A classical ST Elevation Myocardial Infarction (STEMI) is defined as clinical symptoms of an acute coronary syndrome and ≥ 2 contiguous leads showing ST elevation:

• ≥ 2.5 mm in V2-3 if male <40 yrs
• ≥ 2 mm in V2-3 if male >40 yrs
• ≥ 1.5 mm in V2-3 if female
• ≥ 1 mm in other leads

An anterior STEMI is caused by occlusion of the Left Anterior Descending (LAD) artery. This can show ST elevation in the anterior leads V1-4.

An inferior STEMI can be caused by an occlusion of the Right Coronary Artery (RCA, 80%), Left Circumflex (LCx, 18%) or LAD. It is classically associated with ST elevation in the inferior leads II, III and aVF.

A lateral STEMI is associated with ST elevation in the lateral leads (I, aVL, V5-6). It can be more difficult to see at first because these leads are quite spread out on a standard 12-lead ECG. This pattern can be combined with anterior (anterolateral MI) or inferior (inferolateral MI) infarction patterns.

Reciprocal ST depression occurs in the leads that are electrically opposite from those showing ST elevation during an acute infarction.

Inferior infarction is associated with reciprocal ST depression in aVL.

Lateral infarction is associated with ST depression in leads III and aVF.

Posterior infarction is associated with reciprocal ST depression in V1-3.

Posterior MIs can be a little harder to see.

A posterior MI does not produce ST elevation because there are no true posterior leads on a standard 12-lead ECG. Instead, it may show ST depression in the anterior leads V1-3, which is a form of reciprocal changes.

It is also possible to move the electrodes V4-6 to record posterior leads V7-9. If there is at least 0.5mm ST elevation in one or more posterior leads this suggests infarction, but the absence of ST elevation in posterior leads does not exclude a MI.

An isolated posterior MI can be caused by occlusion of a branch from the LCX or RCA. It is rare on its own, and usually accompanies infarction in another territory, i.e. inferior (inferoposterior), lateral (posterolateral) or all 3 of these territories (inferoposterolateral).

A high lateral MI results from occlusion of the first diagonal branch (D1) of the Left Anterior Descending artery (LAD). It may show ST elevation in leads I, aVL and V2 along with ST depression in lead III. This pattern is also known as the South African Flag sign, and it can also be described as a mid anterior MI.

A proximal LAD occlusion that is proximal to the first septal branch S1 may show ST elevation in aVR and V1 and ST depression in V5/V6. This is also known as Precordial Swirl.

A wraparound LAD occlusion may occur if the LAD 'wraps around' the apex of the heart to supply the inferior wall as well as anterior. This occlusion may produce an MI with widespread anterior and inferior ST elevation, and reciprocal ST depression in I & aVL.

An extensive LAD occlusion can produce enormous ST elevations that are known as tombstones because of the associated high mortality.

Extensive LAD occlusion can also affect the conduction system, see the section on QRS patterns including RBBB / bifascicular block.

Right ventricular infarction can be subtle but clinically important to detect, particularly because it is associated with increased risk of hypotension and sensitivity to nitrates.

A right ventricular MI is associated with ST elevation in V1, and III > II. Right sided leads may also show ST elevation.

Some Right ventricular MIs show ST depression in V2, either with ST elevation or an isoelectric ST in V1.

Widespread ST depression with ST elevation in aVR is often stated to be associated with a left main occlusion, but this is a common misconception. It is most important to distinguish between a left main occlusion and a stenosis, but there are many other causes of this pattern.

A true left main occlusion is a disaster with a high risk of cardiac arrest. Many will not survive to have an ECG recorded, and only 0.42% - 3% of patients with an anterior STEMI have a left main occlusion found at the time of catheterisation. If there is a true left main occlusion, it may produce signs of a large proximal LAD occlusion including ventricular conduction blocks along with a circumflex occlusion (posterolateral).

A critical left main stenosis can be associated with widespread ST depression with ST elevation in aVR. This pattern can also be caused by any global mismatch between supply and demand, such as valvular disease, anaemia, hypoxia, hypotension, hypertrophy, extreme tachycardia or hypertension. It may occur more easily if there is coronary stenosis present as well as any of these factors.

The Sgarbossa criteria can help to diagnose MI in the presence of a Left Bundle Branch Block (LBBB). The 3 original criteria were modified by Smith et al. to include any of the following:

1. Concordant ST elevation ≥1 mm
2. Concordant ST depression ≥ 1 mm in any of V1-3
3. Excessively discordant ST elevation ≥ 1 mm and ≥ 25% of the depth of the preceding S-wave.

Unlike the original point scoring criteria, if any of the modified criteria are present then the cath lab should be activated.

This criteria can also be applied to ventricular paced rhythms, and there is some evidence for ventricular ectopic beats and AIVR. It does not apply to a RBBB. It also may not apply to patients with severe hypertension, acute heart failure (pulmonary oedema), extreme tachycardia or hyperkalemia. It is not very sensitive with Left Ventricular Hypertrophy (LVH). None of these criteria have 100% sensitivity or specificity. They are probably most useful in stable patients who present with typical chest pain suggestive of MI. Serial ECGs, careful monitoring and clinical judgement remain very important.

Hyperacute T waves are larger than normal, and are classically associated with early infarction. This increased size can be subtle and there is no strict definition or cutoff, but they are more easily seen in comparison to an old ECG.

Hyperacute T waves may be abnormally tall or just bulky, out of proportion to the QRS complex.

Just like ST changes, hyperacute changes can cause reciprocal changes in opposing leads. Inferior hyperacute T waves may have reciprocal changes in aVL. Posterior hyperacute T waves may be inverted in anterior leads.

Hyperacute T waves can also be present on the way down following an acute occlusion.

De Winter T waves are a special type of hyperacute T waves, accompanied by upsloping ST depression. They are classically associated with LAD occlusion. This pattern is easily missed. It may evolve into or from a classic ST elevation pattern. It is a STEMI equivalent.

Classic de Winter T waves occur in the anterior leads, due to LAD disease.

Occasionally de Winter T waves may be seen in the inferior leads.

Reperfusion T waves evolve with reperfusion to become biphasic with terminal T inversion, and may become fully inverted T waves. They can occur with spontaneous reperfusion, or post intervention.

Just like hyperacute T waves, reperfusion T waves can show reciprocal changes in opposite leads. Inferior reperfusion can have T inversion in inferior leads and large upright T in aVL. Posterior reperfusion can show large upright T in V2-3.

The pattern of T wave inversion may be reversed if there is re-occlusion. Inverted T waves that have become upright again are known as pseudo-normalised.

Wellens Syndrome is a pattern of biphasic or deeply inverted T waves after recently resolved chest pain.

Wellens syndrome is associated with a critical LAD stenosis, and can be thought of as reperfusion waves after a transient MI. The risk of re-occlusion is high.

Two distinct patterns were originally described, though it is now known that type A can evolve to type B over time.

Type A Wellens waves are biphasic T waves.

Type B Wellens waves are deeply inverted T waves.

Just like ST and hyperacute changes, Wellens patterns can be seen in anterior, inferior or lateral distributions. When in a posterior distribution, Wellens waves will be down-up T waves in V2-4.

Pathological Q waves are > 40msec wide (1 small square), >2mm deep or >25% of the QRS height. They can suggest a myocardial infarction, or sometimes a cardiomyopathy or an electrode misplacement. Q waves in the anterior leads can cause poor R wave progression.

Normal Q waves can occur in most leads except V 1-3. They should be present in V5-6.

Transient Q waves are possible. The old model of q waves representing a completed infarct has evolved, and patients with early Q waves can still benefit from primary PCI.

Old anterior Q waves with persistent ST elevation can represent LV aneurysm morphology, which is a common mimic of acute MI.

A fragmented QRS complex has extra waves or notches. This is a nonspecific sign of myocardial scarring, and can be seen after ischemia, nonischemic cardiomyopathy and Brugada syndrome. It can predict arrhythmias and suydden death in arrhythmogenic right ventricular dysplasia, Brugada and acquired long QT syndrome.

Terminal QRS distortion is the absence of an S wave or a J wave in V2 or V3. It is a useful sign suggesting an MI due to LAD occlusion and not early repolarisation.

A new Right Bundle Branch Block (RBBB) can occur with proximal coronary occlusion of the LAD or left main.

An existing RBBB is expected to have discordant ST depression in leads V1-4 and negative T waves. The presence of concordant ST elevation in these leads is abnormal, as is excessive discordance.

The Sgarbossa Criteria do not apply to a RBBB.

Infarction patterns with a new bifascicular block can represent severe proximal coronary occlusion.

Just as T waves can be the first to show signs of infarction, they can be the first to show signs of reperfusion. They may first show subtle terminal T inversion, progressing to biphasic T waves then inverted T waves over time. Large inverted T waves suggest that there is viable myocardium now reperfusing. Whether reperfusion occurs spontaneously or post intervention, the ECG patterns look the same.

ST elevation should come down with reperfusion.

If there is reocclusion, T waves can change from inverted to upright again, and ST elevation may recur. On the way to reforming a hyperacute T wave, the T wave may be briefly flat.

Old infarction can cause pathological Q wave formation in the affected leads. Anterior infarction can also cause a loss of R progression.

An old MI will not have large T waves

Subtle reciprocal changes can be seen in inferior leads (anterior MI) or aVL (inferior).

PR segment changes in a patient with an MI can suggest atrial ischemia or infarction.

Primary repolarisation changes can occur with a normal QRS. They can suggest ischemia/infarction, myo/pericarditis etc. but can also be benign normal variants.

Secondary repolarisation changes occur because of a primary depolarisation abnormality, e.g. Ventricular Hypertrophy, Bundle Branch Blocks, Wolff Parkinson White syndrome or Ventricular Ectopic Beats.

Primary and secondary repolarisation changes can co-exist, e.g. a patient with LVH can also have a myocardial infarction, which can be challenging to interpret.

Repolarisation variants include benign ST changes and benign T wave inversion.

ST changes of early repolarisation can be challenging to distinguish from anterior MI. There are formulae available to assist. Other features of BER include a fishhook pattern, asymmetrical T, STE

T wave inversion can also be a normal variant. T waves may be normally inverted in lead III. Juvenile T waves are inverted in V1-3. Persistent juvenile T waves may be present in adults, most often young AfroCaribbean women with shallow asymmetric T wave inversion in V1-3.

ST elevation can persist as a Left Ventricular (LV) Aneurysm pattern without any ongoing infarction. This includes ST elevation and Q waves in V1-4. There should be at least one QS wave without any R wave. The T waves may be upright or inverted.

Acute MI is more likely if the T:QRS ratio > 0.36 in any of V1-4. Subacute MI is also possible (ie chest pain >6 hours). Both an acute MI and an aneurysm may have akinesis on echo, but a LV aneurysm may have dyskinesis and wall thinning.

Posterior LV aneurysm may have persistent STD after a posterior MI

Pericarditis may closely resemble an acute infarction on the ECG. The classical stages of pericarditis include:

• Stage 1: STE + PR dep first 2 weeks
• Stage 2: T flat, ST normal (1-3 wks)
• Stage 3: inverted T (>3 weeks)
• Stage 4: normal (several weeks)

Ventricular hypertrophy can cause secondary repolarisation changes, but it can also co-exist with acute MI. Important clues for MI include new changes compared to previous (although ST segments can vary over time with LVH alone), terminal QRS distortion and concordant ST changes (though Sgarbossa criteria do not apply).

The secondary repolarisation changes of ventricular hypertrophy are sometimes called a strain pattern.

Electrolyte effects that mimic ischemia and infarction on the ECG include hyperkalemia with its tall peaked T waves, hypercalcemia with a short QT that can resemble pseudo-ST elevation, hypokalemia with ST depression and flat T waves.

Drug/toxin effects that can mimic ischemia and infarction include the digoxin effect with downsloping ST depression, digoxin toxicity with AV blocks, ethylene glycol causing ST elevation...

Not all dynamic changes over serial ECGs represent acute ischemia or infarction. Pseudo-dynamic changes can result rom replacing electrodes / position changes, and normal variants can also have dynamic changes over time. Repolarisation changes can also be rate-related or secondary to intermittent conduction blocks or ventricular pacing.

Non-cardiac illness can affect the ECG, e.g. cerebral T waves are deeply inverted and associated with intracranial haemorrhage.

A type 2 MI can occur secondary to systemic illness e.g. anaemia / traumatic haemorrhage, esophageal rupture / cholecystitis / abdominal complaints..

Sometimes the ST segment is difficult to accurately identify, leading to false reports of ST elevation or depression. This is particularly a problem with a wide QRS e.g. LBBB or RBBB, or with Osborn waves.

The atrial repolarisation waves (Ta) or flutter waves can also mimic ST changes.

Some mimics of ischemia and infarction are impossible to distinguish based on the ECG alone. These may require clinical correlation and cardiology referral to sort out.