Do you understand these T-wave inversions?

Case submitted and written by Alex Bracey, with edits by Pendell Meyers

A man in his 50s without prior medical history was sent to the emergency department from an urgent care facility for concern of an "abnormal ECG" after he had complained of chest pain earlier in the day. He was symptom free at the time of arrival.

Here is the triage ECG at the Emergency Department (we did not immediately have access to the urgent care ECG just yet):

ED ECG#1

What do you think? What do you think his urgent care ECG (done during pain) will show?

This ECG shows sinus bradycardia with terminal ST depressions in II, III, aVF, V3-V6, with reciprocal changes in aVL and I. These findings indicate reperfusion of the inferior and lateral walls, implying that an ECG during active symptoms would likely show OMI.

Note: This is the same pathophysiology and electrophysiology involved in Wellens syndrome, which is simply the name given to reperfusion of anterior wall OMI when the patient is in the pain free state of reperfusion and has not yet lost the anterior wall (requires persistent R-waves to be classic Wellens syndrome). This pattern occurs in any wall of the heart, whichever wall is currently reperfused from a prior occlusion.

On this note, "type A" and "type B" Wellens are useless distinctions that arose before we realized that reperfusion is a progression of findings starting with terminal T-wave inversions ("type A") and progressing to full T-wave inversions ("type B"). My analogy for this misunderstanding of Wellens syndrome that I tell my residents is this: "Imagine you were an alien looking through a microscope and you discovered Earth. You zoom in to a city and look at a single street and you see humans, which happens to be a woman walking with her small child. You watch them for a few hours and then report your findings to your fellow aliens: you declare that there are two types of humans: type A (smaller, helpless ones) and type B (large, smarter ones). If they simply had more knowledge and experience with humans, it would be easy to understand that type A and type B are not different types at all, rather different points along the same progression. If you only look at individual snapshots in time, they appear to be different types, however if you follow them for the full course of their progression the pattern becomes clear.

To make type A and B even more useless, they are misnomers applied by someone who had not carefully read Wellens' papers. They called terminal T-wave inversion type B and deep inversion type A. Wellens called terminal T-wave inversion "Pattern A" and deep "Pattern B."

He reports that today while sitting outside he developed sudden onset bilateral arm “burning” and an “odd feeling” though he was not able to further describe it. He had no chest pain, heaviness, or discomfort at any point and was never short of breath during today’s events. When pressed, he recalls that last week he traveled to Denver where he experienced dyspnea on exertion, though he attributed it to the altitude.

He was alarmed by these symptoms today and presented to an urgent care where this ECG was recorded:

Urgent Care ECG (this was done before arrival to ED, during active symptoms):

STE in II, III, and aVF (which probably barely does meet STEMI critiera) with hyperacute T waves in II, IIII, aVF and reciprocal negative hyperacute T-wave in aVL, with STD in V1-V2

Small R waves in II, III, aVF

This is diagnostic of inferoposterior OMI. The most likely culprit vessel would be the RCA.

Back to the present, in the ED, asymptomatic:

Given that the patient was now asymptomatic in the ED with ED ECG#1, I asked for serial ECGs to be recorded every 30 minutes and for any acute changes in discomfort or clinical condition.

At our facility we have a process to promptly evaluate patients for urgent or emergent PCI that present with ECGs concerning for acute coronary occlusions that do not meet STEMI critieria (OMI) called Heart Alert. We activated this process and the cardiology fellow presented to the bedside.

A third ECG was record at this time with no change, persistent reperfusion pattern.

During this time I received a call from the interventional cardiologist. I discussed the case with him as he reviewed the ECG. We agreed that there were dynamic changes; however, he did not feel that it could represent acute coronary syndrome as the patient did not have chest pain at any time during his prior symptoms. 

This is clearly false.

The patient then reported another episode of diaphoresis. An ECG at this time was recorded:

Redemonstration of small STE in II, III, aVF (not meeting criteria in this ECG) and reciprocal changes in aVL, V2. This ECG demonstrates reocclusion of the affected coronary vessel.

At this time the cardiology fellow again contacted the interventionist who agreed to take the patient for urgent PCI at this time. 

His initial troponin T was 0.02 ng/mL.

Here is what they found on cath:

100% mRCA with TIMI 0 flow

Post DES RCA with TIMI 3 flow

His formal echo performed the next day revealed an EF of 50% and Septal, lateral, and apical wall motion abnormalities.

His troponin T continued to climb over the next day with a peak of 1.4 ng/mL.

He had an uncomplicated post-PCI course and was discharged 3 days later.

Teaching Points:


We must understand the ECG patterns of occlusion and reperfusion because they are not currently taught or understood in the classic STEMI paradigm.

Serial ECGs greatly increase the chances of finding diagnostic features of OMI on ECG.

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MY Comment, by KEN GRAUER, MD (10/10/2019):

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Highly insightful case! Drs. Bracey and Meyers have intentionally changed the time sequence in which the tracings in this case were recorded in order to make a number of important points.

• I limit my comments to discussion of the 1st ECG shown above. This is the initial ECG that was done at the time the patient arrived in the ED.
• I will offer a different perspective on the interpretation of ECG #1. For clarity — I have reproduced and labeled this ECG in Figure-1.

Figure-1: The initial ECG done in the ED (See text).

I propose the following additional Teaching Points regarding interpretation of ECG #1, considering the clinical context in which this patient presented:

• Although I was not surprised by ECG findings on the Urgent Care ECG (which was the 2nd ECG shown above) — I do not think ( = my opinion) that there was any way to be certain there was ongoing acute infero-postero OMI from assessment of ECG #1 alone.
• From an ECG Learning perspective — Systematic interpretation of ECG #1 should result in recognition of at least 4 additional findings not mentioned above. Admittedly, recognition of these findings does not alter management in this case — but there are times when failure to routinely use a systematic approach will result in overlooking ECG findings that are important (as I have shown on prior posts).

At the time ECG #1 was obtained in the ED — all that the ED physician knew was the HISTORY (a 50s man who was previously healthy, had chest pain earlier that day — but was asymptomatic at the time ECG #1 was done). Systematic Interpretation begins with Descriptive Analysis (I’ve put additional findings that should be recognized in BOLD).

• Rate & Rhythm — There is sinus bradycardia (rate in the 50s, perhaps with some sinus arrhythmia).
• Intervals (PR/QRS/QT) — The PR interval is normal. The QRS complex is narrow. The QTc is not prolonged.
• Axis — There is marked left axis deviation — with a predominantly negative QRS in lead II (ie, the axis is more negative than -40 degrees). This is consistent with LAHB (Left Anterior HemiBlock). We don’t know if this is a new finding ...
• Chamber Enlargement — There is no atrial enlargement, and no RVH. But criteria for LVH are met! (ie, R in lead aVL≥12 mm).

Q-R-S-T Changes:

• Q = There are small (normal septal) q waves in leads I and aVL.
• R = There is something strange about R wave progression! There may be a tiny q wave in lead V2? Abrupt transition from the negative QRS in lead V1 — to the predominantly positive QRS complex by V2 — with then loss of R wave by V3, just doesn’t make physiologic sense. Note a much more logical progression of QRS and ST-T wave morphology across the chest leads for the other 2 ECGs done in this case. Recognition that placement of lead V2 may be off in ECG #1 is relevant in this case, given the ultimate evolution of acute infarction.
• ST-T Wave Changes — As emphasized by Drs. Bracey and Meyers, there is terminal T wave inversion in multiple leads in ECG #1 (BLUE arrows highlight this in leads V3 and V4 — but it is also present in leads II, aVF, V5 and V6). As was also emphasized — this ECG finding of a biphasic T wave with terminal T wave inversion (and with frank T wave inversion in lead III) alerts us in a patient with chest pain earlier that day — to the strong possibility that these findings may reflect reperfusion changes. (PINK — then BLUE arrows, highlight the biphasic nature of these T waves.) That said, there really is no ST elevation, no ST depression, and no non-septal Q waves in ECG #1 — and, in the absence of a prior or subsequent tracings — I don’t think ( = my opinion) that a definitive diagnosis of acute infarction can be made. We simply have NO idea as to when these ECG abnormalities may have developed … These ECG changes could certainly be acute — or, they may have developed days (or longer) before ECG #1 was done.
• That said — it should be noted that in addition to these biphasic T waves with terminal inversion (and the frank T inversion in lead III) — ST segments just before these T waves are inappropriately flat in multiple leads (short horizontal BLUE lines in Figure-1). This loss of the normal gradual ST segment upslope is a distinctly abnormal ECG finding, especially in a patient with recent chest pain.

BOTTOM LINE: It should be appreciated that other than leads aVR and V1 — the remaining 10 leads in ECG #1 all show abnormal ST-T wave findings. In a previously healthy middle-aged adult who experienced new chest pain earlier in the day — the overall assessment of ECG #1 alone should clearly justify timely cardiac catheterization.

• Once the earlier ECG from the Urgent Care Center became available — the diagnosis of acute ongoing infero-postero OMI became obvious. But, I thought it important to highlight all of the ECG findings that should be noted on ECG #1 — and, to emphasize that even if no Urgent Care Center ECG had been done, that timely cath would still be indicated.

Our THANKS to Dr. Bracey and Meyers for this insightful case!

A 40-Something male with a "Seizure," Hypotension, and Bradycardia

This is by one of our outstanding 3rd year residents, Aaron Robinson, with some edits and comments by Smith

EMS responded to a reported seizure in a 42 year old male. Per bystanders, he went down after some intense sporting activity, and had “shaking” type movement. He reports no personal or familial history of seizures.

One of our EMS Fellows along with a Senior EM Resident were on duty that evening, and arrived on the scene with the Fire Department. When the physicians approached him, he was ashen, diaphoretic, and appeared in shock. Fire was able to obtain a BP of 60/palp and a pulse in the 40s. The physicians quickly recognized that this was not a seizure and likely cardiac in nature. 

When the paramedics arrived, they obtained a 12 lead ECG and confirmed the unstable vital signs. EKG is pictured below:

What do you think?
There is an obvious inferior STEMI, but what else?
Why is the patient in shock?

Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. He was in profound cardiogenic shock. 

Smith comment: I suspect lead reversal of V2 and V3: the STE is high in V1, lower in V2, and high again in V3. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. It really is an anterior STEMI, but of the Right Ventricular Anterior Wall, not the LV anterior wall.

When there is inferior and anterior STE, the differential is:
1. inferior + RV MI due to RCA occlusion vs.
2. LAD occlusion in a "wraparound LAD" (wraps around to the inferior wall).
In this case, the inferior STE is the most exaggerated, and the anterior STE is highest in V1 and V2. Both of these features make inferior + RV MI by far the most likely (Pseudoanteroseptal MI is another name for this)

There is also sinus bradycardia and the patient is in shock with hypotension. Although the shock is no doubt partly a result of poor pump function, with low stroke volume, especially of the RV, it should be compensated for by tachycardia. Cardiac output is stroke volume x rate, so this patient needs a higher heart rate.

This is a perfect indication for atropine. Atropine may succeed in increasing the heart rate in any narrow complex bradycardia, especially sinus bradycardia, but also with AV block, as AV block with a narrow complex QRS may be a junctional escape. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.

RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. In fact, in inferior MI, sinus bradycardia may be further evidence of Proximal RCA occlusion, which is the occlusion location that results in RV MI. Here is full text of this article.

Case continued

EMS immediately transported, activated the cath lab and gave 324 mg aspirin en route. It was about a 7 minute transport time. EMS  also quickly administered 1L of NS to optimize preload and hopefully boost perfusion. They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas). 

EMS obtained a second ECG one minute later:

It appears the patient’s inferior STEMI has reperfused, as there is resolution of the inferior STE.

The patient arrived at the Emergency Dept critical care area and had this ECG recorded:

The sinus bradycardia persists. As you can see, the STE has returned in the inferior leads and there is now ST depression in the anterior leads concerning for posterior involvement. A right sided ECG was not recorded. STE in V1 with an inferior STEMI is moderately sensitive for right-ventricular involvement but this is only if there is no ST depression in V2! If there is STD in V2, the STE in V1 may be artificially normal! See this paper by Smith et al. Of note, despite the classic teaching, ST depression in Lead I is NOT reliable for the diagnosis of R-sided MI.

A bedside cardiac US was performed and showed an overall decrease in systolic function.

Also, the RV appears large and hypokinetic

The patient kept having recurrent syncopal episodes in the ED and was subsequently intubated for stabilization and airway protecting prior to going to the cath lab. Before transport, a final ECG was recorded:

There is, again, inferior reperfusion, but persistent marked anterior STE. 

He was taken to the cath lab and underwent emergent intervention:

Thrombotic stenosis of the proximal RCA (95% with evidence of plaque

rupture) is the culprit for the patient's inferoposterior STEMI. He was successfully stented. This also confirms right ventricular infarction (RV MI)

A follow up TTE demonstrated a normal LVEF with a “regional wall motion abnormality-posterolateral hypokinetic mild, probable.” His troponin I peaked at 6.107 ng/mL. He was discharged neurologically intact and did very well. He has a history of sudden cardiac death in his family. The patient never arrested during his time at the hospital and his prognosis is good. 

Learning Points:

1. It is easy to mistake syncopal episodes with associated myoclonus as seizures, so have a high index of suspicion for syncope as the etiology. This patient’s shock state upon arrival didn’t fit with seizures and it was quickly recognized.

2. Recognize Right Ventricular STEMI by inferior MI with shock (and clear lungs), sinus bradycardia, and ST elevation in Lead V1 (but it may also be V2 and beyond, with maximal STE in V1 and V2).

3. STE in V1 in inferior MI is moderately sensitive for RV MI (if there is no posterior MI "pulling the ST segment down"). Plus STE in V1 in inferior MI is very specific for RV MI.

4. If time allows, a right sided ECG may help to recognize RV MI, but even this can be falsely negative in the presence of posterior MI (see below).

5. Give atropine for narrow complex bradycardia with hypotension.

6. Give a moderate fluid bolus for Hypotension in RV MI

7. Give norepinephrine for hypotension in spite of the moderate fluid bolus.

I (the senior resident on scene with the EMS Fellow) had a discussion with Dr. Smith regarding this case. During transport, I had debated giving atropine for his bradycardia and cardiogenic shock, but was worried about making an already profoundly ischemic heart more ischemic, and chose instead to optimize preload with pressure bagging 1L NS. Dr. Smith pointed out that while atropine may may result in slightly more oxygen demand, the increase in cardiac output and in blood pressure would increase overall coronary perfusion and decrease ischemia. This is particularly true of RV MI: LV coronary perfusion is dependent on diastolic pressure because the myocardial pressure is too high for perfusion during systole. But RV systolic pressure is low, so the RV perfuses during BOTH systole and diastole. Higher mean arterial pressure improves RV perfusion. Norepinephrine can be very useful adjunct to shock from RV MI, as hypotension is so detrimental to RV perfusion.

So when I find myself in this position again prehospital, I will administer atropine. 

V4R in Right Ventricular MI

As in the Smith study of lead V1 in RVMI, Kosuge et al. studied lead V4R in the context of posterior involvement and found that RVMI was associated with a high rate of STE in V4R in the absence, but not in the presence, of posterior MI. STE V4R had sensitivities of 34% and 96% (p b 0.001), and specificities of 83% and 82% (NS) in the presence and absence of PWI, respectively. They did not study lead V1. Like our study, they used angiographic criteria for RVMI [13]

Kosuge M, Ishikawa T, Morita S, et al. Posterior wall involvement attenuates predictive

value of ST-segment elevation in lead V4R for right ventricular involvement in

inferior acute myocardial infarction. J Cardiol 2009;54(3):386–93.

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MY Comment, by KEN GRAUER, MD (10/7/2019):

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What I like most about this case — is that cath confirmation of acute proximal RCA occlusion as the “culprit” artery allows us to optimally appreciate ongoing events on sequential ECGs done in this case. As such — this case provides unique insight into the interplay between RV vs posterior wall ST-T wave changes from acute occlusion — followed by reperfusion — followed by re-occlusion ...

• For clarity — I’ve put the 4 ECGs done in this case together in Figure-1.

Figure-1: A sequential look at the 4 ECGs in this case (See text).

MY THOUGHTS: In the setting of acute proximal RCA occlusion that produces acute inferior STEMI — it is difficult to predict the net effect of simultaneously-occurring RV and posterior wall infarction.

• Looking first at ECG #1 — As per Dr. Smith, there is an obvious acute inferior STEMI. Acute RCA occlusionas the “culprit” artery is suggested by markedly more ST elevation in lead III > II — and, by an equally marked amount reciprocal ST depression in lead aVL.
• There is also a relatively modest amount of ST elevation in the lateral chest leads (V4, V5, V6) of ECG #1. This can be seen with acute RCA occlusion when there are large postero-lateral branches from the PDA (Posterior Descending Artery) branch of the RCA that supplies the lateral wall. In contrast, when there is infero-postero-lateral MI from acute LCx (Left Circumflex) occlusion — ST elevation in lead V6 tends to be greater than ST elevation in the lead III.
• There is also marked ST elevation in leads V1, V2 and V3 in ECG #1. In the setting of acute inferior STEMI, in which the greatest amount of ST elevation is seen inferiorly (ie, in leads III and aVF) — this anterior ST elevation strongly suggests acute RV MI. And, since the RCA but not the LCx supplies the RV (Right Ventricle) — the diagnosis of acute RV MI confirms that the RCA is the “culprit” artery!
• PEARL: Reasons why Dr. Smith strongly suspected lead reversal of lead V2 with lead V3 in ECG #1 include: i) QRS morphology (Wouldn’t R wave progression be much more logical IF lead V3 was lead V2?); and, ii) ST-T wave morphology (IF lead V3 was lead V2 — Wouldn’t the progression of marked ST elevation in V1, V2 from acute RV MI — with transition to more modest ST elevation by V3 — make much more physiologic sense?).
• BOTTOM LINE: ECG #1 shows bradycardia + marked ST-T wave deviation from acute infero-lateral STEMI + acute RV MI — both being the result of acute RCA occlusion. NOTE: Although we know that acute posterior MI very often accompanies acute inferior STEMI — we would not have known there is posterior involvement if all we had to look at was ECG #1.

ECG #2 was obtained just 1 minute after ECG #1 ...

QUESTION: What if ECG #1 had not been done — and the initial ECG in this case was ECG #2?

ANSWER: If the initial ECG in this case was ECG #2 — then we would not yet have had a definitive diagnosis of acute RCA occlusion. Instead — I would have suspected an LAD “culprit” from the peaked T waves in leads V1-thru-V4 of ECG #2, that without the context of ECG #1 would look like hyperacute anterior changes ...

BACK to sequential evolution in this case.

In light of ECG #1 — How would you interpret ECG #2?

• As per Dr. Smith — ECG #2 shows complete resolution of the inferior wall ST elevation that we saw in ECG #1.
• There is also: i) resolution of high-lateral reciprocal ST depression (in leads I and aVL); ii) resolution of the ST elevation in lateral chest leads (V4,V5,V6); and, iii) beginning T wave inversion in leads III and aVF. These changes strongly suggest spontaneous reperfusion of the occluded RCA.
• In addition — the anterior ST elevation from acute RV MI has also resolved. In its place — we now see T wave peaking in leads V1-thru-V4. MY THOUGHT: Given that the anterior leads show a mirror-image view of the posterior wall of LV — the shape of the ST-T waves that we now see in the anterior leads of ECG #2 to me are most consistent with reperfusion changes from acute posterior MI (that now become visible because ST elevation from acute RV MI has resolved).
• PEARL: Note increased R wave amplitude in leads V2, V3 and V4 of ECG #2 (compared to ECG #1). This is consistent with evolving posterior MI.
• REFLECTION — Isn’t it interesting how quickly the ECG picture can change in the space of 1-minute (the time between ECGs #1 and #2) when there is: i) acute reperfusion of the “culprit” artery; and, ii) interplay between opposing ST-T wave forces of acute RV and acute posterior MI.

Looking at ECG #3:

• As per Dr. Smith (and compared with ECG #2) — there is once again ST elevation in the inferior leads in ECG #3. This is associated with return of reciprocal ST-T changes in the high-lateral leads (leads I and aVL). This strongly suggests re-occlusion of the RCA.
• Although the absolute amount of ST elevation in the inferior leads of ECG #3 is not as much as it was in ECG #1 — it is of interest that once again, the amount of reciprocal ST depression in lead aVL is virtually the mirror opposite of the amount of ST elevation we see in lead III of ECG #3. This reflects that “magic” mirror-image picture for ST-T wave changes in leads III and aVL that is so commonly seen with acute inferior STEMI.
• It is interesting to note that in the chest leads of ECG #3 — the changes of acute posterior infarction now predominate! These include: i) increase in R wave amplitude in leads V2 and V3 (compared to R wave amplitude for these leads in ECG #1); and, ii) the “shelf-like” shape of ST depression in leads V2 and V3 that is so typical of acute posterior MI.
• NOTE: There is no indication at all from ECG #3 that there was acute RV involvement just a little while earlier ...

Finally (ie, just before this patient was taken to the cath lab) — ECG #4 was obtained:

• Limb lead changes once again suggest spontaneous reperfusion of the inferior wall (ie, resolution of inferior ST elevation and high-lateral reciprocal ST depression between ECG #3 and ECG #4).
• BUT in the chest leads for ECG #4 — there is once again ST elevation in leads V1-thru-V4 (most marked in leads V2 and V3). Given that we know from results of cardiac cath that the LAD was not a culprit artery — this means that this return of anterior ST elevation in ECG #4 has to reflect loss of perfusion to the RV.

REFLECTION — So WHY does the shape of anterior ST-T waves look so different in leads V1, V2 and V3 of ECG #1 compared to ECG #4? I think the answer is that in ECG #1 — anterior chest lead ST-T wave changes were dominated by acute RV MI. In contrast, by the time ECG #4 was obtained — we were seeing a combination of ST elevation from acute RV MI + reperfusion changes in the posterior wall (ie, precisely what you might expect to see if you fused the ST-T wave picture for leads V1, V2 and V3 from ECG #1 and ECG #2)!

• Bottom Line: I think it fascinating to reflect on how quickly ST-T wave changes may occur when there is spontaneous reperfusion, which is then followed by re-occlusion of the culprit artery. The ECG picture becomes that much more intriguing when there is interplay between opposing electrical forces, as occurs with acute RV and posterior MI evolving at different tempos.

Our THANKS to Dr. Smith for presentation of this fascinating case!