Chest Pain in the Emergency Department: Diagnostic Pathways

Definition and Clinical Framework

Chest pain is a broad clinical syndrome rather than a narrowly defined symptom. It includes pain, pressure, tightness, heaviness, burning, or discomfort in the chest and may extend to the arms, shoulders, neck, jaw, upper back, abdomen, or epigastrium. Dyspnoea, nausea, vomiting, diaphoresis, fatigue, faintness, and other symptoms may occur without chest pain and should be considered anginal equivalents.

The emergency evaluation of non-traumatic chest discomfort is structured around three principal diagnostic categories:

• Myocardial ischaemia, particularly acute coronary syndrome (ACS).

• Other cardiopulmonary causes, including myopericardial disease, pulmonary embolism, aortic emergencies, and pneumothorax.

• Non-cardiopulmonary causes, including gastrointestinal, musculoskeletal, and anxiety-related disorders.

The immediate objective is not simply to establish whether the patient has ACS. It is to determine whether the patient is clinically unstable, identify life-threatening diagnoses rapidly, and select a safe disposition and diagnostic strategy.

Only a minority of patients presenting with acute chest pain ultimately have ACS; reported rates are generally 5–10%, although some series report 10–20%. Other life-threatening cardiopulmonary conditions account for approximately 5% of presentations in some populations. Despite this relatively low prevalence, missed myocardial infarction remains consequential, and historically 2–6% of patients discharged with presumed non-ischaemic chest pain were subsequently found to have had an infarction.

Pathophysiological Considerations

The central pathophysiological concern in the emergency department is myocardial ischaemia caused by an acute coronary process. Myocardial injury leads to release of cardiac troponin, but troponin elevation is not specific for myocardial infarction. Other conditions may produce cardiomyocyte injury and elevated troponin, so biomarker interpretation must be integrated with the clinical history, ECG, and subsequent investigations.

The emergency differential also reflects distinct mechanisms of acute cardiopulmonary disease:

• Pulmonary embolism and spontaneous pneumothorax may produce abrupt chest pain and respiratory distress.

• Aortic dissection may cause sudden severe pain, often radiating to the back.

• Pericarditis may produce pleuritic or positional pain.

• Myocarditis and pericarditis can present with chest pain, ECG abnormalities, and biomarker elevation; echocardiography and cardiac magnetic resonance imaging may demonstrate inflammatory involvement.

• Gastrointestinal and musculoskeletal disorders may mimic myocardial ischaemia, including severe oesophageal spasm and acid reflux.

Clinical Presentation and Symptoms

Characterising the presenting symptom

The symptom should be classified as cardiac, possibly cardiac, or non-cardiac. The term “atypical” is discouraged because it may understate the possibility of ischaemia.

A focused history should establish:

• Quality of the discomfort.

• Location and radiation.

• Onset and temporal pattern.

• Duration and recurrence.

• Provoking and relieving factors.

• Associated symptoms.

• Similarity to previous documented angina or myocardial infarction.

• Atherosclerotic and thromboembolic risk factors.

• Relevant predispositions, such as connective tissue disease.

No single pain descriptor is diagnostic. The severity of pain also has limited discriminatory value.

Features suggesting myocardial ischaemia

Ischaemic discomfort commonly:

• Is substernal and diffuse.

• Is described as pressure, tightness, heaviness, or squeezing.

• Develops over several minutes.

• Is precipitated by exertion.

• Improves with rest.

• May radiate to the neck, jaw, shoulders, or arms.

• May be accompanied by diaphoresis, dyspnoea, nausea, vomiting, fatigue, faintness, or belching.

Radiation to both arms or shoulders has a particularly strong association with myocardial infarction in the cited clinical data, although right-arm radiation has not shown a consistent association in all studies. Symptoms may be limited to the radiated site, such as aching in an arm or shoulder.

Women and older patients may present with less conventional symptom patterns. Anginal equivalents, including dyspnoea, nausea, or vague anxiety, may occur without perceived pain.

Features suggesting alternative diagnoses

The following patterns should broaden the differential:

Pain that remains constant for many hours or days without ECG abnormalities, elevated cardiac biomarkers, heart failure, hypotension, or other clinical consequences is less likely to be myocardial ischaemia. Conversely, delayed relief more than 10 minutes after nitroglycerin makes an ischaemic explanation less likely, although severe ischaemia remains possible.

Associated symptoms

Dyspnoea is important because it indicates a possible cardiopulmonary process, although it is not specific. Sudden marked respiratory distress should raise concern for pulmonary embolism or pneumothorax. Haemoptysis may occur with pulmonary embolism or severe heart failure, while blood-tinged frothy sputum generally points toward pulmonary disease or pulmonary oedema.

Syncope or presyncope may reflect:

• Haemodynamically significant pulmonary embolism.

• Aortic dissection.

• Ischaemic arrhythmia.

Nausea and vomiting may suggest gastrointestinal disease but can accompany myocardial infarction, particularly inferior infarction. Diaphoresis, fatigue, dizziness, weakness, and loss of consciousness are also important associated symptoms.

Prolonged chest pain lasting more than 15 minutes, or recurrent pain within 1 hour, should prompt urgent medical assessment.

Initial Evaluation and Physical Examination

Immediate priorities

The first assessment should answer three questions:

• Is the patient clinically unstable, with actual or impending circulatory collapse or respiratory insufficiency?

• Is a life-threatening diagnosis likely, including ACS, pulmonary embolism, aortic dissection, pneumothorax, or another acute cardiopulmonary condition?

• If the immediate risk is low, is discharge safe, or are observation and further testing required?

Initial assessment includes:

• Vital signs.

• Focused history.

• Physical examination.

• Immediate 12-lead ECG.

• Chest radiography.

• Measurement of biomarkers of myocardial injury.

Patients with suspected ACS should be assessed systematically and without delay. In the outpatient setting, a patient whose suspicion of ACS is sufficiently high to warrant troponin testing should generally be referred to the emergency department rather than managed through routine outpatient testing.

Physical examination

The supplied material does not provide a detailed organ-system physical examination protocol. It does, however, identify clinical instability and findings that may suggest particular diagnoses. Assessment should therefore focus on:

• Circulatory collapse or hypotension.

• Respiratory insufficiency.

• Evidence of severe heart failure.

• Findings compatible with pneumothorax.

• Findings raising suspicion of aortic dissection.

• Features of pericardial tamponade.

• Signs associated with massive pulmonary embolism.

Physical examination alone cannot reliably rule in or rule out ACS. Its diagnostic value increases substantially when combined with the ECG, cardiac biomarkers, and clinical decision pathways.

Diagnostic Pathway in the Emergency Department

Prehospital assessment

If ACS is suspected in the prehospital setting:

• A 12-lead ECG should be acquired and interpreted as soon as possible.

• Personnel should have access to defibrillation equipment and be trained in basic cardiac life support.

• ECG findings should determine the initial pathway, destination hospital, sequence of investigations, and timing of invasive coronary angiography.

Patients are initially separated into:

• A STEMI pathway, when the ECG shows persistent ST-segment elevation or an equivalent pattern.

• A suspected NSTE-ACS pathway, when there is no ST-segment elevation or equivalent pattern.

A STEMI-pattern ECG indicates a high risk of immediate complications, including ventricular fibrillation, and should prompt emergency reperfusion planning and direct transfer to a centre with continuous percutaneous coronary intervention capability. Patients without ST-segment elevation but with ongoing ischaemic symptoms may still face immediate risks, including ventricular arrhythmias, and should be triaged according to appropriate high-risk protocols.

Emergency department algorithm

A practical sequence is:

• Assess stability and provide immediate stabilisation when required.

• Obtain a 12-lead ECG and chest radiograph.

• Determine whether the ECG demonstrates:

• Measure cardiac biomarkers, particularly high-sensitivity cardiac troponin.

• Evaluate for pulmonary embolism and aortic dissection when suggested by the history, examination, or initial investigations.

• Apply a clinical decision pathway to determine further testing, treatment, observation, or discharge.

The ECG and troponin should be interpreted in the context of the symptom history and clinical risk. A patient with an elevated troponin but a history not compatible with ACS requires assessment for alternative causes of myocardial injury.

Differential diagnosis based on initial testing

Electrocardiography

The 12-lead ECG is a critical early test in suspected ACS and should be obtained rapidly. It serves both diagnostic and triage functions.

The ECG is used to:

• Identify persistent ST-segment elevation or equivalent patterns.

• Direct patients into a STEMI or NSTE-ACS pathway.

• Detect ST-segment depression and T-wave inversion suggestive of ischaemia.

• Support the diagnosis of pericarditis when diffuse ST-segment elevation and PR depression are present.

• Identify arrhythmic or ischaemic complications.

An ECG without ST-segment elevation does not exclude clinically important ACS or immediate risk. Ongoing ischaemic symptoms in such patients may still warrant urgent management.

Cardiac Biomarkers and Laboratory Findings

High-sensitivity cardiac troponin

High-sensitivity cardiac troponin is a central biomarker for the assessment of suspected NSTE-ACS. Rapid rule-in and rule-out algorithms should be used in appropriate patients.

Troponin testing contributes to:

• Identification of myocardial injury.

• Rapid recognition of patients at low risk who may not require additional testing.

• Diagnosis of NSTEMI when interpreted alongside symptoms and ECG findings.

• Risk stratification and selection of further testing or observation.

Troponin elevation does not establish myocardial infarction by itself. Cardiomyocyte injury occurs in conditions other than MI, and alternative diagnoses should be considered whenever the clinical presentation is not compatible with ACS.

Other laboratory findings

The source material does not provide a comprehensive laboratory panel or specific laboratory thresholds. It identifies laboratory assessment as relevant when evaluating alternative diagnoses, such as pneumonia, pulmonary embolism, or eosinophilic myocarditis. In suspected eosinophilic myocarditis, peripheral eosinophilia, asthma, sinusitis, skin lesions, and other systemic features may support the diagnosis.

Imaging

Chest radiography

Chest radiography is part of the initial assessment of acute chest pain. It is not a primary diagnostic test for coronary artery disease, but it may identify or support alternative diagnoses and provide information about cardiac and pulmonary status.

Relevant findings include:

• A lucent space between the lung and chest wall, suggesting pneumothorax.

• Widening of the mediastinum, raising concern for aortic dissection.

• Pulmonary infiltrates, supporting pneumonia in the appropriate clinical context.

• Pulmonary vascular and cardiac silhouette abnormalities in heart failure.

• Pleural effusion and coexisting lung disease.

Echocardiography

Echocardiography may assist in evaluating:

• Cardiac function.

• Heart failure.

• Pericardial disease and tamponade.

• Aortic pathology in selected circumstances.

• Inflammatory involvement in myocarditis and pericarditis.

In suspected aortic dissection, dedicated imaging may include computed tomography, magnetic resonance imaging, or transoesophageal echocardiography, depending on the clinical pathway.

Coronary computed tomography angiography

Coronary computed tomography angiography is recommended as a non-invasive diagnostic option alongside traditional stress testing. Selection should account for the clinical setting, history, and previous investigations. It is particularly relevant after initial assessment when the patient is not immediately directed to an invasive or emergency pathway.

Non-invasive imaging can improve diagnostic accuracy and refine risk assessment. In patients with convincing symptoms but no obstructive coronary disease, testing strategies should also take account of possible microvascular disease.

Cardiac magnetic resonance imaging

Cardiac magnetic resonance imaging may non-invasively confirm inflammatory myocardial involvement in suspected myocarditis or pericarditis. It is particularly relevant when the clinical assessment, ECG, and biomarkers suggest inflammation.

Endomyocardial biopsy

For myocarditis, endomyocardial biopsy is considered on an individual basis in intermediate- and high-risk presentations, specifically when the result is expected to alter management. In eosinophilic myocarditis, diagnosis may be established by biopsy demonstrating eosinophilic myocardial infiltration or by cardiac magnetic resonance evidence of myocarditis accompanied by peripheral eosinophilia and compatible systemic features.

Clinical Decision Pathways and Risk Stratification

Clinical decision pathways combine:

• Clinical characteristics.

• ECG findings.

• Cardiac troponin.

• Patient-specific factors.

Their purpose is to identify patients who require urgent treatment, those who require additional testing or observation, and those who may be safely discharged.

Low-risk patients

High-sensitivity troponin has increased the ability to identify low-risk patients rapidly. Some patients may not need further diagnostic testing after an appropriate clinical, ECG, and biomarker assessment.

Nevertheless, low-risk classification is not equivalent to zero risk. In one population-based study, the estimated 30-day rate of major cardiovascular events among patients with acute chest pain classified as low risk was 2.5%, after exclusion of patients with ST-segment elevation or definite non-cardiac chest pain.

Intermediate-risk patients

Intermediate-risk patients require systematic assessment using clinical decision pathways. Additional testing and management decisions should incorporate shared decision-making. Coronary computed tomography angiography and stress testing are both available non-invasive strategies, and the optimal test depends on the individual clinical context and previous testing.

High-risk patients

High-risk patients include those with:

• STEMI-pattern ECG findings.

• Ongoing ischaemic symptoms despite absence of ST-segment elevation.

• Dynamic or significant ECG abnormalities.

• Compatible symptoms with elevated cardiac troponin.

• Clinical instability.

• Suspected pulmonary embolism, aortic dissection, pneumothorax, or tamponade.

These patients require urgent escalation through the relevant diagnostic and therapeutic pathway.

Acute Management

Immediate stabilisation

Patients with circulatory collapse or respiratory insufficiency require immediate stabilisation while diagnostic assessment proceeds. The initial evaluation should not delay management of clearly life-threatening conditions.

STEMI pathway

The objectives in suspected STEMI are to:

• Control discomfort.

• Identify candidates for urgent reperfusion.

• Minimise the interval from first medical contact to reperfusion.

• Avoid inappropriate discharge.

• Ensure appropriate transfer when the initial hospital lacks percutaneous coronary intervention capability.

Prehospital and emergency systems should support rapid ECG acquisition, interpretation, defibrillation capability, and transfer to a centre capable of continuous PCI. Ventricular fibrillation is a major early cause of death in STEMI, making early recognition, monitoring, and defibrillation capability essential.

In regions remote from PCI centres, prehospital fibrinolysis may be used when the system can transmit a 12-lead ECG, has personnel trained in ECG interpretation and STEMI management, and has online medical oversight capable of authorising treatment.

NSTE-ACS pathway

Patients with suspected NSTE-ACS should undergo rapid high-sensitivity troponin testing with an appropriate rule-in/rule-out algorithm. Management and further investigations depend on the integration of:

• Symptoms.

• ECG findings.

• Troponin results.

• Clinical risk.

• Alternative explanations for myocardial injury.

The source material does not specify antiplatelet, anticoagulant, anti-ischaemic, lipid-lowering, or revascularisation drug regimens or doses for NSTE-ACS.

Chest pain with suspected alternative emergencies

The diagnostic pathway should be redirected promptly when findings suggest:

• Pulmonary embolism: assess risk and proceed to D-dimer testing or imaging according to the clinical pathway.

• Aortic dissection: use dedicated computed tomography, magnetic resonance imaging, or echocardiographic imaging when indicated.

• Pneumothorax: interpret the chest radiograph and manage according to clinical severity.

• Pericardial tamponade: urgent echocardiographic assessment is relevant.

• Pneumonia: integrate radiographic and laboratory evidence with the clinical presentation.

Specific drug treatments and doses for these conditions are not provided in the source material.

Outpatient and Non-Acute Presentations

Although this chapter focuses on the emergency department, some patients present with resolved or chronic discomfort. The pretest probability of an acute cardiopulmonary cause is lower in outpatient practice, and evaluation relies more heavily on the history, physical examination, and ECG.

Testing paradigms are generally less intensive than in the emergency department. However, if clinical suspicion is high enough to justify troponin testing, referral to the emergency department is appropriate.

Patients presenting in an outpatient setting with acute chest pain should undergo ECG assessment if available and should be transported urgently to the emergency department by emergency medical services.

Sex, Age, and Diagnostic Equity

Symptoms may differ in women and older patients, and a lower index of suspicion can contribute to delayed assessment. Observational data indicate that women presenting with chest pain have been less likely than men to receive early clinical review in some emergency department analyses. Young women with myocardial infarction may also experience worse outcomes in settings where the diagnosis is not initially suspected.

These observations support a systematic, symptom-inclusive approach that does not depend on a stereotyped presentation. The assessment should include pressure, tightness, dyspnoea, nausea, epigastric symptoms, and discomfort involving the neck, jaw, arms, shoulders, back, or abdomen.

Drugs and Practical Prescribing Considerations

The source material does not provide specific medication doses for the emergency management of chest pain or ACS.

Nitroglycerin response should not be used as a definitive diagnostic test. Prompt relief may support myocardial ischaemia but can also occur with oesophageal spasm, while delayed relief does not reliably distinguish non-cardiac disease from severe ischaemia.

For prehospital STEMI care, the material supports emergency reperfusion planning and, where appropriate, prehospital fibrinolysis under defined system requirements, but does not provide fibrinolytic agents, doses, contraindications, or adjunctive medication regimens.

Guideline-Based Recommendations

The principal recommendations supported by the source material are:

• Interpret chest pain broadly to include anginal equivalents and symptoms outside the chest.

• Avoid the term “atypical”; classify symptoms as cardiac, possibly cardiac, or non-cardiac.

• Obtain and interpret a 12-lead ECG rapidly in suspected ACS.

• Use high-sensitivity cardiac troponin with rapid rule-in and rule-out algorithms in suspected NSTE-ACS.

• Recognise that troponin elevation indicates myocardial injury but is not specific for MI.

• Use clinical decision pathways to integrate symptoms, ECG findings, biomarkers, and patient characteristics.

• Identify STEMI promptly and transfer directly to a centre with continuous PCI capability when appropriate.

• Treat ongoing ischaemic symptoms seriously even when the ECG lacks ST-segment elevation.

• Use non-invasive imaging to improve diagnostic accuracy and risk assessment.

• Consider coronary computed tomography angiography alongside stress testing, selected according to clinical context and previous investigations.

• Use shared decision-making in intermediate-risk patients when selecting further testing and management.

• In suspected myocarditis or pericarditis, combine clinical evaluation, ECG, biomarkers, echocardiography, and cardiac magnetic resonance imaging.

• Reserve endomyocardial biopsy for selected intermediate- and high-risk myocarditis presentations when the result is expected to change management.

• Maintain a structured differential diagnosis that includes ACS, pulmonary embolism, aortic dissection, pneumothorax, pericardial disease, pneumonia, gastrointestinal disease, and musculoskeletal causes.

Prognosis and Follow-Up

Prognosis depends primarily on the underlying diagnosis, the presence of clinical instability, the speed of recognition, and the timeliness of appropriate treatment. In STEMI, early mortality is strongly related to electrical complications, particularly ventricular fibrillation, and to pump failure. The highest risk of ventricular fibrillation occurs early after symptom onset, with many events occurring during the first day.

Patients discharged after an evaluation judged to be low risk still require appropriate follow-up and clear return precautions because low risk does not eliminate the possibility of subsequent cardiovascular events. The cited population data indicate a 30-day major cardiovascular event rate of 2.5% among a low-risk group defined after excluding patients with ST-segment elevation or definite non-cardiac chest pain.

Intermediate-risk patients require completion of the planned diagnostic pathway, which may include observation, serial troponin assessment, coronary computed tomography angiography, stress testing, or other non-invasive imaging. Decisions should be made in the context of the clinical presentation and shared decision-making.

Patients with myocarditis or pericarditis generally have preserved biventricular function and good outcomes when uncomplicated, although severe heart failure, arrhythmias, persistent disease, recurrence, and constrictive physiology may complicate the course. Persistent symptoms require reassessment and, when indicated, multimodality imaging.

Long-term follow-up should be directed by the identified cause. Patients with confirmed or suspected coronary disease require continued assessment based on their clinical risk and results of non-invasive or invasive testing, while patients with alternative diagnoses require disease-specific follow-up.