Conditions producing the third heart sound can be grouped as physiological

and pathological. Pathological states could further be classified as heart failure
and non-heart failure states. In children and young adults, the third heart sound is
normally heard. It is not heard in normal infants and in adults beyond 40 years of
age. There are no distinctive features by which one can differentiate a physiological
from a pathological third heart sound. However, cardiac enlargement, in association
with loudness and early onset of third heart sound, generally signify a pathological
cause.
Though ventricular failure is the most important cause of third heart sound,
there are many other causes of third heart sound (Table 19.2). In all these states
the presence of the third heart sound should not be used as evidence of heart
failure. An easily audible third heart sound is less common with aortic regurgitation
than mitral regurgitation of similar degree. In fact, a clearly audible third heart
sound in the setting of aortic regurgitation generally suggests heart failure.
The pericardial knock of constrictive pericarditis for all practical purposes is
not distinguishable from the third heart sound. It is usually sharper, earlier in
onset, best heard along the left sternal border and increases during inspiration.
The tumor sound of left or right atrial myxoma can simulate a third heart sound. 337
A sound that is similar to the third heart sound in the presence of mitral stenosis
with little or no mitral regurgitation, may give a clue to left atrial myxoma.
In certain clinical states, the third heart sound occurs early and is close to the
preceding second heart sound. The range of second heart sound to third heart
sound interval at ordinary heart rates is 0.12–0.16 seconds. An early third heart
sound with normal heart rates of 70–90/minute is considered to be a feature of
constrictive pericarditis. Apart from constriction, any condition with very high
Table 19.3: Causes and mechanisms of third heart sound
Causes of early third heart sound Mechanisms of early third heart sound
Constrictive pericarditis High venous or atrial pressures
Severe MR with large V wave Very rapid reversal of pressures during early
Severe TR with large V wave diastole
Acute severe AR Very large V wave as in severe MR with small left
atrium
Any severe ventricular failure Small ventricular cavity with high filling pressures
as in constriction
venous or atrial pressures and quick reversal of pressures in early diastole may
have an early third heart sound.
The large V wave of severe mitral regurgitation is responsible for the early
third heart sound seen in this condition. Any severe ventricular failure with extreme
elevation of venous pressures behind the failing ventricle may cause an early third
heart sound. In a patient with features of congestive heart failure, a third heart
sound is almost always audible. An absent third heart sound in the presence of
‘congestive heart failure’ may suggest the possibility of pericardial tamponade or
AV valve stenosis. Otherwise the diagnosis of heart failure should be rechecked.
Correlations
In the presence of heart failure, the third heart sound correlates well with the
ventricular end diastolic pressures and is usually above 25 mmHg on the left side.
The right sided third heart sound correlates with a rapid y descent in the neck
veins. Other correlations are shown in Table 19.4.
AUSCULTATION TECHNIQUE
338 The third heart sound is a low frequency sound best heard with the bell; it can
occur on either side of the heart (Table 19.5). The left ventricular third heart
sound is best heard at the apex with the bell in the left lateral position during
expiration and is accentuated by isometric hand grip. Unless it is very loud, it is
localized to the apex. The right ventricular third heart sound on the other hand is
best heard along the lower left sternal border, increases during inspiration and
passive leg raising in supine position. It decreases in standing position and during
expiration. As the human ear is least efficient in appreciating low frequency sounds
in the range of third heart sound and fourth heart sound, we must carefully check
Table 19.4: Correlates of third heart sound
Anatomical Dilated ventricle
Functional Systolic dysfunction
(EF <40%)
Hemodynamic
LVEDP > 25 mmHg
Cardiac index < 2 l/min/m2
Symptoms Dyspnea, PND, orthopnea
Doppler flow across AV valves Tall E wave compared to A wave
Table 19.5: Features of left ventricular versus right ventricular third heart sound
Feature LV S3 RV S3
Site Apex LLSB
Respiration Better heard during Inspiration
expiration
Position Left lateral Supine position
Passive leg raising
Isometric hand grip Increases No change
Associated features Left sided cause for S3 Elevated JVP
Rapid y descent
for these sounds when the clinical circumstance demands. One simple method is
to start hearing at the pulmonic area and concentrate in the interval following the
second heart sound. Normally, this period in diastole is impressively silent at the
pulmonary area. After appreciating this silence following the second heart sound,
any extra sound appearing immediately after the second heart sound as the
stethoscope is moved toward apex, is easy to make out. Other sounds can be
heard using a similar method. 339
Once third heart sound is detected, one must mention whether it is right
ventricular or left ventricular, whether it is early or late, and whether it is
physiological or pathological.
SIGNIFICANCE OF THIRD HEART SOUND IN VARIOUS DISORDERS
Normal person
A physiological third heart sound can be heard in practically all healthy children
and adolescents but rarely in people beyond 40 years. This is attributed to vibrations
of the heart muscle arising from prominent early diastolic left ventricular filling
and the subsequent abrupt inflow deceleration. The reason why it fades with age
is unknown. The prevalence of physiological S3 decreases in parallel with the
reduction of the early diastolic left ventricular filling rate. The primary cause is
thought to be an age related increase in blood pressure with the development of
relative left ventricular hypertrophy and altered diastolic compliance. Kupari et al
in a population based study showed that nearly 25 per cent of healthy persons
aged 36–37 years have an audible physiological S3. The presence of this sound is
associated independently with leanness and with a relatively high peak early diastolic
transmitral velocity. With advancing age, the third sound disappears as the left
ventricular early filling decreases. The basic mechanism is probably not left
ventricular hypertrophy caused by increased blood pressure, as is widely believed
but a more primary alteration (ageing) of the left ventricular diastolic properties.
The third heart sound in normal children and during pregnancy can be
confused with mitral or tricuspid diastolic murmurs. The absence of any
abnormality of second sound, or absence of cardiac enlargement, are helpful signs
in diagnosis.
In adults with mitral regurgitation, the third sound helps in assessment of severity
of mitral regurgitation. Any mitral regurgitation beyond mild mitral regurgitation
is generally accompanied by the third heart sound. Moderate or severe mitral
regurgitation is almost always accompanied by the third heart sound. In a diagnosis
of moderate or severe mitral regurgitation, if the third heart sound is not heard
one must suspect an aortic stenosis simulating mitral regurgitation. As the third
340 heart sound is normally heard in children and adolescents, it cannot be used to
estimate the severity of mitral regurgitation. In severe mitral regurgitation, the
loudest sound at the apex is often the third heart sound and is often confused for
the second heart sound. An apical mid-diastolic murmur is common with severe
mitral regurgitation and the accompanying third sound rules out an associated
mitral stenosis. The third heart sound is so consistently present in mitral
regurgitation, that when a lesion, which is generally not accompanied by a third
heart sound, is diagnosed, the presence of the third heart sound makes associated
mitral regurgitation likely, as in aortic stenosis with mitral regurgitation.
Though the third heart sound is expected to occur in aortic regurgitation as in
mitral regurgitation, in actual practice third heart sound is rare in aortic regurgitation in
the absence of left ventricular failure. An easily audible third heart sound in aortic
regurgitation generally means a complicating left ventricular failure or an associated
mitral regurgitation. Aortic regurgitation can produce a third heart sound even in
the presence of associated mitral stenosis as rapid filling can occur through the
aortic valve. In acute aortic regurgitation, the first heart sound is absent or
diminished due to premature closure of the mitral valve and the only sound at the
apex is a loud third heart sound. This third heart sound is often mistaken for the
first heart sound and the short early diastolic murmur of aortic regurgitation
occurring along with third heart sound is mistaken for a systolic murmur. In the
setting of unexplained acute left ventricular failure or pulmonary edema one must
look for this combination of auscultatory findings. The mistake is compounded
by the fact that acute aortic regurgitation is not accompanied by the peripheral
arterial signs of aortic regurgitation, due to a high left ventricular end-diastolic
pressure.
Myocardial disease
In myocardial disease, the third heart sound provides insights into the anatomical
and functional nature of the disorder and allows a classification of the disease as
congestive or restrictive types. The third heart sound in this setting reflects systolic
dysfunction and the ejection fraction is usually less than 40 per cent. In restrictive
cardiomyopathies, the third heart sound occurs only when frank congestive failure
develops.
341
Congenital cyanotic heart disease
The third heart sound is not heard in tetralogy of Fallot, which is the commonest
cyanotic heart disease in children beyond 2 years of age. It is also not a feature of
lesions with a tetralogy like physiology, namely, a ventricular septal defect with
pulmonary stenosis. But the third heart sound is a feature of all cyanotic heart
diseases with increased pulmonary blood flow as in total anomalous pulmonary
venous connection, double outlet right ventricle without pulmonic stenosis, truncus
arteriosus and D-transposition of great arteries with ventricular septal defect. The
third heart sound also occurs in some cyanotic disorders with decreased pulmonary
flow as in Ebstein’s anomaly of tricuspid valve or severe pulmonic stenosis with
intact ventricular septum and right to left atrial shunt with heart failure.
Heart failure
A third heart sound is almost always heard in ventricular failure. This is more
often true in chronic disorders. In a significant number of patients with acute
myocardial infarction, the third heart sound is not easily audible in spite of left
ventricular failure. In this setting, the respiratory rate is a better indicator of LVF
than the third heart sound. In the presence of ‘heart failure’, if the third heart
sound is not heard, one must consider the possibility of cardiac tamponade or
mitral or tricuspid stenosis.
The causes of heart failure without third heart sound are:
• Pericardial tamponade
• Mitral valve obstruction
• Tricuspid valve obstruction
• Acute myocardial infarction with left ventricular failure in some patients
Shock syndrome
In a patient with shock or hypotension, presence of the third heart sound
distinguishes the cardiogenic cause of shock from the non-cardiogenic cause. In
the absence of the third heart sound any of the non-cardiogenic causes of shock
like hypovolemia or septic shock should be considered. Absence of a third heart
sound is a feature of shock due to cardiac tamponade and tension pneumothorax.
The causes of shock without third heart sound are:
• Hypovolemic shock
• Septic shock
342 • Cardiac tamponade
• Tension pneumothorax

In an atrial septal defect the expected right ventricular third heart sound is not heard and
the tricuspid diastolic murmur is a more consistent finding. The combination of
normal variant innocent systolic murmur and audible expiratory split is often
mistaken for an atrial septal defect in children. The physiological left ventricular
third sound in children often excludes an atrial septal defect as the left ventricle is
under filled in atrial septal defect.
A third heart sound in ‘atrial septal defect’ should suggest the possibility of
Ebstein’s anomaly mistaken for atrial septal defect. Other possibilities are, atrial
septal defect with mitral valve disease, and ostium primum atrial septal defect
with mitral or tricuspid regurgitation. In the absence of any of the above conditions,
right ventricular cardiomyopathy due to volume load should be considered.
20 The Fourth Heart Sound
MECHANISM
The fourth heart sound is also called the atrial or pre-systolic gallop. It precedes
the first heart sound and is a low frequency sound, like the third heart sound. The
fourth heart sound arises in the ventricle due to a forcible atrial contraction against
a non-compliant ventricle and can arise on either side of the heart. The requisites
for a fourth heart sound are a healthy atrium in sinus rhythm, a non-stenotic
AV valve and a non-compliant non-dilated ventricle.
Fig. 20.1: Pressure correlations of fourth heart sound (S4). For generation of fourth heart
sound RVEDP has to be more than 12 mmHg and LVEDP has to be more than 15 mmHg.
The fourth heart sound best correlates with ventricular end-diastolic pressure
(EDP) and height of a wave in atrial pressure tracing (Fig 20.1). The fourth heart
sound can be heard when right ventricular EDP is > 12 mmHg on the right side,
and left ventricular EDP > 15 mmHg on the left side. If the EDP is very high,
that is, greater than 25 mmHg, the fourth heart sound may be absent because of
insufficient pumping function of atria.
The requisite factors for a fourth heart sound are:
1. Atrial factors
A healthy atrium
2. Atrioventricular valve factors
Non-stenotic AV valve
3. Ventricular factors
Non-compliant non-dilated ventricle as in
• Ischemia
• Infarction
• Concentric hypertrophy
• Restrictive myopathy
344 • Acute volume load
4. Rhythm: sinus rhythm
When the atrial and ventricular factors are favourable, ventricular non-
compliance is the basis for the fourth heart sound. In a person beyond 60 years of
age, a fourth sound is usually recordable in phonocardiograms. However an easily
audible fourth heart sound at any age is generally abnormal.
Causes
Physiological (recordable not audible)
• Elderly people age above 60 years
Pathological
All causes of concentric left ventricular hypertrophy:
• Systemic hypertension (moderate/severe)
• Aortic stenosis (moderate/severe)
• Hypertrophic cardiomyopathy (obstructive/non-obstructive)
• Restrictive cardiomyopathies
THE FOURTH HEART SOUND
All causes of concentric right ventricular hypertrophy:

• Pulmonic stenosis (moderate/severe)
• Pulmonary arterial hypertension (moderate/severe)
• Restrictive cardiomyopathy
Coronary artery disease:
• Ischemia or infarction
Acute regurgitant lesions:
• Acute aortic regurgitation
• Prolonged P-R interval
CLINICAL RECOGNITION
The fourth heart sound is a low frequency sound and is capable of arising on
either side of the heart. The left ventricular fourth heart sound is best heard at the
apex with the bell of the stethoscope lightly applied during expiration. In contrast
to the third heart sound, the presence of which may mean ventricular failure, the
345
fourth heart sound does not indicate heart failure. It only signifies a ‘hardworking
ventricle’. Of late the importance of diastolic function of the ventricle is increasingly
being realized. Isometric hand grip accentuates it. The right ventricular fourth
heart sound is best heard at the lower left sternal border with the bell, in supine
position. It increases during inspiration and passive leg raising. Unlike its left sided
counterpart the right sided fourth heart sound is more widely audible along the
left sternal border and in the jugular notch.
SIGNIFICANCE IN VARIOUS DISORDERS

The fourth heart sound correlates with a hypertrophied non-dilated ventricle; the
left ventricular end diastolic pressure is usually above 15 mmHg (Table 20.1).
Left ventricular outflow obstruction

All forms of left ventricular outflow obstruction of more than moderate degree
generally result in concentric LVH with reduction in ventricular compliance. The
presence of the fourth heart sound correlates with a gradient of at least 50 mmHg
across the left ventricular outflow. This correlation with the degree of obstruction
is not applicable in hypertrophic cardiomyopathy where the fourth heart sound is
Table 20.1: Correlates of fourth heart sound

Anatomical Concentric ventricular hypertrophy with small cavity
Non-hypertrophied
Ischemia
Infarction
Functional Normal or supernormal systolic function
EF > 50%
Reduction in end-diastolic volume
Hemodynamic LVEDP > 15 mmHg
Electrocardiographic Normal sinus rhythm
P-R interval > 0.14 sec
Echo Doppler Ventricular hypertrophy of pressure loaded pattern
Atrial enlargement
Prominent a wave
Increase in wall thickness to cavity ratio
Exaggerated late diastolic wave pattern in AV valve
flow
Clinical
JVP Prominent a wave
346
Cardiac impulse Pre-systolic impulse
consistently present irrespective of the presence or the degree of obstruction.

With associated coronary artery disease or hypertension, a milder obstruction
may have a fourth heart sound. In the presence of severe aortic stenosis associated
mitral stenosis may be masked due to obliteration of the pressure gradient across
the aortic valve. The presence of the fourth heart sound in this setting rules out
mitral stenosis. The fourth heart sound of aortic stenosis is often better palpable
than audible due to the accompanying loud systolic murmur of aortic stenosis
masking the preceding fainter sound.
Even with severe aortic stenosis, the fourth heart sound may not be audible
in the presence of associated mitral stenosis or a complicating atrial fibrillation.
Right ventricular outflow obstruction

The fourth heart sound occurs when the obstruction is at least moderate. The
RV pressure is usually in the systemic range when a fourth heart sound is heard.
The right ventricular fourth heart sound correlates with a prominent a wave in the
jugular venous pulse measuring more than 15 cm and the right ventricular
end diastolic pressure is usually more than 12 mmHg. The right ventricular fourth
heart sound is more widely audible than its counterpart on the left side. It is heard
along the left sternal border and frequently over the jugular notch. Occasionally,
the fourth heart sound in severe pulmonic stenosis may be relatively long and may
simulate a pre-systolic murmur of tricuspid stenosis. The fourth heart sound of
pulmonic stenosis is better heard during inspiration and supine position or leg
raising. The inspiratory increase in fourth heart sound is accompanied by a
simultaneous decrease or disappearance of the ejection click of pulmonic stenosis.
This is related to the premature opening of the pulmonic valve due to the right
ventricular end diastolic pressures exceeding pulmonary artery diastolic pressures.
The fourth heart sound of pulmonic stenosis is also an indication of an intact
ventricular septum, and generally of the atrial septum too. In the presence of
associated ASD or VSD the right atrial force is dissipated into the left atrium or
the left ventricle respectively.
The fourth heart sound is not a feature of chronic mitral regurgitation as ventricular
dilatation is common in this setting. However, the fourth sound occurs in mitral 347
regurgitation when it is acute or chronic mitral regurgitation with ventricular non-
compliance.
Causes
Papillary muscle dysfunction or rupture
Chordal rupture
Post closed or open commissurotomy
Post balloon dilatation of mitral valve for mitral stenosis
Spontaneous as in mitral valve prolapse
Trauma
Prosthetic malfunction
• Chronic mitral regurgitation
Coronary artery disease with papillary muscle dysfunction
Hypertrophic obstructive cardiomyopathy
Endomyocardial fibrosis
Table 20.2: Mechanisms for absence of fourth heart sound in rheumatic mitral regurgitation
Feature Mechanism
Chronic mitral regurgitation Dilated compliant left ventricle
Associated mitral stenosis Force of atrial contraction cannot be
transmitted to left ventricle
Atrial fibrillation Absence of atrial contraction
Dilated unhealthy left atrium Atrium incapable of generating enough force
In the commonest form of mitral regurgitations, namely rheumatic, the fourth

heart sound is consistently absent (Table 20.2). The mechanisms precluding the
fourth heart sound in rheumatic mitral regurgitation are, the chronicity of mitral
regurgitation with a dilated left ventricle, atrial fibrillation, associated mitral stenosis
and a dilated, unhealthy left atrium.
Chronic aortic regurgitation is not usually accompanied by the fourth heart sound.
The fourth sound occurs when aortic regurgitation is acute or when the ventricular
348 compliance is reduced by an associated disorder. When a fourth sound is heard in
aortic regurgitation, an associated mitral stenosis can be ruled out with confidence
but a third heart sound is possible in spite of mitral stenosis as the ventricle can be
rapidly filled from the aorta.
Causes
Post-balloon dilatation for aortic stenosis
Post-surgical valvotomy
Prosthetic malfunction
Dissecting hematoma of ascending aorta
Retroversion of aortic cusp as in aortic root disease
• Chronic aortic regurgitation
Functional aortic regurgitation with severe systemic hypertension
Severe aortic stenosis with milder aortic regurgitation
Milder aortic regurgitation with associated coronary artery disease
Myocardial disease
The fourth heart sound in this setting allows the distinction between dilated and
restrictive cardiomyopathies. In the dilated form, the fourth heart sound is obviously
not a feature. The most important sound in restrictive cardiomyopathy is the fourth
heart sound. It is a reflection of a well maintained systolic function or ejection
fraction and an impaired diastolic function or relaxation of the ventricle.

Clearly audible and palpable fourth heart sound in coronary artery disease is
common. It usually denotes diastolic dysfunction with left ventricular end diastolic
pressure more than 18 mmHg. The most common cause of diastolic dysfunction
in this setting is myocardial ischemia or myocardial infarction. However, one should
also realize that hypertension which is commonly seen with coronary artery disease
can also generate a fourth heart sound. Additionally, patients with aortic stenosis,
either fixed or dynamic, can also have angina, fourth heart sound. These patients
usually have left ventricular hypertrophy and diastolic dysfunction. In the setting
of myocardial infarction, an audible fourth heart sound indicates that at least
10 per cent of myocardium is at jeopardy. In a patient with shock, a fourth heart 349
sound indicates that hypovolemia is unlikely as wedge pressure will be more than
18 mmHg.
21 Ejection and Non-ejection Clicks
EJECTION CLICKS
Clicks can be ejection or non-ejection. Ejection clicks in turn can be valvular or

vascular in origin. Normally, the semilunar valves open noiselessly. When the aortic
or pulmonic valve open noisily, ejection clicks occur. A valvular ejection click
occurs due to stenosis or deformity of either semilunar valve and is due to an
350 abrupt doming motion of the valve coming to an abrupt halt. The doming and
halting motion seen on echocardiogram coincides with the clinically audible click.
Clicks can result either from abnormality of the valve or the root of the
major vessels (aorta and pulmonary artery). In valvular stenosis, the click results
VALVULAR
VASCULAR
SYSTOLE
DIASTOLE
Fig. 21.1: Mechanism of ejection click (EC)

EJECTION AND NON-EJECTION CLICKS
from abrupt halting of a doming valve at the onset of ejection. The post-stenotic
dilatation contributes in the genesis of ejection click to some extent. Sometimes,
an ejection click can result solely from dilatation of the root due to halting motion
of the compliant root at the time of ejection.
VALVULAR CLICKS
Mechanism
The click is caused by the doming and abrupt halting movement of the valve.
Causes
• Aortic valve
Valvular aortic stenosis
Congenital bicuspid aortic valve
Congenital quadricuspid ‘aortic valve’ as in truncus arteriosus
• Pulmonary
Valvular pulmonary stenosis
VASCULAR CLICKS 351
Vascular clicks on the other hand arise due to sudden distension of the vessel
beyond the valve along with the opening movement of the valve. The mechanism
and significance, and the causes are given in Tables 21.1 and 21.2.
Table 21.1: Mechanism and significance of vascular clicks
Mechanism Significance
Increased pressure beyond Systemic hypertension
the valve Pulmonary hypertension
Increased flow across the Hyperkinetic circulatory states
valve Left to right shunts for pulmonary side
Regurgitation of semilunar valves
Dilatation of the vessel Dilatation or aneurysm of ascending aorta
beyond the valve Dilatation of pulmonary artery due to
Increased flow
Increased pressure
Idiopathic dilatation
Combination of the above factors
Table 21.2: Causes of aortic and pulmonary vascular clicks

Aortic vascular clicks Pulmonary vascular clicks
Systemic hypertension Pulmonary arterial hypertension
Aneurysm of ascending aorta Left to right shunts
Aortic regurgitation Anemia
Tetralogy of Fallot Thyrotoxicosis
Anemia Idiopathic dilatation of pulmonary artery
Thyrotoxicosis
Table 21.3: Vascular versus valvular clicks
Feature Vascular click Valvular click

Second heart sound
Intensity Loud Diminished or normal
Split Normal or close split Abnormal split wide or
or single S2 reversed
Palpable artery Often palpable Impalpable
beyond the valve particularly pulmonary artery
352
The corresponding second heart sound is generally loud in vascular clicks

and is diminished or normal in valvular clicks. Though the aortic sound and
pulmonary sound are often described as diminished or absent in aortic stenosis
and pulmonic stenosis, in mild lesions the corresponding second heart sound is
often normal or even mildly increased. This is related to thickened and mobile
aortic or pulmonary valves. For similar reasons, the aortic sound in a bicuspid
aortic valve is often sharper than normal.
EJECTION CLICK OF AORTIC STENOSIS

The ejection click of valvular aortic stenosis is usually best heard at the left second
space or aortic area and is also widely audible along the left sternal border and
apex. Occasionally it is heard best at the apex in which case it can be mistaken for
a loud first heart sound or a split first heart sound.
It is classically heard in aortic stenosis of bicuspid valve. The intensity correlates
with the pliability of the valve. It occurs earlier as the severity of aortic stenosis
increases and corresponds to the anacrotic wave.
ECG
Fig. 21.2: Aortic ejection click

353
Significance
• Best audible at the aortic area but is widely audible
• Constant
• Localizes the obstruction to the valve
• May be absent when the valve is calcified or immobile
• Is often mistaken for a loud first heart sound
• Absence of ejection click in a child with aortic stenosis makes valvular
aortic stenosis unlikely; sub valvular aortic stenosis or some other
diagnosis is likely
The ejection click of valvular aortic stenosis is constant and does not vary
with respiration unlike that of valvular pulmonic stenosis. Unlike in pulmonic
stenosis, a premature opening of the aortic valve never occurs in aortic stenosis.
(The left ventricular end diastolic pressure is never higher than aortic diastolic
pressure). As the ejection click is often clearly heard at the apex, it can be mistaken
for a loud S1. The ejection click is best heard at the base unlike the first heart
sound, which is best heard at the apex. In children with valvular aortic stenosis the
ejection click is always heard but can be absent in adults with calcified valves.
If an ejection click is not heard in a child with aortic stenosis, either aortic stenosis
is unlikely or there is an obstruction somewhere else (such as sub valvular or supra
valvular aortic stenosis). Calcification of the aortic valve is a rule in aortic stenosis
beyond the age of forty, particularly in males. Persistence of aortic valvular ejection
click in an elderly person with aortic stenosis usually indicates a milder obstruction.
Ejection click of congenital bicuspid aortic valve
A bicuspid aortic valve is one of the commonest congenital anomalies, occurring in
2 per cent of all live births. Its importance lies in its predisposition to infective
endocarditis and the potential development of aortic stenosis or regurgitation or both.
A loud aortic ejection click may be the only manifestation in the absence of
aortic stenosis or aortic regurgitation (Fig. 21.3). In the absence of accompanying
aortic stenosis or aortic regurgitation, the click is often mistaken for a loud first
heart sound. However, whenever the first heart sound is louder at the base than at
the apex, an ejection click is likely. In all patients presenting with fever one must
look for this sign, as it is important to diagnose infective endocarditis early.
The combination of a loud ejection click heard well at the apex resembling a
354 loud S1, and an accompanying early diastolic murmur of aortic regurgitation
heard clearly at the apex, often leads to a mistaken diagnosis of mitral stenosis.
However, the ‘loud S1’, louder at the base than at the apex, and what sounds like
a widely audible S1 split, are clues to aortic regurgitation due to bicuspid aortic
valve (Fig. 21.4).
EJECTION CLICK OF VALVULAR PULMONARY STENOSIS
The ejection click is best heard in the pulmonary area and is usually localized to
that area. In moderate to severe pulmonic stenosis, the click varies with respiration
Fig. 21.4: Congenital bicuspid aortic

Fig. 21.3: Spectrum of auscultatory valve with a loud ejection click and
findings in bicuspid aortic valve aortic regurgitation
and is better heard or audible only during expiration but is diminished or absent
during inspiration. In extremely severe pulmonic stenosis, the click may be heard
only during expiration or may be absent altogether. The variability of the click is
related to the elevated right ventricular end diastolic pressure (RVEDP) in moderate
or severe pulmonic stenosis due to concentric right ventricular hypertrophy
(Fig. 21.5). During inspiration, the increased venous return to the right ventricle
leads to elevation of RVEDP beyond the pulmonary artery diastolic pressure
resulting in premature opening of the pulmonary valve in diastole itself. In milder
degrees of pulmonic stenosis, as the RVEDP is normal, premature opening of the
pulmonic valve is not possible and the click may not vary.
Normally, with inspiration the pulmonary arterial diastolic pressure falls and
right ventricular diastolic pressure may remain unchanged as venous return increases
or may actually fall due to transmission of negative intrapleural pressure. However,
in valvular pulmonic stenosis, as the right ventricle is hypertrophied, the right
ventricular diastolic pressure tends to rise as venous return increases whereas
ECG
355
Fig. 21.5: Mechanism of variable ejection click in valvular pulmonic stenosis

pulmonary arterial pressure falls (as expected). This induces premature opening
of the pulmonary valve before the onset of systole due to elevation of right
ventricular diastolic pressure that exceeds pulmonary diastolic pressure. This
premature opening decreases the intensity of the ejection click in inspiration
(Fig. 21.6).
356
Fig. 21.6: Influence of respiration on pulmonary ejection click in pulmonary stenosis
Fig. 21.7: The ejection click and second heart sound in valvular aortic and pulmonic stenosis.
The ejection click in pulmonic stenosis varies in intensity with respiratory phases (increasing
in expiration and decreasing in inspiration), whereas that of aortic stenosis does not.
Table 21.4: Aortic versus pulmonary ejection clicks

Feature Aortic click Pulmonary click
Site of best audibility Aortic area Pulmonary area
Conduction Widely audible Localized to pulmonary area
Relation to respiration Constant Variable
Better heard during expiration
Accompanying features LVH RVH
Slow rising carotid pulse Prominent a wave in JVP
Systolic thrill at Systolic thrill at pulmonic area
aortic area, neck
Reversed split, Wide split S2 with diminished P2
diminished or
absent A2
357
Fig. 21.8: Expiratory increase of ejection click of pulmonic stenosis
Fig. 21.9: Clicks in mitral valve prolapse may be multiple and vary in timing
Similarly, the second heart sound split is very wide in pulmonic stenosis,
whereas it is either narrow or reversed in aortic stenosis.
NON-EJECTION CLICKS
The term non-ejection click (NEC) is applied to systolic sounds occurring at the
AV valves in prolapse of mitral or tricuspid valves due to myxomatous degeneration
of the valve.
In a normal mitral valve and left ventricle, the mitral valve fits into the left
ventricle like a cone. This conical shape of the mitral valve is a mechanical advantage
as the force of ventricular contraction is mostly expended on the outflow rather
than the inflow. With a flat curtain-like closure of the valve or prolapse, the valve
faces the brunt of left ventricular pressure.
Mitral valve prolapse

Mitral valve prolapse is a common clinical syndrome due to diverse pathogenic
mechanisms affecting the leaflets, chordae tendineae, papillary muscle, and mitral
358 annulus. It is known by vaious names:
• Mitral valve prolapse syndrome
• Systolic click murmur syndrome
• Barlow syndrome
• Billowing mitral cusp syndrome
• Redundant cusp syndrome
• Floppy valve syndrome
• Myxomatous mitral valve
It affects 3–5 per cent of the population. Overdiagnosis by echocardiography
is particularly common.
Determinants of first heart sound–non-ejection click interval

• Left ventricular end diastolic volume
• Rate of left ventricular ejection
The timing of the non-ejection click coincides with the maximal prolapse of the
mitral valve into the left atrium. The click may be single or multiple, with or
without mitral regurgitation.
Based on the degree of abnormality of the valve, the prolapse occurs at a
particular end diastolic volume of the ventricle. This is called the click volume.
The click volume for individual patients is constant unless the lesion progresses.
The ventricular end diastolic volume and the rate of ejection are the important
determinants of S1–non-ejection click (S1–NEC) interval. All the maneuvers that
decrease the ventricular end diastolic volume increase the prolapse and the click is
earlier and louder. On the other hand, the maneuvers that increase the volume of
the ventricle reduce the degree of prolapse and the click occurs later and reduces
in intensity or disappears.
The clicks can be single or multiple, persistent or intermittent. They are best
heard at the apex and being of high frequency are better heard with the diaphragm
of the stethoscope. If loud they can be heard in other areas. The murmur is late
systolic and characteristically changes in length with posture. It is usually best
heard at the apex but sometimes better heard at the lower left sternal border (Fig.
21.10). In contrast to the murmur of rheumatic mitral regurgitation, the murmur
of mitral valve prolapse is relatively rough and rasping in character. Mitral valve
prolapse (MVP) is often mistaken for a variety of other conditions. In view of
chest pain and electrocardiographic ST–T changes, MVP is often mistaken for
coronary artery disease. This mistake is compounded by the exercise test, which is 359
commonly false positive in MVP. While MVP generally carries a good prognosis,
the presence of coronary artery disease has serious implications. A patient with
MVP may present with a wide variety of features and one should look for MVP in
all these clinical situations.
All the maneuvers which decrease in left ventricular size results in movement
of the click towards S1 and which increase in size vice versa. Normally the chordae
prevent the leaflets from prolapsing into the atrium because of tensing movement
Fig. 21.10: Intermittent click murmur in mitral valve prolapse

MANEUVERS
Decrease in Ventricular Size
- STANDING
- VALSALVA PHASE II
- SQUATTING
- NITROGLYCERINE
- AMYL NITRATE
Increase in Ventricular Size
- SUPINE POSTURE
- EXPIRATION
- VALSALVA PHASE IV
- PHENYLEPHRINE
- PROMPT SQUATTING
- BRADYCARDIA
Fig. 21.11: Effect of various maneuvers on S1–NEC interval
due to (contraction of papillary muscles). When the chordae are long and redundant
as in a myxomatous valve, or the papillary muscle function is impaired, the leaflets
lose their support and prolapse into the atrium. As the chordae are stretched with
increase in ventricular size, the amount of prolapse decreases. The opposite
360
mechanism operates when the ventricle becomes small.
Situations in which mitral valve prolapse could occur are:
• Young patient with chest pain
• Unexplained ST–T alterations in inferolateral leads with or without chest
pain
• Recurrent palpitations or unexplained atrial or ventricular arrhythmias
Fig. 21.12: Relationship of ventricular size to the degree of valve prolapse

Table 21.5: Alterations in S1–NEC interval: effect of maneuvers

Maneuvers S1–NEC S1–M
Decrease in ventricular size
Standing
Valsalva phase II
Squatting Decreased Decreased
Nitroglycerine
Amyl nitrate
Increase in ventricular size
Supine
Expiration
Valsalva phase IV Increased Increased
Phenylephrine
Prompt squatting
(Phenylephrine increases the S1–NEC and S1–M interval and also increases the intensity of the murmur.
S1–NEC=First heart sound – non-ejection interval; S1–M=First heart sound murmur interval.)
• Any patient with syncope

• Any patient with fever
• Young patient with stroke
• All patients with mitral regurgitation 361
• All patients with atrial septal defect (Fig. 21.14)
• All patients with Marfan syndrome
• All patients with chest deformity
In all the above situations, auscultation should be performed as a matter of
routine, with the patient in standing position.
Fig. 21.13: Straight back Fig. 21.14: Atrial septal defect with mitral valve prolapse
APPROACH TO PATIENT WITH CLICK SOUND IN SYSTOLE
When an extra sound is heard in systole, one should answer the following questions
(see also Table 21.6).
• Is it a systolic click or some other sound mistaken for it?
• If it is a systolic click, is it an ejection click or a non-ejection click?
• If non-ejection click, is there associated mitral regurgitation?
• If ejection click, is it aortic or pulmonary?
• If aortic, is it vascular or valvular?
• If pulmonary, is it vascular or valvular?
• If pulmonary valvular click, is it due to mild, moderate or severe pulmonic
stenosis?
The loud first sound and split first sound may be mistaken for an ejection
click. The first sound is best audible at the apex and the split first sound is heard
only at the tricuspid area.
Table 21.6: Approach to a patient with clicking sound in systole
362 Finding Inference
Changes significantly with posture Non-ejection click
If NEC Look for the murmur of MR
No change with posture Ejection click either aortic or pulmonary
Best heard at aortic area but is widely Aortic ejection click
audible at LSB and apex
If aortic, A2 is normal or accentuated, Aortic vascular click
second heart sound normally split
If aortic, A2 is diminished, S2 is Aortic valvular ejection click
reversibly split
Best heard at pulmonary area, not Pulmonary vascular or valvular click
widely audible
Loud P2, palpable pulmonary artery Pulmonary vascular click
Wide split S2, diminished P2, Pulmonary valvular click, mild to moderate,
impalpable pulmonary artery with or severe
systolic thrill at pulmonary area
Better heard during expiration in Moderate or severe pulmonic stenosis
standing posture
THE OPENING SNAP
The opening of the normally thin atrioventricular valves is noiseless. However, in

disease the opening of these valves is associated with clicking noises called opening
snaps. The mitral and tricuspid valves, when stenosed cause, opening snaps though
there are many other causes of clicky or high-frequency noises in early diastole:
Mitral
• Mitral stenosis
• Mitral regurgitation (rare)
Tricuspid
• Tricuspid stenosis
• Functional tricuspid stenosis as in atrial septal defect
Tumoursounds
• Right atrial myxoma
• Aneurysm of interventricular septum as in ventricular septal defect 363
Pericardial knock of constrictive pericarditis
Though the opening snap can be recorded in the conditions mentioned above,
for all practical purposes, a clinically audible opening snap almost always means
mitral stenosis. In mitral stenosis, the opening snap is due to thickening of the
valve with a doming motion towards the left ventricle due to high pressure in the
left atrium.
The various mechanisms are (Fig. 21.15):
• Thickening of the valve
• High pressure in the left atrium
• Doming of the stenotic valve (anterior leaflet)
The time at which the opening snap occurs is a function of the left atrial
pressures. The higher the left atrial pressures, the earlier the opening snap. If the
left atrial pressures are lower, the opening snap may occur later. The second heart
sound–opening snap interval (S2–OS) is used to assess the severity of mitral
stenosis. It is inversely related to the severity of mitral stenosis. The shortest
S2–OS interval possible is 0.04 seconds and the longest is 0.12 seconds. At a heart
ECG
Fig. 21.15: Mechanism of mitral opening snap

364
rate of 70–90/min, a mild mitral stenosis has a S2–OS interval of 0.12 seconds, a
moderate mitral stenosis 0.08 seconds and a severe mitral stenosis will have a
S2–OS of 0.04 seconds.
In mitral stenosis, the leaflets are thickened and open with a doming motion.
The left atrial pressures are high at the onset of diastole and result in an abrupt
opening of the valve when the atrial pressure exceeds the ventricular pressure.
This results in the classical opening snap. A calcified valve does not result in
opening sound since the opening excursion is markedly restricted.
The left atrial (LA) pressure is higher with increasing severity of mitral stenosis.
Hence, the crossover point of pressures, that is, the point where the LA pressure
exceeds the LV pressure, occurs earlier and thus closer to the A2. Thus, the
A2–OS interval has an inverse correlation with the severity of mitral stenosis in
most situation (Fig. 21.16). The limitations of this correlation are discussed below.
Though the S2–OS is generally reliable in the estimating severity of mitral
stenosis, it may not be reliable in situations where the diastole is shortened or
prolonged with changes in heart rates, earlier or later occurrence of aortic valve
closure, or elevation of LVEDP, or significant changes in cardiac output (Table 21.7).
Fig. 21.16: Relationship of severity of mitral stenosis to S2–OS interval

365
Mechanisms altering the interval

• Alteration in heart rate
• Alteration in left atrial pressure
• Alteration in left ventricular end-diastolic pressure
• Alteration in aortic pressure
• Conditions affecting the velocity of mitral valve opening
• Aortic regurgitation
• Decreased left ventricular compliance
• Mitral valve calcification
Table 21.7: Second heart sound–opening snap interval in various degrees of mitral stenosis
Degree of mitral stenosis S2–OS LA pressure MVA

Mild mitral stenosis 0.12 sec 15 mmHg 1.5–2.5 cm2
Moderate mitral stenosis 0.08 sec 20 mmHg 1.0–1.5 cm2
Severe mitral stenosis 0.04 sec 25 mmHg < 1.0 cm2
Table 21.8: Conditions where second heart sound–opening snap is unreliable

Condition Shortened/widened Mechanism
Tachycardia Shortened Abbreviation of diastole
Bradycardia Prolonged Prolonged diastole
Hypertension Widened Early aortic closure
Aortic stenosis Shortened/widened Delayed aortic closure
Aortic regurgitation Widened/shortened Early aortic closure
Low cardiac output Widened Lower left atrial pressure
Severe RVF
Severe TR
Severe PAH
Increased LVEDP Widened Obliteration of transmitral
Coronary artery disease gradient
Cardiomyopathy
with systolic or
diastolic dysfunction
The opening snap is virtually pathognomonic of mitral stenosis. An audible

366 opening snap distinguishes mitral stenosis from other conditions simulating it. If
an opening snap is not heard in the setting of mitral stenosis, a calcified valve,
mitral regurgitation, severe aortic regurgitation, aortic stenosis, coronary artery
disease or any condition with left ventricular failure should be considered. In
general, a narrow S2–OS interval always indicates tight mitral stenosis. However,
when the interval is wide, tight mitral stenosis is not ruled out.
Missing opening snap in mitral stenosis

This could be due to:
• Severely calcified mitral valve
• Mitral regurgitation (significant)
• Aortic regurgitation (severe)
• Aortic stenosis (severe)
• Coronary artery disease with left ventricular dysfunction
• Any condition with associated left ventricular failure
• Very close S2–OS (<30 msec)
• Auscultatory incompetence
• OS heard but mistaken for wide split second heart sound
With milder degree of calcification, the opening snap may still be heard.
With all the other lesions, the lesion has to be severe enough to obliterate the
opening snap. For the information of the junior student and the general practitioner
the commonest cause for absence of opening snap is the inability to hear rather
than a real absence. Even when audible, the second heart sound–opening snap is
mistaken for a split second heart sound.
Clinical Recognition of OS and S2–OS Interval

The opening snap is a high-frequency sharp click best heard with the diaphragm of
the stethoscope. It is heard internal to the apex, left sternal border and occasionally
in the pulmonary area. As the murmur of the mitral stenosis is louder at the apex,
the opening snap is difficult to detect at the apex. Exercise may bring it out when
it is not heard at rest. It does not change significantly with respiration. When it is
heard at the pulmonic area, it may be confused for a wide split second heart sound.
Audibility over a wide area and the last of the two components being fainter
differentiate the opening snap from the wide split second sound. The best way for
a student to practice listening for the opening snap is take a patient with classic mitral
stenosis with easily audible opening snap, and auscultate for 20–30 minutes until you 367
get an audible feel of it. Then move away from the site of best audibility to the site
of least audibility when it becomes fainter. This is the type of sound one hears in a
‘difficult’ patient with mitral stenosis (silent mitral stenosis).
The S2–OS interval is best appreciated by the knowing and appreciating the
time intervals of other sounds. For example, the shortest S2–OS interval (0.04
seconds) sounds like a split second heart sound. The widest S2–OS sounds like an
early third heart sound as in severe heart failure, severe mitral regurgitation or the
pericardial knock of constrictive pericarditis (0.12 seconds). The moderate S2–
OS interval sounds like the wide split second heart sound of atrial septal defect.
The sounds following the second heart sound and their time intervals are:
S2 split (inspiration) 0.04–0.05 sec
S2 single (expiration) < 0.03 sec
S2 wide split 0.06–0.12 sec
S2–OS interval 0.04–0.12 sec
S2–pericardial knock 0.10–0.12 sec
S2–S3 interval (pathological) 0.12–0.16 sec
S2–S3 normal (children) 0.12–0.20 sec
368 Fig. 21.17: Sounds around A2 mistaken for OS
Sounds occurring around A2 can be mistaken for an opening snap (Fig. 21.17).
These include a third heart sound (S3), pericardial knock and P2. The normal
intervals between A2 and these sounds are given in Fig. 21.16. We can observe
from the values given, that there can be significant overlap between various intervals.
In mitral stenois the opening snap can give the following information:
• Diagnosis of mitral stenosis
• Differential diagnosis of mitral stenosis from conditions simulating it
• Assessment of severity of mitral stenosis
• Detection of complications like calcifications
• Recognition of associated disorders
If the S2–OS interval is wide but the patient has significant symptoms, one
should consider the possibility of left atrial myxoma as a cause of mitral valve
obstruction. In contrast to the audible opening snap of mitral stenosis or TS,
‘phonographically recordable’ opening snaps are described in a variety of conditions
(Table 21.9).
Table 21.9: ‘Recordable’ opening snaps in the absence of AV valve stenosis

Mitral opening snap Tricuspid opening snap
Mitral regurgitation (may be audible) Atrial septal defect
Mitral valve prolapse (may be audible) Tricuspid regurgitation
Heart block (second and third degree)
Tricuspid atresia
Tetralogy after shunt operation
Thyrotoxicosis
Hypertrophic obstructive cardiomyopathy
Mitral valve prolapse
The basic mechanism in most of these conditions is increased flow across

the AV valve. The degree of thickening and redundancy may play a role in mitral
valve prolapse. Valve thickening is also described as the mechanism in hypertrophic
cardiomyopathy. 369
DIFFERENTIAL DIAGNOSIS OF SOUNDS

In nature, there can never be two things which are exactly alike.
Leibnitz
The various sounds in systole and diastole can be represented as shown in Fig. 21.18.
Fig. 21.18: Clustering of additional sounds around S1 and S2

Table 21.10: Recognition of sounds

Confusion around first heart sound (S1) Confusion around second heart sound (S2)
Split S1 S2 split
S1–ejection click S2–OS
S1–non-ejection click S2–S3
S4–S1 Non-ejection click–S2 (rare)
For the purpose of clarity (confusion!), this can be divided into two groups:
• Confusion around S1
• Confusion around S2
The general principles by which one sound is differentiated from the other are
(Table 21.10):
• Site of best audibility of a sound
• Localized or widely audible
• Character of the sound
• Palpability
• Relation to a physiological act
370 • Accompanying features
Right sided ejection clicks are generally not confused with other sounds as
they are localized to the pulmonary area. These principles can be applied to each
of the sounds (Tables 21.11, 21.12).
Fig. 21.19: Differentiating confusion around S1 and S2

Table 21.11: Sounds around first heart sound (confusion around S1)
Feature Split S1 S1–EC S1–NEC S4–S1
Site of best Tricuspid area Base Apex Apex
audibility
Localized/ Localized Widely audible Widely audible Localized
widely audible
Character Low frequency High frequency, High frequency, Low frequency
sharp, clicky sharp, clicky
Palpability No No No Often palpable
Relation to Best audible No change in NEC loud and Isometric hand grip
physiological act during Aortic click earlier with increases S4
inspiration standing
Associated features Normal Aortic stenosis Mitral valve CAD
RBBB Bicuspid aortic prolapse Cardiomyopathy
ASD valve LVH with HTN
Ebstein’s
anomaly
Table 21.12: Sounds around second heart sound (confusion around S2)
371
Feature S2 split S2–OS S2–S3 NEC–S2
Site of best Pulmonary Internal to Apex Apex
audibility area apex
Localized widely Localized Widely Localized Variable
audible audible
Character High pitch High pitch Low pitch High pitch
Palpability P2 may be Not palpable Palpable Not palpable
palpable
Relation to Inspiration Respiration Expiration Standing posture
physiological act increases has no effect increases increases
Associated Normal Mitral Normal Mitral valve
features: RBBB stenosis Heart prolapse
ASD failure
Ebstein’s MR
anomaly
Though it is unusual for the non-ejection click to be delayed enough to be

close to the second heart sound, errors are common when this happens.
A child with valvular aortic stenosis should always have an ejection click. Absence
of it makes the diagnosis of aortic stenosis suspect, or the stenosis is at another
site, for example, subvalvular or supravalvular. This physical sign may sometimes
be more reliable than some echocardiograms. The following case summary
illustrates this.
Case summary
A 9-year-old girl was referred for evaluation of two echocardiogram reports done within
the same week. One of the reports read congenital bicuspid aortic valve, peak systolic
gradient of 104 mmHg, left ventricular hypertrophy. Another opinion was sought with a
repeat echocardiogram/Doppler. This time the report read congenital bicuspid aortic
valve, superior and inferior orientation, peak systolic gradient 57 mmHg, mild concentric
left ventricular hypertrophy. The cause for referral was the controversy over the gradients
across the aortic valve which was bicuspid.
Five years ealier, she was detected to have patent ductus arteriosus with left to right shunt
and congenital bicuspid aortic valve after two echocardiograms. Cardiac catheterization
confirmed the diagnosis of patent ductus arteriosus and aortic stenosis. The peak systolic
372 gradient across the aortic valve was 10 mmHg. Surgical closure of the ductus was done.
The child was followed up every year by echocardiogram and Doppler.
The child was asymptomatic and the physical examination revealed features of aortic
stenosis. The most remarkable feature was absence of an ejection click thus making Valvular
aortic stenosis unlikely. Yet another echocardiogram was ordered with a request to look
for subvalvular membrane as a cause for aortic stenosis. This time the echocardiographer
could see a thick subvalvular membrane close to the aortic valve. The aortic valve was
normal and tricuspid.
This summary illustrates the value of clinical examination in directing laboratory tests
and also the importance of the absence of ejection click in a child with aortic stenosis.
“You’ve heard about me, Mr. Holmes,” she cried, “else how could you know all that?”
“Never mind.” said Holmes, laughing. “It is my business to know things. Perhaps I have trained
myself to see what others overlook. If not, why should you come to consult me?”
22 Heart Murmurs
Murmurs, unlike sounds, are prolonged vibrations. They are due to disturbance in
blood flow, that manifests as turbulence. Turbulence is defined as an irregular
state of motion in which velocity and pressure show a random variation in relation
to space. The site of maximum intensity of a murmur generally corresponds to
the site of the turbulence (for example, the root of the great vessels in aortic
stenosis and pulmonic stenosis, the left atrium in mitral regurgitation and the
cavity of the left ventricle in aortic regurgitation).
Timing of murmurs
Murmurs are classified by their timing as systolic, diastolic and continuous. Figs. 22.1
and 22.2 show the various types of murmurs and Table 22.1 shows the classification.
Table 22.1: Classification of murmurs
Category Definition
Systolic murmurs Starts with or after S1, and ends before or at S2
Ejection systolic Starts after S1, ends before S2 of that side (A2 or P2)
Pansystolic Starts with S1 and ends with S2 of that side (A2 or P2)
Late systolic Starts after S1, ends with S2 of that side (A2 or P2)
Early systolic Starts with S1, does not reach S2
Diastolic murmurs Starts with or after S2, ends at or before S1
Early diastolic Starts with S2 (A2 or P2), duration in diastole is variable
Mid-diastolic Starts after S2, ends before S1
Late diastolic Starts late after S2 and extends to the S1 of that side
(mitral, tricuspid)
Holodiastolic Early diastolic murmurs occupying whole of diastole
from S2 to S1
Continuous murmur (CM) Beginning anywhere in systole, continues into diastole,
encompassing S2
Fig. 22.1: Definitions of systolic murmurs

PSM: Pansystolic murmur, starts with first heart sound and ends with second heart sound of that side
(A2 or P2); ESM: Ejection systolic murmur, starts after first heart sound and ends with or before
second heart sound of that side; LSM: Late systolic murmur, starts well after first heart sound and
ends with second heart sound of that side; SSM: Short systolic murmur, may start with or after first
heart sound and ends well before second heart sound; EM: Ejection murmur, starts after first heart
sound and ends well before second heart sound.
374
Fig. 22.2: Definitions of diastolic and continuous murmurs

EDM: Early diastolic murmur, starts with second heart sound of that side and ends at a variable
interval; MDM: Mid-diastolic murmur, starts after second heart sound and ends with or before first
heart sound; Pre-SM: Pre-systolic murmur, occurs just before systole ending in first heart sound and
is usually due to atrial booster; Continuous murmur: Begins anywhere in systole and continues into
diastole encompassing second heart sound; Systolo-diastolic: Combination of ejection or pansystolic
murmur with early diastolic murmur and can be mistaken for a continuous murmur.
HEART MURMURS
SYSTOLIC MURMURS
Systolic murmurs are principally classified as ejection systolic and regurgitant

murmurs.
Grading of murmurs
Systolic murmurs are graded, based on their intensity and the presence or absence
of thrill. As systolic murmurs often occur even in the absence of organic heart
disease, it is important to differentiate organic murmurs from functional murmurs.
Murmurs above grade 3 are usually organic; grade 4 murmurs are almost always
organic. As the presence of a thrill makes significant implications in the
interpretation of murmurs, one should be careful in eliciting this physical sign.
The palpable vibrations of the pulmonic sound in the pulmonary area and the
first heart sound at the apex are often mistaken for a thrill. A useful clue is that in
the presence of a thrill, the accompanying murmur is always loud. If the murmur
is faint, an associated thrill is highly unlikely. The original grading was applied for
systolic murmurs whose origin can be organic or functional. Diastolic murmurs
are not generally graded because the very presence of a diastolic murmur signifies 375
heart disease. Some clinicians grade diastolic murmurs by their length. The current
preference is to grade both systolic and diastolic murmurs by the same method.
Functional murmurs may be grade 4 in certain situations. The causes could be:
• Venous hum
• The ejection systolic murmur in the carotid in severe aortic regurgitation
• Mitral mid-diastolic murmur in severe mitral regurgitation
• Early diastolic murmur of pulmonary hypertension (especially in primary PAH)
• Ejection systolic murmur at the pulmonary area in atrial septal defect
Table 22.2: Grading of systolic murmurs
Grade of murmur Basis

Grade 1 Faint murmur heard on careful auscultation
Grade 2 Easily audible but not loud
Grade 3 Easily audible, loud murmur but no thrill
Grade 4 Murmur with a thrill and is usually loud
Grade 5 Murmur audible with the stethoscope partially applied to the chest
Grade 6 Murmur audible with the stethoscope half an inch to an inch away from the chest
The diastolic thrill in pulmonary regurgitation with pulmonary arterial

hypertension is often unexpected and the murmur is mistakenly timed as systolic.
Classification
Ejection systolic murmurs are of two kinds: organic, and functional or innocent.
Organic systolic murmur
LV outflow obstruction
• Valvular
• Subvalvular
Fixed
Dynamic (HOCM)
• Supravalvular
RV outflow obstruction
• Valvular
• Subvalvular
Infundibular
376 Double chambered RV
• Supravalvular
Functional or innocent systolic murmur

LV outflow
• Increased flow
Hyperkinetic states
• Dilation of ascending aorta
Aneurysm
Aortitis
RV outflow
• Increased flow
Left to right shunts (ASD, VSD)
Hyperkinetic states
HEART MURMURS
• Idiopathic dilatation
• Pulmonary artery hypertension
• Innocent systolic murmurs in children
• Chest wall and mediastinal factors
Chest deformities
Thin chest, straight back syndrome, pectus excavatum
Kyphoscoliosis, pulmonary fibrosis
The term organic is used to refer to a structural defect responsible for the
murmur. The terms functional and innocent are used to indicate a non-organic
cause for the murmur. A functional murmur by definition should subserve a
function like increased flow across the aortic valve as in the ejection systolic murmur
of severe aortic regurgitation. For this reason the terms innocent and functional
murmurs should not be used interchangeably. The term ‘innocent’ is used to refer
to murmurs that normally occur in the absence of anatomic or physiologic
abnormalities of the heart or circulation. They can occur at any age but are
particularly more common in children. Innocent murmurs are more common on
the right side of the heart across the RV outflow than on the left side. It is a good 377
practice to routinely look for intrinsic heart disease if a murmur is heard across
the left ventricular outflow in a young person.
Innocent or normal murmurs are of two types: systolic and continuous:
Systolic
• Vibratory murmur (Still’s murmur)
• Pulmonic systolic murmur
• Peripheral pulmonary systolic murmur
• Supraclavicular murmur
• Aortic systolic murmur
• Systolic mammary souffle
Continuous
• Venous hum
• Mammary souffle
EVALUATION OF A MURMUR
A murmur is the most important physical sign in the majority of valvular and
congenital heart diseases. A systematic evaluation is essential to derive maximum
information from this physical sign. Carefully analyzed, each component in the
description of a murmur is valuable in drawing conclusions. The important features
are:
• Site of best audibility
• Timing, configuration or shape
• Grading
• Length
• Character
• Selective conduction
• Relation to a physiological act or maneuver
• Accompanying features
Site
378 Murmurs of right sided origin are generally not heard at the apex. However, when
the right ventricle forms the apex, any of the right sided murmurs can be heard at
apex. The ESM of calcific aortic stenosis in elderly patients with severe emphysema
can be heard only at the apex due to two mechanisms:
a) Severe emphysema does not allow any portion of the left ventricle to
come into contact with chest wall except the region of apex.
Murmurs heard at mitral area or apex
Murmurs heard only at apex MDM of mitral valve origin
Mild or trivial MR
ESM of calcific AS in elderly with emphysema
EDM of AR (rare)
TR of Ebstein’s anomaly of TGA
Murmurs best heard elsewhere EDM of AR
but also heard at apex ESM of AS
MDM of tricuspid origin in ASD or TS
Pansystolic murmur of TR
Pansystolic murmur of VSD
Murmurs which are usually ESM of PS
not heard at apex EDM of pulmonary incompetence
Murmurs which are never heard at apex None
HEART MURMURS
Murmurs heard at tricuspid area (TA)

Murmurs heard only at TA Tricuspid stenosis
Mild tricuspid regurgitation
Small ventricular septal defect
Murmurs best heard elsewhere Mitral regurgitation
but also heard at TA Aortic regurgitation
Aortic stenosis
Pulmonic stenosis
Mitral stenosis (rare)
Murmurs which are generally Mitral stenosis
not heard in TA
Murmurs which are never heard at TA None
Murmurs heard at left sternal border (LSB) (third space)

Murmurs best heard at the LSB Pansystolic murmur of VSD
ESM of AS
EDM of AR
ESM of infundibular PS
Murmurs best heard elsewhere 379
but also along LSB ESM of valvular PS
TR
MR
Murmurs generally not heard along LSB MS
Murmurs never heard along LSB None
Murmurs heard at pulmonary area (left second space)

Murmurs best heard at the ESM of pulmonic stenosis
pulmonary area Flow murmur of pulmonary origin in ASD
Continuous murmur of PDA
VSD
Pulmonary incompetence
Murmurs best heard elsewhere AS
but also heard at pulmonary area VSD
MR
AR
Murmurs which are present but unusual MS
at pulmonary area TS
Murmurs which are never None
heard at pulmonary area
Murmurs heard at aortic area (right second space)

Murmurs best heard at the Valvular AS
aortic area Aortic valve sclerosis
Subvalvular membrane close to the aortic
valve
AR of aortic root origin
Murmurs best heard elsewhere All levels of LV outflow obstruction
but also heard at aortic area MR of mitral valve prolapse
AR of any etiology
VSD
Murmurs rarely heard at the PS
aortic area TR
Murmurs never heard at the MS (almost never)
aortic area
b) The loss of jet effect in a severely calcific valve, which prevents

conduction of the murmur to the carotids.
The mitral diastolic murmur is occasionally heard at the tricuspid area and
along the left sternal border.
380
The commonest murmur heard along the left sternal border is the pansystolic
murmur of ventricular septal defect.
It is extremely unusual for the murmur of mitral stenosis to be audible at the
pulmonary area but is possible in a rare case.
Timing
Timing of the murmur gives clues as to the site of origin of the murmur.
Ejection systolic murmurs: The ejection systolic murmur by definition means a
murmur starting some time after the first heart sound and reaching peak by
mid-systole or later and ending before the second heart sound. The moment the
ventricle begins its contraction, first heart sound occurs due to closure of the
AV valves but takes a while (isovolumic contraction time) to exceed the pressure
in the aorta to open the aortic valve and start ejection (Table 22.3).
Ejection systolic murmur-like murmurs may occur at other sites in some
special situations as listed above. However, the classic mid-systolic peaking and
late systolic tapering is rare.
HEART MURMURS
Table 22.3: Localizing value of ejection systolic murmurs

Site Mechanism
LV outflow Obstruction
RV outflow Increased flow
Increased pressure
Dilatation of vessel beyond
ESM-like murmurs
Small muscular VSD Valve-like mechanism
Large VSD Equalization of pressures/murmur may
actually be across the RV outflow
Acute MR/TR (early systolic) Small atria with obliteration of pressure in
later systole
MR/TR (short systolic) Milder lesions
PAH Equalization of pressures
Large ductus Equalization of pressures
Long narrow ductus Valve-like mechanism
Pansystolic murmurs: A pansystolic murmur is a reflection of a pansystolic 381

pressure difference between the two chambers in the heart. Only three sites in the
heart are capable of pansystolic murmurs, the ventricular septal defect, mitral
regurgitation and tricuspid regurgitation. In actual practice, the murmur of the
ductus may be mistaken for that of a ventricular septal defect when the diastolic
component of the continuous murmur is absent, as in a very large ductus with
either hyperkinetic or fixed pulmonary arterial hypertension. In severe aortic
stenosis or pulmonic stenosis, the very long ejection systolic murmurs may easily
be mistaken for a pansystolic murmur of either ventricular septal defect or mitral
regurgitation. The accompanying features of outflow obstruction help in the
differential diagnosis.
Late systolic murmurs: Late systolic murmurs arise at the mitral valve due to
mitral valve prolapse with mitral regurgitation.
Diastolic murmurs: These are of two kinds:
a) Mid-diastolic/pre-systolic murmurs: These murmurs are called mid-diastolic because
they occur some time after the closure of semilunar valve and before the opening
of the AV valve (isovolumic relaxation time). The pre-systolic murmurs are due to
Table 22.4: Localizing value of pansystolic murmurs

Site Mechanism
VSD Persistent high pressure difference between
LV and RV
MR Persistent high pressure difference between
LV and LA
TR Persistent high pressure difference between
RV and RA as in severe PAH or PS
Pansystolic-like murmurs
PDA (large) High PA pressures obliterate the diastolic
component of CM
Long ESMs of severe AS or PS Very high gradients, with prolonged gradient
and murmur
Table 22.5: Localizing value of mid-diastolic/presystolic murmurs
Site Mechanism
Mitral/tricuspid valve Forward flow of blood occurs at these valves
only after the closure of aortic and pulmonary
382 valves (A2, P2) and opening of mitral and
tricuspid valves. The time interval is called
isovolumic relaxation time.
Mid-diastolic like murmur
Pulmonary regurgitation with normal With low pressure pulmonary regurgitation
PA pressure at the pulmonary area produces turbulence later in the diastole
across the RV outflow
the atrial contraction maintaining flow in pre-systole or the last part of diastole.
Only two sites in the cardiovascular system are capable of these murmurs, the
mitral and tricuspid valves (Table 22.5).
The ‘mid-diastolic-like early diastolic murmur’ is heard in organic pulmonary
regurgitation with normal pulmonary artery pressures.
b) Early diastolic murmurs (EDM): The early diastolic murmurs begin flush with
semilunar valve closure of that side (aortic sound or pulmonic sound). They are
related to backward flow of blood across the semilunar valves under high pressure.
Only two sites in the circulation are capable of murmurs of this timing, aortic and
pulmonary regurgitations (Table 22.6).
HEART MURMURS
Table 22.6: Localizing value of early diastolic murmurs

Site Mechanism
Aortic valve regurgitation Backflow of blood occurs flush with aortic
component of second heart sound
Pulmonary regurgitation of PAH Backflow of blood occurs flush with
(Graham-Steell murmur) pulmonary component of second heart sound
Early diastolic like mid-diastolic murmurs
Tricuspid flow murmurs Tricuspid mid-diastolic murmurs are nearer
to P2 than their counterparts on the left side
Table 22.7: Localizing value of a continuous murmur over the precordium
Site Mechanism
Aorta or systemic artery with another
extracardiac site
PDA/AP window Aorta to pulmonary artery with a systolic and
diastolic pressure difference
Systemic arteriovenous fistula Artery to vein communication with a large
pressure difference continuously
Aorta to one of the cardiac chambers 383
Aorta to RA RSOV to RA
Aorta to RV RSOV to RV
The tricuspid diastolic murmurs appear closer to the pulmonic sound, as the
pulmonic sound occurs later than the aortic sound. Additionally, when the second
heart sound is wide split as in atrial septal defect, the ‘mid-diastolic murmur’ appears
even earlier.
Continuous murmurs: Continuous murmurs by definition start in systole and
continue into diastole overlapping the second heart sound. The continuous murmur
requires a communication between two sites in circulation, which have a continuous
high pressure difference. This type of pressure relationship is possible only with a
communication between two extracardiac sites or an extracardiac site with a cardiac
chamber.
Length
The length of a murmur is generally a reflection of the duration of pressure
difference between two sites in the cardiovascular system if a functional cause for
Table 22.8: Importance of length of the murmur

Condition Significance and mechanisms
All stenotic lesions Directly proportional to length
Exceptions
Conditions which increase flow Anemia, thyrotoxicosis, pregnancy, anxiety
Associated regurgitation Adds to the amount of blood that has to be
moved across the stenotic valve
Conditions which decrease flow Heart failure, low cardiac output as in elderly
people even without obvious heart failure,
diuretics
Proximal severe lesion Stenosis/regurgitation/shunt
Regurgitant lesions Generally unreliable
Pansystolic murmurs (MR/VSD/TR) Long murmur may be associated with lesion
of any degree of severity
Short murmur may be associated with any
degree of severity as in acute MR
Early diastolic murmurs
Aortic regurgitation Length of the murmur is directly proportional
to severity usually
Exceptions
384 Acute AR
LVF
Pulmonary regurgitation Due to PAH is longer and of high frequency
With no PAH is shorter and of low frequency
Continuous murmurs Short or long murmur may be associated with
any degree of severity
In arterial narrowing, the longer the murmur
and higher the frequency, the greater the
narrowing
a murmur is excluded. This is true in all stenotic lesions as in mitral stenosis, aortic
stenosis, pulmonic stenosis or tricuspid stenosis. In lesions producing pansystolic
murmurs, as in mitral regurgitation, ventricular septal defect, and tricuspid
regurgitation, this rule is not applicable. This is because the very presence of these
lesions results in pansystolic murmurs irrespective of the severity of the lesion.
On the other hand, absence of expected pansystolic murmur has important
implications in the evaluation of these lesions and will be discussed in detail under
those conditions. The length of the early diastolic murmur of aortic regurgitation
HEART MURMURS
generally correlates with the severity of aortic regurgitation, but relationship to

length is not as direct as in stenotic lesions. The length of the murmur has no
consistent correlation to the severity of lesions in regurgitant lesions. A short
systolic murmur of mitral regurgitation or tricuspid regurgitation may indicate
anything from a very mild to a very severe lesion or acute lesion. The accompanying
features are important. In aortic regurgitation, the length of the murmur correlates
better than in mitral regurgitation, but is not as reliable as in stenotic lesions.
A short early diastolic murmur may be due to mild, moderate or severe aortic
regurgitation with heart failure or acute severe aortic regurgitation.
Character
The character of the murmur is generally a clue to the lesion responsible. In general,
murmurs with a high pressure difference between the two chambers are of high
frequency or pitch, and those with a low pressure difference are of low frequency
or pitch.
385
Fig. 22:3: Relation between pressure gradients and the frequency of the murmur generated
Table 22.9: Character of the murmur

Feature Mechanism
High frequency (high pitch) High pressure difference between two sites
Soft MR (LV 120 to LA 12 mmHg)
Blowing AR (Aorta 80 to LV 12 mmHg)
Musical
Low frequency (low pitch) Low pressure difference between two sites
Rough MS (LA 20 to LV 5 mmHg)
Rumbling TS (RA 15 to RV 5 mmHg)
Mixed frequency High pressure difference between two sites
Rough AS (LV 200 to Aorta 120 mmHg)
Harsh PS (RV 120 to PA 25 mmHg)
VSD (LV 120 to RV 25 mmHg)
AR, PR (rare)
As a general rule, all regurgitant murmurs (mitral regurgitation, aortic

regurgitation, tricuspid regurgitation, pulmonary regurgitation) are of high frequency
and all stenotic murmurs are rough. The murmurs of AV valve stenosis (mitral
stenosis and tricuspid stenosis) are of low frequency but the murmurs of semilunar
386
valve stenosis are mixed in frequency. This combination of frequencies is a feature
of aortic stenosis, pulmonic stenosis and ventricular septal defect. The low
frequency or rough component of the murmur is best heard at the site of best
audibility of the murmur. The high frequency or soft component of the murmur
is more widely audible and is conducted to the other sites. This is the reason why
the murmur of aortic stenosis is soft at the apex, and is mistaken for mitral
regurgitation.
The character of the murmur depends on the pressure gradient across the
defect, the pressure in the distal chamber and the nature of the defect. The murmur
of aortic regurgitation may be rough in rare cases, be associated with a thrill and is
usually due to a retroverted aortic cusp in aortic root disease as in syphilis or
Marfan syndrome. The Graham Steell murmur of pulmonary arterial hypertension
can occasionally be rough and may have a thrill as in some patients with primary
pulmonary arterial hypertension or severe pulmonary arterial hypertension in
association with patent ductus arteriosus. When these diastolic murmurs sound
rough and have thrill, they can be mistaken for systolic murmurs.
HEART MURMURS
Table 22.10: Effect of physiological and pharmacological maneuvers on murmurs

Murmur Maneuver
Valvular AS vs MR MR murmur does not vary with cycle length,
but AS varies
Amylnitrite decreases MR
Phenylephrine increases MR
Valvular AS vs HOCM Valsalva maneuver, prompt squatting
increase the murmur of HOCM
MR vs TR Inspiratory increase of TR
MS vs Austin Flint murmur (A-F) Amylnitrite increases MS but decreases or
abolishes A-F
Phenylephrine increases A-F
MS vs TS Inspiration increases TS
Expiration increases MS
Pure PS vs tetralogy of Fallot Amyl nitrite decreases Tetralogy murmur
Rheumatic MR vs MR of MVP MR of MVP increases with Valsalva and
standing
PDA vs cervical venous hum Compression of neck veins
Supraclavicular bruit vs AS Extension of shoulder and compression of 387
sub clavian artery increase the bruit
Small VSD vs PS Amyl nitrite increases PS, decreases VSD
Phenylephrine increases VSD, no effect on PS
Large VSD with fixed PAH Amyl nitrite increases VSD murmur
vs hyperkinetic PAH in hyperkinetic PAH
S2–OS vs S2 split (A2–P2) Respiration effects S2 split but has no effect on
S2–OS
Phenylephrine decreases S2–OS
Sudden standing reduces S2 split, but has no
influence on S2–OS
S4–S1 vs S1 split S1 split widens with inspiration and Passive leg
raising
Sudden standing shortens S1 split, decreases S4 (RV)
Ejection click of AS vs PS In PS it is better heard during expiration
(variable)
S3 or S4, LV vs RV Inspiration increases right and expiration left
sided S3/S4
Supine/passive leg raising enhances right sided S3/S4
Standing decreases right sided S3/S4
Ejection click vs Standing, Valsalva enhance the non-ejection
non-ejection click of MVP click and move it towards S1
Physiologic and pharmacological maneuvers

This cannot be overemphasized as failure to use respiration to distinguish a right
sided murmur from a left sided one is similar to the failure to lateralize a hemiplegia
in a patient with neurologic disease.
Accompanying features
The accompanying features in each murmur help in interpreting the murmur
appropriately.
Table 22.11: Interpretation of murmurs: importance of accompanying features
Auscultatory event Accompanying feature Significance

ESM of LV outflow Slow rising pulse Fixed LV outflow obstruction
Bisferiens pulse AS+AR or HOCM
Normal pulse Aortic valve sclerosis or mild AS
EDM along LSB Collapsing pulse AR
Normal pulse PR or mild AR
Long systolic murmur Prominent ‘a’ wave in JVP Severe RV outflow obstruction
at 2nd or 3rd space Sustained parasternal impulse As above
388 Ejection click Valvular PS
Absence of any of the above signs VSD small
MDM at apex OS MS
Loud S1 MS
Diastolic thrill MS
S3 Flow murmur due to MR or post
tricuspid shunts
Severe AR Possible Austin-Flint
Atrial fibrillation MS
Pure RV impulse TR
Biventricular impulse VSD
Pansystolic murmur at LLSB Large ‘V’ wave in JVP TR
Forcible LV impulse MR
Sustained LV impulse AS
Long systolic murmur S3 MR
at apex S4 AS
Though the accompanying features are invaluable in identifying a murmur,

as a student practising auscultation, one should try to evaluate an auscultatory
event in isolation, without the assistance of these features. In actual practice, the
accompanying features are of great value in interpreting any auscultatory sign.
23 Systolic Murmurs
EJECTION SYSTOLIC MURMURS
Mechanism
There is always a time interval between the closure of the atrioventricular valve
and the opening of the semilunar valve. An ejection systolic murmur always
begins a while after the first heart sound. Once ejection begins, it reaches a peak
by mid-systole and hardly any ejection occurs in the late phase of systole. As a
result, these murmurs start after an interval from the first heart sound, reach a
peak by mid-systole and taper off by late systole. The most important members
of this group are the murmurs of aortic and pulmonic stenosis. These murmurs
will be dealt with in some detail.
Various causes of ejection systolic murmurs are depicted in Fig. 23.1. The
location, length, character of murmur, response to various maneuvers, and
associated features like an ejection click or regurgitant murmur will differentiate
the various causes one from the other.
LEFT VENTRICULAR OUTFLOW OBSTRUCTION

Left ventricular outflow obstruction occurs due to a variety of causes (Table 23.1).
Even in India, isolated aortic stenosis is not rheumatic. Calcific degeneration
of congenitally deformed bicuspid valve is a common cause of aortic stenosis. In
rheumatic aortic stenosis, the basic tricuspid architecture of the valve is preserved.
The cusps are fused along the commissures by the rheumatic process leading to
a conical valvular mass with a narrow orifice in the middle.
Fig. 23.1: Ejection systolic murmurs
390 Table 23.1: Causes of left ventricular outflow obstruction
Valvular Supravalvular Subvalvular

1. Rheumatic 1. ‘Hour glass’ type 1. Hypertrophic
cardiomyopathy
2. Bicuspid valve 2. Diffuse type 2. Discrete membranous
3. Unicuspid valve 3. Discrete membrane 3. Tunnel type
4. Acommissural with 4. Aortic dissection
central opening
5. Unicommissural 5. Homozygous
with eccentric opening hyperlipidemia
6. Myxoid dysplasia 6. Healing aortotomy site
7. Annular hypoplasia 7. Rubella
8. Calcific degenerative
9. Hyperlipidemia
10. Fabry’s disease
11. Infective endocarditis
12. Ochronosis
SYSTOLIC MURMURS
Fig. 23.2: Site of left ventricular outflow (LVOT) obstruction
The sites of obstruction can be subvalvular (fixed and dynamic), valvular

391
and supravalvular.
The significance of each of these features will be considered in the setting
of aortic stenosis. It is useful to ask the following questions when a murmur is
being evaluated for aortic stenosis.
Table 23.2: Murmur of valvular aortic stenosis
Site of best audibility Aortic area (second left space)
Also heard at left sternal border, apex
Timing Ejection systolic
Grade Usually 3/6
Length of murmur, time of peaking Short/medium/long
Character Harsh
Relation to physiological act Does not increase during inspiration
Decreases on standing and straining phase of valsalva
Accompanying features Slow rising arterial pulse
Sustained left ventricular impulse
Fourth heart sound, ejection click
Symptoms of angina, syncope, and dyspnea
Fig. 23.3: Ejection systolic murmur of aortic stenosis
Table 23.3: Evaluation of murmur of aortic stenosis
Is it AS or one of the conditions simulating AS?

Conditions simulating AS Aortic valve sclerosis
392 VSD
MR
PS
If AS, what level is the lesion?
Levels of LV outflow obstruction Valvular
Subvalvular
Supravalvular
If subvalvular what is the nature of obstruction?
Nature of subvalvular obstruction Dynamic (HOCM)
Fixed
Subvalvular membrane
Fibromuscular tunnel
If fixed, what is the severity?
Severity of obstruction Mild
Moderate
Severe
Are there any associated defects?
Associated defects in AS AR
Coarctation of aorta
PDA
SYSTOLIC MURMURS
The murmur of aortic stenosis should be evaluated with the issues shown in
Table 23.3 in mind.
MURMUR OF AROTIC STENOSIS
Site of best audibility/selective conduction

The murmur of valvular aortic stenosis is usually best heard at the right second
space, though it is also well heard at the left sternal border and apex (Fig. 23.4).
393
Fig. 23.4: Possible sites of best audibility of the murmur of HOCM

ao: aortic area, pa: pulmonary area, lsb: left sternal border,
llsb: lower left sternal border, sm: systolic murmur
Fig. 23.5: Wide audibility of the murmur of AS

Fig. 23.6: A 60-year-old man, calcific AS; aortic stenosis grade 5/6 aortic area, harsh musical
murmur at apex
It is selectively conducted to the neck vessels particularly to the right carotid (Fig.
23.5). Any deviation from this has significance. When the murmur is heard only
at the apex and nowhere else, a mistaken diagnosis of mitral regurgitation is often
made, but the lack of conduction to the axilla and back is helpful.
394
Timing
The presence of the ejection systolic murmur localizes the lesion to the outflow
from either ventricle. All other causes of ejection systolic murmur need to be
distinguished from the murmur of aortic stenosis.
Table 23.4: Site of best audibility and significance in aortic stenosis
Site of best audibility/selective conduction Significance

Best audible at right second space, Valvular non-calcific AS
conducted to right carotid
Best audible at left sternal border, Subvalvular AS (fixed or dynamic)
no carotid conduction Calcific AS (loss of jet)
Mistaken VSD
Mistaken MR
Carotid murmur with or without Supravalvular AS
right second space murmur Carotid stenosis
Audible only at apex Calcific AS in elderly with emphysema,
where apex is the only part of the heart
coming into contact with chest wall
Mistaken for MR
SYSTOLIC MURMURS
Length of the murmur and time of peaking in systole

The longer the murmur and the later in systole the murmur peaks, the more severe
the aortic stenosis. The duration of the murmur is a reflection of the duration
of pressure difference across the valve. This correlates with the slow rising pulse
and the sustained apical impulse of aortic stenosis. The duration of the murmur
correlates with the severity of aortic stenosis when the cardiac output is within
normal limits. Any significant change in cardiac output makes this sign unreliable.
Overestimation of the severity of aortic stenosis is a feature of high cardiac output
states and underestimation is a feature of low cardiac output states.
Conditions where it may be overestimated are:
• Anemia
• Thyrotoxicosis
• Pregnancy
• Associated aortic regurgitation
• Associated patent ductus arteriosus
• Anxiety
• Tachycardia 395
With a decreased cardiac output, underestimation is likely. With heart failure, the
murmur decreases in intensity and length (Table 23.5). In systemic hypertension
Table 23.5: Conditions where the severity of aortic stenosis is underestimated
Condition Mechanism
Heart failure Low cardiac output
Polycythemia Increased viscosity of blood
Associated proximal obstruction Low cardiac output
Mitral stenosis
Tricuspid stenosis
Associated proximal regurgitation or shunt Low cardiac output
Associated systemic hypertension or coarctation Obliteration of gradient
CAD/myocardial infarction Low cardiac output
Hypothyroidism Low cardiac output
Elderly female Low cardiac output
Higher NYHA class
Atrial fibrillation
and coarctation, as the aortic pressure increases the gradient across the valve
gets obliterated and the murmur may become shorter and less intense. If the
murmur is short with disproportionately severe left ventricular hypertrophy
and prominent S4, hypertrophic cardiomyopathy is likely as the degree of left
ventricular hypertrophy and severity of outflow obstruction may not go hand in
hand in this condition. If the murmur is very short with normal upstroke of the
arterial pulse and no left ventricular hypertrophy, aortic valve sclerosis is likely.
Character
The combination of low- and high-frequency components give the aortic stenosis
murmur its harsh or rough quality. The rough component of the murmur is best
heard at the right second space and is localized to that area, as low-frequency
noises are not widely transmitted. The high-frequency soft component, however,
is widely transmitted especially to the apex. This soft murmur heard at the apex
simulates the murmur of mitral regurgitation closely (Gallavardin phenomenon).
But the lack of conduction to the axilla and back is helpful.
396 Relationship with a physiological act

The useful physiological maneuvers are described below. These maneuvers have to
be tried in all patients with aortic stenosis even if the diagnosis appears certain, as
it permits one to gain experience of how a murmur of fixed obstruction behaves.
Any deviation from this in hypertrophic cardiomyopathy is easy to recognize.
There is significant variation in the response of fixed aortic stenosis to each of
these maneuvers from patient to patient.
• Respiration
• Supine position
• Supine, passive leg raising
• Supine left lateral
• Sitting, leaning forward
• Standing
• Squatting
• Isometric hand grip
• Valsalva maneuver
Maneuvers like inspiration, standing, the straining phase of Valsalva and
prolonged squatting by decreasing the venous return to the left ventricle, reduce
SYSTOLIC MURMURS
Rest Valsalva
Fig. 23.7: Murmur of HOCM increasing by Valsalva and on standing
Table 23.6: Influence of various maneuvers in aortic stenosis
Maneuver Fixed obstruction Dynamic obstruction

Respiration No change May increase with inspiration
Standing Decrease Increase
Valsalva Decrease Increase
397
Squatting Decrease Increase
the cavity size and increase the obstruction in hypertrophic obstructive

cardiomyopathy.
Presence of symptoms such as angina, syncope and dyspnea suggest severe aortic
stenosis and correlate with prolonged ejection systolic murmur with a late systolic
peaking. On the other hand, when the murmur is short in the presence of these
symptoms, hypertrophic cardiomyopathy or associated heart failure should be
considered. In hypertrophic cardiomyopathy, the degree of outflow obstruction
and symptoms are unrelated to each other.
Symptoms Signs
Angina Slow rising arterial pulse
Syncope Sustained apical impulse
Dyspnea Fourth heart sound
Ejection click
The slow rising arterial pulse and a sustained apical impulse go hand in hand
with a long ejection systolic murmur and a delayed peak. A normal arterial pulse
is consistent with a short ejection murmur with an early peak. If the arterial
pulse is normal with a long ejection murmur, murmurs simulating aortic stenosis
are likely (mitral regurgitation, ventricular septal defect). If the apical impulse
is not sustained with a long systolic murmur, mitral regurgitation is likely. A
long systolic murmur is usually accompanied by fourth heart sound in aortic
stenosis due to fixed obstruction. In dynamic obstruction due to hypertrophic
cardiomyopathy (HOCM), fourth heart sound may be heard with a short murmur
or no murmur, as diminished ventricular compliance is a fundamental feature in
hypertrophic obstructive cardiomyopathy with or without obstruction. If fourth
heart sound is not heard with a long murmur, but a third heart sound is heard,
mitral regurgitation is likely. A constant ejection click distinguishes aortic stenosis
from pulmonic stenosis. Again with an ejection click the ventricular septal defect
or mitral regurgitation are unlikely and aortic stenosis is likely.
The ejection click localizes the obstruction to the valve and suggests a
mobile non-calcific valve. Associated aortic regurgitation localizes the obstruction
398 to the valve or subvalvular fixed obstruction and hypertrophic obstructive
cardiomyopathy is unlikely.
The importance of aortic regurgitation in aortic stenosis is:
• Fixed valvular or subvalvular obstruction is likely.
• The accompanying systolic murmur is likely to be due to AS or VSD
and not due to pulmonic stenosis.
• A ‘new murmur of AR’ in AS may mean infective endocarditis in a
febrile patient with AS.
Fig. 23.8: Calcific aortic stenosis, with no ejection click. Note faint A2.
SYSTOLIC MURMURS
Table 23.7: Aortic valve sclerosis (AVS) versus aortic stenosis (AS)
Feature AVS AS
Murmur Short/medium pitch Long/rough
AR Absent May be present
A2 Normal/increased Diminished/absent
S2 Normal split Single/reversed split
LVH Absent Present
S4 Absent May be present
Calcification Rare May be present
Arterial pulse Normal Slow rising
Once the murmur of aortic regurgitation is audible, the systolic murmur is

unlikely to be related to aortic valve sclerosis (Table 23.7).
In addition to the various physiological maneuvers that may be performed
to differentiate various murmurs, changes in relation to ventricular premature
contractions also give clues to proper identification of murmur. Murmur of mitral
regurgitation seldom changes in post-ectopic beat, while aortic stenosis murmur 399
increases in the post-ectopic beat (Fig. 23.9).
In routine clinical practice, the clinical and electrocardiographic evidence
of left ventricular hypertrophy is often used as evidence of aortic stenosis. In
infants with severe aortic stenosis and heart failure, the ECG may show right axis
deviation and right ventricular hypertrophy and can be misleading.
Fig. 23.9: Systolic murmur due to mitral regurgitation remains unchanged in the
beat following a ventricular premature contraction, whereas the murmur increases
in intensity in aortic stenosis.
Table 23.8: Causes of RV outflow obstruction
Valvular Subvalvular Supravalvular

Congenital Congenital Congenital
Domed (42%) Infundibular stenosis Main trunk
Tricuspid (6%) Fibrous band at the junction Right and left pulmonary
Bicuspid (10%) of infundibulum and RV arteries
Unicommissural Tumour (external
(16%) compression)
Hypoplastic annulus Fibromuscular obstruction Thrombus
(6%) beneath the valve Rubella
Double chambered RV
Dysplastic (19%) Neoplasm
Carcinoid
Rheumatic
RIGHT VENTRICULAR OUTFLOW OBSTRUCTION

Unlike aortic stenosis, the commonest cause of pulmonic stenosis is congenital.
400 Acquired RV outflow obstruction is extremely rare (Table 23.8).
The clinical features of RVOT obstruction depend on the level of obstruction.
The presence of ejection click localizes the site to the valve. Isolated infundibular
pulmonic stenosis is a rare condition.
Fig. 23.10: Various levels of right ventricular outflow tract obstructions

SYSTOLIC MURMURS
Table 23.9: Murmur of pulmonic stenosis
Feature Description
Site of best audibility Pulmonary area (right second and 3rd spaces)
Timing Ejection systolic
Grade Grade 4/6
Length, peaking Short, moderate, long covering A2
Peaks in mid-systole, late systole
Selective conduction Supraclavicular, left side of neck
Relationship to physiological act
Respiration Increases with inspiration
Posture Decreases on standing
Valsalva straining phase Decreases or disappears
Accompanying features Ejection click
Wide split second heart sound
Diminished pulmonic sound
Right ventricular fourth heart sound
Sustained left parasternal lift of RVH
Systolic thrill at pulmonary area
Impalpable pulmonary artery
Prominent a wave in JV pulse
Features of right heart failure 401
Symptoms Shortness of breath
Cyanosis/clubbing
Angina
Syncope
Noonan’s syndrome
Hypertelorism
General appearance Moon facies
The significance of each of these features will be considered in the setting

of pulmonic stenosis.
Evaluation
Ask the following questions to evaluate the patient with murmur of pulmonic
stenosis:
With these issues in mind, the murmur of pulmonic stenosis should be
evaluated systematically.
Is it PS or a conditions simulating it? Conditions simulating PS

Innocent systolic murmur
Straight back syndrome
Idiopathic dilatation of pulmonary artery
Tetralogy of Fallot
If it is PS, what is the level of obstruction? Level of obstruction
Valvular
Subvalvular
Supravalvular
What is the severity? Severity of PS with gradient across the valve
Mild (<50 mmHg)
Moderate (50–70 mmHg)
Severe (>70 mmHg)
Is it isolated PS or part of a PS as a part of complex defect
complex defect or syndrome? Tetralogy of Fallot
L-TGA
PS as part of a syndrome
Noonan syndrome
Rubella syndrome
402
Is there pulmonary incompetence? Pulmonary incompetence occurs with
Is it dysplastic valve? Dysplastic valve as in Noonan’s syndrome
Infective endocarditis in PS
Post-surgical valvotomy
Post-balloon valvotomy
As in Noonan’s syndrome
Are there associated defects? Associated defects with PS
ASD
VSD
MURMUR OF PULMONIC STENOSIS
Timing
The murmur of pulmonic stenosis is as a rule an ejection systolic (Fig. 23.11).
A pansystolic murmur is suggestive of either a ventricular septal defect or tricuspid
regurgitation. When the murmur is long, as in severe pulmonic stenosis, the ejection
systolic murmur can be mistaken for the pansystolic murmur of ventricular septal
defect. This confusion is common and is best resolved by the realization that
there is no difficulty in distinguishing mild pulmonic stenosis from moderate or
SYSTOLIC MURMURS
Fig. 23.11: Ejection systolic murmur of pulmonic stenosis
large ventricular septal defect. It is the small ventricular septal defect that is
often confused with moderate or severe pulmonic stenosis because of the long
systolic murmur which is common for both. The accompanying features of
403
severe pulmonic stenosis, like prominent a wave in the neck veins, the sustained
parasternal impulse, audible fourth heart sound, wide split second heart sound,
and the ejection click help in this distinction. A small ventricular septal defect will
have no accompanying features other than the long systolic murmur.
Site of best audibility/selective conduction

The murmur of valvular pulmonic stenosis is generally best audible at the left
second or third space but is also audible at the fourth space along left sternal
border. It is selectively conducted to the supraclavicular area and the left side of
the neck. The murmur of ventricular septal defect is generally not conducted
more to the right side of the neck than left.
The murmur of valvular pulmonic stenosis is usually best heard at the left
second space but can occasionally be better audible at the third space. In other
words, the murmur at the third space may be due to valvular or infundibular
pulmonic stenosis (Table 23.10). The murmur of supravalvular pulmonic stenosis is
better heard superiorly, along the infraclavicular region, and laterally. This murmur
is usually more superficial than that of its valvular counterpart. The murmur of
a double chambered right ventricle is usually best heard at the third space. The
Table 23.10: Significance of the site of best audibility
Site of best audibility/conduction Significance

Left 2nd space Valvular PS
Infraclavicular and away from midline Supravalvular PS
Left 3rd or 4th space Infundibular PS or double chambered RV
Right 2nd or 3rd space PS with L-TGA (PA located to right of aorta)
Valvular PS
Conduction to left side of neck Valvular PS is more likely; ventricular septal defect
is less likely
Failure of conduction to left side of neck Infundibular PS is likely
murmur of pulmonic stenosis in association with L-transposition of great arteries

is best heard along the right sternal border, as the pulmonary artery is posterior
and to the right of the sternum. The pulmonary ejection systolic murmur of atrial
septal defect is often mistaken for pulmonic stenosis. This murmur of atrial septal
defect is usually grade 3/6 or less but is widely audible all over the lung fields. This
disproportion of less intense murmur at the pulmonary area with wide audibility
404 all over the chest is suggestive of atrial septal defect.
Fig. 23.12: Spectrum of auscultatory findings in valvular PS

SYSTOLIC MURMURS
Grade, length of murmur and time of peaking in systole

The murmur of pure pulmonic stenosis is usually at least grade 4/6 (murmur
with thrill). In general, the louder, longer and late peaking murmur, is associated
with more severe pulmonic stenosis. In tetralogy on the other hand, these features
are inversely related to the severity of pulmonic stenosis. This is related to the
associated non-restrictive ventricular septal defect that permits more right to
left shunt as the severity of pulmonic stenosis increases. In other words, in pure
pulmonic stenosis, the right ventricle has the obligation to empty only into the
pulmonary circulation; as the severity of pulmonic stenosis increases the loudness
of the murmur also increases. In tetralogy the right ventricle has no obligation
to empty into the pulmonary circulation, in view of the associated ventricular
septal defect that allows the right ventricle to decompress into the left ventricle
and aorta. The length or the loudness of the murmur is inversely related to the
severity of the tetralogy. The mechanisms that influence the intensity of the
murmur also influence the length of the murmur in a similar fashion. The length
of the murmur is more reliable than the intensity. In adults with thick chest wall,
the murmur is not particularly loud and the thrill is often absent but the length
405
of the murmur correlates with the severity of pulmonic stenosis. In patients with
right ventricular failure and associated right to left atrial shunt the forward cardiac
output across the pulmonary valve decreases and the murmur decreases or may be
absent. This may be mistaken for tetralogy or, surprisingly, for pulmonary arterial
hypertension. The clue lies in looking for the faint murmur (grade 1 to 2/6) of
pulmonic stenosis at the pulmonary area. This murmur though faint, is longer
in duration and is too long for the ejection systolic murmur that can occur with
pulmonary arterial hypertension.
Case summary
A 17-year-old girl was seen in the outpatient clinic for shortness of breath and cyanosis.
She had moderate cyanosis and clubbing of extremities. The arterial pulse and blood
pressure were normal. The JVP was elevated (8 cm above sternal angle) with a prominent
‘a’ wave measuring 12 cm above the sternal angle. The other pulsations were unremarkable.
The apical impulse was diffuse with the point of maximal impulse of grade 2/3 and
sustained with a palpable fourth heart sound. There were no thrills but pulsations were
seen at the 2nd and 3rd spaces on the left. There was no palpable pulmonic sound. The
first heart sound was normal, the second heart sound was single and was interpreted as
a loud pulmonic sound. The right ventricular fourth heart sound was heard. There was
no click. A soft pansystolic murmur (grade 3/6) was heard along the lower left sternal
border. There was grade 2/6 ejection systolic murmur at the pulmonary area. This was
interpreted as the murmur related to pulmonary hypertension. The ECG showed severe
right ventricular hypertrophy and right atrial enlargement. The chest X ray showed cardiac
enlargement of the right atrium and ventricle with prominent main pulmonary artery and
left pulmonary artery. The right pulmonary artery shadow is hidden behind the right atrial
shadow. A diagnosis of:
• Severe pulmonary arterial hypertension, ? primary
• Right heart failure
• Right to left atrial shunt
• Normal sinus rhythm
• Functional class IV
was made. She was discussed in a combined cardiology conference and cardiac catheterization
was decided against due to the high risk involved and also that nothing could be offered
even if it were due to PAH related to Eisenmenger syndrome. While awaiting discharge, she
was seen by one of the trainees who felt that the murmur at the pulmonary area, though
faint, was too long to belong to pulmonary hypertension and the possibility of pulmonic
stenosis existed. It was decided to catheterize her but while awaiting the procedure she
died suddenly in the ward. The autopsy revealed:
• Severe valvular pulmonary stenosis (pin hole)
406 • Patent foramen ovale
This patient illustrates the importance of the duration of the systolic murmur
of pulmonic stenosis. The pulsation in the left second or third space, single second
heart sound, and the dilated main pulmonary artery can be misleading and the
differential diagnosis of pulmonic stenosis involves pulmonary hypertension in
certain clinical settings. Severe right ventricular hypertrophy in pulmonic stenosis
when associated with severe outflow hypertrophy occasionally encroaches or
displaces the main pulmonary artery posteriorly to produce pulsations in the left
second or third space. The second heart sound in primary pulmonary hypertension
is often single and not impressively loud unlike in pulmonary hypertension due
to other conditions. The pulmonary arterial enlargement can be unimpressive
in some patients with primary pulmonary hypertension. This patient was seen
in 1970s when echocardiography was not available. A mistake of this nature is
generally less likely but occurs even today as the following patient illustrates.
SYSTOLIC MURMURS
Case summary
A 20-year-old college girl was evaluated for dyspnea and cyanosis. After a clinical and a
two-dimensional echocardiographic examination, a diagnosis of:
• Primary pulmonary hypertension
• Right to left shunt at atrial level
was made. This girl also had features similar to the described patient above, with a faint
but long systolic murmur suggestive of severe pulmonic stenosis with right to left shunt
at atrial level. A repeat echocardiographic examination suggested severe valvular pulmonic
stenosis. At cardiac catheterization she was found to have:
• Severe valvular pulmonic stenosis
• Dynamic infundibular pulmonic stenosis
• Right ventricular failure
• Right to left atrial shunt
She underwent a percutaneous balloon valvuloplasty with an excellent outcome and is
doing well an year later.
This patient illustrates (over-illustrates) the importance of the length of

systolic murmur at the pulmonary area in a patient with a diagnosis of pulmonary
hypertension or right heart failure, even when the diagnosis was made after an
echocardiographic examination. 407
Selective conduction
The murmur of pulmonic stenosis is selectively conducted to the infraclavicular
region and the left side of the neck. This is related to the direction of the jet and
anatomical bony contiguity. The murmur of ventricular septal defect is generally
not conducted to the neck. The murmur of infundibular pulmonic stenosis and
double chambered RV are usually not conducted to the neck. The pulmonic
stenosis in association with D-transposition of great arteries, is poorly conducted
to the infraclavicular region and is well conducted to the lung fields.
Response to various maneuvers

The murmur of pulmonic stenosis is usually increased during inspiration. This
expected response is seen in only 60 per cent of patients with pulmonic stenosis
and the absence of this sign is common. In the presence of severe right ventricular
failure, the inspiratory increase fails to occur. The murmur decreases or disappears
promptly during the straining phase of the Valsalva maneuver and reappears
promptly after the release. The murmur of aortic stenosis on the other hand,
decreases or disappears after a few seconds of straining and reappears after a lag
period of a few seconds. This is related to the reservoir of pulmonary vascular

bed being available for the left heart.
a) The ejection click (EC): The EC not only distinguishes pulmonic stenosis from
ventricular septal defect but also localizes the obstruction to the valve. Even with
a valvular pulmonic stenosis, the click is absent in patients with dysplastic valve,
absent pulmonic valve with annular stenosis or a very severe pulmonic stenosis.
Conditions with valvular pulmonic stenosis where EC may be absent:
• It may not be valvular pulmonic stenosis
• Dysplastic pulmonary valve
• Absent pulmonary valve
• Very severe pulmonic stenosis
The variability of the click with respiration (expiratory increase) distinguishes
pulmonic stenosis from aortic stenosis. The click is often better appreciated one
intercostal space below the site of best audibility of the murmur.
b) The second heart sound: The wide and variable split of the second heart sound with
408
diminished P2 distinguishes pulmonic stenosis from ventricular septal defect. A
fixed split occurs with associated atrial septal defect or right heart failure.
c) The fourth heart sound: Presence of the fourth heart sound makes a tetralogy
unlikely and pure pulmonic stenosis likely. The gradient across the outflow is
usually more than 70 mmHg when the fourth heart sound is present; the right
ventricular pressures are usually suprasystemic.
d) Prominent a wave in JVP: This has the same significance as the fourth heart sound
but is more easily and frequently appreciable than the fourth heart sound.
e) The parasternal impulse: A sustained parasternal impulse is consistent with
pulmonic stenosis but a hyperkinetic impulse suggests atrial septal defect. Isolated
parasternal impulse without LV impulse rules out ventricular septal defect as the
cause of long systolic murmur.
f) The murmur of pulmonary incompetence: The low frequency murmur of low
pressure pulmonary incompetence localizes the lesion to the valve. Pulmonary
incompetence is also common with dysplastic valve or with infective endocarditis.
A dysplastic valve is not easily amenable for balloon valvuloplasty.
SYSTOLIC MURMURS
OTHER EJECTION MURMURS AT THE BASE
EJECTION SYSTOLIC MURMUR OF AORTIC VALVE SCLEROSIS

The ejection systolic (ESM) murmur is common in the elderly and is due to
thickening and occasionally mild calcification of the valve. It is short in duration,
peaks early in systole, and is softer than the murmur of aortic stenosis. The second
sound is normally split with normal or slight accentuation of aortic sound. This
murmur needs to be distinguished from aortic stenosis (Table 23.7).
EJECTION SYSTOLIC MURMUR OF AORTIC REGURGITATION

Even in the absence of stenosis, aortic regurgitation of moderate or severe degree
is often accompanied by an ejection systolic murmur due to the large stroke
volume that has to be moved across the aortic valve. This murmur may be grade
4/6 or more and may be confused for an associated aortic stenosis with aortic
regurgitation (Table 23.11).
When the diastolic pressure is less than 40 mmHg, free severe aortic
regurgitation is likely, and associated aortic stenosis is unlikely. Systolic thrill 409
over the precordium is not a feature with the ejection systolic murmur of aortic
regurgitation.
EJECTION SYSTOLIC MURMUR IN THE AORTIC AREA IN THE YOUNG

Unlike in the elderly, an ejection systolic murmur in the aortic area in a young
person should be considered abnormal even if the murmur is less than grade 3/6. Once
aortic stenosis is ruled out, one must look for a hyperkinetic state or an underlying
aortic regurgitation. The early diastolic murmur of aortic regurgitation
is more difficult to hear than the systolic counterpart. It is in this setting, that all
Table 23.11: Ejection systolic murmur of aortic regurgitation versus aortic
regurgitation with aortic stenosis
Feature ESM in AS + AR ESM of pure AR

Systolic thrill Precordium + carotid Carotid thrill may occur
No precordial thrill
Murmur length Long Short
Time of peaking Later in systole Early in systole
the maneuvers to bring out the murmur have to be tried. In the setting of rheumatic
heart disease, with mitral and tricuspid valve disease, even a faint 1/6 ejection
systolic murmur at the aortic area suggests associated aortic stenosis. This is
related to the reduction in cardiac output due to two proximal lesions. At cardiac
catheterization, even as low a gradient as 30 mmHg, is considered suggestive of
severe aortic stenosis. The diagnostic possibilities are:
• Underlying aortic regurgitation
• Mild aortic stenosis
• Aortic stenosis in association with tight mitral stenosis
• Congenital bicuspid aortic valve
• All conditions with aortic run-off
• Hyperkinetic heart syndrome
Case summary
A 16-year-old boy presented with palpitation and weakness of 2 months duration. Earlier
he was seen at a hospital in another city where he was evaluated by cardiac catheterization
410 and left ventricular angiography but an echocardiogram was not done. The intracardiac
pressures and flows were found to be normal and the left ventriculogram showed a normally
contracting left ventricle. The cardiovascular system was pronounced normal with an
‘innocent systolic murmur’ of aortic origin. Physical examination revealed an otherwise
normal cardiovascular system but for a short ejection systolic murmur of grade 2/6 at
the aortic area. A short early diastolic murmur was heard along the left sternal border
on prompt squatting and later was also heard with held expiration. A diagnosis of mild
aortic incompetence was made. The patient was advised normal activity and prophylaxis
for rheumatic fever and infective endocarditis.
This patient illustrates the importance of ‘unexplained’ systolic murmur at

the aortic area in the young. Additionally, even at cardiac catheterization, aortic
regurgitation was missed because selective aortic root angiogram was not done as
aortic regurgitation was unsuspected prior to cardiac catheterization. The value
of proper clinical evaluation as a guide to investigation is to be noted.
ESM lower than grade 3/6 at pulmonary area

This is the commonest of murmurs in an otherwise normal cardiovascular
system. A systematic approach to this physical sign often helps in the diagnosis
of conditions of non-cardiovascular origin. Various possibilities are:
SYSTOLIC MURMURS
• Innocent systolic murmur

• Pectus excavatum
• Straight back syndrome
• Kyphoscoliosis
• Pulmonary fibrosis
• Anemia
• Pregnancy
• Thyrotoxicosis
• Mild pulmonic stenosis
• Idiopathic dilatation of pulmonary artery
• Pulmonary arterial hypertension
• Hypertrophic obstructive cardiomyopathy
• Pulmonary AV fistula (increased flow)
• Systemic AV fistula
As the possibilities are manifold, a systematic approach is pertinent.
a) Look for anemia, thyrotoxicosis, pregnancy and AV fistula: As a first 411
step, look for pallor over the tongue and mucus membranes to rule out anemia.
Look at the thyroid gland for any enlargement or other features of thyrotoxicosis.
A venous hum is often a clue to either of these conditions. Absence of pallor
does not always rule out anemia. Reliable hemoglobin estimation is mandatory
for all patients who visit a physician or cardiologist for cardiovascular evaluation.
In all female patients, recheck menstrual history to rule out early pregnancy. All
radiological investigations should be deferred until early pregnancy is ruled out.
A systemic arteriovenous fistula may exhibit an ejection systolic murmur in the
pulmonary area. Looking for an AV fistula involves auscultation over the liver,
skull or any other site of past trauma, needle puncture or surgery. In all patients
who underwent cardiac catheterization from the femoral site, the groin should
be auscultated for a continuous murmur.
b) Look for chest deformity: Look for kyphoscoliosis, pectus excavatum
or straight back syndrome. The last entity is often missed and is best detected by
making the patient stand up and looking for loss of thoracic lordosis. A lateral
view of the chest is confirmatory.
c) Others: Other conditions can be differentiated by the alterations in second

heart sound, presence or absence of additional sounds, and specific chamber
enlargement. It is often not realized that hypertrophic obstructive cardiomyopathy
can simulate an atrial septal defect by the systolic murmur and ‘reversed wide
split’.
If an ejection systolic murmur develops for the first time in patients with
coronary artery disease receiving long term aspirin, significant anemia due to
gastrointestinal bleeding should be considered.
Innocent systolic murmurs are recognized by the company they keep, namely
the normal splitting of S2, and are often accompanied by physiological S3 in
children.
ESM lower than 3/6 at pulmonary area in coronary artery disease

This could have significance in
• Anemia of gastrointestinal origin
• Peptic ulcer
• Aspirin induced peptic ulceration
412
Normal split of second heart sound, P2 normal or mild accentuation
Look for pallor Functional murmur of anemia
Look for thyroid enlargement/signs Functional murmur
of thyrotoxicosis
Last menstrual period/early pregnancy Functional murmur
Chest deformity Functional murmur
Continuous murmur over any site of Functional murmur
AV fistula, high volume pulse
Abnormal split of second heart sound, with additional sounds

Wide ‘fixed’ split S2 , P2 normal or louder, Atrial septal defect
tricuspid MDM
Wide, variable split, decreased P2, EC Mild pulmonic stenosis
Wide variable split, P2 normal, Idiopathic dilatation of pulmonary artery
no tricuspid MDM
Close split or single S2, increased P2 Pulmonary arterial hypertension
Reversed split, LV S4, LVH Hypertrophic obstructive cardiomyopathy
SYSTOLIC MURMURS
Fig. 23.13: Innocent systolic murmur, normal S2 split, physiological S3
• Malignancy of GI tract
• Coronary AV fistula to RA or RV
• Left main coronary arising from pulmonary artery (ALCAPA) 413
• Hypertrophic cardiomyopathy mistaken for CAD
Surprisingly, many patients do not notice malena for long periods.
A 50-year-old man had angina class 2, with angiographic mid left anterior
descending lesion of 75 per cent and normal LV function. He was asymptomatic
with drugs and was on medical follow up. Three months later, he came with
increasing angina with occasional rest angina. Physical examination was otherwise
unremarkable but for an ejection systolic murmur 3/6 at the pulmonary area.
A repeat angiogram revealed findings exactly similar to the previous one. The
intracardiac pressures and LV function were normal. Review of his case revealed
that he had a loud venous hum in addition to ejection systolic murmur 3/6 at the
pulmonary area. His laboratory test was repeated and his hemoglobin was found
to be 6.5 g% only. Upper GI endoscopy revealed an active duodenal ulcer and
he was treated for it; there was prompt recovery. Aspirin was discontinued and
iron was supplemented. This patient’s example should not be used to mean that
the best way to detect anemia is to wait for an ejection systolic murmur at the
pulmonary area. It should be looked for in the long term follow up of all patients
who receive long term oral anticoagulants, aspirin or other analgesics.
PANSYSTOLIC MURMURS
A pansystolic murmur by definition begins with the first heart sound and occupies
all of the systole up to the second sound on its side of origin. The configuration
of the murmur is plateau or even. A pansystolic murmur means a pansystolic
pressure difference between the two chambers. This pressure relationship exists
with left ventricle and left atrium as in mitral regurgitation, right ventricle and right
atrium as in tricuspid regurgitation and between the two ventricles as in ventricular
septal defect. Nowhere else in the heart does a pansystolic pressure difference exist
to permit a pansystolic murmur. The murmurs of mitral regurgitation, tricuspid
regurgitation and ventricular septal defect will be described.
The competence of the normal mitral valve is dependent on the function of the
following structures (Fig. 23.14).
• Leaflets/commissures
• Chordae
414
• Papillary muscles
• Left ventricle
• Mitral annulus
• Left atrium
Abnormal functioning of any of the above structures can result in mitral
regurgitation. The features of the murmur of mitral regurgitation should be
described in full as each one of them have significance in the final assessment
of the patient.
The mitral valve apparatus consists of both anterior and posterior leaflets,
the chordae supporting the leaflets in systole, the papillary muscles that prevent
prolapse of the leaflets due to tension applied to the chordae, the mitral annulus,
the left ventricle (LV) and the left atrium (LA).
When the mitral leaflets become incompetent, blood regurgitates into the
left atrium with a high pressure difference starting with the onset of systole
and continuing to the end of systole. As a result, the V wave in the left atrium
markedly increases.
The commonest cause of mitral regurgitation is rheumatic heart disease.
SYSTOLIC MURMURS
During the acute phase of the rheumatic process due to acute carditis, annular
Fig. 23.14: Components of mitral valve apparatus
dilatation is the principal mechanism and the leaflets show edema with normal
chordae. In chronic rheumatic heart disease, progressive leaflet thickening with
retraction of the cusps occurs. The posterior cusp is involved to a greater extent; 415
as a result; it is retracted and rolled with shortening of chordae. The anterior leaflet
is less thickened and the major chordae are frequently elongated, encouraging
prolapse. The posterior chordae may also elongate and may rupture. Annular
dilatation slowly increases and results in progressive mitral incompetence.
Fig. 23.15: Mechanism of pansystolic murmur of mitral regurgitation (MR)

Table 23.12: Profile of the murmur of mitral regurgitation
Site of best audibility Apex, left sternal border

Timing Pansystolic, late systolic, early systolic
Grading/thrill Grade 3/6, thrill uncommon
Character Soft, blowing, musical, honking
Selective conduction Left axilla, back, left sternal border/aortic area
Relation to maneuvers
Respiration Fails to increase during inspiration
Posture
Standing No change in rheumatic MR
Increases in MVP
Valsalva straining Decrease in Rheumatic MR
Increase in MVP
Cycle length No change in rheumatic MR
Change in murmur in MVP
Associated features Hyperkinetic left ventricular impulse
Diminished first heart sound
Wide, variable second heart sound
416 Third heart sound
Mitral diastolic murmur
Non-ejection click(s)
Fourth heart sound
Timing
The murmur of mitral regurgitation is classically pansystolic and this is true in
most patients with rheumatic mitral regurgitation. Late systolic murmurs occur
in mitral valve prolapse and papillary muscle dysfunction. The murmur of acute
mitral regurgitation is early systolic as the pressure difference between the left
ventricle and left atrium gets obliterated by late systole.
The causes of non-pansystolic murmurs in mitral regurgitation are:
• Papillary muscle dysfunction
• Acute mitral regurgitation (early systolic)
• Trivial or mild mitral regurgitation (even rheumatic)
• ‘Swing’ mitral regurgitation
SYSTOLIC MURMURS
Fig. 23.16: Ruptured chordae tendinae – pansystolic murmur with mid-systolic accentuation
In acute mitral regurgitation due to papillary muscle dysfunction/rupture

as in myocardial infarction, the mitral regurgitation may be faint or even silent.
This is due to the accompanying left ventricular dysfunction and hypotension. In
prosthetic mitral regurgitation the mitral regurgitation occurs around the valve
ring (paraprosthetic) and is often silent.
The causes of silent MR are: 417
• All causes of acute mitral regurgitation
Postsurgical after closed or open commissurotomy
Post-balloon valvuloplasty
Trauma
Fig. 23.17: Mitral regurgitation – chronic (left) and acute (right)

• Para-prosthetic regurgitation
• Trivial mitral regurgitation due to any cause
In trivial mitral regurgitation due to any cause, the murmur is clinically
inaudible but is often detected by Doppler echocardiography. This type of mitral
regurgitation has no influence over the selection of outcome of patients of mitral
stenosis for commissurotomy or balloon valvuloplasty.
Site of best audibility

Rheumatic mitral regurgitation is usually best audible at the apex. In children on the
other hand, the murmur is sometimes best audible at the lower left sternal border.
The murmur of mitral valve prolapse is occasionally best audible at the lower left
sternal border and is possibly suggestive of posterior leaflet involvement.
Grade and presence or absence of thrill

The murmur of mitral regurgitation is usually grade 3/6 and the systolic thrill
is less common because the murmur is soft and of high frequency. Presence of
a systolic thrill usually suggests a chordal rupture, infective endocarditis with
418 vegetations or the systolic murmur of aortic stenosis or ventricular septal defect
mistaken for mitral regurgitation.
Though systolic thrill does not negate the diagnosis of mitral regurgitation,
it is useful to consider the above possibilities before ascribing it to mitral
regurgitation.
Character
The murmur of mitral regurgitation is characteristically soft and blowing. Musical
murmurs occur when there is an unusually vibrating structure in the pathway of
regurgitation, as in ruptured chordae or the vegetations in infective endocarditis.
The murmur of mitral valve prolapse is different in character from rheumatic
mitral regurgitation and is usually rasping in quality. A musical honking murmur
is characteristic of mitral valve prolapse. Medium frequency or harsh murmurs
of mitral regurgitation are usually non-rheumatic and are generally due to mitral
valve prolapse. In general, if the murmur is rough in quality, it is useful to rule
out aortic stenosis or ventricular septal defect simulating mitral regurgitation.
The murmur of rheumatic mitral regurgitation is most commonly conducted
SYSTOLIC MURMURS
selectively to the left axilla and back. This is related to the direction of the jet, which
is generally directed to the left and posteriorly. In some patients with mitral valve
prolapse, the murmur is selectively also conducted along the left sternal border to
the aortic area. The underlying mechanism is that the jet of mitral regurgitation is
directed medially along the aortic root. This type of jet is related to the dominant
involvement of posterior leaflet of mitral valve in mitral valve prolapse. This
type of murmur of mitral valve prolapse is often confused for aortic stenosis.
However, the pansystolic timing of the murmur, the hyperkinetic apical impulse,
and a normal upstroke of the arterial pulse favour mitral regurgitation. This type
of murmur in mitral valve prolapse with a posterior leaflet involvement is easily
amenable to repair of the valve rather than replacement. Rarely, the jet of mitral
regurgitation can be so unusually directed in mitral regurgitation due to mitral
valve prolapse that the murmur is selectively conducted to the right axilla. The
direction of the jet in this case is directed to the interatrial septum. In children
with severe mitral regurgitation, the murmur is heard well even at the pulmonary
area simulating a ventricular septal defect. The basis for this is possibly the jet
of mitral regurgitation reaching the area of left atrial appendage which is closely
related to the pulmonary artery. 419
Maneuvers
Respiration: Contrary to common teaching and belief, the murmur of mitral
regurgitation does not increase with expiration. More importantly, it fails to
increase with inspiration, unlike its counterpart at the tricuspid valve.
Posture: The rheumatic mitral regurgitation decreases on standing or may not
change significantly with posture. The tricuspid regurgitation murmur decreases
with standing and increases with supine position. The mitral regurgitation of
mitral valve prolapse increases on standing (smaller left ventricle) and decreases
with supine position (larger left ventricle).
Valsalva: The mitral regurgitation of mitral valve prolapse increases during the
straining phase of Valsalva whereas rheumatic mitral regurgitation decreases or
disappears.
Phenylephrine: Decreases the mitral regurgitation of mitral valve prolapse due to
reflex bradycardia and larger left ventricular cavity.
In certain situations, the murmur of MR is not obvious and requires to be carefully

sought. This is more likely when the regurgitation is too mild or is due to non-
rheumatic causes.
Significant MR (> 1+) in the setting of acute myocardial infarction is associated
with a five fold increased risk of death and is a function of more extensive infarction,
failure to reperfuse, previous infarction, and concurrent multivessel disease.
After each dilatation during PBMV, one should carefully listen for the
murmur of MR. This murmur is often faint and non-pansystolic, and is often
missed by cursory auscultation. Even a faint murmur should be given importance
(Table 23.13). Other useful clues are non-ejection click audible after dilatation
of the valve and a clearly palpable left ventricular impulse. The non-ejection
click is due to chordal rupture. Ideally the person looking for MR should have
auscultated the patient prior to balloon dilatation. As many auscultators are
unreliable, Doppler echocardio-graphic evaluation in the catheterization laboratory
is recommended.
420 TRICUSPID REGURGITATION

The commonest cause of tricuspid regurgitation is secondary to high right
ventricular pressures either due to pulmonary arterial hypertension or pulmonic
stenosis or dilatation of the right ventricle due to ventricular failure (Fig. 23.18).
Table 23.13: Searching for mitral regurgitation – situations and significance
Circumstance Significance
Any fever of any duration Infective endocarditis
Child suspected of rheumatic fever Acute carditis
All patients with MS Associated MS modifies the intervention
Enhanced risk of infective endocarditis
Acute chest pain Ischemic MR
MVP
Acute MI Ischemic MR
Dilated LV
During PBMV Any degree of MR appearing during the
procedure is a contraindication to further
dilatation of the valve
SYSTOLIC MURMURS
The concept of tricuspid valve complex and underlying pathophysiology is useful

in understanding tricuspid regurgitation.
Right atrium
• Atrial volume
• Atrial pressure
• Atrial compliance
• Annulus
Tricuspid valve (three leaflets)
• Subvalvular apparatus
• 25 chordae (five types)
• Three major papillary muscles, several minor papillary muscles
Right ventricle
• RV volume
• RV pressure
• RV compliance
• RV architecture
421
Derangement of any of these components in isolation, or more often in
combination, results in tricuspid regurgitation.
Fig. 23.18: Mechanisms of tricuspid regurgitation

Table 23.14: Profile of tricuspid regurgitation
Site of best audibility Tricuspid area

Timing Pansystolic
Grading < 3/6
Character Soft and blowing
Selective conduction No selective conduction but is often heard to the right
of sternum
Respiration Increases during inspiration and decreases with expiration
(Carvallo’s sign)
Posture Increases with supine passive leg raising, decreases with
standing
Valsalva straining Disappears
Accompanying features Signs of pulmonary hypertension
Hyperkinetic right ventricular impulse
Prominent v wave in jugular venous pulse
Rapid y descent in jugular venous pulse
Right ventricular third heart sound
422
Tricuspid regurgitation may result from organic tricuspid valve involvement or
functional impairment due to raised right ventricle pressure. In the former, called
low pressure tricuspid regurgitation, the murmur is short as there is equalization
of pressures between the right atrium and right ventricle during late systole. In
high-pressure tricuspid regurgitation, the murmur tends to be of high frequency
and holosystolic due to high pressure gradient between right ventricle and right
atrium. The importance of each of these features is detailed below.

The murmur of tricuspid regurgitation is best heard at the tricuspid area (left
4th space) and is generally not selectively conducted. It may be heard to the right
of the sternum or over the liver. Very rarely, conduction into the neck veins may
occur – when it can be mistaken for an aortic murmur. In Ebstein’s anomaly,
the murmur may be best heard laterally at the apex due to displacement of the
tricuspid valve. In severe tricuspid regurgitation with enlarged right ventricle
forming the apex, the murmur may be audible at the apex and even in the axilla.
In this setting it may be mistaken for mitral regurgitation.
SYSTOLIC MURMURS
Timing and character

The typical murmur of tricuspid regurgitation is pansystolic and is indicative of
tricuspid regurgitation with high right ventricle pressures. The duration of the
murmur is indicative of the duration of pressure difference between the right
ventricle and right atrium in systole. Non-pansystolic murmurs occur with organic
tricuspid valve disease and normal right ventricle pressures. Even with high right
ventricle pressures, a mild or trivial tricuspid regurgitation may be non-pansystolic.
The high frequency murmur is suggestive of high pressures in the right ventricle.
With normal right ventricle pressures, the murmur is lower in frequency.
Causes of short murmur

• Organic tricuspid valve disease without pulmonary hypertension
Rheumatic
Carcinoid syndrome
Tricuspid valve prolapse
Traumatic 423
Following catheter manipulation in right heart
Surgical
Pacemaker wire
Balloon dilatation
Blunt trauma to chest
• Mild or trivial regurgitation even with pulmonary hypertention
The higher the frequency and longer the murmur, the higher the right ventricle
pressure. With high right ventricle pressures, a mild tricuspid regurgitation may
produce a shorter murmur but the frequency is higher. In actual practice, the frequency
is the more reliable indicator of pressures than the length of a murmur.
Grading
As a rule, the murmur of tricuspid regurgitation is less than grade 3/6 and a thrill is
extremely rare. Systolic thrill in tricuspid regurgitation should raise the possibility
of ventricular septal defect mistaken for tricuspid regurgitation or organic
tricuspid regurgitation. Even a functional tricuspid regurgitation when severe
may be associated with a thrill. Such murmurs of tricuspid regurgitation in severe
pulmonary arterial hypertension and mitral stenosis generally indicate the need for
tricuspid annuloplasty in addition to the corrective surgery for mitral stenosis.
The murmur of tricuspid regurgitation usually has no selective conduction, but
may rarely be conducted selectively toward the right sternal border or even into
the neck. The cervical conduction is related to the jet of tricuspid regurgitation
directed into the superior vena cava and can be confirmed by Doppler. The
cervical component of the murmur disappears by compression over the base of
the neck. When tricuspid regurgitation is very severe with extreme right ventricle
enlargement, the right ventricle may form the apex and the murmur may be audible
at the apex or even in the axilla simulating mitral regurgitation. The inspiratory
increase in murmur and pure right ventricle enlargement with apical retraction
favor tricuspid regurgitation.

Respiration: The murmur of tricuspid regurgitation increases or is heard only
424 during inspiration, and decreases or even disappears during expiration. This is
related to inspiratory increase in venous return augmenting right ventricle output
(Fig. 23.19).
Failure of the murmur to increase during inspiration may mean that the murmur
is probably due to an other condition, like ventricular septal defect or mitral
regurgitation. Also, the murmur of tricuspid regurgitation fails to increase
Fig. 23.19: Respiratory variation of tricuspid regurgitation murmur

SYSTOLIC MURMURS
during inspiration when the tricuspid regurgitation is accompanied by organic

tricuspid stenosis or severe right ventricle failure. In the presence of severe right
ventricle failure, the right ventricle fails to take up the challenge of additional
venous return of inspiration, and fails to increase the output and thereby the
murmur. The associated tricuspid stenosis prevents any further increase in venous
return into the right ventricle and the tricuspid regurgitation murmur fails to
increase during inspiration, though the murmur of tricuspid stenosis increases
during inspiration.
In a clinical setting of severe tricuspid regurgitation and right ventricle failure
with the right ventricle forming the apex, the murmur of tricuspid regurgitation
may be heard at the apex and may not increase during inspiration. As a result
the murmur of tricuspid regurgitation is mistaken for mitral regurgitation. This
mistake is most common in pure mitral stenosis with severe pulmonary arterial
hypertension and severe tricuspid regurgitation. A diffuse apical impulse with a
point of maximal impulse along the left sternal border and apical retraction due
to right ventricle volume load rules out mitral regurgitation of any significance.
Accompanying features 425

a) Signs of severe pulmonary arterial hypertension: The functional murmur of
tricuspid regurgitation is almost always accompanied by significant pulmonary
arterial hypertension. The right ventricle systolic pressure is at least 70 mmHg
when high frequency and pansystolic murmur of tricuspid regurgitation occurs.
In the absence of pulmonary arterial hypertension or only mild pulmonary arterial
hypertension, the tricuspid regurgitation is likely to be organic.
b) Sustained, hyperkinetic parasternal impulse: The parasternal impulse is often
grade 3/3 with increased duration of impulse as the right ventricle is both
volume and pressure loaded. A hyperkinetic impulse without increased duration
is suggestive of normal pressure or organic tricuspid regurgitation. Pure right
ventricle enlargement with a pansystolic murmur is suggestive of tricuspid
regurgitation; it is unlikely to be ventricular septal defect.
c) Right ventricular third heart sound: Almost all the patients with tricuspid
regurgitation have right ventricle failure and the rapid filling of right ventricle
results in right ventricle third heart sound. This third heart sound rules out
associated tricuspid stenosis.
d) Tricuspid diastolic murmur: A tricuspid diastolic murmur increasing on

inspiration suggests associated tricuspid stenosis. In severe functional tricuspid
regurgitation, a tricuspid diastolic murmur may occur even in the absence of
tricuspid stenosis due to large flow. This murmur does not increase significantly
with inspiration.
e) Prominent v wave: The v wave in JVP is prominent with significant tricuspid
regurgitation. However, lack of this sign does not rule out tricuspid regurgitation as
significant tricuspid regurgitation can occur with little or no v wave in the neck.
f) Rapid y descent: Pure tricuspid regurgitation is associated with rapid y descent
in the absence of associated tricuspid stenosis.
VENTRICULAR SEPTAL DEFECT

The ventricular septal defect is a hole or multiple holes in the ventricular septum.
It may be primary, part of a complex defect, or acquired.
Classification
426 Setting
• Primary or isolated
• Part of a complex defect
Tetralogy of Fallot
Complete AV canal defect
Corrected transposition of great arteries
Truncus arteriosus
Tricuspid atresia
Sinus of Valsalva aneurysm
D-transposition of great arteries
Size
Small VSD
• VSD restrictive and resistance index is greater than 20 units/m2 BSA
• Normal RV systolic pressure
• Qp/Qs is less than 1.75
Moderate VSD
• Restrictive VSD but may raise RV systolic pressure to approximately
half of LV pressure
SYSTOLIC MURMURS
• Qp/Qs may reach 2 : 1

Large VSD
• The size of aortic orifice or larger
• No resistance to flow
• RV systolic pressure approximates that of LV pressure
Location
• Perimembranous (includes LV-RA defect)
• Subpulmonary
• Below the septal leaflet of tricuspid valve
• Muscular
• With straddling or overriding of tricuspid valve
The typical murmur of ventricular septal defect is pansystolic because there
is a pansystolic pressure difference between the two ventricles in communication
(Table 23.15).
Table 23.15: Profile of the murmur of ventricular septal defect
Timing Pansystolic
427
Site of best audibility Left sternal border 2nd to 4th space
Grade Grade 4/6
Character Rough/harsh
Selective conduction No selective conduction
Relation to physiologic act
Respiration Fails to increase with inspiration
Valsalva straining Increases with expiration
Amyl nitrite Decreases or disappears
Phenylephrine Decreases or increases
Biventricular enlargement
Signs of pulmonary arterial hypertension
Mid-diastolic murmur at apex
Second sound normally split or single
Associated lesions Early diastolic murmur of aortic regurgitation
Continuous murmur of PDA
Age at which murmur is detected Most commonly 2–6 weeks after birth
Table 23.16: Size of ventricular septal defect: definitions
Restrictive defects
(Diameter <1 cm/m2 BSA or RV pressure is normal
orificial area < 0.8 cm2/m2) Left to right shunt is < 1.5:1
No cardiac enlargement
Small ventricular septal defect Pansystolic murmur
No MDM at apex
Moderate ventricular septal defect Elevation of RV pressure to less than 75% of
systemic pressure
Left to right shunt is > 2:1
Pansystolic murmur
Non-restrictive ventricular septal defect
(Diameter > 1 cm/m2 BSA or RV pressure > 75% of systemic pressure
orificial area >0.8 cm2/m2)
Large ventricular septal defect Left to right shunt > 2:1
The importance of each of these features will be discussed. The size of

ventricular septal defect is the most important determinant of the auscultatory
428 findings and the clinical course of patients. Ventricular septal defects are classified
as small, moderate and large not only by physical size but also by alteration in
pressure and flow (Table 23.16).
Fig. 23.20: Role of size of ventricular septal defect

SYSTOLIC MURMURS
The murmur of the ventricular septal defect is determined to some extent

by the size of the defect. In large, non-restrictive defects with equalization of
pressures in left and right ventricles, the murmur may not be pansystolic, especially
with pulmonary vascular disease with decreasing shunt. The loudest and longest
murmur is heard in restrictive defects. A large defect with a large shunt usually
results in associated diastolic mitral flow murmur. When Eisenmenger’s syndrome
develops in a large ventricular septal defect, the murmur disappears entirely.
Evaluation
In the evaluation of ventricular septal defect, the following questions need to be
answered.
Is it VSD or a conditions simulating it? Conditions simulating VSD
Pulmonic stenosis
Aortic stenosis
If it is VSD, what is the size? Small, moderate, large or alternatively
restrictive defect or unrestrictive defect
429
What is the magnitude of left to right shunt? < 1.5:1 or more
2:1 or more
Is there pulmonary arterial hypertension? Mild
If so of what severity? Moderate
Severe
In case of PAH, what type? Hyperkinetic (flow related)
Fixed (resistance related)
What is the site? Perimembranous, inlet, subpulmonic or muscular
Is it single or multiple? Important for surgical correction
Is it isolated VSD or is it part of a Tetralogy of Fallot
complex defect? Transposition of great arteries
Are there any associated lesions? Aortic regurgitation
Pulmonary stenosis
Coarctation of aorta
Timing
The murmur of ventricular septal defect is typically pansystolic and is a reflection
of the pansystolic pressure difference between the two ventricles. This typical
Table 23.17: Conditions under which non-pansystolic murmurs may occur in VSD
Condition Mechanism
Large unrestrictive VSD Right ventricular pressures > 75% of systemic
pressures
Very small VSD Resistance at VSD itself
Muscular VSD Closure of defect by late systole
Multiple VSDs Summation effect as large VSD with
Pulmonary hypertension
Pulmonary hypertension Obliteration of pressure difference
Associated lesions Elevation of right ventricular pressures
Pulmonic stenosis
LV inflow obstruction
murmur is a feature of small and moderate ventricular septal defects. The

determinants of the timing of the murmur of ventricular septal defect are the
size of the defect, the pulmonary arterial pressure, the location of the defect, and
430 the associated defects (Table 23.18).
Site of best audibility and selective conduction

The murmur of ventricular septal defect is best audible along the left sternal
border anywhere from the second to fourth spaces and is not selectively conducted
anywhere (Fig. 23.21). The so-called supracristal ventricular septal defect is best
heard at the pulmonary area and may be selectively conducted to the infraclavicular
area and the left side of neck. The lack of right ventricle enlargement in spite of
a prolonged murmur, absence of prominent a wave in the neck veins, and normal
split and intensity of second heart sound favour a diagnosis of ventricular septal
defect over pulmonic stenosis.
When the murmur of ventricular septal defect is best heard at lower left
sternal border, it may simulate tricuspid regurgitation. The rough murmur, lack
of any ventricular enlargement or biventricular enlargement favor a diagnosis
of ventricular septal defect. A pansystolic murmur with pure right ventricle
enlargement rules out ventricular septal defect and favours tricuspid regurgitation.
The ventricular septal defect of L-TGA may be best audible at apex and be mistaken
for mitral regurgitation. The single second heart sound and evidence of varying
SYSTOLIC MURMURS
Fig. 23.21: The wide audibility of VSD murmur. Note the mid-systolic peaking unlike MR or TR
degrees of AV block (diminished first heart sound, variable first heart sound,
irregular cannon waves in JVP) suggest ventricular septal defect in L-TGA. The
ventricular septal defect of left ventricle to right atrium type (Gerbode’s defect)
431
may be selectively conducted to the right of the sternum or, rarely, even to the
neck.
Character and grade

The murmur of ventricular septal defect is as a rule above grade 4/6 and is almost
always associated with a thrill. Thrill is uncommon with mitral regurgitation and
is extremely rare with tricuspid regurgitation. Absence of thrill does not rule
out ventricular septal defect. The murmur is characteristically rough or harsh in
character. Rarely, it can be high-pitched or soft especially when small and muscular.
This harsh character of the murmur distinguishes it from tricuspid regurgitation
and mitral regurgitation, which are soft and blowing in nature.

The murmur is better heard during expiration and is diminished with inspiration.
This behaviour of the murmur is not consistent. More importantly, the murmur
fails to increase with inspiration; this distinguishes it from tricuspid regurgitation.
Rarely the murmur of ventricular septal defect may appear to increase during
inspiration and decrease during expiration. This unexpected behaviour is related
to the change in the orientation of the heart and interventricular septum with
respiration with changes in the direction of the jet. The jet may be directed
towards the site of auscultation in one phase of respiration and directed away in
another. As this phenomenon is unpredictable from one patient to the other, the
murmur may occasionally be better heard during inspiration. This phenomenon
of directional changes in the jet (‘swing’) may be demonstrated during Doppler
echocardiography. This ‘swing’ ventricular septal defect may explain some of the
unusual auscultatory features of VSD mentioned above. The mitral regurgitation
of mitral valve prolapse may be heard medially and may be confused for ventricular
septal defect but failure of the murmur to increase on standing and Valsalva
straining indicates a ventricular septal defect.
Associated features
Moderate to large ventricular septal defects with left to right shunt produce
biventricular enlargement and favour the diagnosis of ventricular septal defect
over tricuspid regurgitation or pulmonic stenosis. Mild to moderate pulmonary
arterial hypertension can coexist with a pansystolic murmur of ventricular septal
432 defect. In the presence of severe pulmonary arterial hypertension with right
ventricle pressure, systemic or near systemic, a pansystolic murmur of ventricular
septal defect is unlikely.
A pansystolic murmur in the presence of severe pulmonary arterial
hypertension is more likely to be tricuspid regurgitation. The only ventricular septal
defect which may retain its pansystolic timing in spite of severe pulmonary arterial
hypertension is the left ventricular right atrial communication or Gerbode’s defect.
The mid-diastolic murmur at the apex in ventricular septal defect, suggests
that the pulmonary flow is at least twice the systemic flow.
Fig. 23.22: Second heart sound split in VSD

SYSTOLIC MURMURS
Associated lesion
The aortic regurgitation in ventricular septal defect is usually due to a cusp prolapse
(most commonly right cusp, rarely non-coronary cusp) or a bicuspid aortic valve.
To cause aortic regurgitation, the defect has to be perimembranous or should
have at least some degree of perimembranous extension when it is subpulmonic.
The ventricular septal defect is always in the left ventricular outflow portion of
the septum and is subjacent to the aortic valve. The early diastolic murmur of
aortic regurgitation with ventricular septal defect gives a to and fro character to the
murmur. The harsh, rough character of the systolic murmur is distinctly different
from the soft, high frequency nature of the murmur of aortic regurgitation. The
syndrome of ventricular septal defect with aortic regurgitation occurs in more
than one condition.
• Isolated ventricular septal defect with aortic regurgitation
• Tetralogy of Fallot with aortic regurgitation
• Sinus of Valsalva aneurysm with aortic regurgitation
Mechanisms
The mechanisms by which aortic regurgitation may take place are: 433
• Prolapse of aortic cusp
• Bicuspid aortic valve
• Aneurysm of sinus of Valsalva
• Congenital fenestrations of the cusp
It is essential to know the mechanism of aortic regurgitation in ventricular
septal defect because the aortic regurgitation due to prolapse of aortic cusp
is amenable to repair but a bicuspid valve requires valve replacement. The
accompanying loud aortic ejection click suggests bicuspid aortic valve. Onset of
aortic regurgitation in ventricular septal defect is an indication for early surgery.
Even a small ventricular septal defect requires surgery once aortic regurgitation
develops, as aortic regurgitation progresses over a period of time. It is for this
reason, that in all patients with ventricular septal defect, one must check for an
early diastolic murmur of aortic regurgitation carefully. Mild to moderate aortic
regurgitation is often amenable to surgical repair but longstanding severe aortic
regurgitation requires valve replacement. When the aortic regurgitation is mild,
Table 23.18: Determinants of the murmur of ventricular septal defect (VSD)
Size of the defect

Small VSD Pansystolic murmur
Moderate VSD Pansystolic murmur
Large VSD Early systolic or ejection systolic murmur
Pulmonary arterial pressure
No pulmonary hypertension Pansystolic murmur
Pulmonary hypertension Early systolic or ejection systolic murmur
No murmur
Location of the defect
Muscular septum Early systolic or ejection systolic murmur
Supracristal defect Best heard at pulmonary area
Selective conduction to infraclavicular area, left side of neck
Simulates pulmonary stenosis
Left ventricular right atrial May be conducted to the right of sternum or neck
communication (Gerbode’s defect)
Sub-aortic defect May be conducted to aortic area (right 2nd space) or neck
Associated defects
Pulmonic stenosis No murmur across ventricular septal defect
PDA (small to moderate) Continuous murmur masks the pansystolic murmur of VSD
PDA (large with PAH) Short systolic murmur or no murmur
434
Coarctation (pre-ductal) with PAH Short systolic murmur or no murmur
Coarctation (post-ductal) Long systolic or pansystolic murmur in spite of PAH
Ruptured sinus of Valsalva into Continuous murmur masks the pansystolic
right heart murmur of VSD. The murmur may be best heard along
right sternal border
L-transposition of great arteries The systolic thrill may be absent along LSB due to side to
side relation of ventricles
the features of ventricular septal defect dominate the clinical features and aortic
regurgitation is often missed. When aortic regurgitation becomes severe, the
ventricular septal defect is less prominent and is likely to be missed. It is good
practice to look for a ventricular septal defect in all patients with aortic regurgitation
either at physical examination or subsequent investigation. The systolic murmur
of ventricular septal defect in the setting of severe aortic regurgitation may be
mistaken for aortic stenosis, but a systolic thrill along the left sternal border, lack
of carotid conduction, a collapsing pulse, and absence of features of significant
aortic stenosis in spite of long systolic murmur favour the diagnosis of ventricular
septal defect.
SYSTOLIC MURMURS
Fig. 23.23: Ventricular septal defect of acute myocardial infarction. Note alternation of
murmur due to left ventricular failure.
Age of onset of murmur

The murmur of ventricular septal defect most often makes its appearance between
2 and 6 weeks after birth. A murmur appearing before 18 hours of age and later
than 6 months is never due to isolated ventricular septal defect.
A new onset murmur in patients above 40 years in the setting of acute 435
myocardial infarction suggests interventricular septal rupture causing ventricular
septal defect.
DIFFERENTIAL DIAGNOSIS OF PANSYSTOLIC MURMURS
There are only three sites in circulation where pansystolic murmurs are possible.
These are mitral regurgitation, tricuspid regurgitation and ventricular septal defect.
These conditions require to be differentiated from each other (Table 23.19). In
actual practice, not only do these murmurs simulate each other, but other murmurs
may also simulate them.
Table 23.19: Murmurs simulating pansystolic murmurs
Condition Simulated by
Ventricular septal defect Severe pulmonic stenosis
Mitral regurgitation Ductus with diastolic component faint or absent
Tricuspid regurgitation The apical systolic murmur of severe aortic stenosis
Infundibular pulmonic stenosis
Table 23.20: Differential diagnosis of a pansystolic murmur
Feature MR TR VSD
Site of best audibility Apex Tricuspid area LSB, anywhere from
pulmonary to tricuspid
area
Grade Grade 3/6 or 4/6, Thrill does not occur Thrill is common
thrill can occur but rare
Selective conduction Axilla and back No selective conduction No selective conduction
Character Soft, blowing high Soft, blowing high Rough, harsh,
frequency frequency combination of high
and low frequencies
Relation to Fails to increase Increases during Fails to increase
physiological act during inspiration inspiration during inspiration
Accompanying LV enlargement Signs of PAH Biventricular enlargement
features Diminished S1 RV enlargement Signs of PAH
LV S3 Elevated JVP with Apical diastolic murmur
Apical diastolic murmur prominent v wave
436 Once a definitive pansystolic murmur is detected, one must assign it to

one of the three possibilities.
In the majority of patients, it is easy to differentiate the disease from any
other. Occasional difficulty arises when there is variation in the character, site or
radiation of these murmurs. In rare cases, the murmur of mitral regurgitation
or tricuspid regurgitation can be relatively rough simulating ventricular septal
defect but the rest of the features are typical. In children, the murmur of mitral
regurgitation can be best heard at the lower left sternal border and may be heard
clearly at the pulmonary area simulating a ventricular septal defect. The murmur
of ventricular septal defect can be of high frequency and may rarely appear to
increase with inspiration as was discussed earlier.
24 Diastolic Murmurs
Unlike systolic murmurs, diastolic murmurs always signify an abnormal
cardiovascular system either structurally or functionally. It is for this reason that
the diastolic murmurs are generally not graded by their intensity unlike the systolic
murmurs. Diastolic murmurs are often graded by their length. The presence or
absence of thrill should be additionally mentioned.
Fig. 24.1: Diastolic murmurs

Classification
Those arising at the atrioventricular valves
• Mid-diastolic
• Pre-systolic
• Combined
Those arising at the semilunar valves
• Early diastolic
• Mid-diastolic sounding like early diastolic
These murmurs can result either at the AV valves or semilunar valves. Due to
low pressure gradient at the AV valves, the murmur is of low frequency at these
sites. Semi-lunar valve regurgitation on the left side is always of high frequency
because of high pressure difference. However, on the right side it depends on
whether pulmonary hypertension is present or not.
The murmur of pulmonary incompetence with normal pulmonary artery
pressure occurs slightly later in diastole and sounds mid-diastolic.
438 DIASTOLIC MURMURS AT THE LEFT ATRIOVENTRICULAR VALVE
The normal flow of blood across the mitral and tricuspid valves is noiseless. Any
disturbance in the normal flow pattern can result in turbulence and therefore a
murmur.
Mechanisms and causes

Narrowing of mitral valve or left ventricular inflow
• Mitral stenosis
• Cortriatriatum
• Constriction of AV groove as in constrictive pericarditis
• Hypertrophic cardiomyopathy (narrow inflow cavity)
Increased flow across the AV valve
• Left to right shunts (ventricular septal defect, ductus)
• Mitral regurgitation (severe)
• Chronic complete heart block
DIASTOLIC MURMURS
Mechanisms that interfere with mitral valve opening

• Austin Flint murmur with severe aortic regurgitation
• Ventricular aneurysm with a narrow neck
MITRAL STENOSIS
Mitral stenosis (MS) is almost always due to rheumatic heart disease and the stenosis
results from commissural fusion and leaflet thickening. Calcification often occurs
in older patients. The involvement of chordae tendinae is variable. Mitral stenosis
is the commonest of valvular lesions due to rheumatic heart disease.
The murmur of MS is the most important member of this group and will be
considered in detail.
Evaluation
In the evaluation of mitral stenosis the following questions need to be answered at
the end of physical examination. A systematic approach to the various components
of the murmur helps to answer most of the questions.
• Is it mitral stenosis or a condition simulating it? 439
Fig. 24.2: Loud first heart sound, opening snap and mid-diastolic murmur
as heard at the apex in case of mitral stenosis
Fig. 24.3: Murmurs in mitral stenosis. Note loud S1 OS: opening snap; DM: mid-diastolic
murmur following OS; PM; pre-systolic murmur that precedes loud S1
Table 24.1: Features of the murmur of mitral stenosis

Feature Description
Site of best audibility Apex
Timing Mid-diastolic/pre-systolic
Selective conduction Localised to apex
Character Rough, rumbling (low-pitched)
Length Short/moderate/long
Respiration Increases during expiration
Posture Increases in left lateral, decreases on standing
Amyl nitrate inhalation Increases
Isotonic exercise Increases
Isometric hand grip Variable
Accompanying features Loud first heart sound, opening snap, diastolic thrill,
pulmonary hypertension, right ventricular hypertrophy,
absence of left ventricular hypertrophy
Dyspnea/paroxysmal nocturnal
Atrial fibrillation
440
• If mitral stenosis, what is the severity?
• Is the valve pliable or calcified?
• Is there subvalvular fusion?
• What is the rhythm?
• Is there pulmonary hypertension? What is the severity?
• Is there right heart failure?
• Are there associated lesions?
• Is there a discrepancy between symptoms and physical signs?
• Is there a peripheral embolism?
• Is left atrial myxoma, a possibility?
As the mitral valve becomes stenotic, the left atrial pressure gets elevated
with a gradient between left atrium and left ventricle in diastole (Fig. 24.4). The
opening snap (OS) results from abrupt opening of the doming mitral valve. As the
atrial contraction contributes to increased gradients in pre-systole, there is pre-
systolic accentuation of the murmur.
DIASTOLIC MURMURS
ECG
Fig. 24.4: Mechanism of mid-diastolic murmur in mitral stenosis
Timing 441
The mid-diastolic murmur: The murmur of mitral stenosis is mid-diastolic in
timing with a pre-systolic murmur. A mid-diastolic murmur by definition means
that there is a time interval between the second sound and the murmur. When the
ventricle relaxes in diastole, the semilunar valves close first followed by the opening
of AV valves. This time interval between semilunar valve closure and AV valve
opening is called isovolumic relaxation time and the ventricle relaxes like a closed
cavity at this time. Any murmur at the mitral or tricuspid valves in diastole can
only occur after this isovolumic relaxation time. Occasionally, with severe
pulmonary hypertension, the pulmonic sound may be delayed and the aortic sound
may be diminished or absent due to associated aortic valve disease. In such
situations, the mitral diastolic murmur may sound early diastolic. However, the
character of the murmur, the site of best audibility and other features, are of help
in distinguishing mitral stenosis from aortic regurgitation.
The pre-systolic murmur: Though the mid-diastolic murmur often occurs in
conditions simulating mitral stenosis, the pre-systolic murmur is rare in the absence
of mitral stenosis. The pre-systolic murmur of mitral stenosis may be simulated by
a very loud atrial gallop that occurs with hypertrophic cardiomyopathy. In mild
mitral stenosis, a pre-systolic murmur may be the only feature in some patients. It
is not known why in mild mitral stenosis, a mid-diastolic murmur occurs in some
patients and a pre-systolic murmur in others. It may be related to the atrial health,
the pattern of left ventricular inflow, and the nature of subvalvular apparatus.
The pre-systolic murmur is usually absent after the onset of atrial fibrillation.
It must be realized that absence of pre-systolic murmur in atrial fibrillation is not
a rule. In a person with very severe mitral stenosis, the left atrial pressures remain
high even at the end of the diastole. In severe mitral stenosis, in spite of atrial
fibrillation, a pre-systolic murmur may persist. In the short diastolic cycles the
pre-systolic murmur is often heard in atrial fibrillation. However, in long diastolic
cycles if the pre-systolic murmur persists, it is a reliable sign of tight mitral stenosis.
Even a pre-systolic accentuation of the murmur may persist in atrial fibrillation
due to progressive narrowing of the mitral valve funnel due to delayed closure of
the mitral valve in mitral stenosis. The persistence of pre-systolic murmur in atrial
fibrillation is not surprising, since the genesis of pre-systolic murmur is not
dependent on atrial contraction alone.
442 Mechanisms of pre-systolic murmur

The various mechanisms are:
• Atrial contraction
• Persistent atrioventricular gradient
• Left ventricular contraction in pre-systole reducing the mitral funnel
The pre-systolic murmur or accentuation may be absent in conditions other
than atrial fibrillation, like mild mitral stenosis, prolonged P-R interval, elevated
LVEDP (left ventricular dysfunction) or bradycardia.
In first degree heart block with severe prolongation of P-R interval, the pre-
systolic accentuation may actually occur in mid-diastole. With significant
bradycardia, with long diastole, there may not be enough gradient by pre-systole.
With elevated left ventricular end diastolic pressure as in left ventricular dysfunction,
the pre-systolic murmur or accentuation may be absent. An atrial gallop in
hypertrophic cardiomyopathy occasionally simulates the pre-systolic murmur. On
the right side, the right atrial gallop in severe pulmonic stenosis can simulate a pre-
systolic murmur. The length of the diastolic murmur correlates with the severity
of mitral stenosis.
DIASTOLIC MURMURS
Table 24.2: Auscultatory features indicating severity of mitral stenosis

Severity of MS (MVA in cm2) S2–OS interval in seconds Features of murmur
Mild MS (1.6–2.5) 0.08–0.12 Short MDM or pre-systolic murmur
or murmur may appear with exercise
Moderate (1.1–1.5) 0.06–0.08 MDM + Pre-systolic murmur with a gap
Varying length of MDM in atrial fibrillation
Severe (< 1.0) 0.04–0.06 MDM + Pre-systolic murmur with no gap.
Pre-systolic murmur with atrial fibrillation
As depicted in the pressure trace, the onset of OS depends on the left atrial
pressure in early diastole – the higher the pressure, the earlier the OS. Since, LA
pressures correlate with severity of mitral stenosis, the earlier the OS, the more
severe the mitral stenosis (Fig. 24.5, Table 24.2). However, when the cardiac output
is low, the OS may be delayed even with severe mitral stenosis. Conversely, it may
be earlier in the presence of associated mitral regurgitation even with moderate
mitral stenosis due to elevated LA pressures.
With a heart rate of 70–90 per minute, normal cardiac output, and normal
left ventricular end diastolic pressures, the longer the murmur the more severe the 443
stenosis.
Fig. 24.5: Correlation of S2–OS interval with severity of mitral stenosis

Table 24.3: Conditions when the length of the murmur is unreliable in mitral stenosis
Condition Longer/shorter Mechanism
Tachycardia Longer Diastolic abbreviation
Bradycardia Shorter Prolonged diastole
Low cardiac output Shorter Lower left atrial pressure
Severe RVF
Severe TR
Severe PAH
High cardiac output Longer Higher left atrial pressure
Anemia
Pregnancy
Thyrotoxicosis
Anxiety
LVEDP Shorter Obliteration of transmitral gradient
Cardiomyopathy
444 Systemic HTN
Atrial fibrillation Variable Varying diastolic cycle lengths
Mechanisms influencing length of the murmur

• Cardiac output
• Heart rate
• Left atrial pressure
• Left ventricular end-diastolic pressure
• Heart rhythm
When there is alteration in any of the above features, the murmur of mitral
stenosis should not be relied upon to assess the severity of mitral stenosis.
In the presence of any of the features in Table 24.3, the length of the murmur
cannot be used to assess the severity of mitral stenosis.
Site of best audibility and conduction

The murmur of mitral stenosis is usually heard best at the apex and being low-
pitched, is localized to the apex without any selective conduction. The murmur
is so much localized to the apex, that if the apical impulse is missed, the diagnosis
DIASTOLIC MURMURS
of mitral stenosis is also missed. It is for this reason that one must go out of the
way to localize the apex in the left lateral position and check for the diastolic
thrill and the murmur of mitral stenosis. Occasionally, the murmur is audible only
at the tricuspid area, left sternal border and even at the pulmonary area. The
murmur when heard at the tricuspid area can be mistaken for the murmur of
organic tricuspid stenosis. The error is compounded by the mild inspiratory
increase in the murmur due to the attendant increase in heart rates during
inspiration with abbreviation of diastole. Another rare but unique feature of the
murmur of mitral stenosis is that it may be audible only along the left sternal
border. This selective audibility only along the left sternal border may be mistaken
for murmur of aortic regurgitation. However, its low frequency, the mid-diastolic
timing, and lack of peripheral signs of aortic regurgitation, in spite of a long
diastolic murmur, are helpful clues. The 2-D echocardiogram in these patients
shows a shortened anterior leaflet and an elongated posterior leaflet composed
of the tethered posterior wall of left ventricle. In effect, the diastolic jet of mitral
stenosis is directed anteriorly toward the interventricular septum unlike the normal
jet, which is directed towards the apex. This type of valve anatomy does not
permit a closed or open commissurotomy and requires mitral valve replacement. 445
Due to the elevated posterior leaflet by the posterior wall of left ventricle, the
replaced prosthetic valve often abuts close to the left ventricular outflow. The
murmur of mitral stenosis is never heard medially in the presence of right
ventricular failure and dilatation.
Be that as it may, the most common murmur of mitral stenosis is localized to
the apex; an occasional murmur is also heard at the tricuspid area, left sternal
border or pulmonary area. Even more rarely the murmur is best heard along the
left sternal border due to distorted valve anatomy, left ventricular geometry and
unusually directed jet. In patients with severe emphysema, the murmur of mitral
stenosis is best heard at the xiphisternal area as the cardiac impulse is available
only at that site. Even the echocardiographic image can be obtained only by this
view.
Character
The murmur of mitral stenosis is low-pitched, rough and rumbling in character. It
sounds like a bullock cart slowly crossing a wooden bridge. The murmur is low-
pitched because the pressure gradient across the valve is low even if the stenosis is
severe and the highest pressure the left atrium can attain is generally not more
than 30 mmHg. A very low-frequency, loud diastolic murmur with a thrill generally
indicates a pliable non-calcific mitral valve capable of low-frequency vibrations. A
severely calcific immobile valve on the other hand, is not capable of low-frequency
vibrations and gives rise to a higher frequency murmur with lesser intensity and
no thrill. Since the murmur is low-pitched, it is better heard with the bell than with
the diaphragm. This feature is of importance because the high frequency murmur
of aortic regurgitation is also heard at the apex and is best heard with the diaphragm.
In short, the diastolic murmur heard better with the diaphragm suggests aortic
regurgitation, and the murmur heard better with the bell suggests mitral stenosis.
In actual practice, this is applicable only when the bell and diaphragm are of
equally good quality (equisensitive).
Relation to physiologic act or maneuvers

Respiration: The murmur of mitral stenosis is heard best during expiration in
the left lateral position when the venous return to the left heart increases with the
apical impulse nearer to the chest wall. However, respiratory change to the murmur
446 is never as impressive as that of tricuspid stenosis. Occasionally, the expiratory
increase is unimpressive and may actually appear to increase during inspiration.
This is related to the increase in heart rate with inspiration and decrease with
expiration. With the shorter diastole of inspiratory increase in heart rate, the gradient
across the mitral valve increases and the murmur is exaggerated (false positive
Carvallo’s sign). The opposite happens in expiration.
Exercise: In mild mitral stenosis, and even in moderate mitral stenosis, with slow
heart rates, the murmur may be heard only on exertion. Exercise brings in or
increases the murmur by the increase in heart rate and blood flow secondary to
the rise in cardiac output. Even minimal exercise such as turning the patient to the
left lateral position, increases the murmur. Exercise should be used routinely when
mitral stenosis is suspected. Mitral stenosis is not ruled out unless exercise is used
as a maneuver. One must identify the clinical situations in which to look for mitral
stenosis.
• Any patient with unexplained dyspnea
• Loud first heart sound with normal heart rate and P-R interval
• Unexplained pulmonary arterial hypertension
• All patients with rheumatic heart disease
DIASTOLIC MURMURS
• All patients with aortic valve disease

• All patients with tricuspid valve disease
• All patients with atrial fibrillation
• All patients with peripheral embolism
• Unexplained left atrial enlargement/or RVH by ECG.
• All patients with ‘bronchial asthma’
Amyl nitrite inhalation: Inhalation of amyl nitrite results in a fall in systemic
vascular resistance and increase in heart rate. As a result, the degree of aortic
regurgitation decreases, resulting in the disappearance or decrease in the Austin
Flint murmur. On the other hand, the murmur of mitral stenosis increases due to
increase in heart rates. In the setting of severe AR and a mid-diastolic murmur at
the apex, the differential diagnosis lies between mitral stenosis and the Austin
Flint murmur. Unfortunately, amyl nitrite is not available in India.
Posture: The murmur of mitral stenosis is best heard in the left lateral position
and decreases on standing due to reduced venous return. The murmur of mitral
valve obstruction due to left atrial myxoma on the other hand, is better heard on
standing and may be lesser in intensity and duration in the supine position. This 447
expected (or unexpected) variation in the murmur with posture is not diagnostic
of left atrial myxoma and may occur with routine mitral stenosis. The accompanying
tachycardia of standing is responsible for increased gradient across the valve with
an increase in the murmur.
Valsalva maneuver: The Valsalva maneuver results in decrease and disappearance
of the murmur of mitral stenosis, with reappearance post release. However, the
response is delayed in comparison to the murmur of tricuspid stenosis.
Dyspnea/paroxysmal nocturnal dyspnea/orthopnea: The length of the
diastolic murmur of mitral stenosis correlates with the severity of symptoms in
mitral stenosis. In spite of mitral stenosis, if the patient has no significant dyspnea
but has edema or puffiness of face as the dominant feature, associated tricuspid
stenosis should be suspected. When symptoms are out of proportion to the length
of the murmur, the accompanying severe pulmonary hypertension or severe right
ventricular failure with tricuspid regurgitation may be responsible. A rare but
important possibility is left atrial myxoma.
Loud first heart sound: The loud first heart sound calls attention to the underlying
mitral stenosis because this is the easiest of physical signs to detect. In addition,
this sign distinguishes mitral stenosis from other causes of mid-diastolic murmur
at apex (Austin Flint murmur, the mid-diastolic murmur of pure mitral
regurgitation) where the first heart sound is diminished. If the first heart sound is
not loud in mitral stenosis, the following possibilities should be considered.
• Mid-diastolic murmur due to Austin Flint or severe pure mitral
regurgitation
• Calcific mitral stenosis
• Severe subvalvular fusion with fibrous immobile valve
• Associated mitral regurgitation
• Severe right ventricular hypertrophy with masked left ventricular events
• Associated aortic stenosis, coronary artery disease or cardiomyopathy
with elevated left ventricular end diastolic pressure
448
A loud first heart sound generally, but not invariably, suggests a pliable, non-
calcific valve. When the body of the anterior leaflet is mobile, a loud first heart
sound is preserved in spite of calcification and immobility of posterior leaflet.
The opening snap and S2–OS interval: The presence of the opening snap
distinguishes the mid-diastolic murmur of mitral stenosis from all the other causes
of diastolic murmurs at apex. Usually, the longer the murmur of mitral stenosis,
the shorter the S2–OS internal. A short murmur is accompanied by a long S2–OS.
This discordant relationship between the murmur of mitral stenosis and the S2–
OS is a feature of classic mitral stenosis. If the relationship is concordant (long
S2–OS with long murmur and short S2–OS with short murmur), one should
suspect an unusual cause for mitral obstruction, like a myxoma of left atrium.
Though mitral stenosis is the most important cause of diastolic murmur at
the apex, there are many other causes for it (Table 24.4).
In the presence of severe aortic regurgitation, the apical diastolic murmur
may be due to Austin Flint murmur or mitral stenosis. The accompanying features
help distinguish one from the other (Table 24.5). The investigation of choice to
distinguish one murmur from the other in this setting is Doppler echocardiography.
DIASTOLIC MURMURS
Table 24.4: Causes and mechanisms of diastolic murmur at apex

Obstruction to left ventricular inflow Rheumatic mitral stenosis
Left atrial myxoma
Congenital mitral stenosis
Cor triatrium
Constriction around AV groove
Increased flow across the mitral valve Severe mitral regurgitation
Left to right shunts (post-tricuspid shunts)
RSOV in to right ventricle
Aorticopulmonary fistula
Truncus arteriosus
Anemia
Thyrotoxicosis
Pregnancy
Unusual mechanisms at the mitral valve The jet of severe aortic regurgitation preventing
opening of mitral valve
(Austin Flint murmur) 449
Mitral valvulitis of acute rheumatic carditis
(Carey Coombs murmur)
Narrowing of LV inflow due to severe LVH as in
hypertrophic cardiomyopathy
Murmurs produced elsewhere but heard at apex Ventricular aneurysm with a narrow neck
Tricuspid stenosis
Tricuspid flow murmur in atrial septal defect
The murmur of aortic regurgitation
Other physical signs mistaken for mitral Third heart sound for mid-diastolic murmur
diastolic murmur Fourth heart sound for pre-systolic murmur
TRICUSPID DIASTOLIC MURMURS

A variety of conditions produce a diastolic murmur at the tricuspid valve by more
than one mechanism.
Mechanisms and causes

Tricuspid stenosis is most often rheumatic and is associated with mitral stenosis.
The diastolic murmur of tricuspid stenosis is similar to that of mitral stenosis.
Table 24.5: Differentiation of mitral stenosis from Austin Flint murmur

Mitral stenosis Austin Flint murmur
Occurs with organic mitral stenosis Occurs only with severe aortic
in rheumatic heart disease regurgitation, usually non-rheumatic
Long history of dyspnea is the Asymptomatic for long time or
presenting symptom palpitation is the presenting symptom
Signs of pulmonary hypertension are common The aortic regurgitation murmur is best heard along
the left sternal border
First heart sound is accentuated
Opening snap is diagnostic
Third heart sound of LV origin never occurs
Diastolic thrill is common
Amyl nitrite increases the murmur
However, the most important difference is the remarkable increase in intensity of

the murmur with inspiration observed in tricuspid stenosis (Fig. 24.6). In fact,
absence of this feature should raise doubts about the diagnosis of tricuspid stenosis.
450
The importance of each of these features will be discussed
(Tables 24.6 and 24.7).
Fig. 24.6: Mid-diastolic murmur of tricuspid stenosis (TS)
Fig. 24.6: Mechanism of diastolic murmur of tricuspid stenosis

DIASTOLIC MURMURS
Table 24.6: Mechanisms and causes of tricuspid diastolic murmurs

Mechanisms Causes
Obstruction to right ventricular inflow Tricuspid valve stenosis
Rheumatic
Congenital
Carcinoid
Right atrial tumours
Myxoma
Secondary tumours
Ebstein’s anomaly
Increased flow across the valve Pre-tricuspid shunts
TAPVC
RSOV into RA
LV to RA communication
Coronary artery to RA communication
Lutembacher’s syndrome
Partial anomalous venous connection
Interference with opening of tricuspid valve Severe tricuspid regurgitation
Functional
Organic
451
Murmurs produced elsewhere but also heard Severe pulmonary regurgitation with right sided
at tricuspid area Austin Flint murmur
Mitral stenosis
Murmurs mistaken for tricuspid diastolic Normal pressure pulmonary incompetence
murmur Pericardial rub
Right sided S4 may sound like pre-systolic murmur
Table 24.7: Features of the murmur of tricuspid stenosis
Feature Description
Site of best audibility Tricuspid area
Timing Mid-diastolic
Length Short/moderate/long
Character Rough/rumbling
Selective conduction Localised to tricuspid area
Respiration Increases during inspiration
Posture Increases in supine, passive leg raising
Rapid deep breathing Increases

The murmur of tricuspid stenosis is usually best audible at the tricuspid area
(4th space, left sternal border), but is also occasionally heard at the third space, and
therefore can be mistaken for the early diastolic murmur of aortic regurgitation or
pericardial rub. The murmur may occasionally be best heard at the apex in rheumatic
tricuspid stenosis when the right atrium is grossly dilated displacing the tricuspid
valve toward the apex. In Ebstein’s anomaly, the displaced tricuspid valve (towards
the right ventricular apex) and the dilated right atrium together are responsible for
the tricuspid murmurs being best heard at apex.
Timing
The commonest murmur of tricuspid stenosis is pre-systolic with or without the
mid-diastolic component. The length of the murmur is directly related to the
severity of tricuspid stenosis. In general, the tricuspid diastolic murmurs are earlier
in diastole than their counterparts at the mitral valve. For this reason, the tricuspid
diastolic murmurs are often mistaken for the early diastolic murmurs of aortic or
pulmonary incompetence. However, their dramatic increase with inspiration and
452 decrease or disappearance with standing or expiration, distinguish tricuspid stenosis
from aortic regurgitation and pulmonic regurgitation.
Though the length of the murmur is directly related to the severity of tricuspid
stenosis, in Ebstein’s anomaly due to associated atrial septal defect and in rheumatic
heart disease due to associated pulmonary hypertension and elevated right
ventricular end diastolic pressure, the murmur may be shorter for the degree of
tricuspid stenosis.
Causes of short or no murmur

The causes of a short murmur or no murmur could be:
• Rheumatic tricuspid stenosis with accompanying mitral stenosis, severe
pulmonary hypertension, elevated right ventricular end diastolic pressure
• Diuretic therapy in tricuspid stenosis
• Atrial fibrillation (absent pre-systolic murmur)
Character
The murmur of tricuspid stenosis is rough and rumbling and of low frequency.
This is due to low pressure difference between the right atrium and the right
DIASTOLIC MURMURS
ventricle in diastole. The murmur is often mistaken for a pericardial rub due to
this rough character. However in severe tricuspid stenosis particularly in right
atrial tumours, the murmur assumes a higher frequency to resemble the murmur
of aortic regurgitation.
Case summary
A 50-year-old man is seen first in 1979 for a heart murmur and a diagnosis of
cardiomyopathy was made. On repeated follow up in various institutions including the
author’s, he was labeled to have pulmonary incompetence or aortic incompetence as the
murmur was interpreted as high frequency or soft. An echocardiogram was not done as
the facility was not available then. In 1984 the patient was evaluated by echocardiogram
with Doppler and was found to have a large right atrial myxoma, which was surgically
removed. Even at this time the murmur was interpreted as pandiastolic and was higher in
frequency for a murmur of tricuspid stenosis.
Relation to a physiologic act

The murmur of tricuspid stenosis always increases during inspiration. The
inspiratory increase is often so explosive that it is mistaken for a pericardial rub.
453
In some patients it may be heard only during inspiration. If ordinary inspiration
fails to bring in the murmur, passive leg raising in supine position during inspiration
generally brings in the murmur. Another maneuver is to ask the patient to breathe
in and out rapidly 5–6 times and then listening for the murmur during inspiration.
The few rapid breaths increase the venous return which accumulates in the right
atrium enhancing the gradient and thereby the murmur. The inspiratory increase
is so consistent in tricuspid stenosis that if this feature is absent the diagnosis of
tricuspid stenosis is highly unlikely.
The accompanying features are important as they are often the pointers to the
physician to look for the murmur of tricuspid stenosis.
The features in Table 24.8 are expected in classic tricuspid stenosis, but
exceptions are common. Significant pulmonary hypertension can occur in spite
of tricuspid stenosis. The a wave in the jugular venous pulse is absent in atrial
fibrillation and the slow y descent is an unreliable sign. Many patients with milder
degrees of tricuspid stenosis do not present with facial or leg swelling, particularly,
if they are receiving diuretics. Paroxysmal nocturnal dyspnea though rare in the
Table 24.8: Associated features of murmur of tricuspid stenosis

Negative Positive
Absence of paroxysmal nocturnal dyspnea Puffiness of face/edema of legs
Significant dyspnea Prominent a and slow y in JVP
Absence of right ventricular hypertrophy Tricuspid opening snap?
No pulmonary hypertension
No right ventricular third or fourth sounds Associated mitral stenosis
presence of tricuspid stenosis, can occur if the accompanying mitral stenosis is

tight or the tricuspid stenosis is mild.
OTHER MID-DIASTOLIC MURMURS AT THE AV VALVES
This murmur occurs even in absence of mitral stenosis when the mitral regurgitation
is severe. The associated third heart sound rules out mitral stenosis. The
454 pre-systolic component as a rule is absent. A diastolic thrill is rare but can occur in
rheumatic mitral regurgitation even if mitral stenosis is absent. In fact this
mid-diastolic murmur in mitral regurgitation (MR) is most common with rheumatic
mitral regurgitation and is rare with non-rheumatic causes of mitral regurgitation.
If the mid-diastolic murmur of mitral regurgitation is unaccompanied by S3, or is
accompanied by an opening snap, associated mitral stenosis is likely. Other features
are:
• Mid-diastolic and short murmur
• Never pre-systolic
• Suggests severe mitral regurgitation
• Favours rheumatic mitral regurgitation
• May have a diastolic thrill without mitral stenosis but favours rheumatic
MR
• Accompanied by third heart sound
• First sound is usually diminished or absent
Severe mitral regurgitation without mid-diastolic murmur is usually non-rheumatic.
When there is associated atrial septal defect, the mid-diastolic murmur at the mitral
valve may not occur in spite of severe mitral regurgitation. In rheumatic mitral
DIASTOLIC MURMURS
valve disease, some degree of anatomical narrowing of the valve is common though
it is physiologically unimportant. The valve area may be more than 2.5 cm2 but
less than the normal 4 cm2. When flow across this valve is increased as in severe
mitral regurgitation, a flow murmur is easily produced.
The belief that in this setting a diastolic thrill always means mitral stenosis is
not valid.
LEFT TO RIGHT SHUNTS

At the tricuspid valve: In the absence of organic tricuspid valve disease, a diastolic
murmur at the tricuspid valve suggests increased flow across the tricuspid valve,
which is twice the normal. The tricuspid diastolic murmur is best heard at the
lower left sternal border. Sometimes it can be heard at the apex when the right
ventricle forms the apex and the murmur is confused for mitral stenosis.
The tricuspid flow murmur in atrial septal defect is: Best heard at the lower
left sternal border but may be heard at the apex or upper left sternal border; only
mid-diastolic murmur is present, with no pre-systolic murmur; relatively soft or
medium frequency (not rough as in tricuspid stenosis); no significant change with
455
respiration; indicates pulmonary flow to be twice the systemic flow or higher;
more specific sign of atrial septal defect than other signs; always present in
Lutembacher syndrome; can occur in any pre-tricuspid shunt.
Occasionally the murmur is audible slightly higher up along the left sternal
border (third space) and is confused for aortic or pulmonary regurgitation. This
error is enhanced due to the relatively softer character and higher frequency of
this murmur in comparison to the murmur of tricuspid stenosis. It should be
realised however, that this tricuspid diastolic murmur though is more specific
than any other sign of atrial septal defect, is by no means pathognomonic of this
defect. It can occur in any pre-tricuspid shunt (left to right shunt located proximal
to tricuspid valve).
Causes
• Left to right shunts (pre-tricuspid)
Atrial septal defect (secundum/primum defects)
Partial anomalous venous connection
Rupture of sinus of Valsalva in to right atrium
Coronary cameral fistula into right atrium
Left ventricular right atrial communication (Gerbode’s defect)

• Admixture lesions (cyanotic heart disease)
Total anomalous pulmonary venous connection
Single atrium
Hypoplastic left heart syndrome (mitral atresia)
• Severe tricuspid regurgitation
• The right sided Austin Flint murmur in severe functional pulmonary
regurgitation
Unlike the murmur of tricuspid stenosis, the flow murmur in these settings is
usually only mid-diastolic, softer and does not increase significantly during
inspiration.
Increased flow across the mitral valve

When the flow across the normal mitral valve is twice the normal flow, a
mid-diastolic murmur occurs in a variety of states.
Left to right shunts (post-tricuspid shunts)
• Ventricular septal defect
456 • Patent ductus arteriosus
• Aortopulmonary window
• Systemic arteriovenous fistula
• Admixture lesions (cyanotic heart disease)
Increasedpulmonaryflow
• Double outlet right ventricle
• Single ventricle
• Truncus arteriosus
• Tricuspid atresia with large ventricular septal defect but no pulmonic
stenosis
• Extensive bronchopulmonary collaterals in pulmonary atresia or any
cyanotic heart disease with diminished pulmonary flow
• Systemic to pulmonary artery shunts
Diminishedpulmonaryflow
• Tricuspid atresia with pulmonic stenosis
• Severe anemia
• Thyrotoxicosis
DIASTOLIC MURMURS
Severe mitral regurgitation

In a left to right shunt such as ventricular septal defect or PDA, this
mid-diastolic murmur indicates that pulmonary flow is at least twice the systemic
flow and is a definite indication for hemodynamic evaluation and surgery. This
physical sign also distinguishes ventricular septal defect from pulmonic stenosis
and other conditions simulating it. This murmur needs to be distinguished from
the third heart sound often heard in children.
AUSTIN FLINT MURMUR
This murmur can be mid-diastolic/pre-systolic and occurs in the presence of

moderate to severe aortic regurgitation. It is due to the heavy jet of aortic
regurgitation impinging on the anterior leaflet of mitral valve preventing adequate
opening of the valve and creating turbulence at the mitral valve in diastole. Austin
Flint in 1862 described this mitral diastolic murmur in patients with aortic
regurgitation. He ascribed this murmur to flow from left atrium to ventricle. In
1972 Fortuin and Craige described echo-phonocardiographic studies in 15 patients
with moderate to severe pure aortic regurgitation. The murmur occurs while the 457
mitral valve is closing, and terminates at the time of first heart sound. The rapidity
of the closing slope of the valve in diastole is increased by the dual influx from the
atrium and aorta, thus creating a baffle to antegrade flow (Craige). With isometric
hand grip, the degree of aortic regurgitation increases due to elevated peripheral
vascular resistance and the Flint murmur increases. With amyl nitrite inhalation or
administration of vasodilators, the murmur decreases or disappears due to the
reduction in severity of aortic regurgitation. The mitral valve has to be open for
this murmur to occur. In extremely severe aortic regurgitation with premature
closure of the mitral valve in late diastole, the murmur is confined to mid diastole
and the pre-systolic murmur does not occur. Another reason may be that all the
flow from the left atrium must occur in mid-diastole thereby increasing the
turbulence to flow.
Other features are:
• Can be mid-diastolic and/or pre-systolic
• Does not occur with mild aortic regurgitation
• Requires at least moderate aortic regurgitation
Table 24.9: Differentiation of Austin Flint murmur from the murmur of mitral stenosis
Feature Austin Flint Mitral stenosis
Diastolic thrill Rare Common
Amyl nitrite inhalation Decreases/disappears Increases
Isometric hand grip Increases Variable
Vasopressors Increases Variable
First heart sound Decreased/normal Increased
Opening snap Absent Present
LV third heart sound May occur Never occurs
Rhythm Sinus rhythm Atrial fibrillation is common
Diastolic pressure < 40 mmHg Unlikely Likely
with pre-systolic murmur
Significant pulmonary Unlikely Likely
hypertension
• Due to the heavy jet of aortic regurgitation falling on AML preventing

adequate opening and turbulence to flow across mitral valve in diastole
458 • With premature closure of mitral valve as in free severe AR or acute
aortic regurgitation, the pre-systolic murmur does not occur
• Increases with isometric hand grip or vasopressors
• Decreases with amyl nitrite inhalation or vasodilators
• Low-pitched, heard best with the bell, unlike the murmur of aortic
regurgitation which is high-pitched and heard best with the diaphragm
Disappearance of the preexisting pre-systolic Flint’s murmur in an aortic
regurgitation may indicate aggravation of aortic regurgitation or onset of left
ventricular failure with elevated ventricular end-diastolic pressures. The Flint’s
murmur needs to be carefully distinguished from that of mitral stenosis (Table 24.9).
In actual practice check for more than one distinguishing feature. In some patients,
it is not possible to differentiate one from the other by clinical features alone.
Echocardiography is diagnostic in this setting.
OTHER PHYSICAL SIGNS SIMULATING MID-DIASTOLIC MURMURS
Other auscultatory signs, occurring in the diastole can mimic the mid-diastolic
and the pre-systolic murmurs at the AV valves.
DIASTOLIC MURMURS
• Third heart sound as mid-diastolic murmur

• Fourth heart sound as pre-systolic murmur
• Third heart sound and fourth heart sound together as mid-diastolic
murmur
• Pericardial knock of constrictive pericarditis
• Pericardial rub
• Early diastolic murmur of aortic regurgitation at apex
In hypertrophic cardiomyopathy, the loud fourth heart sound can mimic the
pre-systolic murmur. More commonly, the physiological third heart sound of
children is mistaken for mid-diastolic murmur. Rarely, the pre-systolic gallop (fourth
heart sound) in severe pulmonic stenosis can resemble the pre-systolic murmur of
tricuspid valve.
SEMILUNAR VALVE REGURGITATION

Normally, the second heart sound (A2 and P2) marks the closure of the semilunar
valves on either side of the heart. Also, there is no back flow. When these valves
are incompetent, the murmurs start flush with the corresponding second heart 459
sound. It is for this reason these murmurs are called early diastolic murmurs in
contrast to those arising at the AV valves which occur some time later in diastole
(mid-diastolic).
AORTIC REGURGITATION
The competence of the normal aortic valve is maintained by a combined mechanism
of the aortic valve apparatus.
• Aortic valve cusps
• Commissures
• Aortic valve annulus
• Aortic root/sinuses of Valsalva
• LV contractility
Any alteration in the above mechanisms may produce aortic valve incompetence.
Rheumatic heart disease is the commonest cause of aortic regurgitation it affects
the valve cusps. Rarer causes like syphilis produce aortic regurgitation by dilatation
and distortion of the aortic root (Table 24.10).
Table 24.10: Mechanisms of aortic regurgitation

Abnormality of cusp/commissures
Reduction in area Rheumatic fever
Rheumatoid disease
Ankylosing spondylitis
Perforation Infective endocarditis
Commissural fusion Congenital
Rheumatic
Loss of commissural support Congenital
Tetralogy with AR
VSD with AR
Dissection of aorta
Fixed orifice Calcific AS
Distortion of cusps Subvalvular fixed AS
Abnormality of aortic root
Aortic root distortion Nonspecific aortitis
Ankylosing spondylitis
Syphilis
Non specific urethritis (Behcet’s)
460 Rheumatoid disease
Aortic dissection
Aortic root dilatation All disorders with aortitis
Aortopathy (non-inflammatory)
Marfan’s
Familial
Idiopathic
Intimal flap prolapse Ehlers–Danlos
Pseudoxanthoma elasticum
Functional Aortic dissection
Severe systemic hypertension
Evaluation
The questions to be answered when evaluating aortic regurgitation are:
• Is it aortic regurgitation or a condition simulating it?
• If aortic regurgitation, is it due to aortic root disease or valve disease?
Timing
• What is the severity?
• Are there associated lesions?
• Is there heart failure?
DIASTOLIC MURMURS
Table 24.11: Features of the murmur of aortic regurgitation

Features Description
Timing Early diastolic
Site of best audibility Right 2nd space/LSB/apex/right sternal border
Character High frequency/soft/blowing/musical
Length/grading < Grade 3/6, thrill is rare
Respiration Best heard in sitting (or standing) leaning
forward,
Posture Held expiration
Isometric hand grip Increases
Vasopressor (phenylephrine) Increases
Amyl nitrite inhalation or sublingual nitrate Decreases
Prompt squatting Increases
Associated features
Fever/clubbing/recent aggravation of Infective endocarditis
symptoms
Recent/sudden aggravation in severity of Retroversion or prolapse of aortic cusp/
461
AR or symptoms aortic dissection /hypertension
Arterial pulse High volume/collapsing/bisferiens
Blood pressure High pulse pressure/low diastolic pressure/
positive Hill’s sign
LV enlargement Hyperkinetic LV impulse
First sound Normal with mild AR/diminished or
absent in severe AR
Second sound Normal split with mild AR/reversed split
with severe AR or LV dysfunction. A2 is
diminished or absent in valve disease as in
rheumatic. Accentuated with aortic root
disease as in syphilis
Third heart sound Suggests heart failure or associated mitral
regurgitation
Fourth heart sound Acute AR/aortic dissection with past
hypertension and left ventricular hypertrophy
Ejection systolic murmur Occurs with moderate to severe AR commonly
Pulmonary arterial hypertension Rare
Fig. 24.7: Early diagnostic murmur in aortic regurgitation

462
• Is there systemic hypertension?
• Is it chronic/acute or acute or chronic?
• Is there infective endocarditis?
• Is the patient symptomatic?
Many of these questions can be answered by the time one finishes auscultation
in aortic regurgitation, if the auscultation is done systematically.
The murmur of aortic regurgitation is early diastolic starting flush with the
aortic component of the second heart sound (Fig. 24.7). The early diastolic murmur
of pulmonary incompetence starts later with the pulmonary components of second
heart sound. This feature is hardly helpful in differentiating these murmurs from
one another as the two components of second heart sound are difficult to detect
in this setting. With severe pulmonary hypertension due to pulmonary
incompetence, the second heart sound is often single; in aortic regurgitation, the
P2 is covered by the murmur. When transmitted to the apex, the murmur is mistaken
for mitral diastolic murmur. As happens often, when it is difficult to be sure if the
murmur is early diastolic or mid-diastolic, the bell and the diaphragm can be used
to advantage. A diastolic murmur, heard best with the bell is the mid-diastolic
DIASTOLIC MURMURS
Table 24.12: Causes of murmurs at left and right sternal borders in aortic regurgitation
Left sternal border murmurs Right sternal border murmurs
Rheumatic heart disease Syphilis
Congenital bicuspid valve Marfan syndrome
Infective endocarditis Annuloectasia of aortic root
AR in association with valvular AS Ankylosing spondylitis
AR in association with subvalvular fixed AS Rheumatoid arthritis
Reiter syndrome
Prosthetic AR AR in association with tetralogy of Fallot
AR in association with VSD
murmur of mitral valve, and the one heard best with the diaphragm, is the early
diastolic murmur of aortic regurgitation.

The commonest form of aortic regurgitation (rheumatic) due to aortic valve disease,
is heard best along the left sternal border but is also heard well at the right second
space and apex (Table 24.12). In unusual and rare causes of aortic regurgitation
463
(syphilitic) due to aortic root disease, the murmur is heard best along the right
sternal border but is also heard along the left sternal border and apex. The audibility
of the early diastolic murmur at the right second space and apex distinguishes
aortic regurgitation from pulmonary incompetence.
The left sternal border murmur is suggestive of valvular origin for the murmur.
With a dilated aortic root, the murmur is conducted more to the right sternal
border than to the left. In the aortic regurgitation of tetralogy due to the dextroposed
aortic root, the jet of aortic regurgitation may be directed selectively into the right
ventricle and may result in a murmur better audible along the right sternal border.
A similar phenomenon may occur in aortic regurgitation associated with ventricular
septal defect, when the right coronary cusp prolapses into the right ventricle due
to lack of support.
Character and diastolic thrill

The early diastolic murmur of aortic regurgitation is high-frequency, soft, blowing
and may be musical in character. This is related to the high pressure difference
between the aorta and the left ventricle in diastole. This is unlike that of the
mid- diastolic murmur of mitral stenosis where the diastolic pressure difference is
lesser. The early diastolic murmur may assume a musical quality when the cause is
infective endocarditis with vegetations over the aortic valve, or when the aortic
cusp is retroverted as in syphilis. Very rarely, the murmur may be rough in character
like that of aortic stenosis and may have a thrill. This almost always suggests a
retroverted aortic cusp as in syphilis. This unexpected thrill of aortic regurgitation
is often mistaken for a systolic thrill and some other diagnosis may be considered.
However, careful auscultation with simultaneous palpation of the carotid impulse
or ‘inching’ the stethoscope from the base to the apex is helpful.
Length of early diastolic murmur

As a general rule, the length of the murmur correlates with the severity of aortic
regurgitation. However, there are many exceptions to this rule. The length of the
murmur is a reflection of the duration of the pressure gradient between the aorta
and the left ventricle in diastole. In the absence of heart failure in chronic aortic
regurgitation, a short murmur generally indicates mild aortic regurgitation and
a longer murmur is associated with moderate to severe aortic regurgitation.
The length of the early diastolic murmur in aortic regurgitation is a function of
464 aortic pressure, the degree of abnormality at the aortic valve, the left ventricular
end diastolic pressure and probably the direction of the jet of aortic regurgitation.
The length of the murmur is influenced by:
• Aortic pressure (systemic vascular resistance)
• Left ventricular diastolic pressure
• The actual defect at the aortic valve
• The severity of aortic regurgitation
For a given degree of defect at the aortic valve, the longer the murmur the
more severe the aortic regurgitation. Again, for a given defect at the aortic valve,
the higher the aortic pressure, the longer the murmur. The higher the left ventricular
pressure, the shorter the murmur.
Causes of significant AR with short or no murmur are:
• Left ventricular failure
• Tachycardia
• Hypotension
• Vasodilators
• Pregnancy
DIASTOLIC MURMURS
Table 24.13: Causes and clinical settings for acute aortic regurgitation
Cause(s) Clinical setting
Infective endocarditis Fever
Acute pulmonary edema, heart failure
Rheumatic heart disease,
Bicuspid aortic valve
Surgical or balloon dilatation Deterioration after procedure
Blunt injury chest
Trauma
Acute aortic dissection Acute chest pain/back pain
Absent or asymmetry of peripheral pulses
PTCA: Guiding catheter interfering Unexplained hypotension or elevation of PA
with aortic valve closure mechanism diastolic pressures during PTCA
(especially Amplatz catheter)
In acute severe aortic regurgitation, the left ventricular diastolic pressure inevitably
rises and approximates that of aorta, abbreviating or abolishing the murmur. Even
a short murmur should be given importance in the clinical setting when acute
aortic regurgitation is likely. 465
During PTCA, the stiff guiding catheter abutting over the aortic valve may
interfere with its closure and may result in significant acute aortic regurgitation.
This often, manifests not as an auscultatory sign but as an unexplained hypotension
with rise in pulmonary artery diastolic and systolic pressures. Initially, the aortic
diastolic pressure falls; later the systolic pressure falls (Table 24.13).
Tachycardia, of both sinus and ectopic origin, shortens the murmur due to
abbreviation of diastole. With hypotension or vasodilators the driving pressure
for aortic regurgitation is diminished with a decrease in the murmur. In pregnancy
due to hormonally induced reduction in systemic vascular resistance and the
placenta acting like an arterial venous fistula, the murmur may shorten or disappear.
Relation to a physiologic act

The murmur of aortic regurgitation can be very difficult to hear and requires to be
checked through certain maneuvers. Some of these maneuvers help recognise the
murmur when previously audible, and others to differentiate it from murmurs
that simulate it. The early diastolic murmur of aortic regurgitation is most difficult
to hear when it is acute or very mild. Certain disorders are often associated with
Table 24.14: Conditions in which one must check for aortic regurgitation
Condition Significance
Aortic stenosis Localises the lesion to the valve or subvalvular
region
Rules out subvalvular dynamic obstruction
(HOCM)
Helps to distinguish the murmur of AS from PS
Contraindicates balloon dilatation
Mitral valve disease Favours rheumatic heart disease
Ventricular septal defect Early surgery prevents progression of AR
Indication for surgery even with a small VSD
When a murmur of AR is heard the VSD
murmur is mistaken for AS
Tetralogy of Fallot Can precipitate CCF
Repair or replacement of valve
Coarctation of aorta Associated bicuspid valve
Worsening of clinical course
Early surgery for coarctation
Bicuspid aortic valve Associated AR increases the risk of infective
466 endocarditis
Appearance of new murmur when the patient
comes back with fever
Patient with acute chest pain Aortic dissection is likely
Patient with fever Infective endocarditis
Acute pulmonary edema of unknown Acute AR/surgery is life saving
origin
Coronary artery disease Rule out aortic dissection
Contraindication to intra-aortic balloon
High volume pulse or hyperkinetic AR is an important cause
circulatory state
Systemic hypertension AR runs a rapidly progressive course
Vasodilators/ACE inhibitors are the choice
Can be functional with a diastolic pressure above
120 mmHg
aortic regurgitation; one must check for these (Table 24.14). In some clinical
situations, detection of the murmur has important diagnostic and immediate
therapeutic significance.
In all the above situations one must make the patient sit, lean forward and
DIASTOLIC MURMURS
Table 24.15: Maneuvers used to bring out the early diastolic murmur of AR
Maneuver Mechanism
Sitting, leaning forward, held expiration, Aorta nearer to chest
diaphragm firmly applied to the chest Non-interference with the noise of breathing
Improved quality of diaphragm to appreciate the
high-frequency murmur
Prone position Aorta nearer to chest
Prompt squatting Increased systemic vascular resistance
Isometric hand grip As above
Vasopressors (phenylephrine) Increased systemic resistance
The reflex bradycardia with phenylephrine is best
suited for auscultation of aortic regurgitation
murmur
during held expiration with the diaphragm firmly applied to the chest, auscultate
for the early diastolic murmur of aortic regurgitation when it was not audible
earlier. The case of a patient with fever as a presenting manifestation deserves
particular attention. It is often taught that in a patient with fever, one must look
for evidence of infective endocarditis when the fever is of a few weeks duration. It 467
must be realised that infective endocarditis has its beginnings, like any other cause,
in fever. It is now well known that when the diagnosis and therapy are delayed
beyond the first few days or weeks, peripheral embolism and heart failure are
more likely and the chances of medical therapy succeeding are less and less likely.
One must make it a habit to look for the murmur in the heart whether the fever is one day old or
many weeks old. It is in this setting of a febrile patient with tachycardia where a
murmur is not initially heard that one of the maneuvers listed in Table 24.15 must
be used.
Once the murmur of aortic regurgitation is detected, the next step is to
differentiate it from the other murmurs or auscultatory events which closely
simulate it (Table 24.16).
The murmur of aortic regurgitation is one of the most difficult to detect and
requires careful auscultation and use of various maneuvers.
A high volume or collapsing pulse not only supports but also helps quantify aortic
regurgitation. The absence of a collapsing pulse does not rule out aortic regurgitation
Table 24.16: Auscultatory events or murmurs simulating AR

Auscultatory event/murmur Differentiating feature
Pulmonary regurgitation with Not audible at right side of sternum and apex
pulmonary hypertension May increase with inspiration
(Graham Steell murmur) Decreases with standing/expiration
Associated with severe pulmonary hypertension
No peripheral signs of aortic regurgitation
In the setting of valvular disease, occurs only with
severe mitral stenosis
Mid-diastolic murmur of severe mitral Low frequency, better heard with bell
stenosis at apex and occasionally
along LSB
Mid-diastolic murmur of severe mitral As above
regurgitation when heard along left
sternal border
Mid-diastolic murmur of tricuspid Decreases or disappears with sitting, standing,
stenosis during expiration
Increases with supine position, inspiration
Better heard with bell
Prominent a wave with elevated JVP
468 Pericardial friction rub when high Changes with posture/respiration
frequency or musical Never heard to the right of sternum
Primary cause for pericarditis is generally evident
as in mild aortic regurgitation. Similarly, a collapsing pulse does not rule out
pulmonary regurgitation in the presence of significant mitral stenosis and severe
pulmonary arterial hypertension. Ejection systolic murmur of grade 3/6 to 4/6 is
common with moderate to severe aortic regurgitation even in the absence of aortic
stenosis. If the diastolic pressure is less than 40 mmHg, aortic stenosis of any
significance is unlikely even if the ejection systolic murmur is grade 4/6 (Fig. 24.8).
This murmur may have a thrill over the carotid but absence of thrill over the
aortic area or left sternal border and a forcible non-sustained apical impulse with
a diastolic blood pressure of 40 mmHg or less argues against aortic stenosis.
Aortic vascular click is common with aortic regurgitation due to aortic root
disease. This click is usually not very loud, and the accompanying loud A2 and the
early diastolic murmur to the right of the sternum favour a vascular click. A loud
valvular ejection click is common in aortic regurgitation due to bicuspid aortic
valve or the quadricuspid valve of truncal regurgitation in truncus arteriosus. In
DIASTOLIC MURMURS
Fig. 24.8: Grade 4/6 ejection systolic murmur in AR
the absence of impressive cyanosis and clubbing, the last condition may be mistaken
for pure aortic regurgitation or rheumatic heart disease in a grown up child or
adolescent.
PULMONARY REGURGITATION 469
Unlike aortic regurgitation, pulmonary regurgitation (PR) occurs in two settings,

both of which have an important influence on the clinical features of the murmur.
• Pulmonary regurgitation with pulmonary arterial hypertension
• Pulmonary regurgitation with normal pulmonary arterial pressures
The most common form is related to high pulmonary arterial pressures and
will be described first. This murmur is also called the Graham Steell murmur.
Unlike the aortic annulus, which is capable of tolerating very high pressures,
the pulmonary annulus has a weak base and cannot withstand very high pressures.
This murmur generally means that the pulmonary arterial pressures are equal to
or higher than the systemic pressures. Each of the features listed above will be
described.
Timing
The murmur of functional pulmonary incompetence is early diastolic in timing
and needs to be distinguished from aortic regurgitation (Table 24.17). Theoretically,
the murmur of aortic regurgitation starts flush with the aortic component of the
Table 24.17: Murmur of pulmonary incompetence in pulmonary hypertension

Feature Description
Timing Early diastolic
Length Very short to pandiastolic
Site of best audibility Pulmonary area (left 2nd space or 3rd space)
Character High pitched
Conduction Left sternal border 3rd and 4th spaces
Apex if formed by right ventricle
Relation to physiological act/maneuvers
Respiration May increase during inspiration but often fails
to do so; better heard in supine posture,
passive leg raising
Posture Diminishes or disappears in standing posture
Isometric hand grip/vasopressor No influence
Amyl nitrite inhalation No influence/may decrease
Associated features
Signs of severe pulmonary hypertension Loud pulmonic sound
Palpable pulsations in 2nd space
470 Right ventricular impulse
Prominent a wave in JVP
Right ventricular third or fourth heart sound
Right sided Austin Flint murmur
Evidence of mitral stenosis,
Preexisting left to right shunt or Eisenmenger
syndrome
Primary pulmonary hypertension
second sound and that of pulmonary incompetence starts with the pulmonary
component of the second sound. This feature is rarely of use in actual practice
because in the clinical setting when pulmonic regurgitation occurs, the second
heart sound is either closely split or is single, making it difficult to distinguish one
from the other. The organic pulmonic regurgitation due to normal pulmonary
arterial pressures starts some time after the second sound because it takes a while
for the turbulence to occur (Fig. 24.9).
The features of murmur of pulmonic regurgitation depend upon whether
pulmonary arterial hypertension (PAH) is present or not. With pulmonary
hypertension, the murmur is long, decrescendo and of high frequency. However,
DIASTOLIC MURMURS
Fig. 24.9: Mechanism of pulmonary regurgitant murmur
Table 24.18: Features of pulmonary incompetence with normal pulmonary arterial pressures 471
Feature Description
Timing Mid-diastolic
Length Short, never pandiastolic
Site of best audibility Pulmonary area
Character Low frequency, rumbling
Conduction Localized to pulmonary area, may be heard
along the left sternal border
Posture Increases during supine/passive leg raising
Decreases with standing
Respiration Increases with inspiration
Decreases with expiration
Associated features Absence of pulmonary hypertension
Diminished or absent pulmonic sound
Palpable pulmonary artery
Hyperkinetic right ventricular impulse
Signs of valvular pulmonic stenosis
Evidence of infective endocarditis
Tetralogy of Fallot
with normal pulmonary arterial pressures, the murmur is more mid-diastolic and
is of either medium or low frequency across the right ventricular outflow with
lesser pressure gradient (Table 24.18). This murmur sounds mid-diastolic, and
when heard along the left sternal border, may be mistaken for tricuspid stenosis
or even mitral stenosis. In the setting of tetralogy of Fallot with absent pulmonary
valve, the pulmonic regurgitation is accompanied by a rough ejection systolic
murmur due to the annulus narrowing. This combination of murmurs is
occasionally mistaken for a continuous murmur of ductus. The to and fro character
of the murmur and clear time interval between the systolic and diastolic components
help to distinguish one from the other.
Length
The pulmonic regurgitation of pulmonary hypertension may be very short or long
and may even be pan diastolic. The length of the murmur reflects the duration of
pressure difference between the pulmonary artery and the right ventricle in diastole.
In severe pulmonary hypertension where the pulmonary artery diastolic pressures
are usually above 50 mmHg, the right ventricle end diastolic pressure may never
472 equalise that in the pulmonary artery. This permits a long murmur. The pulmonic
regurgitation of normal pulmonary arterial pressures as a rule is short in duration
as the pulmonary artery diastolic pressure is 10–15 mmHg with right ventricle
end diastolic pressure of less than 7 mmHg. This small pressure difference is
rapidly equalised in the later part of diastole, discouraging the possibility of any
murmur.
The length of the murmur also helps in the differential diagnosis of aortic
regurgitation from pulmonic regurgitation of pulmonary hypertension in one
setting. When there is a long early diastolic murmur with no peripheral signs of
aortic regurgitation, pulmonary regurgitation is very likely. This is because a long
murmur means more aortic regurgitation, and should have the peripheral signs of
aortic run off. A long early diastolic murmur with no peripheral signs of aortic
regurgitation for that matter means pulmonic regurgitation.

The murmur of pulmonic regurgitation due to pulmonary hypertension is best
heard at the pulmonary area and may be heard at the apex when formed by the
right ventricle. It is unusual for it to be audible to the right of the sternum. The
DIASTOLIC MURMURS
murmur of pulmonic regurgitation with no pulmonary hypertension is always

localised to the pulmonary area.
Character
The early diastolic murmur of pulmonic regurgitation due to pulmonary
hypertension is of high frequency and that of pulmonic regurgitation with no
pulmonary hypertension is of low frequency. The frequency of the murmur is a
function of the pressure difference between pulmonary artery and right ventricle
in diastole. Rarely, the pulmonic regurgitation of pulmonary hypertension may
have a combination of frequencies with the rough component dominating. This
may, in rare cases, be associated with a diastolic thrill. When the pulmonic
regurgitation murmur is rough with a diastolic thrill, it is often mistaken for a
systolic murmur of ventricular septal defect or pulmonic stenosis. This type of
murmur is more likely in pulmonary hypertension due to patent ductus arteriosus
and primary pulmonary hypertension. This error of mistaking it for a systolic
thrill and murmur is more common than is realized, because one does not expect
a rough early diastolic murmur in pulmonic regurgitation. The rough and long
murmurs are automatically considered systolic and are ascribed to either ventricular 473
septal defect or pulmonic stenosis. It is in this setting that one should carefully
auscultate to identify the sounds first and by inching the stethoscope from the
apex to the base.
Causes of pulmonic regurgitation with no pulmonary hypertension
• Congenital isolated pulmonary regurgitation
• Pulmonic stenosis with dysplastic pulmonary valve
• Tetralogy of Fallot with absent pulmonary valve
• Idiopathic dilatation of pulmonary artery
• Infective endocarditis of pulmonary valve
• After balloon dilatation for pulmonic stenosis
• After surgical valvotomy
• After surgical repair of tetralogy
Relation to a physiological act

The pulmonic regurgitation of pulmonary hypertension has no consistent
relationship to respiration. It may increase during inspiration; this helps to
distinguish it from aortic regurgitation. The murmur fails to increase during
inspiration in a significant number of patients and is related to severe pulmonary

hypertension and possibly right ventricular failure, which prevent further increases
in cardiac output. In the setting of severe pulmonary hypertension, the hangout
intervals on the pulmonic side approximate with that of systemic circulation and
respiration may fail to alter it. Significant inspiratory increase in the murmur is
more often a feature of pulmonic regurgitation of no pulmonary hypertension. As
the murmur of tricuspid stenosis may occasionally be heard nearer the left third
space, it may be confused for pulmonic regurgitation. A dramatic increase with
inspiration is more likely with tricuspid stenosis than with pulmonic regurgitation.
Isometric hand grip and vasopressors increase the murmur of aortic regurgitation
and do not influence pulmonic regurgitation.
Signs of pulmonary hypertension: Severe pulmonary hypertension is a rule with
the Graham Steell murmur. The pulmonic sound is severely accentuated and is
palpable. In rare cases, the pulmonic sound may not be very loud or may even be
interpreted as normal in intensity. This is more likely to happen in patients with
474 primary pulmonary hypertension with right ventricular failure and low cardiac
output. With a reduced flow across the pulmonary valve, the valve excursion is
limited and the subsequent pulmonary valve closure will be less intense.
Other auscultatory signs: The high frequency murmur of tricuspid regurgitation
is common due to high right ventricle pressures, dilated tricuspid annulus, dilated
and dysfunctioning right ventricle. A right sided Austin Flint murmur may occur
and is related to the pulmonic regurgitation jet preventing adequate opening of
tricuspid valve causing relative tricuspid stenosis. A right sided fourth heart sound
and third heart sound may occur. A constant pulmonary vascular ejection click is
common. It is constant because the right ventricle end diastolic pressures can
never exceed the pulmonary artery diastolic pressures in severe pulmonary
hypertension. This relationship between pulmonary artery diastolic pressure and
right ventricle end diastolic pressure prevents premature opening of the pulmonary
valve. The non-pulmonary hypertensive pulmonic regurgitation is accompanied
by normal, diminished or absent pulmonic component of second heart sound.
The right ventricle impulse is hyperkinetic in a purely volume loaded right ventricle
as in pure pulmonary incompetence due to infective endocarditis or idiopathic
DIASTOLIC MURMURS
dilatation of pulmonary artery. The RV impulse is hyperkinetic and sustained,

when pulmonic regurgitation is associated with pulmonic stenosis, as in pulmonic
stenosis with dysplastic pulmonary valve or tetralogy with absent pulmonary valve.
GRAHAM STEELL MURMUR

The Graham Steell murmur in a patient with pulmonary hypertension suggests
that the pulmonary artery pressures are in the systemic or suprasystemic range.
In the setting of valvular heart disease, this murmur as a rule indicates underlying
severe mitral stenosis, or combined mitral stenosis and regurgitation with dominant
mitral stenosis. It rarely occurs with pure mitral regurgitation and almost never
occurs with aortic valve disease. In the setting of left to right shunts, this murmur
is often suggestive of severe pulmonary hypertension near systemic range and
often signifies inoperability. Rarely, this murmur may occur in patients with near
systemic or systemic pulmonary artery pressures and significant left to right shunts
with hyperkinetic shunt dependent pulmonary hypertension (Table 24.19). Never
use this murmur to decide on the operability or inoperability, as a small percentage
of patients with this murmur may be operable. In a patient with cyanosis, this
475
murmur generally indicates Eisenmenger syndrome or, rarely, congenital cyanotic
heart disease with increased pulmonary blood flow and severe pulmonary
hypertension as in transposition of great arteries, double outlet right ventricle,
single ventricle, or total anomalous pulmonary venous connection.
The early diastolic murmur of pulmonary incompetence can occur in atrial
septal defect without any pulmonary hypertension due to dilated pulmonary artery
related to large pulmonary flow.
Table 24.19: Significance of Graham Steell murmur
Clinical setting Significance

Pulmonary artery pressures Near systemic, systemic or suprasystemic range
Valvular heart disease Almost always suggests MS or MS+MR with
dominant mitral stenosis.
Rheumatic heart disease is most likely
Left to right shunts Severe PAH (fixed or hyperkinetic)
No PAH but dilated PA as in atrial septal defect
Cyanotic patient Eisenmenger syndrome
Cyanotic heart disease with PAH
PULMONIC REGURGITATION WITH NO PULMONARY

HYPERTENSION
This type of murmur due to pulmonic regurgitation occurs in a variety of situations.

In the setting of valvular pulmonic stenosis, it means a dysplastic pulmonary valve,
infective endocarditis, post-pulmonary valvuloplasty either surgically or by balloon
valvuloplasty. In cyanotic heart disease, it occurs with tetralogy with absent
pulmonary valve, or after surgical correction of tetralogy with outflow resection
and patch repair (Table 24.20).
Table 24.20: Significance of pulmonic regurgitation with no pulmonary hypertension
Clinical setting Significance
Pulmonary stenosis Localises the lesion to the valve
May suggest a dysplastic valve
Helps to distinguish pulmonic stenosis from
VSD and AS
After balloon dilatation/surgery
476 Tetralogy of Fallot Tetralogy with absent pulmonary valve
After surgical correction
Patient with fever/septicemia Infective endocarditis
It is important to check for the murmur of pulmonic regurgitation in patients

with pulmonic stenosis because, a dysplastic valve is not easily amenable to balloon
dilatation. Infective endocarditis of the pulmonary valve is often mistaken for
bronchopneumonia when the diastolic murmur is not detected. In the differential
diagnosis of systolic murmur at the pulmonary area, the low-frequency
‘mid-diastolic murmur’ suggests pulmonary stenosis and rules out ventricular septal
defect or aortic stenosis.
25 Continuous Murmurs
There are two components in the definition of a continuous murmur. The first
feature is the ability of the murmur to overlap the second heart sound and spill
over to diastole with no respect for the boundaries of the cardiac cycle. The second
feature is that there is no change in character of the murmur from systole to
diastole. The continuous murmur differs from a ‘to and fro murmur’ in one or
both of the features. The murmurs of ventricular septal defect + aortic regurgitation,
aortic stenosis + aortic regurgitation, mitral stenosis + mitral regurgitation belong
to the category of ‘to and fro’ murmurs.
Various sites of left to right communication where continuous murmurs are
possible: patent ductus arteriosus (PDA) (the most common cause), rupture of
sinus of Valsalva (RSOV), systemic arteriovenous (AV) fistula, mammary souffle,
aortopulmonary (AP) window, and so on.
Fig. 25.1: Sites and mechanisms of continuous murmur

Table 25.1: Mechanism of continuous murmurs

Communication between a high and low pressure zone
Systemic AV fistula
Congenital
• Intracranial
• Hepatic
• Lower and upper limbs
Acquired
• AV fistula of hemodialysis
• Post-trauma
• Surgery
• Needle puncture
• After cardiac catheterization
Rupture of sinus of Valsalva aneurysm into
• Right atrium
• Right ventricle
• Left atrium
Coronary cameral fistula
Bronchial to pulmonary arterial collaterals in cyanotic heart diseases with
diminished pulmonary flow
• Pulmonary atresia
478 • Truncus arteriosus
Left to right atrial shunt
• Mitral stenosis with PFO/small ASD
• Mitral atresia + Small ASD
Narrowing of an artery
• Coarctation of aorta
• Renal artery stenosis
• Peripheral pulmonary stenosis
• Truncus arteriosus with pulmonary arterial stenosis
• Coronary stenosis
Increased velocity of flow with turbulence
• Truncus arteriosus with pulmonary arterial stenosis
• Coronary stenosis
• The cervical venous hum
• Over the skull in children with anemia
• TAPVC supracardiac type
• TAPVC infradiaphragmatic/intracardiac
Increased blood flow to an organ
• Thyrotoxicosis, hypernephroma, hepatoma
• Thyroid in thyrotoxicosis
• ‘Tumour blush’ in hepatoma
• Hypernephroma
• Mammary souffle
• Hemangioma
CONTINUOUS MURMURS
The murmur may start any time during systole but should overlap and occupy
a varying duration of the diastole. The murmur need not occupy the whole of
systole and diastole, to fulfill the definition. Continuous murmurs occur due to a
variety of mechanisms. The common mechanisms and the clinical examples are
given in Table 25.1.
PATENT DUCTUS ARTERIOSUS
Patent ductus arteriosus is a communication between the proximal descending

thoracic aorta 2–10 mm beyond the origin of the left subclavian artery to the
origin of the left pulmonary artery from the pulmonary trunk. It is usually 5–10
mm long with a wide aortic orifice and a narrow pulmonary orifice.
At birth, the ductus arteriosus is patent and resembles a muscular artery.
Postnatally, closure occurs in two stages.
The first stage is termed as functional closure. It is complete 10–15 hours after
birth in full term infants and is due to contraction of the smooth muscle in the
media of the ductal wall which produces shortening and increase in wall thickness.
This functional closure is helped by approximation of the intimal cushions. 479
The second stage is called anatomical closure and is completed within 2–3 weeks
after birth. Diffuse proliferation of the intima occurs; this may be associated with
necrosis of the inner layer of the media and hemorrhage into the wall. Small
thrombi may occur within the lumen. This results in permanent closure of the
lumen and results in the formation of a ligamentum arteriosum. The closure most
commonly begins at the pulmonary end and may remain open at the aortic end
resulting in aortic ampulla. The ductus is completely closed in 88 per cent of
children by 8 weeks of age.
Other terms are:
Prolonged patency of ductus: When the process of closure is delayed.
Persistent patency of ductus: When closure fails to occur ultimately.
The factors that influence ductal closure are:
• Release of vasoactive substances (Acetyl choline, bradykinin, endogenous
catecholamines)
• Variations in pH
• Oxygen tension (Increasing tension closing the ductus)
• Prostaglandins (PGE1, PGE2)

• Prostacyclin (PGI2)
The rise in oxygen tension constricts the ductus, and the prostaglandins relax it
keeping it patent. The ductus is hypersensitive to oxygen tension in mature fetus
but is more sensitive to prostaglandins in immature fetus. These factors are
responsible for prolonged patency of ductus in premature infants, especially with
respiratory distress.
In 1900, Gibson described the diagnostic continuous murmur of ductus. As
depicted in Fig. 25.2, there is a continuous pressure difference between the aorta
and pulmonary artery resulting in a continuous murmur. However, if pulmonary
hypertension develops, there may not be any diastolic gradient resulting in isolated
systolic murmur.
Table 25.2: Continuous murmur of patent ductus arteriosus (Gibson’s murmur)
Feature Description
Site of best audibility Pulmonary area (infraclavicular, left 2nd space, 3rd space)
Timing Continuous murmur with a late systolic accentuation
480
with maximal intensity nearer to second heart sound,
and tapers off in diastole
Length Starts a while after first heart sound reaches a peak
nearer to second heart sound and tapers in diastole.
The diastolic component is shorter
Character of murmur Machinery in quality with a combination of high and
low frequencies.
Conduction The systolic component may be widely audible
including the suprasternal notch but the diastolic
component is localized to the pulmonary area.
Respiration May be better heard during expiration
Isometric hand grip Increases in intensity and duration
Vasopressors Increases in intensity and duration
Valsalva Decreases or disappears
Accompanying features High volume or collapsing pulse
Left ventricular or biventricular enlargement
Second heart sound is muffled; or audible
pulmonic sound if PAH
Left ventricular third heart sound
Mid-diastolic murmur at apex
CONTINUOUS MURMURS
Fig. 25.2: The mechanism of continuous murmur of patent ductus arteriosus
With a continuous murmur typical of ductus, the diagnosis is correct almost

all the time. However, once the murmur is atypical, alternative causes for a
continuous murmur should be looked for.
Evaluation
In the evaluation of the continuous murmur of PDA, one should ask the following 481
questions.
• Is it ductus or a condition simulating it?
• If it is ductus, is it isolated, compensatory, or complicated?
• If it is isolated ductus, what size is it?
• What is the size of shunt?
• Is there pulmonary hypertension; if so, what degree?
• Is the pulmonary hypertension hyperkinetic or fixed?
• Are there any associated defects?
A systematic analysis of various features of the murmur will answer most of
the questions.

The murmur of patent ductus arteriosus is best audible at the pulmonary area and
the systolic component is more widely audible at the lower left sternal border,
apex, aortic area and over the suprasternal notch. An accompanying thrill is
common and is often felt over the suprasternal notch. A thrill over the suprasternal
notch is not a feature of ventricular septal defect. Though the systolic component
is widely audible, the diastolic component is restricted to the pulmonary area. If

the diastolic component is clearly heard at the apex, ventricular septal defect +
aortic regurgitation, or some other cause for a continuous murmur, should be
considered. If the murmur of ductus is well heard to the right of the sternum,
either an aortopulmonary window, right sided ductus, or a loud venous hum
transmitted to the infraclavicular area should be considered.
Timing
The typical murmur of ductus is continuous, peaks in late systole, and tapers off
in diastole. Rarely, the murmur may occupy the whole of the systole and diastole.
The late systolic murmur is related to the later rise in pressure in descending aorta
in relation to systole.
The diastolic component is always shorter than the systolic component.
The duration of the murmur is a reflection of the duration of pressure difference
between the aorta and pulmonary artery. As pulmonary pressures start getting
higher, the diastolic component shortens or disappears first followed by
abbreviation or disappearance of systolic murmur. Finally, when systemic and
482 pulmonary pressures become equal, the murmur may be absent altogether.
The murmur of ductus may not be continuous when the patent ductus arteriosus
is too small (valve like), or too large (equalization of pressures), or when there is
pulmonary hypertension (Table 25.3).
Table 25.3: Non-continuous murmurs of patent ductus arteriosus
Cause Mechanism
Severe pulmonary hypertension Equalization of pressures
Large ductus Equalization of pressures
Long, narrow ductus Valve like mechanism
Associated defects
Coarctation (preductal) Lower aortic pressure
Aortic stenosis Lower aortic pressure+elevated LVEDP leading to
PVH and PAH
LV inflow obstruction PVH - pulmonary hypertension
Mitral regurgitation PAH - pulmonary hypertension
Peripheral pulmonary stenosis Central pulmonary hypertension
Ventricular septal defect (large) Equalization of pressures
D-transposition Pulmonary hypertension/posteriorly located PA
Infancy High pulmonary vascular resistance
CONTINUOUS MURMURS
In very young infants, the diastolic component may be very short or absent,
making diagnosis difficult. The murmur is often interpreted as pansystolic and a
diagnosis of ventricular septal defect is often made. Careful auscultation with the
bell of the stethoscope may bring out the diastolic component of the murmur.
Even if this is absent, a high volume pulse with a ventricular septal defect should
raise the possibility of patent ductus arteriosus mistaken for ventricular septal
defect or associated patent ductus arteriosus with ventricular septal defect. The
early diastolic murmur of pulmonary regurgitation of pulmonary hypertension
may be pandiastolic occasionally, and when added to the accompanying pulmonary
ejection systolic murmur, gives an impression of a continuous murmur. However,
the diastolic component being louder than the systolic, the change in character of
the murmur from systole to diastole, and the very long duration of diastolic murmur,
all rule against a ductus.
Character
The murmur of patent ductus arteriosus is machinery in quality and a thrill is
common. It has a combination of frequencies with added multiple clicking sounds.
Though the intensity of the diastolic component is less, the quality of both 483
components is the same. If there is any change in the character of murmur between
the systolic and diastolic components, ductus is unlikely and ventricular septal
defect with aortic regurgitation or some other lesion is likely.
Relation to a physiological act

The murmur of patent ductus arteriosus either fails to change with respiration nor
may increase during expiration. Maneuvers which increase systemic vascular
resistance or aortic pressure, like isometric hand grip or vasopressors increase the
murmur or may bring out the diastolic component when it is not heard earlier.
These features help to look for the murmur when not detected in the initial
evaluation and also help in distinguishing patent ductus arteriosus from other
conditions simulating it.
a) Cyanosis: Central cyanosis with a continuous murmur rules out ductus as an
isolated lesion, or may suggest another cause for a continuous murmur like
bronchopulmonary collaterals.
b) The high volume or collapsing pulse: The high volume pulse is the only clue to the
underlying patent ductus arteriosus when the murmur is non-continuous. When a
diagnosis of left to right shunt is made, a high volume pulse should be used as clue
to the ductus as an isolated lesion or in combination with other shunts. The high
volume pulse is not diagnostic of ductus because it may occur in any condition
with a continuous murmur and aortic run off.
c) Ventricular enlargement: Left ventricular enlargement is common with patent ductus
arteriosus of any significant size and shunt. Right ventricular enlargement occurs
only when pulmonary arterial hypertension sets in. If right ventricular enlargement
occurs without signs of pulmonary hypertension, a diagnosis of ductus is unlikely
and some other condition like rupture of sinus of Valsalva (RSOV) into the right
atrium or right ventricle is likely. This is because the shunt in ductus does not
involve the right ventricle, and right ventricle enlargement occurs only after
pulmonary hypertension sets in. On the other hand, in rupture of sinus of Valsalva,
the aortic run off is directly in to the right heart chambers and right ventricle
enlargement of some degree is a rule.
d) Mid-diastolic murmur at apex: This murmur means that the shunt is more than
484 2:1 in a patent ductus arteriosus, and is a reliable sign of operability in spite of
pulmonary hypertension. In the presence of pulmonary hypertension if this murmur
is audible, the pulmonary hypertension is likely to be hyperkinetic or flow related,
in contrast to fixed pulmonary hypertension which is resistance related with
pulmonary vascular disease.
RUPTURE OF SINUS OF VALSALVA ANEURYSM
The congenital aneurysms of the sinuses of Valsalva is thinning of the wall of the
aortic sinus just above the annulus at the leaflet hinge. Absence of normal elastic
and muscular tissue may be responsible. The weakened area gives way under the
high aortic pressure to form an aneurysm like a ‘wind sock’. This may rupture in
an adjacent low pressure cardiac chamber (either the right ventricle or right atrium).
The aneurysms arising from the right sinus are most common.
The nature of the continuous murmur in this condition depends on two
features: one is the chamber into which the rupture occurs, and the other, the
pressure in the receiving chamber. The common site of rupture is either into the
right ventricle or right atrium. Rupture into left sided chambers is extremely rare.
CONTINUOUS MURMURS
485
Fig. 25.3: Mechanisms of murmur of rupture of sinus of Valsalva. Note that pressure tracings
of the aorta are superimposed on the chambers into which the RSOV is opening. Continuous
pressure difference leads to generation of a continuous murmur.
The character, location and length of the murmur depend upon the site of
rupture. Rupture into the atria always results in a continuous murmur; whereas,
rupture into the right ventricle may modify the murmur due to systolic narrowing
of the tract and elevation of right ventricle systolic pressure due to pulmonary
hypertension. However, the diastolic pressure difference always exists.
The murmur is heard lower along the left sternal border than in PDA and is
more superficial with a very prominent diastolic thrill. The description of purring
of a cat is most applicable to the thrill accompanying this murmur. As described
earlier, the most common murmur is continuous and usually occupies most of the
cardiac cycle; it is generally longer than the murmur of ductus.
From the information in Table 25.5, one can understand why the classic
murmur of rupture of sinus of Valsalva may not be present in all the patients.
Table 25.4: Murmur of rupture of sinus of Valsalva into right heart

Feature Description
Site of best audibility Left sternal border 3rd- 4th spaces
Timing Continuous murmur (CM)
Grade Almost always grade 4/6 or may be 5/6 and
very superficial
Length Very long almost like a pansystolic plus pandiastolic
Character Rough with combination of high and low frequencies
Conduction No selective conduction but is often heard to the right of
sternum. Diastolic component is usually not heard at apex
Respiration No significant change as the murmur is very
Isometric hand grip loud (>grade 4/6) and the pressure difference is large
Vasopressors in either phase of cardiac cycle
High volume or collapsing pulse Confirms aortic run off as the cause of continuous
murmur
Normal intensity S1 First sound is diminished or even absent VSD + AR
(severe), which simulates rupture of sinus of Valsalva
486 Elevated JVP Supports rupture of sinus of Valsalva into right heart
Tricuspid diastolic murmur Rupture of sinus of Valsalva into RA
Evidence of large shunt in chest Ventricular septal defect with aortic regurgitation is
radiograph unlikely/rupture of sinus of Valsalva is likely
Table 25.5: Determinants of the murmur of rupture of sinus of Valsalva

Determinant Nature of murmur
Site of rupture
Right atrium Always continuous/longest of murmurs
Right ventricle Continuous murmur/may vary with right ventricle pressure
Left atrium (rare) Continuous murmur
Left ventricle (rare) Early diastolic murmur
Pulmonary arterial pressure PAH with high RV systolic pressure may shorten or abolish
the systolic murmur with persistence of ‘early diastolic murmur’
RV outflow obstruction Similar as above but the ESM of outflow
obstruction may be added resulting in a to and fro murmur
Associated VSD The rough pansystolic murmur of VSD may overshadow the
systolic component of continuous murmur giving an
appearance of to and fro murmur
CONTINUOUS MURMURS
Table 25.6: Different subsets of murmur of rupture of sinus of Valsalva

Condition Type of murmur
Rupture in right atrium Always a continuous murmur
Rupture in right ventricle Continuous murmur
Pulmonary hypertension (severe) No systolic murmur/to and fro murmur
RV outflow obstruction (severe) To and fro murmur (rough ESM + EDM)
Associated VSD To and fro murmur (rough pansystolic + EDM)
The diastolic component of the murmur of rupture of sinus of Valsalva is

generally not audible at the apex, as the aortic run off is directed in to one of the
right sided chambers. It is often clearly audible to the right of sternum. On the
other hand, the diastolic component of the murmur of ventricular septal defect +
aortic regurgitation is usually audible at the apex, as the left ventricle receives the
aortic run-off in aortic regurgitation.
MULTIPLE LESIONS
Assessment is easier in an isolated lesion than in a combined lesion or a combination 487
of lesions. The term combined lesion is applied to the presence of stenosis and
regurgitation in the same valve (for example, mitral stenosis and regurgitation)
and the term combination of lesions is applied in a broader sense, namely to the
presence of any other lesion in the cardiovascular system (mitral stenosis and
aortic regurgitation or coarctation of aorta with aortic stenosis).
Combined lesions are discussed under the following subsets.
• Valvular lesions
• Combined stenosis and regurgitation
• Mitral stenosis and mitral regurgitation
• Aortic stenosis and regurgitation
• Tricuspid stenosis and regurgitation
• Combination of one valve lesion with another valve
• Mitral valve disease with aortic/tricuspid valve lesions
• Congenital heart disease
• Coexistence of more than one lesion
• Coexistence of valvular lesion with congenital heart disease
• Coexistence of coronary artery disease with valvular or congenital

heart defect
• Coexistence of cardiomyopathy with valvular or congenital defect
COMBINED LESIONS IN VALVULAR HEART DISEASE

As a general principle, any regurgitation adds to the amount of blood that has to
move across the valve. All the features of stenosis are exaggerated as a rule in
combined mitral stenosis and regurgitation.
VENOUS HUM
The normal flow of blood across normal veins in the neck is noiseless. However,
when there is increased velocity of flow (hyperkinetic states such as thyrotoxicosis)
or diminished viscosity of blood (as in anemia) there is a continuous bruit over
the neck veins called the venous hum (Fig. 25.4). In the supine position, with the
veins distended there is little or no turbulence, and therefore no hum is heard.
In a sitting patient, with the bell of the stethoscope lightly applied at the base
488
of the neck in between the two heads of the sternomastoid, the venous hum can
be heard as a continuous murmur. The hum disappears when the venous flow is
interrupted by applying pressure above the stethoscope. The venous hum is heard
in the majority of children and in pregnant women. It is generally abnormal in
other adults. It occurs in hyperkinetic circulatory states like anemia or thyrotoxicosis.
It also occurs in intracranial or head and neck arteriovenous fistulas. If a venous
hum is heard in an adult in the absence of anemia, one should check for
thyrotoxicosis. In a child with congestive heart failure and a high volume arterial
pulse, one should look for a bruit over the head and a venous hum in the neck to
rule out intracranial AV fistula.
Fig. 25.4: Venous hum

CONTINUOUS MURMURS
Causes
Physiological
• Children
• Pregnancy
• Normal adults (rare)
Pathological
• Beri-beri
• Intracranial AV fistula
• Compression of jugular vein by fascia, or bony structures in the neck
An audible venous hum in the presence of congestive heart failure should suggest
the possibility of hyperkinetic states like severe anemia or thyrotoxicosis with heart
failure. Intracranial AV fistula is a rare but important cause of heart failure in
infancy. A cervical venous hum with high volume arterial pulse and bruit over the
skull suggest the diagnosis.
MAMMARY SOUFFLE
489
This is less common than the venous hum and is heard over the breast during
later pregnancy and early postpartum period in lactating women (souffle = ‘puff’
Table 25.7: Mammary souffle
Feature Description
Mechanism Increased blood flow to breast
Timing and length Continuous, late systolic, systolic component
loudest, diastolic component shorter or may be absent
Site of audibility Over the breast on either side or both sides,
2nd or 3rd right or left spaces, no selective conduction
Grade Always less than grade 3/6
Character Medium to high frequency but not musical
Response to physiological manoeuvres
Respiration No significant change
Pressure over the stethoscope Light pressure accentuates,
firm pressure obliterates
Distal pressure Obliterates
Valsalva maneuver No influence
Accompanying features Advanced pregnancy/lactating mother
in French). The murmur most probably is arterial in origin and is a reflection of

increased blood flow to the lactating breast tissue (Table 25.7).
The arterial origin is supported by its delayed onset, systolic accentuation,
and persistence of the murmur during the straining phase of Valsalava.
The mammary souffle should be distinguished from patent ductus arteriosus
and chest wall arteriovenous fistula. Obliteration by distal compression excludes
ductus. The disappearance after stopping lactation is helpful in excluding
arteriovenous fistula.
490
26 The Pericardial Rub
The pericardial rub is a hallmark of pericardial inflammation. It is caused by the
parietal and visceral surfaces of pericardium moving against each other. It is
uniphasic, biphasic or triphasic in timing. The three components when heard are
related to the movement of the heart during ventricular systole, atrial systole (fourth
sound time), and rapid ventricular filling phase (third sound time). The most
commonly audible component is the one during ventricular systole; the atrial systolic
component is the next in frequency and the rapid filling component is the least
commonly audible.
The ‘to and fro rub’ is the most common and is due to the ventricular systolic
and the atrial systolic components. The three component rub is audible in less
than half the cases. The single component rub is very rare and is more likely in the
Table 26.1: Features and description of the pericardial rub
Feature Description
Location Left sternal border
Radiation Pleuropericardial rubs are heard at apex
Timing Uniphasic, biphasic or triphasic
Character Superficial, scratchy, or musical (low- or high-frequency)
Respiration Variable, but is usually better heard with held inspiration
Sitting, leaning forward Better heard
Fever, chest pain Acute pericarditis
Acute MI Post-MI pericarditis
Uremia Uremic pericarditis
Elevated JVP, paradoxus, shock Cardiac tamponade
Acute rheumatic fever Rheumatic pancarditis
setting of atrial fibrillation (lack of atrial contraction) or the resolving stage of

pericarditis. The rub is best heard over the second and third left interspaces over
the ‘bare area’ of the heart. It is best heard in a sitting patient, leaning forward; the
diaphragm of the stethoscope should be pressed close to the chest wall. Respiration
has a variable influence on the rub. The rub can occasionally be evanescent, and
be present in one examination and then surprisingly absent after a few hours.
Unlike a pleural rub, which is absent in the presence of a large pleural effusion, a
pericardial rub can be present even with large pericardial effusion and tamponade.
Differential diagnosis
The pericardial rub has to be carefully differentiated from the following:
• Systolic murmur (single component rub)
• To and fro murmurs (biphasic rub)
• Early diastolic murmur of aortic regurgitation
• Continuous murmur
• Artifact
• Hamman’s sign (mediastinal emphysema)
492 • Ebstein’s anomaly of tricuspid valve
• Tricuspid stenosis
• Right atrial tumour producing RV inflow obstruction
• Means–Lerman scratch in thyrotoxicosis
When very loud and long, the pericardial rub may be mistaken for a continuous
murmur. Uniphasic rubs confined to one phase of the cardiac cycle are often
mistaken for murmurs. Significant change with pressure on the stethoscope,
posture, and localization to the left sternal border help in the differential diagnosis.
Expected alterations with physiological maneuvers also help in the recognition of
error. Recognition of pericarditis in various clinical situations alters the management
and outcome significantly. As the diagnosis of pericarditis is often missed, one
must learn to check for this in various clinical settings (Table 26.2).
Pyogenic pericarditis as a cause of cardiac tamponade is often missed;
unfortunately it is nearly always fatal. For this reason, in all patients presenting
with fever (even if it is of one day duration) or any evidence of septic focus one
must check for the pericardial rub. In patients with fever of unknown origin, apart
from looking for this sign in the initial evaluation, it must be looked for in all
reevaluations as it may appear later in the clinical course of some patients with
THE PERICARDIAL RUB
Table 26.2: When to check for pericardial rub

Clinical setting Implications
Fever, chest pain or septic focus Infective pericarditis, pyogenic pericarditis can
be rapidly fatal and is often missed
Fever of unknown origin Tuberculosis
All patients in shock, ‘heart failure’ Cardiac tamponade
All patients with acute chest pain Post-MI pericarditis/primary pericarditis
Acute rheumatic fever/heart disease Pancarditis/indication for steroids
Infective endocarditis vs rheumatic carditis Rheumatic carditis is likely
Infective endocarditis Ring abscess or myocardial abscess
Chronic renal failure on hemodialysis Cardiac tamponade during dialysis
Amebic liver abscess Abscess communicating with pericardium
Chest pain, fever, after cardiac surgery Post-cardiotomy pericarditis
Any patient with known malignancy Pericardial involvement
tuberculosis or other chronic granulomatous diseases. In all patients with shock,

cardiac tamponade should be ruled out by not only careful clinical examination
493
but also by an echocardiogram.
When patients with established rheumatic heart disease present with fever, it
is often not easy to differentiate infective endocarditis from recurrence of rheumatic
fever. Pericarditis favours the diagnosis of rheumatic fever. In patients with chronic
renal failure with pericarditis on hemodialysis, hypotension during dialysis may
mean relative hypovolemia precipitating cardiac tamponade even at low pericardial
pressures.
If the pericardial rub appears along with the beginning of chest pain, primary
pericarditis as a cause of chest pain is likely. On the other hand, if the rub is heard
24–48 hours after the onset of chest pain, post-MI pericarditis is likely. As the
ECG may fail to show diagnostic changes or even may show features shared by
both conditions, detection of pericardial rub is critical to proper diagnosis and
management of these patients.
In acute MI, the pericardial rub may appear any time after the first day to 6
weeks after MI, and is a more sensitive indicator of pericarditis than even the
echocardiogram. Pericarditis in this setting indicates a transmural myocardial
infarction and is a contraindication to anticoagulant therapy. It gives a clue to the
cause of pain following myocardial infarction. The pain of pericarditis is promptly

relieved by steroids.
Significance of pericardial friction rub after acute MI

• Indicates a transmural myocardial infarction
• Contraindication to anticoagulant therapy
• Cause of persistent pain following myocardial infarction
• May be the cause for post myocardial infarction fever
• Prompt relief with steroids
It is for this reason, that all patients with suspected or diagnosed acute ischemic
syndromes should have careful auscultation to rule out pericardial rub.
494
27 Approach to Auscultation
Auscultation, like any other skill, requires practice. Just like a tennis player does
wall practice, as a student, one must learn to practice auscultation in otherwise
normal hearts. Auscultate your own heart or of patients in the wards without
heart disease to have an idea of the sounds of a normal heart. Patients with typical
disorders like mitral stenosis should be similarly auscultated systematically. For,
example, when the diastolic murmur of mitral stenosis is best heard at the apex,
slowly move away from the apex concentrating on the murmur. Though faint, the
murmur is audible. This is the type of murmur one may encounter in a patient
with ‘silent’ mitral stenosis. Practise similarly with the opening snap. Once the
opening snap is appreciated at the site of best audibility, namely internal to the
apex, by slowly moving away one can appreciate the faint opening snap even to
the right of the sternum. This type of faint opening snap may be the only sign of
mitral stenosis in some situations.
DESCRIPTION OF AUSCULTATORY EVENTS
Note the heart rate

The heart rate influences the duration of various events in cardiac cycle. For
example, with the same degree of mitral stenosis, bradycardia with leisurely diastole
abbreviates the murmur, and tachycardia with a hurried diastole prolongs the
murmur. The S2–OS interval is longer with bradycardia and shorter with
tachycardia.
Note the type of chest

Chest wall thickness influences the intensity of sounds and murmurs. Chest
deformities may produce heart murmurs or exaggerate them. Particularly make

note of pectus excavatum, straight back and kyphoscoliosis.
Identify first and second sounds (and systole and diastole)

This is best done by starting at the pulmonary area where the second heart sound
is louder than the first heart sound. The carotid pulse and apical impulse may also
be used for the same purpose but are probably less reliable. In case of difficulty,
more than one method should be used. When the heart rate is rapid, the carotid
method of identifying can be misleading as the carotid impulse is not as sharp an
event as that of first heart sound or second heart sound. In some situations, the
systole and diastole may be confused with each other, even by experienced
auscultators:
• When the rhythm is irregular or the rate is too fast or too slow
• When both first heart sound and second heart sound are diminished or
absent
• When an additional sound is unusually loud, such as the third heart
sound at the apex in mitral regurgitation
496 • Acute aortic regurgitation with diminished or absent first heart sound
and second heart sound with loud third heart sound mistaken for first
heart sound
• When a loud pericardial knock is heard as in constriction with systolic
retraction of the cardiac impulse. The pericardial knock is mistaken for
the first heart sound
• When a murmur has unexpected features. As in aortic regurgitation with
a thrill and rough quality of the murmur or pulmonary regurgitation
with rough quality and a thrill.
Describe the first and second heart sound

First sound
Intensity
Split
Constancy or variability
Secondsound
Split
Intensity of both components
Describe additional sounds
APPROACH TO AUSCULTATION
Third sound
Right or left sided
Physiological or pathological
Early or late
Fourth sound
Physiological or pathological
Right or left sided
Opening snap
Mitral or tricuspid
S2–OS interval
Ejection click
Right or left sided
Valvular or vascular
If valvular, constant (aortic) or variable (pulmonic)
Non-ejection click
Left or right sided
Single or multiple
497
Describe murmurs
Individual murmurs have already been discussed in Chapters 22 to 25.
Describe presence or absence of pericardial rub

If an auscultatory finding is expected but is not detected, mention it specifically.
This has significance; for instance the absence of ejection click in a child with
aortic stenosis may mean subvalvular aortic stenosis. As a student if you cannot
detect an expected event, mention clearly that you checked for an opening snap
but could not hear it.
Index
A diastolic murmur 459–69

acute myocardial infarction 16–17, 85–88 dyspnea 120
approach 85–88 ejection click 352
thrombolytic therapy 70 ejection systolic murmur 409
vomiting 77 fourth heart sound 348
acute pulmonary embolism 90 jugular venous pulse 250
pain 90 mechanism 460
498 dyspnea 120 peripheral signs 183
afterload 30 pulse 182
alexithymia 78 second heart sound 331
Allen test 198 third heart sound 340
anacrotic pulse 184 aortic stenosis
anaphylactic shock 221 cardiac impulse 278
angina pectoris 16, 64, 69, 72, 80–3 dyspnea 118
CCS classification 81 ejection click 352
chronic stable 64, 69 jugular venous pulse 249
drug precipated 73 pulse 184
linked 72 second heart sound 327
nocturnal 64, 82 syncope 133
postinfarction 64 systolic murmur 396
precipitating factors 72 apical impulse 262–68
Prinzmetal 64, 95 hyperkinetic 264, 268
relieving factors 74 left ventricular enlargement 267
unstable 64, 83–5 localized vs diffuse 268
aortic dissection 91–3 paradoxic septal motion 266
aortic impedance 29 sustained 265, 268
aortic regurgitation systolic retraction 266, 268
blood pressure 224 arterial blood gas analysis 121–23
cardiac impulse 279 arterial bruit 197
INDEX
auscultation 197 acute myocardial infarction 226

arterial pulse 175–205 aortic regurgitation 224
character 182 hypotension/shock 216
alternans 189–93 measurement 206–209
bigeminal 189 auscultation 208
bisferiens 185 Doppler 208
collapsing (water hammer) 182–84 flush technique 209
dicrotic 187 guidelines 210
normal 182 oscillometric 209
paradoxus 193–95 palpation 208
reversed paradoxus 196 postural hypotension 213
post-extrasystolic 189 systemic hypertension 212
slow rising 185 brachiofemoral delay 198, 225
determinants 176 Brockenbrough sign 189, 191
dicrotic notch 177
dicrotic wave 177, 187 C
evaluation 178–82 cannon wave 189, 235–37
rapid irregular 181 cardiac impulse 262–92
rapid regular 179 apical impulse 262
sinus arrhythmia 181 apexcardiogram 263
sinus bradycardia 179 in aortic regurgitation 279 499
sinus tachycardia 179 in aortic stenosis 278
slow pulse 179 in atrial septal defect 280
slow, with fever 180 in cardiomyopathy 290
palpation 178 in congenital acyanotic heart disease 280
percussion wave 177 in congenital heart disease 286
tidal wave 177 in coronary heart disease 288
volume 181 in mitral regurgitation 277
atrial septal defect in mitral stenosis 276
cardiac impulse 280 in patent ductus arteriosus 284
first heart sound 308 in pericardial disease 289
jugular venous pulse 250 in pulmonic stenosis 280
second heart sound 323 in tetralogy of Fallot 286
third heart sound 342 in ventricular septal defect 281, 283
auscultation of the heart 293–96 cardiac output 27
Austin Flint murmur 457 determinants 29
mitral stenosis 450 cardiac tamponade 194
cardiomyopathy 18
B cardiovascular diagnosis 13–20
Bernheim’s syndrome 250 case presentation 8–12
blood pressure 206
chest pain rupture of sinus of Valsalva aneurysm 484

acute 85, 87, 203 venous hum 242, 488
angiography 89 contractility 30
angioplasty 89 coronary arteriography 99, 104
approach 60, 87 chest pain 89
arterial pulse 203 limitations 104
atypical, syndrome 69, 95 coronary artery disease 16
causes 61 arterial pulse in 203
differential diagnosis 87 assessment of severity 97
evaluation 60–104 cardiac impulse 288
myocardial ischemia 63 dyspnea 115
non-acute 96 ejection murmur 412
non-cardiac causes 93 evaluation 98
Cheyne–Stokes breathing 114 fever 171
classification of cardiovascular disability fourth heart sound 349
CCS functional 22 risk factors 63
NYHA functional 21, 25 sex 47
SAS (Goldman) 22 syncope 135
clicks coronary bypass surgery 47
approach 362 coronary anatomy 33
500 ejection clicks 350–57 coronary lesion 39
aortic stenosis 352 cyanotic heart disease 15–16
bicuspid aortic valve 354 jugular venous pulse 253–55
valvular 351 second heart sound 328
valvular pulmonic stenosis 354, 408 third heart sound 341
vascular 351, 352
non-ejection 358–61 D
mitral valve prolapse 358 diastolic murmurs 438
S1–NEC interval 358 aortic regurgitation 459–69
congenital heart disease 14–15, 323 Austin Flint murmur 457
diagnosis 44 Graham Steell murmur 475
second heart sound 323 mid-diastolic murmur 438
congenital cyanotic heart disease mitral regurgitation 454
arterial pulse 202 left to right shunt 455
cardiac impulse 286 mitral stenosis 439–49
jugular venous pulse 253 pre-systolic murmur 441–42
second heart sound 328 pulmonary regurgitation 469–76
continuous murmur 242, 477–90 semilunar valve regurgitation 459
combined lesion 487 tricuspid stenosis 449–54
mammary souffle 489 diastolic thrill 271
patent ductus arteriosus 479
INDEX
dyspnea 105–23 F
anginal equivalents 76 fever
aortic regurgitation 120 cardiovascular signs 173
aortic stenosis 118 coronary artery disease 171
causes 105, 109 definition 159
coronary artery disease 115 equivalents 165
drowsiness 108 infective endocarditis 163–66
drugs 113 in heart disease 159–175
evaluation 106 metabolic changes 163
grading 110 patterns 160–63
mechanisms 106 intermittent 160
mitral regurgitation 118 remittent 162
pulmonary embolism 120 relapsing 162
right heart failure 121 polyarthritis 166–69
post-operative 170
E rheumatic fever 166
Eisenmenger syndrome 253 first heart sound 297–310
jugular venous pulse 253 diminished 305
second heart sound 330 evaluation 303–305
ejection clicks 350–57 in atrial fibrillation 305
aortic stenosis 352 in atrial flutter with variable block 307 501
bicuspid aortic valve 354 in complete heart block 306
valvular 351 in mitral regurgitation 309
valvular pulmonic stenosis 354, 408 in mitral stenosis 308
vascular 351 intensity 297
ejection fraction 29 isovolumic systole 300
ejection systolic murmurs 389–413 loud 304
aortic regurgitation 409 mitral valve 298
aortic valve sclerosis 396, 399, 409 split 308
aortic valve stenosis 393 variable intensity 303
hyperkinetic circulatory states 410 ventricular tachycardia 308
maneuvers 396 fourth heart sound 343–49
severity assessment of aortic stenosis causes 344
395 clinical recognition 345
ventricular premature contractions 399 correlation 344
mechanism 389 in aortic regurgitation 348
pulmonic stenosis 402–408 in coronary artery disease 349
infundibular 403 in left ventricular outflow obstruction 345
L-TGA 404 in mitral regurgitation 347
selective conduction 407 in myocardial disease 349
supravalvular 403 in right ventricular outflow obstruction 346
mechanism 343 in cyanotic heart disease 253–55

in Eisenmenger syndrome 253
G in mitral stenosis 246
Gallavardin phenomenon 396 in mitral regurgitation 248
Gerbode’s defect 431 in pericardial disease 255
in pericardial tamponade 256
H in pulmonic stenosis 246
Hess sign 227 in shock 258
Hill’s sign 182, 225 in SVC obstruction 244
history 40–58 in tetralogy of Fallot 254
checklist 57 in tricuspid regurgitation 246
drug 48–56 in tricuspid stenosis 245
risk factors for heart disease 56–58 in ventricular septal defect 252
hepatojugular reflux 243 liver pulsations 244
normal pattern 229
I phlebostatic access 231
innocent systolic murmur 322, 376, 377
irradiation of impulses 65 K
ischemia Korotkoff sounds 207
total ischemic burden 78 auscultatory silent gap 207
502 Kussmaul’s sign 243
J
jugular venous pulse 228–61 L
a, c, h, v, x, y waves, descent 229, 246 Lutembacher syndrome 247, 251
abnormalities
a wave 234 M
x descent 238 mitral regurgitation
v wave 238 arterial pulse 201
y descent 240 cardiac impulse 277
technique of measurement 232 diastolic murmur 454
cannon wave 235–37 dyspnea 118
angle of Louis 232 first heart sound 309
arterial/venous pulsations 230 fourth heart sound 347
elevated JVP 233 jugular venous pulse 248
hepatojugular reflux 243 second heart sound 331
in aortic regurgitation 250 third heart sound 340
in aortic stenosis 249 mitral stenosis 201
in arrhythmias 258 arterial pulse 201
in atrial septal defect 250 cardiac impulse 276
in cardiomyopathies 255 diastolic murmur 439–49
in constrictive pericarditis 257 dyspnea 116
INDEX
first heart sound 308 clinical recognition 367

jugular venous pulse 246 left atrial myxoma 368
second heart sound 330 missing 366
syncope 137 tumour sounds 363
mitral valve prolapse 358–61 orthopnea 112
chest pain 93 oxygen consumption
murmurs 374 myocardial 71
character 385
continuous 383 P
definition 373–74 palpitation 149–58
diastolic 381 anxiety states 155
evaluation 378 associated symptoms 153
length 383 causes 150
site of best audibility congenital heart disease 157
aortic area 380 nature 152
apex 378 systemic hypertension 158
left sternal border 379 valvular heart disease 156
pulmonary area 379 parasternal impulse 271–72
tricuspid area 379 grading 272
systolic 375 parasternal lift 272–73
effect of maneuvers 387 hyperkinetic left parasternal impulse 271 503
ejection 380 paroxysmal nocturnal dyspnea 111
functional 375 pericardial rub 491–94
grading 375 pericardial tamponade 194
innocent 377 causes of low pressure tamponade 257
late 381 jugular venous pulse 256
pansystolic 381 y wave 240
myocardial infarction pericarditis pain 90
acute 85–88 precordial examination 274
autonomic excess 77 preload 30
painless 77–78 pre-systolic impulse 270
myocardial ischemia 63 pulmonary embolism 120
pathophysiology of discomfort 65 pulsatile exophthalmos 239
pulse
N arterial pulse 176–206
non-ejection clicks 358–61 bigeminal 189
mitral valve prolapse 358 collapsing (water hammer) 182–84
S1–NEC interval 358 dicrotic 187
normal 182
O paradoxus 193–95
opening snap 363–69 post-extrasystolic 189
reversed paradoxus 196 shock 199

slow rising 185 arterial pulse 199
pulsus alternans 189–93, 223 hypotension 216–22
auscultatory alternans 224 causes 219–20
pulsus bisferiens 185 types 219–20
pulsus paradoxus 193–95, 222 sternoclavicular joint pulsations 273
streptokinase 69
R stenosis of coronary artery 38
recanalization rate with streptokinase 69 silent ischemia 66, 79
rest pain 75 syncope 76, 124–48
cardiovascular disorders 127–32
S bradyarrhythmia 130
second heart sound 311–34 complete heart block 131
aortic sound 320 long QT syndrome 129
evaluation 312–19 renal failure 131
hangout interval 311 supraventricular tachycardia 129
in aortic regurgitation 331 ventricular tachycardia 129
in aortic stenosis 327 gastrointestinal 144
in atrial septal defect 323 metabolic and drug induced 143–45
in coarctation of aorta 328 neurological disorders 139–43
504 in congenital cyanotic heart disease 328 brain tumours 142
in Eisenmenger syndrome 330 intracerebral hemorrhage 142
in mitral regurgitation 331 peripheral neuropathy 143
in mitral stenosis 330 subarachnoid hemorrhage 141
in patent ductus arteriosus 326 vertebrobasilar insufficiency 141
in pulmonic stenosis 326 nitrate syncope 136
in shock 333 non-arrhythmic cardiovascular causes
in thromboembolic pulmonary arterial aortic stenosis 133
hypertension 333 catheterization 138
in ventricular septal defect 325 coronary artery disease 135
intensity 319 hypertension 138
pulmonic sound 321 mitral stenosis 137
grading 322 rock concert 127
single 313 vasovagal 125
split 312 systemic hypertension
fixed 317 palpitation 158
paradoxical 318 systolic murmurs 389–436
partial reverse 317 ejection 389
reversed 317 aortic regurgitation 409
wide 314 aortic valve sclerosis 409
seizure 140 aortic valve stenosis 393
INDEX
hyperkinetic circulatory states 410 in atrial septal defect 342

maneuvers 396 in congenital cyanotic heart disease 341
aortic stenosis 396 in heart failure 341
ventricular premature contractions 399 in mitral regurgitation 340
mechanism 389 in myocardial disease 341
pansystolic murmurs 414–36 in normal person 339
differential diagnosis 435 in shock syndrome 342
maneuvers 419 left ventricular 339
mitral regurgitation 414–17 mechanism 335
pulmonic stenosis 401–408 non-heart failure causes 336
double chambered right ventricle 403 right ventricular 339
infundibular 403 tricuspid regurgitation
L-TGA 404 v wave 239
selective conduction 407
supravalvular 403 V
systolic thrill 418 venous hum 241
tricuspid regurgitation 420–25 ventricular septal defect
pulmonary arterial hypertension 425 age 46
right ventricular third heart sound 425 jugular venous pulse 252
tricuspid diastolic murmur 426 second heart sound 325
ventricular septal defect 426–35 spontaneous closure 45 505
systolic murmur 426–35
T ventricular volumes 32
third heart sound 269, 336–42 vomiting 76
causes 336
correlations 338 W
in aortic regurgitation 340 Wenckebach’s phenomenon 259

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Universities Press (India) Private Limited

© Universities Press (India) Private Limited 2009

First published by Orient Longman Private Limited 2003

ISBN 978 81 7371 657 7

Cover and book design

Table: Limitations of cardiac catheterization—patients initially diagnosed to have aortic stenosis

The map is the angiogram and the ground is the patient.

THE OATH OF HIPPOCRATES (MODIFIED)

ABG Arterial blood gas HOCM Hypertrophic obstructive

The importance of becoming a doctor is not fully realized by the majority of

The limits to medicine are best expressed by Trudeau:

To be able to do this we require to cultivate attitudes that enable us to gain a

William Osler maintained that “The practice of medicine is an art, not a

While we do our best we should be prepared to face thanklessness and even

There are two varieties of presentations:

Note the following features (on index card)

5. Past medical history : Note active problems

OUTLINE OF BRIEF PRESENTATION

General principles of brief presentation

Brief presentation (sample)

FORMAL DETAILED PRESENTATION

6. Allergies: Drug reactions

Case presentation guidelines

CONGENITAL HEART DISEASE

b. Size of the defect

CYANOTIC HEART DISEASE

Two forms exist:

Pulmonary arterial hypertension (hyperkinetic),

CORONARY ARTERY DISEASE

The common clinical syndromes are:

Risks: Hypertension mild, and

Table 3.2: Mortality in AMI

Based on clinical examination Based on invasive monitoring

Class Definition GUSTO-I Subset Definition Mortality

PRIMARY MYOCARDIAL DISEASE

18 Is the structural and functional abnormality of heart muscle unrelated to

8. Functional categorization (NYHA)

• Familial storage disease/infiltration

Most diseases have an effect on the functional capacity of the patient. In

NYHA FUNCTIONAL CLASSIFICATION

fatigue, palpitation, dyspnea, or anginal pain.

CCS FUNCTIONAL CLASSIFICATION FOR ANGINA

SPECIFIC ACTIVITY SCALE (SAS)

The intensity of physical activity can be expressed in metabolic units (MET or

Class 2: Patients can perform to completion any activity requiring 5 metabolic

Sedentary work: Sedentary work is defined as ‘lifting maximum 10 lb and

Table 4.2: NYHA functional classification

It is essential to know intracardiac pressures and ﬂows for a proper understanding

Table 5.2: Cardiac output and vascular resistance

Cardiac output 4–8 l/min

The cardiac output is determined by four major factors: preload, afterload,

Table 5.3: Determinants of cardiac output

Table 5.4: Factors inﬂuencing aortic impedance

Physical properties of blood Viscosity of blood

Table 5.5: Alterations in preload, afterload and contractility

Preload Afterload Contractility

Table 5.6: Ventricular volumes

LV end-diastolic volume 72 ± 15 ml/m2

Systemic vascular resistance (SVR) = Mean aortic pressure – Mean RA pressure × 80