STEMI Recognition & Coronary Territories

In STEMI, a coronary artery occludes. The myocardium it feeds loses perfusion. Within minutes, the injured cells fail to repolarize normally. That difference between injured and healthy tissue creates a current of injury in the ST segment. Leads facing the injured wall show ST elevation. Leads facing the opposite wall show reciprocal ST depression.

The ECG shows which wall is injured, so the pattern points to the culprit vessel. A ST change is only as useful as its distribution. Look for one territory, a convex shape and reciprocal change. That is the pattern that drives reperfusion decisions.

1. Identify the J point in each lead as the end of the QRS, on a 12-lead at 25 mm/s with 10 mm/mV.
2. Set the baseline at the TP segment, or the PR segment when the TP is not usable.
3. Measure the ST deviation at the J point in each lead, applying the sex and age threshold to V2–V3.
4. Map the contiguous leads that meet threshold to one territory, then check the reciprocal leads.
5. Add V4R and V7–V9 when the inferior or posterior picture is present.
6. Compare with the prior ECG when one exists.

Start with the leads that meet criteria, then name the territory. The culprit vessel is typical, not certain. Coronary dominance and collateral supply change the map.

• Inferior STEMI: Record V4R and V7–V9 before any preload-reducing drug. You're looking for right ventricular and posterior involvement.
• Anterior STEMI: STE in I and aVL with V1–V4 points to a larger proximal LAD territory. Inferior reciprocal depression backs up the call.
• Posterior STEMI: At least 1 mm of ST depression in V1–V3, with a dominant R wave in V2, is the front view of posterior STE. Confirm with V7–V9.

Reciprocal ST depression is the opposite wall's picture of the culprit injury. It's the main feature that separates regional occlusion from pericarditis and early repolarization. Those usually lack it.

• Inferior STE: depression in I and aVL (the classic pair)
• Anterior STE: depression in II, III and aVF
• Lateral STE: depression in III and aVF
• STE in aVR with diffuse depression: STE in aVR (often with V1) plus widespread ST depression in I, II and V4–V6 points to left main or multivessel ischemia. It doesn't meet single-territory STEMI criteria. It is high-risk NSTE-ACS. Call cardiology early and seek urgent angiography per protocol, especially with hypotension or ongoing pain.

The ECG changes over time, and the stage changes the call. Early changes can come before classic STE. Late changes can look like old infarction.

• Hyperacute T waves: Broad, tall T waves that show up first, often before STE. The 2022 ACC pathway describes them as broad, asymmetric or peaked.
• ST elevation: Develops as the injury current forms. In the territory, it is convex (tombstone) or straight.
• Q waves: Develop in the territory during the acute phase. Their presence alone doesn't date the infarct.
• T-wave inversion: Follows the elevation. The ST segment may normalize while the T inversion stays.
• Old infarct: Persistent Q waves, resolved STE, and inverted or normal T waves. Compare with the prior ECG.

Some patterns point to occlusion even though millimeter STEMI criteria are not met. The 2022 ACC Expert Consensus Decision Pathway counts posterior STEMI, LBBB or paced rhythm with Sgarbossa criteria, de Winter sign and hyperacute T waves as equivalents. For the full criteria, go to the ST Segment & T Wave page. For occlusion without classic STE, see the STEMI Equivalents & Occlusion Signs page.

• De Winter sign: Upsloping ST depression above 1 mm at the J point in precordial leads, with tall, symmetric T waves. It's described with proximal LAD occlusion.
• Posterior pattern: ST depression in V1–V3 with an upright T. Confirm with at least 0.5 mm of STE in V7–V9.
• LBBB or paced rhythm: Apply the Sgarbossa criteria. New LBBB alone is not a STEMI equivalent.
• Wellens pattern (high risk, not a STEMI): Characteristic precordial ST-T changes that point to a critical proximal LAD stenosis, without meeting STEMI criteria. The original report recommends urgent angiography and revascularization when possible.

Acute pericarditis and early repolarization are the main mimics. Both can meet millimeter thresholds, so millimeters alone won't separate them. Look at distribution, morphology and reciprocal change.

Other STEMI Mimics

• LVH: high voltage with discordant STE in V1–V3
• Brugada pattern: coved STE with a negative T wave in V1–V2
• Ventricular aneurysm: persistent STE with Q waves that does not evolve
• Takotsubo: wide-territory change after stress; echo wall motion crosses coronary territories
• Hyperkalemia: peaked T waves with QRS widening can mimic de Winter; check potassium

Artifact & Lead Misplacement

• Limb-lead reversal: changes axis and can create apparent lead I or aVR changes
• Precordial electrodes placed high: can mimic STE in V1–V2
• Tremor or motion: can mimic ST deviation or VT and VF

The ECG sets the pathway. A STEMI or a STEMI equivalent starts reperfusion. A high-risk pattern starts urgent cardiology review. Every drug and threshold below runs on local protocols and online medical direction.

Doses vary by protocol; follow local protocols and medical direction.

Pediatrics

• Pattern: Repolarization varies with age and heart rate. Use age-based pediatric ECG references.
• Cause: In children, ST changes are more often non-ischemic (myocarditis, pericarditis, early repolarization). Think about coronary anomalies and Kawasaki-related coronary disease when suspected.
• Action: Contact pediatric cardiology or medical direction early. Check pediatric vital signs for rate and BP norms.
• Drugs: Pediatric dosing for nitrates, antiplatelets and fibrinolytics is not established. Use weight-based dosing and specialist input.

Other Populations

• Older adults and women: Presentations are often atypical. ST depression may be the only finding.
• Pacemaker or ICD: Paced rhythms need the Sgarbossa criteria. Get a prior ECG.
• Heart transplant: Denervated hearts may have blunted symptoms and abnormal ST-T patterns. Compare with prior tracings.
• Pregnancy: ST-T changes can be normal. In pregnancy or the peripartum period, spontaneous coronary artery dissection should be considered (see reference 10). Involve cardiology and obstetrics early. Follow medical direction for reperfusion.

In transport, a clean tracing is the only reliable input you have. Reduce motion before you record.

1. Identify the J point and TP baseline in each lead before reading any shape.
2. Measure the STE or STD at the J point and note its shape: convex, concave, horizontal or downsloping.
3. Map the distribution to a territory using the lead-group table.
4. Check the reciprocal leads and the STEMI equivalents: de Winter, posterior, Sgarbossa.
5. Add V4R and V7–V9 when the inferior or posterior picture is present.
6. Check the mimics: concave STE with PR depression (pericarditis), early repolarization, LVH, artifact.
7. Decide the pathway and repeat the 12-lead every 15–30 min in ongoing symptoms.

Common Pitfalls

• Waiting for classic STE while a de Winter or posterior pattern is already on the tracing
• Calling isolated V1–V3 depression an NSTEMI without checking V7–V9
• Applying STEMI thresholds in LBBB or a paced rhythm instead of the Sgarbossa criteria
• Giving nitrates to a hypotensive patient with inferior changes and no V4R
• Treating one tracing as the whole answer while symptoms persist
• Missing bradyarrhythmia or heart block in inferior STEMI. Check rate and rhythm continuously, have pacing and atropine ready per protocol, and place pads early when block is likely
• Assuming a fast effect from an oral P2Y12 agent. Opioids such as morphine slow gastric emptying and can delay P2Y12 absorption. Follow protocol on timing
• Transporting to the nearest hospital. When the protocol allows prehospital activation, bypass a non-PCI hospital for a PCI-capable center