Friday, March 27, 2015

The ST Segment in ECG supported by Video:

The ST Segment in ECG

The ST segmentis a flat, isoelectric part of ECG in between the ending from the S wave (J point) and the start of the T wave.
It signifies the actual interval in between ventricular depolarization and repolarization.
The most significant reason for ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.


Causes of ST Segment Elevation:

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  • Acute myocardial infarction
  • Coronary vasospasm (Printzmetal’s angina)
  • Pericarditis
  • Benign early repolarization
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Ventricular aneurysm
  • Brugada syndrome
  • Ventricular paced rhythm
  • Raised intracranial pressure

Morphology of the Elevated ST segment

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Myocardial Infarction
Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology as follows

ST Segment Morphology in Other Conditions:

PericarditisBERLBBBLV aneurysmBrugada

Patterns of ST Elevation

Acute ST elevation myocardial infarction (STEMI)

Causes ST segment elevation and Q-wave formation in contiguous leads, either:
  • Septal (V1-2)
  • Anterior (V3-4)
  • Lateral (I + aVL, V5-6)
  • Inferior (II, III, aVF)
  • Right ventricular (V1, V4R)
  • Posterior (V7-9)
There is usually reciprocal ST depression in the electrically opposite leads. For example, STE in the high lateral leads I + aVL typically produces reciprocal ST depression in lead III (see example below)..
anterior STEMI evolving
Anterolateral STEMI

Coronary Vasospasm (Prinzmetal’s angina)

This will cause a design of ST elevation that's very like acute STEMI - i.e. localized ST elevation with reciprocal ST depression happening throughout attacks of chest pain. Even so, unlike acute STEMI the ECG changes are usually transient, reversible with vasodilators and never commonly ASSOCIATED with myocardial necrosis. It might be difficult to distinguish both of these situations based on the ECG alone.


Pericarditis will cause popular concave  ST segment elevation together with PR segment depression in several leads, usually including I, II, III, aVF, aVL, and V2-6. There's reciprocal ST depression as well as PR elevation in leads aVR and V1. Spodick’s sign - a downward sloping TP segment - can also be seen.


  • Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with depressed PR segments.
  • There is reciprocal ST depression and PR elevation in aVR.
  • Spodick’s sign is present.

Benign Early Repolarization

BER will cause slight ST elevation along with tall T-waves mostly within the precordial leads. Is really a normal variation commonly observed in youthful, healthy and balanced patients. There's frequently notching from the J-point - the “fish-hook” pattern. The actual ST changes might be much more prominent at more slowly heart rates and also disappear in the existence of tachycardia.

Benign Early Repolarization
  • There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the “fish-hook” pattern)

Left Bundle Branch Block

In left bundle branch block, the ST segments and also T waves reveal “appropriate discordance”  i.e. they're directed reverse towards the essential vector of the QRS complex. That creates ST elevation and upright T waves in leads with a negative QRS complex (predominant S wave), whilst developing ST depression as well as T wave inversion in leads along with a positive QRS complex (dominant R wave).

Left Bundle Branch Block
  • Note the ST elevation in leads with deep S waves — most apparent in V1-3.
  • Also note the ST depression in leads with tall R waves — most apparent in I and aVL.

Left Ventricular Hypertrophy

LVH leads to a very similar pattern of repolarization abnormalities as LBBB, with ST elevation within the leads with deep S-waves (usually V1-3) as well as ST depression/T-wave inversion in the leads along with tall R waves (I, aVL, V5-6).
Left Ventricular Hypertrophy
  • Deep S waves with ST elevation in V1-3
  • ST depression and T-wave inversion in the lateral leads V5-6
  • Note in this this case there is also right axis deviation, which is unusual for LVH and may be due to ASSOCIATED left posterior fascicular block.

Ventricular Aneurysm

This is an ECG pattern for residual ST elevation and deep Q waves observed in affected individuals with past myocardial infarction. It's ASSOCIATED with extensive myocardial injury and paradoxical movement of the left ventricular wall during systole.

Ventricular Aneurysm
  • There is ST elevation with deep Q waves and inverted T waves in V1-3.
  • This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI.

Brugada Syndrome

This in an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.

Brugada syndrome
  • There is ST elevation and partial RBBB in V1-2 with a coved morphology — the “Brugada sign”.

Ventricular Paced Rhythm

Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.
AV sequential pacing 1
AV Sequential Pacing

Raised Intracranial Pressure

Raised ICP (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis. More commonly, raised ICP is ASSOCIATED with widespread, deep T-wave inversions (“cerebral T waves”).

ST elevation due to traumatic brain injury
  • Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury.

Less Common Causes of ST segment Elevation

  • Pulmonary embolism and acute cor pulmonale (usually in lead III)
  • Acute aortic dissection (classically causes inferior STEMI due to RCA dissection)
  • Hyperkalaemia
  • Sodium-channel blocking drugs (secondary to QRS widening)
  • J-waves (hypothermia, hypercalcaemia)
  • Following electrical cardioversion
  • Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease

Transient ST elevation after DC cardioversion from VF
Typical Osborn waves
J waves in hypothermia simulating ST elevation

Causes of ST Depression

  • Myocardial ischaemia / NSTEMI
  • Reciprocal change in STEMI
  • Posterior MI
  • Digoxin effect
  • Hypokalaemia
  • Supraventricular tachycardia
  • Right bundle branch block
  • Right ventricular hypertrophy
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Ventricular paced rhythm

 Morphology of ST Depression

  • ST depression can be either upsloping, downsloping, or horizontal.
  • Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria).
  • Upsloping ST depression in the precordial leads with prominent “De Winter’s” T waves is highly specific for occlusion of the LAD.
  • Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction.
  • Posterior MI manifests as horizontal ST depression in V1-3 and is ASSOCIATED with upright T waves and tall R waves.

ST depression: upsloping (A), downsloping (B), horizontal (C)
ST segment morphology in myocardial ischaemia
Reciprocal change
ST elevation in IIIReciprocal change in aVL
ST segment morphology in posterior MI

Patterns of ST depression

Myocardial Ischaemia

ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6 plus leads I, II and aVL. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion and severe triple vessel disease.
NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought. 

LMCA Occlusion

Reciprocal Change

ST elevation during acute STEMI is ASSOCIATED with simultaneous ST depression in the electrically opposite leads:
  • Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
  • Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II).
  • Reciprocal ST depression in V1-3 occurs with posterior infarction (see below).

Reciprocal ST depression in aVL with inferior STEMI

Reciprocal ST depression in III and aVF with high lateral STEMI

Posterior Myocardial Infarction

Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9.

Posterior MI

De Winters T Waves

This pattern of upsloping ST depression with symmetrically peaked T waves in the precordial leads is considered to be a STEMI equivalent, and is highly specific for an acute occlusion of the LAD.
deWinter t waves 2
De Winter’s T Waves

Digoxin Effect

Treatment with digoxin causes downsloping ST depression with a “sagging”  morphology, reminiscent of Salvador Dali’s moustache.
salvador dali digitalis effect


Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval.


Right ventricular hypertrophy

RVH causes ST depression and T-wave inversion in the right precordial leads V1-3.

Right ventricular hypertrophy

Right Bundle Branch Block

RBBB may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.

Right bundle branch block

Supraventricular tachycardia

Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia, provided that it resolves with treatment.
AV-nodal re-entry tachycardia

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