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Teaching Points:

  • What are the signs of ischemia in the ECG
  • Acute ischemia: what are the different stages
  • What are the ECG criteria for STEMI?
  • How to determine the culprit leasion via ECG?
  • Which additional leads need to be recorded if right ventricular infarction is suspected?
  • Which additional leads need to be recorded if LV posterior wall infarction is suspected?
  • What are the criteria for left main infarction?

Signs of ischemia in the ECG

We all know that misdiagnosing a heart attack can have fatal consequences for the patient. The ECG is quickly recorded, and is therefore the number one diagnostic tool for early detection of an infarction: none of the available laboratory parameters can diagnose an infarction nearly as quickly!

The ECG is therefore the most important first-line diagnostic test in any patient with chest pain and/or dyspnea. For patients presenting with chest pain, the guidelines require that an ECG is performed within 10 minutes of medical contact. Thus, without exception, it makes sense for everyone involved in direct patient care to be familiar with the ECG signs of ischemia.

In this lesson, we will discuss all important criteria for the detection of myocardial ischemia.

ECG diagnosis STEMI

The diagnosis of an ST segment elevation myocardial infarction (STEMI, for short) is assigned on the basis of ECG findings. Decisions concerning all subsequent interventions, such as coronary angiography, are dependent on this initial ECG.

Fortunately, the trained ECG expert can diagnose a STEMI in an instant. How long does it take? As long as the ECG recorder needs to print the tracing.

By looking at the ECG leads, we can determine the myocardial region in which the ischemia has occurred, and even the responsible occluded coronary vessel, the so-called "culprit lesion". By looking at the ECG, we can even estimate the time that has passed since the onset of the infarction.

Let’s begin by looking at the signs of an acute STEMI. A fresh STEMI must be recognized immediately. The faster an occluded coronary vessel is reopened, the better the prognosis.

Hyperacute T wave

In the first few minutes of an infarction, so-called "hyperacute T waves" are visible on the ECG. As you can see here, the T-waves are very high and sharp. In an anterior wall STEMI, the hyperacute T waves are particularly pronounced in the chest leads. It is unusual to capture this stage with the ECG, because it occurs very quickly after the onset of symptoms and stops within a very short time period.

ST elevation

Another classical ECG sign during the acute phase of an infarction is the ST-segment elevation which lead to the term “STEMI”. ST elevations usually, but not always, start from the descending R wave and then transition into the T wave. Frequently, the T-wave can no longer be distinguished from the ST segment.

How do these ST elevations actually develop?

In the acute stage of an infarction, cardiac ischemia leads to persistent fluctuations in the electrical activity of the affected myocardial region. Due to these fluctuations, no zero line is visible between excitation and repolarization. From the beginning of the excitation to the end of repolarization, the main vector points to this infarction area, or to put it in terms of ECG-vocabulary, from the beginning of the QRS complex to the end of the T wave. The leads in which the ST elevation is found thus tell us which area is affected.

ST segment depression as indirect signs of infarction

In the leads that are opposite the infarction area, we usually see ST segment depression. These are known as “indirect signs of infarction".

Unfortunately, things are not always black and white, and sometimes we see findings that make us feel very uncomfortable, especially when we are alone with the patient and the ECG. To eliminate all doubts, you should know the universal definition of myocardial infarction:

To be sure about your diagnosis, you need to look at a 12-lead ECG tracing.

To diagnose a STEMI, ST segment elevations must occur in at least two associated leads, and the amplitude of the elevation must be at least 0.1 millivolts. Under usual calibration conditions, this corresponds to just one millimeter or a small box.

In the following, we will look at this definition in more detail.

First, we need to clarify where we actually measure these ST segment elevations.

Perhaps you’ve noticed that the ST segments do not always run horizontally. Instead, they may ascend or descend. To avoid false positive or false negative findings, it is therefore extremely important to measure the elevation in the correct place.

J point

The correct starting point for your measurement is called the "J point". This point marks the transition between the QRS complex and the ST segment.

So far, so good.

Next, we need to clarify how high an elevation needs to be in order to be indicative of a STEMI.

ST elevation amplitudes

Unfortunately, this is not so simple. As mentioned before, ST elevation at the J point must be at least 0.1 mV to be considered relevant. As you know, the left ventricle has much more muscular mass than the rest of the heart.

Accordingly, the definition of the minimum amplitude for the leads representing the left ventricle is dependent on certain factors. Differences arise depending on age and gender.

Here is a summary of the exact reference values:

More than 0.1 millivolts is required to be considered relevant in leads V2 and V3. For men, the minimum amplitude is 0.25 mV for men under the age of 40, and 0.2 mV for men over the age of 40. For women, a minimum amplitude of 0.15 mV is necessary in V2 and V3, irrespective of age.

Before, we talked about “associated leads”. What does this mean? In the chapter on "localization of the infarction", typical infarction patterns are discussed. There you learned that there are specific ECG lead patterns for each coronary vessel or myocardial supply area. The respective ECG lead groups are called "associated leads".

What do we see in the ECG when the patient presents after the acute phase has ended?

Intermediate stage of MI

The acute stage of the infarction is followed by the intermediate stage. Over time, changes in the potentials in the infarction area occur as a result of the transformation from acute necrosis into scar tissue. These changes are reflected in the ECG through the following changes:

- a slow normalization of the ST segment;

- an increase in T wave inversion, leading to terminal T wave inversion; and

- depending on the size of the myocardial scar, the formation of pathological Q-waves.

Terminal T wave inversion is defined as a negative T wave, where the bisector is perpendicular to the isoelectric line, or pointed away from the QRS complex. If such T waves are found in the ECG, this is highly suggestive of an intermediate stage  myocardial infarction.

Chronic stage of MI

Finally, the so-called chronic stage follows. If coronary intervention is performed early, and thus little or no necrosis and subsequent scarring occurs, an infarction ECG normalizes completely. This means that some ECGs look exactly the same as before the infarction.

However, if coronary intervention is delayed, complications arise, such as scars in the myocardium or the formation of an aneurysm.

Scars are reflected in the ECG by deep Q waves and a loss of R waves in the associated leads.

Persistent ST segment elevation, often starting from the ascending S, is a sign of a ventricular aneurysm. Aneurysms are most frequent after large anterior infarctions in the area of the apex. Here, persistent ST segment elevation is found in the anterior leads V1 to V5.

The T wave often normalizes after an infarction, even if coronary intervention is delayed.

The ECG in a patient with myocardial damage following myocardial infarction may look like this:

Pathological Q waves, R loss or delayed R wave progression, and an elevated J point with persistent ST-segment elevation starting from the ascending S wave are found in leads associated with the aneurysmatic myocardium.

Non-ST-elevation myocardial infarction (NSTEMI)

As the name suggests, in non-ST-elevation myocardial infarction or NSTEMI, ST elevation does not occur.

In these patients, myocardial infarction is detected in the laboratory, through determination of the typical increase in cardiac enzymes. In NSTEMI, the ECG can be completely normal. However, other transient signs of ischemia, such as T wave inversion and ST depression, often occur.

Repeated 12-lead ECG evaluation and continuous heart monitoring are essential in patients with NSTEMI to detect possible ECG changes.

Localization of myocardial infarction

In acute myocardial infarction, myocardial ischemia and myocardial necrosis are caused by occlusion or severe stenosis of a coronary artery. The area of the myocardium that is affected is dependent on the perfusion pattern of the corresponding coronary artery. In the ECG leads responsible for the affected myocardial area, characteristic alterations can be found.

Let’s recall our definition of STEMI from the last chapter: ST segment elevation must occur in two associated leads. What exactly do we mean by that?

Let’s take an occlusion of the right coronary artery as an example. As diagnostic criterion for a STEMI, at least two of the ECG leads that represent the RCA supply area must meet the ECG STEMI criteria. If we only find ST elevation in a single lead of the RCA area and another one in a different area, this would not be considered a typical infarction ECG, as those leads are not associated.

As we discussed in an earlier chapter, it helps to think of the ECG leads as cameras, each of which filming a different section of the myocardium. Only if all camera monitors are considered, the entire myocardium can be assessed. If certain sections are not looked at, for example because no chest leads are recorded, no statement can be made about the myocardial sections filmed by the chest leads. Remember, the ECG report cannot be finalized until all 12 ECG leads have been considered.

However, it is important to remember that the 12-lead ECG does not film all myocardial sections. If the patient presents with the typical symptoms of a myocardial infarction but the ECG doesn’t tally with your clinical gut feeling, tracings from additional leads must be recorded. The regular 12 leads do not assess the right ventricle, and neither do they assess the posterior wall. To do this, the additional leads V3R and V4R, and v7-v9 must be used. How to place them exactly is explained in the chapter about the leads.

In the following section, we will go through all of the ischemia-related ECG patterns of importance in your daily clinical work.

Before going through these, we suggest you first go back to the chapter on the nomenclature of the left ventricular walls in case you feel not sure about it.

Myocardial infarction in the left coronary artery

The left coronary artery begins with a relatively short but very important section, the so-called left main artery. It then divides into two large branches: the left anterior descending artery (or LAD) and the circumflex artery (or LCX).


The LAD supplies the anterior wall of the left ventricle, while its septal branches supply the septum. The diagonal branches extend to the lateral wall. The more proximal the LAD stenosis or occlusion, the greater the area of the infarction. In a proximal occlusion of the LAD, the diagonal and septal branches are also affected.

The result is a large anterior infarction, with ECG signs of ischemia in all chest leads from V1 to V6.

The supra apical area of the anterior wall, or simply the tip of the heart, is supplied by distal branches of the LAD.

In a supra-apical infarction, ECG signs of ischemia are typically found in leads V1 to V3.

If the anterior septum is affected without the lateral wall, ECG changes typically occur in V2 and V3, or, if the infarction area is large, even in V1 to V4.

If stenosis occurs in a large diagonal branch with an otherwise open LAD, an infarction of the antero-lateral wall occurs. In this case, ECG signs of ischemia are usually seen in leads I and aVL.


The left circumflex artery also supplies both the antero-lateral and postero-lateral sections of the lateral wall.

Depending on whether the LAD or the LCX is dominant, an infarction of the lateral wall can be caused by stenosis in a large diagonal branch of the LAD or in a marginal branch of the LCX.

Here, too, we usually find ECG changes in leads I and aVL.

As explained earlier, the posterior wall of the left ventricle is not assessed in a conventional 12-lead ECG. Although indirect signs of infarction, namely ST depression, can occur in V1 and V2 in patients with a posterior infarction, we still need "additional cameras" for an exact diagnosis. Thus, in the case of a suspected posterior infarction, leads V7 to V9 are recorded as a continuation of the regular chest leads. It is important to note that in leads V7-9, ST elevations above 0.05 millivolts are considered clinically relevant.

In men aged younger than forty, elevations of 0.1 millivolts or above are considered significant.

Myocardial infarction in the right coronary artery

The inferior wall is supplied by the right coronary artery (RCA), and is represented on the ECG by leads II, III and aVF. ST elevations in these leads are therefore usually associated with deficits in the distribution area of the RCA.

In the event of an inferior infarction, involvement of the right ventricle must always be considered. In this case, an additional ECG recording should be made, using chest leads around the free wall of the right ventricle. These additional leads are called the "right precordial leads" V3R and V4R. Here, an ST elevation of 0.05 mV or above is relevant due to the low mass of the right ventricular myocardium. In men under the age of 30 years, it must be at least 0.1 mV.

In 90% of patients, the RCA supplies the AV node as well as important other sections of the conductive system. Therefore, in RCA infarctions in particular, bradycardiac arrhythmias as well as ventricular fibrillation are a frequent occurrence. Remember that these severe and life threatening arrhythmias can occur in the acute phase of ischemia or in the hours following revascularization. These so-called reperfusion arrhythmias can happen in all myocardial infarctions, not just in RCA infarctions.

It goes without saying that these patients have to be monitored continuously, and you have to be prepared for the worst.

Left main occlusion (LMCA myocardial infarction)

In the case of an occlusion of the left main artery, the oxygen supply in the area of both the LAD and the LCX is disrupted. Due to the size of the affected myocardial area, the prognosis is very poor. Patients with main stem myocardial infarction usually develop cardiogenic shock shortly after the cardiac insult.

Revascularisation of the affected vessels must be carried out immediately. Even if everything appears to be going well, a left main infarction is often lethal.

The following ECG criteria are suggestive of a problem in the distribution area of the left main artery:

- ST elevation in aVR, if it is at least 0.1mV and higher than an elevation in V1 if present.

- The amplitudes of ST elevations and ST depressions in all 12 leads are added to a total sum. The sum of all these ST segment alterations in all 12 leads is more than 18mm.

- Presence of indirect infarction signs in II, III, and v3 to v5

Unfortunately, it is not so easy to pick out these signs on a quick  inspection of the ECG tracing. And, of course, they don’t have a perfect specificity.

We therefore suggest the following practical rule of thumb:

If you find ST elevations or depressions in almost all leads of a 12-lead ECG, or significant depressions in at least 8 leads, you must consider the possibility of a lesion in the territory of the left main artery!