Chest Pain in a 58-Year-Old Diabetic with Atypical Features
A 58-year-old woman with type 2 diabetes and hypertension presents to a rural clinic with 3 hours of epigastric discomfort and nausea, which she attributes to food. She has no chest pain. She is clammy and anxious. Blood pressure is 100/60 mmHg, pulse 105/min regular, respiratory rate 22/min, oxygen saturation 94% on room air, temperature 36.8°C. Heart sounds are soft, lung bases are clear, and the abdomen is soft with mild epigastric tenderness. The clinic has a 12-lead ECG machine, aspirin, glyceryl trinitrate, and a defibrillator, but no troponin assay and no catheter laboratory; the nearest percutaneous coronary intervention centre is 90 minutes away by road. An ECG shows 2 mm ST elevation in leads II, III and aVF.
1. Explain why this presentation is easily misdiagnosed and how the ECG findings localise the problem.
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This is an inferior ST-elevation myocardial infarction presenting atypically. Several factors conspire to mislead:
- Diabetes: autonomic neuropathy blunts anginal pain, so ischaemia presents as epigastric discomfort, nausea, sweating or breathlessness rather than classic central chest pain.
- Epigastric focus: inferior ischaemia commonly produces epigastric pain and nausea, and the mild epigastric tenderness invites a gastrointestinal label.
- Female sex and older age: women more often present with atypical symptoms, and the combination of nausea, clamminess and anxiety is easily dismissed.
- Haemodynamic clues: hypotension (100/60), tachycardia and clamminess suggest a developing cardiogenic or vagally mediated component, not a benign cause.
The ECG localises the infarct: leads II, III and aVF face the inferior wall, supplied by the right coronary artery in most people (or the circumflex). ST elevation in these leads indicates transmural inferior injury. I would also look for reciprocal ST depression in I and aVL, and for right ventricular involvement (ST elevation in V1 or V4R) or posterior extension (ST depression in V1–V3), because right ventricular infarction changes management - nitrates and diuretics can cause profound hypotension.
2. The clinic has no troponin and no catheter laboratory. Outline your immediate management and the decisions you must make before and during transfer.
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Immediate priorities follow an acute coronary syndrome pathway while arranging reperfusion:
- Recognise and treat as STEMI. Aspirin 300 mg chewed (unless truly contraindicated), and a P2Y12 inhibitor if available and not contraindicated. Oxygen only if hypoxic (saturation <90%); she is at 94%, so routine high-flow oxygen is not indicated.
- Assess for right ventricular involvement before nitrates. With hypotension and tachycardia, give glyceryl trinitrate cautiously or not at all until right ventricular infarction is excluded; inferior MI with right ventricular involvement can crash with nitrates. Fluids may be needed if right ventricular infarction is present.
- Arrange urgent transfer for primary PCI, aiming for first medical contact-to-device time within the system's target; call the PCI centre, activate the pathway, and send the ECG. If transfer time would exceed the acceptable window for primary PCI, consider pre-hospital or clinic fibrinolysis if there are no contraindications - this is the key judgement given the 90-minute road transfer and the absence of on-site troponin.
- Treat complications: have the defibrillator attached; treat bradyarrhythmias or heart block (common in inferior MI) with atropine if symptomatic; monitor blood pressure.
- Document and communicate the diagnosis, drugs given, times, and the ECG findings to the receiving team. Do not wait for troponin to act - the ECG is diagnostic here.
3. Six hours later, before transfer is complete, she becomes more hypotensive (80/50 mmHg) with a raised jugular venous pressure and clear lungs. What is your differential and immediate approach?
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The combination of hypotension, raised JVP and clear lungs points to a mechanical or right-sided problem rather than pulmonary oedema:
- Right ventricular infarction: common with inferior MI; the right ventricle fails to pump, so JVP rises while lungs stay clear. Treat with careful fluid loading and avoid nitrates and diuretics.
- Cardiogenic shock from extensive infarction: possible, but usually with pulmonary congestion; still must be considered.
- Mechanical complications: acute mitral regurgitation from papillary muscle rupture, or ventricular septal rupture - both can cause shock, often with a new murmur; they require urgent echocardiography and surgical referral.
- Bradyarrhythmia or heart block: check the rhythm and rate; inferior MI often causes atrioventricular block.
- Tension pneumothorax or pericardial tamponade: less likely here but part of any sudden deterioration.
Immediate approach: ABCDE, attach monitor, obtain a 12-lead ECG and, if available, bedside echo; give a cautious fluid challenge if right ventricular infarction is suspected; stop nitrates; involve the receiving cardiology team urgently and expedite transfer, since mechanical complications and refractory shock need tertiary care. The judgement is to avoid reflexively treating hypotension with diuretics when the lungs are clear.