ECG Blog #540 — Does it "Fit" the Clinical?

The ECG in Figure-1 was recorded from a 60-ish year old woman who presented via EMS (Emergency Medical Services) to a rural hospital for sudden onset of confusion and seizure activity.

• The patient became agitated and combative during transport. She was non-responsive on arrival in the ED (Emergency Department).
• The patient's medical history was unknown at the time she was seen.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Should you activate the cath lab?

 

Figure-1: The initial ECG in today's case — obtained from a 60-ish year old woman who presented with confusion and seizure activity. (To improve visualization — I've digitized the original ECG using PMcardio).

The ECG in Figure-1:

This patient's initial ECG is clearly abnormal:

• The rhythm is sinus tachycardia at a rate of ~130/minute.
• The QRS is narrow and the PR interval is normal.
• While fully acknowledging the difficulty estimating the QTc with marked tachycardia — the QTc is at most "borderline" (Our on-line QTc calculator suggests that the QTc is less than 450 msec.).
• Otherwise — the frontal plane axis is normal, and there is no chamber enlargement.

Regarding Q-R-S-T Wave Changes:

• Q Waves: Considering small size of the QRS in lead aVL — the Q wave in this lead is large in size (deep and wide). In view of the even smaller size of the QRS in lead I — the tiny Q wave in this lead is also likely to be significant.
• R Wave Progression: There is loss of R wave between leads V1 and V2. Although a reasonably sized R wave returns in lead V3 — transition (when the R wave becomes taller than the S wave is deep) is delayed until between leads V5-to-V6.

The above said, the most concerning findings in today's initial ECG are highlighted in Figure-2 (in the 4 leads within the GREEN rectangles). 

• Hyperacute ST elevation is clearly seen in both high-lateral leads ( = leads I and aVL). There is reciprocal ST depression in lead III. 
• In support of this reciprocal change in lead III — ST segment straightening and a lesser degree of ST depression is seen in the other 2 inferior leads ( = leads II and aVF).

In the Chest Leads: 

• Lead V2 is noteworthy because of its slightly elevated and disproportionately enlarged ST-T wave (being both "fatter"-at-its-peak and wider-at-its-base than expected given modest size of the S wave in this V2 lead).
• The picture in this lead V2 stands out in stark contrast to the complete lack of ST-T wave abnormality in the 4 chest leads that follow.

My Impression of ECG #1:

I initially saw today's initial ECG before knowing the history. 

• As suggested by the schematic image that appears above the ECG in Figure-2 — I immediately thought ECG #1 was diagnostic of the South African Flag Sign (See below for review of this important ECG finding). 

Figure-2: Today's ECG "fits" criteria for the South African Flag Sign!

The South African Flag Sign:

The clinical importance of recognizing the South African Flag Sign — is that in a patient with new Chest Pain — this ECG finding strongly suggests acute occlusion of the 1st or 2nd Diagonal Branch of the LAD (Left Anterior Descending) coronary artery. As per the schematic image above the ECG in Figure-2 — the South African Flag Sign is present when there is: 

• i) ST elevation in leads I, aVL and V2; 
• ii) Reciprocal ST depression in lead III (ST depression is also often seen to a lesser degree in neighboring inferior leads II and aVF);
• iii) No ST elevation in any chest lead except for lead V2.

I previously reviewed the South African Flag sign in ECG Blog #320 (See Pearl #1 in that Blog #320 post) — as well as in My Comment at the bottom of the page in the January 18, 2025 post in Dr.Smith's ECG Blog.

• PEARL #1: Sometimes acute proximal LAD occlusion will initially look like an acute occlusion limited to the 1st or 2nd Diagonal Branch. This is because early on — ST elevation may only be seen lead V2, and not yet in leads V1,V3,V4. A tincture of time (and serial ECGs) will usually clarify the situation.
• PEARL #2: The clinical significance of being aware of a Diagonal Branch "culprit" — is that: i) Since only 1 chest lead shows ST elevation (ie, lead V2) — this pattern will not “fit” the definition of a STEMI, because only 1 chest lead shows ST elevation (and by definition, to satisfy criteria for an anterior STEMI — 2 contiguous chest leads must show ST elevation); — and, ii) Recognizing the S. African Flag Sign alerts the angiographer where to look for the “culprit” artery. We have seen cases in which a capable angiographer initially missed the cath finding of Diagonal Branch occlusion — BUT — seeing this ECG pattern conveyed the need for another LOOK at the cath film, with focus on the expected area for Diagonal Branch takeoff then revealing subtle-but-complete occlusion in one of the Diagonals. 

The History Doesn't "Fit" ...

The problem with today's case — is that the history does not "fit" with the ECG picture that strongly suggests acute occlusion of the 1st or 2nd Diagonal Branch of the LAD.

• Today's patient had no chest pain. Instead — this 60-ish year old woman presented with neurologic symptoms, and arrived at the hospital in a non-responsive state.
• While possible for there to be a "silent" MI (ie, in which chest pain is absent) — the clinical presentation of today's case is contrary to what one would expect for an acute cardiac event. Could something else be going on?

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The CASE Continues:

Given the atypical history for an acute MI (especially in view of this patient's non-responsive state on arrival at the hospital) — the cardiologist on call appropriately opted to explore other etiologies before deciding on where best to transfer this patient (as the capability for cardiac catheterization and/or acute stroke management was not available at the rural hospital where this patient was brought to).

• Complicating assessment — an initial Troponin value was moderately elevated!
• The patient was transferred to a facility with cardiac catheterization and acute stroke management capability.
• Initial imaging suggested a necrotic ring-enhancing mass with significant surrounding edema that was thought to represent a brain tumor.

Figure-3 shows the follow-up ECG that was recorded ~4 hours after ECG #1.

• How do you interpret this repeat tracing? 

Figure-3: Comparison between the follow-up ECG recorded ~4 hours after the initial tracing.

Interpretation of ECG #2:

Compared to ECG #1 — the repeat ECG in Figure-3 shows the following:

• Some slowing of the sinus tachycardia (from ~130/minute — down to a rate of ~110/minute).
• Deflation of virtually all hyperacute ST-T wave changes that had been seen 4 hours earlier.

CASE Conclusion:

• The repeat Troponin was essentially unchanged from its initial value (showing similar moderate elevation).
• Cardiac Cath was performed — and showed completely normal coronary arteries — with an abnormal wall motion abnormality typical for Takotsubo (Stress) Cardiomyopathy.
• Further brain imaging suggested that rather than a brain tumor — the patient's neurologic injury was the result of necrotic transformation from a stroke. Given that the patient's neurologic condition returned to near normal — her longterm prognosis was promising.

Lesson-to-be-Learned:

• As discussed on a number of occasions in this ECG Blog — CNS Catastrophes (from CNS bleeds, stroke, tumor, trauma, undifferentiated coma, etc.) — are notorious for producing some of the most bizarre-looking ECGs that are prone to simulate acute infarction (See ECG Blog #299, among others).
• Today's case illustrates just how close the pseudoinfarction pattern from a "CNS catastrophe" may be! (For all the world — Today's initial ECG suggested acute 1st or 2nd Diagonal occlusion).
• Despite the alarming, seemingly acute ST-T wave changes in today's initial ECG — the clinical scenario did not "fit" for an acute MI. While fully aware that some acute MI patients may not necessarily present with chest pain — it was this "disconnect" between the initial ECG and the patient's history that clued to on call cardiologist into the need to explore other potential diagnoses.
• For other examples in which the unexpected clinical presentation suggested that acute-looking ECG changes represented a pseudoinfarction pattern (and not acute infarction) — Check out the February 20, 2025 post in Dr. Smith's ECG Blog (with My Comment at the bottom of the page in that post).
• A common denominator between these CNS catastrophes and the pseudoinfarction patterns they produce on ECG — is greatly increased endogenous catecholamines! This helps to explain the common finding of Takotsubo Cardiomyopathy (Stress Cardiomyopathy) that so often accompanies these conditions. It also explains many of the abnormal ECG findings, as well as the moderately elevated but non-rising Troponin value (See ECG Blog #456 — for review of the ECG findings in Takotsubo Cardiomyopathy).

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Acknowledgment: My appreciation to Paul Carr and Nataliya Szozda (from Toronto, Canada) for contributing this case.

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