ECG Blog #353 — Why the Wide QRS? - T-QRS-D

The ECG in Figure-1 represents a pattern you should recognize — so, NO history is given. How would YOU interpret this tracing?

Figure-1: The ECG in today's case. No history provided ...

MY Thoughts on the ECG in Figure-1:

At first glance — the rhythm in Figure-1 looks like a wide-QRS rhythm. But the QRS is not wide. Instead, the underlying rhythm is sinus, as indicated by upright sinus P waves in lead II (RED arrow in Figure-2).

• The teaching point lies with assessment of QRS duration. The reason the QRS looks wide — is that it "blends in" with neighboring ST segments that are either markedly elevated or depressed. As a result — the boundary between the end of the QRS complex and the beginning of the ST segment becomes indistinguishable in many parts of this tracing.
• This is "Shark Fin" morphology — which most often reflects severe transmural ischemia from acute OMI = Occlusion-based Myocardial Infarction (See ECG Blog #265 and ECG Blog #296 — for additional examples of this phenomenon).

To Confirm Shark Fin Morphology:

The KEY for confirming the presence of Shark Fin morphology — is to find 1 or 2 leads in which you can clearly define the limits (end point) of a QRS complex. 

• The most helpful lead for doing so in today's case is lead I — in which I've drawn in a BLUE line parallel to the heavy grid ECG line in simultaneously-recorded leads I,II,III. Note that I've extended this line down to the corresponding complex in the long lead II rhythm strip (Figure-2).
• The reason for continuing the BLUE line all the way down to the corresponding beat in the long lead II rhythm strip — is that this tells you where the QRS complex ends and the ST segment begins in the long lead II rhythm strip (ie, Blue arrows in the long lead II rhythm strip highlight the end of the QRS complex).
• Knowing this landmark for the complexes in the long lead II rhythm strip — allows us to draw in and extend upward the BLUE lines parallel to the heavy ECG grid line in the other 3 sets of simultaneously-recorded leads.

Putting It All Together:

The ECG in Figure-2 shows sinus rhythm at ~95/minute, with an extreme amount of  "Shark Fin" ST segment deviation in multiple leads: 

• In the 3 inferior leads (II,III,aVF) — there are Q waves with a marked amount of ST elevation (seen to the right of the BLUE lines in Figure-2).
• There is a comparable amount of reciprocal ST depression in lead aVL (with a lesser amount of ST depression in lead I, in which the QRS complex is much smaller).
• 
  
• In the chest leads — ST elevation begins in lead V3, and continues with Shark Fin morphology in leads V4,V5,V6. Small but-definitely-present Q waves are seen in each of these leads.
• An initial positive deflection (r wave) is preseved in leads V1,V2. Shark Fin morphology ST depression is seen in these 2 anterior leads.
• 
  
• BOTTOM Line: In a patient with new chest pain — the ECG shown in Figure-2 is diagnostic of a diffuse, ongoing acute event. IF due to a single "culprit" vessel — I'd suspect acute occlusion of a dominant LCx (Left Circumflex) coronary artery, given infero-postero-lateral involvement. More likely — this patient has severe underlying multi-vessel disease, with acute occlusion of one of the remaining sources of coronary flow.

Figure-2: The rhythm in today's tracing is sinus (RED arrow in lead II). Vertical time lines highlight how to assess QRS duration.

QUESTION:

• Did YOU notice T-QRS-D in lead V3 of Figure-2?

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T-QRS-D: An Underappreciated ECG Sign:

The concept of Terminal QRS Distortion (T-QRS-D) was unknown to me prior to my active participation as an Associate Editor in Dr. Smith's ECG Blog. Since then I've seen many patient cases that validate the clinical utility of this ECG finding promoted by Dr. Stephen Smith. When present — T-QRS-D may provide invaluable assistance for distinguishing between a repolarization variant vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI). I illustrate the ECG finding of T-QRS-D below in Figure-3, which I've excerpted from My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog. To Review:

• T-QRS-D — is defined as the absence of both a J-wave and an S wave in either lead V2 or lead V3. Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.

A picture is worth 1,000 words. I’ve taken the lead V3 examples in Figure-3 from previous cases posted on Dr. Smith’s ECG Blog:

• TOP in Figure-3 — Despite marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
• BOTTOM in Figure-3 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

Regarding Today's Case:

Clearly — We do not need to identify T-QRS-D in today's case to confirm the large acute OMI. That said — I find it helpful to appreciate that T-QRS-D is present in lead V3 (GREEN arrow in Figure-2) because: i) There is no J-wave in this lead; and, ii) There is no S wave (because the last QRS deflection in lead V3 of today's tracing never descends below the baseline)!

Figure-3: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019) — vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (See text).

FOLLOW-Up in Today's CASE:

My follow-up on today's case is limited. Today's ECG is from a 57-year old man who presented for chest pain. Cardiac cath revealed severe multi-vessel disease — including proximal RCA and LAD occlusion, with diffuse LCx disease.

• Prediction of this patient's coronary anatomy is admittedly academic — since prompt cath with acute reperfusion will be indicated regardless of what our prediction might be.
• That said — the reason I suspected that the "culprit" lesion would not only be an acutely occluded proximal LAD (Left Anterior Descending) — was the lack of ST elevation in the more anterior leads (ie, in leads V1,V2).
• While true that LAD occlusion (so-called "wraparound" lesions) can result in ST elevation in both inferior and anterior lead areas — we would not expect this extreme amount of inferior lead ST elevation if the sole lesion was a "wraparound" LAD.
• Dominant LCx occlusion may produce the distribution of acute ST-T wave changes seen in today's ECG. That said — a "Take-Home" Point to keep in mind, is that severe underlying multi-vessel disease is a common setting for extensive areas of acute involvement that don't seem consistent with what you would predict from acute single-vessel occlusion.

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Acknowledgment: My appreciation to Chun-Hung Chen (from Taichung City, Taiwan) for the case and this tracing.

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ADDENDUM (12/28/2022): 

• For review of the concept of Shark Fin ST deviation ...

—  — 

TECG Media PEARL #73 (5:40 minutes Audio) — Reviews the concept of "Shark Fin" ST elevation and depression as a sign of extensive acute infarction.

 

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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 #265 — and ECG Blog #296 — for examples of Shark Fin ST deviation.
• 
  
• The November 22, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was cardiac arrest, ischemic Osborn waves, with massive Shark Fin ST deviation from acute STEMI.
• The June 12, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LPHB), in addition to Shark Fin ST elevation & depression. 
• The January 24, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LPHB) in addition to Shark Fin ST elevation & depression — followed by progressive Low Voltage due to Myocardial Stunning from the huge infarct.
• 
  
• ECG Blog #318 — Reviews the concept of T-QRS-D (Terminal-QRS-Distortion) — as a sign of acute OMI.

ECG Blog #352 — Chest Pain 1 Week Ago ...

The ECG in Figure-1 was obtained from a woman in her 80s — who presented with a history of having had 1 episode of chest pain during the previous week. No chest pain since.

QUESTIONS: 

• Given this history — What happened?
• How would YOU interpret the ECG in Figure-1?

Figure-1: ECG obtained from a woman in her 80s — who presented with 1 episode of chest pain during the previous week. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The mechanism of the rhythm in ECG #1 is sinus (ie, P waves are present and upright in lead II — with a constant PR interval throughout the long lead II rhythm strip). There is slight variability of the R-R interval — with an overall rate of ~60/minute.

• The PR interval is markedly prolonged (ie, to ~0.40 second) — so this is sinus arrhythmia with 1st-degree AV block.

Regarding the other intervals — the QRS is not wide — and the QTc does not appear to be prolonged. The frontal plane axis is normal at about +40 degrees. There is no definite sign of chamber enlargement.

Regarding Q-R-S-T Changes:

• Small and narrow Q waves of uncertain significance are seen in each of the inferior leads. 
• There may in addition, be tiny septal q waves of no significance in the lateral chest leads.
• 
  
• R wave progression in the chest leads manifests a normal "zone" of transition (in that the R wave becomes taller than the S wave is deep between leads V2-to-V3). That said — this transition is more abrupt than usual, with the R wave fairly suddenly becoming predominant in lead V3.

Regarding ST-T Wave Changes:

• In the inferior leads — there is slight ST elevation in lead III — ST-T wave flattening in lead II — and the suggestion of ST coving with slight-but-real terminal T wave inversion in leads III and aVF.
• That these findings are "real" — is supported by recognition of reciprocal changes in high-lateral leads I and aVL (in which there is ST segment flattening with slight depression and terminal T wave positivity).
• 
  
• PEARL #1: Interpretation of the limb lead changes in today's tracing is challenging — because of baseline artifact and resultant variation in ST-T wave morphology between the 2 beats that are seen in each of the limb leads. That said — What counts, is that although the ST-T wave appearance for each of the beats in these 5 limb leads manifests some variation in morphology — the overall (ie, "Gestalt") appearance of ST-T waves in these limb leads is consistent with a common "theme", which is — that in a patient reporting a recent episode of chest pain that has now resolved — these findings suggest a recent event that now manifests reperfusion T waves in the inferior leads.
• 
  
• PEARL #2: Given how common it is for acute or recent inferior OMI to also manifest ECG changes of posterior OMI — I immediately focused my attention on assessing for such changes in the anterior chest leads. Recent posterior OMI is suggested in ECG #1 by: i) Distinctly abnormal ST segment flattening in the anterior chest leads; ii) Surprisingly tall, symmetric T waves in leads V1-thru-V4 (maximal in V2,V3) that are consistent with posterior reperfusion T waves; and, iii) Abrupt development of a predominant R wave in lead V3 (See ECG Blog #351 — for more on these topics).
• 
  
• Completing our assessment for ST-T wave changes — Note that ST segment flattening with slight ST depression continues across the precordium to extend to the lateral chest leads (ie, leads V4,V5,V6).
• 
  
• PEARL #3: As discussed most recently in ECG Blog #350 — there is T wave "imbalance" in the chest leads. That is, when T waves in all 6 chest leads are positive — the T wave in lead V1 is not normally taller than the T wave in lead V6 (as it is in Figure-1). This finding sometimes provides a clue to recent OMI (especially from a LCx culprit artery).

ECG #1 — Putting It All Together:

The series of events and ECG findings described above can be put together to formulate a consistent story:

• The history in today's case (ie, of an older woman who describes an episode of chest pain days earlier — but which has now resolved) — is consistent with a recent event.
• Acute coronary occlusion is often followed by spontaneous reopening of the "culprit" artery. Clinically — these events are suggested by resolution of chest pain at a similar time that reperfusion T waves are seen on ECG. The presence of such reperfusion T waves in the inferior and posterior areas of ECG #1 — suggest that the "culprit" artery was either the RCA (Right Coronary Artery) or the LCx (Left Circumflex). Although a majority of individuals manifest RCA-dominance — the finding of chest lead T wave "imbalance" favors the LCx as the "culprit". KEY Point: Regardless of what the culprit artery turns out to be — the above-described sequence of events is consistent with the spontaneous reperfusion that characterizes Wellens' Syndrome (See ECG Blog #350).
• While Wellens' Syndrome most often involves a high-grade proximal LAD (Left Anterior Descending) stenosis that results in anterior reperfusion T waves — the same pathophysiology of Wellens' Syndrome may also be seen in the form of infero-postero reperfusion waves from recent RCA or LCx occlusion (See ECG Blog #326).
• 
  
• PEARL #4: The importance of recognizing the correlation between ECG findings and the history in today's case (ie, a prior history of chest pain that has resolved at the time the reperfusion T waves in ECG #1 are seen) — suggests the need for timely cath, with expected need for PCI pending cath findings (to prevent reocclusion of the "culprit" artery that spontaneously reopened).

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QUESTION: 

• How likely is it that toda's patient may have had Mobitz I 2nd-degree AV block earlier in the week?

ANSWER:

It is common for patient's with acute inferior MI — to develop a stepwise sequence of AV conduction disturbances, resulting from associated ischemia in the AV node.

• Conduction disturbances in such patients tend to begin with the simple PR interval prolongation of 1st-degree AV block — followed by progression to 2nd-degree AV block of the Mobitz I type (ie, AV Wenckebach). Some patients ultimately progress to 3rd-degree (ie, complete) AV block, most often with a narrow (AV nodal) escape rhythm. 
• In most cases in which AV conduction disturbances develop with acute inferior MI — the progression is sequential (ie, from 1st-degree — to 2nd-degree — to 3rd-degree). Conduction disturbances in such patients tend to be transient — with regression in the reverse sequence over the ensuing period of days to 1-2 weeks, as the patient recovers from their infarction.
• 
  
• BOTTOM Line: The fact that today's patient had a recent inferior MI — and now presents with marked PR interval prolongation — could be perfectly consistent with having had a recent Mobitz I block, that is now in process of resolving as the patient recovers from her infarction.
• 
  
• PEARL #5: Most patients with 1st-degree AV block remain asymptomatic without the need for intervention. This is especially true when the severity of 1st-degree AV block is not great (ie, a PR interval less than 0.30 second). Once the PR interval extends beyond 0.30 second (as is the case in today's patient) — the delay in ventricular contraction that occurs may result in the atria contracting against closed AV valves, with reduction in cardiac output. This may lead to a series of symptoms similar to “pacemaker syndrome” (ie, dizziness, fatigue, light-headedness, presyncope/syncope, dyspnea and/or chest pain).
• On occasion — symptoms in patients with a markedly prolonged PR interval may be severe enough to require implantation of a permanent pacemaker.

Comparison with the Prior ECG:

A previous (baseline) ECG on today's patient was found. For clarity in Figure-2 — I have put this prior ECG (obtained ~3 years earlier — when the patient was asymptomatic) — together with today's initial ECG.

QUESTION:

• Does comparison of the 2 tracings in Figure-2 support our theory regarding the likely sequence of events in today's case?

Figure-2: Comparison of today's tracing — with a baseline ECG from ~3 years earlier. Does this baseline tracing support our theory?

Comparison of the 2 ECGs in Figure-2:

Interpretation of today's initial ECG, in light of the baseline tracing from ~3 years earlier — is insightful. Note the absence of the following findings from ECG #2:

• In the inferior leads of ECG #2 — there was no ST elevation or T wave inversion in this baseline tracing.
• In the high-lateral leads (ie, leads I, aVL) — there was no ST depression with terminal T wave positivity.
• In the anterior chest leads — the ST segments were gently upsloping (as they are supposed to be) in leads V2,V3,V4 — and the T waves in leads V1-thru-V4 were neither tall nor peaked.
• There was no lateral chest lead ST depression (in V4,V5,V6) — and there was no T wave "imbalance" (ie, There was no positive T wave taller in lead V1 than in lead V6).
• R wave progression in the baseline tracing was more natural (ie, Instead of abrupt transition to a predominantly positive QRS by lead V3 — transition to predominant positivity in the chest leads occurred more gradually in ECG #2).

QUESTION:

• Did YOU notice that 1st-degree AV block was present in the baseline ECG? (albeit to a significantly lesser degree = 0.26 second).

CASE Conclusion:

Although I lack specific follow-up to today's case — a number of closing comments can be made.

• The clinical scenario in today's case differs from the more common scenario seen in the ED (Emergency Department) — or in the field by EMS personnel — in that instead of the patient presenting at the time of acute symptoms — the patient presents for care a number of days after their acute chest pain episode. (This is much more consistent with what I used to see as a Primary Care Attending in our Family Medicine Center, where I worked for 30 years.)
• Patients with severe acute chest pain symptoms tend to "self-select" — either calling EMS directly, or getting to the ED by themself or with family. Since the majority of patients who die from acute MI, do so within the first 24-48 hours after onset — it is insightful to appreciate that the patient who only presents a few days after their symptoms, has probably already survived their "highest risk" period.
• 
  
• Given the history in today's case (interpreted in context with the 2 ECGs shown in Figure-2) — We have confirmed that all ST-T wave findings described above for ECG #1 were new since the baseline tracing. This supports our theory that the initial ECG in today's case represents reperfusion following a recent OMI that occurred days earlier. Consistent with Wellens' Syndrome — timely cath is still indicated to clarify the anatomy, albeit the "culprit" artery is most probably open at this time since the patient remains pain-free.
• 
  
• On the other hand — the 1st-degree AV block is not new! — since the PR interval was ~0.26 second on the baseline tracing done ~3 years ago. As a result (unless additional baseline tracings are available) — we really do not know if this patient had been progressively increasing the severity of her 1st-degree AV block over a period of years — or — if her conduction defect had been stable with a PR interval ~0.26 second for the past 3 years, only to increase this past week at the time of her acute OMI. The answer to this question may have implications regarding the potential need for permanent pacing in this older woman (ie, As noted above — it's possible if her severe 1st-degree AV block persists or worsens — that permanent pacing may eventually be needed).

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Acknowledgment: My appreciation to Arron Pearce (from Manchester, UK) for the case and this tracing.

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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 #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 reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).
• 
  
• ECG Blog #285 — and ECG Blog #246 — and ECG Blog #80 — for examples of acute posterior MI (with use of the Mirror Test to facilitate diagnosis).
• ECG Blog #317 — reviews use (or not) of Posterior Leads.
• 
  
• ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.
•  
• The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 
• Diagnosis of an OMI from the initial ECG — Serial tracings with spontaneous reperfusion — then reocclusion! — See My Comment at the bottom of the page in the October 14, 2020 post on Dr. Smith's ECG Blog.
• Acute OMI that wasn’t accepted by the Attending — See My Comment at the bottom of the page in the November 21, 2020 post on Dr. Smith’s ECG Blog.
• Another overlooked OMI (Cardiologist limited by STEMI Definition — OMI evident by Mirror Test) — See My Comment at the bottom of the page in the September 21, 2020 post on Dr. Smith’s ECG Blog.
• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• 
  
• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare Serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• 
  
• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
• ECG Blog #350 — Reviews another case of Wellens' Syndrome (with T wave "imbalance" in the chest leads between leads V1,V6).

ECG Blog #351 — Posterior Leads ...

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 — See ECG Blog #406 — for a Video presentation of this case!

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The ECG in Figure-1 — was obtained from a previously healthy older man who contacted EMS (Emergency Medical Services) because of "chest tightness" that began ~1 hour earlier. Given this history:

QUESTIONS: 

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab ?

Figure-1: The initial ECG in today's case — obtained by EMS at the scene, from an older man with ~1-hour of chest "tightness". (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The rhythm in ECG #1 is sinus at ~75/minute. Regarding intervals — the PR interval is normal — the QRS is not wide — and the QTc is at most borderline prolonged. The frontal plane axis is normal at about +70 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• A large and wide Q wave is seen in lead aVL. There are no other Q waves.
• 
  
• R wave progression is appropriate — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

Regarding ST-T Wave Changes:

• PEARL #1: The most noteworthy findings in today's tracing are in lead V4. The downward sloping "shelf-like" shape of the ST segment in this lead, in association with terminal T wave positivity in a patient with new-onset chest pain — is almost by itself diagnostic of acute posterior OMI (Occlusion-based Myocardial Infarction).
• 
  
• In strong support of my impression from lead V4 — is the shape of neighboring lead V3. Although there is somewhat less ST depression in lead V3 (and its ST segment is now gently upsloping) — there now is significantly more positivity of the terminal T wave.
• The other "neighboring lead" to V4 is lead V5. While not nearly as abnormal as leads V3,V4 — lead V5 shows subtle-but-real "scooped" ST depression. 
• 
  
• PEARL #2: In a patient with new chest pain — the finding of ST depression that is maximal between leads V2-to-V4 should suggest acute posterior OMI until proven otherwise. This provides an important distinction between diffuse SEI (SubEndocardial Ischemia) — in which near comparable ST depression is seen in multiple leads, with ST elevation in lead aVR (See ECG Blog #271).
• 
  
• PEARL #3 (Beyond-the-Core): There is a subtle-but-real abnormality in lead V2 — in that the ST segment in lead V2 is flat (ie, neither elevated nor depressed). This is unusual — because much (most) of the time in a normal tracing, there is slight upsloping ST elevation in lead V2. The finding of a flat ST segment in lead V2 — is most likely the result of an "attenuating" (opposing) effect from acute posterior OMI that produces some ST depression.
• 
  
• The ST segment in lead V1 is coved and slightly elevated. The significance of this finding is uncertain from this tracing.
• Lead V6 is unremarkable.
• 
  
• In the Limb Leads — There is subtle-but-real "scooped" ST depression with terminal T wave positivity in each of the inferior leads.
• The subtle coved shape of the ST segment in lead aVL (with slight ST elevation and suggestion of terminal T wave inversion) — appears to be a reciprocal change to the ST-T wave appearance in the inferior leads.
• I thought lead I was nondiagnostic. 

ECG #1 — Putting It All Together:

As alluded to earlier — in an older patient with new-onset chest pain — the finding of maximal ST depression in leads V3 and V4, with subtle-but-real findings in neighboring leads — is diagnostic of acute posterior OMI until proven otherwise. To Emphasize: In a patient with new chest pain — this single ECG by itself should suffice to merit prompt cath lab activation!

• Although impossible to tell from this single tracing if the large and wide Q wave in lead aVL is new or old — the associated ST coving with slight elevation and hint of terminal T wave inversion — suggests acute high-lateral involvement. This is supported by the finding of reciprocal ST depression in each of the inferior leads.
• Regarding prediction of the "culprit" artery — The finding of suspected acute posterior and high-lateral OMI in the absence of ST elevation in the inferior leads suggests the LCx (Left Circumflex) as the acutely occluded artery (especially of the 1st or 2nd Obtuse Marginal Branch).
• 
  
• BOTTOM Line: Regardless of what turns out to be the "culprit" artery — the important point is that in a patient with new chest pain — ECG #1 by itself is diagnostic of acute OMI until proven otherwise. The cath lab should be activated.

PEARL #4: Use of the "Mirror" Test

I favor use of the "Mirror Test" — as a visual aid to facilitate recognition of acute posterior MI. This adds even more support to the above "Bottom-Line conclusion", that as I emphasize above, should have already been reached.

• The principle of this test is simple: It is based on the fact that the mirror-image view of anterior leads — provides insight to the nature of electrical activity as viewed by the posterior wall of the left ventricle (For more on the "Mirror" Test — See the Audio Pearl in the ADDENDUM below).
• 
  
• Note that I have vertically flipped anterior leads V2 and V3 in the PURPLE inserts that I've added in Figure-2 (to show the mirror-image view of these 2 leads). Doesn't the shape of the "shelf-like" ST depression and terminal T wave positivity seen in leads V3 and V4 of Figure-2, when vertically flipped (as viewed in the Mirror Test) suggest a worrisome shape and amount of ST elevation — as well as already deep T wave inversion?

Figure-2: I've added the mirror-image of leads V3 and V4 to today's tracing — to illustrate how the initial ECG shows a positive "Mirror" Test suggestive of acute posterior OMI (See text).

What Did the Repeat ECG Show?

The EMS team immediately recognized the need to urge cath lab activation and to expedite transport of the patient to the hospital. 

• En route — the EMS team obtained a 2nd ECG (shown in Figure-3) — with substitution of right-sided lead V4R and posterior leads V8 and V9 in place of leads V4,V5,V6.

QUESTIONS:

• How would YOU interpret ECG #2? — considering that it was obtained 18 minutes after ECG #1 (with the patient describing a reduction in chest pain severity).
• 
  
• What are potential Pros & Cons of substituting leads V4R, V8, V9 for V4,V5,V6?

Figure-3: Comparison of the initial ECG — with a repeat ECG done 18 minutes later (substituting leads V4R,V8,V9 — for leads V4,V5,V6). Of note — the patient reported a reduction in chest pain severity around the time ECG #2 was recorded.

Potential Pros & Cons of Additional Leads:

I will never negate the potential benefit of recording additional leads when the purpose for doing so is: i) To increase the confidence of the treating provider in his/her interpretation; — or — ii) Because the treating provider(s) feel the need to "convince" the on-call cardiologist that posterior leads show the ST elevation that is being looked for to "justify" taking the patient to the cath lab. That said — the clinical realities are the following:

• It takes an extra moment of time to record additional leads. As a result — EMS providers must "balance" their need to expedite transport to the ED — vs — spending that extra moment of time because your on-call cardiologist is one who will not activate the cath lab without ST elevation.
• 
  
• The reality is that there is no ST elevation on a standard 12 lead ECG with isolated posterior infarction. That said, as is the case for today's patient — ECG #1 is diagnostic by itself (without the need for ST elevation) — of acute coronary occlusion (ie, of acute OMI = Occlusion-based Myocardial Infarction).
• 
  
• In the April 1, 2018 post in Dr. Smith’s ECG Blog — Drs. Meyers, Weingart and Smith published their OMI Manifesto — in which they extensively document the critically important concept that management of acute MI by separation into a “STEMI” vs “non-STEMI” classification is an irreversibly flawed approach.
• Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! Yet despite this remarkable flaw in the STEMI-paradigm — a substantial number (if not a frank majority) of clinicians continue to apply outdated criteria when interpreting ECGs, by refusing to consider prompt cath for definitive diagnosis and reperfusion therapy just because a millimeter-based definition for acute STEMI is not satisfied.
• The September 3, 2020 post of Dr. Smith's ECG Blog features Dr. Meyers' 17-minute summary of this OMI Manifesto, with all of its documentation.
• 
  
• I summarize KEY points from the OMI Manifesto in the July 31, 2020 post in Dr. Smith's ECG Blog. For clarity, in Figure-4 (below in the ADDENDUM) — I've put the ECG findings to look for that suggest acute OMI — despite the fact that your patient with new chest pain does not satisfy sufficient criteria to qualify as a "STEMI". 

Regarding Posterior Leads:

While many providers (including many cardiologists) favor the use of posterior leads — the reality is that QRST amplitudes with posterior leads are reduced compared to mirror-image anterior lead amplitudes. This is because to assess electrical activity from posteriorly placed V7,V8,V9 electrodes — the thick back musculature (with its significant damping effect) must be traversed before these posterior leads are able to record the heart's electrical activity.

• To Emphasize: I am not against those who prefer to obtain posterior leads because they feel this helps in their interpretation. I am simply saying that with minimal practice using the Mirror Test (See Pearl #4 and Figure-2 above) — that equal information is obtained faster without the need to apply additional leads. (Actually — more information is obtained — since there are times when the Mirror Test is positive despite negative posterior leads).

Regarding Right-Sided Leads:

As discussed in ECG Blog #190 — the BEST way to diagnose acute RV MI is by seeing ST elevation in right-sided leads. The standard 12-lead ECG may hint at acute RV involvement (ie, If in the face of ST depression in leads V2,V3 from acute posterior MI — there is unexpected ST elevation in lead V1). But by itself — the standard 12-lead ECG cannot rule out the possibility of acute RV involvement

• That said — Since acute RV MI is virtually always caused by acute RCA (Right Coronary Artery) occlusion — there should (by definition) — be ST elevation in the inferior leads in patients who also have acute RV involvement. The complete lack of such ST elevation in the inferior leads of ECG #1 — all but negates the possibility of acute RV MI in today's case (ie, isolated RV MI is rare!).

What do We Learn from ECG #2?

The reason I have put the 2 ECGs in today's case together in Figure-3 (shown above) — is that doing so makes it much easier to apply lead-to-lead comparison.

• In the Limb Leads — The frontal plane axis is similar in both ECG #1 and ECG #2. This tells us that lead-to-lead comparison in the limb leads will be valid!
• The heart rate in ECG #2 is a little bit slower.
• There appears to be slightly less ST depression in each of the inferior leads.
• 
  
• In the Chest Leads — We can only compare leads V1,V2,V3, since leads V4R,V8,V9 have replaced lateral chest leads V4,V5,V6 in ECG #2. That said — both the amount of J-point ST depression and the height of the hyperacute T wave in lead V3 are clearly less in ECG #2!
• 
  
• IMPRESSION: In view of the patient's report that chest pain was decreasing at around the time that ECG #2 was recorded — this improvement in ST-T wave appearance suggests that the "culprit" vessel may have been in process of spontaneously reopening.

PEARL #5: Often overlooked (but of critical clinical importance) — is the need for close correlation between serial ECGs and the relative severity of chest pain symptoms at the time that each ECG is obtained. 

• The reason this close correlation is so important — is that it provides KEY insight as to whether the acutely occluded artery has spontaneously reopened — or — is likely to still be occluded. 
• 
  
• KEY Point: The process of acute coronary occlusion is often not "all or none". Instead — many patients have a "stuttering pattern" — in which the acutely occluded artery may spontaneously reopen, only to later spontaneously reocclude. And sometimes, the pattern is of spontaneous opening — followed by reclosure — then reopening — another reclosure — with this process going back-and-forth occurring multiple times — until eventually at some point, a "final" state of either open or closed is reached for the "culprit" vessel.
• Persistent ST elevation with ongoing severe chest pain suggests that the "culprit" artery is still occluded. 
• In contrast — Reduced chest pain that occurs as ST elevation is resolving (and as reperfusion T waves develop) — suggests that the "culprit" artery has spontaneously opened (See the Audio Pearl in today's ADDENDUM below for more on this).

PEARL #6: If the decision is made to obtain additional leads when it comes time to repeat the ECG — Be SURE to obtain a 2nd complete 12-lead ECG before you record right-sided or posterior leads! Otherwise — you lose data.

• Ironically in today's case — If the purpose for obtaining posterior leads in ECG #2 was in the hope of convincing the on-call cardiologist that there is ST elevation in leads V8,V9 — the fact that chest pain was decreasing and acute ST-T wave changes in the inferior leads and in lead V3 seemed to be resolving — will probably also result in less ST elevation in leads V8,V9.
• It probably would have been much easier to establish that acute ST-T wave changes were resolving in ECG #2 if a standard lead V4 would have been recorded in this repeat ECG.
• 
  
• Recording a complete 12-lead ECG before obtaining additional leads would have accomplished 2 things: i) Documenting a change in ST-T wave findings on serial ECGs in a patient with changing severity of symptoms is the definition of "dynamic" ST-T wave change — and, in a patient with new chest pain, this finding alone is indication for prompt cath! — and, ii) Seeing reduced acute ST-T wave changes in a standard lead V4 in ECG #2 — would have better prepared us not to expect much (if any) posterior lead ST elevation.
• 
  
• It turns out that leads V8 and V9 in ECG #2 do show ST coving and slight elevation — but this is minimal.

CASE Follow-Up:

Today's case provides an excellent example of superb care by the EMS team — that quickly recognized acute OMI — and — quickly recognized the need for prompt cath. The on-call cardiologist did perform emergent cardiac catheterization because of persistent chest pain and abnormal ECG changes (I do not have access to subsequent serial tracings on this patient).

• Cardiac cath showed multi-vessel disease — with acute occlusion of the 1st OM (Obtuse Marginal branch) of the LCx (Left Circumflex) artery felt to be the acute "culprit" lesion. A drug-eluting stent was placed — and the patient apparently did well!

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Acknowledgment: My appreciation to Tomasz Numrych (from Maryland, USA) for the case and this tracing.

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ADDENDUM (12/18/2022): 

• Included below are a series of links and other material relevant to detection of the “culprit” artery — and my thoughts for making the case to replace the term “STEMI” with “OMI”, in the hope of substantially increasing detection of acute coronary occlusion. 

 

Free PDF Downloads from relevant Sections in my ECG-2014-ePub:

• PDF File: Overview on the Cardiac Circulation and the “Culprit” Artery in Acute MI —
• PDF File: Posterior MI and the “Mirror Test” —

 

Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.

 

Figure-5: KEY points in the recognition of isolated posterior MI (This figure is taken from ECG Blog #193 — in which I review the "Basics" for predicting the "culprit" artery). 

—  — 

ECG Media PEARL #60 (8:30 minutes Audio) — Reviews use of the "Mirror Test" to facilitate recognition of: i) Acute Posterior MI; ii) Acute High-Lateral or Inferior MI (ie, the "magical" reciprocal relationship between leads III and aVL); and, iii) Anterior ST elevation due to LVH (that is not indicative of anterior MI).

 

—  —

ECG Media PEARL #10 (10 minutes Audio) — 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 "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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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 reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).
• 
  
• 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 (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
• ECG Blog #317 — reviews another case regarding use (or not) of Posterior Leads.
• 
  
• 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.
•  
• The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 
• Diagnosis of an OMI from the initial ECG — Serial tracings with spontaneous reperfusion — then reocclusion! — See My Comment at the bottom of the page in the October 14, 2020 post on Dr. Smith's ECG Blog.
• Acute OMI that wasn’t accepted by the Attending — See My Comment at the bottom of the page in the November 21, 2020 post on Dr. Smith’s ECG Blog.
• Another overlooked OMI (Cardiologist limited by STEMI Definition — OMI evident by Mirror Test) — See My Comment at the bottom of the page in the September 21, 2020 post on Dr. Smith’s ECG Blog.
• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• 
  
• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of the entity of diffuse Subendocardial Ischemia).
• 
  
• ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T-waves).
• 
  
• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
• 
  
• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare Serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• 
  
• ECG Blog #190 — How to diagnose acute RV MI (and use of right-sided leads).