STEMI ECG Teaching Module: Evolution, Territory and the Occlusions Missed

Module orientation

This module belongs to the acute care strand and is delivered to emergency physicians, cardiology residents, intensivists and catheterisation laboratory teams who make activation decisions out of hours. It assumes fluency with the normal tracing. What it teaches is a triage skill: deciding, within roughly thirty seconds of a tracing landing in your hand, whether a vessel is occluded now. The organising idea is that the electrocardiogram in infarction is a moving picture and the single frame you were handed carries a timestamp you must estimate.

Learning objectives

• Place a tracing on the ischaemia-injury-necrosis timeline and estimate how long the vessel has been shut.
• Assign the culprit territory and predict which vessel and which segment is responsible.
• Use reciprocal depression as confirmatory evidence and explain its absence when it does not appear.
• Recognise the occlusion patterns that do not meet conventional elevation thresholds.
• Distinguish infarct patterns from pericarditis, early repolarisation, hypertrophy and conduction disease.

Block 1 — The timestamp question

Participants are given six tracings from the same patient recorded across twelve hours, shuffled, and asked to place them in order. The exercise teaches the sequence far more durably than a list does, because it forces attention to the transitions rather than to the endpoints.

Earliest is the hyperacute T wave — tall, broad-based, symmetrical and confined to the involved leads, often with the ST segment beginning to lift off the J point. It appears within minutes and it is the phase during which reperfusion salvages the most myocardium, which is why it is also the phase most often dismissed as a normal variant. Injury follows: ST elevation of at least 1 mm in two contiguous limb leads, or at least 2 mm in contiguous precordial leads with age and sex adjustment, classically convex or straightened rather than the smiling concavity of benign elevation. Necrosis then declares itself with pathological Q waves, conventionally at least 40 ms wide and deeper than a quarter of the following R wave; after prompt and successful reperfusion these may never develop. As healing proceeds the ST segment settles while T waves invert, and the chronic tracing retains Q waves, poor R wave progression and sometimes persistent inversion. Persisting elevation weeks later should raise the question of aneurysm formation.

The clinical translation taught here is that a patient whose T waves are hyperacute has more to gain from immediate transfer than one whose Q waves are already formed — a point developed in the STEMI and primary PCI course.

Block 2 — Mapping territory to vessel

Territory mapping is taught as a prediction, since the group will see the angiogram afterwards and can score itself.

Two refinements matter clinically. In inferior infarction, elevation greater in lead III than lead II with depression in lead I favours a right coronary culprit and mandates right-sided leads, because right ventricular involvement changes fluid and nitrate management immediately. Extensive anterior elevation accompanied by new right bundle branch block and fascicular block suggests a proximal occlusion with a large territory and a high risk of pump failure. Angiographic correlation for these predictions is supplied by the clinical ECG interpretation course book.

Block 3 — Reciprocal change as evidence

Reciprocal ST depression in leads electrically opposite the injured territory raises diagnostic confidence substantially, and its presence is one of the most useful discriminators between true occlusion and its imitators. Anterior elevation with inferior depression, and inferior elevation with depression in lead I and aVL, are the two patterns participants must recognise instantly.

The teaching caveat is symmetrical: absence of reciprocal change does not exclude occlusion, particularly in isolated lateral or posterior territories where the opposing leads are poorly represented on a standard twelve-lead recording. In those situations the answer is to obtain additional leads rather than to abandon the diagnosis.

Block 4 — Occlusion without obvious elevation

This block carries the highest yield for both examinations and clinical safety, because the patterns it covers are the ones that get discharged. De Winter’s pattern shows upsloping depression at the J point in the precordial leads with tall symmetrical T waves and represents proximal left anterior descending occlusion despite the absence of elevation. Wellens’ pattern — biphasic or deeply inverted T waves in V2 and V3 in a pain-free patient — signals critical proximal stenosis and predicts anterior infarction if managed conservatively; it should never be stress tested.

Posterior infarction presents as horizontal depression in V1 to V3 with tall R waves and upright T waves, and requires posterior leads to confirm. Widespread depression with elevation in aVR and V1 suggests left main or severe multivessel disease rather than a single occlusion, and the management pathway differs. In the presence of left bundle branch block or ventricular pacing, concordance-based criteria of the modified Sgarbossa type are applied. Isolated right ventricular infarction should be sought whenever inferior changes appear. These patterns are drilled repeatedly in the clinical ECG workshop.

Block 5 — The imitators

The final teaching block builds the discriminating features rather than a list of diagnoses. Acute pericarditis produces diffuse, concave elevation with PR depression, PR elevation in aVR and no reciprocal change or territorial logic. Early repolarisation gives concave elevation with notched J points, is stable over serial tracings and follows no coronary distribution. Left ventricular hypertrophy produces secondary repolarisation change proportional to voltage, discordant with the QRS. Takotsubo syndrome can mimic anterior infarction convincingly and is separated angiographically, not electrocardiographically — a point expanded in the Takotsubo course text. Brugada pattern, hyperkalaemia and ventricular aneurysm complete the set.

The governing rule taught is that a tracing suggesting occlusion in a symptomatic patient should trigger serial recording at short intervals. A single equivocal tracing is a snapshot of a process that is still moving.

Self-check

• Tall symmetrical T waves in V2 to V4 with upsloping J-point depression and ongoing pain. Diagnosis? De Winter’s pattern; treat as proximal left anterior descending occlusion.
• Inferior elevation, greater in III than II, with depression in lead I. Next step? Record right-sided leads to look for right ventricular involvement.
• Which infarct pattern should never be provocatively tested? Wellens’ pattern.
• Diffuse concave elevation with PR depression and no reciprocal change. Most likely diagnosis? Acute pericarditis.
• Absent reciprocal depression in a patient with lateral elevation. Does this exclude occlusion? No; opposing leads are poorly represented in that territory.

How this module is taught in the course

The module runs as a timed pattern-recognition session. Tracings are projected for thirty seconds each and participants commit to activate or observe before the angiogram is revealed; scores are tracked across the session so that individual blind spots surface. The shuffled-timeline exercise opens the class and a mixed set of imitators closes it. Supporting reading is the ECG course book, with the wider acute pathway covered in the first hour cardiac emergency course and the diagnosis and imaging collection. A continuous reference treatment of the same material is published as the article on ECG changes in acute myocardial infarction.

Module FAQ

Is this module suitable for non-cardiologists?

Yes, and emergency and acute medicine teams take it routinely. The activation decision is made most often by clinicians who are not cardiologists.

How many tracings are worked through?

Around sixty in the taught session, with a further archive released afterwards for self-directed drilling.

Does the module cover troponin interpretation?

Only where it changes the electrocardiographic decision. The teaching principle is that a tracing suggesting occlusion should not wait for a biomarker result.

What about paced rhythms?

Covered in the fourth block using concordance-based criteria, since ventricular pacing is an increasingly common obstacle in older patients.

Reviewed by Dr A M Thirugnanam, MD, MSICP, FSCAI, Ph.D., Senior Interventional Cardiologist — who selects the tracings for this module from consecutive primary angioplasty activations and pairs each with its angiogram.