Chest Pain
1a. Definition
Chest pain is a symptom — not a diagnosis — defined as any pain, discomfort, pressure, tightness, or heaviness felt in the anterior thorax between the neck and the costal margins. It is one of the most common presentations in both primary and emergency care, accounting for approximately 1% of all GP consultations and up to 20% of emergency admissions in the UK.
The clinical challenge lies in distinguishing immediately life-threatening causes requiring emergency intervention from the much larger volume of benign or non-cardiac aetiologies — without over-investigating low-risk presentations.
1b. Clinical classification
By anatomical origin
Cardiac
- ACS (STEMI, NSTEMI, UA)
- Stable angina
- Pericarditis / myocarditis
- Aortic dissection
- HCM / cardiomyopathy
- Cardiac tamponade
Pulmonary
- Pulmonary embolism (PE)
- Pneumothorax
- Pneumonia / pleuritis
- Pleural effusion
- Lung cancer
- Tracheitis
GI / other
- GORD / oesophageal spasm
- Peptic ulcer disease
- Oesophageal rupture (Boerhaave)
- Pancreatitis / cholecystitis
Musculoskeletal / other
- Costochondritis (Tietze)
- Rib fracture
- Herpes zoster (pre-rash)
- Cervical/thoracic radiculopathy
- Anxiety / panic disorder
- Da Costa syndrome
By clinical urgency (NICE CKS framework)
| Category | Examples | Action |
|---|---|---|
| Immediately life-threatening | STEMI, aortic dissection, tension pneumothorax, massive PE, cardiac tamponade | 999 / immediate admission |
| Potentially serious | NSTEMI/UA, PE, pneumonia, pericarditis, myocarditis | Same-day assessment / urgent referral |
| Non-urgent cardiac | Stable angina (new or worsening) | Rapid access chest pain clinic (RACPC) within 2 weeks |
| Non-cardiac / benign | GORD, MSK, anxiety | Primary care management |
1c. Etiopathophysiology
Ischaemic chest pain (ACS / angina)
- Atherosclerotic plaque in coronary arteries → fixed (angina) or dynamic (ACS) reduction in myocardial oxygen supply
- ACS: plaque rupture or erosion → platelet aggregation → thrombus formation → partial (NSTEMI/UA) or complete (STEMI) occlusion
- Myocardial ischaemia → anaerobic metabolism → lactic acid → stimulates cardiac C-fibres → pain referred to chest, jaw, arm (C8–T4 dermatomes)
- Risk factors: smoking, hypertension, hyperlipidaemia, diabetes, family history, obesity, male sex, age
Key non-ischaemic mechanisms
- Aortic dissection: intimal tear → haematoma propagates in media; hypertension is the primary risk factor
- PE: thrombus (usually DVT) → pulmonary arterial occlusion → ↑ RV afterload, ↓ LV preload, infarction of lung parenchyma (pleuritic pain)
- Pericarditis: inflammation of pericardium (viral most common) → irritation of phrenic nerve → sharp, pleuritic chest pain
- GORD: acid reflux → oesophageal mucosal irritation → visceral pain indistinguishable clinically from angina
- MSK: costochondral inflammation, rib periosteum, intercostal nerve irritation
Assessment
2a. Clinical presentation
Structured history — SOCRATES adapted for chest pain
| Feature | Key differentiating details |
|---|---|
| Site | Central/retrosternal (ACS, GORD, aortic dissection); lateral/unilateral (PE, pleuritis, pneumothorax, MSK, zoster) |
| Onset | Sudden/tearing (dissection, pneumothorax); sudden severe (PE); gradual (angina, GORD, MSK, pericarditis) |
| Character | Crushing/pressure (ACS, angina); tearing/ripping (dissection); sharp/stabbing/pleuritic (PE, pericarditis, pneumothorax, MSK); burning (GORD) |
| Radiation | Left arm/jaw (ACS); back/interscapular (dissection); shoulder tip (diaphragmatic irritation — PE, pneumonia) |
| Associated | Diaphoresis, nausea, vomiting (ACS); dyspnoea, haemoptysis, leg swelling (PE); fever, cough (pericarditis, pneumonia); dysphagia/reflux (GORD); dermatomal rash (zoster) |
| Timing | Exertional + relieved by rest/GTN (angina); rest pain or minimal exertion (ACS); positional (pericarditis worse supine, better leaning forward; GORD worse lying flat) |
| Exacerbating | Exertion (angina, ACS, PE); inspiration (pleuritis, pericarditis, pneumothorax, MSK); palpation (MSK, costochondritis); eating (GORD, peptic ulcer) |
| Severity | Severe unrelenting pain unresponsive to analgesia should raise concern for dissection or massive PE |
Characteristic presentations — key differentiators
| Diagnosis | Classic features | Signs | Distinguishing detail |
|---|---|---|---|
| STEMI | Central crushing pain >20 min, radiation to arm/jaw, diaphoresis, nausea | Pallor, sweating, tachycardia, possible new murmur | ST elevation ≥1 mm in ≥2 contiguous leads or new LBBB |
| NSTEMI / UA | Similar to STEMI but may be briefer or at rest; may be “atypical” | Often normal; may have diaphoresis | Troponin elevated (NSTEMI) or normal (UA); ST depression or T-wave changes |
| Stable angina | Exertional chest tightness, relieved within 5 min by rest or GTN | Often normal between episodes | Reproducible with same level of exertion; NICE: refer to RACPC |
| Aortic dissection | Sudden-onset tearing/ripping pain radiating to back; maximal at onset | BP differential between arms (>20 mmHg), aortic regurgitation murmur, neuro deficit | Wide mediastinum on CXR; D-dimer elevated but non-specific; CT angiography diagnostic |
| PE | Pleuritic chest pain, dyspnoea, haemoptysis, after immobility/surgery/long flight | Tachycardia, tachypnoea, pleural rub, DVT signs, hypoxia | Wells score; D-dimer; CTPA gold standard; S1Q3T3 on ECG (uncommon but classic) |
| Pericarditis | Sharp chest pain, worse lying flat, better leaning forward; recent URTI | Pericardial friction rub; fever | Saddle-shaped ST elevation; PR depression; echo if effusion suspected |
| Pneumothorax | Sudden unilateral pleuritic pain + dyspnoea; young tall thin male | Reduced breath sounds, hyperresonance on affected side; tracheal deviation (tension) | CXR: visible pleural edge with absent lung markings |
| GORD | Burning retrosternal/epigastric; worse post-prandially, lying flat; relieved by antacids | Usually normal; epigastric tenderness | Clinical diagnosis; trial of PPI; no radiation to arm or jaw |
| Costochondritis | Sharp localised pain; worse on palpation and movement | Reproducible tenderness on pressing costochondral junctions | Tietze: swelling present; costochondritis: no swelling |
| Herpes zoster | Dermatomal burning pain; may precede rash by 48–72 h | Vesicular rash in dermatomal distribution (later) | Consider in elderly/immunosuppressed with unexplained unilateral chest pain |
Immediate 999 — do not miss:
- Sudden tearing chest pain radiating to back → aortic dissection until proven otherwise
- Central crushing chest pain >15 min ± diaphoresis, nausea → ACS
- Sudden dyspnoea + pleuritic chest pain + hypoxia + tachycardia → PE
- Absent breath sounds + tracheal deviation → tension pneumothorax (clinical diagnosis — do not wait for CXR)
- Muffled heart sounds + elevated JVP + hypotension (Beck’s triad) → cardiac tamponade
Atypical presentations — do not miss in: women, elderly, diabetics (autonomic neuropathy blunts pain perception). ACS may present as jaw pain, epigastric pain, fatigue, or vomiting alone. Maintain a low threshold.
2b. Relevant investigations
First-line (all chest pain presentations)
- 12-lead ECG: perform within 10 min of presentation — ST changes, LBBB, PR depression, epsilon wave, S1Q3T3
- High-sensitivity troponin (hs-cTnI/T): at 0 h and 1–2 h (ESC 0h/1h pathway); elevated in NSTEMI, myocarditis, PE, aortic dissection, sepsis (non-specific)
- CXR: pneumothorax, pneumonia, pulmonary oedema, widened mediastinum (dissection), pleural effusion
- Oxygen saturation (SpO₂): hypoxia suggests PE, pneumonia, pneumothorax
- Bloods: FBC, U&E, glucose, lipids, LFTs, CRP, D-dimer (if PE suspected + low-to-moderate probability)
Targeted investigations
- CTPA: gold standard for PE
- CT aortography: aortic dissection
- Echocardiogram: pericardial effusion, wall motion abnormality (ACS), tamponade, RV strain (PE), structural disease
- V/Q scan: PE if CTPA contraindicated (pregnancy, CKD, contrast allergy)
- Exercise tolerance test (ETT) / CT coronary angiography (CTCA): stable angina workup — NICE recommends CTCA as first-line imaging for stable chest pain
- Ambulatory Holter / event recorder: if arrhythmia suspected
- Endoscopy / oesophageal pH monitoring: if GORD/oesophageal cause suspected after cardiac exclusion
NICE NG185 (stable chest pain): For patients with stable chest pain and suspected angina, offer CTCA as first-line investigation. Functional imaging (stress MRI, nuclear) if CTCA inconclusive. Invasive angiography only if CTCA shows significant disease or CTCA not feasible.
D-dimer in PE: Use only if Wells score ≤4 (PE unlikely). A negative D-dimer in low/moderate probability effectively excludes PE. Do NOT use D-dimer if pre-test probability is high — proceed directly to CTPA.
Clinical decision tools — AKT favourites
HEART score
- History, ECG, Age, Risk factors, Troponin
- Score ≤3: low risk (0.9–1.7% MACE) — safe discharge
- Score 4–6: moderate — observe, repeat troponin
- Score ≥7: high — early invasive strategy
Wells score (PE)
- Clinical DVT signs (+3), alternative dx less likely (+3), HR >100 (+1.5), immobilisation/surgery (+1.5), previous DVT/PE (+1.5), haemoptysis (+1), malignancy (+1)
- ≤4: PE unlikely → D-dimer
- >4: PE likely → CTPA
TIMI score (ACS)
- 7 variables (age, CAD risk factors, known CAD, ST deviation, anginal events, aspirin use, elevated troponin)
- Score 0–2: low risk; 3–4: moderate; 5–7: high
- Used in UA/NSTEMI risk stratification
GRACE score (ACS)
- Preferred by NICE/ESC for NSTEMI risk stratification
- Variables: age, HR, SBP, creatinine, Killip class, cardiac arrest, ST deviation, troponin
- Score >140: high risk → early invasive strategy
Management — UK NICE CKS / NICE guidelines
3a. Emergency care
Call 999 immediately — do not delay for investigations:
- Suspected STEMI or new LBBB → 999; chew aspirin 300 mg immediately (if not contraindicated); do not give GTN and await
- Suspected aortic dissection → 999; do NOT give antiplatelets or thrombolytics
- Suspected massive PE with haemodynamic instability → 999; IV access, oxygen
- Tension pneumothorax → immediate needle decompression (2nd ICS, midclavicular line) then 999
- Cardiac tamponade → 999; pericardiocentesis in hospital
ACS — immediate primary care actions
- Aspirin 300 mg chewed immediately (crushed if unable to chew)
- GTN sublingual (400 mcg spray or 500 mcg tablet) if SBP >90 mmHg — for symptom relief; repeat every 5 min up to 3 doses
- Oxygen: only if SpO₂ <94% (avoid hyperoxia — worsens myocardial injury)
- IV access if available; monitor; keep patient at rest
- STEMI: primary PCI is preferred reperfusion strategy — must occur within 120 min of first medical contact; if >120 min, consider thrombolysis if PCI not available
- NSTEMI/UA: admit for risk stratification (GRACE score), antiplatelet dual therapy, anticoagulation, and early invasive strategy if high-risk
PE — acute management (in hospital)
- Anticoagulate immediately once PE confirmed (or if high clinical suspicion before imaging)
- DOAC (apixaban or rivaroxaban) preferred — NICE NG158; no need for parenteral bridging
- LMWH if DOAC contraindicated (renal failure, pregnancy, cancer-associated thrombosis → LMWH)
- Massive PE + haemodynamic instability → systemic thrombolysis (alteplase) or surgical embolectomy
Pericarditis — acute management
- NSAIDs (ibuprofen 600 mg TDS) — first line; add colchicine 500 mcg BD for 3 months (COPE trial evidence — reduces recurrence)
- Restrict exercise until asymptomatic + CRP normalised
- Avoid NSAIDs/ibuprofen if STEMI (impair healing) — use aspirin instead
- Admit if: large effusion, tamponade, troponin rise (myopericarditis), immunosuppressed, on anticoagulation
3b. Referral
Same-day / urgent
- Any suspected ACS, PE, dissection, tamponade, pneumothorax → 999 or A&E same day
- NSTEMI with moderate-high GRACE score → admit cardiology
- Suspected myocarditis (young + chest pain + troponin rise + viral prodrome)
- Haemodynamically unstable patient of any cause
- New onset chest pain undiagnosed after initial assessment with any high-risk features
Routine / RACPC
- Suspected stable angina → rapid access chest pain clinic within 2 weeks (NICE NG185)
- New exertional chest pain in patient with known IHD risk factors — do not manage in primary care without specialist input
- Recurrent chest pain with uncertain aetiology after initial workup
- Post-ACS: cardiac rehabilitation referral (NICE NG185)
- Recurrent pericarditis → cardiology
NICE NG185: Do not use exercise ECG to diagnose or exclude stable angina for people without known CAD. Offer CTCA as the first-line diagnostic investigation for stable chest pain when obstructive CAD cannot be excluded clinically.
3c. Primary care management
Post-ACS secondary prevention (NICE NG185)
Antiplatelets
- Aspirin 75 mg lifelong
- Dual antiplatelet therapy (DAPT): aspirin + ticagrelor or prasugrel for 12 months post-ACS
- Clopidogrel if ticagrelor/prasugrel not tolerated
Statin
- High-intensity statin: atorvastatin 80 mg
- Target: >40% reduction in LDL-C; LDL <1.4 mmol/L (ESC)
- Lifelong; do not stop
ACEi / ARB
- Start within 24–48 h post-MI (especially if EF ↓, diabetes, or hypertension)
- Ramipril — titrate to max tolerated
- ARB if ACEi-intolerant
Beta-blocker
- Bisoprolol or metoprolol post-MI
- Continue at least 12 months; longer if HFrEF
- Reduces arrhythmia risk and reinfarction
Stable angina — primary care management (NICE CKS)
- Short-acting nitrate (GTN spray): all patients — prescribe and educate on use; if no relief in 5 min after 2 doses → call 999
- Anti-anginal therapy: beta-blocker (bisoprolol) or rate-limiting CCB (diltiazem/verapamil) as first-line; add second agent if monotherapy insufficient
- Long-acting nitrate / ivabradine / nicorandil / ranolazine: add if 2-drug combination fails — specialist guidance
- Secondary prevention: aspirin 75 mg + statin (atorvastatin 80 mg) in all with confirmed CAD
- Risk factor modification: smoking cessation, blood pressure control (<130/80 target), lipid management, weight, exercise, diabetes control
GORD / oesophageal chest pain
- PPI (omeprazole 20 mg OD) 4–8 weeks — diagnosis and treatment simultaneously
- Lifestyle: head-of-bed elevation, avoid triggers (caffeine, alcohol, fatty foods, late meals), weight loss
- H2 antagonist (famotidine) if PPI not tolerated
- Refer if: alarm features (dysphagia, unintentional weight loss, persistent vomiting, haematemesis, anaemia) → 2WW upper GI endoscopy
MSK chest pain (costochondritis / musculoskeletal)
- Reassurance (once serious causes excluded) is the cornerstone of management
- NSAIDs (ibuprofen 400 mg TDS with food) for 1–2 weeks
- Topical NSAIDs (diclofenac gel) if oral NSAIDs contraindicated
- Local corticosteroid injection if severe/refractory costochondritis
- Physiotherapy referral for thoracic wall dysfunction
Functional / anxiety-related chest pain
- Positive diagnosis — do not over-investigate once serious causes excluded
- Explain mechanism (hyperventilation, somatic amplification) clearly and compassionately
- CBT is most effective treatment (NICE NG197 for generalised anxiety)
- Breathing retraining; consider SSRI if anxiety disorder co-exists
PE — outpatient management (selected low-risk)
- PESI score (or sPESI) — if low risk (class I/II or sPESI 0) and adequate home support → outpatient DOAC treatment appropriate
- Apixaban 10 mg BD for 7 days then 5 mg BD; or rivaroxaban 15 mg BD for 21 days then 20 mg OD
- Duration: provoked PE — 3 months; unprovoked — 3–6 months minimum; recurrent or cancer-associated — extended/indefinite
DVLA considerations: Post-MI — cease driving for 1 week (Group 1) if successfully treated by PCI; 4 weeks if no revascularisation. Stable angina — can drive if symptoms controlled; must stop if symptoms at rest or at the wheel. Group 2 licence (HGV/bus): much stricter — notify DVLA; typically requires satisfactory exercise testing and ejection fraction assessment.
Cardiac rehabilitation: NICE recommends offering cardiac rehabilitation to all patients post-MI and post-revascularisation. Evidence shows it reduces mortality by ~25% and rehospitalisation. GP role: refer, encourage uptake, and monitor completion.
Sources informing these notes
NICE NG185 — Stable chest pain / stable anginaNICE NG89 — Acute MI (ACS)NICE NG158 — Venous thromboembolic diseaseNICE CKS — Chest pain, GORD, Costochondritis, PericarditisESC 2023 ACS GuidelinesESC 2019 PE GuidelinesBMJ Best Practice — Chest painStatPearls — Chest pain evaluationDVLA: Assessing fitness
Oxygen in ACS is a recurring AKT trap — do not give oxygen routinely. It is only indicated if SpO₂ is below 94%. Hyperoxia causes coronary vasoconstriction and worsens myocardial injury.
CTCA is now the first-line investigation for stable chest pain per NICE NG185 — not exercise ECG, which NICE explicitly recommends against for diagnosing or excluding stable angina in those without known CAD.
Aspirin in dissection — giving aspirin or thrombolytics to a patient with aortic dissection can be fatal. The tearing-pain-to-the-back presentation should always make you pause before treating empirically for ACS.
D-dimer is only useful when pre-test probability is low or moderate. A high Wells score mandates CTPA directly — a negative D-dimer in a high-probability patient does not exclude PE.
Colchicine in pericarditis alongside NSAIDs is now standard of care — it halves the recurrence rate and is an increasingly tested prescribing point.
DAPT duration — 12 months post-ACS (aspirin + ticagrelor or prasugrel), then aspirin alone lifelong. Clopidogrel is third choice. This comes up regularly in prescribing and management questions.
