Case 08: Chest Pain

Mr Carter, a 58-year-old male smoker with hypertension and hyperlipidaemia, presents to the emergency department with a 40-minute history of severe, crushing central chest pain radiating to his left arm, associated with profuse cold sweat, nausea, and a feeling of impending doom. His ECG shows ST-segment elevation in leads II, III, and aVF consistent with an inferior ST-elevation myocardial infarction (STEMI).

The differential diagnosis of chest pain includes acute coronary syndrome (unstable angina and myocardial infarction), stable angina, arrhythmia, aortic dissection, pulmonary embolism, pericarditis, oesophagitis, and musculoskeletal pain. Distinguishing features of MI versus angina: MI pain is typically more severe, lasts >20 minutes, is not relieved by rest or nitrates, and is associated with autonomic symptoms (diaphoresis, nausea, vomiting, pallor, haemodynamic compromise).

Atherosclerosis underlies most coronary artery disease. Elevated LDL cholesterol accumulates in the intima of coronary arteries, is oxidised, and taken up by macrophages forming foam cells — the basis of fatty streaks and fibrous plaques. Plaque rupture exposes subendothelial collagen and tissue factor, triggering platelet aggregation and coagulation cascade activation, forming an occlusive thrombus. In STEMI, complete occlusion causes transmural ischaemia of the downstream myocardium; ECG shows ST elevation in the leads reflecting the affected territory.

The coronary circulation: the left anterior descending (LAD) artery supplies the anterior wall and apex; the circumflex artery supplies the lateral wall; the right coronary artery (RCA) supplies the inferior wall and, via the posterior descending artery (PDA), the inferior and posterior surfaces (in 80% of the population who are right-dominant). Inferior STEMI (ST elevation in II, III, aVF) indicates RCA or PDA territory occlusion.

Immediate STEMI management: (1) percutaneous coronary intervention (PCI) is the preferred reperfusion strategy if available within 90 minutes; (2) thrombolysis (e.g. tenecteplase) is used if PCI is not available and symptom onset is within 6 hours. Adjunctive therapy: dual antiplatelet therapy (aspirin + P2Y12 inhibitor such as clopidogrel or ticagrelor), anticoagulation with LMWH during PCI, beta-blockers, ACE inhibitors, and statins. Oxygen should NOT be routinely administered unless the patient is hypoxic (SpO2 <93%), breathless, in heart failure, or in cardiogenic shock.

Ventricular fibrillation (VF) is a common and immediately life-threatening complication of MI. The ECG shows chaotic high-frequency electrical activity with no discernible QRS complexes. Treatment is immediate unsynchronised defibrillation (unlike cardioversion for AF, which is synchronised). CPR is commenced and continued until defibrillation is available.

The haemodynamic consequences of STEMI — pallor, diaphoresis, hypotension, nausea — reflect cardiogenic shock from reduced cardiac output and compensatory sympathetic activation (vasoconstriction, sweating). The Frank-Starling relationship explains why the partially infarcting heart has reduced stroke volume despite elevated end-diastolic pressure (reduced ventricular compliance and contractility). Repeat ECGs and high-sensitivity troponin measurements over 3–6 hours confirm the diagnosis and monitor infarct progression or re-occlusion.