Assessment of chest pain

Overview
Summary Aetiology

Emergencies
Urgent considerations

Diagnosis
Step-by-step Differential diagnosis Guidelines

Resources
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Summary
Chest pain is a common chief complaint, accounting for 5% to 8% of all emergency department visits in the US per year, [1] and is the presenting complaint in 1% to 2% of office-based visits.[2] In general practice in the UK, the incidence of newly diagnosed chest pain is 15.5 per 1000 person-years. [3] Chest pain may be caused by either benign or life-threatening aetiologies and is usually divided into cardiac and non-cardiac causes. Acute coronary syndrome (ACS) encompasses unstable angina and MI. ACS affects only a few of the patients presenting with chest pain, but excluding ACS is vital because of the mortality associated with untreated MI. This monograph concentrates on the assessment of chest pain in the emergency setting.

Differential diagnosis
Sort by: common/uncommon or category Common

Acute coronary syndrome Stable angina Pulmonary embolism Pneumonia Viral pleuritis GORD Costochondritis

Anxiety or panic disorder Uncommon

Pericarditis

Cardiac tamponade Aortic dissection Aortic stenosis Mitral valve prolapse Pneumothorax Pulmonary hypertension Peptic ulcer disease (PUD) Oesophageal spasm Acute cholecystitis Pancreatitis Herpes zoster Gastritis

Aetiology
The common aetiologies of chest pain in the primary care setting are musculoskeletal (36%), gastrointestinal (19%), stable angina (10.5%), unstable angina or MI (1.5%), other cardiac (3.8%), psychiatric (8%), and pulmonary (5%). In 16% of cases the cause is not established. [4] Aetiologies of patients over 35 years of age, admitted to hospital from the emergency department with a chief complaint of non-traumatic chest pain are: [5]
acute myocardial infarction (10.7%) angina/coronary artery disease (22.5%) atypical chest pain (29.4%) aortic dissection (0.3%) other cardiac causes, primarily CHF and atrial fibrillation, (13.8%) pulmonary embolus (0.4%) non-PE pulmonary causes, primarily bacterial pneumonia, (11.2%) but also spontaneous pneumothoraces (0.6%) abdominal causes (1.6%) other (10.2%).

Urgent considerations
See Differential Diagnosis for more details Acute chest pain warrants rapid clinical assessment, as underlying disease can be life-threatening. Continuous monitoring of pulse, BP, and oxygen saturation is standard care. If the patient is in pain or breathless, or oxygen saturation is <90%, high-flow oxygen should be given. Morphine (IV) may also be necessary to relieve severe pain. Initial investigations include a 12-lead ECG, CXR, cardiac biomarkers, FBC, and renal profile. The patient may need to be transferred to an intensive care setting. Once the patient is stable, further tests such as a V/Q scan, echocardiography, CT, or angiography should be requested to confirm clinical suspicion.

Acute coronary syndrome

Acute coronary syndrome (ACS) refers to acute myocardial ischaemia caused by atherosclerotic coronary disease and includes ST-elevation MI (STEMI), non-ST-elevation MI (NSTEMI), and unstable angina (UA). These terms are used as a framework for guiding management. Patients with STEMI need to be urgently triaged, as they may have life-threatening arrhythmias, cardiogenic shock, or pulmonary oedema. STEMI presents with a severe central chest pressure radiating to the jaw or upper extremities. There can be associated nausea and vomiting. Anticoagulation and acute reperfusion therapy with angioplasty (if available within 2 hours) or thrombolytics (if no contraindications and angioplasty not available) should be considered. [6] [7] [8]

Aortic dissection
Aortic dissection typically presents with sudden, severe pain described as a tearing sensation radiating to the mid-back. A CXR may show a widened mediastinum. CT chest with IV contrast or transoesophageal echocardiogram confirms the diagnosis. All patients should immediately receive intravenous beta-blockade for heart rate and BP control. Definitive management depends on the type of aortic dissection and includes urgent surgical replacement or ongoing medical therapy.

Tension pneumothorax
Tension pneumothorax is disruption of the tissues of the lung or pleura causing a 1-way valve that lets air into the pleural space but prohibits its return. In severe cases, the pneumothorax causes mediastinal shift with compression of the great vessels, reducing blood flow to the heart, leading to shock. Tension pneumothorax may begin as acute, sharp, pleuritic pain. Needle decompression followed by tube thoracostomy should be done to prevent acute decompensation.

Pulmonary embolism
PE usually presents with pleuritic chest pain, dyspnoea, and tachycardia. In severe cases, syncope or imminent cardiopulmonary arrest may be presenting signs. CT scan with contrast, pulmonary angiogram, and V/Q scan are key diagnostic modalities. Systemic anticoagulation with heparin or low molecular weight heparin should be

initiated in those patients with PE. D-dimer is helpful in excluding PE. [9] For patients who have a high suspicion for PE, a transthoracic echocardiogram demonstrating right ventricular hypokinesis and paradoxical septal motion may indicate acute right ventricular failure from a PE. [9] In patients with shock, systemic thrombolysis, catheter-directed thrombolysis, or surgical embolectomy should be considered.

Cardiac tamponade
Cardiac tamponade may occur suddenly as a result of trauma, aortic dissection, or gradual accumulation of fluid in the pericardial space. Early recognition and appropriate drainage of pericardial fluid is vital. The condition can present with muffled heart sounds, distended neck veins, and pulsus paradoxus. Diagnosis is made by transthoracic echocardiography.

Red flags
Acute coronary syndrome Pulmonary embolism Pneumonia Cardiac tamponade Aortic dissection Aortic stenosis Mitral valve prolapse Pneumothorax Acute cholecystitis Pancreatitis

Step-by-step diagnostic approach

Chest pain can be triaged into traumatic and atraumatic aetiologies. The evaluation of atraumatic chest pain requires an algorithmic approach that first excludes acute myocardial ischaemia before working through the various aetiologies of chest pain.

History
The character of chest pain should be determined, as this can help differentiate between cardiac, respiratory, musculoskeletal, and other causes. The type, severity, location, and duration of pain; the presence of any radiation; and exacerbating or relieving factors may be helpful in pointing towards a diagnosis. Clinical presentation alone cannot reliably determine acute coronary syndrome (ACS). [10] [11] Past medical history and specific cardiac risk factors such as known cardiac disease, raised cholesterol, hypertension, smoking, and family history support a cardiac cause. [12] Cocaine use also makes cardiac ischaemia more likely. [13] A detailed drug history should also be taken (e.g., use of NSAIDs may result in gastric aetiology). Certain characteristics of chest pain can give clues to the origin. Constricting pain may be due to cardiac ischaemia or oesophageal spasm.

Pain that lasts over 20 minutes and is dull, central, and crushing is likely to be caused by an MI. Pain that radiates to the jaw or upper extremities suggests a cardiac cause. Sharp pleuritic pain that catches on inspiration may originate from the pleura or pericardium and suggests pneumonia, pulmonary embolus, or pericarditis.

A sudden substernal tearing pain that radiates towards the back is the classic presentation of aortic dissection. Precipitating and relieving factors can help distinguish between cardiac and gastrointestinal causes (e.g., GORD, peptic ulcer disease, oesophageal spasm). Pain brought on by food, lying down, hot drinks, or alcohol, and relieved by antacids suggests a gastrointestinal cause. Cardiac pain is more likely to be brought on by exercise or emotion and is typically relieved with rest or nitrates. Abdominal pathology such as acute cholecystitis and pancreatitis may also cause pain referred to the chest. Dyspnoea is an associated symptom in patients with cardiac ischaemia, PE, pneumothorax, or pneumonia. Nausea, vomiting, and sweating may be seen in patients with MI.

Physical examination
Physical examination can further narrow down the differential. Abnormalities revealed in the cardiac examination include abnormalities in pulse or heart sounds (e.g., new onset of aortic stenosis or worsening of existing murmur), hypo- or hypertension, and signs of heart failure. Crepitations revealed by auscultation in one or both bases suggest pneumonia or heart failure. Reduced breath sounds on one side can be caused by a pneumothorax, or focally due to a collapsed lobe. Tenderness on palpation over the area of chest pain usually indicates a musculoskeletal cause, such as costochondritis. However, many patients with MI also have chest wall pain on presentation. A gastrointestinal origin of chest pain is associated with a normal cardiac and respiratory examination, unless there is existing but stable comorbidity. An abnormal abdominal examination (tenderness, rebound, guarding) make a gastrointestinal aetiology more likely.

Basic investigations
Basic observations such as temperature, BP, pulse, and respiratory rate should be monitored. ECG is performed in most patients unless a non-cardiac diagnosis can be made with confidence (e.g., pneumothorax). The ECG should be done as soon as possible after presentation. ST changes such as ST elevation or ST depression, QRS abnormalities, arrhythmias, or tachycardia or bradycardia are characteristic findings in cardiac causes.View imageView imageView imageView image

CXR can confirm respiratory disorders such as pneumothorax or pneumonia. Cardiac ischaemia is often characterised by a normal CXR, but a CXR can provide clues to serious cardiac pathology, such as a widened mediastinum in aortic dissection,View image or a large globular heart in cardiac tamponade. Blood tests Cardiac biomarkers (e.g., CK, CK-MB, troponin I and T) found in skeletal and cardiac muscle are raised in many situations including MI, following a fall or seizure, myositis, hypothermia, or hypothyroidism. CK peaks approximately 48 hours after the event. CK-MB can be requested if the source of the enzyme needs to be determined. Troponins peak at 12 to 24 hours after the event and are more sensitive for cardiac damage. Cardiac biomarkers should be ordered on presentation and at least every 6 to 8 hours after presentation. An FBC should be ordered to screen for anaemia and evidence of infection. A renal profile is useful as a baseline test. Some of the differential diagnoses for chest pain can be excluded or confirmed after history, physical examination, and basic investigations have been carried out. These include ST-elevation MI (STEMI), pneumothorax, pneumonia, pericarditis, and costochondritis. The results of the second set of cardiac biomarkers confirm the diagnosis of non-ST-elevation MI (NSTEMI).

Further investigations
Some differentials need further investigations to confirm the suspected diagnosis. Coronary angiography is required urgently in patients with a STEMI and in patients with an NSTEMI who have high-risk features such as ongoing chest pain and dynamic ECG changes. Once ACS, ventricular arrhythmias, and haemodynamic instability are excluded, patients with chest pain that is clinically considered to be ischaemic in origin should be stratified by their likelihood of having angina and risk for MI. 1. Definite angina: patients with a pretest probability of having CAD of >90% should be directly referred for coronary angiography. 2. Probable angina: patients with a 50% to 90% pretest probability of having CAD may be referred for stress testing with imaging. 3. Possible angina: patients with a 10% to 50% pretest probability of having CAD should be referred for either exercise stress testing (EST) or stress testing with imaging. 4. Non-anginal symptoms with a pretest probability of <10% should be evaluated for alternative causes of chest pain.

Transthoracic echocardiography is a non-invasive way of assessing cardiac function. It is necessary if cardiac tamponade is suspected and is helpful in confirming a diagnosis of pulmonary hypertension. For a diagnosis of aortic dissection to be made, transoesophageal echocardiography is more useful. A CT chest is an alternative if aortic dissection is suspected. Depending on local availability, a V/Q scan, CT pulmonary angiogram, or pulmonary angiogram is necessary if PE is suspected.View image If a gastric diagnosis is the more likely cause for chest pain, then investigations such as oesophagogastroduodenoscopy, oesophageal pH monitoring, oesophageal manometry, barium swallow, and Helicobacter pylori breath test can be considered. A therapeutic trial of proton-pump inhibitors can relieve symptoms in patients with GORD. [14] Further blood tests such as liver profile, serum lipase, and ABG analysis may be necessary if acute cholecystitis or acute pancreatitis is suspected. These diagnoses also require further imaging such as abdominal ultrasound and abdominal CT (for acute pancreatitis).

Chest pain assessment algorithm. NSTEMI: non-ST-elevation MI; STEMI: ST-elevation MICreated by the BMJ Evidence Centre

Differential diagnosis
Sort by: common/uncommon or category Commonhide all Acute coronary syndrome see our comprehensive coverage of Overview of acute coronary syndrome

History
central chest pressure, squeezing, or heaviness; radiation to jaw or upper extremities; associated nausea, vomiting, dyspnoea, dizziness, weakness; occurs at rest or accelerating tempo (crescendo); risk

Exam
examination may be normal; jugular venous distention, S4 gallop, holosystolic murmur (mitral regurgitation), bibasilar rales; hypotensive, tachycardic,

1st test

ECG: ST-elevation MI (STEMI): STsegment elevation >1 mm in 2 anatomically contiguous leads or new left bundle-branch block; non-STelevation MI (NSTEMI) or unstable

Oth

factors: smoking, age (men >45, women >55 bradycardic, or hypoxic depending

years), positive FHx of premature CAD, hypertension, hyperlipidaemia, diabetes, stroke, or peripheral arterial disease [6] [7]

on severity of ischaemia [6] [7]

angina: non-specific; ST-segment depression or T-wave inversionMore

CXR: normal or signs of heart failure, such as increased alveolar markingsMore

cardiac enzymes: elevated in STEMI and NSTEMI; not elevated in unstable anginaMore

Stable angina see our comprehensive coverage of Chronic stable angina

History
known history of coronary artery disease; chest discomfort on exertion; no change in intensity, frequency, or duration; associated diaphoresis, nausea/vomiting, or shortness of breath; risk positive family history of premature CAD, hypertension, hyperlipidaemia, diabetes, stroke, or peripheral arterial disease [7]

Exam
no specific findings for CAD, may have abnormal pulses if peripheral vascular

1st test

ECG: no acute changes; may have evidence of previous infarction, such as Q waves

Other tests

stress testin

sloping ST-s

elevation dur

factors: smoking, age (men >45, women >55 years), disease present

positive for is

CXR: normal or cardiomegaly

regional wall

ventricular d

cardiac biomarkers: not elevated

coronary an

artery narrow

Pulmonary embolism see our comprehensive coverage of Pulmonary embolism

CT coronary

stenosis Mor

History
sharp and pleuritic in nature; shortness of breath; haemoptysis may occur if pulmonary infarction develops; massive PE results in syncope; risk factors: history of immobilisation, orthopaedic procedures, oral contraceptive use, previous PE, hypercoagulable states, or recent travel over long distances;[28] unilateral swollen lower leg that is red and painful suggests DVT; use of the modified Wells criteria can help to screen for risk factors and clinical features suggesting high probability[29]

Exam
tachycardia, loud P2, rightsided S4 gallop, jugular venous distention, fever, right ventricular lift; massive PE may cause hypotension [28]

1st test

ECG: sinus tachycardia; presence of S1, Q3, and T3More

Other tes

D-dimer: non-specific if positive; PE excluded if result negative in patients with low probability of having a PE

th

CXR: decreased perfusion in a segment of pulmonary vasculature (Westermark sign); presence of pleural effusion

CT pulmonary

angiography:identification of thrombus in the pulmonary circulationMore

Pneumonia see our comprehensive coverage of Overview of pneumonia

History
productive or dry cough, fever, pleuritic pain associated with shortness of breath; recent history of travel or infectious exposures [30]

Exam
decreased breath sounds, rales, wheezing, bronchial breath sounds, dullness to observed with severe consolidation [30]

1st test

CXR: pulmonary infiltration, air bronchograms, and pleural effusion

may have rigors, myalgias, and arthralgias; percussion, and increased tactile fremitus

Viral pleuritis

History
prodrome of viral illness (myalgias, malaise, rhinorrhoea, cough, nasal sick contacts

Exam
pleural friction rub with or without low-grade fever; sometimes reproducible tenderness to pleurodynia accompanies pleuritis

1st test

CXR: usually normal but can uncommonly have effusionMore

Oth

congestion, low-grade temperatures); palpation of chest when perichondritis or

GORD see our comprehensive coverage of Gastro-oesophageal reflux disease

History

Exam

1st test

therapeutic trial: relief of symptoms with short trial of proton-pump inhibitors

Other tests

retrosternal burning with eating large no specific or fatty meals that can be reproduced physical with lying supine and relieved by sitting up; relieved by antacids [33] findings

Oesophagogastroduode

inflammation or erosionsM

oesophageal pH monito indicate reflux disease

Costochondritis see our comprehensive coverage of Costochondritis

History
focal chest wall pain, may have known precipitating injury; aggravated by sneezing, coughing, deep inspiration, or twisting of the chest

Exam
reproducible pain, especially at the costochondral junctions

1st test

CXR: no spe

findingsMore

Anxiety or panic disorder see our comprehensive coverage of Panic disorders

History

Exam

1st test

ECG: normal

Other

sharp chest pain with anxiety, dizziness or faintness, palpitations, hyperventilation,

sweating, trembling or shaking, fear of dying or going insane, paraesthesiae, chills or hot flushes, breathlessness or choking sensation

examination otherwise normal

Uncommonhide all
Pericarditis see our comprehensive coverage of Pericarditis

History
usually has viral prodrome; sharp pleuritic chest discomfort provoked by lying supine and improved with sitting up; associated dry

Exam
tachycardia and friction rub; jugular venous distention and pulsus

1st test

ECG: diffuse concave-up STelevation, associated PR depression; changes evolve over timeMore

Other tests

CXR: u

silhoue

cough, fever, myalgias, or arthralgias; history paradoxus indicate effusion of possible causes such as radiation exposure, causing tamponade collagen vascular disease, recent MI, or uraemia

effusion

echoca

small e

Cardiac tamponade see our comprehensive coverage of Cardiac tamponade

History

Exam

1st test

history of underlying cause such as MI, aortic hypotension, distended neck veins, dissection, or trauma; may present insidiously muffled heart sounds; pulsus as a result of hypothyroidism or pericarditis; dizziness; dyspnoea; fatigue paradoxus (a drop of 10 mmHg in arterial BP on inspiration)

ECG: low-voltage QRS; other changes

underlying cause (e.g., ST elevation in specific ST changes in pericarditis)

CXR: globular heart (if large effusion)

echocardiography: pericardial effusio of great vessels, atria, and ventricles

Aortic dissection see our comprehensive coverage of Aortic dissection

History
to interscapular region of the back; pain may migrate with the propagation of the dissection; stroke, acute MI due to obstruction of aortic branches; dyspnoea due to acute aortic regurgitation; hypotension due to cardiac tamponade; history of hypertension, Marfan's syndrome, Ehlers-Danlos syndrome, or syphilis[24] [25]

Exam
diastolic murmur due to aortic regurgitation; muffled heart sounds if the dissection is complicated by cardiac tamponade; new focal neurological findings due to involvement of the carotid or vertebral arteries [24] [25]

1st test

CXR: widened mediastinumMore

Other tes

acute substernal tearing sensation, with radiation unequal pulses or BPs in both arms; new

tr

fla

fla

Aortic stenosis

see our comprehensive coverage of Aortic stenosis

History
age over 60 years; typical angina; chest pain is usually progressive; [27]shortness of breath; syncope (if severe); patients with significant aortic stenosis and heart failure are at high risk of cardiogenic shock or sudden death

Exam
ejection systolic murmur that radiates to the neck; obliteration of S2 indicates severe stenosis; delayed upstroke on palpation of carotid pulse

1st test

ECG: voltage criteria for LVH; enlarged P wave suggesting left atrial enlargement

Other tests

CXR: ca

oedema

echoca

valve le

the aort systolic

Mitral valve prolapse see our comprehensive coverage of Mitral valve prolapse

History
usually asymptomatic, but may cause palpitations, chest pain, dyspnoea, headache, or fatigue

Exam
mid-systolic click and late systolic murmur at the apex

1st test

ECG: usually normal, may show atrial fibrillation or other arrhythmias

Other tests

CXR: usua

pulmonary

echocard

valve prola

Pneumothorax see our comprehensive coverage of Pneumothorax

History
acute, pleuritic chest pain, shortness of breath; primary spontaneous between ages 20 and 40 years; secondary spontaneous in patients with COPD; traumatic due to acute trauma or iatrogenic; [31] shock may occur if rapidly increasing (tension pneumothorax)

Exam
absent breath sounds, increased resonance to percussion; jugular venous distention, trachea deviation, and hypotension if tension pneumothorax (due to compromise of the great vessels) [31]

1st test

CXR: air

visible ple

collapsed

shiftMore

Pulmonary hypertension see our comprehensive coverage of Idiopathic pulmonary arterial hypertension

History
cardiac-sounding chest pain on exertion, dyspnoea; symptoms of right-sided heart failure such as lower extremity oedema, abdominal bloating, or ascites; syncope if severe [32]

Exam
accentuated pulmonic component (P2) to the second heart sound; palpable P2; right ventricular heave; lower extremity oedema; jugular venous distention

1st test

ECG: right axis deviation; RVH or right atrial enlargement

Other tests

CXR: large, prom

echocardiogram

right ventricular s

ventricular and rig effusion

Peptic ulcer disease (PUD) see our comprehensive coverage of Peptic ulcer disease

History
gastric ulcers: epigastric pain or burning with for several hours; duodenal ulcers: epigastric

Exam
epigastric tenderness; if present there may be

1st test

Oesophagogastroduodenoscopy:gastric or duodenal erosions or ulceration

onset 5 to 15 minutes after eating and may last significant bleeding is pain is relieved by eating and may return 1 to 4 tachycardia,

hours postprandially; pain from any ulcer is relieved by antacid; risk factors: cigarette smoking, NSAIDs, and chronic alcohol consumption [34]

hypotension, and conjunctival pallor [34]

Oesophageal spasm

History
crushing substernal chest pain, associated dysphagia, pain does not always correlate with swallowing, dysphagia precipitated by very hot or cold foods, glyceryl trinitrate can relieve the pain [36]

Exam
no specific findings

1st test

barium swallow: corkscrew or rosary bead appearance on barium swallow

Other tests

oeso

man

on >

Acute cholecystitis see our comprehensive coverage of Cholecystitis

History
right upper quadrant pain, radiation to the interscapular area or right shoulder, associated with nausea and vomiting,

Exam
right upper quadrant tenderness (Murphy's sign), abdominal rigidity and guarding if perforation of the

1st test

liver function tests: elevated alkaline phosphatase and gammaGT More

Oth

fevers, anorexia often accompanies pain, gallbladder, rarely have jaundice early signs of peritoneal inflammation such as in the course of cholecystitis [37] abdominal pain with jarring [37]

FBC: leukocytosis with a left shiftMore

abdominal ultrasound:pericholecystic fluid, distended gallbladder, thickened gallbladder wall, and gallstonesMore

Pancreatitis see our comprehensive coverage of Acute pancreatitis

History
epigastric or periumbilical abdominal pain that radiates to the back; may be severe; associated nausea and vomiting; history of alcohol consumption or gallstones [40]

Exam
tachycardic, hypotensive, febrile, acute distress; ecchymosis in the periumbilical region (Cullen's sign) and the flank (Grey-Turner sign)

1st test

serum lipase: double the normal valuesMore

Other tests

FBC: leu

electroly

creatinin

ABG: ac

abdomin

possible

abdomin

the panc

pseudoc

Herpes zoster see our comprehensive coverage of Herpes zoster infection

History
unilateral, burning pain in typical

Exam
vesicular rash on erythematous

1st test

usually no test

Other tests

swab fo

dermatome distribution that may occur before appearance of rash and may persist for >1 month

base, in unilateral distribution of a dermatome

required:diagnosis is clinical

zoster p

immuno

Gastritis see our comprehensive coverage of Gastritis

History
dyspepsia/epigastric discomfort; nausea, vomiting, loss of appetite; history of NSAID use or alcohol misuse; history previous gastric or abdominal surgery

Exam
epigastric gastric discomfort may be present; may have signs associated with vitamin B12 deficiency and pernicious examination, presence of cognitive impairment, angular cheilitis, atrophic glossitis

1st test

Helicobacter pylori urea breath test: positive in H pylori infection

Other te

of Helicobacter pyloriinfection; history of anaemia (e.g., abnormal neurological

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ST changes associated with ischaemia Courtesy of Dr Francis Morris

T-wave changes with ischaemia Courtesy of Dr Channer

ECG showing changes of an acute inferior MI with ST elevation in leads II, III and aVF

Used with permission from Professor James Brown

ECG showing diffuse concave upwards ST elevation with associated PR depression suggestive of pericarditis Used with permission from Professor James Brown

Spiral CT pulmonary angiogram showing a large filling defect within the pulmonary vasculature compatible with a saddle embolus Used with permission from Professor James Brown

CXR showing a widened mediastinum Used with permission from Professor James Brown