American Heart

Association~
Fighting Heart Disease
and Stroke

Examination of the Heart

Part I

Examination of the Heart

The Clinical History

Prepared on behalf of the

Council on Clinical Cardiology
of the American Heart Association
Mark E. Silverman, MD
Professor of Medicine
Emory University School of Medicine
Chief of Cardiology
Piedmont Hospital
Atlanta, Georgia

Part 1

Examination of the Heart

A Series of Booklets
Part 1
The Clinical History
Mark E. Silverman, MD

Part 2
Inspection and Palpation of
Venous and Arterial Pulses
Michael H. Crawford, MD

Part 3
Examination of the Precordium:
Inspection and Palpation
Robert C. Schlant, MD, and J. Willis Hurst, MD

Part 4
Auscultation of the Heart
James A. Shaver, MD, James J. Leonard, MD,
and Donald F. Leon, MD

Part 5
The Electrocardiogram
Masood Akhtar, MD

Available from your local American Heart Association

1972, 1978, 1990 American Heart Association

2 The Basic Structure of History Taking

5 Cardiovascular Data Collection
5
Historical Evidence
6
Symptoms
6
Etiology
8
Severity and Progression of Disease
9
Previous Therapy
10 Common Symptoms of Cardiovascular Disease
10
Chest Pain
10
Angina Pectoris
13
Myocardial Infarction
13
Pericarditis
14
Pulmonary Embolus
15
Aortic Disease
t5
Gastrointestinal Disease
15
The Chest Wall
16
Mitral Valve Prolapse
16
Shortness of Breath
16
Left Ventricular Failure
17
Other Causes of Dyspnea
18
Dizziness and Syncope
19
Cardiovascular Causes
22
Other Causes of Syncope
23
Palpitations
25
Fatigue
25
Edema
26
Intermittent Claudication
26
Cyanosis

Rheumatic Fever
27
29 Conclusion
31 Suggested Reading

The history is the foundation of the clinical diagnosis. The ability and
desire to obtain accurate, unbiased information is a major distinguishing
characteristic of every fine diagnostician. Although standardized
questionnaires, computers, and interviews conducted by paramedical
personnel have become increasingly useful in obtaining information, the
physician must still assume the major responsibility for ensuring that the
information is as complete and accurate as possible.
Despite the obvious necessity of obtaining accurate historical information
and relating that data to the physical examination, the clinical history,
unfortunately, may be neglected or slighted in favor of a glittering physical
finding or a multitude of laboratory tests. A brilliant biochemical diagnosis
may be the simple conclusion of a skilled medical interview.
In addition to accumulating essential historical information, the clinical
interview is the beginning of the patient-physician relationship, an
interaction in which the patient evaluates the physicians patience,
thoroughness, skill, and interest, and the physician seeks subtle clues
from the patients appearance, voice, expression, mannerisms, position in
bed, and breathing pattern. As James Herrick, an early 20th century
American cardiologist of great distinction, remarked, "The doctor may also
learn more about the illness from the way the patient tells the story than
from the story itself."*
This publication provides a basic approach to obtaining clinical history
related to the cardiovascular system. Common symptoms of cardiovascular
disease are also analyzed. A detailed discussion of the interrelations
among symptoms, physical signs, and pathophysiology may be found
among the titles listed under "Suggested Reading."

*Herrick J: Memories of Eight Years. Chicago, University of Chicago Press, 1949, chap
VIII, p 147

The Basic Structure of History Taking

Ideally, ample time should be available to explore the medical history in

depth and in a relaxed manner. If time is short or the patient is too ill or
confused to be questioned at length, a limited interview, focused on the
immediate problem, is desirable. Later, as the patient improves, the history
can be completed.
The conversation might be initiated by asking the patient, "Tell me about
yourself." This friendly opening demonstrates that the physician is genuinely
interested in the person, not the disease. As Sir William Osier, the father of
American medicine, stated, "It is more important to know what sort of
patient has a disease than what sort of disease a patient has." The patient
should then be asked about his or her most important concerns and
current symptoms. At the outset, the physician encourages a spontaneous
flow of information with open-ended questions such as "Tell me about your
chest discomfort; After the patient has elaborated on his or her problem,
the physician can then follow up with more direct questions that favor or
dismiss a specific diagnosis: "Did the pain worsen with activity?"
The physician should be careful to avoid courtroom-type questions that
lead to premature closure of the subject and erroneous conclusions. The
experienced interviewer encourages the spontaneous flow of information
with comments such as "Go ahead; "mm-hmm," "Yes," "1 see," "What
else?" and "Tell me more." This technique, known as passive listening, is
enhanced by nonverbal communication such as open and receptive
posture, eye contact, and head nodding.
The physician should appear interested, sympathetic, and nonjudgmental,
even if the patient becomes upset or hostile. If the patient becomes angry,
it may be helpful to say, "You seem upset." By actively listening to the
underlying feeling in the message and relaying this feeling back to the
patient, the physician demonstrates concern and understanding. For
example, the patient may say, "1 have a minor chest pain, but my wife
insists that you check out my heart." The physician might respond, "Its
alarming to think that your chest pain could be due to a heart condition." It
is important to recognize emotional and psychological overtones and their
implications. Revealing information may be obtained by asking, "What do
you think is wrong with your health?" The physician should also be alert to
the possibility that the patients most distressing symptoms may not be
due to the most serious problem or that the patient may not be willing to
acknowledge certain potentially serious symptoms such as chest pain.
2

The patient may naturally hesitate to trust a stranger with intimate details
of an illness or personal frailties, a reluctance that may be heightened by
differences in age, gender, race, language, or socioeconomic background
between the patient and the physician. Fear and anxiety may lead to
subconscious repression of important information, inability to describe
certain symptoms accurately, faulty memory, or deliberate concealment of
facts such as drinking, poor compliance with medication schedules, and
intense emotional or sexual problems. The physician must try to foster a
relationship of trust by using communication skills. These techniques
require patience and insight and are important in the therapeutic content
of the medical history.
Once the basic symptoms have been identified, each must be teased
apart and examined from all angles. This is accomplished by exploring the
seven basic properties that differentiate a symptom of one disease from a
symptom of another. These basic properties are:
Bodily location. The area of origin of the symptom and the area of
radiation should be defined as precisely as possible.
Quality. The flavor imparted by the symptom may be described as
"sharp," "crampy," or "tingling." Inability to describe the quality may also
be informative.
Quantity. A symptoms quantity includes its severity, the number of
times experienced, and its duration.
Chronology. The chronology of a symptom implies its onset (as
precisely as possible) and sequential development until the present.
Setting. The setting of the symptom includes the time of day or night, if
the patient was active or resting, eating or fasting, emotionally upset or
relaxed, and at home or at work.
Aggravating or alleviating factors. The symptom should be further
clarified by asking what the patient did to gain relief, if a change in
position was sought, and what the effects of movement, respiration,
medication, etc. were.
Associated symptoms. Many diseases are manifested as a
constellation of associated symptoms that support a diagnosis when linked
together. The patient should be asked to describe other sensations
occurring before, during, or after the major symptom.

Using these seven basic properties, the diagnostician can characterize

the symptoms and begin to consider possible disease entities. The history
is gently probed to provide the information necessary to diagnose or
exclude the etiologic possibilities. For example, if the patient is "coughing
up blood," the immediate possible causes may be bronchitis, pneumonia,
tuberculosis, pulmonary embolus, lung tumor, or mitral stenos~s. After the
symptom is delineated as completely as possible, the patient is questioned
in-depth for information that favors a more specific diagnosis or eliminates
several possibilities. The patient is asked to elaborate on each symptom or
illness. Questions such as "When did you last feel well?" or "Did you
consider your health excellent before...?" may be useful.
It is desirable to trace the illness forward, beginning with its clinical
inception and progressing to the present time. Some patients accomplish
this with great skill, embellishing the story with vivid description. However,
many patients are unable to remember dates accurately and may become
confused or flustered if pressed for exact details. Occasionally, a patient is
unable to supply the physician with a clear idea of the illness and its
chronological development. In this situation, the physician may need to
sacrifice chronology to better comprehend the nature of the symptoms.
For example, the physician might say, "Describe a typical attack," "How
long is the shortest/longest/usual attack? .... Tell me approximately how
many attacks of chest pain you have each week. Have these increased in
frequency lately?"
The experienced physician carefully prompts the patient with appropriate
questions so that all necessary information, both positive and negative, is
garnered before a different topic is pursued. Since the physician, not the
patient, has knowledge of disease processes and their clinical
presentations, the physician should structure the clinical interview to allow
a thorough and objective analysis of symptoms without leading the patient
into responses that fit the physicians predetermined conception of the
illness. The physician should also understand his or her own biases to
interact objectively with the patient.
Previous illnesses, past and current therapy, habits, allergies, family
history, occupational and daily living history, and review of systems are
carefully documented. The following questions offer important insight into
the life of the patient: "What do you like to do? .... How do you spend your
day? .... Who is important to you? .... What stresses are you under?"
At the close of the interview, the physician will find it valuable to
summarize his or her understanding of the information so the patient can
correct it before the information is placed in the record.
The patients history may be supplemented by information from relatives
and friends as well as charts and comments from other physicians who
have cared for the patient.

Cardiovascular Data Collection

The history of cardiovascular disease is an inseparable part of the total

medical history, for important information may be overlooked unless all
previous illnesses, symptoms, habits and lifestyle, socioeconomic
considerations, and family history are known. The steps in cardiovascular
data gathering are outlined below.

Historical Evidence
Have you ever had an illness or a problem related to your heart or
blood vessels?
Have you ever been told that you have or have had:
an enlarged heart?
a heart murmur?
a rheumatic heart?
a heart attack?
heart congestion or heart failure?
pericarditis?
a blood clot in the lung?
poor c, irculation?
stroke?
inflamed veins?
Have you ever:
been rejected by the armed services?
failed an insurance exam?
had a high rating on an insurance exam?
had an abnormal electrocardiogram or exercise stress test?
Have you ever taken:
digitalis?
water pills or diuretics?
pills to lower your blood pressure or cholesterol?
nitroglycerin pills under your tongue?
blood thinner?
heart medicines?

The following list of etiologies of heart disease is taken from the New
York Heart Associations Nomenclature and Criteria for Diagnosis of
Diseases of the Heart and Great Vessels.

Symptoms
Do you experience:
chest discomfort or pain?
shortness of breath during moderate exertion?
shortness of breath when recumbent?
swelling of your ankles?
dizzy spells?
fainting spells?
palpitations, skipped heartbeats, or a racing heart?
significant unexplained fatigue?
coughing at night?
coughing up blood?
cramps or pain in your calves, thighs, or hips while walking that is
relieved by rest?
Do you:
have to elevate your head with more than one pillow to breathe
comfortably at night?
have to arise several times during the night to urinate?
have tender or swollen calves?
have varicose veins?
These questions should effectively screen for the presence of heart
disease that is producing physiologic impairment. When chest pains and
palpitations are excluded, the symptoms are traceable to secondary effects
of heart disease on other organs, particularly the lung, brain, kidney, and
blood vessels. If the patient answers any question affirmatively, the
symptom should be explored in more detail, using the approach outlined
in the previous chapter.

Etiology
The clinician should try to establish an etiology by asking questions
directed to known causes of cardiovascular disease. The scope and
number of questions are tailored to the patient, based on symptoms, prior
illnesses, physical findings, and other information gathered.

Acromegaly
Alcoholism
Amyloidosis
Anemia
Ankylosing spondylitis
Atherosclerosis
Carcinoid tumor (argentaffinoma)
Congenital anomaly
Friedreichs ataxia
Glycogen storage disease
Hemochromatosis
Hypersensitivity reaction
Hypertension
Hyperthyroidism
Hypothyroidism
Infection
Marfans syndrome
Mucopolysaccharidosis

Neoplasm
Obesity
Polyarteritis nodosa
Progressive muscular dystrophy
Progressive systemic sclerosis
(scleroderma)
Pulmonary disease (cor pulmonale)
Reiters syndrome
Rheumatic arthritis
Rheumatic fever
Sarcoidosis
Syphilis
Systemic arteriovenous fistula
Systemic lupus erythematosus
Toxic agent
Trauma
Unknown
Uremia

Additional questions are also asked to discover the presence of

coronary risk factors, including age, gender, race, smoking, hypertension,
hypercholesterolemia, diabetes, obesity, inactivity, stress, personality type,
abnormal electrocardiogram, and abnormal exercise test.
Many cardiovascular disorders are genetically determined. The genetic
influence may be obvious, as in Marfans syndrome, or the inheritance may
be indirect and poorly understood, as in atherosclerosis and hypertension.
Familial diseases can affect the vascular system, pericardium, myocardium,
valves, septa, and conduction system separately or in combination. The
abnormality may appear early or late in life, or remain clinically silent. The
possibility of an inherited cardiovascular disorder should be sought by
asking the patient if a family member has a similar problem. A family
pedigree is also obtained and illnesses and causes of death carefully
documented. A family history of birth defects, mental or physical
retardation, or unusual stature is important if congenital heart disease is
present. The possibility of maternal rubella or teratogenic drugs taken
during the pregnancy should be considered. Early death of a family
member may also be significant.

Severity and Progression of Disease

Previous Therapy

This information is necessary so that the patient can be classified

according to the functional severity of the illness. Although there is a
rough correlation between severity of heart disease and the patients
symptoms and limitations, pathophysiologic impairment does not always
correlate closely with symptoms. Many patients with heart disease are
asymptomatic and their activity is unlimited. This is sometimes true even
with advanced heart disease. Before further diagnostic studies and
therapy can be planned, it is essential to learn the patients capacities and
limitations by asking questions such as:

This information provides the foundation for further therapy. It is particularly important to ascertain if the patient understood and followed the
prescribed diet and medications. The patient is often described as failing
to respond to therapy when in reality he or she is not taking medications
correctly nor adhering to prescribed diets. The patient may be confused
about the use of different medications or may not buy medications
regularly because they are too expensive. These problems can often be
resolved by asking the patient to bring his or her medicines to the office
for review.
The patient should be asked if the condition improved after starting a
medication or after cardiovascular surgery. Careful analysis of daily
activities, onset of symptoms, and the medication schedule may provide
essential information for future therapy. The patient should also be
questioned about his or her understanding of the illness so that
appropriate education can be initiated.
In planning a therapeutic program, the physician must also consider the
patients age, interests, other illnesses and limitations, financial needs, home
environment, and willingness to participate and return for follow-up care.

What are your current occupational and recreational activities and

limitations?
What types of activities can you perform in and around the house?
Have you had to curtail any activities?
Do you need to stop and rest before you can finish the activity?
Do you have a regular exercise program?
How much walking/running/climbing can you do before you have
shortness of breath/chest discomfort/fatigue/dizziness?
Over the past year, have your activities become more limited or are your
capabilities about the same?
After the patient has answered these questions, his or her physiologic
cardiac status can be assessed with the following New York Heart
Association classification:
1. Uncompromised
2. Slightly compromised
3. Moderately compromised
4. Severely compromised

Common Symptoms
of Cardiovascular Disease

Chest Pain
Analyzing the many causes of chest pain to arrive at a correct etiology
can vex even the most astute clinician. Although there are numerous
causes of chest pain, the most important are angina pectoris, myocardial
infarction, pericarditis, pulmonary embolus, dissection of the aorta, chest
wall distress, and the pain of gastrointestinal disorders such as hiatal
hernia, esophageal disease or spasm, cholecystitis, pancreatitis, and
peptic ulcer distress.
The features of angina pectoris are described below in detail by using
the seven basic properties that separate angina pectoris from other
causes of chest pain. The distinguishing features of other causes of
chest pain are also discussed.

Angina Pectoris
In 1772, William Heberden described the clinical disorder he called
angina pectoris:
But 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 be
called angina pectoris.
They who are afflicted with it, are seized while they are walking
(more especially if it be uphill, and soon after eating) with a
painful and most disagreeable sensation in the breast, which
seems as if it would extinguish life, if it were to increase or to
continue; but the moment they stand still, all this uneasiness
vanishes.*

*Heberden W: Commentaries on the History and Cure of Diseases. London, L Payne,

News-Gate, 1802
10

This classic account beautifully describes features that are still

considered characteristic of angina pectoris. However, there are variations
on the basic theme. When the patients history is not classic, the
questions must be very penetrating and all possible causes of chest pain
must be considered. The diagnosis of angina pectoris has serious
emotional, prognostic, and economic implications and should not be made
without a full understanding of the symptoms.
Bodily Location. Although the usual origin of the pain is the anterior
midchest, it is not uncommon for pain to originate or even be localized to
the epigastrium, neck or jaw, shoulders, elbows, or arms. Rarely, it may be
felt only in the back. The discomfort is usually limited to the chest but may
radiate to the neck or down the left and sometimes the right arm. On
occasion, it is felt simultaneously in the elbow or wrist. The arm may feel
heavy or lifeless. It is very unusual for the pain to be pinpointed to a small
area or localized to the apex of the heart. The patient usually indicates the
location by a sweep of the hand across or up and down the chest or a
gripped hand over the area.
Quality. The qualities of angina pectoris that most distinguish it from
other causes of chest pain are tightness, squeezing, heaviness, pressure,
and constriction. Sticking, stabbing, throbbing, or needle-like pain is
seldom a symptom of angina pectoris. To complicate matters, some
patients experience angina as indigestion, cramping, burning, aching,
sharp, gas-like, or indescribable. It may be difficult or even impossible to
distinguish angina from other causes of chest pain on the basis of quality
alone. Many patients do not experience angina as "pain" and will stoutly
deny having chest pain. The experienced clinician asks, "Do you have any
discomfort or unusual sensation in your chest?" If the answer remains
negative, the patient should be pressed with more specific questions such
as "Do you have tightening or pressure sensations in your chest?" or ~re
you limited in any way from exerting yourself fully?"
Recent studies have revealed that transient silent ischemia occurs four
to five times more frequently than painful episodes in patients with known
coronary disease. The clinical significance of silent ischemia and its
relation to arrhythmias, infarction, and sudden death are not yet fully
understood, but considerable progress is being made.
Chronology. The usual duration of angina pectoris is brief; it is typically
less than 20 minutes. However, there are patients who describe their chest
discomfort as lasting 30 minutes, an hour, or even more. On close
questioning, some patients have a relatively brief period of significant pain
followed by lingering chest discomfort. Other patients appear to have

11

prolonged myocardial ischemia without electrocardiographic or enzymatic

evidence of myocardial injury. The exact nature and significance of this
sustained pain is not known. It is probably wise to consider myocardial
ischemia as a spectrum, with angina pectoris at one end, myocardial
infarction at the other, and increasing degrees of ischemia in between that
may cause loss of contractile tissue, arrhythmias, heart failure, and death.
Quantity. The severity of angina pectoris varies considerably from an
almost unnoticeable vague discomfort to an intense pain that immediately
grips and immobilizes the patient. Generally, the pain is not unbearable
and can be tolerated and eased by ceasing activities or calming down.
Many patients learn to limit their exertion so that they can live within the
boundaries of their exercise tolerance without experiencing chest pain.
It is important to determine if the frequency of angina pectoris is
increasing, unchanged, or less frequent, and if the angina is now
produced by less effort, no effort, or while sleeping. The number of
nitroglycerin tablets consumed in a day or week may be a good guide.
The patient should be asked if he or she has had to change occupations
or limit recreational or work activities as a result of chest discomfort.
Setting. Although angina pectoris can occur any time or anywhere,
certain times or activities favor its appearance. These include combing
hair or shaving in the morning, walking into a cold wind, running, climbing
stairs, playing with the children, sexual intercourse, tension at work, a
heavy meal, an exciting athletic event, or arguing with a family member.
Angina may also occur while sweeping, changing beds, and raising the
arms overhead to wash windows, brush hair, or place objects in high
cabinets. Angina pectoris is worse with morning activities; similar stresses
later in the day may be easily tolerated. A knowledge of the setting may
permit an alteration of activity, or if the inciting event cannot be avoided,
the prophylactic use of nitroglycerin.
A specific type of angina pectoris, known as Prinzmetals variant angina,
typically occurs during rest and may recur in a nightly cyclic pattern.
ST-segment elevation or depression on the electrocardiogram and
coronary artery spasm have been documented during an attack.
Aggravating or alleviating factors. Angina pectoris is often related to
stress and is relieved by ending or controlling the stress. Cardiac stress
includes not only exertion but emotions such as anger, fear, pain, tension,
excitement, nightmares, exposure to cold weather or wind, a heavy meal,
or isometric exertion such as shoveling snow or lifting heavy objects.
Angina at rest (angina decubitus) is also common and may be explained
by changes in coronary tone, spasm of the coronary artery or platelet
plugs superimposed on fixed coronary obstruction, or, infrequently, in the
absence of significant narrowing.
12

Angina pectoris is usually promptly relieved or lessened by emotional

and physical rest as well as by nitroglycerin. Since the effect of nitroglycerin
is quite rapid, usually immediate or within 3 minutes, the patient should be
asked how quickly the pain left. If the discomfort abates after 10 minutes,
it is unlikely that nitroglycerin was responsible. Nitroglycerin is not effective
for all patients with angina, nor is it specific for angina pectoris since it
can alleviate chest pain of other etiology.
Associated symptoms. While angina may be manifested only as pain,
other symptoms, including dyspnea, palpitations, dizziness, and nausea
may also occur or appear as the sole manifestation. "Silent" ischemia
may appear as an arrhythmia or sudden death.

Myocardial Infarction
The pain of myocardial infarction is usually, though not always, more
intense than angina pectoris and often exceeds 30 minutes in duration. It
often has a different quality, described as heavy, vise-like, crushing,
expanding, or squeezing. The patient may not be able to describe the
pain other than to say it was severe or intolerable. Radiation of pain from
the chest to the shoulders, neck, or arms is common. Associated
symptoms, including nausea, vomiting, sweating, dizziness, syncope,
marked weakness, palpitations, urge to defecate (chezonisus), fear of
death (angor animi), and dyspnea may be prominent.
Because many patients ascribe the discomfort of angina pectoris or
myocardial infarction to indigestion, the complaint of indigestion bears
particular scrutiny. Occasionally, a myocardial infarction is manifested as
acute abdominal pain, tenderness, rigidity, and vomiting. Rarely, the pain
is felt only in the back, neck, or shoulders.
The diagnosis of myocardial infarction often demands that the physician
maintain a high index of suspicion since the pain may be absent, insignificant, or attributed to other causes such as indigestion or gas. Other signs,
including unexplained heart failure, weakness, syncope, or arrhythmias
may be the major manifestation suggesting an acute myocardial infarction.
Patients who have had no recognized symptoms are sometimes found to
have had a myocardial infarction on routine ECG or at autopsy. The
incidence of silent infarction may be as high as 30%. Diagnosis of these
patients may confound even the most astute diagnostician.

Pericarditis
The pain of pericarditis is similar to myocardial infarction in its midchest
location and occasional radiation into the arm. On close questioning, the
patient with pericarditis will usually describe the pain as sharp, unlike the
pain of myocardial infarction. Accentuation of the pain with inspiration,
13

swallowing, on lying down, and with movement, as well as containment of

pain when leaning forward or breathing shallowly, is almost diagnostic.
Radiation of the pain to the left trapezial ridge or scapula and awareness
that the intensity of the pain coincides with the heartbeat is characteristic
but not always present. The pain may be sudden or gradual in onset and
may fluctuate from mild to severe. Relief of the pain with steroids but not
with narcotics is typical. Surprisingly, some patients may have pericarditis
but not experience any chest discomfort.

Pulmonary Emboius
A large pulmonary embolus that produces infarction of the lung is
usually easily diagnosed by the sudden onset of sharp, pleuritic chest
pain, dyspnea, hemoptysis, cyanosis, and tachycardia. More commonly,
pulmonary emboli do not result in pulmonary infarction and may provide a
diagnostic dilemma. The diagnosis of pulmonary emboli should be
considered if there is pleuritic pain, unexplained dyspnea (particularly if
the dyspnea is acute and episodic), atrial arrhythmias, cyanosis,
tachycardia, fever, or congestive heart failure.
The diagnosis is strongly supported by the occurrence of hemoptysis,
which is so infrequent, however, that its absence should not alter the diagnosis. Since pulmonary emboli usually occur in the setting of venous injury,
venous stasis, or alteration of blood coagulation, questions should be directed
to precipitating causes. The following information should be obtained:
Prior history of pulmonary emboli
Presence of leg or calf tenderness
History of heart, lung, or blood disease
Recent surgery (particularly hip surgery), pregnancy, trauma, bed rest, or
long car trip
Use of oral contraceptives
Use of constricting girdle or garter
Occupation (prolonged standing)
Presence of varicose veins or previous vein stripping
By realizing that pulmonary emboli occur in certain settings, particularly
in hospitalized patients, and that their clinical presentation is rarely classic,
the clinician may be able to make the diagnosis.

14

Aortic Disease
A dissection of the aorta is usually announced by sudden, severe,
midline pain often described as tearing or ripping. The pain may radiate
from front to back or down the midline into the abdomen or lower back.
The severity of the pain classically peaks at the onset. Symptoms of
vascular occlusion elsewhere, including myocardial infarction, may follow.
On occasion, this pain cannot be separated from other causes of chest
pain and may even be absent. The association of chest pain with a stroke,
occluded vessel to an extremity, or a new murmur of aortic regurgitation is
highly suggestive of aortic dissection.
An aneurysm of the aorta is usually silent until it expands or ruptures.
When the enlarging aneurysm impinges on the inner surface of the chest
wall, the patient may suffer from a boring, throbbing, or steady pain that is
localized in one area and prolonged or continuous.

Gastrointestinal Disease
Gastrointestinal disease, including esophagitis, esophageal spasm,
hiatal hernia, gastric or duodenal ulcer, erosive gastritis, dyspepsia,
cholecystitis, biliary dyskinesia, and pancreatitis may occasionally appear
as chest pain simulating ischemic heart disease. The most suggestive
clues to gastrointestinal disease are heartburn relieved by antacids,
dysphagia, and painful swallowing (odynophagia). Esophageal disease,
especially esophageal spasm, is particularly difficult to distinguish from
angina pectoris because both cause squeezing or pressure up and down
the midchest and radiation of pain to the neck, jaw, and arms, which is
quickly relieved by sublingual nitroglycerin. Esophageal disease is
suggested when the pain is related to eating, bending over, or
recumbency. Dysphagia is sometimes present. Although biliary disease,
gastric or duodenal ulcer, and pancreatitis can cause chest pain, close
questioning usually reveals that the pain begins in the abdomen and
radiates to the chest.

The Chest Wall

The chest wall is often overlooked as the source of chest pain. There
may be discomfort in the ribs, muscles, costal cartilages, nerves, xyphoid,
breast, pleural lining, or thoracic spine. Specific diagnoses include Tietzes
syndrome, costochondritis, xyphoidalgia, myofascial pain, hyperventilation
syndrome, precordial catch, slipping rib syndrome, cardiac causalgia,
herpes zoster, and trauma. The pain that may result from any of these
problems is often in the midchest or left anterior chest and may radiate to
the neck, shoulders, and arms. An aching or pressing sensation is
common. The patient is naturally alarmed over the possibility of a heart
15

attack and diverts the physicians attention to the heart and away from the
chest wall. Careful questioning of the patient and a thorough examination
of the anterior and posterior chest is essential to make the diagnosis.

Orthopnea. During the day, gravitational effects on the control of fluid

balance may favor a loss of intravascular fluid into the interstitial space.
When the patient is in a horizontal position, the edema fluid may return to
the vascular system, augmenting intrathoracic blood volume and decreasing
the vital capacity of the lung. The patient is unable to breathe easily when
lying down and must elevate his or her head on pillows to breathe
comfortably. Since many people normally sleep on several pillows, the
patient must be asked, "Why do you sleep on several pillows? ....What
happens if you roll off your pillows?" The degree of orthopnea is
measured by the number of pillows used, for example, three-pillow
orthopnea. As cardiac failure becomes advanced, the patient may actually
be forced to sleep in an upright position or in a chair.

Mitral Valve Prolapse

Mitral valve prolapse is now recognized as a common finding, present in
4-6% of the population, with a 2:1 female4o-male prevalence. The vast
majority of these patients are asymptomatic; however, a small subset of
patients complain of chest pain, palpitations, fatigue, and dizzy spells. The
chest discomfort may have some features that suggest angina, such as
heaviness or a midchest location, but it is rarely precipitated by exertion.
The pain is most commonly described as sharp or sticking and is located
near the cardiac apex. It may be fleeting or last for hours.

Paroxysmal nocturnal dyspnea. Some time after retiring, the patient is

suddenly awakened from sleep by a sensation of strangling or smothering.
To gain relief, he or she must sit or stand and may bolt to an open window
for relief. After several minutes the patient is able to return to bed. Paroxysmal dyspnea may recur later in the night.

Shortness of Breath
Dyspnea implies difficulty in breathing and is a symptom common to
many diseases. The patient may describe this discomfort as shortness of
breath, inability to take a deep breath, smothering, cutting off of the wind,
asthma, or wheezing. It may be difficult to separate dyspnea due to
cardiac disease from other causes. This may vary from day to day,
depending on many factors; patients often say that they have "good days
and bad days." With advanced heart failure, shortness of breath is present
at rest or in any minimal activity.

Trepopnea. The patient with cardiac disease is frequently unable to lie

on his or her side, particularly the left side, because he or she experiences
dyspnea, palpitations, or an uncomfortable sensation. This condition,
called "trepopnea," is a common symptom, although it is not usually
mentioned by the patient.
Pulmonary edema. Severe left ventricular failure may produce such
overwhelming pulmonary congestion that the patient actually gurgles forth
pink, frothy sputum with deep, desperate respiratory efforts.

Left Ventricular Failure

The most characteristic features of dyspnea due to left ventricular
failure are:

Wheezing. In some patients, wheezing is a striking expression of pulmonary edema (cardiac asthma). Other causes of wheezing must be excluded.

Other Causes of Dyspnea

Exertional dyspnea. Dyspnea on exertion becomes apparent during

housework, athletic activities, while walking several blocks, or climbing
steps. In assessing severity and progression of heart disease, the
physician must determine the amount of activity necessary to produce
dyspnea and compare current activities with previous capabilities.
Infrequently, the patient with angina pectoris notices chest tightness and
shortness of breath occurring at the same moment of exertion. It may be
difficult to tell if the patients limitation is due to angina, dyspnea, or both.
Indeed, the mechanism of the dyspnea may be an elevation in left
ventricular diastolic pressure related to myocardial ischemia.

16

Pulmonary emboli. Dyspnea caused by pulmonary emboli may appear

dramatically with cyanosis and gasping. More commonly it is recurrent,
less severe, and may be inseparable from congestive heart failure.
Pulmonary disease. Chronic pulmonary disease as a cause of dyspnea
is usually suggested by evidence of lung disease such as a cough, wheezing, sputum, or a history of smoking or bronchitis. Severe bronchospasm
appearing as asthma is occasionally a manifestation of left ventricular
failure. The chest x-ray and presence or absence of heart disease can
usually be used to sort out the cause.
17

Hyperventilation. Dyspnea related to anxiety and attendant hyperventilation is very common and may provide a thorny differential diagnosis,
particularly because hyperventilation often causes chest discomfort
simulating angina. Patients with breathlessness due to hyperventilation
often describe their symptoms as "The air doesnt go all the way down..."
or "1 cant get a full breath." The patient should be carefully observed for
signs of sighing, swallowing of air, and anxiety, and should be asked about
other symptoms of hyperventilation such as tingling or numbness in the
hands ("falling asleep") or around the mouth, dryness of the mouth, and
dizziness. When anxiety is associated with organic heart or lung disease,
determining the major contributing cause of the dyspnea may be perplexing.

Dizziness and Syncope

The symptom of dizziness may cover a multitude of sensations,
including giddiness, a fainting feeling, temporary confusion, unsteadiness,
or vertigo. The patient may substitute other descriptions such as blacking
out, swimming in the head, graying of vision, lightheadedness, or fallingout spells. Vertigo, a spinning sensation, must be carefully differentiated
from dizziness. The term "syncope" implies a temporary loss of
consciousness and postural tone that may or may not be preceded by
dizziness. An episode of dizziness and temporary loss of postural tone
without complete loss of consciousness is referred to as "near syncope."
Since the physician rarely has the opportunity to observe the episode of
syncope, the diagnosis is almost always based on a history provided by the
patient or a witness to the event. The following questions may be useful:
Did you feel as if you would faint, or was the sensation more like spinning
or vertigo?
What was the location and time of the attack? Did it occur more than once?

Did any of the following conditions or activities precede the attack?

a hot, closed room
increased activity
fatigue
hunger
anxiety or other emotion
sight of blood or anticipation of injury
recent illness or flu
What was the relation of the attack to:
position or change of position?
urination?
coughing?
pressure on neck or turning of head?
arm exercise?
taking medication (especially nitroglycerin)?
Did you experience any of the following symptoms before or after an attack?
palpitations or rapid heart rate
chest pain or discomfort
yawning; ringing in the ear; sweating; weakness; sighing; nausea;
numbness; staggering or lack of coordination; confusion; slurred
speech; paralysis of arm, leg, or face; loss of bladder (bowel) control
visual loss
headache
anxiety
What was the duration of symptoms before and after the attack?
Have you had any of the following?
anemia or blood loss
drugs to lower your blood pressure
surgery to cut nerves (sympathectomy)
history of heart murmur, slow or fast heart rate, heart disease
history of stroke, seizure disorder, brain disease, syphilis, diabetes,
pernicious anemia, multiple sclerosis, amyloidosis, syringomyelia
emotional disorder or recent emotional stress
migraine
Cardiovascular Causes
Dizziness or syncope related to the cardiovascular system may be the
consequence of a number of mechanisms, including the following.

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19

Arrhythmias. Very slow ventricular rates, as seen with atrioventricular

block (Morgagni-Adams-Stokes syndrome) or long sinus pauses, and very
rapid ventricular or supraventricular rhythms may impair cerebral blood
flow. Even ventricuiar fibrillation may be brief and self-reverting and attested
to only by dizziness or syncope. Although syncope may be sudden, the
patient often experiences a momentary dizzy spell or a blurring of vision
before loss of consciousness if an arrhythmia is the cause. Attacks can
occur while erect or recumbent. Symptoms related to automatic discharge
such as nausea, sweating, epigastric discomfort, and weakness are not
usually experienced. Convulsions secondary to decreased cerebral blood
flow may occur. Arrhythmias are now recognized as a common cause of
syncope in patients with cerebrovascular disease.
Patients whose ECG shows a prolonged QT interval may be particularly
susceptible to syncope secondary to ventricular arrhythmias, including
ventricular tachycardia and ventricular fibrillation. The prolonged QT interval
syndrome may be an inherited or acquired disorder. A careful family history
may disclose episodes of syncope or sudden death among relatives.
Obstruction to blood flow. Dizziness or syncopal spells can be
produced by an obstruction to blood flow through the heart or lungs
caused by valvular aortic stenosis, hypertrophic subaortic stenosis, mitral
stenosis, atrial myxoma, atrial thrombus, valvular pulmonary stenosis,
tetralogy of Fallot, primary pulmonary hypertension, pulmonary emboli,
pericardial tamponade, and prosthetic valve dysfunction. Arrhythmias and
peripheral vasodilatation related to reflexes or inadequate coronary blood
flow may contribute to the symptoms.
Reflexes affecting heart rate and blood pressure. Vasodepressor
(vasovagal) syncope is a very common cause of dizziness or syncope that
characteristically occurs in response to fear of injury, the sight of blood or
injury, or sudden emotional stress. Anxiety, physical or mental exhaustion,
debility, a heavy meal, stuffy environment, pregnancy, or anemia are
predisposing factors. Syncope is always preceded by warning symptoms
such as nausea, weakness, sweating, epigastric discomfort, blurred vision,
headache, tinnitus, difficulty concentrating, sighing, and dizziness. The
heart rate falls, and the patient appears pale and ill at ease. The syncope
is transient, lasting a few seconds to a few minutes, and may be prevented
by immediately lying down. During recovery the patient is weak, dizzy, and
nauseated, although mentally clear. Symptoms may recur when standing.
Rarely, this form of syncope can occur while the patient is recumbent.

2O

21

Orthostatic hypotension produces dizziness on arising or after prolonged

standing and can be related to reduced effective blood volume, autonomic
nervous system dysfunction, or, rarely, to circulating vasodilator
substances. Dizziness on arising is a common symptom, particularly in the
elderly, and does not necessarily imply an underlying problem requiring
extensive investigation. Contributing causes such as drugs (particularly
antihypertensive or antidepressant medications, vasodilators, and 9blockers), anemia, low blood volume, large varicose veins, and pregnancy
should be considered. Addisons disease is a rare cause of postural
hypotension. Orthostatic hypotension may also be produced by a faulty
autonomic nervous system response to assumption of an upright position.
This can occur after prolonged recumbency or with neurologic diseases
such as diabetic neuropathy, multiple sclerosis, syringomyelia, amyloidosis,
pernicious anemia, and tabes dorsalis. An idiopathic form of orthostatic
hypotension occurs and is often associated with inability to sweat, sexual
impotence, and incontinence.
Hypersensitive carotid sinus is suspected when the patient describes
dizziness or syncope after hyperextension of the neck, turning of the head,
or pressure over the area of the carotid sinus from a necktie or during
shaving. The patient may not be aware of the association or there may be
no obvious reason why the reflex is activated. A faint feeling, weakness,
blurred vision, and nausea may precede the syncopal episode. However,
the syncope often occurs without warning. The syncope is evanescent,
with rapid and complete recovery in a few seconds to several minutes.
Tussive (cough) syncope is rare and occurs with a paroxysm of nonproductive violent coughing. The victims are almost exclusively middle-aged,
overweight men with lung disease.
Micturition syncope is diagnosed when syncope occurs during or after
urination. The person has almost always just arisen from a period of
prolonged recumbency. Onset is abrupt with little or no warning; duration
is brief and followed by full recovery.
Glossopharyngeal neuralgia may result in syncope. In this rare disorder,
the patient suffers pain in the posterior pharynx, bradycardia, hypotension,
and syncope or seizures.

Other Causes of Syncope

Cerebrovascular disease. Syncope may occur with or without warning.
Transient neurologic signs such as unilateral weakness, ataxia, confusion,
slurred speech, numbness of an extremity, or facial asymmetry point to
obstruction to the cerebral blood flow. The syncopal episode is often
prolonged, and the postsyncopal period is characterized by confusion,
weakness, or focal neurologic signs.
Dizziness or syncope associated with upper arm exercise may lead to
diagnosis of a subclavian steal syndrome. This occurs when a severe
obstruction in the proximal subclavian artery allows shunting of blood away
from the cerebral circulation through the vertebral artery to the distal
subclavian artery. Upper arm exercise drops the vascular resistance distal
to the subclavian artery obstruction and enhances the "steal."
Epilepsy. Seizures may be difficult to distinguish from vasodepressor
syncope since both are often precipitated by fatigue and anxiety. An aura
often precedes the epileptic attack. Tonic or cIonic movements may be
witnessed. Loss of bladder or bowel control and biting of the tongue are
common in seizures but also occur with other forms of syncope. The
postictal period is usually prolonged, and the patient is confused or unable
to speak or move with ease.
Hyperventilation. Hyperventilation, a cause of dizziness and,
occasionally, syncope, is very common and a frequent reason for
emergency room visits. Early symptoms include tingling or numbness in
the hands, fingers, and around the mouth, dryness of the mouth, and a
feeling of smothering and apprehension, which may progress to severe
weakness, a sense of unreality, severe chest pain, dizziness, or syncope.
The patient usually breathes deeply, rapidly, and noisily in the later states.
However, hyperventilation may not be apparent. Unconsciousness is not
prolonged unless hyperventilation persists.
Idiopathic syncope. Even after careful historical analysis, the
mechanism of syncope may be unexplained in more than 50% of patients.

Palpitations
Irregularities of the heartbeat or tachyarrhythmias may be silent or experienced by the patient as palpitations, skipping, heart flutter, jumping in the
chest, or a runaway heart. Ambulatory monitoring studies have shown that
these sensations are often due solely to a heightened awareness of the
normal heartbeat, particularly when the patient is lying still in bed or is
emotionally upset, or for no apparent reason. An arrhythmia may also
create a secondary effect such as dizziness, syncope, seizure, blurred
vision, chest discomfort, or dyspnea.
Isolated premature atrial or ventricular beats are common and unnoticed
by most people. However, some people are very aware of the irregularity or
the forceful postextrasystolic contraction and may seek advice and
reassurance.
Atrial tachycardia (AV nodal reentry) is often abrupt in onset and
termination and quite regular in rhythm as contrasted with atrial fibrillation,
which is generally irregular and less striking in the suddenness of its
initiation and termination. When atrial fibrillation is rapid and irregular, the
patient may describe the feeling as a "thumping or fluttering in the chest."
The symptoms caused by these arrhythmias may overlap, or the patient
may not recognize these features.
Ventricular tachycardia may be easily tolerated even if the heart is very
diseased. If the patient has significant coronary or myocardial disease, the
common manifestations are dizziness or syncope, chest pain, and
dyspnea. The patient may or may not appreciate the presence of the rapid
heartbeat. Sometimes the patient comes to the emergency room in shock
or severe heart failure and is discovered to have ventricular tachycardia.
Patients who take digitalis or have permanent cardiac pacemakers or a
large stroke volume (as occurs with aortic regurgitation) are sometimes
frightened by the forcefulness of their heartbeat.
Diagnosis may be difficult because of the diversity of presentation and
the frequent disappearance of arrhythmia by the time the patient sees a
physician. The following questions are often helpful in searching for
occurrence of an arrhythmia:

Recent Attack
When did it start?
Where were you and what were you doing?
Did it start or end abruptly or gradually?
How long did it last?
Were you able to count the pulse rate?
Was the rhythm regular or irregular?
22
23

Can you mimic the rate and rhythm by patting your fingers on top of the
other hand?
Were there associated symptoms such as:
chest discomfort?
weakness?
dizziness?
fainting?
visual blurring?
sweating?

Do you take:
diet pills?
amphetamines?
stimulant pills?

Prior Attacks

Fatigue is a common symptom of heart disease and an important

consequence of heart failure. Unfortunately, the stress and anxiety of daily
life make this symptom so common that the response to the question "Do
you tire easily?" is usually affirmative. A positive response assumes more
importance when the patient has previously enjoyed unlimited exercise
tolerance. In evaluating the progression of cardiac disease, it is helpful to
ask questions that allow the patient to compare current abilities with easily
remembered past events: "Were you able to do all the housework this
Christmas? .... Could you play two sets of tennis last summer?" Some
patients with heart disease will decrease their activities so gradually that
they are not aware of the underlying cardiovascular disease or its
progression. This is particularly true with mitral stenosis.

Have you had similar attacks in the past? (If so, obtain preceding information.)
If so, how frequently do they occur? Have you been examined or given an
ECG during an attack?
Have you found any positions, maneuvers, or medications that have halted
or prevented attacks?

Review of Medical History

Is there a history of:
heart disease?
heart attack?
rheumatic fever?
enlarged heart?
heart murmur or click?
Do you have recurrent chest pain or discomfort?
Is there a history of:
lung disease?
blood clots in the lung?
medication for asthma or lung disease?
Is there a history of chronic anxiety or recent emotional distress?
Is there a history of:
high blood pressure?
thyroid disease?
thyroid medication?
Wolff-Parkinson-White syndrome?
What medications do you take?
What is your consumption of:
cigarettes?
coffee?
tea?
alcohol?
colas?
24

Fatigue

Edema
Retention of salt and water in patients with cardiac disease and heart
failure may result in soft tissue swelling in the feet and around the ankles.
This formation may be described by the patient as swelling of the feet or
puffiness around the ankles. Since gravity promotes fluid extravasation
from intravascular to extravascular spaces, the edema becomes worse as
the day progresses and generally disappears or improves with nighttime
recumbency. The return of fluid to the vascular system at night produces
nighttime diuresis, and patients complain that they frequently arise to
urinate. As heart failure progresses, fluid accumulation may involve other
tissues, particularly the eyelids and sacral areas.
Fluid may collect in the abdomen with advanced right ventricular failure.
As this ascitic fluid increases, the patient may be aware of abdominal distention and bloating. Right upper quadrant pain and tenderness may also
occur as a result of hepatic congestion from high central venous pressure.
Cardiac disease is only one of several possible explanations for fluid
retention. Often several factors contribute to formation of edema.

25

Intermittent Claudication

Rheumatic Fever

Claudication is produced when the blood supply to exercising muscles

is inadequate. This is usually due to significant atherosclerotic obstruction
to the lower extremities but may also be the result of arteritis, embolization,
or extrinsic compression of any vessel. Unless the obstruction is severe,
the limb is asymptomatic at rest. During exercise, the blood supply does
not match the metabolic demands of the tissue, and ischemia results. The
patient notices a cramp, charley horse, ache, or weakness that improves
with rest but recurs when exercise is resumed. The severity and location
of the problem is measured by asking the patient where the discomfort
occurs (foot, calf, thigh, or buttocks) and how much exertion is required to
produce it: "How far can you walk without resting?" This can be quantified
as two-block claudication of the gluteal muscles and calves bilaterally. As
claudication progresses, the patients discomfort when walking increases.
When occlusive disease involves the distal aorta at the iliac bifurcation,
the male patient may also reveal that he is unable to have or maintain an
erection. This is sometimes why the patient seeks medical advice.
When arterial disease is severe, ischemic discomfort may be present at
rest. The pain is described as boring, aching, intense, or steady. The
patient is usually restless, unable to sleep, or forced to dangle the leg over
the side of the bed for slight relief.

At one time, acute rheumatic fever was erroneously diagnosed in many

patients with joint or muscle pain or a heart murmur. For this reason, a
history of rheumatic fever as a child must not be accepted at face value.
Although the patient may not remember details of the illness, the physician
should carefully review the facts and determine if they conform to current
concepts of rheumatic fever. Conversely, many patients who have evidence
of rheumatic heart disease do not have a history of acute rheumatic fever.
The patient or the patients parents should be asked if a sore throat
occurred within 1 month before onset of the illness. Arthritis should be
further defined by asking which joints were involved and the sequence of
the joint involvement. Arthritis, a major criterion, must be distinguished
from the subjective complaint, arthralgia, a minor criterion, by asking if the
joint(s) was swollen, hot, red, tender, or limited in motion. Typically, acute
rheumatic fever causes an inflammation of the larger joints, particularly the
knees and ankles, but also the elbows, wrists, shoulders, and hips, and
more rarely, the small joints of the hand. Arthritis is occasionally
monoarticular but characteristically migrates from joint to joint without
permanent deformity and usually disappears within 3 weeks.
A history of carditis may be difficult to establish. The patient should be
asked if a murmur was heard by the physician during or after the illness
and if the heart was enlarged or symptoms of heart failure were present. A
history of rejection by the military service or an insurance company
because of a heart murmur or a large heart can be important.
Several types of skin eruptions may occur with rheumatic fever,
including erythema marginatum, erythema nodosum, and urticaria. The
patient should be asked if a rash occurred during the illness. If so, the
location, size, and color of the rash should be noted and whether it was
tender or pruritic. Subcutaneous nodules can be a helpful historical clue;
however, they are seldom noticed by the patient.
Rheumatic (Sydenhams) chorea consists of involuntary, brief, nonrepetitive
movements of a body part. Parents may often recognize a change in the
childs usual behavior or coordination, described as frequent grimacing,
nervousness, or awkwardness such as dropping dishes, difficulty buttoning
clothes, or tripping. In mild cases, the parents may describe the child as
being "fidgety." School performance also declines.
Diagnostic criteria for acute rheumatic fever were greatly clarified by
introduction of the Jones criteria in 1944. These criteria were revised in
1982 and include the following.

Cyanosis
Although cyanosis is a physical finding and not a symptom, the patient
or a family member may notice that the skin is blue, dark, or dusky. This
information is extremely important in the infant, as it suggests the
presence of congenital heart disease with right-to-left shunting of the
underoxygenated blood into the arterial circulation. Cyanosis may be
apparent only when the child is crying, feeding, or exercising vigorously.
Additional information is gained by asking if cyanosis was present at birth
or if it appeared later in life.
Cyanosis in the adult has less specific implications and may be due to
lung disease, pulmonary emboli, congenital heart disease, or abnormal
hemoglobins. Cyanosis with dyspnea should always suggest the presence
of a large occluding pulmonary embolus. Cyanosis is not a sign of
congestive heart failure unless there is severe impairment of peripheral
capillary blood flow.

26

27

Major Manifestations
Carditis
Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules

Minor Manifestations
Clinical
Previous rheumatic fever or rheumatic heart disease
Arthralgia
Fever

Conclusion

History-taking is not confined to a single time or location but is a

continuing accumulation of information throughout the patient-physician
relationship. As physical findings are discovered or as laboratory
information is obtained, the clinician should renew the historical pursuit to
expand the original data base and reevaluate the initial diagnosis. In
addition, valuable information not remembered initially may surface as the
patient mulls over the original questions.

Laboratory
Acute phase reactants
Erythrocyte sedimentation rate
C-reactive protein, leukocytosis
Prolonged PR interval

Supporting Evidence of a Preceding Streptococcal Infection

Rheumatic fever is suggested by the presence of two major criteria, or
one major and two minor criteria, if there is evidence of a preceding group
A streptococcal infection such as positive throat culture or serologic
response.
A more detailed discussion of diagnostic criteria can be found in Jones
Criteria (Revised) for Guidance in the Diagnosis of Rheumatic Fever (AHA
publication No. 70-016-B), which was reprinted in Circulation
(1984;69:203A) and is available from the American Heart Association.

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29

Suggested Reading

Beckman HB, Frankel RM: The effect of physician behavior on the collection of data. Ann
Intern Med 1984;101:692-696
Duffy DL, Hamerman D, Cohen MA: Communication skills of house officers. Ann Intern
Med 1980;93:354-357
Enelow A J, Swisher SN (eds): Interviewing and Patient Care, ed 2. New York/Oxford,
Oxford University Press, 1979
Fletcher C: Listening and talking to patients. I: The problem. Br Med J 1980;281:845-847
Fletcher C: Listening and talking to patients. I1: The clinical interview. Br Med J
1980;281:931-933
Fletcher C: Listening and talking to patients. II1: The exposition. Br Med J
1980;281:994-996
Fletcher C: Listening and talking to patients. IV: Some special problems. Br Med J
1980 ;281:1056 - 1058
Hurst JW: The Heart, ed 7. New York, McGraw-Hill Book Co, 1990
Morgan WL Jr, Engel GL (eds): The Clinical Approach to the Patient. Philadelphia, WB
Saunders Co, 1969, pp 1-79
Platt FW, McMath JC: Clinical hypocompetence: The interview. Ann Intern Med
1979;91:898 - 902
New York Heart Association Criteria Committee: Nomenclature and Criteria for Diagnosis of
Diseases of the Heart and Great Vessels, ed 8. Boston, Little, Brown & Co, 1979
Tumulty PA: What is a clinician and what does he do? N EnglJ Med 1970;283:20-24
Walker HK, Hall WD, Hurst JW (eds): Clinical Methods, ed 3. Boston, Butterworth, 1990

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