The following 12-lead ECG was forwarded to me by one of my former Masterclass students.
Chief Complaint: Pressure-like central chest pain with diaphoresis for 45 minutes.
Rhythm: Sinus (Upright P waves in Leads I and II, +/- biphasic P wave in Lead V1)
Rate: Mid- to upper 60’s
Blocks (SA, AV, bundle branch): None
PR Interval: Normal
QT: No measurements, but concerning because it ends near the middle of the R-R interval
ST Deviations: To be discussed.
Aside from the usual measurements and observations, what did you notice first on this ECG? Was it the depressed ST segments with T wave inversions? Or was it the upright T waves?
Most people look for ST elevation which is very minimal on this 12-lead ECG (it’s there in Lead III). But I’m willing to bet that the first thing that caught your eye was the ST depression with T wave inversion in Leads I, aVL, and V1 and V2. Lead V3 also has ST depression but the T wave is biphasic (down/up). T waves are labelled by how they end. Although the T wave in Lead V3 is definitely biphasic… it’s officially an upright T wave because it ends above the baseline.
At this point I would like to introduce you to Jones’s Rule…
“Any ST depression on the ECG of a patient with chest pain compatible with an acute coronary syndrome should be considered a reciprocal change to an acute epicardial ischemia (STEMI) until proved otherwise!”
Corollary to Jones’s Rule
And the Corollary to Jones’s Rule…
“The ST depression of a reciprocal change may appear before the ST elevation is discernible and – even when both are present – the reciprocal change may be more impressive. Remember: the ST elevation is pointing to where the problem is!”
ST Depression and Vascular and Anatomical Areas
We definitely see lots of obvious ST depression on this ECG and that ST depression appears to fit two different anatomical locations: the ST depression in Leads I and aVL represent the basolateral (formerly “high lateral”) area and the ST depression in Leads V1 – V3 represent the left para-apical (formerly “septal”) area.
Here are the anatomical and vascular areas on the ECG:
Leads Anatomical Area Vascular Area
II, III and aVF Inferior Wall (LV) RCA, LCx, LAD
I, aVL Basolateral Wall (LV) LAD, LCx
V1 – V3 (Postero-)Lateral Wall (LV) LCx, RCA
Anterior Wall (LV) LAD
Anterior Wall (RV) RCA
V7 – V9 (Postero-)Lateral Wall (LV) LCx, RCA
V1R – V6R Right Ventricle RCA, LAD
Some of the listings may surprise you: The LAD can certainly cause an inferior wall MI since most (around 80%) of LADs wrap around the apex and supply part of the inferior wall of the left ventricle. The LAD can also result in minor infarctions of the anterior right ventricle because the LAD does send branches over to that area. Those are the branches that “no one ever talks about” and which you very rarely see on any diagrams (mainly because they are very small and usually of no hemodynamic consequence).
The ST depression of subendocardial ischemia does not localize on the ECG! Typically, it includes several vascular territories. When you see ST depression limited specifically to a single vascular territory – consider that a reciprocal change until proved otherwise (once again – Jones’s Rule). Here is an example of true subendocardial ischemia on a 12-lead ECG:
Look at the distribution of ST depression on this ECG! This is called circumferential subendocardial ischemia. Compare the ST depression in this ECG (Figure 2) with that in Figure 1. You can better appreciate the localization of the ST depression in Figure 1.
Remembering Jones’s Rule, we suspect that the leads with ST depression in Figure 1 are NOT indicating subendocardial ischemia, but instead, they demonstrate early acute transmural ischemia in the myocardium opposite those leads. Those ST elevations represent reciprocal changes – not localized subendocardial ischemia.
Reciprocity and Reciprocal Change
Leads I and aVL share reciprocity with the inferior leads (II, III and aVF). Leads V1 – V3 share reciprocity with Leads V7 – V9; but those leads were never recorded, so we don’t know what they looked like. However, we are allowed to diagnose a posterolateral* (formerly “posterior”) STEMI based on ST depression with T wave inversion in Leads V1 – V3. The original description of a “posterior” infarction was a tall R wave in Lead V1 with a flat, depressed ST segment and an upright T wave. What they did not realize at the time is that they were describing a completed infarction with post-reperfusion changes – not an early transmural ischemia. What we see in Leads V1 and V2 on this ECG (Figure 1) is exactly what one would expect of an acute transmural ischemia of the (postero-)lateral wall in progress.
Getting back to the frontal plane (limb) leads, we can definitely suspect that there are reciprocal changes occurring in Leads I and aVL. That means we should be looking for acute ST elevations occurring in Leads II, III and aVF. But all we see is about 1 mm of ST elevation in Lead III only. And we should have STE in at least TWO contiguous leads to diagnose a STEMI.
Hyperacute T Waves
Is there any other hint that we are seeing an acute transmural ischemia in progress? Yes! Look at the T waves in the inferior leads – they all have very wide bases! In fact, the T waves appear to begin at the J point (the termination) of the QRS complexes in those leads. Those are hyperacute T waves. If you spend your career looking for tall, wide hyperacute T waves (as many introductory texts and websites instruct you to do), you are going to miss a lot of hyperacute T waves. (My neighbor owns several “Big and Tall” clothing shops for men. I once asked him if he had many customers over seven feet tall. He replied, “A few – but most are just wide!”) The same with hyperacute T waves. This idea is reinforced in Leads V4 – V6. Those T waves aren’t tall at all – but their bases are certainly wide.
Hyperacute T waves are a subendocardial phenomenon! They indicate that the ischemia is rapidly approaching the epicardial layer – but it’s not there yet! Only when the ST elevation appears has the epicardium been reached and the ischemia has become fully transmural. The hyperacute T waves will usually disappear rapidly after the appearance of the ST elevation, but occasionally some may persist a bit longer. Just remember: if you see hyperacute T waves without ST elevation, the ischemia has not yet become transmural… but expect it very soon!
Deciding on the Culprit Artery
Which coronary artery is our culprit here? I have a pearl for you:
“You can sometimes arrive at a diagnosis much faster if you rule out what did not happen or could not have happened rather than what did happen.”
First, while all three coronary arteries can cause an acute inferior STEMI, the LAD does NOT create posterolateral infarctions. So, that leaves us with either the right coronary artery (RCA) or the left circumflex artery (LCx) as the culprit.
Here’s another pearl for you:
“If there is an inferior MI accompanied by ST depression in Lead aVL – the RCA is the culprit.”
Another somewhat reliable method tells us that if the ST elevation in Lead III is taller than the ST elevation in Lead II – the RCA is the culprit. It appears the RCA is going to be the culprit in this case.
What If the Findings Are Not Diagnostic – But You’re Still Concerned?
How should you manage a patient like this? A normal troponin is not going to be of any help because the patient has had pain for only about 45 minutes. You initiate a work-up for acute coronary syndrome and repeat the ECG every 15 – 20 minutes. Granted, you are in an Urgent Care facility and this patient is going to be transferred – but, due to unforeseen circumstances, you may have this patient remain in your care for longer than you anticipated. With hyperacute T waves like those in the inferior and lateral leads, you probably won’t have to wait long before the ST elevation makes its presence known.
One last pearl: “Although you may diagnose an acute MI by the ST elevation, lack of ST elevation never rules out an acute MI!”
For this issue, I have presented an ECG from my collection. Please feel free to send me an ECG that you would like discussed, along with any specific questions you may have about that ECG. You can email the ECG to me (email@example.com) preferably in a JPG, PNG or PDF format (I cannot use proprietary formats from record-keeping systems). Please remove all identifying data. The ECG should be positioned correctly in landscape format. Do not send ECGs that are sideways or upside down or distributed among two or three separate files. Also, if the ECG paper has been bent, folded or creased it may not be usable. Please state in your email that you want the ECG considered for this publication.
*The correct term for what we used to call a “posterior MI” or “true posterior MI” is actually “lateral MI.” That’s because it has finally been recognized that what we have always considered the lateral wall of the left ventricle is actually located posteriorly in the chest. I have created a video on YouTube that demonstrates this fact using an anatomical 3-D model of the heart. To view it, visit: https://www.youtube.com/watch?v=46_G0SFgSTc