Acute chest pain

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Acute chest pain is a syndrome whose risk depends on the history, physiology and available tests together. Coronary ischaemia commonly causes pressure or heaviness, but symptoms can be less typical in older people and those with diabetes. Shortness of breath, nausea or collapse may dominate. Symptom descriptions change probability rather than providing absolute diagnostic rules.

The initial task is to identify an unstable patient and a treatable emergency. Subsequent testing should answer the remaining clinical question, using the timing of symptoms and assay characteristics. A high troponin indicates myocardial injury; it does not establish plaque rupture without the supporting clinical and electrocardiographic context.

Key points

Assess circulation, respiratory compromise and ongoing pain before applying a low-risk chest-pain pathway.
Obtain an early twelve-lead ECG; a normal initial tracing does not exclude acute coronary syndrome.
Use serial ECGs and the locally validated high-sensitivity troponin pathway when the diagnosis remains uncertain.
Give aspirin 300 mg orally promptly for suspected ACS unless clearly allergic or a relevant contraindication changes the decision.
Consider aortic dissection, pulmonary embolism, tension pneumothorax and oesophageal rupture alongside coronary disease.
Pain relief, reproducible tenderness or a single reassuring test cannot independently exclude a dangerous cause.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Coronary and vascular causes

Coronary thrombosis, acute aortic disease and pulmonary embolism can each present with chest discomfort and require distinct urgent diagnostic and treatment pathways.

Thoracic and extrathoracic causes

Pleural, pulmonary, pericardial, oesophageal and chest-wall conditions produce overlapping symptoms, while upper abdominal disease can be perceived as lower chest discomfort.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Myocardial ischaemia
An imbalance between coronary oxygen supply and myocardial demand activates pain pathways and may progress to injury, ventricular dysfunction and electrical instability.
2
Pleural and pericardial pain
Inflammation or stretching of pain-sensitive thoracic structures can make symptoms vary with breathing or posture, but this pattern does not reliably establish benignity.
3
Aortic wall injury
Disruption within the aortic wall can impair branch-vessel perfusion or cause rupture, explaining why neurological findings or shock can accompany the chest or back pain.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Coronary ischaemic pattern

Central discomfort associated with exertion, sweating, nausea or radiation supports ACS. Persistent or recurrent rest pain and dynamic ECG changes increase concern even if the first troponin is low.

Acute aortic pattern

Abrupt severe pain, neurological findings, limb malperfusion or pulse asymmetry suggests acute aortic disease. The absence of a classic tearing description does not exclude it.

Pulmonary and pleural pattern

Pleuritic pain with breathlessness may reflect embolism, pneumothorax, infection or pericarditis. Hypoxaemia or haemodynamic compromise should determine urgency rather than the adjective pleuritic.

Other dangerous contexts

Severe pain after forceful vomiting suggests oesophageal injury; pain with sepsis, mediastinal features or subcutaneous emphysema requires urgent specialist assessment rather than routine antacid treatment.

Red flags requiring action

Abrupt severe chest or back pain with syncope, pulse asymmetry or a neurological deficit requires urgent assessment for acute aortic disease.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Twelve-lead and serial ECGsFirst step
Why
Identify coronary occlusion, dynamic ischaemia and rhythm disturbances.
Interpretation and limitations
Repeat when symptoms persist or recur and compare previous tracings. A normal resting ECG cannot exclude ACS, and right or posterior leads may be needed for a specific suspected territory.
02
High-sensitivity troponin pathway
Why
Assess myocardial injury using symptom timing and serial change.
Interpretation and limitations
Use the validated assay-specific sampling schedule and thresholds. Very early presentation may need repeat sampling; renal disease, sepsis and tachyarrhythmia can elevate troponin without a primary coronary event.
03
Chest radiograph and targeted CT
Why
Investigate an appropriate non-coronary thoracic question.
Interpretation and limitations
Radiography may reveal pneumothorax or pulmonary disease, but cannot reliably exclude aortic dissection or PE. Select aortic CT angiography or CTPA according to the suspected anatomy.
04
Basic blood tests and bedside assessment
Why
Identify treatment modifiers and serious alternative diagnoses.
Interpretation and limitations
Check haemoglobin, renal function and glucose where relevant; use clinical examination and focused ultrasound in unstable patients while arranging definitive investigation. No routine panel makes all chest-pain causes safe.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Gastro-oesophageal symptoms

Reflux can cause burning retrosternal discomfort, but symptom relief after an antacid does not independently exclude a coexisting or alternative coronary syndrome.

Chest-wall pain

Local tenderness and pain with movement support a musculoskeletal contribution, but the overall history and physiological findings still determine whether urgent investigation is needed.

Panic symptoms

Fear, tingling and rapid breathing may accompany panic or serious cardiopulmonary illness; anxiety should not substitute for an adequate assessment of dangerous alternatives.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Coronary emergencyPersistent pain with an acute ischaemic patternFirst stepThe presentation and ECG support ACS, particularly an acute coronary occlusion requiring reperfusion.

1Monitor rhythm and pressure, obtain IV access, give indicated aspirin and analgesia, and provide oxygen only when hypoxaemia or other immediate critical illness warrants it.
2Activate the appropriate urgent coronary pathway for the ECG and clinical situation; do not wait for a troponin result when an established emergency reperfusion indication is present.
3Reassess for shock, pulmonary oedema and arrhythmia during transfer and treatment, and communicate symptom onset, ECG evolution and medicines already administered.

02Non-coronary emergencyFeatures suggesting aortic or pulmonary vascular diseaseAbrupt severe pain, neurological findings, asymmetric pulses, hypoxaemia or thrombotic risk points toward another dangerous cause.

1EscalationEscalate the concern explicitly and select the appropriate focused imaging and specialist team, checking whether the patient can safely tolerate transport.
2If aortic dissection is strongly suspected, obtain senior input before reflexively administering an ACS antithrombotic package that may worsen bleeding complications.
3For suspected PE, use clinical probability and the diagnostic pathway; unstable patients require urgent specialist consideration of reperfusion and appropriate supportive treatment.

03Uncertain initial assessmentSafe serial evaluation and dispositionThe patient is currently stable and the first ECG or troponin is nondiagnostic.

1AlternativeReview the time course, cardiovascular and thrombotic risks, alternative diagnoses and whether symptoms are ongoing; apply the full validated chest-pain pathway rather than one isolated cutoff.
2Repeat indicated ECG and troponin measurements, reassess the patient during observation, and investigate another cause if the clinical story does not fit a coronary explanation.
3Discharge only when the completed assessment supports it, with a clear working explanation, follow-up and urgent return advice for recurrent prolonged pain, collapse or breathlessness.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Provide early antiplatelet treatment when a coronary thrombotic syndrome is the working diagnosis.

Aspirin loading for suspected acute coronary syndrome

Give a single 300 mg oral loading dose as soon as possible for suspected ACS unless there is clear aspirin allergy or another relevant contraindication; document any prehospital dose before administering.

Assess active bleeding and major alternative diagnoses such as suspected aortic dissection. Further antithrombotic choices depend on the confirmed pathway, bleeding risk and planned intervention.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Electrical instability

Acute ischaemia can trigger ventricular arrhythmia or conduction block, requiring monitoring and prompt access to rhythm-directed treatment while definitive management proceeds.

Pump failure

Loss of effective myocardial function can produce pulmonary oedema or shock, changing both immediate support needs and the urgency of specialist intervention.

Missed alternative pathology

Treating an unrecognised dissection or other bleeding disorder as uncomplicated ACS can delay definitive care and expose the patient to harmful antithrombotic treatment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Monitor rhythm and repeated haemodynamics during ongoing pain or suspected ACS, watching for recurrent symptoms, pulmonary oedema and arrhythmia.
Record the onset and recurrence of pain against ECGs, troponin sampling and treatment to make serial interpretation meaningful.
Reassess after analgesia; relief can improve comfort without resolving the disease that caused the presentation.
Before leaving the acute pathway, communicate outstanding results, the working diagnosis and who is responsible for any further investigation.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Troponin and mechanism

A rise and fall establishes an acute injury pattern, but clinical evidence is still needed to distinguish infarction mechanisms from non-ischaemic injury.

Sex and symptom interpretation

Avoid excluding ACS because symptoms do not match a stereotyped presentation; apply the same careful physiological assessment and appropriate diagnostic testing.

Normal oxygen saturation

A normal saturation is compatible with ACS, aortic dissection or a small PE and is not a global chest-pain rule-out test.

Previous coronary disease

Known disease increases the importance of assessing a change from baseline; it does not mean every new symptom has the same coronary explanation.

11Common pitfallsFrequent interpretation and management errors.

01
Do not use response to glyceryl trinitrate or an antacid as a diagnostic test for the origin of chest pain.
02
Do not let a normal first ECG end investigation when symptoms and risk remain concerning.
03
Do not equate every elevated troponin with an indication for an identical antithrombotic regimen.
04
Do not describe pain as musculoskeletal solely because some chest-wall tenderness can be reproduced.

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