Sunday, January 16, 2022

ECG Blog #276 (81) — What About those T Waves?


You are given the ECG shown in Figure-1 — but without the benefit of any history. 

 

QUESTIONS:

  • How would YOU interpret this tracing?
  • What about those T Waves?

 

Figure-1: You are given this ECG without the benefit of any history. How would YOU interpret this tracing?


=======================================

NOTE: Some readers may prefer at this point to listen to the 9:50-minute ECG Video PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-81).

=======================================



Today's ECG Media PEARL #81 (9:50 minutes Video) — Summarizes my Systematic Approach to 12-lead ECG interpretation (during the first 2:50 minutes of this video) — after which I apply this Systematic Approach to the tracing shown below in Figure-2. I then work through the list of potential Causes of Giant T-Waves shown below in Figure-3.

 

Figure-2: Hard copy of the 12-lead ECG that is discussed in detail in the above ECG Video. The patient was a 50-year old man with chest pain. Which cause(s) of those listed in Figure-3 are most likely to account for the Giant T Waves in leads V4-V6?



Figure-3: Reviews KEY content of the above ECG Video — including the definition of Giant T-Wave Syndrome and, the Differential Diagnosis of this ECG finding.


  

MY Sequential Thoughts on the ECG in Figure-1:

For clarity — I've colored QRST complexes in leads V1, V2 and V3 of today's tracing (Figure-4). As always for interpretation — I favor use of a Systematic Approach (which I review in ECG Blog #205 — as well as during the first 2:50 minutes in today's ECG Video):

  • The rhythm is sinus bradycardia at a rate of ~45-50/minute. The PR, QRS and QTc intervals are all normal (ie, Given the slow heart rate — the QTc is at most no more than minimally prolonged). The frontal plane axis is normal (about +40 degrees).
  • Even though we don't know the age of this patient — QRS amplitudes are increased to such an extent that voltage criteria for LVH are likely to be satisfied regardless of the patient's age (See ECG Blog #245 regarding criteria I favor for ECG diagnosis of LVH).

 

Regarding Q-R-S-T Changes:

  • Q Waves — None.
  • R Wave Progression — Transition occurs early — as a sizeable R wave is already present in lead V1 — and — by lead V2, R wave amplitude equals S wave depth. There follows predominant R wave positivity beginning with lead V3.

 

Regarding ST-T Wave Changes:

  • The most remarkable finding on this tracing is the deep, symmetric T wave inversion that is seen in no less than 9/12 leads in Figure-4. The depth of the T-wave inversion in lead V3 attains nearly 15 mm, which is huge!
  • Additional less obvious findings include slight ST elevation (in leads III and V1) — and — 1-to-1.5 mm of J-point ST depression in virtually all leads that manifest T wave inversion.

 

Figure-4: I've colored QRST complexes in the anterior leads from Figure-1 — so as to highlight the zone of transition in the chest leads (RED, GREEN and BLUE complexes in leads V1, V2 and V3).

 

Clinical Impression: The ECG in Figure-4 shows fairly marked sinus bradycardia — LVH — and — 1-to-1.5 mm of J-point ST depression, followed by deep, symmetric T wave inversion in multiple leads that could be consistent wth LV "strain" and/or ischemia.

  • Clearly — some History is needed for clinical interpretation of this tracing (ie, Is this ECG from a young, relatively asymptomatic athletic adult? — or — from an older patient with recent or new-onset chest pain?). Without any history — we can merely suggest likely possibilities.
  • That said — the following 2 PEARLS can go a long way toward suggesting the most likely possibilities.

  

PEARL #1: More than simply "deep, symmetric T wave inversion" in Figure-4 — there are Giant T-Waves. As defined in today's ECG Video (and above in Figure-3) — the designation of "Giant" T waves is reserved for a limited number of clinical entities that are likely to produce truly deep (>5-10 mm amplitude) T wave inversion.

  • The definition of "Giant" T waves is satisfied for the tracing in Figure-4 by the nearly 15 mm of T wave inversion in lead V3. The T wave in lead V4 is at least 8 mm — and the T wave exceeds 5 mm in leads V2 and V5. 
  • Truly "giant" T waves are not overly common. The advantage of identifying this entity — is that doing so should immediately suggest the diagnostic considerations listed in Figure-3.
  • While impossible to determine WHICH of the entities in Figure-3 is (are) most likely — the lack of significant QTc prolongation would seem to make a severe CNS disorder and Takotsubo Cardiomyopathy less likely. The presence of marked voltage for LVH is in favor of Apical Cardiomyopathy. The 1-to-1.5 mm of J-point ST depression in multiple leads is in favor of ischemia.

  

PEARL #2 — It is tempting on seeing the biphasic T wave with steep downsloping terminal component in lead V2 of Figure-4 (drawn in GREEN) — to think of Wellens’ Syndrome. That said — Wellens’ Syndrome is unlikely to be present in this case

  • While acute coronary disease is a diagnostic possibility when there are Giant T waves (ie, acute ischemia is included among the entities listed in Figure-3) — it is well to remember that there are other causes of the ST-T wave picture seen in lead V2 of Figure-4. These include (among others) — LVH, cardiomyopathy, coronary reperfusion. 
  • In Figure-4 — I suspect the reason for the biphasic T wave in lead V2 (drawn in GREEN) — is simply a reflection of the increased QRS and ST-T wave amplitude that we see, with lead V2 representing a “transition lead” placed between the fairly tall positive T wave in lead V1 (drawn in RED) — and the very deep negative T wave in lead V3 (drawn in BLUE).
  • Remember that the diagnosis of Wellens' Syndrome is far less reliable in the presence of LVH — especially in the presence of ST-T wave changes of LV "strain" and/or ischemia (as is seen in Figure-4).
  • With true Wellens' Syndrome — one would not expect such prominent R wave amplitude in the anterior leads as is seen in Figure-4.
  • T wave inversion is generally not this widespread with Wellens' Syndrome — as it is in Figure-4
  • NOTE: For more on what Wellens' Syndrome is and is notSee ECG Blog #254

 

==============================

I conclude today's ECG Blog post with a final example of Giant T Waves.

  • What differences do you see between the 2 ECGs in Figure-5?

 

Figure-5: Compare this final example of Giant T Waves (TOP Panel) — with the initial ECG in today's post ( = Figure-1shown in the LOWER Panel). Both tracings exhibit Giant T waves. What differences exist between these 2 tracings? (NOTE: I've adapted the ECG in the TOP Panel from the June 22, 2020 post in Dr. Smith's ECG Blog).


ANSWER:

Although both tracings in Figure-5 show Giant T Waves — there are a number of differences between these 2 ECGs.

  • The heart rate is significantly faster in the TOP tracing.
  • QRS amplitude is less in the TOP tracing. That said — voltage for LVH is still satisfied in this TOP tracing by Peguero Criteria (ie, sum of deepest S in any chest lead + S in V4 ≥23 [female] or ≥28 [male]). In this TOP ECG — the S wave in lead V3 (18+ the S in V4 (13) = 31 (See ECG Blog #245 for my review of LVH criteria).
  • The QTc is greatly prolonged in the TOP tracing (it makes up almost 3/4 of the R-R interval) — whereas considering the slow heart rate, the QTc in the LOWER tracing is no more than minimally prolonged.

 

PEARL #3 — While each of the diagnostic considerations for Giant T Waves that are listed in Figure-3 can potentially lengthen the QT interval — the degree of QTc prolongation seen in the TOP tracing of Figure-5 is more likely to result from Takotsubo Cardiomyopathy or from a severe CNS disorder (ie, CNS bleed, stroke, tumor, trauma, seizure, coma).

  • Wellens' Syndrome seems less likely to cause the ST-T wave appearance seen in the TOP tracing — because the excessively prolonged QTc and diffuseness of T wave inversion are not regular features of Wellens' Syndrome. 
  • As was the case in Figure-4 — I suspect the reason for the ST-T wave appearance in lead V2 of the TOP tracing, is that this lead serves as a "transition lead" between notable T wave positivity in lead V1 — and profound T wave inversion in lead V3.
  • Follow-Up: It turns out that the patient whose ECG is shown in the TOP panel of Figure-5 was having alcohol withdrawal seizures, which I suspect was the principal cause of the Giant T Waves and marked QTc prolongation (ie, severe CNS disorder). Additional details with discussion of this case represented by the TOP tracing in Figure-5 can be found in My Comment at the bottom of the page in the June 22, 2020 post of Dr. Smith's ECG Blog. 

 

==================================

Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  •  
  • ECG Blog #245 — Reviews the ECG diagnosis on LVH (with a 9-minute Audio Pearl in this post on this topic).
  •  
  • ECG Blog #254 — Reviews what Wellens' Syndrome is — and what it is not (with a 7:40 minute Audio Pearl in this post on this topic).
  •  
  • ECG Blog #46 — Reviews ECG findings with Takotsubo Cardiomyopathy.
  •  
  • The June 22, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews the case of Giant T-Waves with prolonged QTc that is shown in the TOP panel of Figure-5 above.



No comments:

Post a Comment