Saturday, July 28, 2018

Prehospital OMI recognized immediately by a fantastic paramedic

Written by Pendell Meyers, edits by Steve Smith

This case was sent by a paramedic who wishes to remain anonymous.

"The enclosed case resulted in a positive outcome, and I owe it entirely to the remarkable EKG tutorials on your website."

"A 65 y/o female was found uncomfortable, clammy, and complaining of chest pain. History of HTN, and high cholesterol. She had self medicated with aspirin prior to EMS arrival." 

Here is her first EMS 12 lead:

What do you think?

"12 Lead 1 (21:20:38) - V4 caught my eye as a hyperacute T-wave and indicative of total or at least subtotal occlusion. And the ST/T changes in III and aVF sealed the suspicion. I told the senior officer present to commence STEMI activation."

Meyers comment: This is an excellent interpretation, reflecting years of practice in recognizing hyperacute T-waves vs. normal variants. I agree that V4 is highly suspicious for being hyperacute, which first makes me look at its surrounding neighbors to see if they corroborate this claim. There is some very minimal STE in V2-V4 which, at first glance, might be thought to be a normal variant. However, if normal variant, then there should be good R-wave progression. Instead, there is very poor R wave progression with tiny R waves in V2-V4 which (by the formula) is one of the most important factors and will result in a very high score on the subtle anterior OMI vs. BER formulas.

The T-wave in V3 may not be hyperacute when considered in isolation; however, when considered in the context of V4, I would consider this also suspicious for being a hyperacute T-wave. V2 has a small amount of STE which is inappropriate for its QRS, as well as a possible very small Q-wave which must be assumed to be new in this scenario without a prior ECG for review.

Additionally, lead V2 technically has terminal QRS distortion, because there is no S-wave (never goes back below baseline) and there is also no J-wave. I am not completely convinced of the reciprocal findings inferiorly, but it is possible that these would be convincing if compared to a prior ECG if available.

Because of the possible reciprocal changes, the Q-wave, and the terminal QRS distortion in V2, the formulas would be formally contraindicated. Additionally, the formula technically requires at least 1mm STE in V2-V4 to consider using the formula.

So despite the fact that the formula should not be applied in this case, I will do so anyway to show how profoundly important the reduced R waves and QRS amplitude are:

Any value above 18.2 is LAD occlusion until proven otherwise. 23.08 is far above 18.2.

Two minutes later the paramedic recorded another ECG:

Posterior leads. OMI so obvious that it meets STEMI criteria.
"12 Lead 2 (21:22:58) - technically, a 15 lead, barely two minutes later now showing unequivocal STEMI."

Three more EKGs performed en route to cath center:

"12 Leads 3, 4, and 5 - standard lead placement - were performed en route to cath lab facility."

Here is his EKG on arrival to the cath lab facility ED:

This ECG immediately after the clearly diagnostic STEMI just above suggests that the artery is starting to reperfuse. As Dr. Smith says, the hyperacute T-waves are present "on the way up and on the way down" from total occlusion. V2 in this case is a great example of an unequivocally hyperacute T-wave.

"On arrival, however, the receiving ED physician was unimpressed with the findings on all pre-hospital EKG's. The first hospital EKG (21:41:28) remains pathological for OMI, but the physician merely said "ischemia." 

Nine minutes later, another ECG was recorded:

"The second hospital EKG (21:50:58) was performed just prior to the patient sustaining VF arrest. The physician consulted cardiology, and the patient went to cath. Here is the report:

...A 65 y/o female.  She had a VF arrest and was converted after 1 shock. We found a subtotal occlusion of the mid LAD at the bifurcation of a large diagonal. Wire passed through the soft clot that was present and proceeded to balloon, followed 2 DES stents in the LAD and 1 in the diagonal. Stenting the diagonal was based on the post stent image that showed the vessel to be nearly closed an considering its size and large territory it covered the stent was carefully placed in the diagonal. Activation of the CathLab to balloon = 53min.

Here is the angiogram before intervention:

And after intervention:

Learning Points:

For those of us (like this fantastic paramedic) who care about diagnosing OMI as soon as possible, one must learn to recognize subtle findings like those noticed on the first ECG. In some cases like this one, it will become obvious in minutes, but in other cases it won't happen this quickly or you won't have another ECG available. Until research proves otherwise, it is not acceptable to ignore this education and say "I'm just gonna wait until it turns into a real STEMI." It is an opportunity to save myocardium!

Serial ECGs make bad doctors good and good doctors great.

In addition to hyperacute T-waves and ST-segment deviations, be sure to look for Q-waves, terminal QRS distortion, reduced R-wave amplitude, etc.

Comment by KEN GRAUER, MD (7/28/2018):
Excellent discussion by Drs. Meyers & Smith of this anonymously submitted case, obtained from a 65-year old woman who presented with new chest pain. Serial tracings and cath findings are fully discussed above by Drs. Meyers & Smith. I’ll limit my comments to the initial ECG — which for clarity, I have reproduced in Figure-1.
  • Credit to the paramedic who recognized ECG findings strongly suggests of OMI on this initial ECG in Figure-1 — despite the fact that the receiving ED physician did not. In cases like this, in which there are differences of opinion regarding interpretation of a given tracing — I find it helpful to hone in on ALL features in support of our conclusion that this ECG represents acute evolving OMI until proven otherwise.
  • The reason the ST-T wave in lead V4 “caught the paramedic’s eye” — is that the size of this T wave is disproportionately tall (as well as being “fatter”-at-its-peak-than-expected) relative to the modest QRS dimensions in this lead. T wave inversion in leads III and aVF also caught the paramedic’s eye.

Figure-1: First EMS 12-lead ECG. (See text).

Take another look at the 1st EMS 12-lead ECG in Figure-1How MANY abnormal findings can you identify?
  • I believe the T wave inversion that we see in leads III and aVF is reflective of reciprocal changes — because the 3rd inferior lead ( = lead II) is also abnormal! In the context of our suspicion of acutely evolving anterior STEMI — the horizontal “shelf” that we see for the ST segment in lead II is clearly an abnormal finding — and, support for validity of reciprocal changes is always increased when multiple leads in a given anatomic area are abnormal.
  • It should be noted that that there are QS complexes in both leads III and aVF. The meaning of this finding is uncertain. There is a small r wave in lead II — so this suggests the presence of LAHB. But it’s really impossible to say IF the QS complexes in leads III and aVF represent in addition prior inferior infarction, or merely reflect the markedly leftward axis. In any event, the absence of inferior ST elevation at least tells us the inferior wall is not involved acutely.
  • As noted by Dr. Meyers — there is abnormal ST elevation in leads V1 and V2. But in addition — I strongly suspected lead malposition of leads V1 and V2 because: ithere is a very deep negative component to the P wave in leads V1 and V2, that suddenly becomes positive by lead V3; and iiMorphology of the QRS complex in lead V2 just does not make sense (ie, abruptly changing from a Qr complex in V1 that is predominantly negative — to a predominantly positive [albeit tiny] qR complex in V2 — and then once again abruptly becoming predominantly negative with an rS complex by lead V3). This IS highly relevant — since the findings in Figure-1, which were subtle enough that an experienced ED physician overlooked them — were probably minimized by lead malposition of leads V1 and V2!
  • NOTE: I will mention that my correspondence with the EMS team confirmed that they later realized leads V1 and V2 were in fact placed too high on the chest! And, as we review the serial ECGs above — Note how it is only with the 6th ECG done = which is the 1st ECG done in the hospital ( = the ECG performed on arrival at the cath facility) that the very deep negative P waves and predominantly positive QRS in V2 disappear — supporting my premise that there was lead malposition for all 5 of the EMS tracings shown above. Clearly — this lead malposition does not change our conclusion of ongoing OMI — but it may account for making some of the changes in the 1st ECG (Figure-1) more challenging to recognize.
  • This brings us to assessment of lead V3 in Figure-1. Because lead V2 is malpositioned — it is not truly a “neighboring lead” to V3 … That said, in view of there being at least 6 leads with abnormal ST-T wave findings (leads II,III,aVF; V1,V2,V4) — the T wave in lead V3 also looks disproportionately taller and fatter-at-its-peak-than-it-should-be given the tiny R wave in V3.

COMMENT: Among the most important oversights by the receiving ED physician who failed to appreciate diagnostic changes of OMI on the 1st ECG in Figure-1 — was overlooking the History = a 65yo woman who contacted EMS, who was clammy, who looked obviously uncomfortable, and whose chief complaint was new-onset chest pain. Even before we ever see the 1st ECG — this information tells us we are dealing with a high-prevalence likelihood of an acute coronary syndrome — which should significantly lower your threshold for being concerned about abnormal ECG findings.
  • At least 7/12 leads on the 1st ECG show worrisome findings in association with this high-prevalence situation. That should be more than enough to justify cath lab activation (even without addressing the lead malposition).
  • FINAL Thought: Hopefully constructive feedback was provided to the ED physician. We need to learn from this.

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