American HeartAssociation~Fighting Heart Disease

and Stroke

Examination of the HeartPart I

Examination of the Heart Part 1

The Clinical History

Prepared on behalf of theCouncil on Clinical Cardiologyof the American Heart Association

Mark E. Silverman, MDProfessor of MedicineEmory University School of MedicineChief of CardiologyPiedmont HospitalAtlanta, Georgia

Examination of the HeartA Series of Booklets

Part 1The Clinical HistoryMark E. Silverman, MD

Part 2Inspection and Palpation ofVenous and Arterial PulsesMichael H. Crawford, MD

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

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

Part 5The ElectrocardiogramMasood Akhtar, MD

Available from your local American Heart Association

©1972, 1978, 1990 American Heart Association

2 The Basic Structure of History Taking5 Cardiovascular Data Collection5 Historical Evidence6 Symptoms6 Etiology8 Severity and Progression of Disease9 Previous Therapy

10 Common Symptoms of Cardiovascular Disease10 Chest Pain10 Angina Pectoris13 Myocardial Infarction13 Pericarditis14 Pulmonary Embolus15 Aortic Diseaset5 Gastrointestinal Disease15 The Chest Wall16 Mitral Valve Prolapse16 Shortness of Breath16 Left Ventricular Failure17 Other Causes of Dyspnea18 Dizziness and Syncope19 Cardiovascular Causes22 Other Causes of Syncope23 Palpitations25 Fatigue25 Edema26 Intermittent Claudication26 Cyanosis

27 Rheumatic Fever

29 Conclusion31 Suggested Reading

The history is the foundation of the clinical diagnosis. The ability anddesire to obtain accurate, unbiased information is a major distinguishingcharacteristic of every fine diagnostician. Although standardizedquestionnaires, computers, and interviews conducted by paramedicalpersonnel have become increasingly useful in obtaining information, thephysician must still assume the major responsibility for ensuring that theinformation is as complete and accurate as possible.

Despite the obvious necessity of obtaining accurate historical informationand relating that data to the physical examination, the clinical history,unfortunately, may be neglected or slighted in favor of a glittering physicalfinding or a multitude of laboratory tests. A brilliant biochemical diagnosismay be the simple conclusion of a skilled medical interview.

In addition to accumulating essential historical information, the clinicalinterview is the beginning of the patient-physician relationship, aninteraction in which the patient evaluates the physician’s patience,thoroughness, skill, and interest, and the physician seeks subtle cluesfrom the patient’s appearance, voice, expression, mannerisms, position inbed, and breathing pattern. As James Herrick, an early 20th centuryAmerican cardiologist of great distinction, remarked, "The doctor may alsolearn more about the illness from the way the patient tells the story thanfrom the story itself."*

This publication provides a basic approach to obtaining clinical historyrelated to the cardiovascular system. Common symptoms of cardiovasculardisease are also analyzed. A detailed discussion of the interrelationsamong symptoms, physical signs, and pathophysiology may be foundamong the titles listed under "Suggested Reading."

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

The Basic Structure of History Taking

Ideally, ample time should be available to explore the medical history indepth and in a relaxed manner. If time is short or the patient is too ill orconfused to be questioned at length, a limited interview, focused on theimmediate problem, is desirable. Later, as the patient improves, the historycan be completed.

The conversation might be initiated by asking the patient, "Tell me aboutyourself." This friendly opening demonstrates that the physician is genuinelyinterested in the person, not the disease. As Sir William Osier, the father ofAmerican medicine, stated, "It is more important to know what sort ofpatient has a disease than what sort of disease a patient has." The patientshould then be asked about his or her most important concerns andcurrent symptoms. At the outset, the physician encourages a spontaneousflow of information with open-ended questions such as "Tell me about yourchest discomfort;’ After the patient has elaborated on his or her problem,the physician can then follow up with more direct questions that favor ordismiss a specific diagnosis: "Did the pain worsen with activity?"

The physician should be careful to avoid courtroom-type questions thatlead to premature closure of the subject and erroneous conclusions. Theexperienced interviewer encourages the spontaneous flow of informationwith comments such as "Go ahead;’ "mm-hmm," "Yes," "1 see," "Whatelse?" and "Tell me more." This technique, known as passive listening, isenhanced by nonverbal communication such as open and receptiveposture, 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 theunderlying feeling in the message and relaying this feeling back to thepatient, the physician demonstrates concern and understanding. Forexample, the patient may say, "1 have a minor chest pain, but my wifeinsists that you check out my heart." The physician might respond, "It’salarming to think that your chest pain could be due to a heart condition." Itis important to recognize emotional and psychological overtones and theirimplications. Revealing information may be obtained by asking, "What doyou think is wrong with your health?" The physician should also be alert tothe possibility that the patient’s most distressing symptoms may not bedue to the most serious problem or that the patient may not be willing toacknowledge certain potentially serious symptoms such as chest pain.

The patient may naturally hesitate to trust a stranger with intimate detailsof an illness or personal frailties, a reluctance that may be heightened bydifferences in age, gender, race, language, or socioeconomic backgroundbetween the patient and the physician. Fear and anxiety may lead tosubconscious repression of important information, inability to describecertain symptoms accurately, faulty memory, or deliberate concealment offacts such as drinking, poor compliance with medication schedules, andintense emotional or sexual problems. The physician must try to foster arelationship of trust by using communication skills. These techniquesrequire patience and insight and are important in the therapeutic contentof the medical history.

Once the basic symptoms have been identified, each must be teasedapart and examined from all angles. This is accomplished by exploring theseven basic properties that differentiate a symptom of one disease from asymptom of another. These basic properties are:

Bodily location. The area of origin of the symptom and the area ofradiation 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 alsobe informative.

Quantity. A symptom’s quantity includes its severity, the number oftimes experienced, and its duration.

Chronology. The chronology of a symptom implies its onset (asprecisely as possible) and sequential development until the present.

Setting. The setting of the symptom includes the time of day or night, ifthe patient was active or resting, eating or fasting, emotionally upset orrelaxed, and at home or at work.

Aggravating or alleviating factors. The symptom should be furtherclarified by asking what the patient did to gain relief, if a change inposition was sought, and what the effects of movement, respiration,medication, etc. were.

Associated symptoms. Many diseases are manifested as aconstellation of associated symptoms that support a diagnosis when linkedtogether. The patient should be asked to describe other sensationsoccurring before, during, or after the major symptom.

2 3

Using these seven basic properties, the diagnostician can characterizethe symptoms and begin to consider possible disease entities. The historyis gently probed to provide the information necessary to diagnose orexclude the etiologic possibilities. For example, if the patient is "coughingup blood," the immediate possible causes may be bronchitis, pneumonia,tuberculosis, pulmonary embolus, lung tumor, or mitral stenos~s. After thesymptom is delineated as completely as possible, the patient is questionedin-depth for information that favors a more specific diagnosis or eliminatesseveral possibilities. The patient is asked to elaborate on each symptom orillness. Questions such as "When did you last feel well?" or "Did youconsider your health excellent before...?" may be useful.

It is desirable to trace the illness forward, beginning with its clinicalinception and progressing to the present time. Some patients accomplishthis with great skill, embellishing the story with vivid description. However,many patients are unable to remember dates accurately and may becomeconfused or flustered if pressed for exact details. Occasionally, a patient isunable to supply the physician with a clear idea of the illness and itschronological development. In this situation, the physician may need tosacrifice chronology to better comprehend the nature of the symptoms.For example, the physician might say, "Describe a typical attack," "Howlong is the shortest/longest/usual attack? .... Tell me approximately howmany attacks of chest pain you have each week. Have these increased infrequency lately?"

The experienced physician carefully prompts the patient with appropriatequestions so that all necessary information, both positive and negative, isgarnered before a different topic is pursued. Since the physician, not thepatient, has knowledge of disease processes and their clinicalpresentations, the physician should structure the clinical interview to allowa thorough and objective analysis of symptoms without leading the patientinto responses that fit the physician’s predetermined conception of theillness. The physician should also understand his or her own biases tointeract objectively with the patient.

Previous illnesses, past and current therapy, habits, allergies, familyhistory, occupational and daily living history, and review of systems arecarefully documented. The following questions offer important insight intothe life of the patient: "What do you like to do? .... How do you spend yourday? .... Who is important to you? .... What stresses are you under?"

At the close of the interview, the physician will find it valuable tosummarize his or her understanding of the information so the patient cancorrect it before the information is placed in the record.

The patient’s history may be supplemented by information from relativesand friends as well as charts and comments from other physicians whohave cared for the patient.

Cardiovascular Data Collection

The history of cardiovascular disease is an inseparable part of the totalmedical history, for important information may be overlooked unless allprevious illnesses, symptoms, habits and lifestyle, socioeconomicconsiderations, and family history are known. The steps in cardiovasculardata gathering are outlined below.

Historical EvidenceHave you ever had an illness or a problem related to your heart orblood 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?

SymptomsDo 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 andpalpitations are excluded, the symptoms are traceable to secondary effectsof heart disease on other organs, particularly the lung, brain, kidney, andblood vessels. If the patient answers any question affirmatively, thesymptom should be explored in more detail, using the approach outlinedin the previous chapter.

EtiologyThe clinician should try to establish an etiology by asking questions

directed to known causes of cardiovascular disease. The scope andnumber of questions are tailored to the patient, based on symptoms, priorillnesses, physical findings, and other information gathered.

The following list of etiologies of heart disease is taken from the NewYork Heart Association’s Nomenclature and Criteria for Diagnosis ofDiseases of the Heart and Great Vessels.

AcromegalyAlcoholismAmyloidosisAnemiaAnkylosing spondylitisAtherosclerosisCarcinoid tumor (argentaffinoma)Congenital anomalyFriedreich’s ataxiaGlycogen storage diseaseHemochromatosisHypersensitivity reactionHypertensionHyperthyroidismHypothyroidismInfectionMarfan’s syndromeMucopolysaccharidosis

NeoplasmObesityPolyarteritis nodosaProgressive muscular dystrophyProgressive systemic sclerosis

(scleroderma)Pulmonary disease (cor pulmonale)Reiter’s syndromeRheumatic arthritisRheumatic feverSarcoidosisSyphilisSystemic arteriovenous fistulaSystemic lupus erythematosusToxic agentTraumaUnknownUremia

Additional questions are also asked to discover the presence ofcoronary 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 geneticinfluence may be obvious, as in Marfan’s syndrome, or the inheritance maybe 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. Theabnormality may appear early or late in life, or remain clinically silent. Thepossibility of an inherited cardiovascular disorder should be sought byasking the patient if a family member has a similar problem. A familypedigree is also obtained and illnesses and causes of death carefullydocumented. A family history of birth defects, mental or physicalretardation, or unusual stature is important if congenital heart disease ispresent. The possibility of maternal rubella or teratogenic drugs takenduring the pregnancy should be considered. Early death of a familymember may also be significant.

6 7

Severity and Progression of DiseaseThis information is necessary so that the patient can be classified

according to the functional severity of the illness. Although there is arough correlation between severity of heart disease and the patient’ssymptoms and limitations, pathophysiologic impairment does not alwayscorrelate closely with symptoms. Many patients with heart disease areasymptomatic and their activity is unlimited. This is sometimes true evenwith advanced heart disease. Before further diagnostic studies andtherapy can be planned, it is essential to learn the patient’s capacities andlimitations by asking questions such as:

What are your current occupational and recreational activities andlimitations?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 haveshortness of breath/chest discomfort/fatigue/dizziness?Over the past year, have your activities become more limited or are yourcapabilities about the same?

After the patient has answered these questions, his or her physiologiccardiac status can be assessed with the following New York HeartAssociation classification:

1. Uncompromised

2. Slightly compromised3. Moderately compromised4. Severely compromised

Previous TherapyThis information provides the foundation for further therapy. It is particu-

larly important to ascertain if the patient understood and followed theprescribed diet and medications. The patient is often described as failingto respond to therapy when in reality he or she is not taking medicationscorrectly nor adhering to prescribed diets. The patient may be confusedabout the use of different medications or may not buy medicationsregularly because they are too expensive. These problems can often beresolved by asking the patient to bring his or her medicines to the officefor review.

The patient should be asked if the condition improved after starting amedication or after cardiovascular surgery. Careful analysis of dailyactivities, onset of symptoms, and the medication schedule may provideessential information for future therapy. The patient should also bequestioned about his or her understanding of the illness so thatappropriate education can be initiated.

In planning a therapeutic program, the physician must also consider thepatient’s age, interests, other illnesses and limitations, financial needs, homeenvironment, and willingness to participate and return for follow-up care.

98

Common Symptomsof Cardiovascular Disease

Chest PainAnalyzing the many causes of chest pain to arrive at a correct etiology

can vex even the most astute clinician. Although there are numerouscauses of chest pain, the most important are angina pectoris, myocardialinfarction, pericarditis, pulmonary embolus, dissection of the aorta, chestwall distress, and the pain of gastrointestinal disorders such as hiatalhernia, esophageal disease or spasm, cholecystitis, pancreatitis, andpeptic ulcer distress.

The features of angina pectoris are described below in detail by usingthe seven basic properties that separate angina pectoris from othercauses of chest pain. The distinguishing features of other causes ofchest pain are also discussed.

Angina Pectoris

In 1772, William Heberden described the clinical disorder he calledangina pectoris:

But there is a disorder of the breast marked with strong andpeculiar symptoms, considerable for the kind of danger belongingto it, and not extremely rare, which deserves to be mentionedmore at length. The seat of it, and sense of strangling, andanxiety with which it is attended, may make it not improperly becalled 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 apainful and most disagreeable sensation in the breast, whichseems as if it would extinguish life, if it were to increase or tocontinue; but the moment they stand still, all this uneasinessvanishes.*

*Heberden W: Commentaries on the History and Cure of Diseases. London, L Payne,News-Gate, 1802

This classic account beautifully describes features that are stillconsidered characteristic of angina pectoris. However, there are variationson the basic theme. When the patient’s history is not classic, thequestions must be very penetrating and all possible causes of chest painmust be considered. The diagnosis of angina pectoris has seriousemotional, prognostic, and economic implications and should not be madewithout a full understanding of the symptoms.

Bodily Location. Although the usual origin of the pain is the anteriormidchest, it is not uncommon for pain to originate or even be localized tothe epigastrium, neck or jaw, shoulders, elbows, or arms. Rarely, it may befelt only in the back. The discomfort is usually limited to the chest but mayradiate to the neck or down the left and sometimes the right arm. Onoccasion, it is felt simultaneously in the elbow or wrist. The arm may feelheavy or lifeless. It is very unusual for the pain to be pinpointed to a smallarea or localized to the apex of the heart. The patient usually indicates thelocation by a sweep of the hand across or up and down the chest or agripped hand over the area.

Quality. The qualities of angina pectoris that most distinguish it fromother causes of chest pain are tightness, squeezing, heaviness, pressure,and constriction. Sticking, stabbing, throbbing, or needle-like pain isseldom a symptom of angina pectoris. To complicate matters, somepatients experience angina as indigestion, cramping, burning, aching,sharp, gas-like, or indescribable. It may be difficult or even impossible todistinguish angina from other causes of chest pain on the basis of qualityalone. Many patients do not experience angina as "pain" and will stoutlydeny having chest pain. The experienced clinician asks, "Do you have anydiscomfort or unusual sensation in your chest?" If the answer remainsnegative, the patient should be pressed with more specific questions suchas "Do you have tightening or pressure sensations in your chest?" or ’~reyou limited in any way from exerting yourself fully?"

Recent studies have revealed that transient silent ischemia occurs fourto five times more frequently than painful episodes in patients with knowncoronary disease. The clinical significance of silent ischemia and itsrelation to arrhythmias, infarction, and sudden death are not yet fullyunderstood, but considerable progress is being made.

Chronology. The usual duration of angina pectoris is brief; it is typicallyless than 20 minutes. However, there are patients who describe their chestdiscomfort as lasting 30 minutes, an hour, or even more. On closequestioning, some patients have a relatively brief period of significant painfollowed by lingering chest discomfort. Other patients appear to have

10 11

prolonged myocardial ischemia without electrocardiographic or enzymaticevidence of myocardial injury. The exact nature and significance of thissustained pain is not known. It is probably wise to consider myocardialischemia as a spectrum, with angina pectoris at one end, myocardialinfarction at the other, and increasing degrees of ischemia in between thatmay cause loss of contractile tissue, arrhythmias, heart failure, and death.

Quantity. The severity of angina pectoris varies considerably from analmost unnoticeable vague discomfort to an intense pain that immediatelygrips and immobilizes the patient. Generally, the pain is not unbearableand can be tolerated and eased by ceasing activities or calming down.Many patients learn to limit their exertion so that they can live within theboundaries of their exercise tolerance without experiencing chest pain.

It is important to determine if the frequency of angina pectoris isincreasing, unchanged, or less frequent, and if the angina is nowproduced by less effort, no effort, or while sleeping. The number ofnitroglycerin 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 occupationsor 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 combinghair or shaving in the morning, walking into a cold wind, running, climbingstairs, playing with the children, sexual intercourse, tension at work, aheavy meal, an exciting athletic event, or arguing with a family member.Angina may also occur while sweeping, changing beds, and raising thearms overhead to wash windows, brush hair, or place objects in highcabinets. Angina pectoris is worse with morning activities; similar stresseslater in the day may be easily tolerated. A knowledge of the setting maypermit 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 Prinzmetal’s variant angina,typically occurs during rest and may recur in a nightly cyclic pattern.ST-segment elevation or depression on the electrocardiogram andcoronary artery spasm have been documented during an attack.

Aggravating or alleviating factors. Angina pectoris is often related tostress and is relieved by ending or controlling the stress. Cardiac stressincludes 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 explainedby changes in coronary tone, spasm of the coronary artery or plateletplugs superimposed on fixed coronary obstruction, or, infrequently, in theabsence of significant narrowing.

Angina pectoris is usually promptly relieved or lessened by emotionaland physical rest as well as by nitroglycerin. Since the effect of nitroglycerinis quite rapid, usually immediate or within 3 minutes, the patient should beasked how quickly the pain left. If the discomfort abates after 10 minutes,it is unlikely that nitroglycerin was responsible. Nitroglycerin is not effectivefor all patients with angina, nor is it specific for angina pectoris since itcan alleviate chest pain of other etiology.

Associated symptoms. While angina may be manifested only as pain,other symptoms, including dyspnea, palpitations, dizziness, and nauseamay also occur or appear as the sole manifestation. "Silent" ischemiamay appear as an arrhythmia or sudden death.

Myocardial InfarctionThe pain of myocardial infarction is usually, though not always, more

intense than angina pectoris and often exceeds 30 minutes in duration. Itoften has a different quality, described as heavy, vise-like, crushing,expanding, or squeezing. The patient may not be able to describe thepain other than to say it was severe or intolerable. Radiation of pain fromthe chest to the shoulders, neck, or arms is common. Associatedsymptoms, including nausea, vomiting, sweating, dizziness, syncope,marked weakness, palpitations, urge to defecate (chezonisus), fear ofdeath (angor animi), and dyspnea may be prominent.

Because many patients ascribe the discomfort of angina pectoris ormyocardial infarction to indigestion, the complaint of indigestion bearsparticular scrutiny. Occasionally, a myocardial infarction is manifested asacute abdominal pain, tenderness, rigidity, and vomiting. Rarely, the painis felt only in the back, neck, or shoulders.

The diagnosis of myocardial infarction often demands that the physicianmaintain a high index of suspicion since the pain may be absent, insignifi-cant, or attributed to other causes such as indigestion or gas. Other signs,including unexplained heart failure, weakness, syncope, or arrhythmiasmay be the major manifestation suggesting an acute myocardial infarction.Patients who have had no recognized symptoms are sometimes found tohave had a myocardial infarction on routine ECG or at autopsy. Theincidence of silent infarction may be as high as 30%. Diagnosis of thesepatients may confound even the most astute diagnostician.

Pericarditis

The pain of pericarditis is similar to myocardial infarction in its midchestlocation and occasional radiation into the arm. On close questioning, thepatient with pericarditis will usually describe the pain as sharp, unlike thepain of myocardial infarction. Accentuation of the pain with inspiration,

12 13

swallowing, on lying down, and with movement, as well as containment ofpain when leaning forward or breathing shallowly, is almost diagnostic.Radiation of the pain to the left trapezial ridge or scapula and awarenessthat the intensity of the pain coincides with the heartbeat is characteristicbut not always present. The pain may be sudden or gradual in onset andmay fluctuate from mild to severe. Relief of the pain with steroids but notwith narcotics is typical. Surprisingly, some patients may have pericarditisbut not experience any chest discomfort.

Pulmonary Emboius

A large pulmonary embolus that produces infarction of the lung isusually easily diagnosed by the sudden onset of sharp, pleuritic chestpain, dyspnea, hemoptysis, cyanosis, and tachycardia. More commonly,pulmonary emboli do not result in pulmonary infarction and may provide adiagnostic dilemma. The diagnosis of pulmonary emboli should beconsidered if there is pleuritic pain, unexplained dyspnea (particularly ifthe 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 diag-nosis. Since pulmonary emboli usually occur in the setting of venous injury,venous stasis, or alteration of blood coagulation, questions should be directedto precipitating causes. The following information should be obtained:

Prior history of pulmonary emboliPresence of leg or calf tendernessHistory of heart, lung, or blood diseaseRecent surgery (particularly hip surgery), pregnancy, trauma, bed rest, orlong car tripUse of oral contraceptivesUse of constricting girdle or garterOccupation (prolonged standing)Presence of varicose veins or previous vein stripping

By realizing that pulmonary emboli occur in certain settings, particularlyin hospitalized patients, and that their clinical presentation is rarely classic,the clinician may be able to make the diagnosis.

Aortic DiseaseA dissection of the aorta is usually announced by sudden, severe,

midline pain often described as tearing or ripping. The pain may radiatefrom front to back or down the midline into the abdomen or lower back.The severity of the pain classically peaks at the onset. Symptoms ofvascular occlusion elsewhere, including myocardial infarction, may follow.On occasion, this pain cannot be separated from other causes of chestpain 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 ishighly 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 chestwall, the patient may suffer from a boring, throbbing, or steady pain that islocalized in one area and prolonged or continuous.

Gastrointestinal DiseaseGastrointestinal disease, including esophagitis, esophageal spasm,

hiatal hernia, gastric or duodenal ulcer, erosive gastritis, dyspepsia,cholecystitis, biliary dyskinesia, and pancreatitis may occasionally appearas chest pain simulating ischemic heart disease. The most suggestiveclues to gastrointestinal disease are heartburn relieved by antacids,dysphagia, and painful swallowing (odynophagia). Esophageal disease,especially esophageal spasm, is particularly difficult to distinguish fromangina pectoris because both cause squeezing or pressure up and downthe midchest and radiation of pain to the neck, jaw, and arms, which isquickly relieved by sublingual nitroglycerin. Esophageal disease issuggested when the pain is related to eating, bending over, orrecumbency. Dysphagia is sometimes present. Although biliary disease,gastric or duodenal ulcer, and pancreatitis can cause chest pain, closequestioning usually reveals that the pain begins in the abdomen andradiates to the chest.

The Chest WallThe 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 Tietze’ssyndrome, costochondritis, xyphoidalgia, myofascial pain, hyperventilationsyndrome, precordial catch, slipping rib syndrome, cardiac causalgia,herpes zoster, and trauma. The pain that may result from any of theseproblems is often in the midchest or left anterior chest and may radiate tothe neck, shoulders, and arms. An aching or pressing sensation iscommon. The patient is naturally alarmed over the possibility of a heart

1415

attack and diverts the physician’s attention to the heart and away from thechest wall. Careful questioning of the patient and a thorough examinationof the anterior and posterior chest is essential to make the diagnosis.

Mitral Valve ProlapseMitral valve prolapse is now recognized as a common finding, present in

4-6% of the population, with a 2:1 female4o-male prevalence. The vastmajority of these patients are asymptomatic; however, a small subset ofpatients complain of chest pain, palpitations, fatigue, and dizzy spells. Thechest discomfort may have some features that suggest angina, such asheaviness or a midchest location, but it is rarely precipitated by exertion.The pain is most commonly described as sharp or sticking and is locatednear the cardiac apex. It may be fleeting or last for hours.

Shortness of BreathDyspnea implies difficulty in breathing and is a symptom common to

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

Left Ventricular FailureThe most characteristic features of dyspnea due to left ventricular

failure are:

Exertional dyspnea. Dyspnea on exertion becomes apparent duringhousework, athletic activities, while walking several blocks, or climbingsteps. In assessing severity and progression of heart disease, thephysician must determine the amount of activity necessary to producedyspnea and compare current activities with previous capabilities.Infrequently, the patient with angina pectoris notices chest tightness andshortness of breath occurring at the same moment of exertion. It may bedifficult to tell if the patient’s limitation is due to angina, dyspnea, or both.Indeed, the mechanism of the dyspnea may be an elevation in leftventricular diastolic pressure related to myocardial ischemia.

Orthopnea. During the day, gravitational effects on the control of fluidbalance may favor a loss of intravascular fluid into the interstitial space.When the patient is in a horizontal position, the edema fluid may return tothe vascular system, augmenting intrathoracic blood volume and decreasingthe vital capacity of the lung. The patient is unable to breathe easily whenlying down and must elevate his or her head on pillows to breathecomfortably. Since many people normally sleep on several pillows, thepatient must be asked, "Why do you sleep on several pillows? ....Whathappens if you roll off your pillows?" The degree of orthopnea ismeasured by the number of pillows used, for example, three-pilloworthopnea. As cardiac failure becomes advanced, the patient may actuallybe forced to sleep in an upright position or in a chair.

Paroxysmal nocturnal dyspnea. Some time after retiring, the patient issuddenly 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 windowfor relief. After several minutes the patient is able to return to bed. Parox-ysmal dyspnea may recur later in the night.

Trepopnea. The patient with cardiac disease is frequently unable to lieon his or her side, particularly the left side, because he or she experiencesdyspnea, palpitations, or an uncomfortable sensation. This condition,called "trepopnea," is a common symptom, although it is not usuallymentioned by the patient.

Pulmonary edema. Severe left ventricular failure may produce suchoverwhelming pulmonary congestion that the patient actually gurgles forthpink, frothy sputum with deep, desperate respiratory efforts.

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

Other Causes of Dyspnea

Pulmonary emboli. Dyspnea caused by pulmonary emboli may appeardramatically 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 dyspneais usually suggested by evidence of lung disease such as a cough, wheez-ing, sputum, or a history of smoking or bronchitis. Severe bronchospasmappearing as asthma is occasionally a manifestation of left ventricularfailure. The chest x-ray and presence or absence of heart disease canusually be used to sort out the cause.

16 17

Hyperventilation. Dyspnea related to anxiety and attendant hyperventi-lation is very common and may provide a thorny differential diagnosis,particularly because hyperventilation often causes chest discomfortsimulating angina. Patients with breathlessness due to hyperventilationoften describe their symptoms as "The air doesn’t go all the way down..."or "1 can’t get a full breath." The patient should be carefully observed forsigns of sighing, swallowing of air, and anxiety, and should be asked aboutother symptoms of hyperventilation such as tingling or numbness in thehands ("falling asleep") or around the mouth, dryness of the mouth, anddizziness. When anxiety is associated with organic heart or lung disease,determining the major contributing cause of the dyspnea may be perplexing.

Dizziness and SyncopeThe 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 blackingout, swimming in the head, graying of vision, lightheadedness, or falling-out spells. Vertigo, a spinning sensation, must be carefully differentiatedfrom dizziness. The term "syncope" implies a temporary loss ofconsciousness and postural tone that may or may not be preceded bydizziness. An episode of dizziness and temporary loss of postural tonewithout complete loss of consciousness is referred to as "near syncope."

Since the physician rarely has the opportunity to observe the episode ofsyncope, the diagnosis is almost always based on a history provided by thepatient 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 spinningor 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 roomincreased activityfatiguehungeranxiety or other emotionsight of blood or anticipation of injuryrecent 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 ratechest pain or discomfortyawning; ringing in the ear; sweating; weakness; sighing; nausea;

numbness; staggering or lack of coordination; confusion; slurredspeech; paralysis of arm, leg, or face; loss of bladder (bowel) control

visual lossheadacheanxiety

What was the duration of symptoms before and after the attack?Have you had any of the following?

anemia or blood lossdrugs to lower your blood pressuresurgery to cut nerves (sympathectomy)history of heart murmur, slow or fast heart rate, heart diseasehistory of stroke, seizure disorder, brain disease, syphilis, diabetes,

pernicious anemia, multiple sclerosis, amyloidosis, syringomyeliaemotional disorder or recent emotional stressmigraine

Cardiovascular Causes

Dizziness or syncope related to the cardiovascular system may be theconsequence of a number of mechanisms, including the following.

18 19

Arrhythmias. Very slow ventricular rates, as seen with atrioventricularblock (Morgagni-Adams-Stokes syndrome) or long sinus pauses, and veryrapid ventricular or supraventricular rhythms may impair cerebral bloodflow. Even ventricuiar fibrillation may be brief and self-reverting and attestedto only by dizziness or syncope. Although syncope may be sudden, thepatient often experiences a momentary dizzy spell or a blurring of visionbefore loss of consciousness if an arrhythmia is the cause. Attacks canoccur while erect or recumbent. Symptoms related to automatic dischargesuch as nausea, sweating, epigastric discomfort, and weakness are notusually experienced. Convulsions secondary to decreased cerebral bloodflow may occur. Arrhythmias are now recognized as a common cause ofsyncope in patients with cerebrovascular disease.

Patients whose ECG shows a prolonged QT interval may be particularlysusceptible to syncope secondary to ventricular arrhythmias, includingventricular tachycardia and ventricular fibrillation. The prolonged QT intervalsyndrome may be an inherited or acquired disorder. A careful family historymay disclose episodes of syncope or sudden death among relatives.

Obstruction to blood flow. Dizziness or syncopal spells can beproduced by an obstruction to blood flow through the heart or lungscaused by valvular aortic stenosis, hypertrophic subaortic stenosis, mitralstenosis, atrial myxoma, atrial thrombus, valvular pulmonary stenosis,tetralogy of Fallot, primary pulmonary hypertension, pulmonary emboli,pericardial tamponade, and prosthetic valve dysfunction. Arrhythmias andperipheral vasodilatation related to reflexes or inadequate coronary bloodflow may contribute to the symptoms.

Reflexes affecting heart rate and blood pressure. Vasodepressor(vasovagal) syncope is a very common cause of dizziness or syncope thatcharacteristically occurs in response to fear of injury, the sight of blood orinjury, or sudden emotional stress. Anxiety, physical or mental exhaustion,debility, a heavy meal, stuffy environment, pregnancy, or anemia arepredisposing factors. Syncope is always preceded by warning symptomssuch as nausea, weakness, sweating, epigastric discomfort, blurred vision,headache, tinnitus, difficulty concentrating, sighing, and dizziness. Theheart rate falls, and the patient appears pale and ill at ease. The syncopeis transient, lasting a few seconds to a few minutes, and may be preventedby immediately lying down. During recovery the patient is weak, dizzy, andnauseated, although mentally clear. Symptoms may recur when standing.Rarely, this form of syncope can occur while the patient is recumbent.

Orthostatic hypotension produces dizziness on arising or after prolongedstanding and can be related to reduced effective blood volume, autonomicnervous system dysfunction, or, rarely, to circulating vasodilatorsubstances. Dizziness on arising is a common symptom, particularly in theelderly, and does not necessarily imply an underlying problem requiringextensive investigation. Contributing causes such as drugs (particularlyantihypertensive or antidepressant medications, vasodilators, and 9-blockers), anemia, low blood volume, large varicose veins, and pregnancyshould be considered. Addison’s disease is a rare cause of posturalhypotension. Orthostatic hypotension may also be produced by a faultyautonomic nervous system response to assumption of an upright position.This can occur after prolonged recumbency or with neurologic diseasessuch as diabetic neuropathy, multiple sclerosis, syringomyelia, amyloidosis,pernicious anemia, and tabes dorsalis. An idiopathic form of orthostatichypotension occurs and is often associated with inability to sweat, sexualimpotence, and incontinence.

Hypersensitive carotid sinus is suspected when the patient describesdizziness or syncope after hyperextension of the neck, turning of the head,or pressure over the area of the carotid sinus from a necktie or duringshaving. The patient may not be aware of the association or there may beno 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 nonpro-ductive violent coughing. The victims are almost exclusively middle-aged,overweight men with lung disease.

Micturition syncope is diagnosed when syncope occurs during or afterurination. The person has almost always just arisen from a period ofprolonged recumbency. Onset is abrupt with little or no warning; durationis 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.

2O 21

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 toobstruction to the cerebral blood flow. The syncopal episode is oftenprolonged, and the postsyncopal period is characterized by confusion,weakness, or focal neurologic signs.

Dizziness or syncope associated with upper arm exercise may lead todiagnosis of a subclavian steal syndrome. This occurs when a severeobstruction in the proximal subclavian artery allows shunting of blood awayfrom the cerebral circulation through the vertebral artery to the distalsubclavian artery. Upper arm exercise drops the vascular resistance distalto the subclavian artery obstruction and enhances the "steal."

Epilepsy. Seizures may be difficult to distinguish from vasodepressorsyncope since both are often precipitated by fatigue and anxiety. An auraoften precedes the epileptic attack. Tonic or cIonic movements may bewitnessed. Loss of bladder or bowel control and biting of the tongue arecommon in seizures but also occur with other forms of syncope. Thepostictal period is usually prolonged, and the patient is confused or unableto speak or move with ease.

Hyperventilation. Hyperventilation, a cause of dizziness and,occasionally, syncope, is very common and a frequent reason foremergency room visits. Early symptoms include tingling or numbness inthe hands, fingers, and around the mouth, dryness of the mouth, and afeeling of smothering and apprehension, which may progress to severeweakness, 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 notprolonged unless hyperventilation persists.

Idiopathic syncope. Even after careful historical analysis, themechanism of syncope may be unexplained in more than 50% of patients.

22

PalpitationsIrregularities of the heartbeat or tachyarrhythmias may be silent or expe-

rienced by the patient as palpitations, skipping, heart flutter, jumping in thechest, or a runaway heart. Ambulatory monitoring studies have shown thatthese sensations are often due solely to a heightened awareness of thenormal heartbeat, particularly when the patient is lying still in bed or isemotionally upset, or for no apparent reason. An arrhythmia may alsocreate a secondary effect such as dizziness, syncope, seizure, blurredvision, chest discomfort, or dyspnea.

Isolated premature atrial or ventricular beats are common and unnoticedby most people. However, some people are very aware of the irregularity orthe forceful postextrasystolic contraction and may seek advice andreassurance.

Atrial tachycardia (AV nodal reentry) is often abrupt in onset andtermination and quite regular in rhythm as contrasted with atrial fibrillation,which is generally irregular and less striking in the suddenness of itsinitiation and termination. When atrial fibrillation is rapid and irregular, thepatient may describe the feeling as a "thumping or fluttering in the chest."The symptoms caused by these arrhythmias may overlap, or the patientmay not recognize these features.

Ventricular tachycardia may be easily tolerated even if the heart is verydiseased. If the patient has significant coronary or myocardial disease, thecommon manifestations are dizziness or syncope, chest pain, anddyspnea. The patient may or may not appreciate the presence of the rapidheartbeat. Sometimes the patient comes to the emergency room in shockor severe heart failure and is discovered to have ventricular tachycardia.

Patients who take digitalis or have permanent cardiac pacemakers or alarge stroke volume (as occurs with aortic regurgitation) are sometimesfrightened by the forcefulness of their heartbeat.

Diagnosis may be difficult because of the diversity of presentation andthe frequent disappearance of arrhythmia by the time the patient sees aphysician. The following questions are often helpful in searching foroccurrence 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?

23

Can you mimic the rate and rhythm by patting your fingers on top of theother hand?Were there associated symptoms such as:

chest discomfort?weakness?dizziness?fainting?visual blurring?sweating?

Prior Attacks

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 anECG during an attack?Have you found any positions, maneuvers, or medications that have haltedor 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?

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

FatigueFatigue is a common symptom of heart disease and an important

consequence of heart failure. Unfortunately, the stress and anxiety of dailylife make this symptom so common that the response to the question "Doyou tire easily?" is usually affirmative. A positive response assumes moreimportance when the patient has previously enjoyed unlimited exercisetolerance. In evaluating the progression of cardiac disease, it is helpful toask questions that allow the patient to compare current abilities with easilyremembered past events: "Were you able to do all the housework thisChristmas? .... Could you play two sets of tennis last summer?" Somepatients with heart disease will decrease their activities so gradually thatthey are not aware of the underlying cardiovascular disease or itsprogression. This is particularly true with mitral stenosis.

Edema

Retention of salt and water in patients with cardiac disease and heartfailure 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 orpuffiness around the ankles. Since gravity promotes fluid extravasationfrom intravascular to extravascular spaces, the edema becomes worse asthe day progresses and generally disappears or improves with nighttimerecumbency. The return of fluid to the vascular system at night producesnighttime diuresis, and patients complain that they frequently arise tourinate. As heart failure progresses, fluid accumulation may involve othertissues, 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 dis-tention and bloating. Right upper quadrant pain and tenderness may alsooccur as a result of hepatic congestion from high central venous pressure.

Cardiac disease is only one of several possible explanations for fluidretention. Often several factors contribute to formation of edema.

24 25

Intermittent ClaudicationClaudication is produced when the blood supply to exercising muscles

is inadequate. This is usually due to significant atherosclerotic obstructionto 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 doesnot match the metabolic demands of the tissue, and ischemia results. Thepatient notices a cramp, charley horse, ache, or weakness that improveswith rest but recurs when exercise is resumed. The severity and locationof the problem is measured by asking the patient where the discomfortoccurs (foot, calf, thigh, or buttocks) and how much exertion is required toproduce it: "How far can you walk without resting?" This can be quantifiedas two-block claudication of the gluteal muscles and calves bilaterally. Asclaudication progresses, the patient’s 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 anerection. This is sometimes why the patient seeks medical advice.

When arterial disease is severe, ischemic discomfort may be present atrest. The pain is described as boring, aching, intense, or steady. Thepatient is usually restless, unable to sleep, or forced to dangle the leg overthe side of the bed for slight relief.

CyanosisAlthough 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. Thisinformation is extremely important in the infant, as it suggests thepresence of congenital heart disease with right-to-left shunting of theunderoxygenated blood into the arterial circulation. Cyanosis may beapparent only when the child is crying, feeding, or exercising vigorously.Additional information is gained by asking if cyanosis was present at birthor if it appeared later in life.

Cyanosis in the adult has less specific implications and may be due tolung disease, pulmonary emboli, congenital heart disease, or abnormalhemoglobins. Cyanosis with dyspnea should always suggest the presenceof a large occluding pulmonary embolus. Cyanosis is not a sign ofcongestive heart failure unless there is severe impairment of peripheralcapillary blood flow.

Rheumatic FeverAt one time, acute rheumatic fever was erroneously diagnosed in many

patients with joint or muscle pain or a heart murmur. For this reason, ahistory of rheumatic fever as a child must not be accepted at face value.Although the patient may not remember details of the illness, the physicianshould carefully review the facts and determine if they conform to currentconcepts of rheumatic fever. Conversely, many patients who have evidenceof rheumatic heart disease do not have a history of acute rheumatic fever.

The patient or the patient’s parents should be asked if a sore throatoccurred within 1 month before onset of the illness. Arthritis should befurther defined by asking which joints were involved and the sequence ofthe joint involvement. Arthritis, a major criterion, must be distinguishedfrom the subjective complaint, arthralgia, a minor criterion, by asking if thejoint(s) was swollen, hot, red, tender, or limited in motion. Typically, acuterheumatic fever causes an inflammation of the larger joints, particularly theknees and ankles, but also the elbows, wrists, shoulders, and hips, andmore rarely, the small joints of the hand. Arthritis is occasionallymonoarticular but characteristically migrates from joint to joint withoutpermanent deformity and usually disappears within 3 weeks.

A history of carditis may be difficult to establish. The patient should beasked if a murmur was heard by the physician during or after the illnessand if the heart was enlarged or symptoms of heart failure were present. Ahistory of rejection by the military service or an insurance companybecause 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. Thepatient should be asked if a rash occurred during the illness. If so, thelocation, size, and color of the rash should be noted and whether it wastender or pruritic. Subcutaneous nodules can be a helpful historical clue;however, they are seldom noticed by the patient.

Rheumatic (Sydenham’s) chorea consists of involuntary, brief, nonrepetitivemovements of a body part. Parents may often recognize a change in thechild’s usual behavior or coordination, described as frequent grimacing,nervousness, or awkwardness such as dropping dishes, difficulty buttoningclothes, or tripping. In mild cases, the parents may describe the child asbeing "fidgety." School performance also declines.

Diagnostic criteria for acute rheumatic fever were greatly clarified byintroduction of the Jones criteria in 1944. These criteria were revised in1982 and include the following.

26 27

Major Manifestations

CarditisPolyarthritisChoreaErythema marginatumSubcutaneous nodules

Minor Manifestations

ClinicalPrevious rheumatic fever or rheumatic heart diseaseArthralgiaFever

LaboratoryAcute phase reactants

Erythrocyte sedimentation rateC-reactive protein, leukocytosis

Prolonged PR interval

Supporting Evidence of a Preceding Streptococcal Infection

Rheumatic fever is suggested by the presence of two major criteria, orone major and two minor criteria, if there is evidence of a preceding groupA streptococcal infection such as positive throat culture or serologicresponse.

A more detailed discussion of diagnostic criteria can be found in JonesCriteria (Revised) for Guidance in the Diagnosis of Rheumatic Fever (AHApublication No. 70-016-B), which was reprinted in Circulation(1984;69:203A) and is available from the American Heart Association.

Conclusion

History-taking is not confined to a single time or location but is acontinuing accumulation of information throughout the patient-physicianrelationship. As physical findings are discovered or as laboratoryinformation is obtained, the clinician should renew the historical pursuit toexpand the original data base and reevaluate the initial diagnosis. Inaddition, valuable information not remembered initially may surface as thepatient mulls over the original questions.

2829

Suggested Reading

Beckman HB, Frankel RM: The effect of physician behavior on the collection of data. AnnIntern Med 1984;101:692-696Duffy DL, Hamerman D, Cohen MA: Communication skills of house officers. Ann InternMed 1980;93:354-357Enelow A J, Swisher SN (eds): Interviewing and Patient Care, ed 2. New York/Oxford,Oxford University Press, 1979Fletcher 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 J1980;281:931-933Fletcher C: Listening and talking to patients. II1: The exposition. Br Med J1980;281:994-996Fletcher C: Listening and talking to patients. IV: Some special problems. Br Med J1980 ;281:1056 - 1058Hurst JW: The Heart, ed 7. New York, McGraw-Hill Book Co, 1990Morgan WL Jr, Engel GL (eds): The Clinical Approach to the Patient. Philadelphia, WBSaunders Co, 1969, pp 1-79Platt FW, McMath JC: Clinical hypocompetence: The interview. Ann Intern Med1979;91:898 - 902New York Heart Association Criteria Committee: Nomenclature and Criteria for Diagnosis ofDiseases of the Heart and Great Vessels, ed 8. Boston, Little, Brown & Co, 1979Tumulty 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

Your contributions to theAmerican Heart Associationwill support research thathelps make publications likethis possible.

For more information,contact your local AmericanHeart Association or call1-800-AHA-USA 1(1-800-242-8721).

American Heart ~Association~Fighting Heart Disease

and StrokeNational Center7272 Greenville AvenueDallas, TX 75231-4596

7O- 10296-9490 03 30 A