Sunday, July 26, 2020

Prehospital ECG of a 50-something male with Syncope and Chest Pain

This case was sent by an excellent medic:

A 50-something yo male started to chop wood when he experienced a short syncopal episode followed by 8/10 chest pain.  Ground EMS arrived, administered ASA and sublingual nitro to which he passed out again.

Flight crew was called to transport for signs of shock/syncopal episodes, not ACS.

Ground crew had recorded this prehospital ECG:
Sinus rhythm with one PVC (first complex)
And anything else?























These are hyperacute T-waves diagnostic of LAD occlusion.  They begin at V3, and there is no inferior ST depression, so this is probably a mid-LAD occlusion.  The hyperacute T-waves extend to inferior leads, with a reciprocal down-up T-wave in I and aVL. So it is likely that this LAD wraps around to the inferior wall.  But all of that is not important.  What is important is that one recognizes that there is an occlusion somewhere in some kind of coronary artery. There is some ST depression in V5 and V6.

It is Occlusion Myocardial Infarction (OMI).  But it is not a STEMI, as there is very little ST Elevation.  At most about 50% of OMI meet STEMI criteria.  If you do not recognize this immediately, then you need lots of practice.

See this lecture on electrocardiographically subtle LAD occlusion:

Subtle ECG Findings of Left Anterior Descending Artery (LAD) Occlusion -- LAD Occlusion MI (OMI)


The medic continues:

"Everyone stated this was not a STEMI/ did not fall under STEMI guidelines, however I knew (thanks to your blog) this was an occlusion due to hyperacute T waves V3-V4 and Lead III and aVF.  We airlifted the patient with the LUCAS applied/ STAT pads applied and BVM/airway stuff out and ready.  My partner during the flight was wondering why all the precaution.  I pointed out that the patient was experiencing R on T and to be ready.  The cath lab was activated from the air and we were escorted directly to the lab.  The patient’s pain was treated throughout the flight with bumps of Fentanyl since nitro dumped the patient’s pressure twice before.

"The patient was placed on the table and immediately went in to cardiac arrest with ventricular fibrillation for 5 rounds.  They were able to resuscitate and stent the patients LAD (100% occluded).  We got report a couple days later the patient went home with no deficit.

"Many would not have recognized this as hyperacute and went to the ER.  I want to thank you all again for your teachings as they do not go unappreciated."


Here is the outcome:
It was 35 minutes from symptom onset to ECG.  Then another 31 minutes to activation.

As you can see, there is indeed LAD thrombus with poor flow (arrow on left), re-established by stenting (arrow on right).
The ECG was done at the time of the cath, approximately 60 minutes after the first diagnostic ECG. 


Let's put the two ECGs next to each other:




You can see by the ECG done at the time of cath that the hyperacute T-waves have diminished, but some ST Elevation has developed in V3-V6 over the 90 minutes interval.  



Learning Points:

Learn to recognize electrocardiographically subtle LAD occlusion.  There is no better way to do this than to watch this lecture:

Subtle ECG Findings of Left Anterior Descending Artery (LAD) Occlusion -- LAD Occlusion MI (OMI)




Ken Grauer had these comments:

THANKS so much for writing! So glad Dr. Smith’s ECG Blog has been so helpful! YES — this 12-lead ECG does show hyperacute T waves in each of the inferior leads, as well as in V3-thru-V6 (most marked as you state in V3,V4)  — consistent with 100% LAD occlusion (as per your cath). I’d imagine it was mid-LAD + “wraparound” — given lack of ST elevation in aVL, V1, V2 — with ST elevation in inferior as well as anterior leads.



===================================
MY Comment by KEN GRAUER, MD (7/26/2020):
===================================
Gratifying case for us to see — in which one of our astute medic followers was able to immediately recognize the acuity of this OMI in progress as a result of having learned the pattern from repeated similar cases posted on our blog.
  • Dr. Smith has posted above my immediate impression above (at the end of his discussion) on seeing this tracing and learning that the patient had new-onset chest pain = “this ECG shows hyperacute T waves in each of the inferior leads, as well as in V3-thru-V6 (most marked in V3,V4) — consistent with 100% LAD occlusion. I’d imagine it was mid-LAD + “wraparound” — given lack of ST elevation in aVL, V1, V2 — with ST elevation in inferior as well as anterior leads."

I’d like to add 2 additional points. To do this, I’ve reproduced in Figure-1 the initial ECG in this case.

Figure-1: The initial ECG in this case (See text).



POINT #1: We’ve shown numerous examples of de Winter T waves in Dr. Smith’s ECG Blog. I reviewed features of de Winter T waves in My Comment at the bottom of the page of the May 2, 2019 post — including reproduction of the Figure from the original manuscript by de Winter et al (NEJM 359:2071-73, 2008).
  • I added the following PEARL to that 2019 post — There are many variations on “the theme” of de Winter T waves. In my experience, many of the cases I’ve seen posted that go on to evolve to anterior STEMI do not show J-point ST depression as de Winter et al described (or at most, show minimal J-point depression in only 1-2 leads). The overall pattern is often not “static” — but rather evolves to frank ST elevation in serial tracings. What you see on ECG often depends on when during the process the ECG is obtained ... and, the pattern may evolve!
  • Thus, in ECG #1, the shape of the extremely large, hyperacute T waves (minus the lack of J-point ST depression) resembles the T wave shapes in the Figure I showed in the May 2, 2019 post, which I took from the original manuscript by de Winter et al.

POINT #2: An “R-on-T” phenomenon was said to have been observed in this case. It should be emphasized that this is not what we see for the PVC ( = beat #1) in Figure-1. Unfortunately, we do not see a long lead rhythm strip with onset before the ventricular beat in ECG #1 — but nevertheless, we can still describe what we see in this tracing — and we can still make an accurate determination of the etiology of beat #1.
  • Regular sinus P waves are seen in lead II of ECG #1 (RED arrows).
  • The PR interval preceding beat #1 is clearly shorter than the PR interval preceding sinus-conducted beats #2 and 3.
  • We cannot use lead I in our assessment of the etiology of beat #1 — because artifact distorts the space between the P wave and initial part of the QRS in this lead (BLUE arrow).
  • However, at least in lead II — the very first part of the QRS complex looks identical in beat #1 as in beats #2 and #3 (I’m looking at the initial shape and slope of the very first part of the r wave in lead II). It is the latter part of the QRS complex for beat #1 that becomes very different (at least in leads II and III). These features are characteristic of what happens when there is fusion between a late-cycle ( = end-diastolic) PVC and a sinus-conducted beat.
  • The clinical significance of recognizing late-cycle PVCs in a patient with ongoing acute OMI is comparable to the diagnostic significance of AIVR (Accelerated IdioVentricular Rhythm), when AIVR occurs in the setting of ongoing OMI — which often means there has been spontaneous reperfusion. However, since patients may undergo spontaneous reperfusion — only to be followed a short while later by reocclusion (and then repeat this process over ensuing minutes or hours more than once ...) — it is difficult to correlate events in this patient regarding the repetitive episodes of VFib he experienced, with some resolution of hyperacute T waves, but development of anterior lead ST elevation in the repeat ECG (shown above). This is because we lack more precise awareness of the specific timing of ECG changes correlated to changes in symptom severity. That said — there is a bottom line ...
  • BOTTOM Line: Be aware of the concept of late-cycle PVCs — which can provide insight (in association with symptom and ECG evolution) regarding the likelihood of spontaneous reperfusion (For more on late-cycle PVCs — Please see My Comment at the bottom of the August 13, 2019 post).
  • P.S.: For more on "My Take" regarding late-cycle (end-diastolic) PVCs that result in Fusion Beats (including laddergram illustration) — CLICK HERE


2 comments:

  1. i love this particular post.
    it is all so very clear. and its always wonderful to hear how this blog has led to another life saved; esp in the face of an obvious OMI without STEMI.
    i wonder which hospital is SMMC. and why did it necessitate a chopper? difficult access?
    this medic (i wish i knew his name) performed wonderfully.
    thanks to him, and steve and ken.

    oh... i am prob over-reading, but don't beats number 4 and 5 in lead aVF look a tad Wellen-ish?

    thanks guys.

    ReplyDelete
    Replies
    1. THANKS for your comments Tom! In the Section, “The Medic Continues” — the T waves in leads III and aVF are described as “hyperacute” — which I agree with. The T wave in beat #1 (in lead III) is difficult to assess, given that this is a Fusion beat. But the next 4 T waves (in lead III for beat #2; and in lead aVF for beats #3,4,5) are all fatter-than-they-should-be at their peak, and wider at their base — therefore hyperacute in their appearance. I think the T wave in beat #2 in lead II looks similar + reciprocal changes in lead aVL. So, not-so-much “Wellens-like” in my opinion — but hyperacute inferior lead ST-T wave changes that occur here in association with the acute chest lead changes — :)

      Delete

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