Approach to the adult with nontraumatic chest pain in the emergency department

INTRODUCTION — 

Chest pain is a common emergency department (ED) complaint. Patients present with a spectrum of signs and symptoms reflecting the many potential etiologies of chest pain. Diseases of the heart, aorta, lungs, esophagus, stomach, mediastinum, pleura, and abdominal viscera may all cause chest discomfort.

Clinicians in the ED focus on the immediate recognition and exclusion of life-threatening causes of chest pain. Patients with life-threatening etiologies for chest pain may appear deceptively well, manifesting neither vital sign nor physical examination abnormalities.

This topic review will discuss life-threatening and common causes of chest pain and provide an approach to the evaluation of an adult with chest pain in the ED. The outpatient evaluation of an adult with chest pain is discussed separately. (See "Outpatient evaluation of the adult with chest pain".)

EPIDEMIOLOGY — 

Chest pain is the second most common complaint in adult emergency departments (ED) patients in the United States (US), accounting for 6 to 7 percent (between 7 and 8 million) of annual visits [1]. Most visits result in a diagnosis of noncardiac chest pain, and approximately half do not have a specific cause identified and thus are considered to have nonspecific chest pain [2-4]. Approximately 6 percent are ultimately diagnosed with a life-threatening condition, which is overwhelmingly (>90 percent) acute coronary syndrome. The risk of a life-threatening diagnosis increases with advancing age.

INITIAL ASSESSMENT AND STABILIZATION

Focused history and examination — Evaluation of all patients with acute chest pain in the emergency department (ED) begins with a focused history and examination (eg, triage) to assess hemodynamic stability and for possible life-threatening causes. An algorithm outlining an approach to the ED patient with chest pain is provided (algorithm 1). Causes of chest pain that can pose an immediate threat to life include the following; clinical features are compared in the provided table (table 1):

●Acute coronary syndrome (ACS)

●Acute aortic dissection

●Pulmonary embolism

●Tension pneumothorax

●Pericardial tamponade

●Mediastinitis (eg, esophageal rupture)

●Myocarditis

●Stress (takotsubo) cardiomyopathy

●Perforated peptic ulcer

It is challenging to identify which ED patients with chest pain have life-threatening pathology since the clinical features can significantly overlap with those of benign pathology. Patients with a life-threatening etiology of chest pain may initially have normal vital signs and appear well. Conversely, patients with common, benign etiologies can present with abnormal vital signs (eg, tachycardia from pain or anxiety). In general, it is safest to assume an ED patient with chest pain and any of the following has a life-threatening condition until proven otherwise:

●Abnormal vital signs

●Obvious distress

●Signs of hypoperfusion (eg, diaphoresis, cool/clammy skin)

●Abrupt onset of thoracic or abdominal pain with a sharp, tearing, and/or ripping character (see 'Acute aortic dissection/aneurysm' below)

●Variation in pulse (absence of a proximal extremity or carotid pulse) and/or blood pressure (eg, >20 mmHg difference between the right and left arm)

If there is significant clinical suspicion, life-threatening problems should have treatment initiated immediately, without delay for confirmatory testing. (See 'Life-threatening conditions and presumptive management' below.)

General measures for unstable patients — A patient with chest pain in extremis or with hemodynamic instability requires immediate resuscitation, which includes the following measures:

●Determine the need for airway management and ventilatory support – The initial decision to provide noninvasive or invasive ventilatory support is made based upon clinical grounds, not laboratory values. (See "The decision to intubate" and "Approach to the adult with dyspnea in the emergency department", section on 'Options for oxygenation or ventilatory support'.)

●Provide supplemental oxygen, as needed – An oxygen saturation of 90 to 94 percent is an appropriate target for most patients. (See "Approach to the adult with dyspnea in the emergency department", section on 'General measures'.)

A patient with heart failure may require therapy for volume overload (eg, diuretics) and respiratory distress (eg, supplemental oxygen, positive pressure ventilation), which is discussed separately. (See "Treatment of acute decompensated heart failure: Specific therapies".)

For a patient with ACS and normal oxygen saturation, supplemental oxygen likely does not provide a benefit (and may be harmful), which is discussed separately. (See "Overview of the acute management of ST-elevation myocardial infarction", section on 'Therapies of unclear benefit'.)

●Establish intravenous (IV) access and obtain blood for laboratory measurements – If ACS is being considered, obtain a high-sensitivity troponin if available. (See 'Laboratory studies' below.)

●Begin continuous cardiac monitoring and obtain an electrocardiogram (ECG) – Also, ensure emergency resuscitation equipment (including a defibrillator and airway equipment) are nearby.

●Address any dysrhythmias – Life-threatening dysrhythmias require emergency management (algorithm 2). (See "Advanced cardiac life support (ACLS) in adults".)

The treatment and prevention of dysrhythmias in hemodynamically stable patients with and without ACS are discussed elsewhere. (See "Overview of the acute management of tachyarrhythmias" and "Ventricular arrhythmias during acute myocardial infarction: Prevention and treatment".)

●Provide circulatory support as needed – For a patient in shock, therapies targeted towards specific etiologies (eg, thoracostomy for tension pneumothorax, pericardiocentesis for cardiac tamponade) should be prioritized over crystalloid and/or vasopressor infusion for hemodynamic support. (See "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Volume' and "Use of vasopressors and inotropes" and "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction".)

If right ventricular infarction is suspected, additional management of complications such as bradyarrhythmias, hypotension, and shock may be required. (See "Right ventricular myocardial infarction".)

●Administer aspirin – In a patient without concern for aortic pathology or gastrointestinal tract perforation, give aspirin 162 to 325 mg (nonenteric coated) to be chewed and swallowed. (See "Acute ST-elevation myocardial infarction: Initial antiplatelet therapy", section on 'Aspirin' and "Acute non-ST-elevation acute coronary syndromes: Initial antiplatelet therapy", section on 'Empiric antiplatelet therapy'.)

●Obtain a portable chest radiograph (CXR) – A CXR is obtained in all chest pain patients with hemodynamic instability or a potentially life-threatening diagnosis. However, many life-threatening causes of chest pain may not manifest any abnormality on CXR. (See 'Chest radiograph (most patients)' below.)

●Perform bedside ultrasonography, if indicated – Ultrasound performed by the emergency clinician at the bedside is particularly helpful in a patient with hemodynamic instability and may identify pericardial effusions and tamponade, cardiac wall motion abnormalities (ie, ACS), global left ventricular (LV) dysfunction (ie, myocarditis, cardiomyopathy), right ventricular strain (ie, pulmonary embolism [PE]), absence of lung sliding (ie, pneumothorax), and an intimal flap or dilated aortic outflow tract (ie, aortic dissection). (See 'Bedside ultrasonography' below.)

Rapid ECG (most patients) — A standard 12-lead ECG should be obtained, (ideally by standing order) for all ED patients presenting with potential cardiac chest pain. We agree with guidelines from the American College of Cardiology and American Heart Association (ACC, AHA) that an ECG be obtained and interpreted within 10 minutes of patient presentation in the ED [5].

It can be challenging to identify at triage or early in the ED evaluation which younger adult patients should be evaluated with an ECG. One study suggested an age threshold of 30 years for obtaining an ECG [6]. Even though thresholds for age and noncardiac causes are not universally accepted, the clinician should err on the side of obtaining an ECG since these are inexpensive tests without adverse effects. However, clinical judgement can be used to identify patients who do not need an ECG. For example, a patient with chest pain in the distribution of a herpes zoster rash may not need an ECG, but a young patient with a viral prodrome or pneumonia and pleuritic chest pain may benefit from an ECG given possibility of concurrent pericarditis/myocarditis.

Although the ECG remains the best immediately available test for detecting ACS, its sensitivity for acute myocardial infarction (AMI) is low. A single ECG performed during the patient's initial presentation detects fewer than 50 percent of AMIs. Patients with normal or nonspecific ECGs have a 1 to 5 percent incidence of AMI and a 4 to 23 percent incidence of unstable angina [7-11]. Hyperacute T waves (tall, symmetric, peaked T waves) may be seen early in the course of an ST-elevation myocardial infarction (STEMI) and should prompt rapid serial ECGs (waveform 1 and waveform 2). The ECG should also be repeated if the initial ECG is not diagnostic but the patient remains symptomatic and there remains high clinical suspicion for AMI. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

Initial management and further testing are guided by interpretation of the ECG. The ECG must be interpreted in combination with the patient's signs and symptoms since many ECG findings are not specific. Reviewing prior ECGs, if available, is helpful for determining whether abnormalities are new. The following ECG findings, although a non-exhaustive list, can help focus the evaluation of specific life-threatening diagnoses:

ST-elevation (or STEMI-equivalent) — An ED patient with chest pain and ECG showing ST-elevation or a potential STEMI-equivalent (new left bundle branch block [LBBB], posterior wall STEMI, de Winter sign) requires either immediate treatment for a STEMI (table 2) or determination that the ST-elevation does not represent acute infarction (eg, identifying similar pattern on prior ECG or diagnosing pericarditis). The ST-elevation with pericarditis (waveform 3) is typically more diffuse compared with focal anatomic changes from myocardial ischemia. A patient with a STEMI should have rapid reperfusion therapy (ie, percutaneous coronary intervention, thrombolysis) and not await the result of cardiac biomarker measurement. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Acute pericarditis: Clinical presentation and diagnosis", section on 'Electrocardiogram'.)

A newly identified LBBB (waveform 4) in a patient with chest pain or other ACS symptoms may be a STEMI-equivalent. However, an existing LBBB typically causes ST-elevation and thus makes it difficult to determine if ischemia is present. The Sgarbossa criteria are specific but not sensitive for diagnosis of AMI; these are discussed separately. (See "Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm" and "Overview of the acute management of ST-elevation myocardial infarction", section on 'Rapid diagnosis of STEMI'.)

A posterior wall STEMI can manifest as horizontal ST-depression in leads V1 to V4 and relatively tall R-waves in leads V1 to V3. This should be confirmed by the presence of ST-elevation in the posterior leads V7 to V9 (waveform 5 and figure 1). A de Winter sign, which is associated with left anterior descending artery occlusion and other coronary lesions, consists of relatively tall, symmetric, T waves arising from upsloping ST-segment depression in leads V2 to V6 sometimes with ST-elevation in lead aVR (figure 2). (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Posterior wall MI' and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'de Winter sign' and "Overview of the acute management of ST-elevation myocardial infarction", section on 'Rapid diagnosis of STEMI'.)

ST-elevation can be caused by many conditions other than ischemia/infarction (table 3). (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'ST-segment elevation or depression'.)

Ischemic ECG changes without ST elevation — ST-segment depression and/or T-wave changes in an anatomic distribution suggests myocardial ischemia. (See "ECG tutorial: Myocardial ischemia and infarction", section on 'Acute myocardial ischemia and infarction' and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

A patient with ongoing chest pain, history suggestive of ACS, and ischemic ECG changes that do not meet criteria for ST-elevation should have rapidly instituted medical therapy (eg, aspirin, nitroglycerin, anticoagulation) (table 2). (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Initial assessment and interventions' and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

Nonischemic ECG changes — Examples of nonischemic ECG changes include the following:

●Nonspecific ST/T wave change – Nonspecific ST-segment and T-wave changes are common in patients with pulmonary embolism (PE), aortic dissection, and myocarditis. Patients with acute PE rarely have a normal ECG, but a wide range of abnormalities is possible and most are equally likely to be seen in patients without PE [12]. (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Electro- or echocardiography' and "Clinical features and diagnosis of acute aortic dissection", section on 'Electrocardiogram' and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Electrocardiogram'.)

ECG findings in patients with pericarditis/myopericarditis can include ST segment elevation and T wave inversions (waveform 3) and mimic AMI but are typically more diffuse compared with myocardial ischemia and may vary as the disease progresses. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Electrocardiogram'.)

●"S1Q3T3" or right heart strain – The classically described finding "S1Q3T3" (ie, prominent S wave in lead I, Q wave in lead III, and inverted T wave in lead III (waveform 6)) reflects right heart strain but is neither sensitive nor specific for PE. Right axis deviation, right bundle branch block, right atrial enlargement (ie, "P pulmonale") can all occur with a PE. If the clinical scenario suggests PE, evidence of right heart strain further increases suspicion. (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Electro- or echocardiography' and "ECG tutorial: Chamber enlargement and hypertrophy", section on 'Right atrial abnormality/enlargement'.)

●PR depression – Widespread PR segment depression (and elevation in aVR) is seen early in the course of acute pericarditis, but not in all patients (waveform 3). (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Electrocardiogram'.)

●Low-voltage QRS complex or electrical alternans (waveform 7) – These ECG findings suggest the presence of a pericardial effusion. (See "Cardiac tamponade", section on 'Electrocardiogram'.)

●Ectopy, dysrhythmias – Ventricular tachycardia (VT) and ventricular fibrillation (VF) are infrequent but life-threatening complications of a STEMI; premature ventricular beats (PVC), VT, and VF are common in the immediate post-infarction period. Atrial or ventricular ectopic beats, complex ventricular dysrhythmias (couplets or nonsustained VT), or rarely, atrial tachycardia or atrial fibrillation can occur with myocarditis. Atrial dysrhythmias (eg, atrial fibrillation) can occur with a PE. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Arrhythmias' and "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Electro- or echocardiography'.)

●Atrioventricular (AV) blocks – High grade AV blocks can occur with ACS, Lyme disease, cardiac sarcoidosis, and idiopathic giant cell myocarditis. (See "ECG tutorial: Atrioventricular block" and "Conduction abnormalities after myocardial infarction" and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Electrocardiogram'.)

Normal ECG or sinus tachycardia — A normal ECG does not exclude a life-threatening condition but makes the diagnosis of some (eg, ACS, stress cardiomyopathy) less likely. Sinus tachycardia can occur with any life-threatening cause of chest pain and is a common ECG finding in patients with a PE or pericardial tamponade.

A normal ECG (or sinus tachycardia) should prompt evaluation for noncardiac life-threatening causes of chest pain (eg, pneumothorax, mediastinitis, perforated peptic ulcer, PE, aortic dissection). For example, one-third of patients with aortic dissection will have a normal ECG. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Electrocardiogram'.)

SUBSEQUENT EVALUATION — 

Often, a definitive diagnosis cannot be made during the initial focused history and examination and additional testing is performed in parallel with management. The patient's history, comorbidities, and description of symptoms help to narrow the scope of potential diagnoses and to stratify the patient's risk for life-threatening disease. The physical examination focuses on vital sign abnormalities and cardiac or pulmonary findings and may support a diagnosis. If not already obtained, an electrocardiogram (ECG) and chest radiograph (CXR) are obtained for most patients, unless an obvious noncardiac or nonpulmonary cause (eg, zoster) is identified.

History — In a patient with chest pain, it is difficult to distinguish which organ system is involved purely on the basis of history. Symptoms significantly overlap when thoracic organs develop disease because thoracic organs share afferent nervous system pathways. Patient descriptions of their symptoms can be helpful in some instances, but emergency clinicians must guard against premature diagnostic closure based upon history. Several studies demonstrate that so-called "atypical" presentations occur more often than was previously thought, and misinterpretation of such presentations increases the risk for misdiagnosis and adverse outcomes [13,14].

A detailed history of the patient's chest pain includes the following characteristics:

●Onset and timing of pain – The rapidity of the onset (eg, abrupt or gradual) of chest pain can help to narrow the differential diagnosis. Pain that starts suddenly and is severe at onset is associated with acute aortic dissection, pneumothorax, and pulmonary embolism. Abrupt onset of pain was reported in 85 percent of patients in one registry of patients with acute aortic dissection [15]. Chest pain associated with pulmonary embolism can also begin suddenly but may worsen over time. Nontraumatic pneumothorax most often occurs suddenly at rest, without any precipitating event.

Ask about the timing of the pain, such as constant or episodic in nature, duration of episodes, and whether it is ongoing. Establish when the pain began, as that may influence timing and interpretation of cardiac biomarker testing. Ask whether the discomfort is similar to prior illness.

Ask about symptoms or events that preceded the pain, such as trauma, major surgery or medical procedures (eg, endoscopy, aortic catheterization), or periods of immobilization (eg, long plane ride). A history of forceful vomiting preceding symptoms in a toxic-appearing patient raises concern for a ruptured esophagus and mediastinitis. However, a significant portion of patients who rupture their esophagus give no history of vomiting, and presentations vary [16-18].

Conversely, discomfort from an acute coronary syndrome (ACS) typically starts gradually and may start or worsen with exertion. With stable angina, discomfort occurs only when activity creates an oxygen demand that outstrips supply limited by a fixed atherosclerotic lesion. This occurs at relatively predictable points and changes slowly over time. Unstable angina represents an abrupt change from baseline functioning, which may manifest as discomfort that begins at lower levels of exercise or at rest.

●Pain quality, location, radiation, provocation, and palliation – Patients often describe the symptoms of an ACS as discomfort rather than pain. The discomfort may be a pressure, heaviness, tightness, fullness, or squeezing. Ischemia is less likely if the discomfort is knifelike, sharp, pleuritic, or positional. The classic location is substernal or in the left chest, and radiation to the arm, neck, jaw, back, abdomen, or shoulders may occur. Pain that radiates to the shoulders (including bilateral arms) or occurs with exertion significantly increases the relative risk for ACS.

Relief of pain following the administration of sublingual nitroglycerin does not reliably distinguish between cardiac ischemia and noncardiac causes of chest pain [19,20]. Beware of "atypical" presentations of ACS, which are common and occur more often in older adults, diabetics, and women. Patients with "atypical" symptoms (eg, dyspnea, nausea, weakness) associated with their myocardial infarction fare worse than patients who experience typical symptoms, likely due to delays in diagnosis and treatment. These issues are discussed in greater detail separately. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'History' and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Atypical presentations'.)

An acute aortic dissection most often presents with the sudden onset of sharp, severe pain [15,21]. Patients may describe the pain as tearing or ripping. However, according to the International Registry of Acute Aortic Dissection (IRAD), presentations can be diverse, and classic findings absent. The pain most often occurs in the chest but can begin in the back and may migrate or radiate into other areas of the chest, back, or abdomen, depending upon the portion of the aorta involved and the extent of the dissection. Pain extending beyond the thorax should significantly raise concern of an aortic dissection. We recommend calculation of an aortic dissection detection (ADD) score. In a study with 2538 patients with acute aortic dissection, 96 percent (2430) were identified as having at least one of the clinical risk markers [22]. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Aortic dissection detection risk score (ADD-RS)'.)

Sharp pain may also accompany pulmonary embolism, pneumothorax, or pericarditis.

A pulmonary embolism (PE) can create different kinds of pain, or painless dyspnea. Pain associated with PE may worsen with deep inspiration and may localize to the chest wall. Patients with pneumothorax report ipsilateral chest pain, which may initially be sharp and pleuritic but may become dull or achy over time. The discomfort of pericarditis is classically positional: worse when lying supine and relieved somewhat when leaning forward. It may also worsen with deep inspiration.

Sharp, well-localized pain clearly reproduced with movement or palpation of the chest wall is characteristic of musculoskeletal causes. Often the patient relates a history of trauma or strenuous activity prior to developing pain.

Burning pain in the chest and epigastrium is commonly associated with gastrointestinal causes. Esophageal rupture can cause chest and/or abdominal pain. Cardiac disease can cause identical symptoms, however, and emergency clinicians must avoid prematurely attributing such symptoms to gastrointestinal disease.

●Associated symptoms – Diaphoresis, nausea, and vomiting frequently accompany chest discomfort associated with, but are not predictive of, ACS [23]. These symptoms may also occur with nonischemic chest pain, including aortic dissection, PE, acute heart failure, and esophageal spasm. Nausea and belching frequently accompany gastrointestinal causes of chest pain, but can also occur in patients with inferior myocardial infarction (MI).

Acute aortic dissection has a wide range of potential associated symptoms depending on the arterial branches involved, which may confound the diagnosis (table 4). According to one review, syncope accompanies 13 percent of dissections involving the ascending aorta [24]. Neurologic symptoms, ranging from hoarseness to paraplegia and altered mental status, occur in 18 to 30 percent of patients with aortic dissection [24]. ACS can occur when the dissection involves the coronary arteries.

Dyspnea frequently accompanies pulmonary causes of chest pain and may be the predominant symptom in PE, pneumothorax, and pneumonia. Tachypnea is common with PE and may be accompanied by wheezing and fever. Young healthy patients may manifest only a relative tachypnea or tachycardia despite the presence of pneumonia or pulmonary embolism. Dyspnea is often the only complaint among older adults with ACS.

Cough, syncope, and hemoptysis may occur with PE or valvular heart disease (particularly mitral stenosis), although cough and hemoptysis are more common with bronchitis, pharyngitis, or COPD exacerbations. Dyspnea and cough may accompany pericardial and pleural effusions regardless of etiology.

Preceding or concomitant pain and swelling in an extremity suggests deep venous thrombosis (DVT) complicated by PE. DVT occurs most often in the lower extremities, but clots may also originate in the upper extremities and the large veins of the pelvis, where they may produce bilateral lower extremity swelling if the inferior vena cava becomes occluded.

Fever raises concern for infectious causes, but is also associated with pericarditis, myocarditis, and rarely, acute myocardial infarction (AMI). A low-grade fever may accompany PE.

●Risk factors – Risk factors for ACS include male sex, age over 55 years, family history of coronary artery disease, peripheral artery disease, diabetes mellitus, hypercholesterolemia, hypertension, prior abnormal stress test, and tobacco use [25]. The presence of chest pain concerning for ACS or ischemic ECG changes is much more predictive of ACS compared with just the cardiac risk factors [26]. The absence of cardiac risk factors does not identify patients that can safely be discharged from the emergency department (ED). Cocaine or amphetamine use raises concern for ACS regardless of other risk factors. Cocaine increases the metabolic demands of the heart via its stimulant effects, and also causes coronary artery vasoconstriction and promotes thrombus formation in patients who may otherwise be at low risk for ACS. (See "Overview of established risk factors for cardiovascular disease" and "Cocaine: Acute intoxication" and "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine use" and "Acute amphetamine and synthetic cathinone ("bath salt") intoxication".)

Aortic dissection occurs most often in older patients with systemic hypertension and atherosclerotic disease but also occurs in patients with acquired or congenital conditions that weaken the structural architecture of the aortic wall. Patients younger than 40 years of age with connective tissue disorders (eg, Marfan syndrome), bicuspid aortic valve, cocaine use, or pregnancy (particularly in combination with bicuspid aortic valve or connective tissue disease) are at risk for aortic dissection. Other factors that predispose to aortic dissection include previous aortic surgery and recent cardiac surgery or aortic instrumentation. (See "Clinical features and diagnosis of acute aortic dissection", section on 'High-risk conditions' and "Overview of acute aortic dissection and other acute aortic syndromes".)

An increased risk for DVT/PE exists among patients with a recent history of prolonged immobilization (eg, long distance travel), surgery (particularly an orthopedic procedure of the lower extremity lasting more than 30 minutes), central venous catheterization, trauma, pregnancy, patients with cancer, lung, or chronic heart disease, and those with a personal or family history of hypercoagulability. Use of certain hormonal contraceptives [27] or chemotherapeutic agents that raise serum levels of estrogen and, to a lesser extent, progestin also confer increased risk. A significant number of patients with PE may have no identifiable risk factor at the time of diagnosis, but subsequent evaluation reveals a hematologic predisposition for venous thrombosis (eg, Factor V Leiden mutation) or anatomic predisposition (eg, thoracic outlet syndrome). (See "Pulmonary embolism: Epidemiology and pathogenesis in adults", section on 'Pathogenesis and pathophysiology'.)

Tobacco use increases risk for cardiovascular and pulmonary disease and is an independent risk factor for spontaneous pneumothorax, regardless of underlying lung disease. A high prevalence of spontaneous pneumothorax exists among patients with HIV and pneumocystis carinii (P. jirovecii) pneumonia. Young females with endometriosis may experience menses-related pneumothoraces (ie, catamenial pneumothorax) if pleural involvement exists [28]. Activities, such as self-contained underwater breathing apparatus (SCUBA) diving can precipitate a spontaneous pneumothorax, and air travel may precipitate recurrence in patients with an incompletely healed pneumothorax [29]. (See "Complications of SCUBA diving" and "Pneumothorax and air travel in adults" and "Pneumothorax in adults: Epidemiology and etiology", section on 'Subpleural blebs' and "Clinical presentation and diagnosis of pneumothorax".)

●Prior testing – Ask about prior diagnostic studies (eg, stress test or coronary computed tomography [CT] angiography) or procedures (eg, cardiac catheterization) performed to evaluate similar symptoms. For example, a recent cardiac catheterization or coronary CT angiogram with normal or minimally diseased vessels virtually eliminates the possibility of ACS. A study of 1977 consecutive patients with coronary arteriograms documenting minimal (ie, less than 25 percent) stenosis or normal coronary arteries found that 98 percent had a 10-year interval without an MI [30]. Other studies have found similar results [31]. Conversely, a prior negative stress test is not useful to rule out ACS in a patient with active chest pain in the ED. Testing in patients with recurrent chest pain is discussed further below. (See 'Cause of chest pain not identified and clinically well patient' below.)

Physical examination — Patients with an immediately life-threatening cause for their chest pain tend to appear anxious and distressed and may be diaphoretic and dyspneic. Significant vital signs abnormalities (eg, hypoxia, tachycardia, bradycardia, hypotension) should be addressed immediately. (See 'General measures for unstable patients' above.)

Physical examination findings in patients with acute aortic dissection may be absent or suggestive of end-organ ischemia due to aortic branch vessel occlusion (depending on the affected arteries), including myocardial infarction, stroke, acute intestinal ischemia, or extremity ischemia (table 4). Discrepancies in pulses or blood pressure are notable findings when present but occur infrequently. In the International Registry of Acute Aortic Dissection (IRAD), signs of dissection included: murmur of aortic insufficiency (32 percent), pulse deficit (15 percent), signs of shock or cardiac tamponade (8 percent), acute heart failure (7 percent), and cerebrovascular accident (5 percent) [15]. Up to 30 percent of patients may have neurologic findings (eg, Horner syndrome, paraparesis, paraplegia). (See "Clinical features and diagnosis of acute aortic dissection", section on 'Clinical features'.)

Chest pain associated with focal wheezing or asymmetric extremity swelling raises concern for PE. Most often patients with PE have a normal extremity examination. Unilateral decreased breath sounds may be noted with pneumothorax; subcutaneous emphysema is uncommon. Pneumonia can cause adventitious breath sounds, including rales/crackles and rhonchi.

Most often the physical examination is not helpful in distinguishing patients with ACS from those with noncardiac chest pain. ACS is characterized by a paucity of examination findings. The presence of pulmonary crackles, with or without an S3 gallop, is associated with left ventricular dysfunction and left-sided heart failure, possibly due to ACS. Jugular venous distention (movie 1), hepatojugular reflux, and peripheral edema suggest right-sided heart failure, possibly due to ACS or PE. A new systolic murmur is an ominous sign that may signify papillary muscle dysfunction or a ventricular septal defect. Clinicians may hear a pericardial friction rub in patients with pericarditis.

In some instances, physical findings suggest a specific noncardiac diagnosis. For example, epigastric tenderness and heme positive stool suggest a possible gastrointestinal source for pain. Hamman's crunch is a crackling sound (movie 2) similar to a pericardial friction rub heard over the mediastinum in patients with mediastinal emphysema.

General measures if concern for life-threatening condition — If there is a concern that the patient may have a life-threatening condition (table 1) following the history and examination, the patient should have the same general measures as described above (if not performed during initial stabilization), with the exception that the CXR does not have to be portable. (See 'General measures for unstable patients' above.)

Diagnostic testing — An ECG and CXR are obtained for most ED patients with chest pain, and further testing is based on clinical suspicion. However, there is wide variation in diagnostic testing and ultimately depends upon clinical judgement. For example, in one study of 1341 ED patients with chest pain and a noncardiac discharge diagnosis, 89 percent had an ECG, and 81 percent had at least one troponin [4].

ECG interpretation is discussed above. (See 'Rapid ECG (most patients)' above.)

Chest radiograph (most patients) — A posterior-anterior (PA) and lateral CXR is obtained for most patients, unless an obvious nonpulmonary cause (eg, ST-elevation MI, zoster) is identified. If a single-view CXR was obtained as part of the initial stabilization and is diagnostic, a two-view CXR may not be necessary.

The CXR may be diagnostic (eg, pneumothorax), but even in the presence of a life-threatening condition it may be normal (eg, ACS, PE) or have nonspecific findings that increase suspicion for a process (eg, atelectasis for PE). Approximately 90 percent of patients with an acute aortic dissection will have some CXR abnormality [32]. The vast majority of patients with a PE or ACS have a normal or nonspecific CXR.

The following CXR findings, although a non-exhaustive list, can help focus the evaluation of specific life-threatening diagnoses (see "Evaluation of diffuse lung disease by conventional chest radiography"):

●Parenchymal processes – Signs of heart failure that may appear on a CXR include alveolar and/or interstitial (eg, "Kerley B" lines, peribronchial cuffing) pulmonary edema, cephalization of blood vessels, and vascular congestion (image 1). An ACS can also cause sudden impairment in systolic and/or diastolic function, resulting in decreased cardiac output, elevated filling pressures, and the development of pulmonary edema. (See "Heart failure: Clinical manifestations and diagnosis in adults".)

In the appropriate clinical context, an infiltrate on CXR is diagnostic of pneumonia (image 2). (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Chest radiograph (preferred)'.)

Atelectasis is a common finding in patients with a PE. Classically described but rare findings associated with PE include pleural-based wedge-shaped defect (representing infarcted lung parenchyma, so-called Hampton hump (image 3)) or paucity of vascular markings distal to the site of embolus (Westermark sign (image 4)). (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Chest radiograph'.)

●Pleural effusion – The presence of a pleural effusion is nonspecific and can be seen with PE, aortic dissection, pneumonia, mediastinitis, heart failure, and many other processes. Once a life-threatening condition is excluded (typically with CT imaging), an unexplained pleural effusion requires further evaluation, which is discussed separately. (See "Diagnostic evaluation of the hemodynamically stable adult with a pleural effusion" and "Imaging of pleural effusions in adults", section on 'Conventional radiography'.)

●Mediastinal widening/pathology – The classic findings of a widened mediastinum or aortic knob occur in up to 76 percent of patients with an aortic dissection [32]. If clinical suspicion is high, these findings are associated with an odds ratio of 11 for aortic dissection (95% CI 6.1-19.8). Displacement of the aorta may also be seen. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Chest radiograph'.)

In patients with severe vomiting or recent instrumentation of the esophagus, mediastinal emphysema suggests esophageal rupture. (See "Boerhaave syndrome: Effort rupture of the esophagus".)

A hiatal hernia or mediastinal mass may also explain the patient's symptoms. (See "Approach to the adult patient with a mediastinal mass".)

●Cardiomegaly – An enlarged cardiac silhouette on CXR can occur with a pericardial effusion (typically >200 mL) (image 5), myocarditis, cardiomyopathy, and other causes. (See "Pericardial effusion: Approach to diagnosis", section on 'Chest radiograph' and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Chest radiograph' and "Heart failure: Clinical manifestations and diagnosis in adults".)

●Pneumothorax – The presence of a pneumothorax is established by demonstrating a white visceral pleural line without peripheral bronchovascular markings (image 6). (See "Clinical presentation and diagnosis of pneumothorax", section on 'Chest radiography'.)

●Pneumoperitoneum – Free air under the hemidiaphragm on upright radiograph confirms the diagnosis of a perforated abdominal viscus (image 7). (See "Overview of gastrointestinal tract perforation", section on 'Chest imaging'.)

Directed studies based on clinical suspicion

Laboratory studies

●Cardiac biomarkers – Troponin is the preferred laboratory test for the diagnosis of acute myocardial infarction (AMI). We prefer high-sensitivity troponin assays, when available. In the setting of AMI, assays for cardiac troponin I and T detect elevations within 2 to 3 hours, peak at 12 hours, and remain elevated for 7 to 10 days. (See "Troponin testing: Clinical use" and "Diagnosis of acute myocardial infarction".)

Unless the patient has symptoms for more than 2 hours and the initial value of a high-sensitivity troponin T is below the level of detection (<6 ng/L), a single set of negative cardiac biomarkers is not sufficient to rule out AMI [33]. Initial cardiac biomarker determinations above the level of detection cannot be used to determine discharge, but abbreviated interval testing (at 0 and 1, 2 or 3 hours) using high-sensitivity troponins may allow for safe discharge and reduce additional testing in patients otherwise at low risk for ACS [34-36]. Interpretation of troponin results for diagnosing ACS and timing of serial troponin testing are discussed separately. (See "Evaluation for suspected non-ST-segment elevation acute coronary syndromes".)

Troponin can also be elevated from mechanisms other than acute thrombotic occlusion of a coronary artery (table 5). (See "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".)

●D-dimer – In patients with a low-or moderate pretest probability for PE (table 6), a D-dimer test with high sensitivity can rule out the diagnosis, obviating the need for further testing. The utility of the D-dimer test depends upon both patient baseline characteristics and the sensitivity and specificity of the assay employed. Patients likely to have an elevated D-dimer at baseline are those with advanced age, malignancy, sepsis, recent major surgery or trauma, or pregnancy (table 7). The interpretation of a D-dimer result (eg, fixed cut-off, age-adjusted, YEARS criteria) is discussed separately. (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'D-dimer with standard fixed cutoff'.)

D-dimer in combination with the Aortic Dissection Detection Risk Score (ADD-RS) may be useful to rule out suspected aortic dissection (table 8) [37]. (See "Clinical features and diagnosis of acute aortic dissection", section on 'ADD-RS plus D-dimer'.)

●Complete blood count – The white blood cell count may be elevated in any of the inflammatory or infectious etiologies of chest pain, such as myocarditis and pericarditis, mediastinitis, and pneumonia. Anemia in a patient with exertional chest pain is suggestive of myocardial ischemia, but also consistent with aortic rupture.

●B-type natriuretic peptide (BNP) and NT-proBNP – BNP levels above 100 pg/mL are highly sensitive for acute heart failure (HF), while levels below 50 pg/mL have a high negative predictive value for HF. When used in conjunction with other clinical information, natriuretic peptide concentrations can help to identify or exclude acute HF as the cause of dyspnea and chest pain, but other conditions can also elevate the plasma concentrations of natriuretic peptides. (See "Natriuretic peptide measurement in heart failure" and "Natriuretic peptide measurement in non-heart failure settings".)

●Coagulation indices – These should be obtained in a patient taking an anticoagulant medication or if there is concern for hemorrhage.

●Basic electrolyte concentrations, kidney function studies – These are helpful in a patient who may need intravenous contrast, such as for a CT or coronary angiography.

●Liver biochemical tests, lipase – The serum aminotransferases and lipase are helpful in patients with clinical suspicion for biliary tract disease or pancreatitis (eg, associated epigastric or right upper quadrant pain or tenderness, radiation to back or right shoulder). (See "Clinical manifestations, diagnosis, and natural history of acute pancreatitis", section on 'Pancreatic enzymes and products' and "Acute calculous cholecystitis: Clinical features and diagnosis", section on 'Laboratory studies'.)

●Arterial blood gas – An arterial blood gas is not routinely indicated for patients with chest pain, even when PE is suspected. The arterial-alveolar oxygen gradient provides little help in diagnosing or excluding PE or in distinguishing PE from other causes of ventilation-perfusion mismatch. (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Laboratory tests'.)

●Acute phase reactants – Erythrocyte sedimentation rate (ESR) and/or c-reactive protein (CRP) are often elevated in acute myocarditis. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Acute phase reactants'.)

●Other tests – Several biomarkers are being studied for use in early diagnosis of aortic dissection, but their role remains unclear. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Other experimental tests'.)

Bedside ultrasonography — Ultrasound performed by the emergency clinician at the bedside often helps to exclude or support certain diagnoses in a patient with chest pain, such as the following:

●Pericardial tamponade – Pericardial effusion, cardiac chamber collapse, abnormal septal motion with respiratory variation, inferior vena cava plethora (movie 3) (see "Emergency ultrasound in adults with abdominal and thoracic trauma", section on 'Pericardial and limited cardiac examination' and "Cardiac tamponade", section on 'Echocardiography')

●Acute coronary syndrome (ACS) – Cardiac wall motion abnormalities supports ischemia in the appropriate clinical setting (see "Role of echocardiography in acute myocardial infarction", section on 'Use of echocardiography')

●PE – Right heart strain, McConnell sign, or deep vein thrombosis supports the diagnosis (see 'Pulmonary embolism' below and "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Echocardiography' and "Echocardiographic assessment of the right heart" and "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity", section on 'Diagnostic compression ultrasonography (CUS)')

●Aortic dissection – Pericardial effusion, intimal flap, or aortic outflow track diameter >35 mm [38] (see "Clinical features and diagnosis of acute aortic dissection", section on 'Cardiovascular imaging')

●Pneumothorax – Presence of lung point, absence of lung sliding (image 8 and movie 4) (see "Bedside pleural ultrasonography: Equipment, technique, and the identification of pleural effusion and pneumothorax", section on 'Evaluation for pneumothorax' and "Clinical presentation and diagnosis of pneumothorax", section on 'Diagnostic imaging')

●Pneumonia – Focal B-lines ("comet tails"), irregular pleural morphology, hypoechoic areas appearing similar to hepatic parenchyma, air bronchograms [39] (see "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Evaluation of the etiology of cardiopulmonary failure' and "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Ultrasound and other studies')

●Pleural effusion – Anechoic area within appropriate anatomic boundaries (eg, diaphragm, lung) (image 9) (see "Bedside pleural ultrasonography: Equipment, technique, and the identification of pleural effusion and pneumothorax", section on 'Identification of pleural effusion using ultrasonography' and "Imaging of pleural effusions in adults")

●Heart failure – Multiple diffuse bilateral B-lines, smooth pleural morphology, pleural effusions, reduced left ventricle (LV) function (see "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Lung ultrasound' and "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Thoracic ultrasonography')

●Myocarditis/cardiomyopathy – LV dilation, global systolic dysfunction, and occasionally wall motion abnormalities in the appropriate clinical setting suggest these diagnoses (see "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Echocardiography')

Advanced imaging studies — CT is the preferred imaging modality in most ED patients with chest pain not suspicious for ACS who require advanced imaging for diagnosis. CT can identify aortic dissection, PE, mediastinal pathology, distinguish a pulmonary bleb from true pneumothorax, parenchymal processes (eg, pneumonia), and chest wall pathology (eg, rib fracture). CT may thus identify an alternate diagnosis when performed to exclude aortic dissection or PE. Advanced imaging based on suspicion by diagnosis includes the following:

●Acute aortic dissection – Several modalities diagnose aortic dissection with high sensitivity, including CT (98 percent), magnetic resonance imaging (MRI) (98 percent), and transesophageal echocardiography (TEE) (94 percent).

The patient's clinical presentation (likelihood of ascending aortic dissection, hemodynamic status) and the availability and institutional expertise with particular imaging modalities determine the approach to diagnostic imaging. CT angiography is the most common initial study given that it is widely available and enables prompt diagnosis, but may be contraindicated in patients with a contrast allergy or kidney insufficiency. The decision to give contrast must be balanced against the need for immediate diagnosis, weighing the clinical index of suspicion, the hemodynamic stability of the patient, and the availability of other modalities. TEE allows for rapid beside diagnosis of the hemodynamically unstable patient but requires an experienced echocardiographer. MRI may provide the greatest anatomic detail about the site of the intimal tear and branch vessel involvement, but it is not universally available in EDs, requires more time to perform than CT, cannot accommodate patients with indwelling metallic hardware, and often requires transport from the ED to another department. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Diagnosis' and "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)

●Pulmonary embolism – PE can be diagnosed by CT, nuclear imaging (ventilation/perfusion scan), or pulmonary angiography.

Chest CT angiogram with contrast (CTPA) is the most widely used study for the diagnosis of PE. Imaging with multidetector CT scanners allows for visualization of PE in the subsegmental pulmonary arteries, although smaller emboli are of questionable clinical significance. CTPA combined with venography can detect a deep vein thrombosis (DVT) using a single dose of contrast agent. Duplex ultrasonography can be helpful in patients at risk for PE with physical findings suggestive of DVT. Nuclear ventilation/perfusion lung scanning is mostly reserved for patients in whom CTPA is contraindicated or inconclusive, but frequently results in subsequent imaging because of the high number of indeterminant studies. Pulmonary angiography, once the gold standard, is rarely used. (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'CTPA' and "Pulmonary embolism in pregnancy: Clinical presentation and diagnosis", section on 'Diagnostic imaging'.)

●Acute coronary syndrome – The diagnosis of ACS can be facilitated or excluded with CT coronary angiography (CCTA) or cardiac stress testing. At institutions where 64-slice cardiac CT scanner or better and local expertise are available, CCTA can be used in symptom-free patients with nonischemic ECGs and one initial negative troponin. (See "Noninvasive imaging for diagnosis in patients at low to intermediate risk for acute coronary syndrome", section on 'Patients whose symptoms have resolved'.)

CCTA can identify obstructive coronary artery stenosis and studies suggest excellent accuracy compared with invasive coronary angiography (ie, cardiac catheterization). Trials have found that CCTA can safely facilitate higher rates of discharge from the ED [40,41]. CCTA can be combined with protocols to exclude PE and dissection (ie, triple rule out CT) but have been associated with increased radiation exposure [42]. (See "Cardiac imaging with computed tomography and magnetic resonance in the adult", section on 'Cardiac CT'.)

Many EDs have chest pain observation units that can perform cardiac stress testing. The most commonly used and widely available stress testing modalities are exercise ECG (non-imaging) and exercise or pharmacologic stress combined with imaging (stress echocardiography or stress radionuclide myocardial perfusion imaging). A main objective of stress testing is to assess the functional or physiological consequences of anatomic coronary artery disease and can assist in the risk stratification of ED patients with suspected ACS. (See "Stress testing for the diagnosis of obstructive coronary artery disease" and "Evaluation for suspected non-ST-segment elevation acute coronary syndromes", section on 'Indeterminate testing or elevated risk'.)

●Myocarditis, pericarditis, pericardial effusion/tamponade, stress (takotsubo) cardiomyopathy – Specific patterns on transthoracic echocardiogram (TTE) can raise suspicion and aid in the diagnosis of these processes. For example, the presence of apical ballooning suggests stress cardiomyopathy, and global left ventricular dysfunction suggests myocarditis. Echocardiography plays a key role in identification of a pericardial effusion and assessing its hemodynamic significance (eg, diastolic right atrium collapse). Additionally, the presence of regional wall dysfunction may point to ischemia as a diagnosis. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Echocardiography' and "Acute pericarditis: Clinical presentation and diagnosis", section on 'Echocardiogram' and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Identification of wall motion abnormalities' and "Cardiac tamponade", section on 'Echocardiogram' and "Role of echocardiography in acute myocardial infarction".)

●Mediastinitis, perforated peptic ulcer – Imaging is discussed above and separately. (See 'Mediastinitis' below and 'Perforated peptic ulcer' below and "Boerhaave syndrome: Effort rupture of the esophagus", section on 'Diagnosis' and "Overview of complications of peptic ulcer disease" and "Overview of gastrointestinal tract perforation".)

CAUSES OF CHEST PAIN — 

Many processes can be the cause of chest pain in emergency department (ED) patients (table 9).

Life-threatening conditions and presumptive management — Life threatening conditions include the following:

Acute coronary syndrome — Acute coronary syndrome (ACS) is the most common potentially life-threatening cause of chest pain encountered in the ED.

The 28-day case mortality rate for an ACS among patients in resource-abundant settings can be as high as 10 percent, depending upon the severity of disease and the treatment provided [43,44]. Older adults, patients with diabetes, and women are more likely to manifest "atypical" symptoms with ACS. A summary of immediate treatment interventions for patients with ACS is provided in the table (table 2). (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

Unless a high-sensitivity troponin is available, do not rely on a single electrocardiogram (ECG) or a single set of cardiac biomarkers to rule out ACS, unless symptoms have been continuous and prolonged (ie, over six to eight hours). (See 'Diagnostic testing' above and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Disposition'.)

The use of risk scores (eg, HEART score) and care pathways to stratify risk for ACS in ED patients with chest pain is discussed separately. (See "Evaluation for suspected non-ST-segment elevation acute coronary syndromes".)

Assume that any patient who presents with symptoms of an ACS within a few days or weeks following percutaneous coronary interventions (eg, angioplasty or stent placement) or coronary artery bypass grafting has an abruptly occluded coronary artery or graft until proven otherwise. (See "Coronary artery stent thrombosis: Clinical presentation and management" and "Early cardiac complications of coronary artery bypass graft surgery", section on 'Early graft occlusion'.)

Acute aortic dissection/aneurysm — The incidence of aortic dissection is estimated at 3 per 100,000 patients per year, which may be an underestimation, as many patients die prior to diagnosis. Aortic dissection most commonly affects patients with systemic hypertension in their seventh decade of life, but it can affect younger individuals, particularly those with known aortic valve or connective tissue abnormalities. Dissection typically begins with a tear in the inner layer of the aortic wall allowing blood to track between the intima (inner layer) and media (middle layer). Pulsatile blood flow causes propagation of the dissection with subsequent obstruction of branch arteries (eg, coronary, carotid, mesenteric) leading to ischemic injury to areas perfused by those vessels. A thoracic aortic aneurysm typically does not cause symptoms unless it rapidly expands, dissects, ruptures, or compresses other intrathoracic structures. The clinical picture of aortic intramural hematoma and other acute aortic syndrome (eg, penetrating aortic ulcer, aortic rupture, thoracic aortic aneurysm) is similar to classic acute aortic dissection. (See "Clinical features and diagnosis of acute aortic dissection" and "Overview of acute aortic dissection and other acute aortic syndromes" and "Clinical manifestations and diagnosis of thoracic aortic aneurysm".)

High-risk conditions include Marfan syndrome, family history of aortic disease, known aortic valve disease, known thoracic aortic aneurysm, or previous aortic manipulation, including cardiac surgery. The presence of one or more of the following factors significantly increases the probability of aortic dissection, but the absence of all three does not exclude the diagnosis (see "Clinical features and diagnosis of acute aortic dissection", section on 'High-risk clinical features'):

●Abrupt onset of thoracic or abdominal pain with a sharp, tearing and/or ripping character

●Variation in pulse (absence of a proximal extremity or carotid pulse) and/or blood pressure (>20 mmHg difference between the right and left arm)

●Chest radiograph (CXR) with mediastinal and/or aortic widening

The use of the Aortic Dissection Detection Risk Score (ADD-RS) (table 8) with or without D-dimer testing is discussed in detail separately. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Aortic dissection detection risk score (ADD-RS)'.)

Definitive diagnostic testing is determined by the patient's hemodynamic stability and the imaging modalities available. For a hemodynamically unstable patient, a transesophageal echocardiography (TEE) is generally preferred since it can be performed at the bedside. For a hemodynamically stable patient, compute tomography (CT) angiography is preferred, but magnetic resonance (MR) angiography is an alternative. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Cardiovascular imaging'.)

For a patient with an aortic dissection, immediate treatment involves anti-impulse therapy with blood pressure (<120/80 mmHg) and heart rate (<60 beats per minute) control to reduce shearing forces and intensity of pulsatile cardiac flow (table 10). If high clinical suspicion, anti-impulse therapy should be started before the diagnosis is confirmed with imaging. Combination antihypertensive drug therapy (eg, beta-blocker and vasodilator) is usually required and provided in the table (table 11). (See "Management of acute type B aortic dissection", section on 'Medical management'.)

Emergency cardiac and/or vascular surgery consultation is obtained. Aortic dissection affecting the ascending thoracic aorta and complicated dissection involving the descending aorta (figure 3) require endovascular or surgical intervention. (See "Management of acute type A aortic dissection" and "Management of acute type B aortic dissection", section on 'Approach to intervention'.)

Pulmonary embolism — The incidence of pulmonary embolism (PE) is estimated at 0.4 per 1000 patient years. Mortality rates vary widely based upon comorbid conditions and the size of the embolus. Early diagnosis and treatment reduce mortality. Pulmonary embolism occurs when a dislodged venous clot migrates through the right side of the heart and becomes lodged at the branch point of the pulmonary arteries (saddle embolus) or more distally. Occlusion of pulmonary blood flow results in pulmonary hypertension, right ventricular dysfunction, poor gas exchange, and ultimately parenchymal infarction. (See "Pulmonary embolism: Epidemiology and pathogenesis in adults".)

PE can be challenging to diagnose because of its wide range of presentations and nonspecific findings on examination, ECG, and CXR. PE can be missed if the diagnosis is not considered; PE should be considered a potential diagnosis in any patient with acute chest discomfort or dyspnea who lacks a firm alternative diagnosis (eg, myocardial infarction [MI] diagnosed by history and elevated ST segments, pericardial tamponade diagnosed by ultrasound).

The approach to patients with potential PE focuses on risk stratification. Patients with a high Wells score (table 6) (calculator 1) or signs of right ventricular heart dysfunction or hemodynamic instability are at high risk and should have a CT angiogram or ventilation perfusion (V/Q) scan (algorithm 3). For all other patients, risk stratification depends on the pretest probability for PE. Patients with a negative Pulmonary Embolism Rule-out Criteria (PERC) score (table 12) (calculator 2) can be ruled out for PE without D-dimer testing. Patients at low or moderate risk for PE according to a validated scoring system (eg, Wells score, YEARS criteria) and a negative D-dimer can be ruled out for PE without further testing (algorithm 4 and algorithm 5). Detailed discussions of risk stratification and diagnosis are found separately. (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism" and "Pulmonary embolism in pregnancy: Clinical presentation and diagnosis".)

Bedside ultrasonography or echocardiography can provide important confirmatory findings, particularly in hemodynamically unstable patients. The presence of right heart strain is approximately 50 percent sensitive and 83 percent specific for PE in the proper clinical setting [45]. McConnell sign (normal motion at the right ventricular apex relative to akinesis or hypokinesis of the right ventricle free wall) appears to be more specific for PE than global right ventricular dysfunction [46]. (See "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Echocardiography' and "Echocardiographic assessment of the right heart".)

Initial management for confirmed pulmonary embolus involves anticoagulation (algorithm 6). For a patient at low-clinical risk, it is generally reasonable to withhold anticoagulant therapy pending the evaluation. A patient with hemodynamic instability may require thrombolytic therapy or embolectomy (algorithm 7). In a patient with a presumptive diagnosis of PE, and definitive diagnostic testing is unsafe or not feasible, thrombolytic therapy may need to be administered based on clinical suspicion combined with bedside ultrasonography or echocardiography findings (if available). Detailed discussions of treatment is found separately. (See "Acute pulmonary embolism in adults: Treatment overview and prognosis".)

Pneumothorax — Pneumothorax can occur following trauma or pulmonary procedures. It also occurs spontaneously in patients with underlying lung disease (secondary pneumothorax) and without (primary pneumothorax) (image 6). Patients with primary spontaneous pneumothorax tend to be younger males who are tall and thin. Secondary spontaneous pneumothorax occurs with greatest frequency in patients with chronic obstructive pulmonary disease, cystic fibrosis, and asthma. Regardless of etiology, the accumulation of air in the pleural space can lead to tension pneumothorax with compression of the mediastinum, causing rapid clinical deterioration and death if unrecognized. (See "Pneumothorax in adults: Epidemiology and etiology".)

Tension pneumothorax is diagnosed clinically by hemodynamic compromise and unilateral diminished breath sounds. Treatment should not be delayed for confirmation by chest radiograph. Pneumothorax can also be identified by bedside ultrasonography (image 8). (See "Bedside pleural ultrasonography: Equipment, technique, and the identification of pleural effusion and pneumothorax", section on 'Evaluation for pneumothorax' and "Clinical presentation and diagnosis of pneumothorax", section on 'Diagnostic imaging'.)

Tension pneumothorax is treated with immediate finger, needle, or tube thoracostomy. (See "Thoracostomy tubes and catheters: Placement techniques and complications" and "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Role of needle/finger chest decompression'.)

Symptomatic pneumothoraces not under tension are treated with tube thoracostomy, aspiration, or observation. (See "Treatment of primary spontaneous pneumothorax in adults" and "Treatment of secondary spontaneous pneumothorax in adults".)

Mediastinitis — Common causes of mediastinitis include odontogenic infections, esophageal perforation, and iatrogenic complications of cardiac surgery or upper gastrointestinal and airway procedures. Mortality for patients with mediastinitis remains high (14 to 42 percent) even when treated with operative debridement and antibiotics [47-50]. Delays in diagnosis further increase mortality. (See "Boerhaave syndrome: Effort rupture of the esophagus" and "Postoperative mediastinitis after cardiac surgery".)

The initial plain chest radiograph is almost always abnormal in patients with esophageal perforation and mediastinitis and usually reveals mediastinal or free peritoneal air. CT scan may show extraesophageal air, periesophageal fluid, mediastinal widening, and air and fluid in the pleural spaces, retroperitoneum or lesser sac. The diagnosis is confirmed contrast esophagram or CT scan. (See "Boerhaave syndrome: Effort rupture of the esophagus", section on 'Diagnosis'.)

Broad spectrum antibiotics are given early in suspected mediastinitis. Consultation with cardiothoracic surgery is obtained for surgical debridement and possible repair. (See "Boerhaave syndrome: Effort rupture of the esophagus", section on 'Management'.)

Pericardial tamponade — Pericardial tamponade occurs when there is accumulation of pericardial fluid under pressure, leading to impaired cardiac filling. Tamponade covers a spectrum of clinical severity. Some patients have mild compromise, while others develop a severe compromise in cardiac filling, producing a picture resembling cardiogenic shock that requires immediate reduction in pericardial pressure by pericardiocentesis. Tamponade may occur with aortic dissection, after thoracic trauma, or as a consequence of acute pericarditis from infection, malignancy, uremia, or some other cause. (See "Cardiac tamponade".)

Bedside ultrasonography can diagnose (movie 3) or rule out cardiac tamponade and should be performed in every ED patient with chest pain and signs of shock. (See "Emergency ultrasound in adults with abdominal and thoracic trauma", section on 'Pericardial and limited cardiac examination'.)

Tamponade with overt hemodynamic compromise requires immediate removal of pericardial fluid, which produces a rapid and dramatic improvement in cardiac and systemic hemodynamics. Early tamponade with only mild hemodynamic compromise may be treated conservatively, with careful monitoring, serial echocardiographic studies, avoidance of volume depletion, and therapy aimed at the underlying cause. (See "Pericardial effusion: Approach to management".)

Myocarditis — Myocarditis is an inflammatory disease of cardiac muscle caused by a variety of infectious and noninfectious conditions (table 13). Myocarditis can occasionally be severe and cause dilated cardiomyopathy with left ventricular (LV) dysfunction, cardiogenic shock, dysrhythmias, and sudden death. Diagnosis typically involves measurement of cardiac biomarkers, acute phase reactants, and cardiac imaging (echocardiography, coronary angiography, and/or cardiac magnetic resonance). Depending on the etiology and severity, management can include anticoagulation, antibiotics, antivirals, immunosuppressives, glucocorticoids, heart failure therapy, circulatory support and/or transplantation. (See "Clinical manifestations and diagnosis of myocarditis in adults" and "Treatment and prognosis of myocarditis in adults".)

Stress (takotsubo) cardiomyopathy — This syndrome mimics myocardial infarction (MI) and is associated with intense emotional or physical stress. It is characterized by transient regional systolic dysfunction, typically of the LV, but without angiographic evidence of obstructive coronary artery disease or acute plaque rupture. Stress cardiomyopathy occurs in approximately 1 to 2 percent of patients with troponin-positive ACS or suspected ST-elevation MI. The risk of severe in-hospital complications is similar to that in patients with ACS and includes acute heart failure with cardiogenic shock, dysrhythmia, ventricular and papillary muscle rupture, tamponade, and stroke. The definitive diagnosis generally requires coronary angiography and serial assessment of LV systolic function. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)

Perforated peptic ulcer — Peptic ulcer disease (PUD) can occasionally cause perforation of the stomach or duodenum causing both chest and abdominal pain, depending on the location of the ulcer. Initial management includes broad-spectrum antibiotic therapy and immediate surgical consultation since most patients will require urgent surgery to limit ongoing abdominal contamination and manage the perforated site. (See "Overview of complications of peptic ulcer disease" and "Overview of gastrointestinal tract perforation".)

Other conditions — Among commonly occurring diseases in ED patients complaining of chest pain, gastrointestinal problems (eg, gastroesophageal reflux disease) comprise a significant percentage [43]. Common causes of non-life-threatening chest pain in adults are discussed below and in greater detail separately. (See "Outpatient evaluation of the adult with chest pain", section on 'Other etiologies'.)

●Cardiac causes – Acute heart failure is frequently associated with chest discomfort. Patients with stable angina can usually identify their anginal chest pain and relay a history of exertional triggers. Valvular heart disease, such as aortic stenosis, can cause chest discomfort, which may signify worsening valvular function. Infectious or inflammatory causes of chest discomfort include pericarditis and myopericarditis. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults" and "Chronic coronary syndrome: Overview of care" and "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Acute pericarditis: Clinical presentation and diagnosis".)

●Pulmonary/pleural causes – Respiratory infections, such as pneumonia, tracheitis, and bronchitis, are frequently accompanied by chest discomfort and cough. Chest tightness is a common complaint with asthma exacerbations. A number of disease processes can result in increased pulmonary arterial pressures and resultant right sided heart dysfunction (cor pulmonale). Pulmonary malignancy can cause chest pain particularly if there is pleural involvement. Chest heaviness or discomfort may be noted with pleural effusions. Pleuritis is an inflammation of the lung pleura that causes pleuritic chest pain but should be a diagnosis of exclusion in an ED patient. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Acute exacerbations of asthma in adults: Home and office management" and "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Epidemiology, pathogenesis, and diagnostic evaluation in adults" and "Pleural fluid analysis in adults with a pleural effusion" and "Clinical manifestations of lung cancer".)

●Gastrointestinal causes – Gastroesophageal reflux ("heartburn"), esophageal spasm, and gastritis/esophagitis can all present as chest discomfort. A hiatal hernia may result in chest pain. Pain from gallstones or pancreatitis can be referred to the chest. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults" and "Gastritis: Etiology and diagnosis" and "Evaluation of the adult with chest pain of esophageal origin" and "Clinical manifestations and evaluation of gallstone disease in adults" and "Clinical manifestations, diagnosis, and natural history of acute pancreatitis".)

●Musculoskeletal causes – Musculoskeletal causes of chest pain include rib contusions and fractures, intercostal muscle strains, and costochondritis (table 14). (See "Major causes of musculoskeletal chest pain in adults".)

●Psychiatric disorders – Anxiety disorders are a common cause of chest pain. Patients with a panic attack often complain of chest tightness and a sense of impending doom. Chest pain can be a somatic symptom associated with depression or somatic symptom disorder. Patients with a serious medical etiology of their chest pain can also have concomitant anxiety. Anxiety disorders as a cause of the symptoms remain a diagnosis of exclusion in the ED. (See "Panic disorder in adults: Epidemiology, clinical manifestations, and diagnosis" and "Minor depression in adults: Epidemiology, clinical presentation, and diagnosis" and "Somatic symptom disorder: Epidemiology, clinical features, and course of illness".)

●Other conditions – Herpes zoster and postherpetic neuralgia in thoracic dermatomes can cause chest pain; prodromal pain typically precedes the rash by two to three days. Chest pain can be referred, such as from abdominal organs or cervical disc disease. Chest pain is associated with various inflammatory/autoimmune conditions and collagen vascular diseases including fibromyalgia, systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis, scleroderma, polyarteritis nodosa, and Takayasu arteritis. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster" and "Postherpetic neuralgia" and "Fibromyalgia: Clinical manifestations and diagnosis in adults" and "Pulmonary manifestations of systemic lupus erythematosus in adults" and "Overview of pleuropulmonary diseases associated with rheumatoid arthritis" and "Clinical manifestations and diagnosis of sarcoidosis" and "Clinical manifestations and diagnosis of systemic sclerosis (scleroderma) in adults" and "Clinical manifestations and diagnosis of polyarteritis nodosa in adults" and "Clinical features and diagnosis of Takayasu arteritis".)

DISPOSITION — 

The patient's condition, preliminary diagnosis, and risk assessment determine disposition.

Cause of chest pain identified or clinically ill patient — Any patient with hemodynamic instability or significant respiratory distress is admitted to the intensive care unit (ICU). Patients with acute aortic dissection, acute coronary syndrome, cardiac tamponade, perforated peptic ulcer, myocarditis, or mediastinitis require admission and appropriate consultation. Most patients with a pneumothorax need admission, but some can be managed as an outpatient (eg, not enlarging, treated with aspiration or a one-way valve device). Patients with stable angina do not require inpatient evaluation. (See "Management of acute type B aortic dissection" and "Management of acute type A aortic dissection" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Cardiac tamponade" and "Boerhaave syndrome: Effort rupture of the esophagus" and "Treatment and prognosis of myocarditis in adults" and "Overview of complications of peptic ulcer disease" and "Treatment of primary spontaneous pneumothorax in adults" and "Chronic coronary syndrome: Overview of care".)

Patients with pulmonary emboli with hemodynamic instability or significant hypoxia are admitted to the ICU. Stable patients with pulmonary embolism do not require admission to an ICU or telemetry monitoring. Some low-risk patients can be treated as an outpatient. (See "Acute pulmonary embolism in adults: Treatment overview and prognosis".)

Patients with ST-elevation myocardial infarction (STEMI) are admitted following reperfusion therapy via fibrinolytics or percutaneous coronary intervention. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy".)

Cause of chest pain not identified and clinically well patient — Any patient without a clear explanation for their chest pain after the initial workup (ECG, imaging, laboratory studies) is completed may still have an acute coronary syndrome (ACS). Risk stratification for potential ACS includes two parallel strategies: identify patients at such low risk that they can be safely discharged home with follow-up, and identify patients at sufficiently high risk to require admission and acute management. High-sensitivity troponins may allow for safe discharge and reduce additional testing in patients otherwise at low risk for ACS. If discharged without provocative testing, low-risk patients should have clear follow-up encouraged, ideally within a few days of discharge. Follow-up within 72 hours is safe [51].

Patients not at low risk for ACS but without known coronary artery disease or obvious signs of myocardial infarction and without a clear alternative diagnosis should be observed further, and myocardial ischemia ruled out using serial cardiac biomarkers, ECGs, and possibly further testing. Using a validated instrument (eg, HEART score) can aid risk stratification and urgency of provocative testing [52-56]. Exercise treadmill or pharmacological testing with or without nuclear imaging, as well as stress echocardiography and CT coronary angiography (CCTA), can further assist cardiovascular risk stratification in the emergency department (ED). (See "Evaluation for suspected non-ST-segment elevation acute coronary syndromes" and "Cardiac imaging with computed tomography and magnetic resonance in the adult".)

Patients less than 40 years old with normal ECGs and no prior cardiac history have less than a one percent risk of ACS and less than a one percent risk of death, acute myocardial infarction, or revascularization at 30 days [57]. They can be discharged with follow-up.

Determining disposition in patients with recurrent ED visits for chest pain and low-risk for ACS (eg, HEART score ≤3) can be challenging. We agree with the Guideline for Reasonable and Appropriate Care in the Emergency Department from the Society for Academic Emergency Medicine that the following low-risk patients (with negative troponin testing) can be managed on an outpatient basis [58]:

●A normal stress test within the previous 12 months (we do not believe that repeating another stress test is necessary, but CCTA may be appropriate if concern for inadequate or false-negative previous stress test)

●Nonobstructive (<50 percent stenosis) or no occlusive (zero percent stenosis) coronary artery disease on prior angiography within 5 years

●Prior CCTA within the past 2 years with no coronary stenosis AND a negative single, high-sensitivity troponin

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Adult with chest pain in the emergency department".)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Chest pain is the second most common complaint in adult emergency departments (EDs) patients in the United States. Most visits result in a diagnosis of noncardiac chest pain, and approximately half with nonspecific chest pain. Approximately 6 percent are ultimately diagnosed with a life-threatening condition, which is overwhelmingly (>90 percent) acute coronary syndrome (ACS). (See 'Epidemiology' above.)

●Initial assessment and stabilization – Clinicians in the ED focus on the immediate recognition and exclusion of life-threatening causes, which starts with a focused history and examination. Patients with life-threatening etiologies for chest pain may appear deceptively well, manifesting neither vital sign nor physical examination abnormalities. An algorithm outlining an approach to the ED patient with chest pain and a table allowing for quick comparison of findings in life-threatening causes are provided (algorithm 1 and table 1). (See 'Initial assessment and stabilization' above.)

A standard 12-lead ECG should be obtained for all ED patients presenting with chest pain who are hemodynamically unstable or who do not have an obvious noncardiac cause. (See 'Rapid ECG (most patients)' above.)

In general, it is safest to assume an ED patient with chest pain and any of the following has a life-threatening condition until proven otherwise:

•Abnormal vital signs

•Obvious distress

•Signs of hypoperfusion (eg, diaphoresis, cool/clammy skin)

•Abrupt onset of thoracic or abdominal pain with a sharp, tearing, and/or ripping character

•Variation in pulse (absence of a proximal extremity or carotid pulse) and/or blood pressure (>20 mmHg difference between the right and left arm)

•ECG with ST-segment elevation

●History – Significant overlap exists among the symptoms experienced by patients with life-threatening and common causes of chest pain. Emergency clinicians must guard against premature diagnostic closure based upon the history or results of nonspecific diagnostic testing. So-called "atypical" presentations occur often; misinterpretation of such presentations increases the risk for adverse outcomes. (See 'History' above.)

●Physical examination – The physical examination is often not helpful in distinguishing ACS from noncardiac chest pain. In some instances, physical findings suggest a specific noncardiac diagnosis. Patients with an immediately life-threatening cause tend to appear anxious and distressed and may be diaphoretic and dyspneic. (See 'Physical examination' above.)

●Diagnostic testing – An ECG and chest radiograph (CXR) are obtained for most ED patients with chest pain, and further testing is based on clinical suspicion. The CXR may be diagnostic (eg, pneumothorax), but even in the presence of a life-threatening condition it may be normal (eg, ACS, pulmonary embolism [PE]) or have nonspecific findings that increase suspicion for a process (eg, atelectasis for PE). (See 'Chest radiograph (most patients)' above.)

Serial cardiac biomarkers (preferably high-sensitivity troponin) are used to diagnose or exclude ACS. A D-dimer can exclude a PE in patients with a low or moderate pretest probability (table 6). D-dimer in combination with the Aortic Dissection Detection Risk Score (ADD-RS) may be useful to rule out suspected aortic dissection (table 8). (See 'Laboratory studies' above.)

Bedside ultrasound is particularly helpful in a patient with hemodynamic instability and can identify pericardial effusions and tamponade, cardiac wall motion abnormalities (ie, ACS), global left ventricular dysfunction (ie, myocarditis, cardiomyopathy), right ventricular strain (ie, PE), and pneumothorax. (See 'Bedside ultrasonography' above.)

Advanced imaging studies can diagnose or exclude aortic dissection (CT, MRI, transesophageal echocardiography), PE (CT angiogram, ventilation/perfusion scan, pulmonary angiography), ACS (cardiac stress testing, CT coronary angiography), and pericardial processes (transthoracic echocardiogram). (See 'Advanced imaging studies' above.)

●Causes of chest pain – Diseases of the heart, aorta, lungs, esophagus, stomach, mediastinum, pleura, and abdominal viscera may all cause chest discomfort (table 9). Causes of chest pain that pose an immediate threat to life include ACS, aortic dissection, PE, tension pneumothorax, pericardial tamponade, mediastinitis (eg, esophageal rupture), myocarditis, stress (takotsubo) cardiomyopathy, and perforated peptic ulcer. (See 'Life-threatening conditions and presumptive management' above.)

Common, non-life-threatening causes include gastroesophageal reflux disease, anxiety disorders, and musculoskeletal processes; these are typically a diagnosis of exclusion in an ED patient, especially in the presence of ACS or PE risk factors. (See 'Other conditions' above.)

●Disposition – The patient's condition, preliminary diagnosis, and risk assessment determine disposition. A clinically well patient without the cause of chest pain identified following ECG, imaging, and laboratory studies may still have an ACS. Using a validated instrument (eg, HEART score) can aid risk stratification and urgency of provocative testing. (See 'Disposition' above.)