## Friday, March 15, 2019

### A 50-something with chest pain presents to a Non-PCI capable facility

An avid reader sent me this case.  He learned to read subtle ECGs here.

Case

A 50-something presented with chest pain.  A triage ECG was recorded and shown to the ED physician:
 What do you think?The QTc-B was 427 ms

This was texted to me with no information, and here is my reply:

"I think it looks like an LAD occlusion."

Why did I say this?
--There is minimal STE in V2, but in the presence of a tiny QRS.
--The ST segment in V2 is convex upward, or at best straight
--The QRS starts with a Q-wave
--There is a fragmented QRS (down-up-down-up-down-up)
--There is ST elevation in V3 with a rather straight ST segment

If you ignore the convexity, and use the 4-variable formula, we get:

STE60V3 = 3.0
QTc = 427
RAV4 = 12.5
QRSV2 = 2

Value = 21.73.  This is a very high value and strongly supports LAD occlusion.  The best cutoff was 18.2 with approximately 85-90% sensitivity and specificity.

The reader then told me the details:

"The ECG was shown to my partner, who thought it was normal.  He signed it as "No STEMI" (which is technically true)."

"I then signed up for the patient on the board without having seen the ECG."

"Then I saw the ECG and thought to myself "Oh, my God!""

"I too thought it looked like an LAD occlusion."

"I then saw the patient clutching his chest."

"I gave aspirin and heparin bolus, and called for a helicopter to transfer to the PCI facility."

"I was afraid they would not even accept the patient."

"The helicopter arrived and we recorded another ECG 25 minutes after the first, just as he was being loaded onto the stretcher:
 Now it is an obvious STEMI (see leads V3 and V4)

Then I gave 50 mg (full-dose) TNK-tPA (tenecteplase)

Outcome:

The cardiologist at the receiving institution reported that the patient was pain free on arrival.  [No EKG data was provided. This is important because if the ECG does not show evidence of reperfusion, immediate angio +/- PCI is indicated regardless of pain status]

"He said the patient was nearly pain free on arrival to their ER because of the TNK-tPA and thus, since he got TNK, protocol is to wait 3-24 hours because of the risk of bleeding.  If he were still having significant chest pain, they would have taken him immediately."

Because he was pain free, they waited 14 hours (until the next AM) to take him to CATH:

Angiogram:

100% occlusion of the old stent in the LAD (with a 95% stenosis proximal to the stent), 90% stenosis of RCA, and 70% stenotic circumflex, so he stented all three.

Whether there was TIMI 3 flow was not stated.

His troponin I peaked at 76 ng/mL.

===================================
Comment by KEN GRAUER, MD (3/15/2019):
===================================
This is an important example of shape recognition. The case was submitted by an avid follower of Dr. Smith’s ECG Blog. The patient was a man in his 50s, who presented to the ED with chest pain. His initial triage tracing is shown in ECG #1. Forty-five minutes later — a 2nd ECG (ECG #2) was obtained. For clarity — I have put both tracings together in Figure-1.
• Dr. Smith has expertly detailed the reasons why the QRST appearance in leads V2 and V3 of ECG #1 is diagnostic (until proven otherwise) of acute LAD occlusion.
QUESTION: Aside from leads V2 and V3 — How many other leads in ECG #1 are abnormal?
• ALSO  Do you think there may be a problem with lead placement in ECG #1?
 Figure-1: The 2 ECGs shown in this case (See text).
===================
COMMENT: As per Dr. Smith — considering that this ECG was obtained in an ED, leads V2 and V3 are all but diagnostic of acute LAD occlusion. That said, this tracing was interpreted as “normal” when first seen. As a result — it is worth dissecting the findings in ECG #1.
• In addition to the findings noted by Dr. Smith — the SHAPE of the QRST complex in lead V2 should “jump out” at you! The frowny” shape (ie, coved) ST segment that is topped off by a fatter-than-it-should-be T wave peak is simply disproportionate to the tiny QRS complex in this lead. This is a “picture” that in a patient with new chest pain — should be saying to you, “I’m an acute OMI until you prove that I am not."
• To support the presumption that lead V2 is acute — we need to find at least one neighboring lead with ST elevation. As noted by Dr. Smith — the 2mm of J-point ST elevation with “rather straight” takeoff in lead V3 is clearly abnormal. NO more than these 2 neighboring leads in this patient with new chest pain should be needed to justify prompt transfer to the closest PCI facility.
BUT — it is Important to Recognize the OTHER Findings:
• With proximal (as opposed to mid- or distal) LAD occlusion, in addition to anterior chest lead ST elevation — there will often be associated limb lead changes in the form of ST elevation (which may be subtle) in lead aVL inferior lead ST-T wave depression. In ECG #1 — there is suggestion of slight ST elevation in lead aVL — and, there are subtle-but-real ST segment flattening changes in each of the 3 inferior leads. Of these, lead aVF is the most marked — in that it clearly shows a straightened (if not slightly depressed) ST segment, with abrupt angulation that leads into a taller-than-it-should-be T wave given the tiny amplitude of the QRS complex in this lead aVF. NOTE: These limb lead changes are subtle! Butin the context of clearly abnormal ST elevation in V2 and V3 in this patient with new chest pain — I believe they strongly support the likelihood of acute proximal LAD occlusion.
• Next in the context of clearly abnormal ST elevation in leads V2 and V3 — I interpreted the slight-but-real ST elevation in neighboring leads V1 and V4 as abnormal. I felt this offered further support that acute proximal LAD occlusion was ongoing. Retrospectively — I felt a look at ECG #2 (in Figure-1confirmed that the subtle ST elevation that I just alluded to for leads V1 and V4 of ECG #1 was real — because abnormalities in both leads V1 and V4 have clearly become more evident in this 2nd ECG obtained 45 minutes later.
Finally — I suspect there is malposition of at least lead V2 in ECG #1. This is because R wave progression as we move from lead V1-to-V2-to-V3 in ECG #1 just doesn’t make physiologic sense (ie, practical disappearance of the S wave in lead V2, with this multiphasic, almost null QRS complex — that then shows return of a substantial S wave in lead V3). Realizing that much has changed in ECG #2 with evolution of the infarct and development of deep anterior Q waves (QS complexes) — Doesn’t progression of QRS complexes and ST-T waves across chest leads in ECG #2 appear to be more logical?
• Given that ECG abnormalities were initially not recognized in ECG #1 — it is quite possible that suspecting malposition of one or more chest leads, and immediately repeating the ECG might have resulted in a repeat tracing with more leads showing abnormal findings that might have been picked up earlier.
BOTTOM LINE: The fact that ECG #1 was initially interpreted as “normal” in this patient with new chest pain — means there is still “work to be done” in the area of ECG interpretation education.Rather than strict adherence to numerical stemi guidelines:
• Remember that the prevalence of acute cardiac disease is greatly increased in an adult of a certain age who presents to an ED with new-onset chest pain.
• When the amount of ST segment deviation is modest — ST segment SHAPE takes on much greater importance.
• Although changes may be subtle — it’s essential to scrutinize all 12 leads, to see if a consistent “story” is being told. Doing so reveals that no less than 8 of the 12 leads in ECG #1 show at least subtle abnormal findings — which, when interpreted together in association with the clearly abnormal appearance of leads V2 and V3, make a convincing case for acute LAD occlusion until proven otherwise.
Our THANKS to the avid reader who shared with us this insightful tracing!

1. This seems quite obvious to me. Probably because I've been following your blog.

1. Yes. It is far from obvious to most physicians!

2. @ Swagata — GREAT that this now seems quite obvious to you! The "next step" is how well did you in recognizing the subtler abnormal findings in the other 6 leads (beyond V2,V3) — and did you suspect possible lead malposition of at least lead V2 in ECG #1 (These fine points discussed in My Comment above — :)

2. @Steave Smith; In my locality this is indeed hard to diagnosis such subtle MI. We are not taught this in college and since this a poor third world country with slow transport; most MI patients come with evolved or old mi. In my 14 days of cardiology rotation, Ive never seen one hyperacute MI.

3. @Dr. Ken, I did see the slight st elevation in lead aVL and st depression in lead aVF. But I did not suspect the malposition of lead V2. From ECG #1; since the diagnosis was primarily based on V2; if there is malposition of V2; then isn't V2 invalid ? In that case; was other changes significant enough to make a diagnosis of LAD occlusion ?

1. @ Swagata — In my opinion (others may feel different) — it is the COMBINATION of findings in ECG #1 (as I describe above) in this patient with new chest pain that strongly suggest acute OMI until you prove otherwise. My point about V2, is that its placement may be off. I DO think we definitely CAN (and should) use lead V2 — and it is by far the most abnormal lead. My point is that perhaps IF lead placement did turn out to be off, and another ECG was done with corrected lead placement — that this might yield an even MORE abnormal ECG that would be easier to diagnose. I hope this makes sense — :)

2. I understand your point. Thanks for the clarification.