Sunday, April 30, 2023

ECG Blog #377 — Is the 1st ECG Normal?

The patient whose initial ECG is shown in Figure-1 — is a middle-aged man who presented to the ED (Emergency Department) for new-onset CP (Chest Pain). He was hemodynamically stable at the time this tracing was done.
  • The patient was still having CP at the time ECG #1 was obtained — although the severity of his CP was unclear (ie, It is not known IF this patient’s CP was increasing — the same — or decreasing — at the time the ECG in Figure-1 was recorded).

  • In view of the above history — How would YOU interpret the initial ECG?
  • WHY is it important to correlate severity of this patient’s CP with ECG #1?

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

MY Thoughts on the Initial ECG in Figure-1:
Sinus rhythm at ~60/minute is seen in ECG #1. All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement (ie, Although R wave amplitude is a bit tall in lead V5 — QRS amplitude does not quite satisfy voltage criteria for LVH). 

Regarding Q-R-S-T Changes:
  • Q Waves — are not seen on this tracing.
  • R Wave Progression — is normal, with transition (where height of the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

S-T T Wave Changes — These are non-diagnostic …
  • In the Limb Leads — QRS voltage is fairly low. There is non-specific ST-T wave flattening, but this does not look acute.

  • In the Chest Leads — The most abnormal-looking lead is lead V5, in which there is a sagging ST segment, but without J-point depression. The overall ST-T wave appearance in this lead looks more like LV “strain” than ischemia. There is non-specific ST-T wave flattening in neighboring leads V4 and V6.
  • T waves are upright and peaked in anterior leads V1,V2,V3. The slight J-point ST elevation that is seen in these leads is not abnormal in leads V2 and V3 (that commonly manifest slight ST elevation as a normal phenomenon) — but lead V1 usually does not manifest any ST elevation (and the J-point is slightly elevated in lead V1 of ECG #1). Finally — it is difficult to determine if T wave amplitude in lead V2 is slightly disproportionate to S wave depth in this lead.

PEARL #1: When T waves in the chest leads are upright (as they are in Figure-1 — with the exception of the T wave in lead V5) — 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).

BOTTOM LINE Regarding ECG #1:
The initial ECG in today's case is not diagnostic of an acute event. That said — in this middle-aged man who presented to the ED with new-onset CP — there are a number of ECG findings of potential concern. These include.

  • Subtle-but-real nonspecific ST-T wave flattening in 5 of the limb leads. 
  • T wave "imbalance" in the chest leads — in which the upright T wave in lead V1 is not only taller than the T wave in lead V6 — but, there is slight ST elevation in lead V1 — and a potentially disproportionately tall T wave in lead V2.
  • Support that these findings may be acute — is forthcoming from the uncharacteristically flat ST-T waves in lateral chest leads V4,V5,V6. Against the sagging ST-T wave in lead V5 being a reflection of LV "strain" — is the positive T wave and lack of any ST segment sagging in more-lateral lead V6.

  • To Emphasize: As isolated findings — None of the above ST-T wave abnormalities are diagnostic of an acute event. But taken together, in association with the history of new-onset CP — We can not rule out an acute (or recent) cardiac event on the basis of this single tracing. Therefore — ECG #1 is not a "normal" tracing (and close clinical follow-up is essential!).

PEARL #2: It's important to appreciate that 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 reason it is important to always correlate 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 — 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 — ST elevation and reciprocal ST depression significantly improve.
  • Somewhere in between the phase of acute ST elevation and return of ST segments to baseline, followed at some point by development of reperfusion (ie, inverted) T waves — may be a "transition" phase of pseudo-normalization, during which the ECG may look relatively normal (or show no more than nonspecific ST-T wave flattening).

How Does Pearl #2 Relate to Today's Case?
As stated above — ECG #1 in today's case is non-diagnostic. The patient was still having CP at the time this initial ECG was obtained — but how severe his CP was is unclear from the information we have available (ie, it was not known IF his CP was increasing — the same — or decreasing).
  • IF this patient's CP was still severe at the time ECG #1 was recorded — then the peaked anterior T waves with subtle ST elevation and a potentially disproportionate T wave in lead V2 might reflect early proximal LAD (Left Anterior Descending) occlusion.

  • IF on the other hand, the patient's CP was significantly less than it was at the time symptoms began — then the peaked anterior T waves and diffuse ST-T wave flattening elsewhere might reflect reperfusion T waves in a patient with posterior OMI.

  • Alternatively — ECG #1 may simply reflect nonspecific ST-T wave abnormalities in a patient who was not having an acute event. 

What To Do Clinically?
The point to emphasize — is that we simply can not arrive at any conclusion on the basis of the single tracing shown in Figure-1. Instead — optimal management would include the following:
  • Repeat the ECG soon! (ie, within 10-20 minutes of the initial tracing). IF the patient is evolving an acute event — it often takes no more than minutes for dynamic ST-T wave changes to become evident that confirm the diagnosis. Additional repeat ECGs are indicated (as might be needed)until such time that a definitive ECG diagnosis (of either acute OMI or no OMI) is made!
  • Look for a prior ECG on the patient (which may provide insight as to whether subtle ECG findings, as were described above for ECG #1 — are new or old).
  • Follow-up closely with serial troponins — to see if there is any elevation.
  • Ideally obtain a stat Echo at the bedside (which if this shows a regional wall motion abnormality during chest pain — would confirm an acute evolving event).

Today's CASE Continues:
The repeat ECG (that was done ~2 hours later) — is shown together with the initial tracing in Figure-2. The patient was apparently still having CP at the time ECG #2 was done (although  it was unclear if the patient's CP had persisted at the same intensity — or — had waxed and waned during the 2 hours that passed between obtaining these 2 tracings).

  • In light of the above historical information (and in light of the initial ECG in Figure-1) — How would you interpret ECG #2?

  • Has there been an acute OMI? IF so — What is the "culprit" vessel?  

Figure-2: Comparison of the repeat ECG with the initial tracing. (To improve visualization — I've digitized the original ECG using PMcardio).

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 disease — versus — 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 — and this may alter QRST appearance]).
  • After full interpretation of the initial ECG you have looked at — I go lead-by-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.

  • Finally (as per PEARL #2 above) — I do my best to correlate the presence and relative severity of CP to ECG findings in each of the serial tracings. 

In Today's CASE: Comparing ECG #1 and ECG #2:
As noted above — a good 2 hours passed before the repeat tracing was obtained. Unfortunately — how severe symptoms were during this 2-hour period is uncertain.
  • To Emphasize: Our goal in repeating the ECG, is to see if there have been dynamicST-T wave changes since the initial tracing was done, since IF there has been significant change — this would confirm that an acute event was ongoing.

  • How Valid is Our Comparison? — Comparison between ECG #1 and ECG #2 with regard to QRS amplitude and morphology in the 6 limb leads — reveals no significant change. In the chest leads — R wave progression is similar in the 2 tracings, with no more than slight reduction in lateral chest lead R wave amplitude. This suggests that any differences in ST-T wave morphology between the 2 tracings will be clinically significant!

What are the Changes?
Comparison of ECG #1 and ECG #2 reveals a number of significant changes:
  • The most "eye-catching" change in ST-T wave appearance between the 2 ECGs in Figure-2 — is in lead V2. The slight upsloping J-point ST elevation with prominent upright T wave that had been present in ECG #1 — has been replaced by slight-but-real shelf-like J-point ST depression, with reduction in the size of the terminally positive T wave. In a patient with new chest pain — this ST-T wave appearance in lead V2 of ECG #2 is consistent with a positive "Mirror" Test (as described in ECG Blog #285 — as well as in other Related ECG Blog links provided below).
  • Support that this change in ST-T wave appearance in lead V2 of the repeat ECG is real — is forthcoming from clear ST-T wave changes in each of the other 5 chest leads!

  • In lead V1 — the ST segment is no longer elevated, as it had been in ECG #1. Note that the "imbalance" of precordial lead T waves is no longer present! (ie, The T wave in lead V6 of ECG #2 is now clearly taller than the T wave in lead V1).
  • In lead V3 of ECG #2 — instead of slight upsloping ST elevation, leading to a large positive T wave — there is now flat ST depression leading to a biphasic T wave with terminal negativity.
  • In lead V4 of ECG #2 — ST depression becomes more marked than it was in lead V3, now with frank T wave inversion.
  • In lead V5 — the sagging ST segment seen in the initial ECG — has been replaced by straightening of the ST segment takeoff, now with a clearly positive T wave. This effect continues in lead V6 of ECG #2 — in which there is now unmistakeable J-point ST elevation, with straightening of the ST segment takeoff that leads into a hyperacute T wave.

PEARL #3: The fact that there are such definite differences in multiple leads of the repeat ECG in today's case — defines these differences as "dynamic" ST-T wave changes. In a patient with new CP — this ECG finding indicates acute OMI until proven otherwise (and provides clear indication for prompt cath!).

PEARL #4: Did YOU appreciate the change in ST-T wave appearance between the 2 ECGs in Figure-2 in leads I and aVL? To emphasize — the change is subtle. That said — recognition of this change illustrates the important concept of comparing tracings in the context of the entire ECG. The fact that there is no doubt about the changes in each of the 6 chest leads compared to ECG #1, makes me look that much closer at the remaining leads in ECG #2, for additional findings that may be more subtle. The fact that there is no doubt about new hyperacute ST-T waves in lateral chest leads V5,V6 in ECG #2 — tells me that the increased volume of the positive T waves in high-lateral leads I and aVL of this repeat tracing is real!

Putting It All Together:
Although it would have been helpful to know how this patient's symptoms correlated to the timing of ECGs #1 and #2 — Knowing there was ongoing CP of some degree in association with these 2 tracings done 2 hours apart strongly suggests the following:
  • Dynamic ST-T wave changes are seen. ST depression that is maximal between leads V2-to-V4 is diagnostic of acute posterior OMI. Hyperacute ST-T waves in all lateral leads (ie, in leads I,aVL; V5,V6) with new ST elevation in lead V6 of ECG #2 — is diagnostic of acute lateral OMI.
  • Acute postero-lateral OMI in the absence of inferior lead ST elevation strongly suggests acute LCx (Left Circumflex) Occlusion as the "culprit" artery. Prompt cath with PCI is clearly indicated.

Today's CASE Concludes:
The cath lab was activated after ECG #2. Cardiac catheterization revealed total occlusion of the LCx — which was successfully reperfused with PCI (Percutaneous Coronary Intervention). There was insignificant disease in the RCA (Right Coronary Artery) and the LAD (Left Anterior Descending) coronary artery. 
  • In Figure-3 — I've added the final ECG in today's case, done the day after PCI, with the patient pain-free.

  • How would YOU interpret the likely status of the "culprit" LCx artery at the time that each of the ECGs in Figure-3 were done?

Figure-3: Comparison of all 3 tracings obtained in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

How to Interpret the 3 ECGs in Figure-3?
The results of cardiac catheterization proved that the "culprit" vessel was the LCx — with occlusion of this vessel causing postero-lateral infarction.
  • The initial ECG in today's case ( = ECG #1) — did not show expected findings of acute LCx occlusion, in that there is no ST depression in leads V1-thru-V4 — and no lateral lead ST elevation. 
  • Instead — there is precordial lead T wave "imbalance", with the T wave in lead V1 taller than the T wave in lead V6 — and, with a disproportionately tall T wave in lead V2 (compared to S wave amplitude in this lead). This suggests that the "culprit" LCx had spontaneously reopened at the time ECG #1 was recorded. The surprisingly tall T waves in leads V1,V2,V3 are consistent with reperfusion T waves in the posterior wall distribution. The nonspecific ST-T wave flattening seen in the other leads in ECG #1 are consistent with probable "pseudo-normalization" on the way to developing reperfusion T wave changes.

  • As discussed in detail above — ECG #2 was obtained ~2 hours after ECG #1, without clear indication as to the relative severity of CP compared to CP severity at the time of symptom onset. I suspect the patient's CP had increased in severity at the time ECG #2 was recorded — since maximal ST depression in leads V2-to-V4, in association with hyperacute ST-T waves in all lateral leads (with new ST elevation in lead V6) strongly suggests that the "culprit" vessel had spontaneously reoccluded at the time this repeat ECG was obtained.

  • The final ECG in today's case ( = ECG #3) was obtained the day after successful PCI, at a time when the patient was pain-free. The fact that ST-T waves in ECG #3 look so similar in appearance to ST-T waves in ECG #1 — supports my presumption that the "culprit" vessel had already spontaneously reopened by the time the initial ECG in today's case was done.

PEARL #5: One of the KEY "Take-Home" Points from today's case — is how correlation between the presence and relative severity of CP with ECG findings on each serial tracing can provide invaluable information regarding the status (open or closed) of the "culprit" vessel at the time each ECG is done.


Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) 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 #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 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 #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 — 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 (4/30/2023):
  • 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

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