Saturday, April 20, 2019

How long would you like to wait for your Occlusion MI to show a STEMI? Sometimes serial ECGs minimizes the delay.

Written by Pendell Meyers


An elderly woman presented with acute onset chest pain and shortness of breath. 

EMS showed us their ECG on arrival at her house:

What do you think?







There is sinus rhythm with minimal STE in V1-V3, not meeting STEMI criteria. However, this STE is definitively abnormal in the setting of a normal QRS complex and hyperacute T-wave morphology in V2. There is a small amount of reciprocal STD in V6 with a negative T-wave.

This is subtle but diagnostic for anterior Occlusion MI. V2 never has this appearance in the absence of full thickness ischemia.

We called for emergent cath lab activation.

The cardiologist arrived quickly and was skeptical about these findings on EMS ECG. So while they were trying to explain their interpretation I simply recorded another ECG:



This ended the discussion.


100% mid-LAD occlusion.


LAD now open after intervention.
Peak troponin T was 1.76 ng/mL.



Repeat ECGs after intervention were consistent with successful reperfusion without significant Q-wave development:





Convalescent echo showed EF 41% with anterior, lateral, and apical wall motion abnormalities. 

Given the relatively rapid reperfusion, and the absence of QS-waves, much of the abnormality on echo could be reversible (myocardial stunning, not infarction). 



Learning Points:

Serial ECGs can sometimes turn a difficult decision into a very easy one, but not all OMIs will develop into clear STEMIs quickly, and some OMIs never will manifest STEMI at all. The delay between OMI and STEMI sometimes causes unacceptable loss of myocardium or worse.

Make sure to burn the morphology of lead V2 from the initial ECG into your brain so that you can recognize this pattern in the future.

STE in V1 with STD in V6 in the presence of a normal QRS complex is another piece of evidence consistent with LAD occlusion.


===================================
Comment by KEN GRAUER, MD (4/20/2019):
===================================
With this case — Dr. Meyers addresses a common theme of this ECG Blog = HOW LONG to wait for your OMI ECG to show a STEMI? As we’ve emphasized before, the important “lesson-to-be-learned” — is that there should not be a need to wait! As soon as there is evidence of acute OMI — your cardiology colleague should be called to expedite cath with the goal of acute reperfusion.
  • For clarity — I’ve reproduced the first 3 ECGs that were done in this case in Figure-1. In addition to review of why acute OMI is evident from ECG #1 ( = the initial ECG in this case, that was done by EMS on arrival at the patient’s house— I found serial observation of the lead Vappearance on these 3 sequential ECGs to be insightful and important to note!
Figure-1: The first 3 ECGs shown in this case (See text).
=================
WHY ECG #1 is Diagnostic of Acute OMI (Until You Prove Otherwise )
Dr. Meyers correctly notified the cardiologist-On-Call as soon as he saw ECG #1 because:
  • 1The clinical setting was worrisome ( = an elderly woman with new-onset chest pain).
  • 2Given this history — there is NO way that the ECG appearance of lead Vin ECG #1 is normal. Relative to the very small QRS amplitude in lead V2 — the ST segment in this lead is disproportionately large, coved in shape (ie,“frowny” configurationwith some ST elevation. This ST-T wave in lead V2 of ECG #1 is clearly hyperacute.
The appearance of other leads in ECG #1 is much less remarkable compared to the appearance of lead V2. The T wave in neighboring leads V1 and V3 looks a bit more-prominent-than-it-should-be given QRS amplitude in these leads — but this change is subtle, and far from diagnostic! (Of the 5 QRS complexes in these leads — some suggest slight ST elevation in leads V1 and V3 — but others don’t). Otherwise, there is no more than nonspecific ST-T wave flattening in the remaining leads. Therefore — Lead Vis the KEY to the diagnosis in ECG #1. To this, I’d add the following points:
  • It is good to be aware that with acute OMI of the 1st (or 2nddiagonal branch of the LAD — the only chest lead that may show ST elevation is lead V2. There may be a lesser amount of ST elevation in lead aVL, in association with inferior lead reciprocal ST depression — or — early on, the ECG might look similar to what we see in ECG #1.
  • Things can change very quickly during the course of an actively evolving acute OMI (See THIS CASE — in which just 8 minutes passed between the 1st and 2nd ECGs). So, early on — acute OMI of the LAD might (and in this case, did) look like ECG #1.
  • I suspect one or more of the 3 anterior leads (V1,V2,V3in ECG #1 are malpositioned. My reason for this suspicion is that I wouldn’t expect the S wave in lead V2 to decrease by as much as it does from neighboring lead V1 — and then, to become deeper at the same time the r wave is becoming taller, as we move from V2-to-V3. In addition, transition of ST-T wave shape from an upsloping ST segment in V1 — to a downward coving ST segment by V2 — and then back again to an upsloping ST segment by V3, is not the pattern of a usual physiologic progression as one moves from V1-to-V3.
=================
The Take-Home” Point: As per Dr. Meyers — Use of frequent serial ECGs can be invaluable until the clinical picture is clarified.
  • Chest lead malposition is surprisingly common — even when experienced ECG technicians are the ones doing the tracings.
  • Given that the cardiologist in this case was skeptical about the diagnosis of acute OMI from ECG #1 — I would have immediately repeated the ECG as soon as I saw this initial tracing because: iSome form of anterior lead malposition is suggested (See above) — andimmediate repeat ECG after verifying electrode lead placement might have clarified the true status of acute ST-T wave changes; andiiGiven this patient’s acute symptoms + strong suggestion of hyperacute ECG changes in lead V2 of ECG #1 — there is a definite possibility that you might already see some evolution of ST-T wave changes within the brief time frame between when ECG #1 was done — and when the repeat ECG is completed. NOTE: The reason I’m suggesting to immediately repeat the ECG — is because we are trying to expedite convincing the cardiologist on this case to take this patient to cath as soon as this can be done.
  • PEARL #1: There is an easy way to eliminate the possibility of chest electrode lead placement variability when serial tracings are done. Simply mark the spot on the  chest where electrode leads are placed in cases in which lead malposition is suspected. This should guarantee consistency of electrode lead placement for subsequent serial tracings.
  • PEARL #2: Be aware that change in the ANGLE of the patient’s bed may alter QRS and ST-T wave appearance in any number of leads. This factor is typically ignored (Have you ever seen notation on an ECG that the patient was too dyspneic to lie flat? — and that as a result, his/her bed was raised to 30 degrees [or to whatever angle the bed has been raised to ... ] at the time the ECG was done).
Comment on Lead VVariability in the 3 ECGs in Figure-1:
Dr. Meyers has capably discussed the evolution of serial ECGs done in this case — and then correlated this with cath findings. I wanted to focus on the changing appearance of the QRS complex in lead V2 for ECGs #1, #2 and #3 (Figure-1):
  • It is likely that a different technician recorded each of the 3 ECGs in Figure-1 — since more than one ECG machine was used (black vs red grid lines), and the 3 tracings were recorded at different locations (ie, the patient’s house; the ED; and the cath lab). Lead malposition becomes much more likely when a different person is recording repeat tracings.
  • I’ve already described why I thought lead malposition is likely for ECG #1.
  • Lead malposition is almost certain for ECG #3. One simply would not expect progression from predominant negativity of the QRS in lead V1 — to predominant positivity by lead V2 — to an equiphasic QRS complex by lead V3.
  • And yet another QRS morphology is seen in lead V2 of ECG #2 — in which there is a multiphasic, almost null net QRS complex.
  • Realizing that this patient has just undergone a PCI procedure — I would not expect the marked variation in lead V2 QRS morphology across these 3 tracings to have been caused by coronary reperfusion. Especially in view of fairly consistent QRS morphology in the lateral chest leads (leads V4, V5 and V6) across these 3 tracings — I think it virtually certain that there has been lead malposition (at least for lead V2) in at least one or two of these 3 tracings.
  • BOTTOM Line: As per Dr. Meyers — "Serial ECGs" can sometimes turn a difficult decision (regarding acute cath lab activation or not) into a very easy one. Awareness of how common chest lead malposition is — and, appreciation of when to suspect lead malposition — may prompt earlier repeat ECGs that may help to expedite you being able to convince a reluctant cardiologist of the need for immediate cath.


No comments:

Post a Comment

Recommended Resources