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.


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.

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.


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!

Thursday, August 15, 2019

5 Cardiologists said this is not a STEMI. But was it an OMI?

Written by Pendell Meyers

A male in his early 50s presented with waxing and waning chest pain starting at rest. He had multiple cardiovascular risk factors and the EM physician strongly suspected ACS.

Here is his initial ECG:
What do you think?

Sinus rhythm
-STE in V1-V5, possibly a tiny amount in V6, and small amount in I and aVL, and II
-Reciprocal STD (although perhaps isoelectric at J point, immediate STD after the J point) with very ischemic appearance in lead III (down-up T-wave is strongtly suggestive)
-Large T-waves in V2-V4, which may be either a normal variant or hyperacute
-Very tiny Q wave in lead V2, as well as V6, I, and aVL, which is not seen in normal variant
-STEMI criteria are not formally met; although V2 has sufficient STE (greater than 2.0 mm), neither of it's neighbors have enough STE to meet criteria (V1 is close at 0.5 mm of the "required" 1.0 mm)

This is all highly diagnostic of acute anterior MI, with the most likely etiology being OMI of the proximal-mid LAD.

The formulas would be formally contraindicated because of the Q-wave in V2, but if we use them anyway the results are (using QTc 397 ms):

4 Variable formula: 20.32
3 Variable formula: 24.08

Both formulas predict LAD occlusion.

The physician called the on-call cardiologist immediately to discuss this ECG, but the cardiologist reportedly said not to activate the cath lab because he/she was not convinced by the ECG. Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI."

The first troponin I returned elevated at 0.11 ng/mL.

Serial ECGs were obtained, including this one several hours later:
Slightly more STE and longer QT than prior.

Although I do not see much difference between the ECGs, for some reason (perhaps ongoing pain or rising troponins) the case was reevaluated at this time and the decision was made to perform cath.

They found 100% acute mid-LAD Occlusion MI, stented with excellent angiographic result.

Peak troponin I was greater than 75 ng/mL (the assay does not measure higher than this apparently).

Learning Points:

STEMI criteria misses 25-40% of OMI, like this case for example.

Due to our paradigm which lags far behind the current achievable skill level, cases like this will continue to be missed or delayed until we solve the problem by replacing the paradigm.

This is another case demonstrating OMI with all ST segments concave.

Pay attention to even the tiniest Q-waves in the right context and assume they are new until proven otherwise. New Q-waves during MI are NOT wide ("greater than 40 ms") until later.

Any Q-wave in V2 in the presence of an otherwise normal QRS complex is abnormal.

Repeat ECGs are almost always helpful.

Use of the formulas would have improved recognition of this OMI.

Ongoing ischemia (by symptoms, ECG, or troponin) despite maximal medical management is an indication for emergent cath lab activation.

Comment by KEN GRAUER, MD (8/15/2019):
Once again, the wrong question was asked in this case. That's because it should not matter IF the initial ECG in this case ( = ECG #1 in Figure-1) represents an acute STEMI or an acute OMI — since initial management should be the SAME:
  • Considering that this patient had multiple cardiac risk factors good story for ongoing new ischemic-sounding chest pain and, the ECG abnormalities seen in ECG #1 — prompt cath to define the anatomy, with goal of acute reperfusion if acute OMI is confirmed is the treatment of choice.
  • Unless a prior ECG on this patient can be found that shows identical findings as we see in ECG #1 — there is NO way to rule out acute OMI. As a result — it’s hard to justify not doing acute cath ...
Figure-1: The 2 ECGs in this case (See text).

MTHOUGHTS on ECG #1: Dr. Meyers has skillfully detailed the abnormal ECG findings. To facilitate visualization — I’ve put both tracings together and labeled the following key points:
  • There is loss of the initial r wave in lead V1 — with development of a small-but-real Q wave in lead Vof ECG #1. Overall QRS morphology in lead V2 is strange, with this qRS complex being “sandwiched in” between an rS complex in lead V1, and an rS complex in lead V3 — so there may be some lead misplacement of lead V2. That said — the small q in V2 is almost certainly a real finding, and clearly abnormal.
  • There is more than 2 mm of ST elevation in lead Vof ECG #1 (Compare the RED horizontal baseline with the RED arrow in this lead). The very wide T wave base, with T wave peak clearly exceeding R wave amplitude in this lead clearly defines the T waves in V2 as being hyperacute.
  • Disproportionate T wave amplitude (compared to R wave height) in leads V3 and V4 define those T waves as also being hyperacute.
  • Note that there is more ST elevation in lead V4 of ECG #1, than there is in lead V3 (Compare the RED horizontal baseline with the RED arrow in these leads). There shouldn’t be more ST elevation in V4 than in V3.
  • Finally (as per Dr. Meyers) — the ST-T wave in lead III is clearly abnormal (curved RED line) — with the scooped ST segment ending in a biphasic (negative-then-positive) T wave.
BOTTOM LINE: Without an identical-looking prior tracing — there is NO way to rule out the possibility (if not probability) of acute ST-T wave findings in at least leads V2-thru-V4 Q in V2 reciprocal change in lead III, in this patient with new chest pain. A millimeter definition of acute STEMI should not be needed to justify the need for prompt cardiac catheterization.
  • NOTE: With proximal LAD OMI — one typically sees: isignificant ST elevation beginning in leads V1,V2; iireciprocal ST depression in each of the 3 inferior leads (II,III,aVF); andiiisignificant ST elevation in lead aVL. Because we only partially see these features in ECG #1 — I would interpret this tracing exactly as Dr. Meyers did = probable “proximal-mid acute LAD occlusion”.

MTHOUGHTS on ECG #2: Several hours later — ECG #2 was obtained. As per Dr. Meyers — for the most part, there has been little change between the 2 tracings. That said:
  • I think there is now more ST elevation in lead Vof ECG #2 than there was in ECG #1 (Compare the BLUE horizontal baseline with the BLUE arrow in this lead).
  • Note that there is once again more ST elevation in lead V4 than in lead V3 of ECG #2. This is not a normal finding.
BOTTOM LINE: Given the clinical history — ECG #2 should not have been needed for making the decision to take this patient to the cath lab ...

Our THANKS to Dr. Meyers for this insightful case!

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