Wednesday, June 2, 2021

ECG Blog #230 (46) — Are there Serial ECG Changes?


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NOTE: Interpretation of the tracings in today's case involves multiple subtleties. But I felt it an excellent case for teaching purposes — since it provides many insights to real-life clinical decision-making when the answers are not obvious. Are YOU up for the challenge? YOUR input is welcome if you disagree with any of my assessments!

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The patient is a woman in her 50s with known coronary disease — including prior stenting of a proximal LAD lesion. She presented to the ED (Emergency Department) with typical chest pain of several hours duration

  • The patient's initial ECG is shown in Figure-1 — at which time she rated severity of her chest pain at 6/10.
  • No prior tracing was available for comparison at the time this patient was seen.

 

QUESTION:

  • In light of the above clinical history — HOW would you interpret this patient's initial ECG?

 

 

Figure-1: The initial ECG obtained from a woman with known coronary disease and new chest pain of several hours duration.


 

 

My THOUGHTS on ECG #1:

As always — I interpreted ECG #1 by use of a Systematic Approach (See ECG Blog #205 for details):

  • Rate & Rhythm: There is a regular sinus rhythm (with upright conducting P waves in lead II) — at a rate of ~70/minute.
  • Intervals (PR, QRS, QTc) — The PR interval is normal, and the QRS complex is not widened. I estimate the QTc to be prolonged at ~480 msec.
  • Axis: Normal (about +10 degrees).
  • Chamber Enlargement: None. (Although not shown — standardization is normal at 10 mm/mV. The P wave is peaked in lead II, but falls slightly short of criteria for RAA).

 

Regarding Q-R-S-T Changes:

  • Q Waves: There is a Q wave in lead aVL that is wider than is usually seen for a septal q wave. QS complexes are seen in leads V1V2 and V3.
  • R Wave Progression: Transition (where height of the R wave exceeds depth of the S wave in the chest leads) is delayed (occurs between lead V5-to-V6). R wave progression is poor as a result of the anterior QS complexes.
  • ST-T Wave Changes: There is ST segment flattening in multiple leads, some of which show a hint of slight ST depression. There is ST segment coving with minimal ST elevation and modest, symmetric T wave inversion in leads V2, V3 (and to a lesser extent in lead V4). There is ever-so-slight ST elevation in lead aVR.


IMPRESSION: This is not a normal tracing — as the QTc is prolonged, and there are nonspecific ST-T wave abnormalities in virtually every lead.

  • The QS complexes in leads V1-thru-V3 — with no more than a tiny r wave in lead V4 and a small fragmented r wave in lead V5 — are consistent with prior anteroseptal MI.
  • While the above-described ST-T wave changes could clearly be consistent with ischemia — my impression was that these changes were not diagnostic of an acute process. That said — no prior ECG was available for comparison at the time this patient was seen.


PEARL #1: In the absence of a prior ECG for comparison — it is not possible to rule out an acute process on the basis of this single tracing. On occasion — one may see the phenomenon of "pseudo-normalization"— in which on-the-way to evolving acute ST elevation — prior ST depression passes through a stage in which ST segments are nearly isoelectric. 

  • KEY Point: The history in this case is that of a “high-prevalence” situation (ie, one with higher likelihood for an acute event) — since the patient has known coronary disease, and now presents to the ED with report of new typical chest pain of several hours duration. Therefore — despite the fact that ST-T wave changes in ECG #1 do not look particularly acute — the burden of proof remains on the medical team to rule out an acute event, rather than the other way around.

 

PEARL #2: As stated — we can not rule out the possibility of an acute ongoing event on the basis of the single ECG shown in ECG #1. Close follow-up, serial troponins, and several repeat ECGs will be needed to determine the patient’s course.

  • ECG findings may evolve quickly — sometimes over the space of minutes rather than hours (See ECG Blog #115 — for an example of dramatic ST-T wave evolution over a period of less than 10 minutes). As a result — the 2nd ECG in a patient with ongoing chest pain should probably be obtained within ~15-30 minutes — with additional repeat tracings being indicated until one can be comfortable that an acute process is not actively evolving.
  • As discussed in ECG Blog #222 — a "coming-and-going" of chest pain severity, associated with a 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. 
  • 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.


PEARL #3: When available — Echo at the bedside (looking for a localized wall motion abnormality during an episode of chest pain) — can be an excellent way to provide immediate support of the need for prompt cardiac cath. 

  • It should be emphasized that the diagnostic value of bedside Echo is markedly reduced IF the patient is not having chest pain at the time the Echo is done (ie, Nothing is ruled out by a normal Echo if the patient is no longer having symptoms). 

 


The CASE Continues:

2nd ECG was done ~2 hours after ECG #1. Severity of chest pain had decreased to 4/10 at the time this 2nd ECG was obtained (Figure-2).

 

QUESTION:

  • HOW would you interpret ECG #2 in light of the tracing obtained 2 hours earlier?
  • In Figure-2: Are there clinically significant changes between the 2 tracings?

 

 

Figure-2: Comparison of the initial ECG in this case — with a 2nd ECG obtained ~2 hours later (See text).


 

 

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NOTE: Some readers may prefer at this point to listen to the 7:20 minute ECG Audio PEARL before reading My Thoughts regarding the 2nd ECG that is shown in Figure-2

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Today’s ECG Media PEARL #46 (7:20 minutes Audio) — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?").

  • For review of the 3 Clues that suggest chest lead malposition of leads V1 and V2 — See My Comment at the bottom of the page in the November 4, 2018 post on Dr. Smith’s ECG Blog.

 



My THOUGHTS on ECG #2:

The most relevant way to interpret ECG #2 — is by lead-to-lead comparison with ECG #1 — which is why I've placed these 2 tracings together (Figure-2). I'll often compare leads in a similar anatomic distribution together. Looking first in the Limb Leads:

  • Q waves are decidedly deeper in both of the high lateral leads ( = leads I and aVL) in ECG #2. In addition, the ST segments in these 2 leads are more coved, with a hint more T wave inversion in the 2nd ECG.
  • There is clearly more ST depression in each of the inferior leads ( = leads II, III, aVF) in ECG #2.
  • CAVEAT #1: There has been a shift in frontal plane axis between ECG #1 and ECG #2. This is evident from the fact that the QRS complex in lead III is predominantly negative in ECG #1 — but it is predominantly positive in ECG #2.
  • CAVEAT #2: Interpretation of the meaning of these limb lead ST-T wave changes is complicated by the fact that 2 hours passed between the time that ECGs #1 and #2 were done — so we don't know the full story about how these ECG changes evolved.

 

Looking next in the Chest Leads:

  • There is slight-but-real ST segment coving and elevation in leads V2 and V3, that seems to be less in ECG #2 compared to ECG #1. T wave inversion also seems more shallow in ECG #2.
  • There is slightly more J-point ST depression in leads V5 and V6 in ECG #2.
  • CAVEAT #3: There has definitely been a change in R wave progression between these 2 tracings. In ECG #1 — No r wave at all was seen in leads V1, V2 and V3 — and transition (where the R wave becomes taller than the S wave is deep) did not occur until between leads V5-to-V6. In contrast, in ECG #2 — a small r wave develops by lead V3 — and transition occurs much earlier (between leads V3-to-V4).

 

Putting It All Together: I found it difficult to know what to make of my serial comparison between ECG #1 and ECG #2.

  • There has been change in the severity of this patient's chest pain (ie, a decrease from 6/10 to 4/10).
  • There has been slight increase in ischemic changes in the limb leads of ECG #2.
  • There has probably been no overall change in the chest leads.
  • Comparison between the 2 tracings was clearly made more difficult by slight change in frontal plane axis and definite change in R wave progression that was probably caused by somewhat different precordial lead electrode placement
  • BOTTOM Line: I wish we had a repeat ECG showing similar frontal plane axis and similar R wave progression that was done much sooner than 2 hours after ECG #1. Without this — it is hard to draw conclusions. I was not convinced from comparison of ECG #1 and ECG #2 that an acute event had occurred.

 

 

The CASE Continues:

Serum troponins never reached significance. By the next morning — the patient's chest pain had virtually resolved — and a 3rd ECG was done (Figure-3). On seeing this 3rd ECG — the cardiology team discharged the patient. Cardiac cath was not performed.

 

QUESTION:

  • HOW would you interpret ECG #3 in light of ECG #2?
  • In Figure-3: Are there clinically significant changes between the 2 tracings? If so — WHAT is the most likely explanation for these changes?

 

 

Figure-3: Comparison of ECG #2 — with a 3rd ECG obtained the following morning (See text).



 

 

My THOUGHTS on ECG #3:

Once again — there are technical issues that complicate interpretation of ECG #3, and comparison of this 3rd ECG with ECG #2:

  • The frontal plane axis in ECG #3 is clearly different than that in ECG #2 (Compare the different QRS appearance in leads III and aVF in these 2 tracings). The frontal plane axis in ECG #3 resembles that seen in ECG #1.
  • I suspect the lead V1 and V2 electrodes in ECG #3 were placed too high on the chest because: i) For the 1st time — P waves in both of these leads are negative; andii) There is a distinct r' complex in lead V2 that wasn't previously seen (See My Comment at the BOTTOM of the page in the November 4, 2018 post on Dr. Smith’s ECG Blog).
  • Transition occurs later in ECG #3 compared to ECG #2.
  • BUT Despite these Technical Differences — I think it is unmistakable that symmetric T wave inversion is clearly deeper in multiple leads in ECG #3 compared to ECGs from the day before!

 

Putting It All Together: Brief coronary occlusion followed by rapid spontaneous reopening of the "culprit" artery may not always result in serum troponin elevation. The patient in today's case had known coronary disease — she presented with a very typical story of new chest pain — and showed a series of subtle ECG changes in association with her symptoms. Her chest pain resolved the next morning — in association with diffuse deepening of symmetric T wave inversion not fully explained by modest technical differences between the tracings.

  • I interpreted this diffuse T wave inversion as most consistent with reperfusion T waves following a transient event (See ECG Blog #194 — for more on this subject).
  • While clinically — this patient may not have suffered any lasting damage from her brief coronary occlusion — the risk is that what once spontaneously occluded and reopened, might reocclude again without necessarily reopening the next time. I thought cath should have been performed to see if PCI (Percutaneous Coronary Intervention) was needed.
  • I suspect the ECG story may have been more convincing had the 2nd tracing been done sooner, and additional serial tracings obtained.

 

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Acknowledgment: My appreciation to Kris Walpot (from Leuven, Belgium) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
  • ECG Blog #115 — Shows an example of how drastically the ECG may change in as little as 8 minutes
  • ECG Blog #222 — Reviews the concept of dynamic ST-T wave changes, in the context of a detailed clinical case. 
  • 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.

  • An Example of R Wave Progression that Does Not Make Sense (therefore probable malposition of 1 or more chest leads): See My Comment at the BOTTOM of the page in the May 3, 2020 post on Dr. Smith’s ECG Blog.

  • 3 Clues that Suggest Too-High Placement of Leads V1 & V2 Electrodes: See My Comment at the BOTTOM of the page in the November 4, 2018 post on Dr. Smith’s ECG Blog.

  • Another Example of Too-High Placement of the Leads V1 & V2 Electrodes: See My Comment at the BOTTOM of the page in the March 29, 2020 post on Dr. Smith’s ECG Blog.





4 comments:

  1. Interesting case, Dr. Grauer. I agree those changes on the last strip might suggest spontaneous reperfusion. Would it be possible to comment a little bit more on the QTc prolongation and its importance when considering ischemia? Thank you! T.

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    1. Good Question you ask! — although unfortunately, it is one without a definite answer. It IS true that QTc prolongation may be caused (and/or exacerbated) by acute or chronic ischemia. The problem is that MANY things may prolong the QTc interval (ie, certain medications/low K+ or low Mg++/ CNS disorders/ hypertrophy-“strain”) — plus we don’t have a baseline ECG that might tell us if the prolonged QTc is a longterm finding. So the prolonged QTc doesn’t really help me in this particular case.

      What I CAN say — is that 2 less-commonly-thought-of factors that might favor a repolarization variant instead of early anterior infarction can be normal R wave progression and a shorter-than-expected QTc interval. That said — even in this setting, those are nonspecific findings — and by itself, a slightly short vs normal vs prolonged QTc would NOT be decisive for me when assessing a chest pain patient’s ECG.

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  2. Strange, why suddenly a Q in I and aVL in the second ECG and not in ECG 1 and 3. Something went wrong with leads placement I think.

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    1. My favorite “Go-To” site for quick review of the most common forms of lead misplacement is from Life-In-The-Fast-Lane (GO TO — https://litfl.com/ecg-limb-lead-reversal-ecg-library/ ) — but the picture we see “come-and-go” in ECGs 1,2,3 does NOT resemble any of these common lead placement errors. Now, it is possible that a “multiple lead mix-up” occurred — and those are more difficut to predict … though that is not overly common once you are in a hospital with experienced technicians …

      In my 7-minute ECG Audio Pearl in today’s blog post ( = MP-46, above) — I discuss some factors to keep in mind — one of which that is usually NOT considered is the angle of the bed — which CAN change QRST morphology. I have no idea of knowing if this might be a possibility in today’s case. Other than that (as I explain in detail above) — YES, there IS an axis shift — but the cause of this is not apparent …

      BOTTOM LINE — As per my above Audio Pearl — it IS important to realize that we are “not comparing apples with apples” when we compare ECG #1 and #2 — nor when we compare ECG #2 and #3 for the many reasons I described in detail above. WHY the limb leads in ECG #2 are so different though is not something we are able to retrospectively explain …

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