The current STEMI paradigm: Because STEMI criteria are not met, let's wait until the myocardium is dead!!

This was sent to me by an inpatient nurse who reads this blog but wants to remain anonymous.

An inpatient rapid response was called for a patient with hypotension.  

The patient was originally admitted for pneumonia and had been transferred out of the ICU a day prior. He had a history of HFrEF, HTN, and AML. 

"When I arrived his blood pressure was 70s/40s and he was pale and profusely diaphoretic." 

"He spoke Spanish but we did deduce that he had 7/10 chest pain radiating to the back." 

"We couldn’t initially get a hold of the primary physician but our hospital allows the rapid response nurses to begin a work-up through protocols/standing orders so I obtained serial EKGs, a high sensitivity trop, and administered aspirin."

Here is the ECG:

The conventional computer read was "Normal sinus rhythm.  Right Bundle Branch Block"

What do you think?

Smith: this ECG with RBBB is diagnostic of proximal LAD Occlusion (OMI).  Absence of ST Elevation is irrelevant.  There is ﹤1 mm of STE in I, aVL, V5 and V6 (no STEMI "criteria", and hyperacute T-waves in I, aVL, V5 and V6.

This nurse, who reads this blog regularly, immediately recognized OMI, in spite of absence of ST Elevation criteria.

Nurse: "I compared it to an admission EKG from four days prior which made me even more concerned." 

Here is that previous ECG:

No RBBB, and no hyperacute T-waves

Finding and viewing this previous ECG should not be necessary to make the diagnosis!

"I called interventional cardiology and sent them pictures of the baseline EKG as well as the serial EKGs during the call, and explained the patient presentation." 

"They replied by saying that the EKG "doesn’t meet STEMI criteria" but that they would come and evaluate at bedside." 

"They agreed with me that the presentation was highly concerning but were initially planning on waiting a few hours (!!) to take the patient for cath later in the afternoon." 

Smith: waiting only makes for more irreversible myocardial loss with attendant heart failure and death.  Why would anyone want to wait??  Don't wait!!

"Luckily, after we moved the patient to the CCU, the critical care team performed a bedside echo that revealed LV hypokinesis and they immediately took the patient to the cath lab."

Delay due to absence of STEMI criteria: The time delay had they not done the echo in the ICU would have been several hours; as it was, there was an extra hour of delay.

Nurse: "They found a thrombotic occlusion of the proximal LAD with TIMI 0 flow and the patient received two stents." 

The initial high sensitivity troponin I was 15 ng/L (below the URL). Depending on troponin would have delayed intervention -- do not use troponin to make the decision when the ECG is diagnostic!.

Smith: I sent the diagnostic ECG to the Queen of Hearts:

And here is the explanation:

You can see that the Queen sees the hyperacute T-waves in I, aVL, V5 and V6.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

Learning points:

1. One's credentials have little to do with one's ability to read an ECG for OMI.  It takes a certain visual talent and lots of practice and, most of all, the ability to free one's mind of the old ways of seeing things.  Some of the best are EKG techs with who have no medical training at all.  Nurses, medics, interns.  All can be expert at this. 

2.  The Queen of Hearts is amazing.

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MY Comment, by KEN GRAUER, MD (4/16/2024):

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Important case for the reasons put forth above by Dr. Smith. I'll add the following thoughts regarding interpretation of the initial ECG in today's case, that I've reproduced and labeled in Figure-1.

• First — to emphasize the presentation of today's patient: This patient had just been discharged from the ICU a day earlier — and now presented with new CP (Chest Pain) and hypo-tension. His past medical history included HFrEF and hyper-tension — and he is tachycardic. It is hard to imagine a more concerning clinical presentation scenario (ergo — our need to rule out rather than rule "in" an acute event).

Even before looking at this patient's prior ECG, done just 4 days earlier — We see the following in Figure-1:

• Sinus tachycardia (in association with new CP and hypotension) = a very worrisome finding!
• Bifascicular block (RBBB/LPHB).
• 
  
• ST-T wave abnormalities in multiple leads — which as per Dr. Smith (even before comparing with the ECG from 4 days earlier) is diagnostic of acute proximal LAD OMI.

Looking closer at the specific ECG findings I have labeled in Figure-1:

• Typically with simple RBBB — there is ST-T wave depression in at least several anterior leads. There should not be the ST segment coving seen in ECG #1 (which I highlight with the "frowny"-shape coved BLUE curved lines that I've drawn in leads V1,V2,V3).
• I've superimposed with a dotted BLUE line in leads V1,V2 the approximate depth I'd expect to see for the ST depression in these leads with uncomplicated RBBB (especially given the surprisingly tall R' deflection in lead V1). The absence of any ST-T wave depression in lead V2 (and to a lesser extent, the less-than-expected amount of ST-T depression in V1) is almost certainly the result of attenuation by what would otherwise probably be anterior ST elevation.
• RED dotted lines in leads I, aVL; V4,V5,V6 are drawn at the ST segment baseline. Because of the ST segment coving in each of these leads (which as per Dr. Smith — clearly reflects hyperacute ST-T waves in these leads) — it is difficult with these smooth ST segments to know where the "J-point" truly lies — but although not great in terms of amount — I interpreted the ST segments in each of these 5 leads as elevated (especially in lead V4).
• RED dotted lines in inferior leads III and aVF are also drawn at the ST segment baseline. I interpreted the ST-T wave depression in these 2 inferior leads as consistent with reciprocal changes in acute proximal LAD OMI. 
• 
  
• BOTTOM Line: If we add in the abnormal ST-T wave flattening in lead II — then, in addition to sinus tachycardia and bifascicular block (RBBB/LPHB) in this patient with a very worrisome clinical presentation — there are worrisome, acute-looking ST-T wave changes in 11/12 leads (ie, in all leads except aVR).
• As per Dr. Smith — it's hard to imagine why anyone would want to delay immediate cardiac cath and PCI in this patient who by all evidence, appears to be in the throes of progressing to cardiogenic shock.

Figure-1: The initial ECG in today's case.