📋 Key Information Summary
- Chest pain is the single most common presenting complaint in Australian emergency departments, accounting for >700,000 presentations annually; the primary goal is rapid identification of life-threatening causes while avoiding unnecessary admissions.
- The HEART pathway and EDACS (Emergency Department Assessment of Chest Pain) are validated for Australian practice and can safely discharge low-risk patients within 2–3 hours using serial troponins.
- Acute coronary syndromes (ACS) encompass STEMI, NSTEMI, and unstable angina — always consider ACS first because missed MI carries a 2.5-fold increase in 30-day mortality.
- Red-flag features requiring immediate action: crushing central chest pain radiating to the left arm or jaw, diaphoresis, haemodynamic instability, new ST-elevation ≥1 mm in two contiguous leads, or new left bundle branch block.
- High-sensitivity troponin (hs-cTn) with a 0/1-hour or 0/2-hour algorithm is the standard of care in Australian EDs; troponin I or T assays must be interpreted with sex-specific 99th-percentile upper reference limits.
- STEMI management: door-to-balloon PCI ≤90 minutes if PCI-capable; if not, fibrinolysis (tenecteplase) within 30 minutes of first medical contact followed by transfer for angiography within 2–24 hours.
- NSTEMI / unstable angina risk-stratify with GRACE or TIMI score; dual antiplatelet therapy (aspirin + ticagrelor or prasugrel/clopidogrel), anticoagulation (heparin), and timely invasive strategy per GRACE risk.
- GTN (sublingual spray 400 µg) and IV morphine remain first-line symptom relief for ischaemic chest pain; routine oxygen is NOT recommended unless SpO₂ <94%.
- Non-cardiac causes account for 50–70 % of ED chest-pain presentations: musculoskeletal (costochondritis, Tietze), gastrointestinal (GORD, oesophageal spasm), anxiety/panic, and pulmonary embolism must be systematically excluded.
- Stress testing (exercise ECG, stress echo, or CT coronary angiography) is recommended for intermediate-risk patients within 72 hours of ED discharge and is funded via MBS item numbers 11204–11224.
- Aboriginal and Torres Strait Islander Australians have 1.7× the rate of ACS hospitalisation and higher out-of-hospital cardiac death; culturally safe assessment, outreach cardiology, and ACCHS-facilitated follow-up are essential.
- Women, older adults, and people with diabetes frequently present with atypical symptoms (dyspnoea, fatigue, nausea, back pain) rather than classic chest pain — maintain a low threshold for investigation.
- All suspected ACS patients should receive aspirin 300 mg (chewed) immediately unless contraindicated; PBS authority-required ticagrelor or clopidogrel are added per interventional cardiologist or local protocol.
Introduction & Australian Epidemiology
Chest pain is one of the most frequent reasons for emergency department (ED) attendance and general practice consultation in Australia. It encompasses a broad differential diagnosis ranging from immediately life-threatening conditions (acute coronary syndrome, aortic dissection, pulmonary embolism, tension pneumothorax, oesophageal rupture) to benign and self-limiting disorders (musculoskeletal strain, gastro-oesophageal reflux, anxiety). A structured, evidence-based diagnostic approach is essential to minimise missed acute coronary events while avoiding unnecessary hospital admissions and invasive investigations.
Australian burden of disease: According to the Australian Institute of Health and Welfare (AIHW, 2023), ischaemic heart disease remains the leading single cause of death in Australia, responsible for approximately 17,500 deaths per year. Acute coronary syndromes account for roughly 70,000 hospitalisations annually. Chest pain presentations to EDs exceed 700,000 per year, yet only 10–15 % of these patients receive a final diagnosis of ACS. This low diagnostic yield underscores the importance of efficient risk stratification pathways that are safe, cost-effective, and feasible in the Australian healthcare context.
Key national datasets:
- AIHW Cardiovascular Disease Statistics — hospital separations, mortality, and prevalence data.
- National Heart Foundation of Australia / Cardiac Society of Australia and New Zealand (CSANZ) clinical guidelines.
- ACSQHC Acute Coronary Syndromes Clinical Care Standard (2019, updated 2023).
- MyHeartMap and Australian Stroke and Heart Atlas for geographic variation.
Sex and age differences: Women are more likely to present with atypical symptoms such as dyspnoea, fatigue, nausea, and upper-back or jaw pain. Older adults (≥65 years) and those with diabetes mellitus may also lack classic ischaemic features, leading to delayed diagnosis. Indigenous Australians experience ACS at younger ages and with higher case-fatality rates than non-Indigenous Australians, highlighting the need for targeted screening and culturally safe care pathways.
Chest Pain Diagnostic Model
A systematic approach to the undifferentiated chest-pain patient integrates clinical history, electrocardiography, and serial high-sensitivity cardiac troponin (hs-cTn) measurement. Two validated decision aids are widely used in Australian emergency departments:
HEART Pathway
The HEART score allocates points across five domains (History, ECG, Age, Risk factors, Troponin). A score of 0–3 identifies low-risk patients suitable for early outpatient investigation; 4–6 denotes moderate risk warranting observation and serial troponins; 7–10 is high risk and mandates inpatient cardiology assessment and likely invasive strategy.
| Domain | 0 points | 1 point | 2 points |
|---|---|---|---|
| History | Slightly suspicious | Moderately suspicious | Highly suspicious |
| ECG | Normal | Non-specific repolarisation disturbance | Significant ST deviation |
| Age | <45 years | 45–64 years | ≥65 years |
| Risk factors | No known risk factors | 1–2 risk factors | ≥3 risk factors or history of atherosclerotic disease |
| Troponin | ≤ normal limit | 1–3× normal limit | >3× normal limit |
EDACS (Emergency Department Assessment of Chest Pain Score)
EDACS was developed and validated in New Zealand and Australian cohorts (Than et al., 2014). Combined with serial hs-cTn at 0 and 2 hours, EDACS-low-risk patients can be safely discharged for outpatient stress testing within 72 hours. This pathway reduces ED length of stay by a median of 3.5 hours compared with traditional troponin-only strategies.
Differential Diagnosis Framework
The clinician should systematically categorise chest pain into four urgency tiers:
Acute Coronary Syndromes (STEMI, NSTEMI, Unstable Angina)
Acute coronary syndromes result from acute disruption of an atherosclerotic coronary plaque leading to thrombus formation, myocardial ischaemia, and variable degrees of myocardial necrosis. The three ACS subtypes are defined by ECG findings and cardiac biomarker results:
| ACS Subtype | ECG Finding | Troponin | Pathology |
|---|---|---|---|
| STEMI | ST elevation ≥1 mm in ≥2 contiguous leads (≥2 mm in V1–V3) or new LBBB | Elevated (but treat on ECG — do NOT wait) | Complete coronary occlusion → transmural infarction |
| NSTEMI | ST depression, T-wave inversion, or non-specific changes | Elevated above 99th percentile with rising/falling pattern | Subtotal occlusion or microvascular occlusion → subendocardial necrosis |
| Unstable angina | May be normal or show ischaemic changes | Normal (no necrosis) | Plaque disruption without sufficient necrosis to raise biomarkers |
STEMI — Emergency Management
Reperfusion strategy:
- Primary PCI (percutaneous coronary intervention): Preferred when available within 120 minutes of FMC. All Australian metropolitan tertiary hospitals and many regional centres (e.g., Geelong, Wollongong, Gold Coast) have 24/7 catheterisation laboratory capability.
- Fibrinolysis: Tenecteplase (weight-adjusted single IV bolus) is the recommended agent when PCI is not accessible within 120 minutes. Administer within 30 minutes of arrival. Arrange urgent transfer for rescue PCI if fibrinolysis fails (persistent ST elevation at 60–90 minutes) or routine angiography within 2–24 hours if successful. PBS Authority Required for tenecteplase.
NSTEMI / Unstable Angina — Risk Stratification & Management
Patients with NSTEMI or unstable angina should be risk-stratified using the GRACE 2.0 score (Global Registry of Acute Coronary Events) to guide the timing of invasive management:
- GRACE score >140 (very high risk): Immediate invasive strategy (angiography within 2 hours). Features: haemodynamic instability, ongoing ischaemia, life-threatening arrhythmia, mechanical complications.
- GRACE score 109–140 (high risk): Early invasive strategy (angiography within 24 hours).
- GRACE score <109 (low/intermediate risk): Invasive strategy within 72 hours or conservative strategy with ischaemia-guided approach based on clinical judgement.
Pharmacotherapy for ACS — Drug Cards
Secondary Prevention Post-ACS
All ACS patients should be discharged on:
- Dual antiplatelet therapy (DAPT) — aspirin 100 mg daily + ticagrelor 90 mg BD (or clopidogrel 75 mg daily) for ≥12 months.
- High-intensity statin — atorvastatin 80 mg PO nocte (PBS General Benefit) or rosuvastatin 20–40 mg PO daily.
- Beta-blocker (bisoprolol 1.25–10 mg or metoprolol succinate 23.75–190 mg) if LVEF ≤40 % or ongoing ischaemia.
- ACE inhibitor (ramipril 2.5–10 mg) or ARB (valsartan 40–160 mg BD) if LVEF ≤40 %, anterior MI, diabetes, or hypertension.
- Mineralocorticoid receptor antagonist (eplerenone 25–50 mg) if LVEF ≤40 % with heart failure symptoms.
- Smoking cessation support (PBS-listed nicotine replacement or varenicline) and cardiac rehabilitation referral (MBS item 93050–93053).
Red Flags & Investigations
Red-Flag Features Demanding Immediate Escalation
- Crushing, pressure-like, or tight central chest pain radiating to the left arm, jaw, or epigastrium.
- Associated diaphoresis, nausea, or dyspnoea.
- Haemodynamic instability: SBP <90 mmHg, HR >100 bpm, signs of cardiogenic shock.
- ECG: ST elevation ≥1 mm (≥2 mm V1–V3) in ≥2 contiguous leads, new LBBB, Wellens syndrome (deep symmetric T-wave inversion in V2–V3), de Winter T-waves.
- New-onset heart failure: pulmonary oedema, raised JVP, S3 gallop.
- Syncope or sustained ventricular arrhythmia in the setting of chest pain.
- Tear-type chest pain radiating to the back with pulse differential — consider aortic dissection (call vascular surgery and perform CT aortogram).
ECG Interpretation — Key Patterns
A 12-lead ECG must be obtained within 10 minutes of first medical contact for all patients presenting with chest pain.
| ECG Pattern | Significance | Action |
|---|---|---|
| ST elevation ≥1 mm in ≥2 contiguous leads | STEMI | Activate Code STEMI; immediate reperfusion |
| New left bundle branch block (LBBB) | Suspected STEMI equivalent | Treat as STEMI until proven otherwise |
| ST depression ≥0.5 mm, T-wave inversion | NSTEMI / ischaemia | Serial troponins, cardiology consult |
| Deep symmetric T-wave inversion V2–V3 (Wellens) | Critical LAD stenosis | Urgent angiography; avoid stress testing |
| De Winter T-waves (upsloping ST depression + tall T-waves precordial) | LAD occlusion equivalent | Treat as STEMI |
| Diffuse concave ST elevation, PR depression | Pericarditis | NSAIDs, colchicine; echo for effusion |
| Low voltage, electrical alternans | Large pericardial effusion / tamponade | Urgent echocardiography; consider pericardiocentesis |
High-Sensitivity Troponin (hs-cTn)
High-sensitivity cardiac troponin assays (hs-cTnT and hs-cTnI) are the standard of care in all Australian hospital laboratories. Key principles:
- Sex-specific 99th percentile upper reference limits (URL): hs-cTnT: 15.5 ng/L (female), 21.7 ng/L (male); hs-cTnI (Abbott Architect): 16 ng/L (female), 34 ng/L (male).
- 0/1-hour algorithm (ESC-recommended): If baseline hs-cTn is below the rule-out threshold and the 1-hour delta is minimal → low risk; if above the rule-in threshold or significant delta → high risk; intermediate values require 3-hour retest.
- 0/2-hour algorithm (ADAPT-ADP / EDACS protocol): Used widely in Australian EDs; validated by Than et al. in Australasian cohorts.
- Chronic troponin elevation: Common in CKD (eGFR <30), heart failure, and LVH. Serial delta change (rise and/or fall) is essential to distinguish acute from chronic elevation.
Stress Testing & CT Coronary Angiography
Oesophageal & MSK Causes of Chest Pain
Non-cardiac chest pain accounts for 50–70 % of all chest-pain presentations in Australian EDs. Musculoskeletal and gastrointestinal aetiologies are the two most common categories. Systematic evaluation prevents both missed cardiac diagnoses and unnecessary invasive investigation.
Gastro-Oesophageal Causes
| Condition | Clinical Features | Diagnosis | Management |
|---|---|---|---|
| Gastro-oesophageal reflux disease (GORD) | Burning retrosternal pain worse after meals, lying flat, or bending; relieved by antacids; associated with regurgitation | Clinical diagnosis; 24-h pH monitoring if atypical; upper endoscopy if alarm features | PPI (esomeprazole 20–40 mg PO daily); lifestyle modification; PBS General Benefit |
| Oesophageal spasm | Severe, squeezing central chest pain mimicking angina; may be triggered by hot/cold food or stress | High-resolution oesophageal manometry (referral) | GTN sublingual (empirical), CCBs (diltiazem 60 mg TDS PO), PPI |
| Boerhaave syndrome (oesophageal rupture) | Severe chest pain after forceful vomiting; subcutaneous emphysema; Mackler's triad (vomiting, chest pain, subcutaneous emphysema) | CT chest with oral contrast (gold standard); water-soluble contrast swallow | Surgical emergency — immediate cardiothoracic/upper-GI surgical consultation; IV antibiotics, NBM |
Musculoskeletal Causes
Musculoskeletal chest pain is the most common non-cardiac aetiology, affecting up to 30–50 % of ED chest-pain patients. It is characterised by:
- Reproducible chest-wall tenderness on palpation (high negative predictive value for ACS).
- Pain exacerbated by movement, deep breathing, or specific postures.
- No associated dyspnoea, diaphoresis, or haemodynamic compromise.
| Condition | Features | Management |
|---|---|---|
| Costochondritis | Pain at costochondral junctions (usually 2nd–5th ribs); localised tenderness without swelling | NSAIDs (ibuprofen 400 mg PO TDS with food or naproxen 250–500 mg PO BD); heat packs; reassurance |
| Tietze syndrome | As costochondritis but with visible swelling at the costochondral junction | NSAIDs; local corticosteroid injection if refractory |
| Muscle strain (intercostal, pectoralis) | History of physical exertion or repetitive movement; pain with resisted muscle contraction | Rest, simple analgesia (paracetamol 1 g QID PRN), graduated return to activity |
| Rib fracture | History of trauma; focal bony tenderness; pain with inspiration | Analgesia (stepwise: paracetamol → NSAIDs → opioids); incentive spirometry; chest X-ray (may miss non-displaced fractures) |
| Cervical / thoracic radiculopathy | Dermatomal pain; paraesthesia; reproduced by neck/spinal movements | Physiotherapy, simple analgesia; MRI spine if persistent (MBS item 63210) |
Other Important Non-Cardiac Causes
- Pulmonary embolism: Pleuritic chest pain, tachycardia, hypoxia; Wells score and D-dimer screening (MBS item 65120); CT pulmonary angiography (CTPA) if indicated. Refer to PE article.
- Pneumothorax: Sudden-onset pleuritic pain with dyspnoea; reduced breath sounds; CXR or POCUS. Refer to pneumothorax article.
- Herpes zoster: Dermatomal burning or lancinating pain preceding vesicular rash; may mimic cardiac pain if left-sided. Treat with valaciclovir 1 g PO TDS for 7 days (PBS General Benefit).
- Anxiety / panic disorder: Often associated with hyperventilation, perioral tingling, and palpitations. Diagnosis of exclusion. Consider referral to GP Mental Health Treatment Plan (MBS item 80110).
Special Populations
Pregnancy
Paediatrics
Older Adults (≥65 years)
Renal Impairment
Hepatic Impairment
Immunocompromised
Aboriginal and Torres Strait Islander Health Considerations
Cardiovascular disease is the leading cause of the health gap between Aboriginal and Torres Strait Islander Australians and non-Indigenous Australians. The AIHW reports that Indigenous Australians experience acute coronary syndromes at 1.7 times the rate of non-Indigenous Australians and are significantly more likely to die from ischaemic heart disease before the age of 65. Culturally safe, community-centred approaches are essential to improving outcomes.
📚 References
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