ACS recognition and ECG localisation

Key Takeaways

  • New left bundle branch block alone does not diagnose STEMI.

  • Record right-sided leads when inferior STEMI raises concern for right ventricular infarction.

  • Normal initial troponin or ECG does not exclude evolving ACS.

Last updated: October 2026

Acute Coronary Syndromes & ECG Localization

Acute coronary syndromes (ACS) represent a critical continuum of myocardial ischaemia resulting from acute disruption of an atherosclerotic plaque, subsequent platelet aggregation, and intracoronary thrombus formation. Rapid clinical triage, electrocardiographic localization, and adherence to time-critical reperfusion pathways are essential competencies for practice in Australian emergency and acute medical settings.


Spectrum of Acute Coronary Syndromes

The clinical spectrum of ACS is traditionally subdivided based on electrocardiographic findings and circulating biomarkers of myocardial necrosis:

  1. STEMI: An ischaemic presentation with a qualifying ST-elevation or occlusion-equivalent ECG pattern needs immediate reperfusion assessment without waiting for troponin. ECG categories do not precisely define transmural versus subendocardial histology; occlusion can occur without conventional ST elevation.
  2. NSTEMI: Acute myocardial injury with a rise/fall in troponin and evidence of ischaemia, without a qualifying ST-elevation pattern. Troponin elevation alone is not proof of coronary thrombosis. Serial ECGs, symptoms and risk assessment determine urgency.
  • Unstable angina: Ischaemic symptoms without biomarker evidence of acute myocardial injury. Serial ECGs and high-sensitivity troponin are needed because an initially normal result does not establish this diagnosis.

Australian Biomarker Pathways

Australian guidelines endorsed by the National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (NHFA/CSANZ) prioritize high-sensitivity cardiac troponin (hs-cTnI or hs-cTnT) assays. Accelerated diagnostic protocols utilize validated 0/1-hour or 0/2-hour rapid triage algorithms:

  • Troponin rule-out: Apply the validated assay-specific accelerated pathway, accounting for onset, serial change and clinical/ECG findings. Very early presentation or ongoing concerning symptoms may require further testing. A low initial troponin is not permission to ignore an occlusion ECG pattern.
  • Troponin rule-in: A substantial rise/fall supports acute injury, but myocardial infarction also requires evidence of ischaemia. Evaluate ACS risk and other causes such as sepsis, myocarditis or renal disease; a single elevated result does not mandate angiography for everyone.

Coronary Anatomy and 12-Lead ECG Localization

Accurate lead localization allows direct correlation between surface ECG leads, anatomical myocardial regions, and the culprit epicardial coronary artery:

  • Anteroseptal (V1–V4): Supplied by the Left Anterior Descending (LAD) coronary artery. Occlusion leads to loss of anterior wall contractility, anterior Q waves, and significant reduction in left ventricular ejection fraction.
  • Extensive Anterior / Anterolateral (V1–V6, I, aVL): Supplied by the proximal LAD or the Left Main Coronary Artery (LMCA). Carries the highest risk of acute pulmonary oedema, cardiogenic shock, and life-threatening ventricular arrhythmias.
  • Lateral (I, aVL, V5, V6): Supplied by the Left Circumflex (LCx) artery or the diagonal branch of the LAD. Isolated high lateral infarction manifests as ST elevation in leads I and aVL with reciprocal ST depression in leads III and aVF.
  • Inferior (II, III, aVF): Supplied by the Right Coronary Artery (RCA) in approximately 85% to 90% of individuals (right-dominant circulation) and by the Left Circumflex (LCx) in 10% to 15% (left-dominant circulation). In RCA occlusion, ST elevation in lead III typically exceeds ST elevation in lead II (ST↑III>ST↑IIST\uparrow \text{III} > ST\uparrow \text{II}), accompanied by ST depression in lead I and aVL.

Right Ventricular Myocardial Infarction (RVMI)

Approximately 30% to 50% of inferior STEMIs involve the right ventricle due to proximal RCA occlusion proximal to the acute marginal branches.

  • Diagnostic Rule: In all patients presenting with acute inferior STEMI, a right-sided 12-lead ECG (leads V1R to V6R) must be recorded immediately.
  • ECG Hallmark: ST-segment elevation ≥1.0 mm\ge 1.0\text{ mm} (or ≥0.5 mm\ge 0.5\text{ mm} in older adults) in lead V4R is the single most sensitive and specific marker of acute RV involvement.
  • Haemodynamic Triad: Hypotension, elevated jugular venous pressure (often with Kussmaul sign: a paradoxical rise in JVP during inspiration), and completely clear lung fields on auscultation.
  • RV infarction with hypotension: Stop nitrates; give a cautious small crystalloid bolus with reassessment of perfusion and lungs. Avoid interventions worsening hypotension or excessive preload reduction, and obtain urgent reperfusion support. RV failure is not a reason for unlimited fluid or a permanent ban on all beta-blockade after stabilisation.

True Posterior Myocardial Infarction

Occlusion of the distal circumflex artery or the posterior descending artery (PDA) causes transmural ischaemia of the posterior wall of the left ventricle. Because standard precordial leads look at the posterior wall from the anterior chest, they record electrical activity in reverse (mirror-image changes):

  • Standard Leads (V1–V3): Horizontal ST-segment depression, tall and wide R waves (R/S ratio>1.0R/S \text{ ratio} > 1.0), and upright, tall T waves.

  • Confirmation: Place posterior leads V7 (left posterior axillary line), V8 (tip of left scapula), and V9 (left paraspinal border) at the fifth intercostal space. ST elevation ≥0.5 mm\ge 0.5\text{ mm} in leads V7 to V9 confirms acute posterior STEMI and represents a STEMI-equivalent requiring immediate reperfusion.

  • Left bundle branch block or ventricular pacing: Concordant ST elevation, concordant anterior ST depression, or disproportionately discordant elevation using the modified Sgarbossa approach supports acute coronary occlusion. The modified proportional criterion is distinct from the original weighted score. Seek urgent expert ECG review; new LBBB alone is not diagnostic of STEMI.

  1. Concordant ST elevation ≥1 mm\ge 1\text{ mm} in any lead with a positive QRS complex (Score 5).
  2. Concordant ST depression ≥1 mm\ge 1\text{ mm} in leads V1, V2, or V3 (Score 3).
  3. Excessively discordant ST elevation characterized by an ST/S ratio ≤−0.25\le -0.25 (the ST elevation measured at the J-point is at least 25% of the preceding negative S-wave amplitude) (Smith modification).

Primary references (checked 7 October 2026): Heart Foundation ACS guideline.

Test Your Knowledge

A 62-year-old man presents with persistent severe retrosternal chest pressure lasting two hours. His standard 12-lead ECG reveals no ST-segment elevation, but shows 2 mm of horizontal ST-segment depression in leads V1, V2, and V3, accompanied by prominent R waves (R/S ratio > 1) and upright, broad T waves in the same leads. Repeat troponin I at 1 hour is significantly elevated above the 99th percentile. Which of the following is the most appropriate next diagnostic step?

A

Record posterior ECG leads V7 through V9 to evaluate for true posterior ST elevation

B

Arrange an urgent outpatient exercise stress echocardiogram within two weeks

C

Perform immediate transthoracic echocardiography to assess aortic root dimensions

D

Discharge home with an ambulatory 24-hour Holter monitor and general practice review

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