Diagnostic approach to chest pain in adults
James L Meisel, MD, FACP
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Updates are added as important new information is published. The literature review for version 14.2 is current through April 2006; this topic was last changed on April
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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-lifethreatening etiologies, which may be functionally disabling, are much more common in the primary care setting and require a cost-effective approach to diagnosis [ 1,2 ].
The correct diagnosis is most often derived from a vigilantly obtained, detailed history that is supported by specific physical findings, an electrocardiogram, and/or chest x-ray.
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" ).
ETIOLOGY 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 ( show table 1 ) [ 3 ]:
 Approximately 60 percent of chest pain diagnoses were not "organic" in origin
(eg, 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 nonorganic chest pain in primary care practice [ 1,2,4 ].
The prevalence of chest pain etiologies varies according to the population studied.
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 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
[ 5 ]. In contrast, the incidence of cardiac diagnoses may exceed 50 percent in patients with chest pain after the age of 40 [ 6-8 ].

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 supplemental oxygen, intravenous access, and placement of a cardiac monitor. A 12lead electrocardiogram and a blood sample for cardiac enzyme measurement should be obtained if possible.
Patients who are thought to be experiencing a myocardial infarction should chew a
325 mg aspirin tablet. Sublingual nitroglycerin should be given 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 "Evaluation and management of suspected acute coronary syndrome in the emergency department" ).
EVALUATION — The initial goal in the office evaluation of chest pain in stable individuals is to exclude CHD and other potentially life-threatening conditions. This is usually accomplished using clinical judgment, and less frequently exercise testing, other noninvasive testing, or invasive angiography. ( See "Stress testing for the diagnosis of 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 diagnosis of
"noncardiac" or "atypical" chest pain is not very useful outside of a coronary care setting. A diagnostic pattern will frequently emerge, based upon the patient's risk factors and a description of the pain and associated symptoms. ( See "Evaluation and management of suspected acute coronary syndrome in the emergency department" , section on Characteristics of chest pain and associated symptoms).
In the primary care setting, the history 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 ( show table 2 ). As an example, one study found that physicians were able to correctly diagnose a nonorganic (eg, 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. No organic diagnosis was missed.
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 lung perfusion scanning to detect pulmonary embolism) [ 9,10 ]. Pretest probability is an important component of the interpretation of these test results. ( See
"Stress testing for the diagnosis of coronary heart disease" and see "Diagnosis of acute pulmonary embolism" ).
As discussed above, this utility of the history and physical examination applies to stable patients after emergent diagnoses have been excluded. ( See "Emergency

response to chest pain in the office" above ). The chest pain history is less useful in patients suspected of having an acute coronary syndrome (ACS). 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 [ 11 ]. 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 [ 12 ]. ( See "Evaluation and management of suspected acute coronary syndrome in the emergency department" ).
The patient's style of presentation may influence the physician's subjective judgment and clinical reasoning. 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 actress and script presented in a "histrionic" fashion; a third group read a verbatim transcript of the interview [ 13 ]. 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 patient interview.
Description of chest pain — A thorough description of the pain is an essential first step in the diagnosis of chest pain ( show table 3 ). ( See "Differential diagnosis of chest pain" ).
Quality of the pain — 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"). Patients with a history of coronary heart disease tend to have the same quality of chest pain with recurrent ischemic episodes.
The chest pain of myocarditis can be pleuritic, but it can also mimic that of myocardial ischemia. ( See "Clinical manifestations and diagnosis of myocarditis in adults" , section on Clinical manifestations).
One study of patients presenting to the emergency department with chest pain found that "sharp" or "stabbing" was a low-risk description only if the pain had a pleuritic or positional component, was fully reproducible by palpation, and the patient had no history of angina or myocardial infarction. No patients who presented with these findings had a cardiac etiology of pain [ 8 ]. However, all three of these characteristics were present in only 48 of 596 patients studied. It is important to clarify with patients who use the word "sharp" that they actually mean "knife-like" or "stabbing" rather than "severe".
Cultural and sex differences may affect descriptions of angina. As an 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 [ 14 ]. 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.
Region or location of pain — Ischemic pain is a diffuse discomfort that may be 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. Referred pain is an exception (see below).
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 [ 9,15,16 ]. Although pain radiating to the left arm is classically associated with coronary ischemia, radiation to the right arm may be a particularly useful finding. In one study, as an 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 [ 16 ]. Radiation to both arms is another strong predictor of acute myocardial infarction ( show table 3 ) [ 9,12 ].
Acute cholecystitis can present with right shoulder pain, although concomitant right upper quadrant or epigastric pain is more typical than chest discomfort. ( See "Clinical features and diagnosis of acute cholecystitis" ). 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 "Evaluation and management of acute pericarditis" , section on Chest 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 typically has an abrupt onset with the greatest intensity of pain at the beginning.
 The onset of ischemic pain is most often gradual with an increasing intensity over time. A crescendo pattern of pain can also be caused by esophageal disease
[ 15 ]. ( See "Chest pain of esophageal origin" ).
 "Functional" or nontraumatic musculoskeletal chest pain might have a much more vague onset ( show table 4 ). ( 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 ( show figure 1A-1B ) [ 17 ]. ( See "Psychosocial and other social factors in acute myocardial infarction" ).

Provocation — The patient should be asked about factors that provoke or make the pain worse:
 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) [ 18 ].
 Chest discomfort provoked by exertion is a classic symptom of angina, although esophageal pain can present similarly [ 15 ].
 Other factors that may provoke ischemic pain include cold, emotional stress, meals, or sexual intercourse. ( See "Pathophysiology and clinical presentation of ischemic chest pain" ).
 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 ( show table 5 ). ( See "Evaluation and management of acute pericarditis" and see "Diagnosis of acute pulmonary embolism" and see "Diagnostic approach to community-acquired pneumonia in adults" ).
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 [ 19 ]. 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) [ 20 ].
 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 [ 11,21,22 ].
 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 CHD [ 6 ]. As many as onethird of myocardial infarctions may go unnoticed by the patient [ 23 ]. The patient's level of concern about his symptom may be greater than that of his physician but 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 [ 15,22,24 ].
 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) [ 25 ], 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 is more frequently associated with myocardial infarction than esophageal disease [ 9,26 ].
The presence of other associated symptoms may aid the diagnosis of chest pain:
 Dyspnea — Exertional dyspnea is common when chest pain is due to myocardial ischemia and may predate the sensation of angina [ 27 ]. 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 [ 28 ]. Dyspnea is an important warning symptom whether or not chest pain is present [ 29 ].
 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 [ 30,31 ]. The differential diagnosis of chest pain and palpitations due to new atrial fibrillation includes pulmonary embolism. ( See "Causes of atrial fibrillation" ).

 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 [ 32 ]. ( See
"Differential diagnosis of chest pain" , 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 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 see "Clinical manifestations and diagnosis of familial Mediterranean fever" ).
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 ( show figure 2 ) [ 33 ]. 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 factors for cardiovascular disease" ).
 The presence of hyperlipidemia, left ventricular hypertrophy, or a family history of premature CHD increase the risk for myocardial ischemia ( show figure 2 and show table 6 ).
 Hypertension is a risk factor for both CHD and aortic dissection ( show figure 2 ).
 Cigarette smoking is a nonspecific risk factor for serious pathology; it is associated with CHD, thromboembolism, aortic dissection, pneumothorax, and pneumonia ( show figure 2 ). ( See "Preventive cardiology: Cardiovascular risk of smoking and benefits of smoking cessation" and see "ATS guidelines: Cigarette smoking and health" ).
 A history of cocaine use may increase the suspicion of myocardial infarction
[ 34 ]. In one study of 3946 patients with an acute myocardial infarction, 1 percent had used cocaine within the prior year; the risk of a myocardial infarction was increased 24 times over baseline in the 60 minutes after cocaine use ( show figure 3 )
[ 35 ]. ( See "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 surgery, and the use of certain drugs such as procainamide , hydralazine , or isoniazid . ( See "Etiology of pericardial disease" ).
 Age 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. 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" and see "Coronary heart disease in the elderly: Risk factors; presentation; and evaluation" ).
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 [ 36 ]. Sympathomimetic drug use accounted for 7 percent of cases, and other, non-traditional risk factors were infrequently noted ( show table 6 ).
Age can also can 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 see "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 blunt trauma to the chest, which 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 "Pericardial and postpericardial injury syndromes" ).
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.
 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. As an example, a marked difference in blood pressure between the two arms suggests the presence of aortic dissection, although most patients with a dissection do not have a pulse deficit. ( 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 [ 8 ]. Hyperesthesia, particularly when associated with a rash, is often due to herpes zoster. ( See "Postherpetic neuralgia" ).

 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 see "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.
Ancillary studies — Ancillary studies including an ECG (when a cardiac etiology is possible) and chest radiography (when cardiac 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 ( show table 2 and show table 7 ). ( See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and see "Imaging of pneumothorax" ). The absence of any acute or diagnostic ECG changes may therapeutically allay patient anxiety and reduce shortterm disability [ 37 ]. 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 ( show table 8 ).
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 [ 38 ]. 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 [ 8 ]. ( See
"Evaluation and management of suspected acute coronary syndrome in the emergency department" , section on Characteristics of chest pain and associated symptoms).
 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 [ 9 ]. 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 [ 9 ]. Other series have found that 1 to 4 percent of patients with normal ECGs will have an acute infarction.
 A normal ECG in a patient with the recent onset of chest pain can also be found in patients with a less acute coronary syndrome such as stable angina. Aortic dissection should be considered in patients with ongoing pain and a normal ECG.

Abnormal electrocardiogram — An abnormal ECG that contains specific findings (eg,
ST segment elevation, ST segment depression, or new Q waves) remains an important predictor of an acute coronary syndrome (acute myocardial infarction or unstable angina) ( show table 7 ) [ 8,9,39 ]. 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 [ 40,41 ]. ( See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" ).
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 [ 8 ].
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 help avoid missing infrequent but dangerous diagnoses such as aortic dissection ( show radiograph 1 ), pneumothorax ( show radiograph 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 [ 42,43 ].
In one prospective series, 23 percent of chest x-rays had an abnormality that influenced therapy [ 42 ].
Other studies — The history, physical examination, and, in some individuals, an ECG and chest radiograph should be sufficient to allow the physician to form a hypothesis regarding the etiology of pain (eg, musculoskeletal, cardiac, gastrointestinal, pulmonary, psychogenic, or other etiology). More specific studies or therapeutic trials may occasionally be required at this point to arrive at a specific diagnosis.
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, type 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. A primary goal of the initial evaluation is to identify patients with potentially life-threatening etiologies of chest pain, and the results of the history and physical are central to guiding the remaining evaluation once life-threatening etiologies have been excluded.
 Step 1 (Evaluate need for emergent care) — Consider potentially lifethreatening 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 "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 CHD appears likely based on symptoms that are typical for stable angina and/or a history of cardiac risk factors ( see "Risk factors" above ), proceed to Step 3; otherwise, proceed to Step 5.
 Step 3 (Symptoms consistent with stable angina) — Evaluate the patient for
CHD ( see "Stress testing for the diagnosis of coronary heart disease" ), and consider starting outpatient management (therapy may include aspirin , beta blockers, nitroglycerin , and education about the need for emergency care). If there is a concern for angina secondary to valvular heart disease (eg, critical aortic stenosis), perform an echocardiogram prior to stress testing. 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 classic for 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, arrange for an evaluation for CHD
( see "Stress testing for the diagnosis of 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" ); 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); 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" ).
 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. 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. The table ( show table 9 ) can help with estimating the likelihood of an acute coronary syndrome [ 44 ]. It is reasonable to then skip to a suspected 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 coronary heart disease" ).
The primary care physician's response to the patient with possible ischemic chest pain may include emergent hospitalization, immediate or scheduled stress testing, or cardiology consultation [ 45 ]. An AHA/ACC Task Force on Practice Guidelines has published recommendations for the clinical assessment of patients with ischemic chest pain ( show algorithm 1A-1B and show table 8 ) [ 46,47 ].
 Emergent hospitalization is necessary for patients with suspected acute myocardial infarction or, usually, unstable angina [ 44 ]. ( See "Diagnosis of an acute myocardial infarction" and see "Overview of the management of acute ST elevation (Q wave) myocardial infarction" and see "Overview of the management of unstable angina and acute non-ST elevation (non-Q wave) 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 coronary heart disease" ).

 Although not recommended in the ACC/AHA guidelines [ 47 ], 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 myocardial perfusion imaging (MPI) 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 MPI is limited in patients with a previous myocardial infarction. ( See "Acute rest myocardial perfusion imaging for the evaluation of suspected non-ST elevation acute coronary syndrome" ).
 Cardiology consultation should be considered when the diagnosis of chest pain is not clear.
The likelihood of CHD can be estimated on clinical grounds. As an example, in the
Coronary Artery Surgery Study (CASS), chest pain symptoms were categorized into three groups ( see "Stress testing for the diagnosis of coronary heart disease" , section on
Estimating pretest risk) [ 48 ]:
 Definite or classic angina — Substernal chest discomfort with a characteristic quality and duration, which is provoked by exertion or emotional stress and relieved by rest or nitroglycerin
 Probable or atypical angina — Chest pain with two of the three above characteristics
 Nonanginal or nonischemic chest pain — Chest pain with one or none of the above characteristics
When patients were divided into subgroups based upon gender and the characteristics of their chest pain, the pretest probability of CHD varied between 5 and 89 percent ( show table 10 ). CASS and other studies have shown that, within each of these subgroups, the frequency of CHD increases with age, while women with the same symptoms are less likely to have CHD than men of the same age ( show table
11 ) [ 49,50 ].
Empiric treatment with aspirin , beta blockers, and/or sublingual nitroglycerin or longacting 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 "Overview of the management of stable angina pectoris" ).
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 [ 51,52 ]. An adequate trial of acid suppression for gastroesophageal disease may obviate the need for further diagnostic testing and is probably cost-effective [ 52 ]; if more extensive diagnostic

testing is necessary, it should be performed while the patient is still on acid suppression therapy [ 53 ]. ( See "Chest pain of esophageal origin" ).
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 [ 8,54 ].
 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 [ 55 ]. 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 [ 56,57 ]. 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 [ 58 ]. 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. ( See "Overview of panic disorder" ). Such patients may also feel reassured if a specific diagnosis and therapy can be offered.
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REFERENCES
Martina, B, Bucheli, B, Stotz, M, et al. First clinical judgment by primary care physicians distinguishes well between nonorganic and organic causes of abdominal or chest pain. J Gen Intern Med 1997; 12:459.
Svavarsdottir, AE, Jonasson, MR, Gudmundsson, GH, Fjeldsted, K. Chest pain in family practice. Diagnosis and long-term outcome in a community setting. Can Fam
Physician 1996; 42:1122.
Klinkman, MS, Stevens, D, Gorenflo, DW. Episodes of care for chest pain: A preliminary report from MIRNET. Michigan Research Network. J Fam Pract 1994;
38:345.
An exploratory report of chest pain in primary care. A report from ASPN. J Am Board
Fam Pract 1990; 3:143.
Luke, LC, Cusack, S, Smith, H, et al. Non-traumatic chest pain in young adults: A medical audit. Arch Emerg Med 1990; 7:183.
Pryor, DB, Harrell, FE, Lee, KL, Califf, RM. Estimating the likelihood of significant coronary artery disease. Am J Med 1983; 75:771.

7.
8.
9.
10.
13.
14.
11.
12.
Goldman, L, Weinberg, M, Weisberg, M, et al. A computer-derived protocol to aid in the diagnosis of emergency room patients with acute chest pain. N Engl J Med 1982;
307:588.
Lee, TH, Cook, F, Weisberg, M, et al. Acute chest pain in the emergency room.
Identification and examination of low-risk patients. Arch Intern Med 1985; 145:65.
Panju, AA, Hemmelgarn, BR, Guyatt, GH, Simel, DL. Is this patient having a myocardial infarction? JAMA 1998; 280:1256.
Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED
Investigators. JAMA 1990; 263:2753.
Servi, RJ, Skiendzielewski, JJ. Relief of myocardial ischemia pain with a gastrointestinal cocktail. Am J Emerg Med 1985; 3:208.
Swap, CJ, Nagurney, JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA 2005; 294:2623.
Birdwell, BG, Herbers, JE, Kroenke, K. Evaluating chest pain. The patient's presentation style alters the physician's diagnostic approach. Arch Intern Med 1993;
153:1991.
D'Antono, B, Dupuis, G, Fortin, C, et al. Angina symptoms in men and women with stable coronary artery disease and evidence of exercise-induced myocardial perfusion defects. Am Heart J 2006; 151:813.
15.
16.
17.
18.
Davies, HA, Jones, DB, Rhodes, J, Newcombe, RG. Angina-like esophageal pain:
Differentiation from cardiac pain by history. J Clin Gastroenterol 1985; 7:477.
Berger, JP, Buclin, T, Haller, E, et al. Right arm involvement and pain extension can help to differentiate coronary diseases from chest pain of other origin: A prospective emergency ward study of 278 consecutive patients admitted for chest pain. J Intern
Med 1990; 227:165.
Cohen, MC, Rohtla, KM, Lavery, CE, et al. Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death. Am J Cardiol 1997; 79:1512.
Berlinerblau, R, Shani, J. Postprandial angina pectoris: Clinical and angiographic correlations. J Am Coll Cardiol 1994; 23:627.
19. Gibbons, RJ. Nitroglycerin: should we still ask?. Ann Intern Med 2003; 139:1036.
20. Henrikson, CA, Howell, EE, Bush, DE, et al. Chest pain relief by nitroglycerin does not predict active coronary artery disease. Ann Intern Med 2003; 139:979.
21. Castrina, FP. Unexplained noncardiac chest pain. Ann Intern Med 1997; 126:663;.
22. Ros, E, Armengol, X, Grande, L, et al. Chest pain at rest in patients with coronary artery disease. Myocardial ischemia, esophageal dysfunction, or panic disorder? Dig
Dis Sci 1997; 42:1344.
23. Sigurdsson, E, Thorgeirsson, G, Sigvaldason, H, Sigfusson, N. Unrecognized myocardial infarction: Epidemiology, clinical characteristics, and the prognostic role of angina pectoris. The Reykjavik Study. Ann Intern Med 1995; 122:96.
24. Voskuil, J, Cramer, MJ, Breumelhof, R, et al. Prevalence of esophageal disorders in patients with chest pain newly referred to the cardiologist. Chest 1996; 109:1210.
25. Ingram, DA, Fulton, RA, Portal, RW, Aber, CP. Vomiting as a diagnostic aid in acute ischaemic cardiac pain. Br Med J 1980; 281:636.
26. Tierney, WM, Roth, BJ, Psaty, B, et al. Predictors of myocardial infarction in emergency room patients. Crit Care Med 1985; 13:526.
27. Cook, DG, Shaper, AG. Breathlessness, angina pectoris and coronary artery disease.
Am J Cardiol 1989; 63:921.
28. Bergeron, S, Ommen, SR, Bailey, KR, et al. Exercise echocardiographic findings and outcome of patients referred for evaluation of dyspnea. J Am Coll Cardiol 2004;
43:2242.
29. Abidov, A, Rozanski, A, Hachamovitch, R, et al. Prognostic significance of dyspnea in patients referred for cardiac stress testing. N Engl J Med 2005; 353:1889.

30.
31.
32.
33.
Friedman, HZ, Weber-Bornstein, N, Deboe, SF, Mancini, GB. Cardiac care unit admission criteria for suspected acute myocardial infarction in new-onset atrial fibrillation. Am J Cardiol 1987; 59:866.
Crenshaw, BS, Ward, SR, Granger, CB, et al, for the GUSTO-1 Trial Investigators.
Atrial fibrillation in the setting of acute myocardial infarction: The GUSTO-1 experience. J Am Coll Cardiol 1997; 30:406.
Fleet, RP, Dupuis, G, Marchand, A, et al. Panic disorder, chest pain and coronary artery disease: Literature review. Can J Cardiol 1994; 10:827.
Clinical policy for the initial approach to adults presenting with a chief complaint of chest pain, with no history of trauma. American College of Emergency Physicians.
Ann Emerg Med 1995; 25:274.
34.
35.
Lange, RA, Hillis, LD. Cardiovascular complications of cocaine use. N Engl J Med
2001; 345:351.
Mittleman, MA, Mintzer, D, Maclure, M, et al. Triggering of myocardial infarction by cocaine. Circulation 1999; 99:2737.
36.
37.
38.
39.
Kanitz, MG, Giovannucci, SJ, Jones, JS, Mott, M. Myocardial infarction in young adults: risk factors and clinical features. J Emerg Med 1996; 14:139.
Sox, HC, Margulies, I, Sox, CH. Psychologically mediated effects of diagnostic tests.
Ann Intern Med 1981; 95:680.
Norell, M, Lythall, D, Cheng, A, et al. Limited value of the resting electrocardiogram in assessing patients with recent onset chest pain: Lessons from a chest pain clinic.
Br Heart J 1992; 67:53.
Rude, RE, Poole, K, Muller, JE, et al. Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients. Am J
Cardiol 1983; 52:936.
40. Goldman, L, Cook, EF, Johnson, PA, et al. Prediction of the need for intensive care in patients who come to emergency departments with acute chest pain. N Engl J Med
1996; 334:1498.
41.
42.
43.
Brush, JE, Brand, DA, Acampora, D, et al. Use of the initial electrocardiogram to predict in-hospital complications of acute myocardial infarction. N Engl J Med 1985;
312:1137.
Templeton, PA, McCallion, WA, McKinney, LA, Wilson, HK. Chest pain in the accident and emergency department: Is chest radiography worthwhile? Arch Emerg Med
1991; 8:97.
Russell, NJ, Pantin, CF, Emerson, PA, Crichton, NJ. The role of chest radiography in patients presenting with anterior chest pain to the Accident & Emergency
Department. J R Soc Med 1988; 81:626.
44.
45.
Braunwald, E, Mark, DB, Jones, RH, et al. Diagnosing and managing unstable angina. Quick reference guide for clinicians, number 10. AHCPR Publication No. 94-
0603. Rockville, MD. U.S. Department of Health and Human Services, Public Health
Service, Agency for Health Care Policy and Research and National Heart, Lung, and
Blood Institute. March 1994.
Kirk, JD, Turnipseed, S, Lewis, WR, Amsterdam, EA. Evaluation of chest pain in lowrisk patients presenting to the emergency department: the role of immediate exercise testing. Ann Emerg Med 1998; 32:1.
46.
47.
Gibbons, RJ, Abrams, J, Chatterjee, K, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee on the Management of Patients With Chronic Stable
Angina). Circulation 2003; 107:149.
Gibbons, RJ, Chatterjee, K, Daley, J, et al. ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina. A report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines

(Committee on Management of Patients with Chronic Stable Angina). J Am Coll
Cardiol 1999; 33:2092.
48.
49.
50.
Weiner, DA, Ryan, TJ, McCabe, CH, et al. Exercise stress testing. Correlations among history of angina, ST- segment response and prevalence of coronary-artery disease in the Coronary Artery Surgery Study (CASS). N Engl J Med 1979; 301:230.
Diamond, GA, Forrester, JS. Analysis of probability as an aid in the clinical diagnosis of coronary- artery disease. N Engl J Med 1979; 300:1350.
Chaitman, BR, Bourassa, MG, Davis, K, et al. Angiographic prevalence of high-risk coronary artery disease in patient subsets (CASS). Circulation 1981; 64:360.
51.
52.
Wang, WH, Huang, JQ, Zheng, GF, et al. Is Proton Pump Inhibitor Testing an
Effective Approach to Diagnose Gastroesophageal Reflux Disease in Patients With
Noncardiac Chest Pain?: A Meta-analysis. Arch Intern Med 2005; 165:1222.
Borzecki, AM, Pedrosa, MC, Prashker, MJ. Should noncardiac chest pain be treated empirically? A cost-effectiveness analysis. Arch Intern Med 2000; 160:844.
53. Castell, D, Katz, P. The acid suppression test for unexplained chest pain (editorial).
Gastroenterology 1998; 115:222.
54. Wise, CM. Chest wall syndromes (Editorial review). Curr Opin Rheum 1994; 6:197.
55. Stein, PD, Terrin, ML, Hales, CA, et al. Clinical, laboratory, roentgenographic and electrocardiographic findings in patients with acute pulmonary embolism and no preexisting cardiac or pulmonary disease. Chest 1991; 100:598.
56. Lantinga, LJ, Sprafkin, RP, McCroskery, JH, et al. One-year psychosocial follow-up of patients with chest pain and angiographically normal coronary arteries. Am J Cardiol
1988; 62:209.
57. Roll, M, Kollind, M, Theorell, T. Five-year follow-up of young adults visiting an emergency unit because of atypical chest pain. J Intern Med 1992; 231:59.
58. Chernen, L, Friedman, S, Goldberg, N, Feit, A. Cardiac disease and nonorganic chest pain: factors leading to disability. Cardiol 1995; 86:15.