ECG Blog #341 — WHY are the T Waves Peaked?

The ECG in Figure-1 — was obtained from a 60-ish year old man who was admitted following a syncopal episode in the bathroom. He complained of a short episode of abdominal pain a few weeks earlier — but had not had chest pain. He was hemodynamically stable at the time the ECG in Figure-1 was recorded.

• How would YOU interpret this patient’s initial ECG?
• Are ECG findings likely to be the result of hyperkalemia?

Figure-1: The initial ECG in the ED — obtained from a 60-ish year old man with a syncopal episode and abdominal pain. No chest pain.

MY Thoughts on ECG #1:

As always — I favor a systematic approach to 12-lead ECG interpretation (See ECG Blog #205).

• There is significant artifact — especially in the limb leads.
• The rhythm is sinus at ~65-70/minute. All intervals (PR, QRS, QTc) appear to be normal. There is marked LAD (Left Axis Deviation) — with at most, no more than a tiny initial positive deflection in the inferior leads.
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• PEARL #1: Although difficult to be certain because of the marked baseline artifact — it appears that QRS complexes in the inferior leads are fragmented (ie, notched). The combination of predominant negativity of the QRS + fragmentation — suggests that in addition to LAHB (Left Anterior HemiBlock) — there has also been infarction at some point in time.

Continuing with systematic assessment:

• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q waves: As already stated — while difficult (because of artifact) to determine if the initial QRS deflection in inferior leads is positive or negative (ie, Q wave or r wave) — this is an academic distinction, since predominant negativity with fragmentation in all inferior leads at the least qualifies as a “Q-wave-equivalent” pattern.
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• R Wave Progression: There is early transition (with R>S already by lead V2).
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• PEARL #2: Did YOU notice the rSr’ pattern in lead V1? (and the R-s-r’ pattern in lead V2?). While possible that this represents incomplete RBBB conduction — the finding of a similar terminal r’ deflection in lead aVR and the negative P wave deflection in lead V1 suggests that the V1 and V2 electrode leads in ECG #1 may have been placed too high on the chest (See ECG Blog #274 for clues how to quickly recognize V1,V2 misplacement). This is relevant to today’s case — because of how prominent T wave changes are in the anterior leads!

Continuing with S-T Changes:

• The most remarkable finding in ECG #1 — relates to the presence of tall, peaked and pointed T waves in the anterior chest leads. While their symmetric appearance, narrow base and extreme point at the peak of the T wave in leads V3 and V4 could clearly be consistent with hyperkalemia (and I would definitely want to check the serum K+ level) — lack of this extreme morphology in most other leads suggests something other than hyperkalemia as the cause.
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• The other remarkable lead area with prominent ST-T wave changes is in the inferior leads — where leads II,III,aVF all show ST segment coving (albeit no ST elevation) with moderately deep, symmetric T wave inversion.

ECG #1: Putting It All Together:

The patient in today’s case did not have chest pain. Instead — he was admitted to the hospital for a syncopal episode that occurred while he was in the bathroom. The patient also reported having an episode of abdominal pain several weeks earlier. Although less typical — these symptoms could represent an alternative presentation of recent or acute coronary disease.

• I did want to rule out hyperkalemia — but I thought the lack of more generalized T wave peaking to be against this electrolyte disorder as full explanation for the ST-T wave changes in this tracing.
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• Chest lead T wave peaking (with giant T waves >10 mm tall in leads V3,V4) could represent a form of deWinter-like T waves from LAD (Left Anterior Descending) coronary artery occlusion — BUT — the J-point ST depression of deWinter-like T waves is missing — leads with peaked T waves are not “fatter”-at-their peak and wider-at-their-base, as is typical with deWinter T waves — and, rather than ST elevation in the inferior leads, there is symmetric T wave inversion (See ECG Blog #183 — regarding the concept of deWinter-like T waves).
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• Alternatively, instead of hyperacute anterior T waves — T wave peaking in the chest lead distribution shown could reflect posterior wall reperfusion. This would be consistent with the symmetric T wave inversion in leads II,III,aVF of ECG #1, that might represent inferior wall reperfusion changes (See ECG Blog #266 — regarding distinction between deWinter T waves vs Posterior MI).
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• BOTTOM Line: I initially was not certain of the cause of the ST-T wave changes in ECG #1. That said, although today's patient did not present with new chest pain — he did present with other symptoms that could reflect recent or acute coronary disease. Regardless of my uncertainty about the potential presence and location of a "culprit" artery — the ST-T wave changes in ECG #1 looked acute!

The CASE Continues:

The patient remained hemodynamically stable. Serum K+ was normal ( = 4.5 mEq/L). Two troponins showed similar slightly elevated values. A 2nd ECG was obtained 30 minutes after the initial tracing (Figure-2).

• What (if any) ECG changes do you see in ECG #2?

Figure-2: Comparison of the initial ECG in today's case — with the repeat ECG obtained 30 minutes later. What (if any) ECG changes do you see?

The Repeat ECG:

There are some subtle changes in ECG #2, compared to the initial tracing. Appreciation of these changes is best accomplished by lead-to-lead comparison of both ECGs placed next to each other (as I have done in Figure-2). Note the following:

• QRS morphology and the frontal plane axis is similar in both ECGs shown in Figure-2. However, QRS morphology is different in the chest leads! Note that the terminal r' that was present in leads V1 and V2 of ECG #1 — is no longer present in ECG #2. In addition — there is no longer a negative P wave in lead V1. As a result — I suspect that the too-high lead V1,V2 placement of ECG #1 has been corrected in ECG #2. This is relevant — because the location of maximal T wave peaking has shifted more anteriorly in ECG #2.
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• BOTTOM Line: I found it difficult to determine IF there was (or was not) any significant change in ST-T wave morphology between the 2 tracings in Figure-2. That said — while the predominantly negative and fragmented QRS complexes in the inferior leads may have represented prior infarction — the tall, peaked chest lead T waves "looked" acute — with need to assume that they are acute until proven otherwise!

A Prior ECG was Found!

It turns out that a previous "baseline" ECG from 2016 was found. For clarity — I put this previous tracing together with ECG #2 in Figure-3.

• HOW does this baseline tracing help for understanding the probable time sequence of events in today's case?

Figure-3: Comparison of ECG #2 — with a prior ECG (ECG #3) from today's patient, obtained in 2016. How does this baseline tracing help in understanding the time sequence of events in today's case?

What the Prior ECG Tells Us:

A number of significant ECG changes have occurred in the 6 years since the prior (2016) ECG was obtained. These include the following:

• Although fragmentation and predominant negativity of the QRS in leads III and aVF was present in 2016 — a definite R wave was present in lead II of the baseline tracing. T waves in all 3 inferior leads were upright in 2016, with at most minimal J-point depression. This suggests that while a 1st inferior infarction may be "old" (those fragmented, predominantly negative QRS complexes in leads III and aVF of ECG #3) — loss of the R wave in lead II, with associated symmetric T wave inversion in all 3 inferior leads of ECG #2 are new findings since 2016!
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• Early transition with a prominent (nearly 15 mm tall) R wave already in lead V2 was present in the 2016 tracing. Whether this tall R wave in lead V2 of the 2016 tracing was serving as a marker of prior posterior infarction was uncertain from review of this baseline tracing.
• Note how deep the S wave in lead V2 of ECG #3 is (ie, >20 mm, with overlap into the lead V3 R wave). As a result — the tall anterior T waves (between 5-10 mm in height) that are seen in the 2016 tracing are not disproportionate. KEY Point: Seeing this 2016 baseline tracing helps explain why the T waves in ECG #2 are so very tall (and now so pointed). There has been superimposition of an acute T wave change on top of what previously was already quite tall anterior T waves.

Putting Together the Story from Figures-1, -2 and -3:

• There is no history of chest pain in today's case. Therefore — we are missing a very important "clue" to the timing of the acute event (assuming that retrospective questioning of today's patient does not yield recall of any additional symptoms in recent days-to-weeks).
• Against an acutely evolving event — is the lack of significant change in ST-T wave morphology between ECGs #1 and #2 — and the finding of 2 troponin values showing similar values that are only slightly elevated above normal.
• Presumably — a recent event occurred, given how tall and pointed the chest lead T waves are in ECG #2 (especially in comparison to their non-acute appearance in the 2016 baseline tracing).
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• Conclusion: From the information known — I think the most logical explanation for the above described ECG findings — is that ECGs #1 and #2 represent recent infero-postero MI (that probably occurred days-to-1-to-2 weeks ago) — with inferior T wave inversion and anterior tall, peaked T waves representing spontaneous reperfusion changes.

Cardiac Cath was Performed:

Angiography performed a number of days later — revealed extensive multi-vessel coronary disease (Figure-4).

• The main trunk of the LAD was patent. There was a ~70% stenosis of the 1st Diagonal Branch of the LAD.
• A critical 90% stenosis was present in the LCx (Left Circumflex). This was felt to be the "culprit" artery responsible for the patient's recent event.
• An 80% stenosis was present in the distal RCA (Right Coronary Artery).
• Two ~80% stenoses were present in the PDA (Posterior Descending Artery).

Figure-4: Cath images showing 90% narrowing of the LCx (the presumed "culprit" artery for the patient's recent event) — with additional high-grade lesions in the RCA and PDA.

Lessons To Be Learned:

• Multi-vessel disease can often explain unusual ECG findings (I was not initially sure of the culprit lesion from my review of the initial ECG in today's case).
• Not all patients with acute (or recent) MI have chest pain (See ECG Blog #228 — which includes an Audio Pearl on this subject). Among non-chest-pain symptoms that have been associated with "Silent" MI are syncope and abdominal pain (both of which were associated with today's case).
• The deWinter-like T waves of acute LAD occlusion vs tall anterior T waves from posterior wall reperfusion — can sometimes be very difficult to distinguish from one another. 
• Regardless of the cause and precise sequence events in today's case — ST-T wave changes in the initial ECG were obviously acute, with need for prompt investigation.
• The history is often KEY to explaining complex cases like this one (the brief recent episode of abdominal pain could represent the "silent MI" non-chest-pain equivalent symptom that explains all facets of 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).
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit" artery. NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI. 
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• ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.
• ECG Blog #80 — Reviews determination of the "culprit" artery and application of the Mirror Test for recognition of acute Posterior MI. 
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• ECG Blog #248 — Reviews a case that illustrates Causes of a Tall R Wave in Lead V1 (with the Audio Pearl in this post devoted to this subject).
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
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• ECG Blog #262 — Reviews a case of recent acute Infero-Postero MI with group beating from Wenckebach conduction and Low Voltage (with a list of the causes of Low Voltage).
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• ECG Blog #266 — Reviews some considerations when distinguishing between deWinter T Waves vs Posterior MI.
• ECG Blog #183 — Reviews a case of deWinter T Waves (with the Audio Pearl in this post discussing some variants of the deWinter T wave pattern). 
• ECG Blog #53 — Reviews another case of deWinter T Waves.
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• ECG Blog #318 — Provides another variation of de-Winter-like T waves — and — Reviews (and illustrates) the concept of T-QRS-D (Terminal-QRS-Distortion).
• ECG Blog #215 — Reviews a case with T-QRS-D.
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• ECG Blog #340 — Reviews yet another variation of deWinter-like T waves (with downsloping ST segments and ischemic-induced J-waves).
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• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 
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• The November 22, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the BOTTOM of the page for My Comment regarding ischemia-induced Osborn Waves).
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• ECG Blog #274 — Reviews the concept of R Wave Progression (and how to quickly recognize lead V1,V2 misplacement).