Monday, March 21, 2022

ECG Blog #292 — Why Did the Patient Die?


The 2 ECGs shown in Figure-1 were obtained from a man in his 30s — who presented to the ED (Emergency Department) with chest pain that began several hours earlier. ECG #2 was recorded 1 hour after ECG #1. Initial troponin was negative.

Cardiac cath was advised — but the patient refused. Instead, he left the hospital — only to be found dead at home 36 hours later
  • How would YOU interpret the serial tracings shown in Figure-1?
  • WHY did the patient die?

Figure-1: The 2 ECGs in today's case (See text).


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NOTE: I'm repeating the following Audio PEARLS that are relevant to today's case. Some readers may prefer at this point to listen to these Audio Pearls before reading My Thoughts that appear below, regarding the ECGs in today's case.

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ECG Media PEARL #39a (4:50 minutes Audio) — Reviews the concept of Dynamic ST-T Wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated).

 

 


ECG Media PEARL #46a (6:35 minutes Audio) — Reviews HOW to compare Serial ECGs (ie, Are you comparing "Apples with Apples" — or — with Oranges?).




My THOUGHTS on Today's Case:
There are lessons to be learned from today's case. These include:
  • What is meant by the term, "dynamic" ECG changes?
  • How to compare serial tracings?
  • Are "dynamic" ECG changes seen in Figure-1?
  • What is the most likely reason this patient died?
  • Can we determine a "culprit" artery?

What is Meant by the term, "Dynamic" ECG Changes?
The goal of obtaining serial ECGs in patients suspected of evolving an acute coronary event — is that tracings obtained early on may look relatively normal. This picture may rapidly change, sometimes over the course of minutes! When initial ECG changes are subtle — they may be most easily recognized by lead-to-lead comparison of 1 tracing with another.
  • IF ECG changes evolve in a way that corresponds to the coming and going of chest pain symptoms — this is important information. It tells us there is an active, ongoing process — and that prompt cath with acute reperfusion is likely to be needed regardless of whether or not the millimeter-definition of a STEMI has been satisfied.
  • The problem is — that the "culprit" artery may spontaneously open and close more than once during its process of arriving at a final result — so that even if ST elevation resolves in association with resolution of chest pain — this spontaneous reopening of the vessel, may just-as-easily be followed by spontaneous closure again — and this time, perhaps without spontaneous reopening.
  • It is this active evolution of ST-T wave changes that may occur with the coming and going of symptoms that we define as "dynamic" ECG changes. ST segments elevate with the onset of chest pain (signaling acute coronary occlusion) — and ST segments return toward their baseline, often followed by "reperfusion" changes of T wave inversion that signal reopening of the "culprit" vessel. The importance of recognizing these "dynamic" ECG changes — is that this indicates an unstable situation at risk of evolving further to permanent coronary occlusion.

How to Compare Serial Tracings?
The method I favor for comparing serial tracings — is to pick one of the ECGs — and to interpret that tracing in its entirety by whatever systematic approach you are using. I usually start with the earliest tracing that was recorded — because you then know that any changes seen on a subsequent tracing are "new".
  • We are looking for changes in the shape and amount of ST elevation and depression between the tracings that we are comparing.
  • The challenge with ECG comparison — is that we have to distinguish between differences from one ECG to the next that are likely to be due to a worsening or improvement in the patient's coronary diseaseversus — ECG changes that are likely the result of technical factors (ie, a shift in frontal plane axis or QRS morphology changes due to a difference in lead placement or in the degree of elevation of the patient's bed [some acutely ill patients are unable to lie flat]).
  • After full interpretation of the initial ECG you looked at — I go lead-to-lead when I compare serial tracings, holding both tracings right next to each other. This is because IF, for example — the QRS complex is predominantly positive in lead III or in lead aVF on the 1st tracing — but then becomes more-negative-than-positive on the 2nd tracing — then the frontal plane axis has shifted!and — you'll need to consider this axis shift when determining whether any differences in ST-T wave morphology are likely to be due to technical factors or "true" evolution of the patient's cardiac condition.



My THOUGHTS on the Initial ECG in Figure-1:

I began assessing today's case with interpretation of the initial ECG in the ED ( = ECG #1). As always — I used a Systematic Approach (See ECG Blog #205 for details):

  • Rate & Rhythm: There is a fairly regular sinus rhythm at ~80-85/minute.
  • Intervals (PR, QRS, QTc) — Normal.
  • Axis: Normal (about +65 degrees — given slight negativity of the QRS in lead aVL).
  • Chamber Enlargement: None. 

 

Regarding Q-R-S-T Changes:

  • Q Waves: No Q waves of note. There appears to be a small initial r wave in lead III (which manifests an rsR' complex). The Q waves seen in leads aVR and V1 are so common (and normal) that I generally don't mention them. No other Q waves.
  • R Wave Progression: Normal. Transition (where height of the R wave exceeds depth of the S wave in the chest leads) occurs normally (ie, here between leads V3-to-V4).

 

Regarding ST-T Wave Changes:

  • There is nonspecific ST-T wave flattening in leads III and aVF.


IMPRESSION: Overall, I thought ECG #1 was unremarkable for a patient who presented with new chest pain. The nonspecific ST-T wave flattening seen in leads III and aVF is often seen in patients without chest pain.



My THOUGHTS on ECG #2:

As noted in Figure-1ECG #2 was obtained 1 hour after ECG #1 in this 30-something year-old man, who presented to the ED with several hours of chest pain.

  • Once again — My assessment of the ST-T wave appearance in ECG #2 for this patient with chest pain was fairly unremarkable — and by itself, did not suggest acute changes. 




CHALLENGE:
What I did not do in my description above — was to compare these 2 tracings, looking for changes that may have occurred during the hour after ECG #1 was done. Please go back and TAKE ANOTHER LOOK at these 2 tracings (which for clarity, I reproduce below in a 2nd look at Figure-1). Please GO lead-by-lead in your comparison.
  • Do YOU see any differences in ST-T wave morphology in any of the 12 leads?
  • What clinical information do we need to know in order to optimally interpret these 2 tracings?

Another Look at Figure-1: The 2 ECGs in today's case.



ANSWER: Comparison of ECG #1 and ECG #2:
As emphasized in the above Audio Pearl-46a — the KEY for accurate comparison of serial tracings is to assess whether the frontal plane axis and chest lead electrode placement are comparable.

  • In the Limb Leads: QRS morphology and amplitude, as well as the frontal plane axis — are virtually identical in ECG #2, compared to what was seen in ECG #1.
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  • In the Chest Leads: Considering that half-standardization was used to record the chest leads in ECG #2 — I saw no significant difference in R wave progression or QRS morphology between the 2 tracings.

  • KEY Point: Knowing that frontal plane axis and chest lead electrode placement is comparable in ECG #1 and ECG #2 greatly facilitates comparison of these serial tracings. This tells us that any significant change that we see between ECG #1 and ECG #2 is likely to be real.


Lead-by-Lead Comparison:
Careful comparison between the 2 tracings shown in Figure-1 does show a number of differences:
  • In the High-Lateral Leads: The T waves in leads I and aVL of ECG #1 were slightly larger (more upright) in this earlier tracing — than they are in ECG #2.
  • In the Inferior Leads: Although I do not see any difference in the ST-T wave appearance in lead II — T waves in the other 2 inferior leads (leads III and aVF) are more upright in ECG #2, compared to what they were in ECG #1.
  • In the Chest Leads: Even accounting for the change in standardization — the T waves in leads V2-thru-V6 are flatter in ECG #2 than they were in ECG #1. The T wave in lead V1 is less deeply inverted in ECG #2.
Conclusion: Admittedly — the above described differences in ST-T wave appearance between ECG #1 and ECG #2 are subtle. But the fact that despite no appreciable change in either frontal plane axis or chest lead QRS morphology — no less than 10/12 leads do show differences is undeniable!
  • The KEY clinical information missing in this case — is an account of what happened to the severity of this patient's chest pain between the time that these 2 ECGs were recorded.
  • IF there was in fact a change in the severity of this patient's symptoms — this would strongly support the premise that there are ongoing dynamic ST-T wave changes. For example — IF chest pain was significantly less at the time ECG #2 was recorded, this might indicate evolution of acute LAD (Left Anterior Descending) occlusion, in which spontaneous reperfusion signaled what was soon to become anterior reperfusion T waves ( = anterior T wave inversion).
  • In this case — IF an ECG had been recorded a bit before ECG #1, perhaps it might have revealed "tell-tale" anterior ST elevation.
  • BOTTOM Line: Without knowing details about the course of this patient's chest pain — it's impossible to predict a probable "culprit" artery. But IF there was indeed a significant change in the severity of this patient's symptoms between the time that ECGs #1 and #2 were recorded — this would have been clear indication for prompt cath.

  • "Take-Home" Message #1: The course of acute coronary occlusion is sometimes stuttering. That is, the "culprit" artery may completely occlude — only to spontaneously open a short time later. IF the duration of complete occlusion is brief (ie, minutes) — then even high-sensitivity troponin may not necessarily elevate. When ST-T wave changes correlate with the "coming-and-going" of symptoms — these ECG findings strongly suggest onging change in the patency of the "culprit" artery. The reason these dynamic ST-T wave changes are indication for prompt cath — is that what was totally occluded (and is now open) — might just as easily occlude again at any time, until the final state of the culprit artery is ultimately reached.
  • "Take-Home" Message #2: The ECG findings in today's case are subtle — and neither ECG #1 nor ECG #2 alone suggested an ongoing acute event. But when one considers that no less than 10/12 leads show a subtle-but-real difference in ST-T wave morphology in this patient with new chest pain — the strong indication for prompt cath that was advised is undeniable. This patient might still be alive IF he had not ignored this recommendation.

  • Final "Take-Home" POINT: Recognition of dynamic ST-T wave changes sometimes requires meticulous lead-by-lead comparison of serial ECGs, interpreted in association with the serial course of the patient's symptoms.

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Acknowledgment: This case was anonymously sent to me ...
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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
  • ECG Blog #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEJM manuscript). 
  • ECG Blog #222 — Reviews the concept of Dynamic ST-T wave changes, in the context of a detailed clinical case. 
  • ECG Blog #260 — Reviews another case that illustrates the concept of "dynamic" ST-T wave changes.

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
  • ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

  • ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culpritartery.

  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.

  • ECG Blog #115 — Shows an example of how drastically the ECG may change in as little as 8 minutes.
  • The January 9, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case is remarkable for the dynamic ST-T wave changes that are seen. It's helpful to appreciate: i) That acute ischemia/infarction is not the only potential cause of such changes (cardiac cath was normal); ii) That changes in heart rate, frontal plane axis and/or patient positioning can not always explain such changes; and, iii) That entities such as repolariztion variants, LVH and/or acute myopericarditis may all contribute on occasion to produce an evolution of challenging dynamic ST-T wave changes on serial ECGs.

  • The August 22, 2020 post in Dr. Smith's ECG Blog — which illustrates another case of dynamic ST-T wave changes that resulted from a repolarization variant

  • The July 31, 2018 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case provides an excellent example of dynamic ST-T wave changes on serial tracings (that I illustrate in My Comment) in a patient with an ongoing acutely evolving infarction.
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