Acute Coronary Syndrome (ACS) does not refer to an adorable coronary artery too cute for it’s own good; it refers to a group of conditions that result in decreased coronary blood flow to the myocardial tissue. With a decreased coronary blood flow, there is a decreased supply of oxygen to the myocardial tissue. And nothing is as bad to the myocardial tissue than a lack of oxygen! If you are the superstitious type, you will believe that all bad things come in threes. No truer words have ever been spoken, with the 3 issues that result from a lack of oxygen to the myocardial tissue all starting with a capital “I”…
Myocardial Ischaemia occurs when there is a mismatch between the myocardial oxygen supply and demand – it is reversible if the oxygen supply and demand issue is rectified
Myocardial Injury occurs secondary to prolonged myocardial ischaemia but prior to death of myocardial tissue – it is also reversible if the supply and demand issue is rectified
Myocardial Infarction is the death of myocardial tissue secondary to prolonged ischaemia – it is not reversible and results in permanent myocardial tissue damage even if the ischaemia is resolved
If you haven’t already read this post on the 12 lead ECG, do yourself a favour and read it before continuing with this post (it will make things a WHOLE lot clearer)! If you are after an article that helps you diagnose the various cardiac rhythms out there, have a look at the flowchart that can be found in “How to Diagnose ANY Cardiac Rhythm Systematically“. If not, read on…
As we learnt in the previous post, the 12 lead ECG gives us a view of the anterior, lateral and inferior portions of the heart (especially the left ventricle):
- Leads V1 – V6 are anterior leads, with V5 and V6 also having lateral properties
- Leads I and aVL are lateral leads
- Lead II, III and aVF are inferior leads
These areas of the heart are perfused by particular coronary arteries:
So for instance, if the left circumflex artery that deviates from the left coronary artery and wraps around the side of the heart has a blockage…which leads of our ECG are we going to see changes consistent with ischaemia, injury and/or infarction in? Take your time and have a look at both the images above to try and figure it out…
What about if there was a blockage of the left anterior descending artery somewhere lower down towards distal end of it? Or perhaps if there was a blockage higher up in the left anterior descending artery just after it deviates from the left coronary artery? Once again, take your time and have a look at both images above to figure it out…
- Circumflex artery blockage: lateral leads I and aVL, and possibly V5 and V6
- Low left anterior descending artery blockage: inferior leads aVF, II and III
- High left anterior descending artery blockage: inferior leads AVF, II and III along with anterior leads V2, V3 and V4
The beauty of ECG changes consistent with myocardial ischaemia, injury and infarction is that they all show up differently on a 12 lead ECG. But before we talk about these changes, we should quickly brush up on what the normal components of an ECG trace look like:
Analysing the length of various segments such as the PR interval and QRS complex are important for rhythm analysis. But when it comes to analysing ECG changes consistent with ischaemia, injury or infarction; it is more the height of things and the return to baseline that we are concerned about. It is important to note the following:
- The Q wave is the first negative inflection that deviates from baseline, but may not always be present (even on a normal ECG)
- If the first deflection from the baseline is positive, that means you have no Q wave and that positive deflection is actually your R wave
- If a Q wave is present, it is usually quite small in height (less than 25% of the height of the QRS complex)
- The R wave is the first positive inflection that deviates from baseline
- The S wave is the negative inflection that follows the R wave and should return to baseline prior to an upright T wave
What Do We See On ECG When There Is Myocardial Ischaemia?
The earliest ECG change to occur with myocardial ischaemia are tall, peaked and often wide T waves:
These are known as hyper acute T waves and are usually present for only 5 to 30 minutes after the onset of myocardial ischaemic symptoms. For this reason, this is rarely seen as the only ischaemic change on an ECG as patients are usually not having an ECG recorded at the moment one of their coronary arteries occlude. It is important to note that there are other conditions that can cause hyper acute T waves, such as hyperkalaemia. However, if the changes have occurred and your patient is complaining of chest pain…you know what they say about something that looks like a duck and walks like a duck; it’s probably a duck!
What Do We See On ECG When There Is Myocardial Injury?
If myocardial ischaemia is not rectified, myocardial injury will ensue. This presents on an ECG with the following: ST elevation, ST depression and/or T inversion.
ST elevation is usually evident within hours of the onset of myocardial ischaemic symptoms. The morphology of an ST elevated complex can be convex (coved), concave (saddleback), plateaued (tombstone) or obliquely straight (ski slope).
In order to be classified as ST elevation, two contiguous leads must be affected by ≥ 0.2 mV in precordial leads and/or ≥ 0.1 mV in the other leads at the J-point. Yes, I just said a whole bunch of things that will likely have some people scratching their heads. Let me explain:
- Contiguous leads mean leads that are right next to each other (viewing the same part of the heart) – an example would be if there were ischaemic changes in lateral lead aVL, it makes sense that I would also expect ischaemic changes in lateral lead I
- Precordial leads are leads V1 – V6 which are the closest to the heart and therefore you would expect a slightly higher amplitude with the ECG waveforms when compared to the other leads
- J point is the point that the QRS complex ends and the ST segment begins, which normally will be at baseline
It is important to note that like hyper acute T waves, ST elevation may not always be associated with myocardial ischaemia/injury. There are many differential diagnoses for ST elevation including pericarditis, benign early repolarisation, left bundle branch block, left ventricular hypertrophy, ventricular aneurysm, Brugada syndrome, ventricular paced rhythm and raised intracranial pressure. The general rule of thumb is this: a “smiling” ST elevation is usually benign if the patient shows no signs of myocardial ischaemia; a “frowning” ST elevation usually indicates something more sinister such as an imminent myocardial infarction.
But also remember that any ST elevation (whether it is smiling or frowning) in the setting of chest pain must be treated as such until proven otherwise – if it looks like a duck, and it walks like a duck; treat it like a duck!
ST depression is usually evident within hours of the onset of myocardial ischaemic symptoms. In order to be classified as ST depression, two contiguous leads must be affected by ≥ 0.5 mV at the J-point. The morphology of an ST depressed complex can either up-sloping (A), down-sloping (B), or horizontal (C).
T wave inversion usually indicates worsening myocardial injury. In order to be classified as T wave inversion, two contiguous leads must be affected by ≥ 0.1 mV in leads with prominent R waves (positive waveform).
I associate the ECG changes associated with myocardial ischaemia/injury with a person being punched. If I punch a really annoying person once, but someone pulls me away before I can do more damage…there will most likely be a reddened area that will disappear very shortly after I am removed from the scene, never to punch them again. Think of this as your hyper acute T wave seen in myocardial ischaemia. If I managed to get in a good few punches prior to someone coming and pulling me away, chances are that I would have left a small bruise. This small bruise will eventually clear up, but it will take a little longer than if it was merely a reddened area from one punch. Think of this as your ST elevation or ST depression seen in myocardial injury. However, if I was able to get a couple of kicks in there before someone pulled me away…that bruise is going to bigger and hang around a lot longer. Think of this as your T inversion, which can sometimes persist on the ECG for many months after the initial myocardial ischaemic event.
What Do We See On ECG When There Is Myocardial Infarction?
Remember that myocardial ischaemia and injury is reversible, if the myocardial oxygen supply and demand issue is rectified. If it is not rectified in time, myocardial infarction will ensue. I think of this as me holding a really annoying person underwater (wow, I am really violent today). If I held someone underwater for 30 seconds, and then let them above water to breathe for 30 seconds and keep repeating this…they will be annoyed, but they will survive if I stop (like myocardial ischaemia). If I held someone underwater for a minute, then only let them above water to breathe for 10 seconds before dunking them under again…they will be gasping for air, but they will survive if I stop (like myocardial injury). However, if I held someone underwater for 10 minutes…they will no longer be annoyed or gasping, they would be dead even if I stopped after 10 minutes (like myocardial infarction).
Myocardial infarction presents on an ECG in the form of pathological Q waves. Pathological Q waves are defined as Q waves that are more than 25% the height of the QRS complex (remember, a Q wave can only be classified a Q wave if it is the first negative inflection away from baseline). Once a pathological Q wave forms on an ECG, it will always be on that ECG. So how do we tell an acute myocardial infarction apart from an old myocardial infarction?
- Pathological Q waves in the presence of ST elevation, ST depression and/or T wave inversion indicate an ACUTE myocardial infarction – that means that it is happening right now!
- Pathological Q waves may develop within 1 to 2 hours of the onset of acute myocardial infarction symptoms, though they often take 12 hours and occasionally up to 24 hours to appear
- Pathological Q waves without ST elevation, ST depression and/or T wave inversion indicate an OLD myocardial infarction – that means it has happened in the past at some point!
Notice how in the acute picture, I have a Q wave that is about 8 little boxes down from the baseline? Compare this with the R wave that is about 4 little boxes up from the baseline? This gives me a total QRS complex height of approximately 12 little boxes. 8 divided by 12 is equal to approximately 67% (way more than 25% and therefore a pathological Q wave)! Have a go with the old myocardial infarction picture and tell me what the percentage height of the Q wave is…
The Q wave is how many little boxes away from baseline?
About 2 little boxes…
The R wave is how many little boxes away from the baseline?
About 5 little boxes…
That gives us a total of how many little boxes?
About 7 little boxes…
Which means the percentage of the Q wave in relation to the QRS complex is?
2/7 = 29% (more than 25% and therefore a pathological Q wave)!
What Are Reciprocal Changes?
ST elevation, T inversion and pathological Q waves are called the indicative changes of myocardial ischaemia/injury/infarction and occur in the ECG leads looking at the damaged myocardial tissue. Reciprocal changes are the mirror image of the indicative changes and are often seen in leads recording from the opposite area of the heart, picked up on the ECG as ST depression. For this reason, ST depression does not always mean myocardial injury…it could just mean that those ECG leads are picking up on a large surge of energy from the indicative changes occurring in the opposite ECG leads.
Reciprocal changes may include taller than normal R waves (mirror image of Q waves), ST depression (mirror image of ST elevation), and tall T waves (mirror image of T wave inversion). Reciprocal changes tend to be seen in up to 70% of inferior infarctions and 30% of anterior infarctions.
It is important to note the following:
- Reciprocal changes only potentially apply if there is ST depression evident on an ECG
- If ST depression is evident on the ECG without any sign of concurrent ST elevation, it should be treated as an ECG change consistent with ischaemia/injury in the area of the heart that the affected leads are viewing
- If ST depression is evident on the ECG in the presence of concurrent ST elevation, it may merely reflecting a reciprocal change – however, myocardial injury in that area cannot be completely ruled out!
Let’s Practice What You Have Learnt…
We are going to analyse the following 12 lead ECG in terms of changes consistent with myocardial ischaemia, injury or infarction; inclusive of which areas of the heart are affected:
- Let’s group the leads first
- Let’s assess the anterior leads first (red box)
- ST depression in lead V2
- Let’s assess the lateral leads next (blue box)
- ST depression in leads I and aVL
- Let’s assess the inferior leads last (green box)
- ST elevation in leads II, III and aVF
- Despite lead III looking like it may have a pathological Q wave, notice the very small upstroke directly from baseline (R wave) prior to the larger down stroke (S wave)
- Let’s diagnose the whole picture
- Anterior leads do not have contiguous leads affected, so let’s not include it within our diagnosis
- We have no pathological Q waves, so we do not have infarction yet
- ST elevation is an indicative change so we can say that we have inferior myocardial injury
- The ST depression in the lateral leads could be a reciprocal change, but we cannot completely exclude concurrent lateral myocardial injury
- The answer?
- INFERIOR MYOCARDIAL INJURY WITH RECIPROCAL CHANGES IN LATERAL LEADS, however cannot exclude lateral myocardial injury
I hope that this has made understanding ECG changes consistent with myocardial ischaemic changes a bit clearer for you.
- Abbott Northwestern Medical Education Department. (2015). Student ECG: Ischemia, injury and infarction. Retrieved from: http://www.anwresidency.com/students/talks/ekg/ischemia.pdf
- Goldberger, A. L., & Prutkin, J. M. (2016). Electrocardiogram in the diagnosis of myocardial ischemia and infarction. Retrieved from: http://www.uptodate.com/contents/electrocardiogram-in-the-diagnosis-of-myocardial-ischemia-and-infarction
O’Brien, T. E. (2014). Ischemia, injury and infarction. Retrieved from: http://ekg.academy/learn-ekg.aspx?seq=1&courseid=323
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