Monday, August 26, 2019

An ECG sent to me with concern for hyperacute T-waves

Written by Pendell Meyers


A woman in her 70s with diabetes, hypertension, and hyperlipidemia suddenly developed nausea, diaphoresis, and brief syncope while eating at a restaurant. She did not report any chest pain or pressure.

She was brought to the Emergency Department and this ECG was recorded while she was still feeling nauseous but denied chest pain, shortness of breath, or other symptoms:

What do you think? No baseline was available for comparison.











Sinus rhythm
Grossly normal QRS complex
Less than 1mm STE in II, III, and aVF, as well as V4-6, all with extremely upward concavity
aVL has the smallest possible amount of STD in aVL with a shallow negative T-wave
The T-waves in the inferior leads seem to have potentially large amplitude compared to their QRS complexes
STEMI criteria are not met

Although inferior OMI commonly presents with submillimeter STE in the inferior leads with very subtle reciprocal STD and/or T-wave inversion, the morphology of this ECG is not convincing to me. The T-waves have significant amplitude but they are not "fat" enough to be hyperacute. The morphology of STE is not diagnostic of being due to acute transmural ischemia. It is difficult to describe exactly why, but is something that simply comes with time, after following up hundreds of cases to see the ECG progression and patient/angiographic outcomes.


This ECG was texted to me with no clinical information, with the sender being concerned for possible hyperacute T-waves and STE in the inferior leads.

I replied: "I see why you would be worried about hyperacute T-waves, but they just don't look fat enough to be hyperacute. There is definite STE inferior and lateral but it just doesn't look like true positive STE to me. I wouldn't activate the lab for this EKG alone, but if the patient is clinically compatible with ACS you could call a heart alert. I would do echo for WMA, q15 min EKGs - if it's real it will be dynamic and become clear soon. Let me know what happens." If I had known there was no definite chest pain or pressure this would have been slightly more confident.



I later found out that the cath lab was activated soon after arrival.

The patient went emergently to the cath lab, where all coronary arteries were found to be normal.

Note: Normal coronary arteries at the time of cath of course does not rule out the possibility of OMI. There can be OMI at the time of the ECG followed by spontaneous (or medication induced) lysis, such that the artery is open at the time of cath. This can be so brief that even troponins do not significantly rise. Of course that is very rare. But it demonstrates the point that the angiogram alone cannot be used to adjudicate the presence or absence of OMI. The ECG progression, clinical picture, and biomarkers are also involved in the full diagnosis of OMI. The ECG progression in particular is important: True positive OMI findings on ECG must always resolve or evolve. Conversely, an ECG that remains static throughout the entire clinical course means that the ECG findings were not due to OMI (even if OMI was truly present!).


Serial troponins were negative.

Echo showed no wall motion abnormality.

Most importantly, several repeat ECGs were basically unchanged:
This is the ECG the next day. This one likely does meet STEMI criteria in II, III, and aVF. But it is the same morphology as the first ECG. Absolute STE is irrelevant - the fact that the prior ECG did not meet criteria and this one does, is meaningless in my opinion.



Learning Points:

This was an example of a false positive cath lab activation due to ECG findings that were thought to represent OMI.

Learning how to differentiate hyperacute T-waves from normal variants like this is difficult and requires comparing cases like this with our database of true positive hyperacute T-waves. True hyperacute T-waves are tall, fat, wide, symmetric, and by these properties have large area under the curve compared to the size and morphology of the QRS complex. 

Take this example: first I'll show you a close up of leads II, III, aVF, and aVL from a true positive inferior hyperacute case. Below you'll see the same leads from this case.

These are fat, symmetric, true positive hyperacute T-waves in III and aVF, with their reciprocal counterpart in aVL. This patient had RCA OMI. From: 

A female in her 60s who was lucky to get expert ECG interpretation



This case. False positive, proven by no evolution and no evidence of OMI, negative trops, and normal angiogram.


Use these cases to see more true positive inferior hyperacute T-waves:

You have two hours to save this patient's life











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Comment by KEN GRAUER, MD (8/26/2019):
===================================
I find this an important case for helping to clarify the semantics surrounding use of the term hyperacute” when referring to T wave appearance. I fully AGREE with Dr. Meyers astute ECG assessment and management plan for the initial ECG in this case ( = ECG #in Figure-1).
  • That said — I offer a different perspective on the semantics that I favor to describe the ECG findings in this case.
Figure-1: The 2 ECGs shown in this case (See text).



MTHOUGHTS on ECG #1: The most remarkable findings in ECG #1 are seen in the inferior leads. That said, systematic assessment of this tracing reveals a number of additional findings of interest:
  • There is baseline artifact in several leads. In ECG #1 — this is most marked in leads II, III and aVF. Since electrical derivation of these 3 leads is shared by involvement of the left leg electrode — this is the probable source of this artifact. I’ll emphasize that despite the artifact — this tracing is clearly interpretable. The reason I note the artifact, is that on occasions when artifact does impair interpretation, it may be helpful to recognize from which extremity the artifact arises (Details on this subject are beautifully described in this article by Rowlands and Moore.)
  • Beyond-the-Core: In contrast, the limb lead artifact in ECG #2 is maximal in leads I, II and aVR, with electrical derivation of these 3 leads shared by involvement of the right arm electrode — which is the probable source of artifact in ECG #2.
Additional findings of interest in ECG #1 include the following:
  • There are multiple small and narrow Q waves. These are seen in leads I, II, aVL, aVF; and V3-thru-V6. There appears to be a small-but-present initial r wave in lead III. The clinical significance of these Q waves is uncertain — but their presence should be noted because this finding might be relevant if there was ongoing infarction.
  • There is early transition — because the R wave becomes predominant (ie, taller than the S wave is deep) as early as lead V2. This finding could also be relevant — because posterior infarction is among potential causes of early transition.
  • Finally — I was struck by how similar the appearance is for QRS complexes and ST-T waves in leads V3-thru-V6 of ECG #1. This made me wonder if there might not be a potential technical mishap in this recording.

AGREE completely with Dr. Meyers that:
  • There is <1 mm ST elevation in the inferior and lateral chest leads.
  • There is ST segment flattening with no more than minimal T wave inversion in lead aVL. Lead aVL does not have the appearance of a true “reciprocal change”.
  • The T waves in the inferior leads of ECG #1 are each taller-than-expected considering the appearance of the QRS complex in each of these leads.
  • Criteria for a STEMI are definitely not met in ECG #1.
  • The T waves in each of the inferior leads in ECG #1 are not as “fat” as the T waves in the true positive example of inferior hyperacute T waves that Dr. Meyers shows above.
  • Although this 70yo woman with cardiac risk factors did have acute symptoms (ie, nausea, diaphoresis and syncope) — she did not report any chest discomfort! On the whole — her history is not convincing for acute OMI (although we need to remember that not all acute MIs are associated with chest pain).
  • I would not activate the cath lab on the basis of ECG #1 alone.

Where MPerspective Differs: While the history for this patient is not at all convincing for acute OMI — and, reciprocal changes are lacking — and, chest leads fail to show acute changes — we still have the unescapable finding of waves that are taller-than-they-should-bin each of the 3 inferior leads. That said:
  • ECG #1 is not diagnostic of acute OMI.
  • I would not have activated the cath lab on the basis of ECG #1 alone.
  • BUT — this patient did present to the ED with new non-chest pain symptoms (including syncope) that could reflect an acute cardiac event.
  • AND — in my opinion, in the absence of a prior ECG for comparison — we can not rule out the possibility that these might be hyperacute T wave changes in the inferior leads of ECG #1.
Why this is all Symantics: Regardless of how one classifies the T waves in the 3 inferior leads of ECG #1 — optimal management will be similar:
  • A definitive diagnosis can not be made from ECG #1 alone.
  • Continued close observation of this patient frequent serial ECGs stat Echo in the ED (looking for wall motion abnormalityserial troponins — will almost certainly yield the correct diagnosis in very short order.


MTHOUGHTS on ECG #2: There is essentially NO change in the appearance of ECG #2 compared to ECG #1. We are told that several other ECGs done after the initial tracing all looked the same.
  • I find it of interest that both early transition and similar appearance of the QRS complex and ST-T waves in lateral chest leads persist in ECG #2 done the next day. This makes a technical mishap much less likely — and makes me wonder if an unusual body habitus might account for these findings ...

BOTTOM LINE: Dr. Meyers and I are essentially saying the same thing. Considering this patient presented to the ED with new symptoms (including syncope — albeit without chest pain) — ECG #1 is not a normal tracing.
  • Regardless of whether or not you classify the inferior T waves in ECG #1 as possibly hyperacute or not — additional testing, including repeat serial ECGs, troponin + stat Echo are all needed to arrive at a more certain diagnosis.
  • “Ya gotta be there” to make the decision of whether or not to activate the cath lab on the basis of the history and ECG #1. While fully acknowledging that “hindsight is 100% in the retrospectoscope” — for learning purposes, I’ll put forth the thought that repeat ECG, stat Echo and initial troponin could probably have been enough to dissuade the decision to activate the cath lab in this case.

Our THANKS to Dr. Meyers for presenting this case!




Friday, August 23, 2019

Editorial by Meyers and Smith, full text: Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)

Tuesday, August 20, 2019

Elderly with Paced Rhythm, Possible Ischemic symptoms, and an Equivocal Smith Modified Sgarbossa ECG

An 80 year old presented with a couple days of SOB, weakness, and diaphoresis.  There was no chest pain.

Here was her initial ECG:
What do you think?

















-There is a paced rhythm.
-There is some concordant ST Elevation (STE) in V5 and V6.
-There is ST depression in V2.
-There is minimal concordant ST depression in V3 (remember there should be, if anything, appropriately discordant ST Elevation).

The treating physician did not think that there was sufficient concordant STE in V5 and V6.  He saw the ST depression in V2, but did not see it as concordant or excessively discordant because the R-wave and S-wave were equal.

However, when the QRS is isoelectric in LBBB or paced rhythm, there should be zero ST shift!  
Non-ischemic (baseline, normal) ST shift in Paced Rhythm and LBBB is due to Appropriate Discordance.  If there is no dominance of the R-wave or S-wave, there cannot be appropriate discordance.  Any ST shift in these cases is abnormal (ischemic).

So this is clearly ischemic ST depression.

In addition: While it is true that the concordant ST Elevation in V5 and V6 is not quite 1 mm, any concordant STE is highly suspicious.  Moreover, this is in the context of a very low voltage R-wave, so a small amount of concordant STE is much more significant.

This ECG is diagnostic of Occlusion MI (OMI).

The provider did not immediately activate the cath lab.

There were a couple subsequent ECGs before angiogram which show some evolution (worsening)


Increased ST depression in V2


Clinical Course

An initial troponin T returned at 2.1 ng/mL.  This is very high for an initial troponin, and nearly diagnostic of OMI by itself, but of Subacute OMI, consistent with this patient's long duration of symptoms.

She did then later go to the cath lab (uncertain how much later) where she went was intubated, and put on a balloon pump.

Circumflex was the culprit, as expected.

The RCA and LAD were also diseased (3-vessel disease).

They decided to do bypass surgery; but would do PCI if surgery considered too high risk.

She then developed cardiogenic shock and returned to the cath lab for PCI of the circumflex.

The doctor wrote:

She had a rocky course with pain and was eventually transitioned to hospice

"I am trying to learn from this case.  Looking at it objectively—was a really criteria to activate the lab or was this an NSTEMI. I cannot make up my mind about V5 V6 but I don’t think there are any criteria in the other leads.

"From the catheter report and presentation I also don’t think she has OMI unless I am wrong….."

He is to be greatly commended for sharing this and trying to learn from it.

Comment:

This is a late presentation MI and it is unlikely that earlier treatment would have made a large difference.

Learning Point:

In LBBB and Paced rhythm, if the S-wave and R-wave are of equal amplitude, there should be zero ST shift, since there is no "appropriate discordance."  Thus, any ST shift is likely to be ischemia.



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Comment by KEN GRAUER, MD (8/21/2019):
===================================
Excellent example by Dr. Smith of a pacemaker tracing that is diagnostic of recent infarction in a patient with new chest pain. My comments are brief, and offer a slightly different perspective on the superb discussion by Dr. Smith.
  • For clarity — I’ve put the first 2 tracings in this case together, and have labeled some KEY findings (Figure-1).
Figure-1: The first 2 ECGs done in this case (See text).



MTHOUGHTS on ECG #1: Assessment of pacemaker tracings for acute ST-T wave changes is challenging. I find this even more difficult than ST-T wave assessment with complete LBBB — because of tremendous variability in what a normally paced tracing will look like. Often, it will be difficult (if not impossible) to detect acute MI when all beats are paced. That said, sometimes the SHAPE of the ST-T wave in one or more leads will clearly look abnormal. My preference focuses on identifying such clearly abnormal ST-T wave morphology.
  • There is an underlying sinus rhythm in ECG #1. Following a PR interval of ~0.20 second — all QRS complexes are paced. For the most part — QRS morphology resembles a LBBB pattern.
There are 3 leads in ECG #1 that manifest ST-T waves that are clearly not normal:
  • Leads Vand Vshow coved (convex down) ST segments that appear to be elevated by at least 1 mm (coved RED lines in these leads — with the horizontal RED lines indicating the PR segment baseline). These are primary ST-wave changes — because the shape and direction of these elevated ST segments is opposite expected ST-T wave morphology in a lateral lead with LBBB-like morphology (ie, the ST-T wave in leads I and aVL show the expected ST-T wave shape in a lateral lead).
  • Lead Valso manifests a primary ST-wave change — because the SHAPE of the depressed ST segment in this lead is clearly abnormal (curved RED line in V2).
  • Given the definite ST-T wave abnormality of leads V2, V5 and V6 in ECG #1 — we can suspect that the curved and slightly depressed ST segments in neighboring leads V1 and V3 — as well as the ST coving (albeit without any ST elevation) that we see in lead V4 are also abnormal. That said, in isolation (ie, without the definite ST-T wave abnormalities in leads V2, V5 and V6) — I wouldn’t be able to call a recent MI from the subtle abnormalities seen in leads V1, V3 and V4.
  • I see no acute changes in the limb leads of ECG #1.
It should be noted that this elderly woman presented with a several-day history of dyspnea, weakness and diaphoresis — but no chest pain. As a result — I would have NO idea from the appearance of ECG #1 as to WHEN an event may have occurred ...
  • Clearly, the above described chest lead ECG changes could be very recent, if not still actively ongoing. On the other hand — an MI could have occurred at the onset of symptoms, or even a few days before that. The patient did not have chest pain — and shortness of breath from MI-induced heart failure sometimes takes a number of days to develop.
  • Timely cardiac catheterization would help clarify the situation — although from the information given and the appearance of ECG #1 — cardiac cath might not need to be immediate. “Ya gotta be there … “.


MTHOUGHTS on ECG #2: Some time after ECG #1 — and 2nd tracing was done (ECG #2). Details of this case, including when ECG #2 was obtained, and how this 2nd ECG was interpreted are lacking.
  • The point to emphasize, is that IF decision to perform cardiac catheterization was not made after seeing ECG #1 — it definitely should have been made after ECG #2 was done. The shape and amount of ST depression in lead V2 has dramatically worsened. There is probably also slightly more ST depression in leads V1 and V3 of ECG #2 — but, it is the appearance of lead V2 in ECG #2 that tells us acute OMI is in progress until we prove otherwise.
BOTTOM LINE: Assessment of acute ST-T wave changes is often quite difficult in pacemaker tracings. This case is insightful in illustrating how leads V2, V5 and V6 in ECG #1 should have prompted more rapid recognition of potential acute change.
  • In my experience — SHAPE of ST-T wave changes is often more important than the amount of ST deviation.

Our THANKS to the clinician who presented this soul-searching case!



Saturday, August 17, 2019

Acute Chest pain in a 50-something, and a "Normal" ECG

Chris Mondie of the Newark Beth Israel Emergency Medicine Residency sent this case

A 50-something man presented with acute chest pain.

Here is his ECG:
As you can see, the computer called it completely normal
What do you think?


















The computer did not even mention the ST elevation.  It could at least say: "ST Elevation, consistent with normal variant," or "consistent with ischemia or normal variant," or "consistent with early repolarization."  But it simply says "normal."

An interpretation of "normal" could, of course, deceive many providers.

Analysis

This could be normal variant ST Elevation in V2 and V3.  There is 1.5 mm STE in at the J-point in lead V2 (relative to QRS onset, otherwise known as PQ junction).  There is 1.0 mm in V3.

So this is a normal amount of STE in V2 and V3, defined by Universal Definition of MI as up to 2.0 mm in men over age 40.  So there is definitely no STEMI, and the STE is normal.  So the computer is correct in calling it normal.

But after reading this blog, you all know that most OMI do NOT meet STEMI criteria.  Some patient's baseline ECG has zero STE.  Some patient's baseline has normal variant STE.  You don't know which kind of patient this is.

Some normal STE is actually due to OMI.  Some normal STE is not due to ischemia at all.

It is your responsibility to determine if STE is ischemic or not.

How do we do so?

Use the formula.

QTc = 385
STE60V3 is at least 4.0 mm, maybe more
RAV4 = 6
QRSV2 = 18

Formula value = 19.94 (very high, indicating LAD occlusion).

Any value greater than 18.2 is likely to be LAD occlusion.

For graphs of sensitivity, specificity, and accuracy at various cutoffs, see this post:

More precise interpretation of the results of the 4-variable formula.


12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion


Chris Mondie's note:

"My read: Acute proximal LAD occlusion. Hyperacute T waves which tower above the preceding R waves, poor precordial R wave progression. Large T in V1.  Smith subtle LAD equation indicative of acute LAD occlusion. 

"Bedside echo revealed anteroseptal wall motion abnormality at which point I activated a code STEMI. 

"Cardiology agreed to take the pt to the lab but thought it would likely be negative. 

"100% proximal LAD successfully stented. 
Defibrillated out of v fib in the cath lab. 
Initial TnI was negative. 

"I thank you for constantly updating your blog and allowing free open access education on EKG interpretation. I recognized this as a STEMI immediately and I was only able to do so solely because of your blog."


===================================
Comment by KEN GRAUER, MD (8/18/2019):
===================================
Our thanks to Dr. Chris Mondie for providing this case. Credit to him for performing stat Echo in the ED — which, with the finding of anteroseptal wall motion abnormality immediately confirmed the need for prompt cath, even before a 2nd tracing was done.
  • For clarity — I’ve labeled a number of KEY findings in the initial ECG performed in the ED ( = ECG #1 in Figure-1).
Figure-1: The initial ECG done in the ED (See text).



MTHOUGHTS on ECG #1: This is not a normal tracing. The remarkable ECG findings are multiple:
  • There are small-but-definite Q waves in each of the inferior leads (RED arrows). These Q waves in leads III and aVF are surprisingly wide — and to me are suggestive of inferior infarction at some point in time (possibly acute).
  • It is difficult to assess ST-T waves in the inferior leads — because we only have 2 QRST complexes in each lead — and, there is baseline wander in lead aVF obvious artifact with a different appearance of the ST-T wave for each of the 2 beats in leads II, III and aVF. IF clarification of these findings was important (as to whether something acute was ongoing in the inferior leads) — I would immediately repeat this ECG. That’s because despite lack of reciprocal ST-T wave changes in lead aVL — it looks like there may be slight-but-real ST elevation with slightly fatter-than-they-should-be T waves (probably hyperacute) in each of the 3 inferior leads (Compare the elevated J-point to the horizontal RED baseline in each of these leads).
That said, there is NO urgency for clarifying what is going on in the inferior leads — because clear indication for immediate cath is already forthcoming solely from the appearance of the chest leads in this patient with new-onset worrisome chest pain. Among the remarkable chest lead ECG findings include:
  • As per Dr. Mondie — the T waves in leads Vand especially in V“tower over” the respective R waves in these leads. These are hyperacute waves.
  • Whereas the base of these T waves in leads V2 and V3 does not seem all that wide — the base of the overly tall T wave (compared to its respective R wave) in lead Vis wide. So, until proven otherwise — we need to assume hyperacute waves in at least leads V2-thru-V4.
  • There are Q waves in leads V4, V5 and V6 (RED arrows in these leads). Although these lateral chest lead Q waves are not that deep — the do appear to be wider-than-expected for “septal Q waves”.
  • Two other reasons to suspect that these are not “normal septal Q waves” in leads V4-thru-V6 are: iAlthough normal septal Q waves may occasionally be seen in lead V4 — they are generally not as large in lead V4 as the septal Q waves in leads V5 and V6. However, the Q wave that we see in lead V4 of ECG #1 IS equally large and wide as the Q waves in V5 and V6. This most probably is not normal; andiiInstead of the usual progressive increase in R wave amplitude as we move from lead V2-to-V3 — there is slight decrease in R wave amplitude. While I can’t rule out lead placement as the reason for this slight decrease in lead V3 R wave amplitude — the finding of a larger-than-expected Q wave in neighboring lead V4 makes me suspect that this is a real phenomenon related to ongoing anterior OMI.
  • There appears to be slight-but-real ST elevation in leads V4 and V5 (I’m uncertain about V6). The amount of ST elevation in lead V4 (even if it doesn’t satisfy stemi criteria) looks more than what I’d normally expect in this lead (Compare the elevated J-point to the horizontal RED baseline in these 2 leads).
  • Of the 2 QRST complexes that we see in lead V1 — the T wave of the 1st complex is taller-than-normally-expected for an upright T wave in lead V1 (V1 usually does not have tall T waves). Once again, due to technical issues — we do not know which of the 2 QRST complexes that we see in lead V1 is accurate ...
BOTTOM LINE: Some of the above abnormalities I mention are subtle. Individually — they probably would not mean much. BUT:
  • In a patient with new-onset worrisome chest pain — the potentially hyperacute T waves in leads V2V3 and V4 should be more-than-enough to merit prompt cath.
  • Once determined that stat Echo shows an anterior wall motion abnormality — the diagnosis of acute ongoing OMI is confirmed!
  • The possibility of something acute ongoing in the inferior leads is real. Support for the likelihood of acute ECG changes is then strengthened by identifying the additional subtle ECG abnormalities that I describe above in other leads on this tracing.

Once again — our THANKS to Dr. Chris Mondie for presenting this case!



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