Wednesday, June 21, 2017

Patient presentation is important, and so is R-wave amplitude

Two Histories, One ECG


Story number one:

An athletic 20-something presents with chest pain and has this ECG at triage:
QTc = 362 ms
What do you think?





















In a 20-something, this is a tough ECG.  Is it anterior MI?

Being young does not rule it out: 

An intoxicated, agitated, 20-something with chest pain


There is sinus bradycardia at a rate of 44.

There is 2 mm of ST elevation in V2 and V3 (at the J-point, relative to the PQ junction), which is below the "criteria" for men under 40 (2.5 mm).

There is upward concavity
There is no ST depression
There are no Q-waves
There is no terminal QRS distortion

So early repolarization is a possibility.

However, there is very suspicious STE in III and aVF, with ST depression in aVL.    To me, this makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III and aVL, so it is a bit confusing.  Unless you consider a wraparound LAD. 

There is also an upright T-wave in V1, larger than V6.  This is a very soft sign of LAD occlusion, and did not add any diagnostic improvement over our formula model for diagnosing LAD occlusion vs. early repol.  In that study, this finding was present in 39% of LAD occlusion and 15% of early repol.

What do the formulas have to add?
Computerized QTc
RAV4 = R-wave amplitude in lead V4
STE60V3 = ST Elevation relative to the PQ jct at 60 ms after the J-point
QRSV2 = total QRS amplitude (Q, R, and S) in lead V2

The 3-variable formula is: 
(1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).

The 4-variable formula is: 
(1.062 x STE at 60 ms after the J-point in V3 in mm) + (0.052 x computerized QTc) - (0.151 x QRSV2) - (0.268 x R-wave Amplitude in V4 in mm).

 In its derivation study, the 4-variable formula performed better than the 3-variable formula, with an AUC of  0.9538 vs. 0.9686, and was both more sensitive and specific.

Driver BE and Smith SW: A new 4-variable formula to differentiate normal variant ST segment elevation in V2-V4 (early repolarization) from subtle left anterior descending coronary occlusion - Adding QRS amplitude of V2 improves the model

Both formulas can be calculated at this link on an excel applet:
http://hqmeded-ecg.blogspot.com/p/rules-equations.html

The measurements are:

RA V4 = 6.5
STE60V3 = 3.0
QRSV2 = 12.5
QTc = 362 ms

The formula values are thus:

3-variable: 22.83 (less than 23.4; the most accurate, but not most sensitive, cutoff).  I still worry when the value is above 22.0 (still misses 4% of LAD occlusion when below 22.0)

4-variable 18.38 (greater than 18.2; the most accurate, but not most sensitive, cutoff). So this is strongly indicative of LAD occluson.

Computerized QTc = 362 ms (this is VERY short for LAD occlusion, but is so short because of correction for slow heart rate; the measured QT was 413 ms.)  This is the main reason the formula value is not very high.

Thus, the ECG is early repolarization by the old formula and is LAD occlusion by the new one.

Even though the ST Elevation is not diagnostic, and T-waves of this size can be seen in early repolarization, but low QRS and R-wave amplitude is not.

The inferior ST findings also make this ECG diagnostic.

In case you were wondering about the T-waves and bradycardia, the K was normal.

Why bradycardia?  Think about that inferior ST elevation.  Maybe there is also inferior MI from wraparound LAD with associated sinus bradycardia.


Story number 2: the real story

I was at triage when a 60-something man who had history of elevated cholesterol and hypertension appeared, clutching his chest, diaphoretic and pale, stating he had had sudden onset of substernal CP 30 minutes prior.

I looked at him and thought to myself: "this man is having an anterior MI".  I almost activated the cath lab without an ECG, but we recorded one within 1 minute of arrival.

Here is that same ECG again:

I actually only saw lead V2 on the screen of the machine when I activated the cath lab.  It had not yet even been printed out.

14 minutes later, just before going to the cath lab, the patient's pain went from 10/10 to 7/10.

Another ECG was recorded:
The T-waves in V2 and V4 are slightly smaller

The patient went to the cath lab:

A large proximal LAD thrombus with TIMI-1 flow was found.  Thus, there had been some minimal spontaneous reperfusion (autolysis).  It was a wraparound LAD, explaining the inferior ST elevation with reciprocal ST depression in aVL (the opposite of what you expect with a proximal LAD occlusion).  It was stented.

The post-cath ECG is here:
ST elevation is resolved.
T-waves have normalized
There is T-wave inversion in III with resolution of ST elevation.

The cardiologists were not impressed by the ECG.  This is the cardiology note:

"Pt's ECGs were not convincing but presentation was extremely concerning for ACS."

Summary

So this was an anterior and inferior STEMI due to an LAD that wraps around to the inferior wall. We do not see evidence of the ischemia of the first diagonal (which is distal to the occlusion and usually is revealed by STE in I and aVL).  This is because that STE was cancelled out by reciprocal ST depression due to the inferior STE.  The sinus bradycardia may be due to the inferior wall ischemia, although this happens primarily when there is occlusion of the RCA.

The 4-variable formula was correct.

The door to balloon time was 57 minutes.

This was recorded the next day:
Now there are Wellens' waves (terminal T-wave inversion), although with a poor R-wave.
The poor R-wave suggests quite a bit of anterior infarction, probably permanent.

Peak cTnI = 51 ng/mL

The echo next day showed:

The estimated left ventricular ejection fraction is 63 %.
Regional wall motion abnormality-distal septum anterior and apex akinetic
Regional wall motion abnormality-distal inferior wall .
Left ventricular hypertrophy concentric .
Regional wall motion abnormality-anterior akinetic.


Learning Points:

1. The pretest probability is important
2. R-wave amplitude is important
3. The 4 - variable formula is more accurate than the 3-variable
4. Look at the inferior leads.
5. Remember that a wraparound LAD can hide the findings of a proximal occlusion.




15 comments:

  1. Is there a cut point at which we can say that T is large in relation to QRS?

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    Replies
    1. There are no criteria for hyperacute T-waves. What I can say is that in our study, the T-waves in LAD occlusion and in early repol BOTH averaged 7 mm in leads V2-V4 (average sum = 21 mm). However, because the average R-wave amplitude is so much higher in early repol, the mean T/R ratio was 3.1 in LAD occlusion and 0.7 in early repolarization. This is why the formulas work so well: they rely heavily on R-wave amplitude in V4 and QRS in V2. STE60V3 relies on the slope of ST elevation, which is related to T-wave height.
      Steve Smith

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  2. Very useful information, especially for medical students.

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  3. In the first 12 lead, there are inverted P-waves in leads II, III, and aVF; would that be a low atrial rhythm or high junctional rhythm, as opposed to a sinus brady?

    P.S. These cases are really great! Please keep up the excellent posts.

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    Replies
    1. It could be either.
      Thanks! Will do.

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  4. Another question, regarding QTc in AMI. In pathophysiology of ischemia the earliest response is opening of I Katp channels which has a shortening effect on action potential duration and consequent "early repolarization". Later, however, both AP amplitude and the speed of phase 0 diminish, resulting in conduction slowness. Is it possible that some of subtle STEMI cases like the one presented here with short QTc be explained by first mechanism, while other cases with longer QTc by the second mechanism?

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    1. I am not certain, but look at this reference: Kenigsberg DN, Khanal S, Kowalski M, Krishnan SC. Prolongation of the QTc interval is seen uniformly during early transmural ischemia. J Am Coll Cardiol 2007;49:1299-305.

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  5. Nice case illustrating KEY Learning points that include: i) Pre-test probability is important; ii) The ECG is the “net” effect of ongoing events — which if multiple, may lead to a “cancelling out effect” that sometimes makes it more difficult to identify each individual event … So while true that IF the 1st ECG here was obtained from a young, seemingly healthy adult, one might be tempted to called it a repolarization variant — a more careful look at this tracing should definitively tell you this is NOT a normal tracing. Virtually every lead on this ECG is abnormal. In the chest leads — the T wave in V1 should not be so upright (and as per Dr. Smith, it should not be of greater amplitude than the T wave in V6). The peak of those T waves in V2,V3,V4 is “fatter-than-it-should-be” for a repolarization variant, and these T waves are disproportionately tall compared to the QRS in these leads. And there is subtle-but-present ST segment “straightening” in V5,V6 that is not “normal” — just as there is subtle-but-abnormal ST segment straightening in leads I, II and aVL. There is a big Q wave in lead III with subtle suggestion of ST elevation + terminal T inversion, which is the “mirror-image” of what we see in lead aVL — and despite how tiny the complex is in lead aVF, there is inappropriate ST elevation in this lead, with a hint of terminal T inversion. The learning point I would add to this case, is to always look at all 12 leads when contemplating whether findings in one or two leads are significant. There will often be subtle-but-real findings in one or more other leads that support your suspicion of something acute in progress. In this particular case, in the context of our concern about those T waves in leads V2,V3 — ALL other leads are actually abnormal … THANKS to Dr. Smith for presenting this highly illustrative case.

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    Replies
    1. Thanks, Ken, and sorry for delay in publishing!

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  6. Steve...

    Two great cases, but something just doesn't smell right here. Did you notice that the P waves are negative (or isoelectric) in the inferior leads and visibly much larger in Lead I than in Lead II in both cases? This is distinctly abnormal. Is there a LA/LL lead wire switch? Those are definitely not retrograde P waves because the P wave in Lead I would be either isoelectric or barely visible as a positive deflection.

    Also, in the first case, did you get a cath report? In the presence of a wraparound LAD, if the occlusion is proximal to D1, the simultaneous STE in aVL and Lead III will tend to cancel each other out. However, in my experience, it usually doesn't bring the ST segment in aVL all the way down to the baseline. I suppose there's no reason it couldn't, but as I said, I've never encountered that in my experience. What seems more likely to me is that in this patient D1 was probably proximal to S1. If the occlusion were between the two branches, that would result in the STE in V1 and leave aVL to react reciprocally to the inferior changes. Marriott was always adamant that a flat ST with an acute T wave ascent from the baseline could constitute a reciprocal change. The STE in the inferior leads caused by an occlusion of a Type III LAD is usually not quite as impressive as an inferior MI caused by an RCA or LCx occlusion.

    Also, in both cases, aVF exhibited a very small, nearly isoelectric QRS with an ST segment that was virtually a straight line from the J point to the peak of the T wave. I refer to this as "Jones's Sign." In the setting of a patient with chest pain compatible with ACS, I have found that it often represents a middle stage in the migration of the ST segment from a normal upward concavity to a more diagnostic upward convexity. It may or may not precede reciprocal changes in other leads. Is it pathognomonic? I have no idea. But I have observed this phenomenon for over 30 years and if you see it, you'd better take a very close look for other signs of an MI. So many people pay no attention to this particular ST segment morphology and consider it "normal."

    Another thing to consider here is that the primary repolarization changes of an acute epicardial ischemia may precede or lag behind the changes in the reciprocal leads. They may not always appear concurrently.

    Thanks for such an excellent website and an incredible educational resource!

    Jerry W. Jones, MD FACEP FAAEM

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  7. Sorry Steve but there is one more thing...

    I'm confused about the sequence of the ECGs. Is the first ECG from the 20 y/o and the second ECG from the 60 y/o? You have included the same ECG for both. Click on the first ECG, then when you see the four ECGs at the bottom of the screen, if you click on the second, then the first, then the second etc. there is no difference that I can see.

    Jerry W. Jones, MD FACEP

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    1. Jerry,
      sorry if I was unclear.
      The ECG was really from a 60 something.
      But I wanted people to see the same ECG from both perspectives: 20 and 60.
      OK?
      Steve

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  8. How did you recognize that it is anterior and not, for example, lateral MI? Does lateral MI have different presentation? I know that inferior MI has complains on nausea, gastric acid reflex...

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    Replies
    1. I recognized it as anterior and inferior because that is where the ST elevation is

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  9. Very useful information on ECG, keep it up

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