ECG Basic – ST Segment
ST Segment Interpretation
Learn how to identify and measure the ST segment, recognize patterns of elevation and depression, and distinguish acute ischaemic changes from common non-ischaemic mimics.
Learning objectives
1. What is the ST segment?
The ST segment is the portion of the ECG tracing that extends from the end of the QRS complex to the beginning of the T wave. Its starting point is the J point, where ventricular depolarisation ends and the ST segment begins.
At the cellular level, the ST segment broadly corresponds to the plateau phase of the ventricular action potential. In a normal tracing it is usually close to the isoelectric baseline. Displacement above or below baseline may reflect myocardial ischaemia or injury, but it can also arise from a range of structural, electrical, inflammatory, metabolic, or neurological conditions.
The J point is the reference point for measuring ST displacement. Do not confuse the J point with the beginning of the QRS complex or the peak of the T wave.
How to assess the ST segment
Confirm the tracing. Check calibration, paper speed, lead labels, artefact, and baseline stability. Standard ECG calibration is commonly 25 mm/s and 10 mm/mV.
Choose the baseline. The TP segment is generally the preferred isoelectric reference when it can be identified reliably. The PR segment may be used when the TP segment is not clear, while remembering that pericardial or atrial abnormalities can shift it.
Locate the J point. Identify the transition from the terminal QRS complex to the ST segment.
Measure displacement. Measure vertically from the selected baseline to the J point, then assess the contour and the subsequent ST-T morphology.
Compare leads and time points. Look for changes in anatomically contiguous leads, reciprocal changes, prior ECGs, and dynamic evolution on serial tracings.
| ECG paper measurement | At 25 mm/s | At 10 mm/mV |
|---|---|---|
| 1 small square (1 mm) | 0.04 seconds | 0.1 mV |
| 1 large square (5 mm) | 0.20 seconds | 0.5 mV |
2. ST-segment elevation
ST elevation describes a shift of the ST segment above the isoelectric baseline. In a patient with a compatible clinical presentation, new ST elevation in contiguous leads can indicate acute coronary occlusion and requires urgent assessment. However, ST elevation is not synonymous with acute myocardial infarction: several non-ischaemic conditions can produce similar appearances.
STEMI ECG thresholds
The 2023 ESC acute coronary syndrome guideline defines ECG findings suggestive of ongoing coronary occlusion as new J-point elevation in at least two contiguous leads, using the thresholds below in the appropriate clinical context and in the absence of LVH or LBBB:
| Lead group | Threshold |
|---|---|
| Leads other than V2–V3 | ≥1 mm |
| V2–V3, men younger than 40 years | ≥2.5 mm |
| V2–V3, men 40 years or older | ≥2 mm |
| V2–V3, women (any age) | ≥1.5 mm |
These cut-offs support ECG classification; they do not replace clinical assessment. Acute coronary occlusion may be present without meeting conventional STEMI thresholds. Persistent symptoms, haemodynamic instability, dynamic ECG changes, and occlusion-equivalent patterns require urgent clinical evaluation.
ST elevation morphology
ST elevation may appear concave, convex, or relatively straight. Although morphology can guide the differential diagnosis, no single contour reliably rules myocardial infarction in or out.
Contiguous lead territories
| Territory | Typical leads | Additional leads to consider |
|---|---|---|
| Septal | V1–V2 | — |
| Anterior | V3–V4 | — |
| Lateral | I, aVL, V5–V6 | High lateral: I, aVL |
| Inferior | II, III, aVF | Right-sided leads V3R–V4R if RV involvement suspected |
| Posterior | V7–V9 | Standard ECG may show reciprocal ST depression in V1–V3 |
Inferior, lateral, anterior, septal, right ventricular, and posterior territories are useful descriptive patterns rather than perfect maps of a single coronary artery. Coronary anatomy and individual perfusion territories vary.
Important ST elevation patterns
Acute coronary occlusion / STEMI
New ST elevation in contiguous leads, often with reciprocal depression in electrically opposite leads. Q waves may develop, but their absence early in the presentation does not exclude acute infarction.
Coronary vasospasm
Transient, localised ST elevation can occur during episodes of chest pain and may resolve with relief of spasm. The ECG alone may not reliably distinguish spasm from acute coronary thrombosis.
Acute pericarditis
Often produces widespread concave ST elevation with PR-segment depression. Reciprocal ST depression and PR elevation may be seen in aVR and sometimes V1.
Early repolarisation pattern
May show mild, often concave ST elevation with J-point notching or slurring, particularly in precordial leads. Clinical context and comparison with previous ECGs are essential.
Brugada pattern
Type 1 morphology includes coved ST elevation in the right precordial leads, followed by a negative T wave. This is a channelopathy pattern associated with risk of ventricular arrhythmia.
Takotsubo syndrome
Can mimic acute MI with chest pain, ST elevation or T-wave inversion, and troponin elevation. Echocardiography demonstrates characteristic regional wall-motion abnormalities.
3. ST-segment depression
ST depression is a downward shift of the ST segment below the isoelectric baseline. It may represent subendocardial ischaemia, reciprocal change from ST elevation in another territory, or a secondary repolarisation abnormality.
Three common morphologies
New horizontal or downsloping ST depression of at least 0.5 mm in two contiguous leads is an ECG finding suggestive of myocardial ischaemia in the Fourth Universal Definition of Myocardial Infarction, although lesser changes may still be clinically meaningful in a high-risk context.
Important patterns associated with ST depression
Subendocardial ischaemia
May produce ST depression across several leads, often prominent in I, II, aVL, and V4–V6. Widespread ST depression with ST elevation in aVR and/or V1 may indicate extensive ischaemia, including left main or multivessel disease, particularly in an unstable patient.
Reciprocal change
ST depression in leads electrically opposite an area of acute ST elevation. It may be an important clue when the primary elevation is subtle or overlooked.
Posterior infarction
Posterior occlusion may appear as horizontal ST depression in V1–V3, often with a relatively tall R wave and upright T wave. Record V7–V9 when suspicion remains.
De Winter pattern
Upsloping ST depression at the J point in the precordial leads with tall, symmetrical T waves is a recognised pattern associated with acute LAD occlusion and should prompt urgent assessment.
Common non-acute-coronary causes
- Digoxin effect: characteristic downsloping, “scooped” ST depression.
- Hypokalaemia: ST depression with T-wave flattening or inversion, prominent U waves, and apparent QU prolongation.
- Supraventricular tachycardia: rate-related ST depression can occur and may resolve after termination of tachycardia; persistent changes still require clinical assessment.
- RBBB or RVH: secondary ST depression and T-wave inversion may occur in right precordial leads.
- LBBB, LVH, or ventricular pacing: secondary repolarisation changes may cause discordant ST shifts.
4. Distinguishing ischaemia from common mimics
ST-segment deviation should never be interpreted from contour alone. Consider the distribution of changes, associated PR and T-wave findings, QRS morphology, symptoms, haemodynamic state, previous ECGs, and serial evolution.
| Condition | Typical ECG clues described in the source | Interpretive caution |
|---|---|---|
| Acute MI / STEMI | Localised ST elevation in contiguous leads; reciprocal ST depression may be present. Concave, convex, or straight contours can occur. | Do not exclude occlusion because the ST segment is concave or because Q waves are absent. |
| Pericarditis | Widespread concave ST elevation, PR depression; reciprocal ST depression and PR elevation in aVR and V1. | Spodick sign (downsloping TP segment) may support the diagnosis but is not independently diagnostic. |
| Early repolarisation | Mild ST elevation, often precordial, tall T waves, and J-point notching or slurring (“fish-hook”). | Compare prior ECGs and assess symptoms; a benign pattern must not be assumed in an acute presentation. |
| LBBB / ventricular pacing | Appropriate discordance: ST-T direction generally opposite to the dominant QRS direction. | Standard ST-elevation criteria are difficult to apply; symptoms and validated approaches to occlusion assessment matter. |
| LVH | ST elevation may accompany deep S waves in V1–V3; ST depression and T inversion may accompany tall lateral R waves. | Secondary repolarisation changes can obscure superimposed acute ischaemia. |
| Ventricular aneurysm | Persistent ST elevation with deep Q waves after previous MI; T-wave inversion may coexist. | Compare with previous ECGs and assess the clinical timeline. |
| Brugada pattern | Coved ST elevation in V1–V2 with a right bundle branch block-like appearance. | Recognise the pattern and assess arrhythmic risk; do not label as STEMI solely from the elevation. |
| Raised intracranial pressure | May cause ST elevation or depression; widespread deep T-wave inversion (“cerebral T waves”) is more typical. | Consider neurological context and other causes of repolarisation abnormalities. |
| Takotsubo syndrome | ST elevation or T-wave inversion, chest pain, and possible troponin rise; characteristic regional wall-motion abnormality on echocardiography. | It is a STEMI mimic and requires urgent assessment to exclude coronary occlusion. |
Other reported causes of ST elevation
The supplied ECG reference also lists pulmonary embolism or acute cor pulmonale, acute aortic dissection involving a coronary artery, hyperkalaemia, sodium-channel-blocking drugs with QRS widening, J waves in hypothermia or hypercalcaemia, changes after electrical cardioversion, myocarditis, cardiac tumours, and abdominal conditions such as pancreatitis or gallbladder disease.
Reciprocal ST changes
| Primary ST elevation | Common reciprocal lead(s) |
|---|---|
| Inferior STEMI (II, III, aVF) | aVL (sometimes I) |
| High lateral STEMI (I, aVL) | III and aVF (sometimes II) |
| Posterior infarction | V1–V3 may show ST depression as a mirror-image pattern |
When ST depression is confined to inferior or high lateral leads, actively inspect the electrically opposite leads for subtle ST elevation. What appears to be isolated depression may be reciprocal change.
5. A systematic approach to ST-segment interpretation
- Start with the patient. Assess symptoms, onset and duration, haemodynamic status, and clinical probability of acute coronary syndrome.
- Check technical quality. Confirm calibration, lead placement, artefact, and baseline stability.
- Find the J point. Measure ST displacement relative to a stable isoelectric reference, preferably the TP segment when clear.
- Assess the pattern. Identify elevation or depression, morphology, magnitude, and whether changes occur in contiguous leads.
- Search for reciprocal changes. Review electrically opposite leads and consider posterior or right ventricular involvement.
- Consider mimics and secondary changes. Review QRS width and voltage, pacing, LVH, bundle branch block, pericarditis, electrolyte disturbance, and other clinical conditions.
- Compare and repeat. Retrieve prior ECGs and repeat the ECG when symptoms persist, recur, or evolve. Add right-sided or posterior leads when indicated.
- Act on the whole picture. A non-diagnostic initial ECG does not exclude acute coronary occlusion. Escalate promptly when clinical suspicion remains high.
In suspected acute coronary syndrome, obtain and interpret a 12-lead ECG promptly. Ongoing ischaemic symptoms, instability, dynamic changes, or an occlusion-equivalent pattern warrant urgent senior/cardiology assessment and reperfusion-pathway consideration according to local protocols. Do not delay escalation while waiting for a textbook pattern to appear.
Posterior and right ventricular leads
Posterior leads V7–V9
Consider when there is ongoing suspicion of posterior occlusion, especially with ST depression in V1–V3 or an inconclusive standard ECG. The 2023 ESC guideline recommends a low threshold for supplemental leads in this setting.
Right-sided leads V3R–V4R
Record in suspected inferior MI when right ventricular involvement is a concern. Right-sided ST elevation may be transient, so early recording is useful.
6. Key takeaways
- The ST segment extends from the J point to the onset of the T wave and is normally close to the isoelectric baseline.
- Measure ST displacement at the J point against a stable baseline, preferably the TP segment when identifiable.
- ST elevation can be concave, convex, or straight in acute MI; morphology alone cannot exclude infarction.
- New J-point elevation in at least two contiguous leads should be assessed using lead- and sex/age-specific thresholds in the appropriate clinical setting.
- Horizontal or downsloping ST depression may indicate ischaemia; reciprocal changes and posterior infarction are important patterns to recognise.
- Pericarditis, early repolarisation, LVH, bundle branch block, pacing, Brugada pattern, Takotsubo syndrome, neurological disease, and metabolic disturbances can mimic or alter ST segments.
- Clinical context, serial ECGs, comparison with prior tracings, and supplemental leads are essential when the first ECG is inconclusive.
References
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