Saturday, July 22, 2023

ECG Blog #387 — 2 Minutes Later ...

The ECG in Figure-1 was obtained from an elderly man with a history of coronary disease — who contacted EMS for "burning" chest discomfort that woke him at 3am. Unlike his "usual" anginal episodes — this chest discomfort was not relieved by NTG. Some amount of time passed at home — during which his chest discomfort persisted
  • The patient was hemodynamically stable at the time he was seen by EMS, when ECG #1 was recorded.

  • How would YOU interpret the initial ECG in today's case?
  • In view of the above history — Does ECG #1 suggest an acute event? Should the cath lab be activated?

Figure-1: The initial ECG in today’s case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on ECG #1: 
In view of the history — the initial ECG in today's case is clearly of concern! I see the following:
  • Although there is no long lead rhythm strip — we can see that the rhythm is AFib with a controlled ventricular response (ie, irregularly irregular rhythm without P waves — and with a heart rate between ~70-110/minute).
  • Regarding Intervals: There is no PR interval (since the rhythm is AFib). The QRS complex is narrow. The QTc is at most slightly prolonged. 
  • Axis: Slightly leftward — but not leftward enough to qualify as LAHB (ie, predominantly negative QRS in lead aVF — but not predominantly negative in lead II).
  • No chamber enlargement.
  • Large, wide Q waves are present in leads III and aVF — consistent with this elderly patient's known history of coronary disease (ie, prior inferior infarction).

The most remarkable changes in ECG #1 relate to ST-T waves:
  • In the Limb Leads — ST-T wave changes do not look acute. There is no more than minimal upsloping ST elevation in leads III and aVF — with volume of the upright T wave in these leads not disproportionate to the very wide and deep Q waves that are present. 
  • The ST segment in the other inferior lead ( = lead II) is flat, but not elevated at all.
  • There is some downsloping ST depression in high-lateral leads I and aVL — which is consistent with a mirror-image opposite ST-T wave picture compared to what we see in leads III and aVF.

  • BUT — in the Chest Leads There definitely are ST-T wave changes of concern! This is especially true given the History in today's case.

PEARL #1: Normally, there will be slight, upward sloping ST elevation in anterior leads V2 and V3. Not only is this slight ST elevation missing from leads V2,V3 in ECG #1 — but the ST segment in these leads (as well as in neighboring leads V1; and V4,V5) is distinctly flat! 
  • This picture of ST segment flattening (with loss of the normal slight ST elevation in V2,V3) — should be instantly recognized as abnormal, especially in a high-risk patient (such as in the elderly man with known coronary disease in today's case — whose episode of new chest discomfort was not relieved by NTG).

PEARL #2: When T waves in anterior chest leads are upright (as they are in Figure-1) — then, the T wave in lead V1 will usually not be taller than the T wave in lead V6
  • Although this "Imbalance" of precordial T waves is not seen very often — in the “right” clinical setting, it has been associated with recent OMI (Occlusion-based MI), most often from a LCx culprit artery (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM — and ECG Blog #350).

  • NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly much taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized. 

PEARL #3: The course of acute MI from acute coronary occlusion — is often staggered. By this, I mean that even without PCI or thrombolytic therapy — the "culprit" vessel may spontaneously reopen. Sometimes the "culprit" vessel stays open — but at other times, it may at any point in time reocclude. And, sometimes this process of spontaneous reopening and reclosing may occur multiple times in short succession.
  • The importance of correlating the presence (and relative severity) of CP with each serial ECG recorded on the patient — is that doing so may provide insight as to whether the "culprit" vessel at any time during the process is likely to be open or closed.
  • The "culprit" coronary artery is more likely to be occluded IF — the patient has ongoing severe CP (Chest Pain), especially if this occurs in association with ST elevation over the area of infarction.
  • Spontaneous reperfusion is likely IF — in association with reduction (or resolution) of CP, the ST elevation and reciprocal ST depression significantly improve.
  • Reperfusion of the "culprit" artery is even more likely IF — in association with CP resolution, one sees "reperfusion" T waves (ie, T wave inversion) in areas where there had been ST elevation.

  • KEY Point: Somewhere in between the phase of acute ST elevation and return of ST segments to baseline — may be a "transition" phase of pseudo-normalization, during which time the ECG may look relatively normal (or show no more than nonspecific ST-T wave flattening). IF attention is not paid to the presence and relative severity of CP in association with each serial ECG — it could be extremely EASY to overlook recent OMI if the initial ECG is being viewed during this phase of pseudo-normalization.

PEARL #4: Perhaps the most difficult infarction location to recognize — is acute posterior MI. This is because none of the leads in a standard 12-lead tracing directly view the posterior wall.
  • As emphasized in many of these ECG Blogs (See ECG Blog #285 and Blog #193among many others) — use of the "Mirror Test" facilitates recognition of acute posterior MI (ie, Instead of ST elevation — there is mirror-image opposite ST depression in anterior leads that provide a "mirror-image opposite" view of the posterior left ventricular wall). The message is clear — If, in a patient with new chest pain — ST-T wave depression is maximal in leads V2, V3 and/or V4 — consider acute posterior MI until proven otherwise.

  • KEY Point: In areas of the heart where an acute STEMI produces ST elevation — reperfusion T waves (that develop after the "culprit" artery reopens) will appear as T wave inversion. The opposite occurs with posterior MI — in which instead of T wave inversion, development of tall, upright T waves in leads V2, V3 and/or V4 signal the presence "reperfusion" T waves.

As emphasized in ECG Blog #317 — Although posterior leads (ie, V7,V8,V9) are often advocated to facilitate recognition of acute posterior MI — use of posterior leads is not essential for this purpose.
  • QRST amplitudes with posterior leads are reduced compared to mirror-image anterior lead amplitudes — because electrical activity from posteriorly placed V7,V8,V9 electrodes has to traverse the thick back musculature before it can pick up the heart's electrical activity. 
  • MY Observation: In my experience over the past 40+ years of diligently looking for posterior MI — I have virtually never seen posterior leads diagnose a posterior infarction that wasn't already evident to me from application of the Mirror Test to the standard 12-lead ECG. NOTE: With just a little bit of practice — it becomes EASY to apply the Mirror Test to facilitate recognition of posterior MI.


Putting It All Together:
Given the History in today's case (ie, of an elderly man with known coronary disease — who a number of hours before ECG #1 was obtained, was awakened by new CP that was not relieved by NTG) — I would interpret ECG #1 as suggestive of acute posterior OMI ( = Occlusion-based MI) — until proven otherwise.
  • The modest amount of ST depression (which is maximal in lead V4) — in association with the T wave imbalance (T in V1>T in V6), with flat ST segments and disproportionately tall, peaked T waves in leads V1-thru-V4 — suggest there has been spontaneous reperfusion.
  • The very deep and wide Q waves in leads III and aVF indicate that there has been inferior infarction at some point in time. Whether this inferior infarction is part of the recent posterior OMI is uncertain from the single ECG shown in Figure-1. After all — the onset of symptoms occurred some hours earlier — and there is still some ST elevation in lead III with reciprocal changes in leads I and aVL — so there could be an associated acute (or recent) inferior infarction. 

  • PEARL #6: Availability of a prior ECG on today's patient could have answered the question as to whether limb lead changes are "new" or "old". Finding a prior tracing on today's patient would also confirm my impression of recent (and/or ongoing) posterior OMI.

  • PEARL #7: Even without availability of a prior ECG — the history and ECG findings described above in the initial tracing justify cath lab activation. This is because even though the "culprit" artery may have spontaneously reperfused — What has spontaneously reopened might just as easily spontaneously close again — which is why prompt cath with PCI of the "culprit" artery is indicated to prevent reclosure.


The CASE Continues:
En route to the hospital — another tracing was done 2 minutes after ECG #1. For clarity and ease of comparison — I've put this repeat ECG together with today's initial tracing in Figure-2.

  • How would YOU interpret the repeat ECG — which was recorded 2 minutes after ECG #1?
  • Does this repeat ECG support my impression of recent (and/or ongoing) posterior OMI? 
  • What important piece of clinical information are we missing in association with ECG #2?

Figure-2: Comparison between the initial ECG — and the repeat ECG done ~2 minutes later. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Repeat ECG: 
The frontal plane axis and QRS morphology is virtually the same in all 12 leads for both of the tracings in Figure-2. This tells us that lead-by-lead comparison for any change in ST-T wave morphology is valid!
  • The AFib with controlled ventricular response is unchanged.
  • I see no difference in limb lead ST-T wave appearance between the 2 tracings. 

  • BUT — there has been a definite change in ST-T waves in the chest leads! Specifically — there has been a significant increase in the amount of ST depression in leads V2-thru-V6 in ECG #2. This ST depression is now clearly downsloping — with reduced T wave amplitude.

  • PEARL #8: The fact that there has been unmistakable change in ST-T wave appearance between the serial tracings in Figure-2 — defines this development as a "dynamic" ST-T wave change. In a patient with new symptoms — the finding of ischemic-looking "dynamic" ST-T wave change by itself — is indication for prompt cath, with probable need for PCI (See ECG Blog #222 for more on this topic).
  • As previously noted — acute posterior OMI produces ST depression in anterior leads (ie, a positive "Mirror" Test). The disproportionately tall (and abnormal-looking) T waves in several chest leads of ECG #1 are consistent with "reperfusion" T waves in this posterior infarction — which suggest that the "culprit" vessel had spontaneously reopened at some point before ECG #1 was recorded. The fact that ECG #2 now shows ischemic-looking increased ST depression in multiple chest leads, in association with reduced T wave amplitude — strongly suggests that the "culprit" vessel has now reoccluded!

PEARL #9: There unfortunately is no information in this case as to whether this patient's "burning" chest discomfort was increasing — was stable — or, was decreasing at the time that ECG #2 was recorded. 
  • It's important to appreciate, that IF chest pain was increasing at the time ECG #2 was recorded — that this would strongly support our theory that the reason for the increased ST depression and decreased T wave amplitude in multiple chest leads, is that the "culprit" vessel has now reoccluded!
  • The clinical importance of this association — is that indication for immediate cath becomes absolute (!) — IF chest pain increased at the time the "dynamic" ST-T wave changes that we see in ECG #2 were recorded.


CASE Conclusion:
On their way to the hospital, the EMS crew requested cath lab activation — because they recognized the above "dynamic" ST-T wave changes.
  • Unfortunately, the clinical significance of the serial ECG changes in Figures-1 and -2 were not recognized by providers in the ED. Cath lab activation was cancelled when the initial troponin was not elevation.
  • Additional troponins were not ordered.
  • Additional follow-up on this case is lacking ...

COMMENT: It is always difficult to attempt reconstruction of a case when information is lacking. That said — there are important lessons to be learned from events in this case. To the above 9 Pearls — I add the following.
  • PEARL #10: There are several reasons why the initial troponin with acute OMI may fall within the "normal" range (ie, spontaneous reopening of the "culprit" artery may have occurred soon enough after acute occlusion — such that there is no initial troponin elevation). Despite the initial normal troponin in today's case — additional troponins should have been ordered on this high-risk patient with a worrisome history of new chest pain.

  • PEARL #11: There is no mention in today's case of a prior ECG ever becoming available. While understandable that previous ECGs for comparison will usually not be available to the EMS team dispatched to attend to the patient — it should have been EASY to find a prior tracing for comparison purposes in the ED on this patient with known coronary disease and prior anginal episodes. The chances are excellent that comparison of a prior tracing with ECG #1 — could have confirmed that the ST-T wave changes in today's initial tracing were acute. In 2023 — it should be EASY to locate and transmit previous ECGs for comparison from established patients.

  • Final PEARL: Appreciation of the pathophysiology described above in Pearl #3 is essential for optimal assessment of patients suspected of having an acute coronary event. Cath lab activation should not have been cancelled in today's case.

Beyond-the-Core: Are there N-Waves in ECG #1?
I reviewed the concept of "N-Waves" in ECG Blog #354
  • While writing up this case — it dawned on me that the best explanation for the extra positive "notch" that we see in leads III and aVF of ECG #1, but which disappears in ECG #2 (despite essentially no other change in inferior lead QRS morphology) — is that these small deflections in ECG #1 reflect N-waves.
  • IF so — this subtle ECG finding would be consistent with recent OMI, most likely with the LCx as the "culprit" artery.
  • Oppositely-directed small negative deflections are seen in high-lateral leads I and aVL in both ECG #1 and ECG #2.

What is an "N-Wave"?
In 2011 — Niu et al described the presence of an "N-Wave" — or delayed activation wave of the left ventricular basal region. Because this area of the heart is typically supplied by the LCx — this is likely to be the "culprit" artery when N waves are seen as part of the pattern of acute ischemia (Int J Cardiol 162(2): 107-111, 2013).
  • As highlighted in the March 26, 2022 post in Dr. Smith's ECG Blog — N waves are recognized by the transient appearance of notching (usually ≥2 mm in size, with respect to the PR segment) — with resultant slight widening of the QRS complex. Because N-waves typically last <24 hours after acute occlusion — they may be smaller than 2 mm, depending on when during the process they are seen.
  • As opposed to J-wave notching (that is more likely seen in the chest leads) — N-waves are usually seen in one or more of the inferior leadsand/or in leads IaVL.

  • MY Thoughts: When I first read about N-waves — I was hesitant to use this ECG finding in my assessment, for fear of "overcalling" occasional QRS fragmentation as being something else. But I thought both the case I presented in ECG Blog #354, as well as today's case — are consistent with being probable N-waves in these 2 patients with chest pain and ECG signs consistent with posterior OMI from a LCx culprit. I wish we had cath confirmation on these 2 cases.


Acknowledgment: My appreciation to David Baumrind (from Eastern Long Island, NY, USA) for the case and this tracing.


Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery — as well as the importance of the term, "OMI" ( Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
  • ECG Blog #367 — for another example of acute LCx OMI

  • ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
  • ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.

  • ECG Blog #260 — ECG Blog #222 — and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamicST-T wave changes.

  • ECG Blog #230 — How to compare serial ECGs.

  • ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...

  • ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (with another case to illustrate the Mirror Test for diagnosis of acute Posterior MI).
  • ECG Blog #317 — reviews why posterior leads are not essential for diagnosis of acute posterior MI.

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.

  • ECG Blog #350 and ECG Blog #377 — regarding T Wave Imbalance in the Chest Leads.

  • ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

  • The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.


ADDENDUM (7/22/2023):
  • I've added several Audio Pearls below with material relevant to today's case.

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?).

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MIshould replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria


  1. This is another masterly interpretation and your eagle sharp eyes caught the N waves, lovely

    1. And YOUR "eagle eyes" caught that I caught those N waves! I thought of YOU as I added this comment on N waves! — :)