IM2.6-9 | ACS Clinical Evaluation — Summary & Reflection

KEY TAKEAWAYS

Clinical indication: Structured ACS evaluation is indicated for any new, unexplained chest, jaw, arm, or upper abdominal pain. Cannot-miss diagnoses: STEMI, NSTEMI/UA, aortic dissection, PE, tension pneumothorax.

Structured history (SOCRATES + IHD risk factors):
- Central pressure/heaviness, radiation to jaw/arms, onset at rest, duration >20 min, incomplete GTN response, diaphoresis, vomiting → high ACS probability
- Tearing at onset, back radiation, maximal at onset → dissection screen (unequal arm BP, pulse deficits)
- Pleuritic + dyspnoea + tachycardia + thrombophilia risk → PE screen

Focused examination:
- Vital signs: unequal arm BP (dissection), Killip class assignment, RR and SpO2
- Praecordium: S3 (LV failure), S4 (stiff LV), new pansystolic murmur at apex (papillary muscle MR), harsh murmur left sternal border (VSD), pericardial rub
- JVP elevated + clear lungs + hypotension in inferior MI → RV infarction (give fluids, not diuretics)
- Peripheral pulses: pulse deficits (dissection, PAD)

Killip classification: I (no HF) → II (mild HF, basal crepitations, S3) → III (pulmonary oedema) → IV (cardiogenic shock)

Clinical ACS classification:
- Stable angina: exertional, <5 min, complete GTN response
- UA: rest/crescendo, >20 min, incomplete GTN, troponin negative
- NSTEMI: clinically same as UA, troponin positive
- STEMI: severe sustained rest pain >30 min, haemodynamic compromise, diaphoresis, vomiting (inferior)
- Atypical ACS (diabetics, elderly, women): epigastric pain, dyspnoea, jaw pain — ECG and troponin mandatory

REFLECT

Return to the opening scenario: the 55-year-old man with chest pressure, radiation, diaphoresis, and vomiting at 11 PM. Having worked through this module, map your clinical reasoning: which features in the history raise the pre-test probability of STEMI to near-certainty before the ECG arrives? Which examination finding — if present — would make you abandon the plan to give thrombolysis and escalate immediately to CT aortography? And if the ECG were to show inferior ST elevation with an elevated JVP, clear lung fields, and hypotension — what mechanistic explanation would you give for that haemodynamic triad, and how would it change your fluid management? The ability to reason in real time through this cascade — history to examination to differential to ACS classification to immediate management — is the competency this module equips you with.