Chest Pain

Chest discomfort in the community is a frequently reported symptom. It has a broad differential diagnosis, ranging from benign musculoskeletal pain to life-threatening cardiac events. The underlying cause is often not obvious on first assessment, so a working diagnosis routinely needs a combination of history, examination, and targeted investigation. Most turn out benign: among those presenting to their primary care doctor with chest pain, the final diagnosis was not ischaemic heart disease in 83%. The epidemiology of chest pain in primary care and emergency department settings was reported as musculoskeletal, including costochondritis in 36% of cases, gastrointestinal in 19%, cardiac in 16%, stable angina in 10.5%, unstable angina or myocardial infarction (MI) in 1.5%, other cardiac in 3.8%, psychiatric in 8%, pulmonary in 5% and other/unknown in 16%. Only a small minority are ACS: 2 to 4% of patients presenting with chest pain will have acute coronary syndrome.

Immediate life-threatening causes:

• STEMI/NSTEMI
• Unstable angina
• Pulmonary embolism
• Aortic dissection
• Tension pneumothorax.

Also consider: pericarditis, GORD ± spasm, biliary colic, hyperventilation/ anxiety.

Terminology

Atypical chest pain is often used to describe non-cardiac chest pain, but it lacks specificity. Using the terms ‘cardiac,’ ‘possibly cardiac’ or ‘non-cardiac’ is the preferred terminology. Patients themselves describe their discomfort in all kinds of ways — pressure, tightness, squeezing, heaviness, burning — so chest discomfort is often the more accurate term to use when talking with a patient, rather than assuming pain is what they’d call it.

Red flags

• Lightheadedness/syncope (ACS, PE, dissection)
• Pain radiating to the arm(s) or jaw (ACS)
• Thoracic back pain (dissection)
• Sweating (ACS)
• Palpitations
• Haemoptysis (PE)
• Dyspnoea (ACS, PE)
• History of IHD, diabetes, or hypertension (ACS)
• Pulse asymmetry or inter-arm blood pressure difference (dissection)
• Subcutaneous emphysema/crepitus (oesophageal rupture)
• Pulsatile abdominal mass (AAA).

Certain groups, such as women, elderly patients, those with dementia and individuals with diabetes, might not exhibit typical symptoms of ischaemic chest pain. A reassuring-sounding history doesn’t rule out ACS in these groups. Women are more likely to be misdiagnosed with non-cardiac chest pain, and are more likely to experience procedure delays once admitted. First Nations people have a rate of coronary events twice that of non-Indigenous Australians, and cardiovascular disease in this population is more common and presents at a younger age — factor this into risk assessment rather than relying on standard age cutoffs alone.

History

The mnemonic OLDCAAR — onset, location, duration, character, alleviating/aggravating factors, associated symptoms, and radiation — is a useful structure for the history.

• Onset: abrupt, maximal-at-onset pain raises concern for aortic dissection, pneumothorax, or PE.
• Associated syncope → ACS, PE, dissecting aneurysm.
• Pleuritic pain → pleurisy, pericarditis, mediastinitis, pneumothorax, chest wall pain.
• Character: ischaemic pain is typically a deep, diffuse, hard-to-localise pressure/heaviness/squeezing rather than a sharp, well-localised pain; sharp, stabbing, or tearing pain is more consistent with dissection, pneumothorax, PE, or (after oesophageal rupture) mediastinitis, and less likely due to ACS. Pain reproduced or worsened by chest-wall palpation makes ACS substantially less likely, though it doesn’t exclude it.
• Duration: pain lasting only seconds, or continuous and unchanging for many hours or days, is less likely to be ACS — stable angina classically lasts 2–3 minutes and eases with rest, while ACS pain classically persists beyond 20 minutes. Relief with nitroglycerin is not a reliable diagnostic test for cardiac origin — oesophageal spasm can also respond to it.
• Radiation to the back, particularly midscapular, suggests aortic dissection but also occurs in ACS and pancreatitis; radiation to either arm, the jaw, neck, or epigastrium can all occur with ACS (classic teaching that only left-arm radiation is specific for ACS is outdated — right-arm and bilateral radiation are also concerning).
• Worse stooping or lying down at night → GORD; worse with deep inspiration or lying supine → pericarditis or PE, not ACS.
• Ask specifically about recreational drug use (cocaine/amphetamines — associated with ACS, dissection, and Prinzmetal’s angina) and, before giving nitrates, PDE-5 inhibitor use (sildenafil/tadalafil within the last 24–48 hours — risk of profound hypotension).

Risk factors

Standard cardiovascular risk factors (age, known CAD or premature family history of CAD, hypertension, hyperlipidaemia, diabetes, smoking) and vascular disease (peripheral arterial disease, stroke/TIA) raise ACS risk, as do less classic associations — HIV, systemic inflammatory disease, cocaine/cannabis use, chronic kidney disease, and chronic alcoholism. Separately, ask about risk factors for aortic aneurysm/dissection (Marfan syndrome or other connective tissue disorder, SLE, RA, longstanding hypertension) and for VTE (see Pulmonary embolism, below).

Examination

Vital signs first — hypotension or shock should prompt immediate consideration of an obstructive/life-threatening cause.

• Absent femoral pulses or a significant inter-arm BP difference → dissection.
• Focal, reproducible chest wall tenderness → chest wall pain.
• A friction rub → pleurisy or pericarditis.
• Muffled heart sounds or a diastolic murmur → tamponade or aortic regurgitation from a Type A dissection.
• Raised JVP → tamponade, PE, tension pneumothorax, or heart failure.
• Reduced/absent breath sounds with hyper-resonance → pneumothorax.
• Subcutaneous emphysema → oesophageal rupture/mediastinitis.

Diagnostic strategy

Probability diagnosis: musculoskeletal/chest wall pain, psychogenic, angina/ACS.

Serious disorders not to miss:

• Cardiovascular — ACS, aortic dissection, pulmonary embolism/infarction.
• Spontaneous coronary artery dissection (SCAD) — a rare cause of ACS, more common in women with few or no atherosclerotic risk factors; easily missed if not specifically considered.
• Malignant — lung cancer, spinal cord/meningeal tumour.
• Infective — pneumonia, pericarditis (not necessarily infective), mediastinitis.
• Pneumothorax — diagnosed on a standard upright chest X-ray; an expiratory film does not necessarily increase the diagnostic yield and is no longer routinely recommended.
• Oesophageal rupture — classically Boerhaave’s syndrome (severe chest or epigastric pain after forceful vomiting/retching, in a middle-aged man with recent excess food/alcohol intake; pain may radiate to the back or left shoulder and worsens on swallowing).

Pitfalls: mitral valve prolapse, oesophageal spasm (notoriously difficult to diagnose), GORD, biliary colic, herpes zoster, rib fracture, muscular tear (e.g. from coughing).

Masquerades: depression/anxiety, anaemia, drugs (e.g. cocaine), spinal dysfunction.

Investigations outside a tertiary centre

ECG immediately — within 10 minutes of presentation for anyone with chest pain or an ischaemic equivalent (dyspnoea, unexplained fatigue). An initial ECG is often non-diagnostic (roughly a fifth of eventual MIs present with a normal first ECG), so repeat every 15–30 minutes in the first hour if suspicion persists, and again with any change in status or a new episode of pain — a normal ECG does not rule out ACS if clinical suspicion remains.

Troponin testing might have a limited role in the primary care setting, except when working in an emergency department in the regional areas. Where it genuinely is available and has a fast turnaround, it may still have a place: low-risk patients whose symptoms completely resolved more than 24 hours ago; atypical, low-likelihood-of-ACS symptoms, where a troponin essentially covers clinical uncertainty; or recent symptoms where the patient can be appropriately monitored in the practice while awaiting the result. A normal troponin doesn’t exclude unstable angina, and troponin shouldn’t be ordered at all unless there’s a mechanism to review the result as soon as it’s available — don’t draw a sample that won’t result before the patient leaves.

D-dimer is useful for excluding PE in patients who are genuinely low-to-intermediate pretest probability (see Wells/PERC below) — a negative D-dimer combined with a low Wells or Geneva score has around 99% sensitivity to rule out DVT/PE, but the test itself has only about 50% specificity, so it isn’t useful, and shouldn’t be drawn, in a high pretest-probability patient (unacceptable false-negative rate) or if the result can’t be promptly obtained or acted on.

CXR is often normal or non-specific in ACS and PE; it’s more useful for alternative diagnoses — pneumonia, pneumothorax, and (with clinical correlation) a widened mediastinum in dissection or mediastinal air in oesophageal rupture.

Risk-stratification scores

HEART score (for undifferentiated chest pain, estimating major adverse cardiac event risk) — 0–2 points each for: History (slightly/moderately/ highly suspicious), ECG (normal/non-specific repolarisation change/ significant ST depression), Age (<45/45–64/≥65), Risk factors (0, 1–2, or ≥3 traditional risk factors or known atherosclerotic disease), Troponin (normal, 1–3× upper limit, or >3× upper limit). Total score 0–10: 0–3 low risk (consider early discharge), 4–6 moderate risk (admit for observation/further testing), 7–10 high risk (early invasive management). Where troponin genuinely isn’t available (many urgent-care settings), the same tool without its troponin component — sometimes called HEAR — is not formally validated for this use, but a HEAR score of 0–1 has been associated with a very low (~0.1%) 30-day major-adverse-cardiac-event rate in a retrospective ED study, and can reasonably inform shared decision-making about whether ED referral is needed.

Wells score for PE — points for: clinical signs of DVT (3); PE is the most likely diagnosis (3); heart rate >100 (1.5); immobilisation ≥3 days or surgery in the past 4 weeks (1.5); previous DVT/PE (1.5); haemoptysis (1); active malignancy (1). ≤4 = PE unlikely (consider D-dimer to rule out); >4 = PE likely (proceed to CT pulmonary angiogram).

PERC rule — for patients with a low pre-test probability of PE, used to avoid unnecessary D-dimer testing/imaging: age <50, heart rate <100, SpO2 ≥95% on room air, no haemoptysis, no oestrogen use, no prior DVT/PE, no unilateral leg swelling, no surgery/trauma requiring hospitalisation in the past 4 weeks. If all 8 criteria are met, PE can be excluded without further testing (in a genuinely low-pre-test-probability patient — PERC is a rule-out tool, not a substitute for Wells scoring in higher-probability patients).

Pulmonary embolism

See Pulmonary Embolism for the full page — probability scoring, DOAC choice and dosing, duration, and follow-up.

Presentation is often non-specific and can be subacute — “PE may present with very few clinical signs or symptoms and can easily be missed. Symptoms to ask about: “Chest pain (especially if pleuritic)”, “Dyspnoea (especially if sudden onset)”, cough, haemoptysis, presyncope or syncope, and unilateral leg/arm pain or swelling suggesting a DVT. Red flags: haemodynamic instability (hypotension, tachycardia, shock); reduced oxygen saturation — either warrants urgent escalation. VTE risk factors are cumulative — strong (recent hip/knee replacement, hip/leg fracture, major surgery or trauma within 6 weeks, spinal cord injury), intermediate (active cancer/chemotherapy, pregnancy/puerperium, prior VTE, known thrombophilia, stroke, COC/HRT), and weak (prolonged immobility, obesity, increasing age, varicose veins).

Pneumothorax

Spontaneous pneumothorax is classified as primary (PSP — no underlying lung disease, “often young, tall, thin males”) or secondary (SSP — pre-existing lung pathology such as COPD, cystic fibrosis, or interstitial lung disease). Smoking is the dominant modifiable risk factor for PSP. Clinical presentation typically includes acute onset of pleuritic chest pain, dyspnea, and sometimes tachycardia — larger pneumothoraces (>15% of the hemithorax) add reduced chest wall movement and ipsilateral decreased/absent breath sounds. Tension pneumothorax is a rare but life-threatening progression, “characterized by hypoxemia, hypotension, and tracheal deviation away from the affected side” — treat with emergent needle decompression as a bridge to tube thoracostomy where that’s within the treating clinician’s scope, while arranging emergency transfer.

Aortic dissection

Aortic dissection is a rare condition that can be difficult to diagnose and needs to have a high index of suspicion. The typical presentation of aortic dissections involves an abrupt and intense tearing pain that spreads through the back. Hypertension is a common finding among patients with aortic dissections, and approximately 20% of cases might present with neurological deficits. Suspicions of aortic dissection might increase when the two arms’ blood pressure differs by more than 20 mmHg. Also suspect it from the other red flags above (absent femoral pulses, syncope) — classified by where it starts:

• Type A — starts in the ascending aorta. Life-threatening (risk of cardiac tamponade, aortic regurgitation, coronary or cerebral malperfusion) — needs emergency cardiothoracic surgery.
• Type B — starts distal to the left subclavian artery (descending aorta/arch). Less immediately life-threatening and usually doesn’t need same-day surgery unless complicated (malperfusion, rupture, refractory pain/hypertension).

It has a high mortality rate — around 20% of patients die before reaching hospital, and a further 30% die during admission — which is why it warrants same urgency as ACS despite being far rarer. Risk factors beyond hypertension include cocaine use, Marfan syndrome, known aortic valve disease or thoracic aortic aneurysm, recent aortic manipulation (surgery, catheterisation), and a family history of aortic disease.

In a GP, urgent-care, or rural/peripheral hospital setting: this is an emergency-transfer diagnosis, not one to manage locally. Phone for an ambulance and clearly state the patient has (suspected) acute aortic dissection requiring urgent transfer; while arranging transfer — analgesia, IV access if available, and (only where the treating clinician has the training, drugs, and monitoring to do it safely) heart-rate control before any blood-pressure-lowering agent, since lowering pressure first can reflexively increase aortic wall shear stress. Don’t delay transfer to pursue further local workup once dissection is suspected, and send a full summary, any ECGs, and a record of what’s been given with the patient. Before an automatic emergency transfer, it’s still worth briefly considering the patient’s own goals of care — an advanced care plan, or frailty/aged-care-facility residence — since that context can change what “appropriate management” means for this particular patient.

Non-cardiac chest pain — the gastrointestinal/musculoskeletal/psychiatric differential

Once cardiac and other immediately life-threatening causes are excluded, noncardiac chest pain (NCCP) is common — “an estimated prevalence of approximately 13% (95% confidence interval: 9%, 16%) globally” — and is by definition a diagnosis of exclusion, not a positive one. Even after cardiac disease is “excluded,” vigilance for a changed pain pattern remains warranted: patients with NCCP who have traditional cardiac risk factors still carry a measurably higher cardiovascular mortality than those without.

Gastro-oesophageal causes are the most common — the prevalence of GORD as a cause of NCCP is believed to be between 30% and 60%, depending on the population, and as it is low-cost and low-risk to investigate it should be the first condition considered. In the absence of red flags warranting endoscopy, “an appropriate initial step is to perform a proton pump inhibitor (PPI) test, which has an acceptable sensitivity and specificity (both approximately 80%)” — typically eight weeks of double-dose PPI (e.g. pantoprazole 40 mg twice daily), with a positive test defined as >50% symptom reduction. Persistent dysphagia should prompt consideration of oesophageal dysmotility (nutcracker oesophagus, achalasia, distal oesophageal spasm) — oesophageal manometry is the best diagnostic tool, though it is low-yield (a specific cause is found in around 10% of patients tested).

Musculoskeletal chest wall pain is a diagnosis of history and examination, given the lack of a gold-standard diagnostic test — useful features include tenderness to palpation and positional changes in symptoms.

Functional/psychiatric causes are common and often coexist with other functional GI disorders (irritable bowel syndrome, bloating). Contributing psychological factors are also found in up to 75% of patients with functional chest pain, over half of whom have panic disorder, anxiety or major depression.

Urgent care and rural/peripheral practice

The limited existing evidence suggests that the decision to present to urgent care for chest pain is associated with a markedly lower risk of adverse outcomes relative to ED patients. The reported incidence of ACS/major adverse cardiac events within 30 days among urgent care chest-pain presentations is under 2%, including moderate-risk patients by HEAR/HEART. Still:

• For patients who appear acutely unwell or in distress, or who have significantly abnormal vital signs, the first priority should be emergency medical service (EMS) activation. Given that urgent-care staffing is limited in quantity and scope, it’s prudent for the treating clinician to remain with the patient and delegate the EMS call to staff.
• EMS transport should be recommended for all patients being referred to an ED for chest pain. In patients going to an ED by private vehicle, it’s strongly advised that they don’t drive themselves, and they should be directed to the most appropriate nearby facility. Document that EMS transport was suggested and the patient declined, if that’s what happens. Send a paper copy of the ECG and any other documentation with the patient, and try to notify the ED directly once the patient has left.
• While awaiting transport for a concerning presentation: 300 mg chewable/dissolved aspirin (unless contraindicated — hypersensitivity, a bleeding disorder, active peptic ulcer disease/gastric haemorrhage; use a lower dose, e.g. 150 mg, in pregnancy) and an ECG if it can be obtained without delaying transfer. Keep a defibrillator near the patient if available.
• Routine oxygen is not beneficial, and may be harmful, in suspected ACS without hypoxaemia — it’s a coronary vasoconstrictor. Only give it if oxygen saturation is ≤90% (aiming for SpO2 ≤96%, or 88–92% if there’s a risk of hypercapnia e.g. COPD), and use low-flow via nasal prongs.
• Nitroglycerin should be used cautiously outside a monitored setting — it has never been shown to improve mortality in ACS and can cause clinically significant hypotension, which is harder to manage without IV access on hand. Always check for PDE-5 inhibitor use first (see History, above).
• Immediately available troponin and D-dimer testing is uncommon in urgent care — most centres don’t have it. Drawing D-dimer or troponin tests that will not result while the patient is in urgent care is not advised — use clinical gestalt plus a score that doesn’t depend on troponin (HEAR, above) to guide the transfer/shared decision-making conversation instead.
• Point-of-care ultrasound, where available and the operator is experienced, can be more sensitive than plain radiography for pneumothorax, pericardial effusion, and pulmonary oedema — useful if the skill and equipment exist locally, not a reason to delay transfer if they don’t.
• Give every discharged patient clear, specific safety-netting: what symptoms mean “come back/call an ambulance now,” not a vague “return if it gets worse” — a heart-attack action plan, where available, is a good vehicle for this. In very-low-risk patients, urgent cardiology follow-up (within a few days) is ideal, but primary-care follow-up is reasonable where cardiology access is limited, as is common in rural practice.

Disposition

Most chest pain seen in the community is not life-threatening, but the practical rule is the reverse of “innocent until proven guilty”: the burden is on the clinician to demonstrate a genuinely low-risk picture (history, exam, and — where available — a validated score) before treating a patient as safe for outpatient management, and to ensure reliable follow-up once the serious differentials have been reasonably excluded. Anyone with a red flag above, an unstable vital sign, or a high-risk score needs same-day emergency assessment; most acute aortic dissection, tamponade, tension pneumothorax, and STEMI need emergency transfer for definitive (usually surgical or interventional) care that isn’t deliverable in a GP/urgent-care/rural setting. A new-onset or unstable angina, or a positive troponin where one was drawn, is also an emergency-department trigger in its own right, even without a red flag. Low-risk, reassuring presentations — stable angina, a HEART/HEAR score in the low-risk band with a negative troponin where available, PE excluded by Wells/PERC/D-dimer, or a confidently benign non-cardiac cause (GORD, musculoskeletal, resolved minor pneumothorax) — are appropriate for community management with safety-netting and appropriate follow-up.