ECG Blog #467 — The Cath Lab was Deactivated

I was sent the ECG in Figure-1 — obtained from a previously healthy man his 60s, who contacted EMS (Emergency Medical Services) for new-onset severe “burning” CP (Chest Pain) that radiated to the jaw and throat.

On seeing the ECG in Figure-1 — the EMS crew activated the cath lab.

• QUESTION: Do you agree with this decision by the EMS crew to activate the cath lab?

Figure-1: The initial ECG in today's case — done by EMS at the scene. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Today’s CASE:

Sometimes — “Ya gotta be there!” The words on paper in my initial paragraph (written above) — voice concern that this man in his 60s may be having an acute cardiac event. If similar concern is perceived by the EMS team in the field — then even before seeing the initial ECG, the patient is in a higher-risk category for having an acute cardiac event.

• As a result — any abnormalities on the initial ECG should prompt significant concern.

And — the initial ECG in Figure-1 is not normal ...

• The rhythm is sinus (small, but upright P wave in lead II ) — with some R-R interval variability (probable sinus arrhythmia).
• All intervals (PR, QRS, QTc) are normal — as is the frontal plane axis (about +50 degrees). No chamber enlargement.
• Regarding Q-R-S-T Wave Changes: There are no Q waves — and R wave progression is normal (with transition where the R wave becomes taller than the S wave is deep occurring normally between leads V3-to-V4). 

BUT — there are subtle-but-important findings regarding ST-T wave appearance. I've highlighted these in Figure-2. 

• Do you agree?

Figure-2: I've labeled the initial ECG in today's case.

Abnormal Findings in Figure-2:

• My "eye" was immediately drawn to lead V2 (within the RED rectangle). There should be slight gentle upsloping ST elevation in leads V2 and V3 in a normal tracing. This is not seen in lead V2 (the straight RED line that I've drawn in this lead highlighting this abnormal straightening of the ST segment). In a patient with new CP — recognition of this subtle-but-important finding is what prompts me within seconds to suspect an ongoing posterior OMI (Occlusion-based MI).
• In addition — the T wave in lead V2 looks taller-than-it-should-be given modest size of the QRS in this lead (RED arrow in lead V2). This suggests that there may already be some spontaneous reperfusion of an ongoing posterior OMI.
• In support of my suspicion of an ongoing posterior OMI — is the similar finding in neighboring lead V2 of another T wave that looks taller-than-it-should-be (within the BLUE rectangle).
• Any doubt that I may have had that these admittedly subtle lead V2 and V3 findings are real — was immediately dispelled by the shelf-like ST depression in lead V4. There is no way this shape and this amount of ST depression in this mid-chest lead is "normal" (especially since lack of increased R wave amplitude in this tracing rules out LV "strain" from LVH as a cause of ST depression).
• Additional findings of subtle but abnormal ST segment straightening are also seen in leads V5, I and aVL.
• And then there is the coved but non-elevated ST segment in lead III — that I felt was noteworthy, though of uncertain significance.

What do these Subtle Findings Mean?

When interpreting ECGs such as the initial tracing in today's case — We need to remember that we are not trying to "rule in" an acute STEMI.

• Instead — We need to remember that this man in his 60s presents with new cardiac-sounding CP that immediately places him in a higher-risk category for having an acute cardiac event. Therefore, in the absence of a prior baseline ECG for comparison — any abnormal findings on his initial tracing must be interpreted as acute until proven otherwise.
• Not to accept that the process of acute coronary occlusion is "fluid" and not "static" — is to ignore the pathophysiology of this process. It is also the best way to miss a lot of acute OMIs in need of prompt cath with PCI (ie, See recent publications by Ricci, Smith et al — Ann Emerg Med, 2025 — and — McClaren, Smith et al — JACC Adv. 2024,3:101314 — with detailed review of this pathophysiology in Podcast #2 in My ECG Podcast tab at the top of each page in this ECG Blog). 

Impression: In this patient with new CP — the ECG in Figure-1 should suggest the possibility of an evolving posterior OMI. 

• While fully acknowleding that STEMI criteria are not satisfied in this initial ECG (and that many interventionists would not take this patient to the cath lab on the basis of this single ECG unless the patient was having refractory CP) — the physiologic reason for the lack of more obvious abnormalities may be the result of some spontaneous reperfusion (suggested by disproportionately taller-than-expected T waves in anterior leads V2,V3).
• This could account for the lack of ST elevation on this tracing (ie, "pseudonormalization" phase — that occurs between the stage of ST elevation and reperfusion ST-T wave changes). 
• Whether ST coving in lead III is the result of associated inferior OMI is uncertain from this single ECG. 
• Finally, given this patient's age and the diffuseness of the above-noted ST-T wave abnormalities — there may be underlying multivessel disease. 
• Bottom Line: Additional evaluation (serial ECGs, Troponins) with prompt transport to a cath-capable facility is needed.

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The CASE Continues:

The patient was promptly transported to the nearest ED facility. The ECG was repeated on arrival in the ED — as shown in Figure-3.

• The ED physician interpreted the patient's "burning" CP that was with associated nausea as GERD (esophageal reflux). As a result — initial treatment consisted of a GI cocktail.
• The patient's CP had decreased at the time the repeat ECG (shown at the bottom of Figure-3) was recorded. As a result — the cath lab was deactivated.

QUESTIONS:

• Do you agree with this management in the ED?
•     — Is ECG #2 an unremarkable tracing?

Figure-3: Comparison between the initial ECG vs the repeat ECG in the ED.

My Thoughts on Figure-3:

There are subtle-but-important differences between the 2 ECGs that are seen in Figure-3.

• KEY Point: It would be easy to overlook these differences if these tracings were not placed side-by-side to facilitate lead-by-lead comparison.
• There has been a slight change in the frontal plane axis (ie, The isoelectric QRS that is now seen in lead aVF of ECG #2 indicates a more horizontal axis). This slight axis shift probably accounts for the intermittent QS that we now see in lead III. That said — I do not think there has been any significant ST-T wave change in the limb leads.

In the chest leads:

• The T waves in leads V2 and V3 appear less prominent in ECG #2.
• There is less baseline wander and less baseline artifact in leads V4,V5,V6 of ECG #2. As a result — assessment of ST-T wave appearance is much more reliable in this repeat ECG. Whereas I put a BLUE question mark over the variable ST-T wave appearance in lead V6 of ECG #1 — there is now no doubt that there is abnormal ST segment flattening with slight ST depression in leads V4,V5,V6.

Bottom Line: Overall – I think ST-T wave changes in ECG #2 may be slightly less. This may be explained by the decrease in the patient's CP at the time of the repeat ECG. But the definite ST segment flattening and depression in leads V4,V5,V6 is real — and given the history of new severe CP — this has to be assumed as acute ischemia until proven otherwise.

• The call for cath lab activation should not have been deactivated on the basis of this 2nd ECG.

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The CASE Continues:

• The initial Troponin was negative.
• Although the patient's CP had decreased on arrival in the ED — it never went away.
• A bit later, while still in the ED — the patient's CP worsened, at which time ECG #3 was recorded (which I've placed next to ECG #2 in Figure-4).

QUESTIONS:

• How to interpret the 2 ECGs in Figure-4 given the clinical context of this case?
•     — What to do?

Figure-4: The ECG was repeated while the patient was still in the ED because of worsening of his CP.

ANSWER:

Looking at ECG #3 — the answer is now obvious.

• In ECG #3 — We now see definite hyperacute ST-T waves in leads III and aVF — with marked reciprocal changes in high-lateral leads I and aVL.
• The previously taller T waves in leads V2 and V3 — have been replaced by marked ST depression that begins in lead V2 and extends through until lead V6.
• There is now more ST elevation in lead aVR.
• IMPRESSION: There is an obvious acute infero-postero OMI in progress. Correlating the timing of the severity of this patient's CP with serial ECG changes suggests that the taller-than-expected T waves that were initially seen in leads V2,V3 did reflect spontaneous reperfusion — BUT — recurrence of CP severity in association with ECG #3 and worsening of ECG changes in virtually all 12 leads suggests there has been spontaneous reocclusion. The diffuseness of these ST-T wave changes in ECG #3 suggest there may be underlying multi-vessel disease.

Cardiac Cath was performed:

• The patient had multi-vessel disease — including a 90% LAD lesion — 70% LCx lesion — and "chronic near-occlusion" of the RCA.
• The patient was scheduled for CABG.

Lessons To Be Learned:

• In a higher-risk patient (such as the patient in today's case) — detection of subtle ECG abnormalities on the initial ECG may be extremely important. Frank ST elevation will not be seen in 1/3 or more cases of acute coronary occlusion. Especially if the history of symptoms is fluctuating — ECG changes may be subtle if the tracing is recorded during the period "pseudo-normalization".
• The initial Troponin may be negative despite ongoing acute infarction (even when high-sensitivity Troponins are used). Physiologically — this may occur as a result of very brief coronary occlusion, followed so soon after by spontaneous reperfusion. This is why clinical correlation of each ECG recorded with notation of the presence and severity of CP is so important.
• What spontaneously opens — may just as easily spontaneously reclose. For this reason — even though CP may decrease and the ECG may "improve" — if an ongoing OMI is in process, the patient still needs prompt cath with PCI to prevent reocclusion.
• In a patient with an ongoing OMI — reduced CP is not the same as completely resolved CP. As long as any CP continues — the acute event is still ongoing (such that prompt cath with reperfusion is still needed).
• The paradigm of waiting until STEMI criteria are satisfied is outdated and dangerous. Even when cardiac cath is ultimately performed — precious time is wasted, with potential loss of precious myocardium as a result of this delay (as occurred in today's case).

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Acknowledgment: My appreciation to Cortland Ashbrook (from Spokane, WA, USA) for the case and this tracing.

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