ECG Blog #222 — Are Changes Dynamic?

The ECG in Figure-1 was obtained from a 50-ish year old man — who presented to the ED (Emergency Department) with new-onset chest pain.

• HOW would you interpret this tracing in light of this clinical history?
• Should you immediately activate the cath lab?
• OR — Could the anterior T waves represent a repolarization variant?

 

 

Figure-1: Initial ECG obtained from a 50-ish year old man — who presented with new-onset chest pain (See text).

 

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NOTE #1: Some readers may prefer at this point to listen to the 4:45 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-39a).

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Today’s ECG Media PEARL #39a (4:45 minutes Audio) — Reviews the concept of Dynamic ST-T Wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated).

 

 

MY Approach to this Tracing:

As always — I favor a Systematic Approach for every ECG I encounter (This Systematic Approach reviewed in ECG Blog 205). My descriptive analysis of the ECG shown in Figure-1 is as follows:

• There is fine baseline artifact present in virtually all leads. Although suboptimal — this in no way impairs interpretation of the major findings on this ECG.
• The rhythm is regular at ~60-65/minute. Although tiny in amplitude — upright P waves with a constant PR interval appear to be present in lead II (as well as in other leads) — so the rhythm is sinus. All intervals (PR, QRS, QTc) are normal. There appears to be slight left axis deviation (the QRS more negative than positive in lead aVF) — but not nearly enough to qualify as LAHB (because the QRS is predominantly positive in lead II). There is no chamber enlargement.

 

Regarding Q-R-S-T Changes:

• There appears be a tiny Q wave in lead aVL (This is probably a normal septal q wave).
• R wave progression is normal — with “transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-to-V4. 

 

Assessment of ST-T waves:

• Given the history (ie, new-onset chest pain in this middle-aged adult) — careful scrutiny for even subtle ST-T wave changes is indicated. There are a number of clearly abnormal ECG findings. These include: i) Hyperacute T waves in leads V2 and V3 — that are clearly disproportionately tall with respected to R wave amplitude in these leads; ii) The suggestion of slight ST depression with sagging ST segment in lead III; iii) Subtle flattening of the ST segment in lead aVF, with sugestion of a subtle biphasic T wave in lead aVF with terminal T wave positivity; iv) Suggestion of slight ST elevation in lead aVL; and, vi) Suggestion of slight ST elevation in lead V1 (See ECG Blog #218 for a similar case, with discussion of when a T wave is deemed to be "hyperacute" in ECG MP-35).

 

FIGURE-1: Putting It All Together:

There are some important lessons to be learned from assessment of ECG #1:

• This middle-aged man presented to the ED with new-onset chest pain. This immediately puts him in a higher-prevalence group. It places the "burden of proof" on us to prove that he is not having an acute cardiac event — rather than the other way around.
• In the context of this history — there should be NO doubt that the T waves in leads V2 and V3 of ECG #1 are disproportionately tall (!) with respect to R wave amplitude in these leads. These T waves must be assumed hyperacute (ie, indicative of an acutely evolving event) — until proven otherwise. 
• As a Result — unless a prior baseline tracing was available showing identical T wave changes in leads V2 and V3 — immediate cath lab activation is indicated solely on the basis of the history and ECG findings described in the 2 bullets above this one.
• The suspected "culprit" artery is the proximal LAD (Left Anterior Descending) coronary artery (See ECG Blog #193 — for more on prediction of the "culprit" artery).
• Additional support that the ECG changes in Figure-1 are indeed acute could be forthcoming from: i) Looking very carefully at the other 10 leads on this tracing, to see if there were additional subtle ST-T wave changes; ii) Obtaining a positive troponin (though it will take at least a few minutes for troponin assay to return); iii) Performing an Echo at the bedside during chest pain — IF this shows a wall motion abnormality (Echo will only be helpful for ruling out an acute event IF obtained during chest pain); and/or, iv) Repeating the ECG as soon as a few minutes later! (See ECG Blog #115 — for an example of how drastically an ECG may change in as little as 8 minutes).

PEARL #1: I have noted above subtle ECG findings in leads III, aVF; aVL and V1. I will emphasize that none of these 4 leads shows definite abnormalities — and were it not for the worrisome history (of new-onset chest pain) and the clearly abnormal T waves in leads V2 and V3 — no conclusions could be drawn from what we see in these other 4 leads. 

• T wave inversion in leads III and aVF is not necessarily abnormal when the QRS is predominantly negative (as it is in Figure-1). 
• Slight ST elevation may normally be seen in both leads aVL and V1.
• It is only because we know the T waves in leads V2 and V3 are definitely abnormal in this patient with new-onset chest pain — that the subtle findings I note in leads III, aVF, aVL and V1 add to my suspicion of an acute cardiac event.

The CASE Continues:

The cath lab was not activated. Another ECG was obtained 10 minutes after ECG #1. For clarity — I have placed both tracings, together with clinical chest pain scores in Figure-2.

• Do you see any potentially significant difference in ST-T wave appearance between these 2 tracings?
• Does ECG #2 and the associated chest pain scores shown in Figure-2 further support the indication for immediate cath lab activation? IF so — WHY?

Figure-2: Comparison between the first 2 ECGs obtained in this case. Note marked reduction in chest pain at the time the 2nd ECG was recorded (See text).

PEARL #2: As emphasized in today's Audio Pearl (MP-39) — the process of acute coronary occlusion is not always "all or none" — but instead, may involve occlusion of the "culprit artery" — only to be followed a short while later by spontaneous reopening of the occluded coronary vessel.

• Spontaneous reopening of the occluded vessel may be recognized clinically by reduction of chest pain and simultaneous improvement in ischemic ECG findings.
• Some patients manifest a stuttering course — in which the "culprit artery" may open and close a number of times. 
• Reocclusion of the "culprit" artery may be recognized clinically by return of chest pain and worsening of ECG ischemic changes.
• This "coming-and-going" of chest pain severity, associated with corresponding increase or decrease in ischemic ECG changes constitutes what is known as "dynamic" ST-T wave changes. Recognition of this phenomenon is clear indication for prompt cardiac catheterization, with goal of acute reperfusion before fixed coronary occlusion becomes established.
• Dynamic ST-T wave changes may be subtle! The challenge is to rule out artifact, axis shift, and/or variation in lead placement as the cause of any change in ECG appearance that you see. This is not always easy to do.

 

MY Thoughts on FIGURE-2:

The chest pain scores in Figure-2 show marked improvement in the patient's symptoms. That said — the ECG changes I note are extremely subtle! I find the most effective way to compare serial tracings when looking for interval change — is to go lead-by-lead.

• The "good news" — is that there is virtually no difference in frontal plane axis or QRS morphology in any of the 12 leads for the 2 tracings shown in Figure-2. This means that any difference we note between these 2 ECGs (no matter how small) is likely to reflect a "real" change in ST-T wave appearance.
• There appears to be slightly more ST-T wave depression in leads III and aVF in ECG #1 (at the time the CP score was 7/10) — compared to ECG #2 (CP score = 1/10).
• The T wave in lead aVL looks slightly flatter in ECG #2 (CP score = 1/10).
• The T wave in lead V2 of ECG #1 looks taller (clearly greater than 1 large box) — compared to T wave amplitude in lead V2 in ECG #2 (for which the T wave is definitely not more than 1 large box in amplitude).
• I did not see any significant change in the other 8 leads.

IMPRESSION: The difference in ST-T wave appearance between ECG #1 and ECG #2 is exceedingly subtle — and I had to look lead-by-lead at these tracings several times before satisfying myself that: i) There is slight improvement in ST-T wave appearance in ECG #2; and, ii) This corresponds to the marked reduction in chest pain — therefore qualifying as a "dynamic" ST-T wave change. 

• These findings support my earlier impression that immediate cath lab activation was indicated.
• Anatomically — it is likely that there has been at least partial reopening of the LAD. This is all the more reason to proceed with prompt cardiac catheterization before reocclusion can occur.

 

The CASE Continues:

The cath lab was not activated. The patient's chest pain returned 3 hours later — and another ECG was obtained at this time (Figure-3). Troponin came back positive.

• How would you interpret the 2 ECGs shown in Figure-3 in the context of events of this case that occurred previously?

 

Figure-3: Comparison between the 2nd ECG — and ECG #3, obtained 3 hours later after chest pain returned (See text).

 

MY Thoughts on FIGURE-3:

Increased progression of ST-T wave changes are now obvious in Figure-3!

• PEARL #3: The BEST way to get really good at recognizing even subtle ST-T wave abnormalities — is to review serial tracings on cases in which you learn the results of cardiac catheterization and — for which you then GO BACK to the initial tracing to look again at those lead areas where subtle changes have now become obvious.
• The amplitude of T wave peaking that we saw in leads V2 and V3 of ECGs #1 and #2 — has dramatically increased in ECG #3 (to more than 10 mm in lead V3).
• Note that lead V1 now shows more ST elevation in ECG #3, as well as a hint of beginning terminal T wave inversion. This confirms that the subtle ST elevation that I suspected was present in lead V1 of ECG #1 was indeed an early and "real" sign.
• Note that the hyperacute T wave appearance in leads V2 and V3 has now extended in ECG #3 to also involve leads V4, V5 and V6 (all of which manifest definite flattening of their ST segment, with slight ST depression in V5,V6 and disproportionate T wave peaking that was not present previously). 
• Taken together — the 6 chest leads in ECG #3 are consistent with deWinter-like T waves from proximal LAD occlusion in this patient with new chest pain (See ECG Blog #183 for more on recognition of deWinter-like T waves).
• The T waves in leads I and aVL of ECG #3 are more peaked than they were in ECG #2 when the patient's chest pain had almost resolved. This supports my suspicion that the ST-T wave in lead aVL of ECG #1 was indeed a subtle-but-real early sign.
• The shape of the ST-T waves in each of the inferior leads (II,III,aVF) in ECG #3 clearly looks more acute than it did in ECG #2 when the patient's chest pain had almost resolved.

 

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FOLLOW-UP on Today’s Case:

Cardiac catheterization was performed after ECG #3 was obtained.

• As shown in Figure-4 — there was 100% occlusion of the proximal LAD — with achievement of excellent reperfusion following successful PCI.

Figure-4: Cath films on this patient before and after PCI:

• LEFT: WHITE arrows in the before-PCI picture highlight 100% proximal occlusion of the LAD (Left Anterior Descending) coronary artery. The LCx (LeftCircumflex) coronary artery is a large vessel, and is intact. Of interest — a Ramus Intermedius (ie, Ramus) coronary artery is present (the origin of the Ramus seen within the 2 dotted red lines). In ~10-20% of subjects — the Ramus may be seen as an anatomic variant, in which the LMain (Left Main Coronary Artery) trifurcates into the LAD, LCx and a Ramus branch of variable size. 
• RIGHT: RED arrows show successful reperfusion of the LAD following PCI — in which we now see good flow to the LAD and to the 1st Diagonal Branch. Of interest, the Ramus Intermedius branch is less well seen after reperfusion of the LAD — presumably because this vessel is no longer as needed, now that excellent flow to the LAD and its branches has been restored.

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Concluding NOTE: There is much to be learned from this case. It is always easier to look back in the "retrospectoscope" — but the important point is to learn from our experience.

• In a patient with new-onset chest pain — the hyperacute T wave appearance in leads V2 and V3 in ECG #1 should be all that is needed to prompt immediate cath lab activation.
• Given the corresponding reduction in chest pain 10 minutes later — the subtle-but-real ST-T wave changes noted in ECG #2 qualify as a "dynamic" ST-T wave change — which adds further support to the indication for prompt cardiac catherization.
• But in the event (for whatever reason) that the treatment team is not yet convinced of the indication for cath lab activation after seeing ECG #2 — a 3rd ECG should have been repeated long before the 3-hour delay in this case. This is among the most important lessons to be learned from today's case.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205). 
• ECG Blog #218 — Review of a case similar to today's (with the subject of Audio Pearl MP-35 in this Blog being WHEN T waves are "hyperacute"). 
• ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the “culprit” artery. 
• ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data. 
• ECG Blog #115 — Shows an example of how drastically the ECG may change in as little as 8 minutes. 
• ECG Blog #183 — Reviews recognition of deWinter-like T waves vs repolarization variants. 
• ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome.

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• The January 9, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case is remarkable for the dynamic ST-T wave changes that are seen. It’s helpful to appreciate: i) that acute ischemia/infarction is not the only potential cause of such changes (cardiac cath was normal); ii) that changes in heart rate, frontal plane axis, and/or patient positioning can not always explain such changes; and, iii) that entities such as repolarization variants, LVH, and/or acute myopericarditis may all contribute on occasion to produce an evolution of challenging dynamic ST-T wave changes on serial ECGs. 
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• The August 22, 2020 post in Dr. Smith's ECG Blog — which illustrates another case of dynamic ST-T wave changes that resulted from a repolarization variant. 
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• The July 31, 2018 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case provides an excellent example of dynamic ST-T wave changes on serial tracings (that I illustrate in My Comment) in a patient with an ongoing acutely evolving infarction.