Thursday, January 20, 2022

ECG Blog #277 — WHY those T Waves?

The ECG in Figure-1 was obtained from an older man with abdominal pain. He was alert, but hypotensive at the time this tracing was done. No chest pain.



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




Figure-1: This ECG was obtained from an older adult with abdominal pain. How would YOU interpret this tracing?


MY Sequential Thoughts on the ECG in Figure-1:

Although artifact and curvature of this tracing make assessment more challenging — I believe that accurate interpretation still is possible.

  • The rhythm is sinus tachycardia at a rate of ~110/minute. Regarding intervals — the PR interval is normal and the QRS complex is narrow. Assessment of the QT interval is clearly more difficult with tachycardia. That said — despite the fast heart rate, the QTc appears to be markedly prolonged!
  • The frontal plane axis is normal (about +80-85 degrees). No chamber enlargement.


Regarding Q-R-S-T Changes:

  • Q Waves — Small but-definitely-present q waves are seen in each of the inferior leads (II,III,aVF). There is loss of r wave between lead V2-to-V3 — with development of a narrow but deep Q wave in lead V3, with persistence of small q waves through to lead V6.
  • R Wave Progression — Transition is normal (ie, the R wave becomes taller than the S wave is deep between leads V2-to-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-1 (ie, leads I, II,III,aVF; V2-V6). The depth of the T-wave inversion in lead V3 attains nearly 15 mm, which is huge! T wave depth measures 10 mm in lead V4 — and 9 mm in lead V2.
  • Additional important findings include 1 mm of ST elevation in each of the inferior leads, with suggestion of slight reciprocal ST depression in lead aVL — and — meaningful ST elevation in each of the chest leads showing T wave inversion.


COMMENT: The most remarkable finding in today's case is the presence of Giant T-Waves. As was discussed in detail in ECG Blog #276 — 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.

  • PEARL #1: The clinical importance of recognizing the presence of Giant T Waves in today's tracing — is that this should immediately suggest the diagnostic considerations listed in Figure-2.
  • Despite the fact that the patient in today's case did not have chest pain — the 2 entities among those listed in Figure-2 that seem most likely to account for the Giant T waves in today's tracing are: i) Acute MIand iiTakotsubo CMP (CardioMyoPathy).
  • Unfortunately — a definitive diagnosis was never obtained in this case, because the decision was made to treat this severely ill patient conservatively. Details of management are lacking. It is known however, that among the complications that developed — Hyperkalemia (ie, K+ = 6.4 mEq/L) was present near the time that the ECG in Figure-1 was obtained.


Figure-2: This graphic reviews the definition of Giant T-Wave Syndrome and — the Differential Diagnosis of this ECG finding (For more on Giant T Waves — See ECG Blog #276).


My thoughts on this case are the following:


ECG Findings in Favor of Acute MI:

The Q waves, ST elevation and T wave inversion in each of the 3 inferior leads in Figure-1 certainly suggests acute MI. Similarly — chest lead Q waves and diffuse ST elevation with deep T wave inversion could clearly be the result of a large infarction from acute LAD (Left Anterior Descending) coronary artery occlusion.

  • Acute LAD occlusion with a "wraparound" distribution to supply the inferior wall — could account for the presence of Q waves and ST-T wave changes in both inferior and antero-lateral leads in Figure-1.
  • The deep, diffuse T wave inversion could represent reperfusion T-waves occurring at a point in the process in which residual ST elevation was still present.


My HUNCH: Takotsubo Cardiomyopathy:

Realizing that I do not have access to definitive information in this case — I still think it interesting to speculate about what the final diagnosis might have been.

  • Although certainly possible that the ECG in Figure-1 could reflect the result of acute "wraparound" LAD occlusion, now in the stage showing deep reperfusion T waves — certain ECG findings go against this theory. These include: i) The markedly prolonged QTc interval in an alert patient; ii) The lack of chest pain in the history; andiii) The lack of localization of ECG findings (ie, deep T wave inversion is seen in no less than 9/12 leads).
  • Instead — I feel the ECG in Figure-1 and the clinical picture in today's case is more suggestive of Takotsubo Cardiomyopathy (See Figure-3which I've reproduced from ECG Blog #46). Findings in this case suggestive of Takotsubo CMP include: i) The markedly prolonged QTc interval; ii) The lack of chest pain in the history; iii) Sinus tachycardia (which is nonspecific, but common with Takotsubo CMP — related to increased sympathetic tone/catecholamine surge associated with this disorder)iv) A lack of reciprocal ST depression (because the area of myocardial dysfunction with typical Takotsubo CMP is mainly in the apex)andv) Diffuse ST elevation with deep T wave inversion without localization to a specific anatomic area (as would be expected with acute MI). Also relevant, is the fact that these ST-T wave changes are most marked in the chest leads of Figure-1 (as would be expected with Takotsubo CMP — because the area of myocardial dysfunction is mainly in the apex).
  • PEARL #2: Takotsubo CMP is easy to overlook — because there are no specific ECG findings to confirm the diagnosis. Instead, a variety of non-localized Q waves and ST-T wave changes may be seen (as suggested in Figure-3). Because these ECG abnormalities may be marked, there is a tendency to diagnose acute MI instead of Takotsubo.
  • Think of the possibility of Takotsubo CMP when confronted with a patient who presents with a markedly abnormal ECG that doesn't quite "fit" the clinical picture — as in today's case.


PEARL #3: As noted earlier — the patient in today's case developed renal failure, and was found to have a serum K+ = 6.4 mEq/L around the time that the ECG in Figure-1 was obtained.

  • While we expect to see tall, peaked T waves with hyperkalemia — negative T waves may sometimes be seen! The fact that many of the inverted T waves in the chest leads of Figure-1 are pointed at their deepest descent makes me wonder if hyperkalemia may have been contributing to this T wave appearance.

Figure-3: ECG Findings in Takotsubo Cardiomyopathy (For more on Takotsubo Cardiomyopathy — See ECG Blog #46).



Acknowledgment: My appreciation to Anil Kumar Kolli (from Indiafor the case and this tracing.


Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #276 — Reviews the syndrome of Giant T-Waves (and the most common causes of this disorder).

  • ECG Blog #46 — Reviews ECG findings with Takotsubo Cardiomyopathy.

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