Prehospital Cath Lab Activation. What happened when the medics and patient arrived at this Academic ED?

This was texted to me by a paramedic while I was out running one day:

"54 yo male chest pain started at 1pm. History of diabetes type II and stent placement in 2018. I’m seeing hyperacute T waves III, aVF, down sloping depression I and aVL. Thoughts?"

What do you think?

I responded: "Definite inferior OMI.  And Right Ventricular.  Activated the Cath Lab."

He responded: "Copy that...Cath Lab activated. thank you"

Smith analysis: There is a massive hyperacute T-wave in lead III, and a massive reciprocally inverted hyperacute T-wave in aVL (and I).  There is minimal STE in III and reciprocal STD in aVL (and I).  There is some minimal STE in V1 (suggesting RV MI) and minimal STD in V2 (suggesting posterior OMI, and also mitigating the evidence of RV MI -- the posterior OMI pulls down the ST segment in V1 so there is less STE than there would otherwise be).  There are hyperacute T-waves in V3 and V4, further evidence of RV MI.  there is a bit of STD in V6 which is identical to "precordial swirl" which can be due to LAD OMI involving the septu, or to RV MI.

Let's see how the PMCardio Queen of Hearts AI Model performs:

"Acute Occlusive Myocardial Infarction"

She gave this a score of 1.0 (100% probability of acute OMI)

Here is the explainability map:

He arrived at the ER (this is a place with an Emergency Medicine Residency).

"We're in the ER now and they said 'the elevation is not convincing.'"  

They de-activated the cath lab.

This ECG is so obvious to me that it is hard to imagine that there are doctors who do not recognized it.  But it is true.  Many, if not most, doctors are so brainwashed by "1 mm of ST Elevation in 2 consecutive leads" that they cannot see OMI without it.

I contacted a doctor there whom I know to tell him about it and to get some follow up:

He wrote: "That is disappointing. Kudos to the medics."

"I found out that the interventionalist had just finished a case and came to the ED to see about the de-activated case. He saw the ECG and ordered an ED ECG."

Here it is:

Obvious inferior OMI, and now the STE in V1 is huge, with huge hyperacute T-waves of Right ventricular OMI

The cath lab was re-activated:

Angiogram:

100% occlusion mid-RCA occlusion (in-stent thrombosis). TIMI 0. Aspiration thrombectomy and DES x1. LVEDP 31.

The RV marginal branch must have a takeoff that is more distal than usual, as this is definitely an RV MI.

My friend also wrote this:

"Yeah. Apparently the intern also recognized it (he is an avid reader of the blog), but the staff overruled him." 

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My Comment, by KEN GRAUER, MD (11/14/2024):

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I share Dr. Smith's disappointment with regard to the failure to recognize the obvious acute OMI evident on today's initial ECG (that I've reproduced and labeled in Figure-1).

• The patient is a 54yo man with diabetes and a known history of coronary diseae (prior stent placement) — who presented with new CP (Chest Pain) — therefore very high likelihood for having an acute coronary event. This should mean that the initial ED physician should be looking for the slightest abnormalities — that need to be taken as acute until proven otherwise (and not the other way around).
• The initial ECG shows definite ST-T wave abnormalities in 11/12 leads — with marked hyperacute T waves in lead III (within the 1st RED rectangle in Figure-1). Given tiny size of the fragmented QRS complex in this lead (which I interpreted as a "Q-wave equivalent" given predominant negativity with notching on the S wave downslope) — this QRS complex could literally "swim" around within the huge ST-T wave in this lead (ie, that is clearly "hypervoluminous" ) .
• Confirmation of T wave hyperacuity in lead III is immediately forthcoming from mirror-image opposite ST-T wave depression in lead aVL (within the 2nd RED rectangle in Figure-1).
• In the context of these marked ST-T wave abnormalities in leads III and aVL — the T waves in leads II and aVF are also clearly hyperacute ("bulkier"-than-they-should-be given relative size of the QRS in these leads).
• 
  
• IMPRESSION: In this very high likelihood patient with new CP — the total time to diagnose acute inferior OMI with need for prompt cath should be no more than seconds, given the findings in these 4 limb leads. The paramedics on this case immediately recognized these findings. As per Dr. Smith — I also found it difficult to understand why the admitting ED physicians cancelled the cath lab activation.

QUESTION:

I've mentioned 4 specific leads (leads II,III,aVL,aVF) that show diagnostic changes of acute inferior OMI.

• Why did I say that 7 additional leads also show abnormal ST-T wave findings? 

Figure-1: I've labeled the initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWER:

The following describes ST-T wave abnormalities in 7 additional leads:

• Lead I — also shows reciprocal ST-T wave depression. We have often emphasized the "magical" mirror-image opposite ST-T wave picture between leads III and aVL in the setting of acute inferior OMI. This is such a consistent finding — that we have to question whether inferior lead ST elevation truly indicates acute inferior OMI if we do not see this reciprocal relationship between leads III and aVL. Although usually not as marked as the ST-T wave depression that we see in lead aVL with acute inferior OMI — we will often also see indication of reciprocal ST depression in lead I (which together with aVL, is the other high-lateral lead).
• Lead V1 — shows ST segment coving of a broader-than-usual T wave for this lead, with slight-but-real ST elevation. In the setting of acute inferior OMI — seeing ST elevation in lead V1 suggests associated RV MI. This can be confirmed by obtaining right-sided chest leads (See the May 30, 2023 post in Dr. Smith's ECG Blog for more on the ECG diagnosis of RV MI).
• Lead V2 — shows ST segment flattening with ST depression. This is definitely abnormal — because leads V2 and V3 normally show a slight amount of gentle upsloping ST elevation — such that ST segment flattening with depression in association with acute inferior OMI is diagnostic of associated posterior OMI. Note that despite the marked hyperacute limb lead changes — the relative amount of ST depression in lead V2 is minimal. The reason for this is that what would have been much more ST depression from this posterior OMI — has been attenuated by the ST elevation produced in leads V1 and V2 (which correspond to right-sided leads V2 and V1).
• Leads V3,V4 and V5 — all show "bulkier"-than-they-should-be ST-T wave in these leads. They are also hyperacute T waves (ie, fatter-at-their-peak and wider-at-their-base than they should be given modest QRS amplitude in these leads). What is unusual about these hyperacute changes — is that usually this is seen with acute LAD OMI — though the "culprit" artery on cath was the RCA (mid-stent thrombosis). Since this patient has known coronary disease as well as diabetes — we can speculate that these changes in this anterior lead distribution may be the result of some compromise in collateral flow to the anterior wall. Regardless of its cause — the "answer" regarding these hyperacute changes in leads V3,V4,V5 is that it adds further support to the need for prompt cath.
• Lead V6 — shows abnormal ST segment "scooping" with slight depression — which I interpreted as an additional sign of diffuse, underlying coronary disease.

BOTTOM Line in Today's CASE: In a very high likelihood patient with new CP — the ECG changes in leads II,III,aVL and aVF (at the very least) — need to be promptly recognized (as they were by the paramedic on this case).

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