Assessment of Chest Pain

Assessment
of chest pain
Straight to the point of care
Last updated: Jan 31, 2020

Table of Contents
Overview 3
Summary 3
Theory 4
Aetiology 4
Emergencies 6
Urgent considerations 6
Diagnosis 8
Approach 8
Differentials overview 20
Differentials 22
Guidelines 36
References 38
Images 49
Disclaimer 57
Assessment of chest pain Overview
Summary
Chest pain is a common chief complaint, accounting for approximately 5% of all emergency department
visits in the US per year.[1] It is the presenting complaint in 1% of clinic-based visits.[2] In the UK, 1% to 2%
OVERVIEW
of adults attend primary care each year with a new presentation of chest pain.[3] [4] [5] In Belgium and the
Netherlands, chest pain was present in about 1% of patient consultations across 118 primary care centres
over a 2-week period.[6]
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), encompassing unstable angina, ST-elevation myocardial infarction, and
non-ST-elevation myocardial infarction, may not be the most common aetiology in patients presenting
with chest pain, but excluding ACS is vital because of the mortality associated with untreated myocardial
infarction.
This topic concentrates on the assessment of acute chest pain in the emergency setting.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jan 31, 2020.
BMJ Best Practice topics are regularly updated and the most recent version
3
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2020. All rights reserved.
Assessment of chest pain Theory
Aetiology
A retrospective study in the US, conducted over a 5-year period, of patients aged over 35 years, with a chief
complaint of non-traumatic chest pain admitted to hospital from the emergency department, found that chest
THEORY
pain most frequently had a coronary cause.[7] Pulmonary embolism and aortic dissection were rare but
important causes.[7]
Distribution of final diagnoses in people over 35 years admitted to hospital from one US hospital emergency
department with chief complaint of non-traumatic chest pain, over a 5-year period (PE, pulmonary embolism)
Created by BMJ; based on data from Kohn MA, Kwan E, Gupta M, et al. Prevalence
of acute myocardial infarction and other serious diagnoses in patients presenting to an
urban emergency department with chest pain. J Emerg Med. 2005 Nov;29(4):383-90
Reports have indicated that up to 3.5% of patients with a diagnosis of acute coronary syndrome have the
diagnosis missed in the emergency department.[8] [9] [10]
The distribution of aetiologies is different in primary care. Common aetiologies of chest pain include:[2]
• Musculoskeletal causes
• Reflux oesophagitis
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jan 31, 2020.
Assessment of chest pain Theory
• Costochondritis.
An observational study found that most final diagnoses in people presenting with chest pain in primary care
are non-life-threatening; however, 8.4% have a life-threatening final diagnosis.[6]
THEORY
Another study in general practice settings found that most patients had no diagnosis assigned at
presentation (72.4%) or within the next 6 months following a first episode of chest pain (no previous record of
cardiovascular disease).[11] Those patients who had no diagnosis attributed to their chest pain at 6 months
had higher long-term incidence of cardiovascular events compared with patients who had been diagnosed
with non-coronary pain.
5
Assessment of chest pain Emergencies
Urgent considerations
(See Differentials for more details)
Acute chest pain warrants rapid clinical assessment, as underlying disease can be life-threatening.
Continuous monitoring of pulse, blood pressure, and oxygen saturation is standard care. Use an ABCDE
(airway, breathing, circulation, disability, exposure) approach to systematically assess and treat the patient.
Treat life-threatening problems before moving onto the next part of the assessment.[12]
If the patient with acute chest pain (undiagnosed aetiology) has an oxygen saturation below 94%,
supplemental oxygen should be given initially, pending investigation.[13] [14] All patients require oxygen
saturation measurement using pulse oximetry. One systematic review and meta-analysis found that the
liberal use of oxygen was associated with increased mortality in acutely ill patients when compared with a
conservative oxygen strategy.[15] [16] Recommendations regarding supplemental oxygen and target ranges
may vary depending on each guideline and/or disorder.
Supplemental oxygen has not been proven to be helpful and may be harmful in patients with acute coronary
EMERGENCIES
syndrome (ACS) who have normal oxygen saturations.[14] [17] Guidelines recommend that oxygen should
not be routinely administered in normoxic patients with suspected or confirmed ACS.[14] [18]
European guidelines do not recommend oxygen routinely if the oxygen saturation is ≥90% for patients with
presumed ACS.[19] British Thoracic Society guidelines recommend a target oxygen saturation of 94%
to 98% for most acutely ill patients, or 88% to 92% (or a patient-specific target range) for those at risk of
hypercapnic respiratory failure.[13]
Opiates (e.g., morphine) may be necessary to relieve severe pain.
Immediate investigations include a 12-lead ECG, chest x-ray, cardiac biomarkers, full blood count, 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 ventilation-perfusion (V/Q) scan, echocardiography, computed tomography, or angiography
should be requested to confirm the diagnosis.
Acute coronary syndrome

ACS refers to acute myocardial ischaemia caused by atherosclerotic coronary disease and includes ST-
elevation myocardial infarction (STEMI), non-STEMI, and unstable angina. These terms are used as a
framework for guiding management.
Patients with STEMI need to be urgently assessed, as they may have life-threatening arrhythmias,
cardiogenic shock, or pulmonary oedema. STEMI typically presents with a severe central chest pressure
radiating to the jaw or upper extremities. There can be associated nausea and vomiting. The treatment is
anticoagulation and acute reperfusion therapy with angioplasty (if available within 2 hours) or thrombolytics (if
no contraindications and angioplasty not available).[19] [20] [21]
Aortic dissection
Aortic dissection typically presents with sudden, severe pain described as a tearing sensation radiating
to the mid-back. A chest x-ray may show a widened mediastinum. Computed tomography chest scan
with intravenous contrast or transoesophageal echocardiogram confirms the diagnosis. Patients should
immediately receive intravenous beta-blockade for heart rate and blood pressure control. Additional, titratable
agents such as sodium nitroprusside or calcium-channel blockers may be required. Definitive management
Assessment of chest pain Emergencies
depends on the type of aortic dissection and includes urgent surgical replacement or ongoing medical
therapy. Dissections involving the ascending aorta (Stanford A) are generally managed surgically and
necessitate urgent surgical consultation. Uncomplicated dissections involving solely the descending aorta
(Stanford B) are generally managed medically. Complicated Stanford B dissections may be managed
endovascularly.[22]
Tension pneumothorax
Tension pneumothorax occurs when there is a disruption of the tissues of the lung or pleura causing a one-
way valve that lets air enter, but not exit, the pleural space. In severe cases, the tension 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 immediately to prevent acute decompensation.
Pulmonary embolism
Pulmonary embolism (PE) typically presents with pleuritic chest pain, dyspnoea, and tachycardia.
EMERGENCIES
Haemoptysis occurs less commonly. In severe cases, syncope or imminent cardiopulmonary arrest may
be presenting signs.[26] Computed tomographic pulmonary angiography 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.
Patients with suspected PE can be classified into distinct categories of clinical (pre-test) probability that
correspond to confirmed PE prevalence using the original Wells criteria (modified), simplified Wells criteria
(modified), original Geneva score (revised), or the simplified Geneva score (revised).[27] [28] [29] Each of
these clinical decision tools assigns a value (a single point, or points) to a series of historical and physical
examination features, the sum of which determines whether PE is likely or unlikely.
The simplified versions of the modified Wells criteria or revised Geneva score may be preferred in clinical
practice because of their ease of use.[30] Both simplified versions have been validated; neither has been
shown to be superior to the other.[31] [32] However, the Geneva score is based entirely on objective clinical
items and may be more reproducible (the Wells criteria [original and simplified] include the subjective clinical
item 'alternative diagnosis less likely than PE').[33]
In low-risk patients, guidelines from the American College of Physicians recommend the Pulmonary
Embolism Rule-out Criteria (PERC) to help exclude PE.[34] [35] [31] In those patients with moderate risk or
who are PERC rule positive, D-Dimer may be helpful in excluding PE.[26] [36] [27] For patients who have a
high suspicion for PE, a transthoracic echocardiogram demonstrating right ventricular dilation may indicate
acute right ventricular failure from a PE.[27] 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 point-of-care ultrasonography or transthoracic echocardiography. Patients presenting in shock from
tamponade require emergency pericardiocentesis.[37]
7
Assessment of chest pain Diagnosis
Approach
Patients with chest pain can be triaged according to whether the aetiology is traumatic or atraumatic. 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. It is important to check whether the
patient still has pain, and if not, to find out when his or her last episode of pain occurred.[18]
History
The character of chest pain 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).[38] [39] [40]
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 15 minutes and is dull, central, and crushing is a feature of ACS.
• Pain that radiates to the jaw or upper extremities suggests a cardiac cause.[41]
• Pain that is new in onset, or a change to the usual pattern in a patient with previously stable angina,
including recurrent episodes occurring frequently with little or no exertion, or lasting longer than 15
minutes, suggests possible ACS.[18]
• 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). Cardiac pain is more likely to be brought on by exercise
or emotion and is typically relieved with rest or nitrates. However, response to glyceryl trinitrate should not
be used to make a diagnosis.[18] Pain brought on by food, lying down, hot drinks, or alcohol, and relieved
DIAGNOSIS
by antacids suggests a gastrointestinal cause. Heartburn and acid regurgitation are typical symptoms of
GORD.[42]
Abdominal pathology, such as acute cholecystitis and pancreatitis, may also cause pain referred to the
chest. Associated symptoms may help to narrow the diagnosis. Acute cholecystitis may cause symptoms of
fever, nausea, vomiting, persistent severe right upper quadrant pain, and jaundice. Acute pancreatitis pain is
typically sudden in onset, constant, may radiate to the back, and worsens with movement. The onset of pain
is sudden and is associated with vomiting in 80% of cases.[43]
Dyspnoea is an associated symptom in patients with cardiac ischaemia, pulmonary embolism (PE),
pneumothorax, or pneumonia. Nausea, vomiting, and sweating may be seen in patients with ACS.
Despite these more typical features, it should be remembered that some patients with ACS may present with
atypical symptoms: pre-syncope/syncope, nausea and vomiting, or dyspnea in the absence of chest pain.
This occurs more commonly in women, people with diabetes, and those aged 75 years or more.[44] [45] [46]
[47] [48] [49]
Past medical history and specific cardiac risk factors, such as known cardiac disease, elevated cholesterol,
hypertension, smoking, and family history, support a cardiac cause.[50] Cocaine use also makes cardiac
ischaemia more likely.[51] It is helpful to determine if the patient has had any previous investigations or
treatment for chest pain.[18]
A detailed drug history should also be taken (e.g., use of non-steroidal anti-inflammatory drugs may result in
a gastric cause of pain due to gastritis, gastric ulcer, or duodenitis).
Physical examination
Physical examination can further narrow down the differential.
Patients with chest pain may present in acute shock, such as those with:
• Tension pneumothorax
• Cardiac tamponade
• Massive PE
• ACS with cardiogenic shock
• Pancreatitis
• Sepsis from pneumonia or cholecystitis
• Oesophageal rupture.
Abnormalities revealed in the cardiac examination include abnormalities in pulse or heart sounds (e.g., new
onset of aortic stenosis, mitral regurgitation, or worsening of existing murmur, pericardial friction rub), hypo-
or hypertension, and signs of heart failure. Cardiac examination is often normal in ACS. Aortic dissection
may cause a pulse deficit, indicated by reduced pulse force or volume, or clinical signs of hypoperfusion
(e.g., cold, blue, mottled limb) affecting the extremities.[52] This is particularly common in a proximal
dissection affecting the aortic arch, and may be unilateral or bilateral. Interarm systolic blood pressure
differences of more than 20 mmHg may be present with aortic dissection.
Crepitations on 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
DIAGNOSIS
costochondritis. However, many patients with myocardial infarction also have chest wall pain on presentation.
Tenderness unilaterally, in a dermatomal distribution (with or without the typical rash), may be indicative
of herpes zoster. The pain typically presents 2 to 3 days before the development of a rash in the affected
dermatome. However, some patients present with pain for up to 1 week before development of a rash.[53]
Typically, the rash is vesicular on an erythematous base in a unilateral distribution of one dermatome.
9
Varicella zoster virus

Courtesy of Daniel Eisen, MD; used with permission
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)
makes a gastrointestinal aetiology more likely. Possible disorders include: GORD, peptic ulcer disease,
DIAGNOSIS
cholecystitis, pancreatitis, and gastritis. In acute cholecystitis, physical examination may reveal a right upper
quadrant mass. A positive Murphy's sign (the examiner’s hand rests on the right costal margin and deep
inspiration causes pain) has a specificity of 79% to 96% for acute cholecystitis.[54]
Features of a connective tissue disease such as Marfan's syndrome (tall stature, arachnodactyly, pectus
excavatum, joint hypermobility, high-arched palate and narrow face) or type IV Ehlers-Danlos syndrome
(translucent skin, easy bruising, small joint hypermobility) may be present in patients with aortic dissection.
Unilateral leg tenderness or swelling may indicate a deep vein thrombosis in patients with suspected PE.
Basic investigations
Basic observations include temperature, blood pressure, pulse, and respiratory rate. In addition, the following
should be monitored, using clinical judgement on the frequency of monitoring required, until a firm diagnosis
has been made.[18]
• Heart rhythm
• Oxygen saturation by pulse oximetry
• Repeated resting 12-lead ECGs
• Any exacerbations of pain and/or other symptoms
• Pain relief; checking that this is effective.
ECG
• A 12-lead 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 segment changes such as ST elevation or ST depression, QRS abnormalities, arrhythmias, or
tachycardia or bradycardia are characteristic findings in cardiac causes.
• ST segment elevation, measured at the J point, >1 mm in contiguous leads, indicates ST-elevation
myocardial infarction (STEMI). ST-wave depression or T wave inversion in contiguous leads may
indicate coronary ischaemia. Patients with ACS may have normal or nearly normal ECGs; where there
is concern for ACS, serial ECGs should be performed.
ECG showing changes of an acute inferior myocardial infarction with ST elevation in leads II, III, and aVF DIAGNOSIS
From the collection of Professor James Brown; used with permission
11
ECG showing ST depression

From the personal collection of Dr Syed W. Yusuf and Dr Iyad N. Daher,
Department of Cardiology, University of Texas, Houston, TX; used with permission
• Pericarditis may be present with diffuse ST elevation or PR depression.[55]
• ECG findings that may be present in patients with PE include sinus tachycardia (most commonly) and
S wave in lead I with Q wave and T wave inversion in lead III (S I, Q III, T III pattern).
• Patients with pericardial tamponade may demonstrate electrical alternans (alternate-beat variation in
the amplitude or axis of the QRS complex).
Chest x-ray
• A chest x-ray can confirm respiratory disorders such as pneumothorax or pneumonia. If pneumonia
is a concern (and the patient is clinically stable enough to travel to radiology), posterior-anterior and
lateral projections increase the sensitivity of diagnosis. Cardiac ischaemia is often characterised by a
normal chest x-ray, but a chest x-ray can also provide clues to serious cardiac pathology, such as a
DIAGNOSIS
widened mediastinum in aortic dissection, or a large globular heart in cardiac tamponade.
Chest x-ray showing a widened mediastinum

DIAGNOSIS
13
Chest x-ray showing a large globular heart in a patient with pericardial tamponade
DIAGNOSIS
Blood tests
• In patients with concern for ACS, cardiac biomarkers should be ordered on presentation and at least
every 6 to 8 hours after presentation. There is considerable variability in protocols, depending on types
of biomarkers available.[21] [56]
• Cardiac biomarkers (e.g., troponin I and T, creatine kinase [CK], creatine kinase-MB [CK-MB]) found in
skeletal and cardiac muscle are raised in many situations including myocardial infarction, following a
fall or seizure, myositis, hypothermia, or hypothyroidism. Troponin is more specific for myocardial injury
than CK or CK-MB. Troponin is the preferred biomarker in the evaluation of patients with chest pain.
• High-sensitivity troponins, where available, may allow for earlier diagnosis of ACS.[57] Patients with
a non-ischaemic ECG and a negative high-sensitivity troponin T, particularly if they have had pain for
over 3 hours, have a very low risk of major adverse cardiac events (MACE).[58] [59] In the UK, the
2016 update of the National Institute for Health and Care Excellence guideline on the assessment of
chest pain recommends that high-sensitivity troponin tests should not be used in people in whom ACS
is not suspected.[18]
• One cohort study of patients who presented to the emergency department with chest pain but no
ACS found that any elevation of high-sensitivity troponin was associated with an increased risk of
cardiovascular events and death over a mean follow-up of three years. [60] CK should only be used if
troponin is unavailable.
• A full blood count should be considered 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 STEMI, pneumothorax,
pneumonia, pericarditis, and costochondritis. The results of the second set of cardiac biomarkers usually
confirm the diagnosis of non-STEMI (NSTEMI). Patients with normal serial ECGs and 2 sets of normal
troponin measurements at least 3 hours apart may be considered for management with outpatient testing
within the next 72 hours.[21]
Coronary angiography with percutaneous coronary intervention (PCI)
• Coronary angiography with PCI is required urgently in patients with STEMI and in patients with
NSTEMI who have high-risk features such as ongoing chest pain and dynamic ECG changes.
DIAGNOSIS
15
DIAGNOSIS Assessment of chest pain Diagnosis
Angiogram showing occluded right artery

From the personal collection of Dr Mahi Ashwath; used with permission
• If PCI is unavailable or delayed more than 2 hours, then systemic fibrinolysis should be given for
STEMI, but not for NSTEMI.
Risk stratification
The HEART score has been developed for risk stratification of patients in the emergency department.
Patients with a low HEART score (0-3) have a low risk of MACE at 6 weeks. Patients with a high HEART
score (7-10) are at significant risk for MACE.[41] [61] [62] One 2017 systematic review and meta-analysis
found that the HEART score had a sensitivity of 96.7%.[63]
Composition of the HEART score for chest pain patients in the emergency department
Six AJ, et al. Neth Heart J. 2008;16:191-6; used with permission
DIAGNOSIS
There are many other risk scores available. Guidelines vary in their recommendations on risk stratification in
people presenting with acute chest pain to the accident and emergency department.[64]
Further investigations
Some patients need further investigations to confirm the suspected diagnosis.
Once ACS, ventricular arrhythmias, and haemodynamic instability are excluded, patients with chest pain that
is clinically considered to be ischaemic in origin can be stratified by their likelihood of having angina and risk
for coronary artery disease (CAD).[65] [66] [67] [68] [69] [70]
1. High pre-test probability of CAD (>90%): should be referred for coronary angiography.
2. Intermediate pre-test probability of CAD (10-90%): should have stress testing with imaging
(radionuclide, echocardiography, or magnetic resonance imaging).
3. Low pre-test probability of CAD (<10%): if the patient has an interpretable ECG (not left bundle branch
block, pre-excitation [Wolff-Parkinson-White], or ventricular paced rhythm) and is able to exercise,
he or she should have an exercise stress test. Otherwise the patient should have a stress test with
imaging.[65]
17
Guidelines differ in their recommendations on use of risk stratification and further specific investigations so
it's important to check local protocols.
Patients without symptoms of angina 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, computed tomography (CT) angiography is more useful.[71]
This allows rapid imaging and detection of life-threatening aortic pathology. Magnetic resonance aortography
has a sensitivity and specificity equivalent to CT. This imaging modality also provides information on aortic
valve pathology and left ventricular function, but the images take longer to acquire so it is only suitable for
haemodynamically stable patients.[71] A trans-oesophageal echocardiogram is an alternative if a dissection-
skilled operator is readily available.[72]
PE can be difficult to diagnose. A high index of suspicion is required. Initial tests include chest x-ray,
ECG, and arterial blood gases, but results of these tests do not definitively establish or eliminate PE
as a diagnosis. Validated scores help to predict the likelihood of PE. These include the Wells score
and the Geneva score (and their simplified versions).[73] [29] D-dimer blood testing by enzyme-linked
immunosorbent assay (ELISA) has a sensitivity and negative predictive value >95%, regardless of the
calculated clinical probability, making it useful to rule out the presence of venous thromboembolism.
However, specificity is much lower, with estimates from 23% to 63%. It is particularly useful in patients with a
low or intermediate clinical probability assessment.[74] [75] [76]
For patients identified to be at very low risk of PE, the Pulmonary Embolism Rule-Out Criteria may be used.
If the patient meets all criteria (age <50 years; initial heart rate <100 bpm; initial oxygen saturation >94% on
room air; no unilateral leg swelling; no haemoptysis; no surgery or trauma within the last 4 weeks; no history
of venous thromboembolism; no oestrogen use), the risk for PE is considered to be lower than the risk of
testing, and so a D-dimer is not indicated. D-dimer should be done for patients who do not meet all of the
criteria.[31]
A diagnosis of PE can effectively be ruled out in patients with a low probability of PE on clinical scoring with a
DIAGNOSIS
D-dimer that is not elevated. The risk of PE within 3 months in these patients is less than 1%.[77]
For patients with a high probability of PE on clinical scoring (i.e., PE likely) or an abnormal D-dimer, imaging
is required. Multiple-detector computed tomographic pulmonary angiography (CTPA) scanning of the chest is
the imaging study of choice.
Spiral computed tomography pulmonary angiogram showing a large filling

defect within the pulmonary vasculature compatible with a saddle embolus
If CTPA is contraindicated or not available, other imaging studies may be used, such as a ventilation-
perfusion scan.
DIAGNOSIS
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, once cardiac causes of the chest pain have been ruled out.[78]
Further blood tests such as liver profile and either serum lipase or amylase may be necessary if acute
cholecystitis or acute pancreatitis is suspected. These diagnoses may also require further imaging such as
abdominal ultrasound and abdominal CT (for acute pancreatitis).
19
Differentials overview
Common
Stable angina
Pneumonia
Viral pleuritis
GORD
Costochondritis
Anxiety or panic disorder
Uncommon
Pulmonary embolism
Pericarditis
Cardiac tamponade
Aortic dissection
DIAGNOSIS
Aortic stenosis
Mitral valve prolapse
Pneumothorax
Pulmonary hypertension
Peptic ulcer disease
Oesophageal spasm
Acute cholecystitis
Acute pancreatitis
Herpes zoster
Uncommon
Gastritis
DIAGNOSIS
21
Differentials
Common
History Exam 1st Test Other tests
central chest pressure, examination may »ECG: ST-elevation »B-type natriuretic

squeezing, or be normal; jugular myocardial infarction peptide: >99th
heaviness; radiation venous distention, S4 (STEMI): ST-segment percentile of normal
to jaw or upper gallop, holosystolic elevation >1 mm Measurement of B-
extremities; associated murmur (mitral in ≥2 anatomically type natriuretic peptide
nausea, vomiting, regurgitation), bibasilar contiguous leads or
dyspnoea, dizziness, rales; hypotensive, new left bundle-branch (BNP) or N-terminal
weakness; occurs at may be tachycardic, block; non-STEMI pro-BNP (NT-pro-BNP)
rest or accelerating bradycardic, or hypoxic (NSTEMI) or unstable may be considered
tempo (crescendo); risk depending on severity angina: non-specific; to supplement
factors: smoking, age of ischaemia[20] [21] ST-segment depression
(men >45, women >55 or T-wave inversion assessment of global
years), positive family ECG should be risk in patients with
history of premature obtained in all patients suspected ACS.[21]
coronary artery [56]
disease, hypertension, with chest pain
hyperlipidaemia, within 10 minutes of
»coronary
diabetes, stroke, or presentation. angiography: STEMI:
peripheral arterial critical occlusion of
disease;[20] [21] Serial ECGs are a coronary artery;
women, older people NSTEMI and unstable
extremely important, as
(>75 years), and people angina: evidence
with diabetes may be many cases of acute
of coronary artery
more likely to present coronary syndrome narrowing
with atypical symptoms (ACS) present with If the patient has a
such as nausea or
DIAGNOSIS
normal initial ECGs.[20] STEMI and there are

dyspnoea
[21] no contraindications,
urgent coronary
angiography with
possible re-perfusion
therapy should be
considered.[19]
ECG showing Patient with unstable

changes of an acute angina or NSTEMI
inferior myocardial must proceed to urgent
infarction with ST coronary angiography if
elevation in leads they demonstrate high-
II, III, and aVF risk features: ongoing
From the collection chest pain, new
of Professor James congestive heart failure,
Brown; used ventricular arrhythmias,
with permission hypotension, dynamic
Common

»CXR: normal or signs ECG changes, and
of heart failure, such elevated cardiac
as increased alveolar
markings, blood enzymes.[20] [21]
diversion to upper
lobes, cardiomegaly,
Kerley B lines, pleural
effusions
Pulmonary oedema
and congestive heart
failure is an important
high-risk feature in
ACS.
»cardiac enzymes:
elevated in STEMI and
NSTEMI; not elevated
in unstable angina
Elevated troponins
are highly specific and
sensitive for myocardial
damage, but not all
elevated troponins are
secondary to coronary
ischaemia.[79]
DIAGNOSIS
Other diagnoses
that may elevate
troponins include
severe hypertension,
sepsis, pulmonary
embolism, myocarditis,
pericarditis, and cardiac
contusion.
◊ Stable angina
may be known no specific findings »ECG: no acute »stress testing:

history of coronary for CAD, may have changes; may have ≥1 mm of horizontal
artery disease; abnormal pulses if evidence of previous or down-sloping ST-
chest discomfort on peripheral vascular infarction, such as Q segment depression or
exertion, relieved disease present waves ST-segment elevation
by nitroglycerine or during or after exercise
23
Common
◊ Stable angina

rest; no change in »CXR: normal or is considered positive
intensity, frequency, or cardiomegaly for ischaemia; high-risk
duration; no associated disease: regional wall
»cardiac
diaphoresis, nausea/ motion abnormalities
biomarkers: not
vomiting, or shortness and left ventricular
elevated
of breath; risk factors: dysfunction
smoking, age (men Guidelines differ in their
>45, women >55 recommendations on
years), positive family
history of premature use of risk stratification
coronary artery disease and further specific
(CAD), hypertension, investigations so it's
hyperlipidaemia, important to check local
diabetes, stroke, or
peripheral arterial protocols. Modalities of
disease[21] stress include exercise
or pharmacological
agents, such as
adenosine or
dobutamine.
Imaging modalities
include nuclear (single
photon emission CT) or
echocardiogram.
Exercise stress
DIAGNOSIS
testing has medium

sensitivity (50%)
and high specificity
(90%).[80] Stress
testing with imaging
has a high sensitivity
and specificity (80% to
90%).[81]Differentiates
between angina and
non-cardiac chest pain
in patients with possible
or probable angina.
UK guidance on chest
pain recommends
that exercise ECG
should not be used to
diagnose or exclude
Common
◊ Stable angina

stable angina for
people without known
CAD.[18]
»coronary
angiography:
evidence of coronary
artery narrowing
Definitive test for
diagnosis of CAD.
»CT coronary
angiography:
identification of stenosis
Recently developed,
non-invasive
investigative modality.
The ability to quantify
stenosis is not well
established.[82] [83]
Pneumonia
DIAGNOSIS
productive or dry decreased breath »CXR: pulmonary »WBC count: elevated
cough, fever, pleuritic sounds, rales, infiltration, air with left shift (increased
pain associated wheezing, bronchial bronchograms, and neutrophil count)
with shortness of breath sounds, pleural effusion »sputum culture:
breath; may have dullness to percussion, may reveal culprit
rigors, myalgias, and increased organisms, but not
and arthralgias; may tactile fremitus sensitive or specific;
be recent history of observed with severe recommended in
travel or infectious consolidation[90] patients with severe
exposures[90] disease as well as in
all patients empirically
treated for MRSA
or Pseudomonas
aeruginosa [91]
Sometimes helpful for
choosing antibiotics.
»blood culture:
may reveal culprit
organisms, but not
sensitive or specific;
recommended in
25
Common
Pneumonia

patients with severe
disease as well as in
all patients empirically
treated for MRSA or P
aeruginosa [91]
Sometimes helpful for
choosing antibiotics.
◊ Viral pleuritis
prodrome of viral illness pleural friction rub »CXR: usually normal »FBC: normal,
(myalgias, malaise, with or without but can uncommonly or leukocytosis
rhinorrhoea, cough, low-grade fever; have effusion with lymphocytic
nasal congestion, low- sometimes reproducible Viral pleuritis is a predominance
grade temperatures); tenderness to diagnosis of exclusion.
contacts with others palpation of chest
having apparent when perichondritis
infectious disease or pleurodynia
accompanies pleuritis
◊ GORD

DIAGNOSIS
may have chest pain, no specific physical »therapeutic trial: »oesophagogastroduodenoscopy:

typically retrosternal findings relief of symptoms with oesophageal
burning with eating short trial of proton- inflammation or
large or fatty meals pump inhibitors, but erosions
that can be reproduced consider cardiac Indicated if long-
with lying supine and work-up to exclude standing symptoms or
relieved by sitting up; cardiac cause before
relieved by antacids; presuming GORD associated features
reflux symptoms and commencing such as anaemia,
therapeutic trial[42] dysphagia, or
involuntary weight loss.
◊ Costochondritis
focal chest wall reproducible pain on »CXR: no specific

pain, may have chest wall palpation, findings
known precipitating especially at the Should be performed
injury; aggravated by costochondral junctions to assess for
Common
◊ Costochondritis

sneezing, coughing, possible fractures or
deep inspiration, or malignancies as the
twisting of the chest
aetiology of patient's
chest wall pain.
◊ Anxiety or panic disorder
sharp chest pain with hyperventilation, »ECG: normal »CXR: normal

anxiety, dizziness or examination otherwise »HADS (hospital
faintness, palpitations, normal anxiety and
sweating, trembling depression scale)
or shaking, fear score: may have a
of dying or going score >11
insane, paraesthesiae,
chills or hot flushes,
breathlessness or
choking sensation
Uncommon
Pulmonary embolism
DIAGNOSIS
chest pain that is sharp may have tachycardia, »ECG: sinus »echocardiography:
and pleuritic in nature; loud P2, right-sided tachycardia; usually may show acute right
shortness of breath; S4 gallop, jugular nonspecific but may ventricular dilation or
haemoptysis may occur venous distention, show S1, Q3, and T3 hypokinesis
if pulmonary infarction fever, right ventricular pattern »ventilation-
develops; massive lift; massive PE may »D-dimer: non-specific perfusion (V/Q)
pulmonary embolism cause hypotension[84] if positive; PE excluded scan: may show V/Q
(PE) results in syncope; if result negative in mismatch
risk factors: history patients with low
of immobilisation, »pulmonary
probability of having a
orthopaedic angiography: may
PE
procedures, oral identify thrombus in the
contraceptive »CXR: may show pulmonary circulation
use, previous PE, decreased perfusion Definitive test, rarely
hypercoagulable states, in a segment of performed because is
or recent travel over pulmonary vasculature
(Westermark sign); may invasive.
long distances;[84]
unilateral swollen lower show pleural effusion
leg that is red and »CT pulmonary
painful suggests deep angiography: may
venous thrombosis;
27
Uncommon
Pulmonary embolism

use of the modified identify thrombus in the
Wells criteria can pulmonary circulation
help to screen for risk First-line test in
factors and clinical patients with high
features suggesting
high probability[73] probability of PE
provided there are no
contraindications.[83]
[84]
Spiral computed
tomography
pulmonary
angiogram showing
a large filling defect
within the pulmonary
vasculature
compatible with a
saddle embolus
From the collection
DIAGNOSIS
of Professor James
Brown; used
with permission
◊ Pericarditis
usually viral prodrome; tachycardia and friction »ECG: diffuse concave- »CXR: usually normal;
sharp pleuritic chest rub; jugular venous up ST-elevation, enlarged cardiac
discomfort provoked distention and pulsus associated PR silhouette (globular
by lying supine and paradoxus indicate depression; changes heart) if pericardial
improved with sitting effusion causing evolve over time effusion present
up;[55] associated dry tamponade ECG changes occur in »echocardiography:
cough, fever, myalgias, >80% of patients.[85] normal or shows small
or arthralgias; history effusion
of possible causes
such as radiation
exposure, collagen
Uncommon
◊ Pericarditis

vascular disease,
recent myocardial
infarction, or uraemia
Cardiac tamponade
history of underlying hypotension, distended »ECG: low-voltage

cause such as neck veins, muffled QRS; electrical
myocardial infarction, heart sounds; pulsus alternans; other
aortic dissection, or paradoxus (a drop of changes depend on
trauma; may present ≥10 mmHg in arterial underlying cause (e.g.,
insidiously as a result blood pressure on ST elevation in acute
of hypothyroidism or inspiration) myocardial infarction
pericarditis; dizziness; or non-specific ST
dyspnoea; fatigue changes in pericarditis)
»CXR: globular heart (if
large effusion)
DIAGNOSIS
Chest x-ray showing
a large globular
heart in a patient
with pericardial
tamponade
From the collection
of Professor James
Brown; used
with permission
»echocardiography:
pericardial effusion
causing collapse of
great vessels, atria, and
ventricles
29
Uncommon
Aortic dissection
acute substernal unequal pulses or »CXR: widened »transoesophageal

tearing sensation, blood pressures mediastinum echocardiography:
with radiation to in both arms; new Limited sensitivity false lumen or flap
interscapular region diastolic murmur due (64%) and specificity in the ascending or
of the back; pain to aortic regurgitation; descending aorta; new
may migrate with the muffled heart sounds (86%) for aortic aortic regurgitation or
propagation of the if the dissection is disease.[88] pericardial tamponade
dissection; stroke, complicated by cardiac »CT chest with
acute myocardial tamponade; new focal contrast: false lumen
infarction due to neurological findings or flap in the ascending
obstruction of due to involvement of or descending aorta
aortic branches; the carotid or vertebral
dyspnoea due to acute arteries[86] [87] »MRI angiography:
aortic regurgitation; false lumen or flap
hypotension due to in the ascending or
cardiac tamponade; descending aorta
history of hypertension, Chest x-ray Very accurate, but
Marfan's syndrome, showing a widened limited availability in the
Ehlers-Danlos
mediastinum acute setting.
syndrome, or
syphilis[86] [87] From the collection
of Professor James
Brown; used
with permission
Aortic stenosis
DIAGNOSIS
age over 60 years; ejection systolic »ECG: voltage criteria »CXR: calcified aortic
typical angina; murmur that radiates to for left ventricular valve; pulmonary
chest pain is usually the neck; obliteration hypertrophy; enlarged oedema
progressive;[89] of S2 indicates severe P wave suggesting left »echocardiogram:
shortness of breath; stenosis; delayed atrial enlargement poor excursion of aortic
syncope (if severe); upstroke on palpation valve leaflets; elevated
patients with significant of carotid pulse velocities through the
aortic stenosis and aortic valve; possible
heart failure are at left ventricular systolic
high risk of cardiogenic dysfunction
shock or sudden death
Uncommon
Mitral valve prolapse
usually asymptomatic, mid-systolic click and »ECG: usually normal, »CXR: usually normal,
but may cause late systolic murmur at may show atrial may show enlarged
palpitations, chest pain, the apex fibrillation or other pulmonary artery or left
dyspnoea, headache, arrhythmias atrium
or fatigue »echocardiogram:
mitral regurgitation and
valve prolapse
Pneumothorax
acute, pleuritic chest absent breath sounds, »CXR: air in the pleural
pain, shortness increased resonance space, visible pleural
of breath; primary to percussion; jugular line from collapsed
spontaneous between venous distention, lung, or mediastinal
ages 20 and 40 tracheal deviation, and shift
years; secondary hypotension if tension The diagnosis of
spontaneous in patients pneumothorax (due tension pneumothorax
with COPD; traumatic to compromise of the
due to acute trauma or great vessels)[92] should be made on
iatrogenic;[92] shock clinical grounds, not
may occur if rapidly radiographically.
increasing (tension
pneumothorax)
◊ Pulmonary hypertension
DIAGNOSIS
cardiac-sounding accentuated pulmonic »ECG: right axis »CXR: large, prominent

chest pain on exertion, component (P2) to deviation; right pulmonary arteries
dyspnoea; symptoms of the second heart ventricular hypertrophy »echocardiogram:
right-sided heart failure sound; palpable or right atrial tricuspid regurgitation;
such as lower extremity P2; right ventricular enlargement estimated right
oedema, abdominal heave; lower extremity ventricular systolic
bloating, or ascites; oedema; jugular pressure >35 mmHg;
syncope if severe[93] venous distention right ventricular and
[94] right atrial dilation;
pericardial effusion
31
Uncommon
◊ Peptic ulcer disease
gastric ulcers: epigastric tenderness; »Helicobacter pylori

»oesophagogastroduodenoscopy:
epigastric pain or if significant bleeding gastric or duodenal breath test: may be
burning with onset 5 to is present there erosions or ulceration positive
15 minutes after eating may be tachycardia, Breath test has a
and may last for several hypotension, and sensitivity of 93% and
hours; duodenal ulcers: conjunctival pallor[95]
epigastric pain is specificity of 97% for H
relieved by eating pylori .
and may return 1 to 4
hours postprandially; Sensitivity and
pain from any specificity are too
ulcer is relieved by
low for the test to be
antacid; risk factors:
cigarette smoking, clinically useful for the
non-steroidal anti- diagnosis of peptic
inflammatory drugs, ulcer disease but
and chronic alcohol
aid in management
consumption[95]
of patients who do
not need endoscopy.
Repeat to test for
eradication.
Note that test is

sensitive and specific
for H pylori , but
not for peptic ulcer
DIAGNOSIS
disease.[96]
◊ Oesophageal spasm
crushing substernal no specific findings »barium swallow: »oesophageal

chest pain, associated corkscrew or rosary manometry:
dysphagia, pain does bead appearance on simultaneous
not always correlate barium swallow contractions on >30%
with swallowing, of wet swallows[97]
dysphagia precipitated
by very hot or cold
foods, glyceryl trinitrate
can relieve the pain[97]
Uncommon
Acute cholecystitis
right upper quadrant right upper quadrant »liver function »hydrox y-

pain, radiation to the tenderness (Murphy's tests: may be elevated iminodiacetic
interscapular area sign), abdominal alkaline phosphatase acid (HIDA) scan:
or right shoulder, rigidity and guarding and gamma glutamyl decreased radionuclide
associated with if perforation of the transferase uptake in the
nausea and vomiting, gallbladder, rarely Suggests biliary gallbladder due to
fevers, anorexia often have jaundice early obstruction. Not specific cystic duct obstruction
accompanies pain, in the course of Sensitivity is 95% and
signs of peritoneal cholecystitis[98] for cholecystitis.
specificity is 99%.[100]
inflammation such as
»FBC: leukocytosis
abdominal pain with
with a left shift
jarring[98]
Helpful in judging the
severity of illness in a
patient.
»abdominal
ultrasound:
pericholecystic fluid,
distended gallbladder,
thickened gallbladder
wall, and gallstones
The reported sensitivity
and specificity
of ultrasound in
the diagnosis of
acute cholecystitis
DIAGNOSIS
approaches 95%.[99]
Acute pancreatitis
epigastric or tachycardic, »serum lipase: »FBC: leukocytosis

periumbilical abdominal hypotensive, febrile, double the upper limit Important in
pain that radiates to the acute distress; of normal values determining the short-
back; may be severe; ecchymosis in the The diagnostic value
associated nausea and periumbilical region term mortality of
of lipase is greatest
vomiting; history of (Cullen's sign) and the pancreatitis (Ranson's
alcohol consumption or flank (Grey-Turner sign) up to 1 day after the
score).
gallstones[101] onset of pain and has
a 95% sensitivity and »electrolytes and
specificity.[102] renal function:
elevated creatinine,
high anion gap
»ABG: acidosis, low
pH
33
Uncommon
Acute pancreatitis

Important prognostic
marker.
»abdominal
ultrasound:
determines possible
cause, such as
gallstones
Should be done
regularly to work
up the aetiology of
pancreatitis.
»abdominal CT
scan: stage the
severity of the
pancreatitis; pancreatic
necrosis; pseudocyst
Used in patient with
severe pancreatitis to
look for complications.
◊ Herpes zoster

DIAGNOSIS
unilateral, burning pain vesicular rash on »usually no test »swab for viral
in typical dermatome erythematous base, in required: diagnosis is culture and
distribution that unilateral distribution of clinical polymerase chain
may occur before a dermatome reaction (PCR):
appearance of rash varicella-zoster
and may persist for >1 positive on culture,
month immunofluorescence,
or PCR
◊ Gastritis
dyspepsia/epigastric epigastric gastric »Helicobacter pylori »oesophagogastroduodenoscopy:

discomfort; nausea, discomfort may be urea breath test: results can be variable;
vomiting, loss of present; may have positive in H pylori may show atrophy and/
appetite; history of signs associated with infection or erosions
non-steroidal anti- vitamin B12 deficiency »gastric mucosal
inflammatory drug use and pernicious biopsy: variable;
or alcohol misuse; anaemia (e.g., positive for H pylori
history of Helicobacter abnormal neurological
Uncommon
◊ Gastritis

pylori infection; history examination, presence ; features of acute or
of previous gastric or of cognitive impairment, chronic gastritis
abdominal surgery angular cheilitis,
atrophic glossitis
DIAGNOSIS
35
Assessment of chest pain Guidelines
Guidelines
Europe
2017 ESC guidelines for the management of acute myocardial infarction in

patients presenting with ST-segment elevation (ht tps://www.escardio.org/
Guidelines/Clinical-Practice-Guidelines)
Published by: European Society of Cardiology

Last published: 2017
Chest pain of recent onset: assessment and diagnosis (ht tps://

www.nice.org.uk/guidance/cg95)
Published by: National Institute for Health and Care Excellence

GUIDELINES
Myocardial infarction (acute): early rule out using high-sensitivity troponin

tests (Elecsys Troponin T high-sensitive, ARCHITECT STAT High Sensitive
Troponin-I and AccuTnI+3 assays) (ht tps://www.nice.org.uk/guidance/dg15)
Published by: National Institute for Health and Care Excellence

North America
ACR appropriateness criteria: chest pain - possible acute coronary syndrome

(ht tp://www.acr.org/Quality-Safety/Appropriateness-Criteria)
Published by: American College of Radiology

ACR appropriateness criteria: chronic chest pain-noncardiac etiology

unlikely: low to intermediate probability of coronary artery disease (ht tp://
www.acr.org/Quality-Safety/Appropriateness-Criteria)

ACR appropriateness criteria: chronic chest pain - high probability of

coronary artery disease (ht tps://www.acr.org/Clinical-Resources/ACR-
Appropriateness-Criteria)

Assessment of chest pain Guidelines
North America
ACR appropriateness criteria: suspected pulmonary embolism (ht tp://

www.acr.org/Quality-Safety/Appropriateness-Criteria)

ACR appropriateness criteria: acute nonspecific chest pain - low

probability of coronary artery disease (ht tp://www.acr.org/Quality-Safety/
Appropriateness-Criteria)

GUIDELINES
ACR appropriateness criteria: acute chest pain - suspected aortic dissection
(ht tp://www.acr.org/Quality-Safety/Appropriateness-Criteria)

Multimodality appropriate use criteria for the detection and risk assessment
of stable ischemic heart disease (ht tp://www.onlinejacc.org/content/63/4/380)
Published by: American College of Cardiology; American Heart Association; American Society of
Echocardiography; American Society of Nuclear Cardiology; Heart Failure Society of America; Heart
Rhythm Society; Society for Cardiovascular Angiography and Interventions; Society of Cardiovascular
Computed Tomography; Society for Cardiovascular Magnetic Resonance; Society of Thoracic Surgeons
37
Assessment of chest pain References
Key articles
• Ibanez B, James S, Agewall S, et al. 2017 ESC guidelines for the management of acute myocardial
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• Kline JA, Kabrhel C. Emergency evaluation for pulmonary embolism, part 2: diagnostic approach. J
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syndrome? The rational clinical examination systematic review. JAMA. 2015 Nov 10;314(18):1955-65.
Abstract
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Assessment of chest pain Images
Images
IMAGES
Figure 1: Distribution of final diagnoses in people over 35 years admitted to hospital from one US hospital
emergency department with chief complaint of non-traumatic chest pain, over a 5-year period (PE, pulmonary
embolism)
Created by BMJ; based on data from Kohn MA, Kwan E, Gupta M, et al. Prevalence of acute myocardial
infarction and other serious diagnoses in patients presenting to an urban emergency department with chest
pain. J Emerg Med. 2005 Nov;29(4):383-90
49
IMAGES Assessment of chest pain Images
Figure 2: Varicella zoster virus

Courtesy of Daniel Eisen, MD; used with permission
IMAGES
Figure 3: ECG showing changes of an acute inferior myocardial infarction with ST elevation in leads II, III, and
aVF
Figure 4: ECG showing ST depression
51
From the personal collection of Dr Syed W. Yusuf and Dr Iyad N. Daher, Department of Cardiology, University
of Texas, Houston, TX; used with permission
IMAGES
Figure 5: Chest x-ray showing a widened mediastinum

IMAGES
Figure 6: Chest x-ray showing a large globular heart in a patient with pericardial tamponade
53
Figure 7: Angiogram showing occluded right artery

From the personal collection of Dr Mahi Ashwath; used with permission
IMAGES
Figure 8: Composition of the HEART score for chest pain patients in the emergency department
Six AJ, et al. Neth Heart J. 2008;16:191-6; used with permission
55
Figure 9: Spiral computed tomography pulmonary angiogram showing a large filling defect within the
pulmonary vasculature compatible with a saddle embolus
Assessment of chest pain Disclaimer
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Assessment of chest pain Disclaimer
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Contributors:
// Authors:
James E. Brown, MD, MMM

Professor and Chair
Emergency Medicine, Wright State University Boonshoft School of Medicine, Kettering, OH
DISCLOSURES: JEB declares that he has given expert testimony in matters related to this topic.
// Acknowledgements:
Dr James E. Brown would like to gratefully acknowledge Dr Marvin H. Eng and Dr Mori J. Krantz, previous
contributors to this topic.
DISCLOSURES: MHE declares that he has no competing interests. MJK is a consultant for
GlaxoSmithKline.
// Peer Reviewers:
Michael Jelinek, MD, FRACP, FACC

Cardiologist
St Vincent’s Hospital Melbourne, Associate Professor, Department of Medicine, University of Melbourne,
Melbourne, Australia
DISCLOSURES: MJ declares that he has no competing interests.
Debabrata Mukherjee, MD
Gill Foundation Professor of Interventional Cardiology
Director of Cardiac Catheterization Laboratories, Gill Heart Institute, Division of Cardiovascular Medicine,
University of Kentucky, Lexington, KY
DISCLOSURES: DM declares that he has no competing interests.
Martin Bocks, MD
Clinical Lecturer
University of Michigan Congenital Heart Center, Ann Arbor, MI
DISCLOSURES: MB declares that he has no competing interests.
Ethan Cumbler, MD
Assistant Professor
Department of Internal Medicine, University of Colorado Health Sciences Center, Denver, CO
DISCLOSURES: EC declares that he has no competing interests.
Davendra P.S. Sohal, MBBS, MPH

Research Fellow
Internal Medicine, Albert Einstein College of Medicine/Jacobi Medical Center, Bronx, NY
DISCLOSURES: DS declares that he has no competing interests.

Assessment of Chest Pain

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Assessment of Chest Pain

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Assessment

Straight to the point of care

Last updated: Jan 31, 2020

Opiates (e.g., morphine) may be necessary to relieve severe pain.

Acute coronary syndrome

Certain characteristics of chest pain can give clues to the origin.

• Constricting pain may be due to cardiac ischaemia or oesophageal spasm.

Varicella zoster virus

ECG showing ST depression

widened mediastinum in aortic dissection, or a large globular heart in cardiac tamponade.

Chest x-ray showing a widened mediastinum

From the collection of Professor James Brown; used with permission

Coronary angiography with percutaneous coronary intervention (PCI)

Angiogram showing occluded right artery

Transthoracic echocardiography is a non-invasive way of assessing cardiac function. It is necessary if

Spiral computed tomography pulmonary angiogram showing a large filling

Acute coronary syndrome

Anxiety or panic disorder

Mitral valve prolapse

Peptic ulcer disease

Acute coronary syndrome

History Exam 1st Test Other tests

central chest pressure, examination may »ECG: ST-elevation »B-type natriuretic

normal initial ECGs.[20] STEMI and there are

ECG showing Patient with unstable

Acute coronary syndrome

History Exam 1st Test Other tests

History Exam 1st Test Other tests

may be known no specific findings »ECG: no acute »stress testing:

History Exam 1st Test Other tests

testing has medium

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

may have chest pain, no specific physical »therapeutic trial: »oesophagogastroduodenoscopy:

History Exam 1st Test Other tests

focal chest wall reproducible pain on »CXR: no specific

History Exam 1st Test Other tests

◊ Anxiety or panic disorder

History Exam 1st Test Other tests

sharp chest pain with hyperventilation, »ECG: normal »CXR: normal

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

history of underlying hypotension, distended »ECG: low-voltage

History Exam 1st Test Other tests

acute substernal unequal pulses or »CXR: widened »transoesophageal

History Exam 1st Test Other tests

Mitral valve prolapse

History Exam 1st Test Other tests

History Exam 1st Test Other tests

cardiac-sounding accentuated pulmonic »ECG: right axis »CXR: large, prominent

◊ Peptic ulcer disease

History Exam 1st Test Other tests

gastric ulcers: epigastric tenderness; »Helicobacter pylori

Note that test is

History Exam 1st Test Other tests

crushing substernal no specific findings »barium swallow: »oesophageal

History Exam 1st Test Other tests