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Official reprint from UpToDate


www.uptodate.com 2015 UpToDate

Diagnostic approach to chest pain in adults


Author
James L Meisel, MD, FACP

Section Editor
Mark D Aronson, MD

Deputy Editor
Lee Park, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2015. | This topic last updated: May 22, 2014.
INTRODUCTION The patient who describes chest pain to the primary care physician represents an immediate
challenge. The symptom is usually of benign etiology, but rarely it may portend imminent catastrophe. Although
standard textbooks of medicine often emphasize the high-risk nature of chest pain, non-life-threatening etiologies,
which may be functionally disabling, are much more common in the primary care setting and require a
cost-effective approach to diagnosis [1-3]. The correct diagnosis is most often derived from a vigilantly obtained,
detailed history (pain description; associated symptoms; and in some cases disease risk factors) that is supported
by specific physical findings, an electrocardiogram, and/or chest x-ray.
Importantly, the prevalence of chest pain etiologies varies according to the population studied [4]. The causes of
chest pain that are most common in primary care practice and the diagnostic approach in the office for chest pain
of uncertain etiology are reviewed here. A more complete discussion of the differential diagnosis of chest pain is
found separately. (See "Differential diagnosis of chest pain in adults".)
EPIDEMIOLOGY IN PRIMARY CARE POPULATIONS A prospective study of 399 episodes of chest pain in
patients seen in multiple outpatient centers over a one-year period noted the following prevalences of various
causes of chest pain (table 1) [5]:
Approximately 60 percent of chest pain diagnoses were not "organic" in origin (ie, not due to cardiac,
gastrointestinal, or pulmonary disease).
Musculoskeletal chest pain accounted for 36 percent of all diagnoses (of which costochondritis accounted for
13 percent) followed by reflux esophagitis (13 percent).
Stable angina pectoris was responsible for 11 percent of chest pain episodes; unstable angina or myocardial
infarction occurred in only 1.5 percent. Nevertheless, most of the ancillary diagnostic testing used was
directed toward finding or excluding a cause of coronary disease.
These observations are consistent with other reports of the frequency of etiologies of chest pain in primary care
practice [1,2,4,6,7].
The presence of risk factors and the age of the patient population are important contributors to coronary artery
disease (CHD) prevalence. (See "Overview of the risk equivalents and established risk factors for cardiovascular
disease".) In one retrospective review, as an example, only 7 percent of patients less than age 35 who had chest
pain were diagnosed with CHD [8]. In contrast, the incidence of cardiac diagnoses may exceed 50 percent in
patients with chest pain after the age of 40 [9-11].
A more complete discussion of the differential diagnosis of chest pain is found separately. (See "Differential
diagnosis of chest pain in adults".)
EMERGENCY RESPONSE TO CHEST PAIN IN THE OFFICE Chest pain due to myocardial infarction,
pulmonary embolus, aortic dissection, or tension pneumothorax may result in sudden death. Any patient with a
recent onset of chest pain, especially when the symptoms are ongoing, who may be potentially unstable based
upon history, appearance, or vital signs, should be transported immediately to an emergency department in an
ambulance equipped with a defibrillator. Stabilization of such patients should begin in the prehospital setting and
includes intravenous access, placement of a cardiac monitor, and supplemental oxygen if breathlessness,
hypoxemia, or signs of heart failure or shock are present [12]. Noninvasive monitoring of oxygen saturation may be
used to decide on the need for oxygen administration. A 12-lead electrocardiogram and a blood sample for cardiac
enzyme measurement should be obtained if possible. (See "Evaluation of the adult with chest pain in the
emergency department".)

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Patients who are thought to be experiencing an acute coronary syndrome (ACS) should chew a 325 mg aspirin
tablet. Sublingual nitroglycerin should be given for chest pain unless the patient has relatively low blood pressure
without intravenous access or has recently taken a phosphodiesterase inhibitor such as sildenafil (Viagra).
Further assessment should be conducted in the emergency department. (See "Initial evaluation and management
of suspected acute coronary syndrome in the emergency department".)
EVALUATION The office evaluation of new onset chest pain in stable individuals should begin with the
consideration of imminently life-threatening causes (including acute coronary syndrome, pulmonary embolus, aortic
dissection, pneumothorax, and esophageal rupture). This is usually accomplished using clinical judgement, along
with ECG testing, and less frequently exercise testing, other noninvasive testing, or invasive angiography. (See
"Evaluation of the adult with chest pain in the emergency department", section on 'Life-threatening conditions' and
"Initial evaluation and management of suspected acute coronary syndrome in the emergency department", section
on 'Clinical presentation' and "Primary spontaneous pneumothorax in adults", section on 'Clinical presentation' and
"Clinical presentation, evaluation, and diagnosis of the adult with suspected acute pulmonary embolism" and
"Boerhaave syndrome: Effort rupture of the esophagus", section on 'Clinical manifestations' and "Stress testing for
the diagnosis of obstructive coronary heart disease".)
Once a life-threatening etiology has been excluded, attempts should be made to identify the specific cause of
symptoms and begin treatment. A diagnostic pattern will frequently emerge, based upon the patient's risk factors,
description of the pain, and associated symptoms.
In the primary care setting, the history (description of chest pain, associated symptoms and risk factors) and
physical examination, complemented by selected tests such as an electrocardiogram or chest radiograph, allow
the physician to accurately diagnose most causes of chest pain and to judge which patients likely have a benign
etiology. As an example, one study found that physicians were able to correctly diagnose a nonorganic (ie, not due
to cardiac, gastrointestinal, or pulmonary disease) versus organic cause of chest pain in 88 percent of patients
using only the history and physical examination [1]. In the remaining 12 percent who were misdiagnosed as having
chest pain of organic etiology, most of the diagnoses were made with little confidence.
Several studies suggest that a diagnosis of "nonspecific" chest pain carries risk of increased mortality, especially
due to ischemic heart disease [13-16]. Thus, a diagnosis of nonspecific chest pain should be made cautiously and
may indicate the need for vigilant follow-up. A diagnosis of "noncardiac" or "atypical" chest pain is not very useful
outside of a coronary care setting.
The clinical evaluation is also useful to estimate the pretest probability of organic causes of chest pain prior to
undergoing diagnostic tests (eg, stress ECG testing to detect CHD or d-dimer, CT-angiography or lung perfusion
scanning to detect pulmonary embolism) [17,18]. Pretest probability is an important component of the
interpretation of these test results. (See "Stress testing for the diagnosis of obstructive coronary heart disease"
and "Clinical presentation, evaluation, and diagnosis of the adult with suspected acute pulmonary embolism".)
The chest pain history is less useful in patients suspected of having an acute coronary syndrome (ACS) [19,20]. As
an example, one article reviewed studies in which at least one chest pain characteristic was described in patients
subsequently found to have an ACS [19]. Although certain elements of the chest pain history were associated with
increased or decreased likelihoods of ACS, none of them alone or in combination identified a group of patients in
whom the diagnosis could be safely excluded. (See "Initial evaluation and management of suspected acute
coronary syndrome in the emergency department".)
Conversely, in patients with stable, intermittent chest pain, a description of typical angina (ie, substernal
discomfort, precipitated by exertion, improved with rest or nitroglycerin in less than ten minutes with many patients
reporting radiation to shoulders, jaw, or inner arm) was a moderately strong predictor of obstructive epicardial
CHD [20]. Other causes of anginal chest pain include valvular heart disease, pulmonary hypertension, and cardiac
syndrome X. (See "Angina pectoris: Chest pain caused by myocardial ischemia" and "Valvular heart disease in
elderly adults" and "Overview of pulmonary hypertension in adults" and "Cardiac syndrome X: Angina pectoris with
normal coronary arteries".)
The patient's style of presentation will influence the physician's subjective judgment and clinical reasoning [21]. This
was illustrated in a study of 44 male internists who were randomized to watch a video of an actress with classical
angina symptoms interacting with a physician in a "businesslike" fashion, using a scripted interview, or the same

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actress and script presented in a "histrionic" fashion; a third group read a verbatim transcript of the interview [22].
A cardiac cause for the chest pain was suspected by 50 and 13 percent of physicians viewing the businesslike and
histrionic portrayals, respectively; the estimated incidence of CHD was 20 versus 10 percent. The internist's
assessment of the risk of CHD was similar among the different groups after viewing some objective data.
Nevertheless, the physicians viewing the histrionic portrayal were far less likely to pursue a cardiac workup (53
versus 93 percent). This study illustrates the importance of maintaining a high degree of diagnostic objectivity
during the evaluation.
Description of chest pain A thorough description of the pain is an essential first step in the diagnosis of chest
pain (table 2). (See "Differential diagnosis of chest pain in adults".)
Descriptions of chest discomfort due to myocardial ischemia may differ depending on patients' culture [23], gender,
age and presence of comorbid conditions such as diabetes. The Women's Ischemia Syndrome Evaluation (WISE)
study clearly documented gender differences in the diagnosis, prognosis and pathophysiology of ischemic heart
disease [24]. As another example, a study of patients undergoing exercise stress testing with perfusion imaging
reviewed symptoms in 38 women and 94 men who had both angina and imaging evidence of ischemia [25].
Compared with men, women rated their chest pain as more intense, used different terms to describe the pain
(more often "sharp" and "burning"), and more frequently had pain and other sensations in the neck and throat.
Quality of the pain Certain descriptors of chest pain (pleuritic, positional, sharp, reproducible with
palpation) are weakly correlated with decreased likelihood of ACS, whereas as other characteristics (radiation to
shoulders/arms or precipitated by exertion) are associated with an increased likelihood [19]. However, these
characteristics are only weakly-associated with ACS. Thus, no symptom alone or in combination allows safe
discharge of patients without physical examination and diagnostic testing.
The patient with myocardial ischemia often denies feeling chest "pain." More typical descriptions include squeezing,
tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest, a band-like sensation, knot in
the center of the chest, lump in the throat, ache, heavy weight on chest (elephant sitting on chest), like a bra too
tight, and toothache (when there is radiation to the lower jaw).
In some cases, the patient cannot qualify the nature of the discomfort but places his or her fist in the center of the
chest (the "Levine sign") or makes some other gesture indicating the location or type of pain (see 'Region or
location of pain' below). Patients with a history of coronary heart disease tend to have the same quality of chest
pain with recurrent ischemic episodes.
Acute chest pain with a classically ripping or tearing quality may be helpful in diagnosing acute aortic dissection
[26]. (See "Clinical manifestations and diagnosis of aortic dissection".)
Pulmonary embolism presents with pleuritic chest pain in only 40 to 48 percent of patients [27]. The chest pain of
myocarditis can be pleuritic, but it can also mimic that of myocardial ischemia. (See "Overview of acute pulmonary
embolism in adults", section on 'Clinical presentation, evaluation, and diagnosis' and "Clinical manifestations and
diagnosis of myocarditis in adults", section on 'Clinical manifestations'.)
Region or location of pain Ischemic pain is often a diffuse discomfort that is difficult to localize. Pain that
localizes to a small area on the chest is more likely of chest wall or pleural origin rather than visceral [28]. Referred
pain is an exception as described in the next section.
Patients may indicate the location and/or nature of discomfort with a gesture. In an observational study in 202
patients admitted with chest pain [28], the following observations were noted about the predictive value of such
findings:
Gestures such as placing a fist in the center of the chest (the "Levine sign") or an open palm over the chest in
response to questions about the type or location of chest pain had low predictive value for ischemic pain.
Pointing at a single location with one finger (felt to be a sign indicating nonischemic pain) occurred in only
eight patients, one of whom had an elevated troponin consistent with myocardial infarction.
Patients who indicated larger areas of discomfort were more likely to have an ischemic etiology of pain than
patients who indicated smaller areas of discomfort.

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This study was performed in inpatients, so the prevalence of ischemic chest pain was probably much higher than
would be seen in a primary care setting.
Radiation The pain of myocardial ischemia may radiate to the neck, throat, lower jaw, teeth, upper
extremity, or shoulder. A wide extension of chest pain radiation increases the probability that it is due to myocardial
infarction [17,29,30]. Although pain radiating to the left arm is classically associated with coronary ischemia,
radiation to the right arm may be a more useful finding. In one study, for example, 48 of 51 patients who presented
to an emergency department with chest pain that radiated to the right arm suffered from coronary disease; 41 had
a myocardial infarction [30]. Radiation to both arms is another predictor of acute myocardial infarction (table 2)
[17,19].
Pain radiation may provide a clue to other etiologies of chest pain. As an example, acute cholecystitis can present
with right shoulder pain, although concomitant right upper quadrant or epigastric pain is more typical than chest
discomfort. (See "Acute cholecystitis: Pathogenesis, clinical features, and diagnosis".) Chest pain that radiates
between the scapulae may be due to aortic dissection. (See "Clinical manifestations and diagnosis of aortic
dissection".) The pain of pericarditis typically radiates to one or both trapezius ridges. (See "Clinical presentation
and diagnostic evaluation of acute pericarditis", section on 'Chest pain'.) Cervical radiculopathy may present with
chest, upper back or upper extremity pain.
Temporal elements The time course of the onset of chest pain may be a very useful distinguishing feature:
The pain associated with a pneumothorax or a vascular event such as aortic dissection or acute pulmonary
embolism classically has an abrupt onset with the greatest intensity of pain at the beginning.
The onset of ischemic pain is more often gradual with an increasing intensity over time. A crescendo pattern
of pain can also be caused by esophageal disease [29]. (See "Chest pain of esophageal origin".)
"Functional" or nontraumatic musculoskeletal chest pain might have a much more vague onset (table 3). (See
"Clinical evaluation of musculoskeletal chest pain".)
The duration of pain is also helpful. Chest discomfort that lasts only for seconds or pain that is constant over
weeks is not due to ischemia. A span of years without progression makes it more likely that the origin of pain is
functional. The pain from myocardial ischemia generally lasts for a few minutes; it may be more prolonged in the
setting of a myocardial infarction.
Myocardial ischemia may demonstrate a circadian pattern. It is more likely to occur in the morning than in the
afternoon, correlating with an increase in sympathetic tone (figure 1A-B) [31]. (See "Psychosocial factors in acute
myocardial infarction".)
Provocation The patient should be asked about factors that provoke or worsen the pain:
Discomfort that reliably occurs with eating is suggestive of upper gastrointestinal disease. Postprandial chest
pain may be due to gastrointestinal or cardiac disease; in the latter case it can be a marker of severe
myocardial ischemia (eg, left main or three-vessel CHD) [32].
Chest discomfort provoked by exertion is a classic symptom of angina, although esophageal pain can present
similarly [29].
Other factors that may provoke ischemic pain include cold, emotional stress, meals, or sexual intercourse.
(See "Angina pectoris: Chest pain caused by myocardial ischemia".)
Pain made worse by swallowing is likely of esophageal origin. (See "Chest pain of esophageal origin".)
Body position or movement, as well as deep breathing, may exacerbate chest pain of musculoskeletal origin.
(See "Clinical evaluation of musculoskeletal chest pain".)
Truly pleuritic chest pain is worsened by respiration and may be exacerbated when lying down. Causes of
pleuritic chest pain include pulmonary embolism, pneumothorax, viral or idiopathic pleurisy, pneumonia, and
pleuropericarditis (table 4). (See "Clinical presentation and diagnostic evaluation of acute pericarditis" and
"Clinical presentation, evaluation, and diagnosis of the adult with suspected acute pulmonary embolism" and
"Diagnostic approach to community-acquired pneumonia in adults" and "Clinical manifestations and diagnosis

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of enterovirus and parechovirus infections", section on 'Pleurodynia'.)


Palliation Factors that make the pain better should be established:
Pain that is reliably and repeatedly palliated by antacids or food is likely of gastroesophageal origin.
Pain that responds to sublingual nitroglycerin is frequently thought to have a cardiac etiology or to be due to
esophageal spasm. However, pain relief with nitroglycerin in an acute care setting is not helpful in
distinguishing cardiac from noncardiac chest pain [33]. In a study of 459 patients who presented to an
emergency department with chest pain and were admitted to the hospital, the percentage of patients who
had relief of chest pain with nitroglycerin was similar among the 141 patients with active CHD and the 275
patients without active CHD (35 versus 41 percent experienced relief) [34].
Similarly, relief of pain following the administration of a "GI cocktail" (eg, viscous lidocaine and antacid) does
not reliably distinguish gastrointestinal from ischemic chest pain [35-37].
On the other hand, pain that abates with cessation of activity strongly suggests an ischemic origin.
The pain of pericarditis typically improves with sitting up and leaning forward.
Severity The severity of pain is not a useful predictor of the presence of CHD [9]. As many as one-third of
myocardial infarctions may go unnoticed by the patient [38]. The patient's level of concern about his symptom may,
however, be commensurate with its severity.
Associated symptoms Associated symptoms may not reliably distinguish between a cardiac and
gastrointestinal origin of chest pain, which can coexist in up to 35 percent of patients [29,37,39].
Belching, a bad taste in the mouth, and difficult or painful swallowing are suggestive of esophageal disease,
although belching and indigestion also may be seen with myocardial ischemia.
Vomiting may occur in the setting of myocardial ischemia (particularly transmural myocardial infarction) [40],
in addition to gastrointestinal problems such as peptic ulcer disease, cholecystitis, and pancreatitis. Diabetic
ketoacidosis, which can be precipitated by acute myocardial infarction, is another cause of vomiting.
Diaphoresis has been more frequently associated with myocardial infarction than esophageal disease
[17,20,41].
The presence of other associated symptoms may aid the diagnosis of chest pain:
Dyspnea Exertional dyspnea may occur when chest pain is due to myocardial ischemia and may predate
the sensation of angina [42]. Dyspnea that occurs concurrently with chest pain may be due to myocardial
ischemia or a number of pulmonary disorders including pathology of the airways, lung parenchyma, or
pulmonary vasculature. In one report, patients with chest pain and dyspnea referred for exercise
echocardiography had a higher incidence of exercise-induced ischemia and a poorer long-term prognosis than
patients with chest pain alone [43]. Dyspnea may be an important warning symptom whether or not chest
pain is present [44]. However, in one review, dyspnea did not usefully discriminate the diagnosis of acute
myocardial infarction (Likelihood ratio [LR] = 1) [20].
Cough The differential diagnosis of chest pain and cough includes infection, as well as congestive heart
failure, pulmonary embolus, and neoplasm. Cough, hoarseness, or wheezing may also be the result of
gastroesophageal reflux disease. (See "Gastroesophageal reflux and asthma".)
Syncope The patient with myocardial ischemia may describe presyncope. However, syncope associated
with chest pain should raise a concern for aortic dissection, a hemodynamically significant pulmonary
embolus, a ruptured abdominal aortic aneurysm, or critical aortic stenosis (particularly if the patient has a
history of exertional dyspnea).
Palpitations Patients with ischemia can feel palpitations resulting from ventricular ectopy or may have an
abnormal awareness of their sinus rhythm. While atrial fibrillation is associated with chronic CHD, new onset,
isolated atrial fibrillation is uncommon in patients with acute myocardial infarction [45,46]. The differential
diagnosis of chest pain and palpitations due to new atrial fibrillation includes pulmonary embolism. (See
"Epidemiology of and risk factors for atrial fibrillation".)

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Psychiatric symptoms Symptoms of panic disorder, generalized anxiety, depression, or somatization may
occur in patients with chest pain. A review of the literature found that panic disorder is present in 30 percent
or more of patients with chest pain who have no or minimal CHD; it also may coexist with CHD [47].
In a subgroup analysis of the Women's Health Initiative Observational Study, panic disorder was an
independent risk factor for CHD in postmenopausal women [48]. Because panic disorder clearly has a
negative long-term effect on the psychological and physical well-being of patients with chest pain [49], it is
among the psychosocial diagnoses (including domestic violence, discussed below) that should be actively
considered rather than labeling the patient with "noncardiac" or "atypical" chest pain. (See "Differential
diagnosis of chest pain in adults", section on 'Psychogenic/psychosomatic causes of chest pain'.)
Constitutional symptoms The elderly in particular may describe profound fatigue as the presenting
complaint of myocardial infarction. More diffuse constitutional symptoms raise the concern for cancer, which
is a rare cause of isolated chest pain in the primary care setting. Pleuritic chest pain and systemic symptoms
prompt an evaluation for causes of serositis such as systemic lupus erythematosus or familial Mediterranean
fever. (See "Pulmonary manifestations of systemic lupus erythematosus in adults" and "Clinical manifestations
and diagnosis of familial Mediterranean fever".)
Symptoms associated with coronary heart disease in women In a report of 515 women with an acute MI,
only 57 percent reported acute chest pain; the other presenting symptoms were shortness of breath (58
percent), weakness (55 percent), and fatigue (43 percent) [50]. Only 30 percent reported prodromal chest
discomfort, meaning that women with underlying coronary heart disease are unlikely to report chest
discomfort.
Other specific symptoms and association with domestic violence In a diverse, community-based population
of 1900 primary care patients, chest pain was one of many specific physical symptoms associated with
current domestic violence [51].
True chest wall pain is not usually associated with systemic symptoms. Exceptions include pain due to chest wall
neoplasm, associated intrathoracic trauma, and the constitutional symptoms or rash of herpes zoster.
Risk factors The clinical impression raised by the patient's description of pain must be interpreted together with
other aspects of the history, including risk factors for various etiologies of chest pain (figure 2) [52]. Knowledge
about such risk factors provides important information regarding disease likelihood, which may ultimately guide the
type and extent of evaluation performed. (See "Overview of the risk equivalents and established risk factors for
cardiovascular disease" and "Overview of the causes of venous thrombosis" and "Clinical manifestations and
diagnosis of aortic dissection", section on 'Risk factors'.)
A history or lack of classical coronary risk factors does not usefully discriminate ischemic causes of chest
pain in the acute setting [53,54].
The presence of hyperlipidemia, left ventricular hypertrophy, or a family history of premature CHD increase
the risk for myocardial ischemia (figure 2).
Hypertension is a risk factor for both CHD and aortic dissection (figure 2).
Cigarette smoking is a nonspecific risk factor for serious pathology; it is associated with CHD,
thromboembolism, aortic dissection, pneumothorax, and pneumonia (figure 2). (See "Cardiovascular risk of
smoking and benefits of smoking cessation".)
Chest pain is the symptom most commonly reported by cocaine users [55]. A history of cocaine use may
increase the suspicion of myocardial infarction [56] and, less commonly, aortic dissection [57], pulmonary
hypertension [58], and acute pulmonary syndrome (crack lung) [59]. In one study of 3946 patients with an
acute myocardial infarction, the risk of a myocardial infarction was increased 24 times over baseline in the 60
minutes after cocaine use (figure 3) [60]. Cocaine-associated myocardial infarction may also present without
chest pain [61]. (See "Evaluation and management of the cardiovascular complications of cocaine abuse".)
A recent infection, especially viral, may precede an episode of pericarditis or myocarditis. Other risk factors
for pericarditis include a history of chest trauma, autoimmune disease, recent myocardial infarction or cardiac

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surgery, and the use of certain drugs such as procainamide, hydralazine, or isoniazid. (See "Etiology of
pericardial disease".)
Age alone is an important risk factor for CHD; among patients older than age 40, chest pain resulting from
stable CHD or an acute coronary syndrome (unstable angina or myocardial infarction) becomes increasingly
common [54]. On the other hand, elderly patients, especially women, are more likely to have non-classic
presentations of coronary disease. (See "Clinical features and diagnosis of coronary heart disease in
women".)
The majority of younger patients with chest pain due to CHD have traditional risk factors for atherosclerosis
other than age. In a retrospective study of 209 patients under age 40 presenting with an acute myocardial
infarction, 98 percent had at least one of the conventional coronary risk factors; 80 percent smoked
cigarettes, 40 percent had a family history, 26 percent were hypertensive, and 20 percent had hyperlipidemia
[62]. Sympathomimetic drug use accounted for 7 percent of cases, and other, nontraditional risk factors were
infrequently noted (table 5).
Age can also help establish other diagnoses. As examples, men older than age 60 are most likely to suffer
aortic dissection, while young men are at highest risk for primary spontaneous pneumothorax. (See "Clinical
manifestations and diagnosis of aortic dissection" and "Primary spontaneous pneumothorax in adults".) Young
adults of both sexes are diagnosed with viral pleurisy more often than are their elders.
A past history of CHD, symptomatic gastroesophageal reflux, peptic ulcer disease, gallstones, panic
disorder, bronchospasm, or cancer is very helpful. It is important to establish if the present symptoms are
similar to those which occurred when the diagnosis was previously established. A history of diabetes mellitus
should heighten the concern for a nonclassic presentation of CHD. (See "Prevalence of and risk factors for
coronary heart disease in diabetes mellitus".)
It is important to exclude recent trauma to the chest. Blunt trauma can result in pneumothorax, disruption of
the aorta, tracheobronchial tree and esophagus, myocardial or pulmonary contusion, or chest wall injury with
associated musculoskeletal discomfort. (See "Post-cardiac injury syndromes".) Esophageal perforation or
rupture, albeit rare, may be a complication of recent upper endoscopy.
Physical examination The focused physical examination is used to support or disprove hypotheses generated
by the history. Thus, the extent of the examination is primarily determined by the diagnoses that are being
considered. A brief, "core" examination may suffice to diagnose life-threatening and common etiologies of chest
pain.
If acute coronary syndrome is suspected neither the physical examination nor the history is as potentially valuable
as a diagnostic tool as the initial serial ECG [19,20]. In this setting, the physical examination can be more useful for
identifying patients at higher risk of adverse outcomes [63].
The general appearance of the patient suggests the severity and possibly the seriousness of the symptoms.
A full set of vital signs can provide valuable clues to the clinical significance of the pain and may in some
cases aid in establishing its origin. Vital signs can also help with risk stratification and patient disposition
decisions in some cases (eg, acute myocardial infarction, pulmonary embolism or pneumonia).
As an example, a marked difference in pulse or blood pressure between the two arms suggests the presence
of aortic dissection [26], although most patients with dissection do not have a pulse deficit. However,
according to one study, the combination of findings of acute pain that is classically ripping or tearing in quality,
the pulse or blood pressure differential, and mediastinal or aortic widening on chest film is virtually
pathognomonic for aortic dissection (LR = 66) [26]. (See "Clinical manifestations and diagnosis of aortic
dissection".)
Palpation of the chest wall may evoke pain; if so, the patient should be asked if this sensation is identical to
the chief complaint. Chest wall tenderness may be present concomitantly with myocardial ischemia [11].
Hyperesthesia, particularly when associated with a rash, is often due to herpes zoster. (See "Postherpetic
neuralgia".)

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A complete cardiac examination including auscultation and palpation should be performed in a sitting and
supine position to establish the presence of a pericardial rub or signs of acute aortic insufficiency or aortic
stenosis. Ischemia may result in a mitral insufficiency murmur or an S4 or S3 gallop; there may also be
abnormal precordial movement, especially at the apex. (See "Auscultation of cardiac murmurs" and
"Auscultation of heart sounds".)
Determine if the breath sounds are symmetric and if wheezes, crackles or evidence of consolidation is
present.
A careful examination of the abdomen is important, with attention to the right upper quadrant, epigastrium,
and the abdominal aorta.
Focal neurologic signs in the setting of acute chest pain may be helpful in diagnosing acute aortic dissection
[26].
Ancillary studies Ancillary studies including an ECG (especially during an episode of chest pain or when there
is no obvious noncardiac cause of chest pain) and chest radiography (when cardiac, pericardial, aortic, or
pulmonary disease is a consideration) may support the initial diagnosis and help avoid missing serious etiologies of
chest pain such as acute myocardial infarction or pneumothorax (table 6) [64]. (See "Electrocardiogram in the
diagnosis of myocardial ischemia and infarction" and "Imaging of pneumothorax".)
The absence of any acute or diagnostic ECG changes may therapeutically allay patient anxiety and reduce
short-term disability [65]. Other specific clinical laboratory tests may be useful. As an example, pulmonary
embolism may be unlikely if a d-dimer test is negative, while an initial positive troponin may help diagnose
myocardial infarction. Further investigations, such as exercise ECG, myocardial perfusion, or echocardiographic
stress testing, a diagnostic course of acid suppression, or lung perfusion, bone, or chest CT scanning may
occasionally be required to establish specific etiologies for the chest pain. (See "Stress testing for the diagnosis of
obstructive coronary heart disease".)
Normal electrocardiogram A normal ECG markedly reduces the probability that chest pain is due to acute
myocardial infarction, but it does not exclude a serious cardiac etiology (particularly unstable angina). ECG findings
must be considered in the context of the history and physical examination.
Patients with unstable angina are much more likely to have a normal ECG than those with acute myocardial
infarction. In a retrospective series of 250 patients who presented to a cardiology clinic for evaluation of
recent onset chest pain, 20 percent of those with normal ECGs were found to have unstable angina; one-third
of patients diagnosed with unstable angina had a normal ECG [66]. The false-negative rate was lower in a
prospective series of emergency department patients presenting with chest pain; only 4 percent of those with
a normal ECG were found to have unstable angina, but strict criteria were used to define the "normal" ECG
[11]. (See "Initial evaluation and management of suspected acute coronary syndrome in the emergency
department", section on 'Clinical presentation'.)
One review found that the likelihood ratio of acute myocardial infarction in a patient with a normal initial ECG
was 0.1 to 0.3 [17]. However, if the history and physical examination suggest a high pretest probability of an
acute myocardial infarction, a normal ECG does not fully eliminate this diagnosis [17]. Other series have
found that 1 to 4 percent of patients with normal ECGs will have an acute infarction.
Aortic dissection and pulmonary embolus are among the diagnoses that should be considered in patients with
ongoing pain and a normal ECG.
Abnormal electrocardiogram The ECG is valuable both for risk stratification and diagnosis of acute
myocardial infarction. An abnormal ECG that contains specific findings is the most important predictor of acute
myocardial infarction (LR = 22 for ST elevation not known to be old, LR = 22 for Q waves, and LR = 4.5 for ST
depression) (table 6) [11,17,20,67]. Patients with an acute myocardial infarction who present with a positive initial
ECG are more likely to require invasive therapy, have a complicated hospital course, or die [68,69]. (See
"Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)
Among patients with a non-ST elevation ACS, the ECG can identify patients in different risk categories. The major
factors are the presence, extent, and location of ST segment depression. (See "Electrocardiogram in the

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prognosis of myocardial infarction or unstable angina", section on 'ECG for prognosis in UA and NSTEMI'.)
An ECG that is nonspecifically abnormal (eg, there are nonspecific ST and T wave abnormalities) is commonly
seen and may or may not indicate heart disease. (See "ECG tutorial: ST and T wave changes".) In one series of
patients seen in the emergency department for chest pain, more than two-thirds with a nonspecifically "abnormal"
ECG ultimately had a noncoronary diagnoses [11].
Chest radiograph A chest radiograph may assist in the diagnosis of chest pain if a cardiac, pulmonary, or
neoplastic etiology is being considered. It is also useful in the acute setting to evaluate for a pleural effusion in
patients with pleuritic pain and to help avoid missing infrequent but dangerous diagnoses such as aortic dissection
(image 1), pneumothorax (image 2), and pneumomediastinum. In the case of aortic dissection, however, other
studies are typically necessary to make the diagnosis. (See "Clinical manifestations and diagnosis of aortic
dissection".)
Approximately 20 percent of correctly interpreted chest films performed on patients with chest pain in an
emergency setting yield clinically relevant information [70,71]. In one prospective series, 23 percent of chest x-rays
had an abnormality that influenced therapy [70].
Other studies The history, physical examination, and, in some individuals, an immediate ECG and chest
radiograph should be sufficient to allow the clinician to form a hypothesis regarding the etiology of pain (eg,
musculoskeletal, cardiac, gastrointestinal, pulmonary, psychogenic, or other etiology). For select patients with
possible low-risk ACS or chronic stable CAD, an accelerated diagnostic protocol or rapid outpatient stress testing
may provide important risk or diagnostic information [63]. More specific studies or therapeutic trials (such as
myocardial perfusion or echocardiographic stress testing, a diagnostic course of acid suppression, or lung
perfusion, bone, or chest CT scanning) may be required to establish specific etiologies for chest pain. (See
'Expanded information for algorithm' below.)
Other tools for diagnosing acute, potentially life-threatening chest pain are available, including clinical prediction
rules [26,72,73], coronary artery calcium score, and other biomarkers for ACS (eg, brain natriuretic peptide)
[74-76]. Since none have been shown to be sensitive enough to be fully relied upon in the acute setting, clinical
judgment and traditional diagnostic testing remain a central part of the evaluation.
ALGORITHM FOR THE APPROACH TO THE DIAGNOSIS OF CHEST PAIN One approach to the diagnosis
of chest pain is outlined in the algorithm below. The approach is not regimented since the specific diagnosis of
chest pain requires integration of data about the patient's risk factors, description of pain, and associated
symptoms, as well as the physical examination and electrocardiogram or chest radiograph. The components of this
algorithm are evidence based wherever possible, but the sum of its parts has not been validated by any clinical
studies. It should not be construed as a practice guideline.
Diagnostic algorithm The initial step prior to following the algorithm below is to perform a focused history and
physical examination, and consider performing an ECG and/or chest x-ray. Once a life-threatening etiology has
been excluded, attempts should be made to identify the specific cause of symptoms and begin treatment.
Step 1 (Evaluate need for emergent care) Consider potentially life-threatening causes of chest pain.
Patients in whom an acute coronary syndrome (acute myocardial infarction or unstable angina) is
suspected should receive emergent care (this generally includes chewing an aspirin while awaiting transport
to an emergency department, ideally via an ambulance equipped with a defibrillator). (See 'Emergency
response to chest pain in the office' above and "Initial evaluation and management of suspected acute
coronary syndrome in the emergency department".)
Emergent care should also be provided to patients who appear to be seriously ill and to patients in whom
there is a suspicion of a critical noncoronary diagnosis such as pulmonary embolus, pneumothorax, aortic
dissection, esophageal rupture, or acute abdomen. For patients who do not require emergent care, proceed
to Step 2.
Step 2 (Emergent care not needed) In patients in whom a diagnosis of stable CHD appears likely based
on symptoms that are suggestive of angina and/or a history of cardiac risk factors (see 'Risk factors' above),
proceed to Step 3; otherwise, proceed to Step 5.

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Step 3 (Symptoms consistent with stable angina) Evaluate the patient for CHD (see "Stress testing for the
diagnosis of obstructive coronary heart disease"), and consider starting outpatient management (therapy may
include aspirin, beta blockers, nitroglycerin, and education about the need for emergency care) or admitting
the patient to the hospital, especially if symptoms are progressive. If there is a concern for angina secondary
to valvular heart disease (eg, critical aortic stenosis), perform an echocardiogram prior to stress testing.
Consider other causes of anginal chest pain, such as cardiac syndrome X and pulmonary hypertension. If the
results of the evaluation do not demonstrate CHD, proceed to Step 4; otherwise, proceed to step 8.
Step 4 (Evaluation for CHD was negative) Evaluate the patient for gastrointestinal disease. This evaluation
may initially involve a trial of acid suppression. (See "Chest pain of esophageal origin".) If there is no
diagnosis and symptoms persist, proceed to step 6; otherwise, proceed to step 8.
Step 5 (Symptoms not suggestive of angina)
Step 5a For patients who are felt not to have an ischemic etiology for chest pain but who have
significant risk factors for CHD, consider arranging for an evaluation for CHD
(see "Stress testing for the diagnosis of obstructive coronary heart disease") while proceeding to Step 5b.
Step 5b If symptoms suggest a musculoskeletal etiology, a trial of an NSAID is appropriate;
otherwise, proceed to step 5c. If pain persists, consider rib films, a bone scan, and plain or CT chest
radiography.
(See "Clinical evaluation of musculoskeletal chest pain".) If there is no diagnosis and symptoms persist, proceed to
step 6; otherwise, proceed to step 8.
Step 5c If symptoms suggest a gastrointestinal etiology, evaluate the patient for gastrointestinal
disease; otherwise, proceed to step 5d. This evaluation may initially involve a trial of acid suppression.
(See "Chest pain of esophageal origin".) If there is no diagnosis and symptoms persist, proceed to step 6;
otherwise, proceed to step 8.
Step 5d If symptoms suggest a psychogenic etiology, evaluate the patient for a psychosocial source
of chest pain
(see "Differential diagnosis of chest pain in adults"); otherwise, proceed to step 5e. Diagnostic strategies may
include a therapeutic trial of an antidepressant medication or a psychiatric referral. If there is no diagnosis and
symptoms persist, proceed to step 6; otherwise, proceed to step 8.
Step 5e Consider chest anatomy as a guide to other less common causes of non-life-threatening
chest pain including: chest wall pain (eg, zoster, breast disease); other cardiac pain such as pericarditis;
pathology of the lung parenchyma, vasculature, or pleura; and pain referred to the chest from the
gallbladder, diaphragm, or from a disc herniation.
(See "Differential diagnosis of chest pain in adults".)
Step 6 (Persistent chest pain) If chest pain persists and evaluations for CHD (as in step 5a),
musculoskeletal pain (as in step 5b), gastrointestinal pain (as in step 5c), psychogenic pain (as in step 5d),
and other causes (as in step 5e) have not all been performed, those evaluations should now be undertaken.
If there is no diagnosis and symptoms persist, proceed to step 7; otherwise, proceed to step 8.
Step 7 (Diagnostic evaluations negative) Patient likely has chronic idiopathic chest pain. Since this is
known to cause significant disability, consider referral to a pain management center or medical symptom
reduction program. No further evaluation is required unless the patient has a change in symptoms or the
symptoms are disabling.
Step 8 (Cause of chest pain diagnosed) Proceed with therapy or additional evaluation as appropriate for
the diagnosed condition.
Expanded information for algorithm The clinician's first step in the evaluation of any patient with recent chest
discomfort is to exclude life-threatening illness, including ACS, pulmonary embolism, aortic dissection,

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pneumothorax and esophageal rupture. ACS is the most common of the etiologies requiring immediate
hospitalization. One study found that patients may present to the primary care provider for evaluation in the month
preceding admission for acute myocardial ischemia, suggesting the need for clinicians to be vigilant for and
correctly interpret early or nonclassic symptoms of ACS [77]. The primary care provider may therefore play an
important role in early diagnosis.
Consideration of all information in the history, physical examination, ECG, and chest radiograph will determine
whether ACS or alternative diagnoses are more or less likely. In these patients for whom the likelihood of ACS is
neither high nor low, decisions will need to be made in part based upon other factors such as patient proximity to a
health care facility, ability to comply with specific provider recommendations, family support system, patient and
practitioner preferences, and the ability to perform an outpatient stress testing promptly [63].
Patient features, any one of which should alert the clinician to a high likelihood of ACS in a patient who does not
have clear ST elevations on ECG, include [78]:
Worsening in the frequency, intensity, duration, and timing (eg, nocturnal pain, rest pain) of prior anginal or
anginal equivalent symptoms
New onset symptoms of shortness of breath, nausea, sweating, extreme fatigue in a patient with a known
history of cardiovascular disease
Onset of typical anginal symptoms in a patient without a history of cardiovascular disease
New findings on physical examination of murmur (or worsening of a previously noted murmur), hypotension,
diaphoresis, rales or pulmonary edema
Transient ST deviation ( 1 mm) or T wave inversion in multiple precordial leads.
Features that need to be considered but are not as predictive as the high likelihood ones include [78]:
Age greater than 70 years
Diabetes mellitus
Extracardiac vascular disease
Either fixed Q waves or ST depression of 0.5 to 1 mm or T-wave inversion > 1mm on ECG.
The primary care clinician's response to the patient with possible ischemic chest pain may include emergent
hospitalization, immediate or scheduled stress testing, or cardiology consultation [79] (See 'Emergency response
to chest pain in the office' above.). An AHA/ACC Task Force on Practice Guidelines has published
recommendations for the clinical assessment of patients with possible ischemic chest pain [63,64,80].
Emergent hospitalization is necessary for patients with suspected acute myocardial infarction or, usually,
unstable angina [81]. (See "Criteria for the diagnosis of acute myocardial infarction" and "Overview of the
acute management of ST elevation myocardial infarction" and "Overview of the acute management of
unstable angina and non-ST elevation myocardial infarction".)
Exercise stress testing is indicated for patients with a suspected ischemic heart disease who do not have an
unstable coronary syndrome (eg, acute myocardial infarction or unstable angina). The indications and options
for exercise testing are discussed in detail separately. (See "Stress testing for the diagnosis of obstructive
coronary heart disease".)
Although not recommended in the ACC/AHA guidelines [80], transthoracic echocardiography (TTE) can
identify regional wall motion abnormalities within seconds of acute coronary artery occlusion and thus may be
a useful adjunct to the standard evaluation for cardiac ischemia. TTE is also appropriate to assist in the
identification of other causes of chest pain, such as pericarditis with effusion, aortic dissection, and possibly
pulmonary embolism. (See "Transthoracic echocardiography for the evaluation of chest pain in the emergency
department".)
Similarly, acute rest radionuclide myocardial perfusion imaging (rMPI) is a sensitive test for detecting acute
myocardial infarction, particularly if the chest pain is ongoing at the time of the study. It can be used to assist in
emergency department triage of patients with chest pain. The specificity of acute rest rMPI is limited in patients
with a previous myocardial infarction. (See "Acute rest radionuclide myocardial perfusion imaging for the evaluation
of suspected non-ST elevation acute coronary syndrome".)

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Cardiology consultation should be considered when the diagnosis of chest pain is not clear.
Empiric treatment with aspirin, beta blockers, and/or sublingual nitroglycerin or long-acting nitrates is indicated in a
patient who has a high likelihood of ischemic coronary disease on the basis of the clinical evaluation while awaiting
an outpatient diagnostic test. (See "Stable ischemic heart disease: Overview of care".)
Once ACS and other life-threatening etiologies are not felt to be reasonable diagnostic considerations, one may
then skip to evaluation and management of the most likely etiology. An exception is new anginal-quality pain that is
suspected to be of gastrointestinal origin in patients at risk of coronary disease; in this case, a cardiac evaluation
should be considered even as other therapy is begun. (See "Stress testing for the diagnosis of obstructive
coronary heart disease".)
Evaluation for gastrointestinal disease follows if the cardiac work-up is negative since up to 60 percent of patients
with angina-like chest pain and normal coronary angiograms will have evidence of gastrointestinal disease [82,83].
An adequate trial of acid suppression for gastroesophageal disease may obviate the need for further diagnostic
testing and is probably cost-effective [83]; if more extensive diagnostic testing is necessary, it should be performed
while the patient is still on acid suppression therapy [84]. Further diagnostic testing should be considered for
patients with concerning symptoms or signs for cancer, such as unexplained weight loss, anemia, or
gastrointestinal bleeding. (See "Chest pain of esophageal origin" and "Clinical manifestations of peptic ulcer
disease".)
A diagnosis of chest wall pain should not be made until other causes have been thoughtfully excluded:
Patients with active myocardial ischemia can also have chest wall tenderness that may or may not be
reproducible by palpation [11,85].
Other causes of "pleuritic" chest pain, such as pulmonary embolism, must also be considered. A reduced
PaO2 or increased alveolar-arterial gradient may suggest the diagnosis of pulmonary embolism; however, the
PaO2 is between 85 and 105 mmHg in approximately 18 percent of patients with pulmonary embolism, and
up to 6 percent may have a normal alveolar-arterial gradient for oxygen [86]. Of note, chest pain due to
pulmonary embolism may be persistent rather than pleuritic.
If the evaluation of isolated chest wall pain reveals no evidence of rheumatic disease, infection, tumor, or other
systemic illness, it is reasonable to defer ancillary studies and prescribe a therapeutic trial of antiinflammatory
medication. (See "Clinical evaluation of musculoskeletal chest pain".)
Chronic noncardiac chest pain has an excellent physical prognosis, but it is associated with significant long-term
psychosocial debility [87,88]. One study found that patients with functionally disabling chest pain, both with and
without heart disease, were much more likely to suffer from a host of debilitating psychiatric conditions and
demand more frequent medical attention than were patients who remained active despite chest pain [89]. Given
the disability suffered by patients with chronic chest pain, a psychiatric (eg, panic disorder) or psychosocial
diagnosis should be explored if there is other supporting clinical evidence. Such patients may also feel reassured if
a specific diagnosis and therapy can be offered.
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and
Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable
with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
patient info and the keyword(s) of interest.)
Basics topics (see "Patient information: Chest pain (The Basics)")
Beyond the Basics topics (see "Patient information: Chest pain (Beyond the Basics)")

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SUMMARY AND RECOMMENDATIONS


The most common etiologies of chest pain in primary care practice include musculoskeletal and
gastrointestinal causes, followed by cardiac, psychiatric, pulmonary, and other causes. (See 'Epidemiology in
primary care populations' above.)
Any patient with a recent onset of chest pain who may be potentially unstable based upon history,
appearance, or vital signs, should be transported immediately to an emergency department. (See
'Emergency response to chest pain in the office' above and "Evaluation of the adult with chest pain in the
emergency department".)
The initial goal in the office evaluation of chest pain in stable individuals is to exclude acute coronary
syndrome (ACS) and other potentially life-threatening conditions. This is usually accomplished with the history,
physical examination, and certain ancillary studies (eg, ECG, chest radiograph, and further testing for ACS,
pulmonary embolism, or aortic dissection as indicated). (See 'Evaluation' above and "Stress testing for the
diagnosis of obstructive coronary heart disease" and "Stable ischemic heart disease: Overview of care".)
After life-threatening conditions have been ruled out, evaluation of other causes of chest pain is warranted.
The evaluation should be guided by the results of the initial clinical assessment, including history and physical
examination. (See 'Algorithm for the approach to the diagnosis of chest pain' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
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GRAPHICS
Causes of nonemergent chest pain in Michigan Research Network
(MIRNET) primary care practices
Cause

Prevalence, percent

Musculoskeletal, including costochondritis

36

Gastrointestinal

19

Cardiac

16*

Stable angina

10.5

Unstable angina or MI

1.5

Other cardiac

3.8

Psychiatric

Pulmonary

Other/unknown

16

MIRNET: Michigan Research Network.


* As high as 50 percent in older populations.
Adapted from Klinkman MS, Stevens D, Gorenflo DW. J Fam Pract 1994; 38:345.
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Likelihood ratios for myocardial infarction (MI) based on components


of the chest pain history
Description of pain

Positive likelihood ratio (95%


CI)

Descriptions increasing the likelihood of MI


Radiation to right arm or shoulder

4.7 (1.9-12)

Radiation to both arms or shoulders

4.1 (2.5-6.5)

Exertional

2.4 (1.5-3.8)

Radiation to left arm

2.3 (1.7-3.1)

Associated with diaphoresis

2.0 (1.9-2.2)

Associated with nausea or vomiting

1.9 (1.7-2.3)

Worse than previous angina or similar to


previous MI

1.8 (1.6-2.0)

Described as pressure

1.3 (1.2-1.5)

Descriptions decreasing the likelihood of MI


Pleuritic

0.2 (0.1-0.3)

Positional

0.3 (0.2-0.5)

Sharp

0.3 (0.2-0.5)

Reproducible with palpation

0.3 (0.2-0.4)

Inframammary location

0.8 (0.7-0.9)

Nonexertional

0.8 (0.6-0.9)

CI: confidence interval.


Data from: Swap, C, Nagurney, J. Value and limitations of chest pain history in the evaluation of
patients with suspected acute coronary syndromes. JAMA 2005; 294:2623.
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Important features of the history in musculoskeletal chest pain


Features suggestive of visceral causes
Middle aged or elderly patient
Risk factors for coronary disease
Exertional pain
Cough
Fever
Dyspnea
Atypical location

Features suggestive of musculoskeletal cause


Insidious onset
Recent repetitive unaccustomed activity (trunk and arms)
Positional component
Persistent and prolonged (lasting hours-days)

Features suggestive of associated condition


Neck, thoracic, or shoulder pain (pain referred to chest)
Chronic low back pain, young patient (ankylosing spondylitis)
Ocular inflammation (ankylosing spondylitis or related disease)
Diffuse musculoskeletal pain/sleep disturbance (fibromyalgia)
Peripheral joint pain and swelling (rheumatoid arthritis)
Skin lesions (psoriasis), (psoriatic arthritis)
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Circadian pattern of nonfatal myocardial infarction and


sudden death

A meta-analysis was performed using trials that reported the timing for an
acute myocardial infarction (N=66,635 patients) and sudden death (N=19,390
patients). An excess number of infarctions and sudden deaths occurred in the
morning between the hours of 6 am and 12 pm, indicating a circadian pattern
to their occurrence.
Data from Kangro, T, Henriksen, E, Jonason, T, et al. Am J Cardiol 1997; 79:1507.
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Circadian variation in unstable angina and non-Q wave


myocardial infarction

Prospective analysis of patients entered into the TIMI III registry shows that there is a
circadian variation in the onset of pain in patients with unstable angina and non-Q
wave myocardial infarction (AMI); the greatest number of patients experience the
onset of pain between 6 am and 12 pm.
Redrawn from Cannon, CP, McCabe, CH, Stone, PH, et al, for the TIMI III Registry and
TIMI IIIB Investigators, AM J Cardiol 1997; 79:253.
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Causes of pleuritic chest pain


Viral pleurisy
Pneumonia
Acute pulmonary embolus
Pneumothorax
Pericarditis
Collagen vascular diseases, including systemic lupus erythematosus, mixed connective tissue
disease, and rheumatoid arthritis
Drug-induced lupus
Inflammatory bowel disease
Familial Mediterranean fever
Radiation pneumonitis
Pulmonary histoplasmosis, infection with the lung fluke Paragonimus
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Additive effects of risk factors on cardiovascular disease at five


years

Cumulative absolute risk of CVD at five years according to systolic blood pressure and
specified levels of other risk factors. The reference category is a nondiabetic, nonsmoking
50-year-old woman with a serum TC of 154 mg/dL (4.0 mmol/L) and HDL-cholesterol of
62 mg/dL (1.6 mmol/L). The CVD risks are given for systolic blood pressure levels of
110, 130, 150, and 170 mmHg. In the other categories, the additional risk factors are
added consecutively. As an example, the diabetes category is a 50-year-old diabetic man
who is a smoker and has a TC of 270 mg/dL (7 mmol/L) and HDL-cholesterol of 39
mg/dL (1 mmol/L).
CVD: cardiovascular disease; TC: total cholesterol.
Adapted from: Jackson R, Lawes CM, Bennett DA, et al. Lancet 2005; 365:434.
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Relative risk of myocardial infarction onset after


cocaine use

Relative risk of myocardial infarction onset is plotted on a logarithmic


scale for each of the three hours after cocaine use. Relative risks were
estimated by comparing the frequency of cocaine use in each of the 3
hours before myocardial infarction onset to its expected frequency based
on each patient's reported usual frequency of cocaine use over the prior
year. Error bars indicate 95 percent CI. Dotted line represents baseline
risk during periods of nonexposure to cocaine. The risk of myocardial
infarction was increased 24 times over baseline in the first 60 minutes
after cocaine use.
Adapted from: Mittleman MA, Mintzer D, Maclure M. Circulation 1999;
99:2737.
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Nontraditional risk factors for myocardial infarction in younger


adults*
Risk factor

Percent

Physical stress with MI

39

Obesity alone

30

Sympathomimetic drug use

Estrogen or oral contraceptive pill use

Valvular heart disease

Collagen vascular disease

Cardiomyopathy

History chest irradiation

Myocarditis

Chronic dysrhythmia

Sickle cell anemia

<1

Coronary artery spasm

6.5

* 209 young adults, 98 percent of whom also had traditional coronary risk factors. Data from Kanitz,
MG, Givannucci, SJ, Jones, JS, Mott, M, J Emerg Med 1996; 14:139.
Occurrence of myocardial infarction (MI) in 277 patients with documented spasm. Data from Bory M,
Pierron F, Panagides D, Bonnet JL, et al, Eur Heart J 1996; 17:1015.
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Features of electrocardiogram that increase the probability of a


myocardial infarction in patients presenting with acute chest pain
Likelihood ratio
ST-segment elevation
New

6-54*

Any

11

Q-waves
New

5-25*

Any

New conduction defect

ST-segment depression

3-5*

T-wave inversion

2-3*

*In heterogeneous studies the likelihood ratios are repeated as ranges.


Adapted from: Panju, AA, Hemmelgarn, BR, Guyatt, GH, Simel, DL. JAMA 1998; 280:1256.
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Aortic dissection

PA chest film in a patient with the sudden onset of excruciating


interscapular pain and hypotension. The ascending aortic arch is dilated,
displacing the trachea to the right (black arrow). A left lower lobe
density is suggestive of a pleural effusion. Surgery revealed a dilated
ascending aorta with a dissection approximately 3 cm distal to the aortic
valve.
Courtesy of Robert A Novelline, MD.
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Pneumothorax

Left panel: A left-sided, simple pneumothorax is seen on this PA chest radiograph


(large white arrows). Right panel: On the expiratory film, the pneumothorax is larger
and more easily seen (small white arrows).
Courtesy of Robert A Novelline, MD.
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