Author: Mr Vik Veer MBBS(Lond) MRCS(Eng) DoHNS(Eng) — December 2007. Updated 2025.
Cardiovascular Causes
Angina and Acute Coronary Syndromes (ACS)
Spectrum: Stable angina, unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).
Typical features: Central or left-sided chest tightness or pressure ("like a heavy weight"), radiating to the left arm, jaw, or neck. Associated with diaphoresis, nausea, dyspnoea, and sometimes syncope. Typically precipitated by exertion or stress (stable angina), or at rest (UA/NSTEMI/STEMI). Lasts 2–20 minutes in stable angina; more than 20 minutes in ACS.
Discriminating features: Relieved by GTN spray in angina; not fully relieved in ACS. Women, diabetics, and the elderly may present atypically with epigastric pain, fatigue, or dyspnoea without chest pain (equivalents).
Key investigation: 12-lead ECG (ST changes, new LBBB), serial high-sensitivity troponin (at 0 and 3 hours), echocardiogram to assess wall motion abnormalities.
Initial management: STEMI — aspirin 300 mg, P2Y12 inhibitor (ticagrelor 180 mg), activate primary PCI pathway. NSTEMI — aspirin 300 mg, P2Y12 inhibitor, anticoagulation (fondaparinux or LMWH), risk stratification with GRACE score, early angiography.
Pericarditis
Typical features: Sharp, positional pleuritic chest pain — worse lying flat, improved by sitting forward. Often with a history of a recent viral illness (Coxsackievirus B, influenza, EBV). May be associated with fever. A pericardial friction rub may be heard on auscultation.
Discriminating features: Positional nature (better leaning forward) is very characteristic. Diffuse saddle-shaped ST elevation with PR depression on ECG. No troponin rise (or mild, non-significant rise in myopericarditis).
Key investigation: ECG (diffuse concave ST elevation, PR depression), ESR/CRP (elevated), echocardiogram (to exclude effusion).
Initial management: NSAIDs (ibuprofen 600 mg three times daily) plus colchicine (0.5 mg twice daily for 3 months); restrict exercise; exclude pericardial effusion and tamponade.
Mitral Valve Prolapse
Typical features: Atypical chest pain, often sharp, left-sided, not related to exertion. Palpitations are common. Typically in young, tall, slender females.
Discriminating features: Mid-systolic click followed by a late systolic murmur on auscultation. Echocardiogram is diagnostic.
Aortic Causes
Aortic Dissection
Typical features: Sudden onset of severe, tearing or ripping pain, maximal at its onset — classically described as "the worst pain I have ever felt." Radiates to the back (interscapular region) as the dissection propagates down the descending aorta. Associated with hypertension (the most common risk factor), Marfan syndrome, bicuspid aortic valve, or pregnancy.
Discriminating features: Pain is maximal at onset (unlike MI, which builds up over minutes). Blood pressure differential between arms (>20 mmHg). Pulse deficit. Neurological signs (carotid or spinal artery involvement). A new aortic regurgitation murmur (Type A dissection involving the aortic root). The ECG is typically normal unless the dissection extends to occlude a coronary ostium (most commonly the right).
Key investigation: CT aortogram (gold standard). Do NOT give thrombolytics if dissection is possible — this will cause catastrophic haemorrhage.
Initial management: Urgent cardiothoracic referral. Tight blood pressure control (target systolic <120 mmHg) with IV labetalol or esmolol. Type A (ascending) — emergency surgery. Type B (descending only) — medical management unless complicated.
Aortitis
Inflammation of the aortic wall — causes include syphilis (now rare), giant cell arteritis, Takayasu arteritis, ankylosing spondylitis, and rheumatoid arthritis. Can cause chest pain, aortic regurgitation, and aneurysm formation.
Pulmonary Causes
Pulmonary Embolism (PE)
Typical features: Sudden-onset pleuritic chest pain (worse on inspiration), dyspnoea, and tachycardia. Haemoptysis occurs in pulmonary infarction (<15% of cases). Risk factors include immobility, recent surgery, malignancy, thrombophilia, oral contraceptive pill, and pregnancy.
Discriminating features: Pleuritic pain (worsened by breathing) is very suggestive. Oxygen saturation may be reduced. DVT signs in the leg (in approximately 30% of cases). ECG may show sinus tachycardia (most common), right heart strain (S1Q3T3 pattern — large S in I, Q wave and T wave inversion in III), right bundle branch block, or AF.
Key investigation: Wells score (clinical pre-test probability), D-dimer (if low probability — a negative D-dimer excludes PE), CT pulmonary angiogram (CTPA, gold standard). V/Q scan if CTPA is contraindicated (e.g., severe renal failure, contrast allergy, pregnancy).
Initial management: Oxygen if SpO2 <94%. Anticoagulation (LMWH, fondaparinux, or DOAC — rivaroxaban or apixaban). Massive PE with haemodynamic compromise requires systemic thrombolysis (alteplase) or embolectomy.
Pneumothorax
Typical features: Sudden-onset sharp, unilateral pleuritic chest pain and dyspnoea. Most common in tall, thin young men (primary spontaneous pneumothorax) or in patients with underlying lung disease (COPD, asthma — secondary pneumothorax). Tension pneumothorax presents with rapid deterioration, tracheal deviation away from the affected side, absent breath sounds, hypotension, and raised JVP — a medical emergency.
Key investigation: Chest X-ray (visible pleural edge and absent lung markings beyond it). If tension pneumothorax is clinically suspected — do not wait for imaging: immediate needle decompression (2nd intercostal space, mid-clavicular line) followed by chest drain insertion.
Pneumonia / Pleuritis
Typical features: Pleuritic chest pain (worse on breathing and coughing), fever, productive cough with purulent or rust-coloured sputum, and dyspnoea. Lobar consolidation on examination (reduced air entry, bronchial breathing, dullness to percussion, increased vocal resonance).
Key investigation: Chest X-ray (consolidation), sputum culture, blood cultures, CRP, FBC, urea (CURB-65 score for severity assessment).
Initial management: Antibiotics according to severity and local guidelines (community-acquired pneumonia: amoxicillin ± clarithromycin; hospital-acquired: broader spectrum cover).
Tracheitis, Tuberculosis, Malignancy, Connective Tissue Disease
Tracheitis causes a central, burning, retrosternal pain worsened by coughing. TB can cause pleuritic pain from pleural involvement, and chest pain from mediastinal lymphadenopathy. Pulmonary malignancy may cause pain from pleural invasion, rib metastases, or Pancoast tumour (apical lung cancer invading the brachial plexus — causing pain radiating down the medial arm). Connective tissue diseases (SLE, rheumatoid arthritis) can cause serositis (pleuritis and pericarditis).
Oesophageal and Upper GI Causes
Gastro-oesophageal Reflux Disease (GORD)
Typical features: Retrosternal burning pain ("heartburn"), worse after meals, when lying flat, and when bending over. Associated with acid regurgitation. May be precipitated by spicy food, alcohol, caffeine, and fatty meals. Relieved by antacids or sitting upright.
Discriminating features: The burning quality and relationship to meals and posture helps distinguish from cardiac pain, though GORD and angina can coexist and mimic each other. GTN will relieve oesophageal spasm as well as angina, so this test is not specific.
Key investigation: Trial of proton pump inhibitor (PPI), 24-hour oesophageal pH monitoring, endoscopy if alarm features present (dysphagia, weight loss, haematemesis, anaemia).
Oesophageal Spasm
Diffuse oesophageal spasm causes severe, cramp-like retrosternal chest pain that may radiate to the back or jaw, closely mimicking cardiac pain. It may be precipitated by swallowing cold liquids. It is relieved by GTN (which relaxes smooth muscle) and calcium channel blockers. Barium swallow shows the characteristic "corkscrew oesophagus".
Peptic Ulcer Disease and Pancreatitis
Peptic ulcer pain is typically epigastric but can radiate to the chest. It is related to meals (duodenal ulcer pain is relieved by food; gastric ulcer pain is worsened by food). Pancreatitis causes severe epigastric pain radiating to the back, with nausea and vomiting, raised serum amylase and lipase.
Mallory-Weiss Tear
A longitudinal tear at the gastro-oesophageal junction following forceful vomiting or retching. Presents with haematemesis after an episode of vomiting. Chest pain may be present. Managed with proton pump inhibitors; rarely requires endoscopic or surgical intervention.
Abdominal Causes
Gallstones (Biliary Colic)
Typical features: Severe, constant right upper quadrant pain radiating to the right shoulder tip or scapula, often after a fatty meal. Associated with nausea and vomiting. Murphy's sign is positive in acute cholecystitis. Gallstones can occasionally cause referred pain to the right lower chest.
Chest Wall and Musculoskeletal Causes
Tietze's Syndrome (Costochondritis)
Typical features: Localised tenderness over the costochondral junctions (most commonly 2nd and 3rd rib cartilages). Pain is sharp, worsened by movement and palpation, and there is no swelling. Tietze's syndrome specifically refers to the variant with visible or palpable swelling at the junction; in costochondritis without swelling, the term "costochondritis" is preferred.
Discriminating feature: Precise, reproducible tenderness on palpation of the affected costochondral junction — this is a very useful discriminating feature that strongly suggests a musculoskeletal cause.
Bornholm Disease (Epidemic Myalgia / Pleurodynia)
Bornholm disease is caused by Coxsackievirus B and presents with sudden-onset severe pleuritic chest or upper abdominal pain, often in epidemics. Associated with fever and myalgia. Pain is paroxysmal and severe. Treatment is supportive. Named after the Danish island of Bornholm where an epidemic was first described.
Rib Fracture and Intercostal Muscle Injury
Typical features: Localised chest wall pain, worsened by movement, palpation, inspiration, and coughing. History of trauma or, in the elderly, low-energy trauma (rib fracture from coughing in osteoporosis).
Skeletal Causes
Thoracic Outlet Syndrome
Compression of the neurovascular bundle (brachial plexus, subclavian artery and vein) as it passes between the first rib and clavicle. Causes chest pain, arm pain, paraesthesia in the medial arm and hand (C8/T1 distribution), and vascular symptoms.
Herniated Intervertebral Disc
Thoracic disc herniation can cause dermatomal chest pain that wraps around the chest wall. It may be accompanied by neurological signs in the legs (if spinal cord is compressed).
Ankylosing Spondylitis
An inflammatory arthropathy affecting the sacroiliac joints and spine. Thoracic involvement can restrict chest wall expansion and cause chest pain. Aortitis and aortic regurgitation are recognised cardiac associations.
Osteoarthritis and Tabes Dorsalis
Degenerative disease of the thoracic spine can cause referred chest pain. Tabes dorsalis — a late manifestation of syphilis affecting the dorsal columns — causes severe, brief, "lightning" pains in the chest (tabetic crises), along with Argyll Robertson pupils and ataxia.
Neurological and Other Causes
Anxiety and Panic Disorder
Typical features: Diffuse, variable chest tightness or pressure associated with palpitations, dyspnoea, tingling in the extremities, dizziness, and a feeling of impending doom. May mimic ACS. Occurs in the context of anxiety or panic attacks. Important not to dismiss as "just anxiety" without excluding organic pathology — anxiety and ACS can coexist.
Key investigation: Diagnosis of exclusion — exclude cardiac, pulmonary, and metabolic causes first. Formal psychiatric assessment.
Herpes Zoster (Shingles)
Typical features: Dermatomal pain (often burning or stabbing) following a thoracic dermatome. The key diagnostic feature is the appearance of the rash (vesicles on an erythematous base) several days after the pain begins — zoster is often misdiagnosed as cardiac or pleural pain before the rash appears. Post-herpetic neuralgia can persist for months after the rash resolves.
Frequently Asked Questions
What are the most important causes of chest pain to exclude immediately in A&E?
The five immediately life-threatening causes of chest pain are: (1) STEMI/ACS — requires immediate ECG and troponin; (2) aortic dissection — requires CT aortogram and urgent cardiothoracic input; (3) pulmonary embolism — requires clinical pre-test probability score (Wells), D-dimer, and CTPA; (4) tension pneumothorax — a clinical diagnosis requiring immediate needle decompression before imaging; and (5) oesophageal perforation — rare but presents with severe chest pain after instrumentation or vomiting (Boerhaave syndrome). Every patient with chest pain should have an ECG, pulse oximetry, and a focused history within minutes of arrival.
What is the classic presentation of aortic dissection and how does it differ from MI?
Aortic dissection presents with severe chest or back pain that is maximal at its very onset — like a "tearing" or "ripping" sensation. This is in contrast to MI, where the pain builds over minutes. Dissection pain radiates to the interscapular region of the back as the dissection propagates down the descending aorta. There may be pulse deficits, blood pressure differential between arms, neurological signs, and a new aortic regurgitation murmur. The ECG is typically normal in dissection (unless the right coronary ostium is involved, causing inferior STEMI). Critically, thrombolytics given for a misdiagnosed MI can be fatal in dissection — always check for dissection clinically and radiologically before thrombolysis.
How do you differentiate pericarditis from STEMI on an ECG?
The key ECG differentiators are: (1) Distribution — pericarditis causes ST elevation in virtually all leads (diffuse/global), whereas STEMI causes ST elevation only in leads corresponding to the infarcted coronary territory; (2) Shape — pericarditis causes concave (saddle-shaped) upward ST elevation, whereas STEMI causes convex (tombstone or dome-shaped) ST elevation; (3) PR depression — pericarditis characteristically causes PR segment depression (most specific ECG sign of pericarditis), which is not seen in STEMI; (4) Reciprocal changes — STEMI produces reciprocal ST depression in the "mirror" leads; pericarditis does not. Clinically, pericarditis pain is positional (worse lying flat, better sitting forward), whereas MI pain is not positional.
What is Bornholm disease and how does it present?
Bornholm disease (epidemic pleurodynia or epidemic myalgia) is a viral illness caused by Coxsackievirus B, which preferentially infects intercostal and diaphragmatic muscles. It presents with sudden-onset severe paroxysmal chest or upper abdominal pain (from intercostal and diaphragmatic muscle involvement), fever, headache, and myalgia. The pain is described as "devil's grip" because of its severity. It typically occurs in epidemics, is self-limiting (1–2 weeks), and treatment is supportive with NSAIDs. The virus can also cause pericarditis, myocarditis, aseptic meningitis, and orchitis — so it should be considered in patients with atypical chest pain presenting in an epidemic context.
How useful is the chest pain character in distinguishing cardiac from non-cardiac causes?
Pain character is a useful but imperfect discriminating factor. Classic features that increase the probability of cardiac pain include: central or left-sided location; pressure or tightness quality; radiation to the left arm, jaw, or neck; association with exertion or stress; relief with GTN; and associated diaphoresis and nausea. Features that decrease the probability of cardiac pain include: sharp or stabbing quality; pleuritic character (worsened by breathing); precise localisation to a small area; reproduction by palpation; and onset after meals or when lying down. However, up to 20% of MI patients present atypically — particularly women, diabetics, and the elderly — so a low threshold for ECG and troponin measurement is essential.
What is the GRACE score and when is it used?
The GRACE (Global Registry of Acute Coronary Events) score is a risk stratification tool for patients with NSTEMI and unstable angina. It uses variables including age, heart rate, systolic blood pressure, serum creatinine, cardiac arrest on presentation, Killip class (degree of cardiac failure), ST deviation on ECG, and elevated cardiac biomarkers. The score stratifies patients into low, intermediate, or high risk of in-hospital and 6-month mortality. High-risk patients (GRACE score >140) should receive early invasive angiography (within 24 hours). Intermediate-risk patients should receive angiography within 72 hours. Low-risk patients may be managed conservatively with elective investigation.
What is costochondritis and how is it diagnosed?
Costochondritis is inflammation of the costochondral junctions — the cartilaginous joints where the ribs meet the sternum. It is a very common and benign cause of chest pain that is frequently encountered in A&E and general practice. The diagnosis is clinical: the key feature is precise, reproducible tenderness on palpation of the costochondral junction. The 2nd and 3rd junctions are most commonly affected. The pain is worsened by movement, deep breathing, and coughing. There is no swelling (if there is visible swelling, the diagnosis is Tietze's syndrome — a distinct entity). Management is reassurance, NSAIDs, and physiotherapy.
ST3 interview: A 55-year-old man presents with tearing back pain radiating to the chest. He is hypertensive. What is your differential and initial management?
The top priority diagnosis is aortic dissection. I would immediately call for senior assistance and perform an ABCDE assessment. I would place two large-bore IV cannulas, take blood for FBC, U&E, clotting, crossmatch, and troponin. I would obtain a 12-lead ECG — if there is inferior ST elevation, I must consider that the dissection has extended to involve the right coronary ostium, and I must NOT give thrombolytics. I would measure blood pressure in both arms — a differential of >20 mmHg is suggestive of dissection. I would arrange an urgent CT aortogram. While awaiting imaging, I would control blood pressure with IV labetalol or esmolol to a target systolic of less than 120 mmHg, and ensure adequate analgesia with IV morphine. I would contact cardiothoracic surgery immediately if Type A dissection is confirmed on CT, as this requires emergency surgery. Type B without complications may be managed medically, with endovascular intervention (TEVAR) reserved for complications.
How does herpes zoster cause chest pain and how is it recognised?
Herpes zoster (shingles) is caused by reactivation of the varicella-zoster virus in a sensory dorsal root ganglion. When it affects a thoracic dermatome (most commonly T3–T10), it presents as burning, shooting, or stabbing unilateral chest pain that strictly follows a dermatomal distribution and does not cross the midline. The critical diagnostic feature is the rash — vesicles on an erythematous base that appear within a few days of the pain's onset. Before the rash appears ("pre-eruptive" or "zosteriform" pain), the presentation can mimic cardiac or pleural disease. Antiviral therapy (aciclovir or valaciclovir) should be started within 72 hours of rash onset to reduce the duration of illness and the risk of post-herpetic neuralgia.
References
- Ibanez B, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal. 2018; 39(2): 119–177.
- Collet JP, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. European Heart Journal. 2021; 42(14): 1289–1367.
- Erbel R, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. European Heart Journal. 2014; 35(41): 2873–2926.
- Konstantinides SV, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. European Heart Journal. 2020; 41(4): 543–603.
- British Thoracic Society. BTS Guidelines for the Management of Spontaneous Pneumothorax. Thorax. 2010; 65(Suppl 2): ii18–ii31.
- Adler Y, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. European Heart Journal. 2015; 36(42): 2921–2964.
- Longmore M, Wilkinson I, Davidson EH, Foulkes A, Mafi AR. Oxford Handbook of Clinical Medicine. 10th ed. Oxford: Oxford University Press; 2022.