Chest Pain

Differentiation of Cardiac vs Non-Cardiac Causes: Thorough Evaluation Frameworks

Cardiac causes

• Ischaemic: ACS (unstable angina, NSTEMI, STEMI), stable angina, coronary vasospasm (Prinzmetal angina)

• Non-ischaemic: Pericarditis, myocarditis, aortic dissection, cardiomyopathy, significant arrhythmias (e.g. tachyarrhythmias)

Non-cardiac causes

• Gastrointestinal: GORD, oesophageal spasm, peptic ulcer disease, pancreatitis

• Musculoskeletal: Costochondritis, rib fracture, Tietze’s syndrome

• Respiratory: PE, pneumothorax, pneumonia, pleuritis

• Psychogenic: Panic attack, anxiety disorders, hyperventilation

Evaluation

• History: Nature of pain (sharp, crushing, burning), duration, triggers (exertion, stress), associated features (SOB, diaphoresis, palpitations), risk factors (age, smoking, diabetes)

• Examination: Vital signs (BP in both arms if dissection suspected), chest wall tenderness, heart/lung auscultation, signs of heart failure or shock

• Investigations: ECG, troponins, chest X-ray, bloods (FBC, UECs, possibly D-dimer if PE suspected), consideration of risk scores (e.g. HEART, GRACE, TIMI in acute presentations)

With Chest Pain

Low-risk chest pain

• Perform stress ECG if no high-risk features, normal baseline ECG, and stable symptoms

• Useful for detecting inducible ischaemia in suspected stable angina

High-risk chest pain

• Consider stress echocardiography to visualise regional wall motion abnormalities under stress

• Pharmacological stress (dobutamine) if patient cannot exercise

• If suspicion of ACS, proceed with immediate hospital assessment

Without Chest Pain

Low risk

• No immediate investigation required if completely asymptomatic and no significant risk factors

Intermediate risk (10–20%)

• Consider coronary CT angiography (CTCA) for anatomical assessment of coronary arteries

High family history risk

• CTCA can be helpful if no prior CAD diagnosis and the patient has a strong family history of premature coronary artery disease

ACS Pathways: Management Based on Guidelines

Initial assessment

• ECG within 10 minutes of arrival or symptom presentation

Troponins at 0 hours and repeat at 3 hours if needed (hs-troponin can facilitate earlier diagnosis)

Risk stratification

• High risk: Immediate cardiology referral ± urgent angiography

• Intermediate risk: Admit for serial troponins, continuous monitoring, possible inpatient stress testing

• Low risk: Outpatient stress testing or CTCA if no ongoing chest pain, normal ECG, and stable vitals

Management

• Antiplatelets: Aspirin 300 mg loading, add clopidogrel or ticagrelor if ACS confirmed

• Symptom relief: GTN sublingual or IV for persistent pain, IV morphine if severe

• Long-term therapy: Beta-blockers (if no contraindications) and statins for secondary prevention, consider ACE inhibitors in LV dysfunction, hypertension, or diabetes

Imaging Modalities: Stress Tests, Coronary CT Angiography, and Echocardiography Indications

Stress ECG

• Low-risk patients with a normal baseline ECG and suspected stable angina

• Limited utility if baseline ST/T changes, LBBB, or paced rhythm

Stress Echocardiography

• Intermediate to high-risk chest pain to detect wall motion abnormalities

• Useful when baseline ECG abnormalities limit interpretation of a standard stress ECG

CTCA

• Intermediate-risk chest pain (~10–20% estimated pre-test probability)

• No prior diagnosis of CAD but equivocal or atypical symptoms

• Strong family history of early coronary artery disease

• Helps rule out significant stenoses, can reduce need for invasive angiography

Echocardiography

• Assess LV function, valve pathology, or pericardial effusion

• Evaluate suspected structural heart disease such as dilated or hypertrophic cardiomyopathies

Additional Considerations

• Rapid identification of red flags (ongoing chest pain at rest, hypotension, arrhythmias, syncope, signs of heart failure) dictates urgent ED referral

• GORD or oesophageal spasm can mimic cardiac chest pain; a trial of proton pump inhibitors may help clarify diagnosis

• Panic attacks may present with chest tightness, palpitations, hyperventilation; differentiate from cardiac aetiologies through thorough assessment and risk stratification

• Chronic stable chest pain in the setting of known CAD warrants optimisation of anti-anginal therapy (beta-blockers, nitrates, possibly calcium channel blockers) and risk factor management (lipids, BP, diabetes control, smoking cessation)

• Thorough GP follow-up for borderline or recurrent symptoms ensures timely escalation if patients deteriorate or new features emerge

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