Wednesday, June 26, 2019

Serial Evolving ECGs all diagnostic of LAD OMI, but never meet STEMI criteria

A 60-something called 911 for chest pain.

Medics recorded an ECG at time zero:

What to you think?



There is no ST elevation, but V2 has a definite hyperacute T-wave.  Inferior leads have a tiny bit of ST depression (this is very significant).  aVL has a tiny amount of coved ST elevation in the presence of a tiny QRS.  These are all very very suspicious for proximal LAD OMI.

They recorded another at 20 minutes:
 
Evolving anterior OMI, but with barely any ST Elevation.
 Look at the huge size of the T-wave in V4 relative to the R-wave.
Increasing STE in aVL
Increasing inferior reciprocal ST depression

If you doubted LAD occlusion on the first one, there is no doubt any more.
This is diagnostic
Repeat at 25 Minutes:

Further evolution.
Absolutely diagnostic of acute LAD occlusion.



And another at 30 minutes:

The computer never noticed the myocardial infarction on any of these ECGs.


The patient arrived in the ED.

This is the first ED ECG (at t = 40 minutes):
Computer did not comment on acute MI.
The attending physician brought this to me without any of the other ECGs and asked my opinion:
With 3 seconds, I said:
Acute LAD Occlusion.
It is diagnostic of LAD occlusion all on its own, without even comparing to the others.

This is what my partner thought also, but just wanted confirmation.

The cath lab was activated.

2nd ED ECG 60 minutes
Now there is diagnostic ST Elevation, but barely.
Computer still did not comment on STEMI



A Proximal LAD occlusion was found and stented.

ECG after reperfusion
Typical Reperfusion T-waves, similar to Wellens' waves (and same pathophysiology), but different in that true Wellens' waves have preservation of R-wave.   This has a QS-wave in V2 because of extensive infarction, in spite of rapid reperfusion.


Next day
QS-waves with reperfusion T-waves again

Peak trop I 85.6 ng/mL (very large OMI)

Anterior Wall Motion Abnormality

At no point in time did the computer read a STEMI

Learning Points:

1. Acute LAD occlusion frequently does not manifest ST Elevation that meets "criteria"
2.  Look for hyperacute T-waves (relative to QRS amplitude/voltage)
3. Look for any inferior ST depression, even minimal
4. Do serial ECGs.


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Comment by KEN GRAUER, MD (6/26/2019):
===================================
Our THANKS to Dr. Smith for this superb example of serial evolution of acute LAD occlusion (OMI— starting in the prehospital phase — passing through the ED — and following reperfusion of the occluded artery.
  • I limit my comments to ECG#1 = the initial ECG done by medics in the field on this 60-something patient with new-onset chest pain. For clarity — I’ve put the 2 parts of this tracing together, and have added a few aids for ST segment shaping to facilitate visualization (Figure-1).
Figure-1: The initial ECG in this case, done by medics in the field (See text).

MTHOUGHTS on ECG #1  Dr. Smith has done a great job with his tracing-to-tracing description of important findings for the 8 ECGs in this case.
  • KEY Take-Home POINT: Given the history of new-onset chest pain in this patient — you should be 100% certain of the need for prompt cath from this 1st ECG alone. Your clinical assessment of ECG #1 in Figure-1 should be acute LAD occlusion until proven otherwise!
KEY ECG Findings in Figure-1:
  • Leads V2 and V3 were the 1st to catch my eye! That the T waves in these 2 leads are hyperacute should be obvious from how disproportionate these waves are compared to the tiny r wave in V3, and lack of any r wave at all in lead V2. Note how fat-at-their-peak and wide-at-their-base these T waves are. Note also straightening of the ST segment upstroke in lead V2 (angled BLUE line in this lead) — such that the normal upward concavity of the ST segment in lead V2 has been lost.
  • There is loss of anterior wavesA tiny initial r wave seems to be present in lead V1. This is completely lost by lead V2 (which manifests a deep QS complex). The r wave returns in lead V3 — but is still considerably smaller-than-it-should-be for a lead V3.
  • Next, looking at neighboring leads” — There is at least 1mm of ST elevation with definite coving of the ST segment in lead V1 (frowny”-shaped BLUE line in V1). This is not a normal lead V1 appearance — but rather reflects extension of the ongoing process (ie, the hyperacute T waves in leads V2 and V3). Thus, acute ST-T wave changes begin as early as lead V1.
  • Continuing with the concept of neighboring leads” — hyperacute wave changes are clearly seen in lead V4 (with a disproportionately large T wave in V4, that is more than half the height of the R wave in this lead — as well as this T wave in V4 being fat-at-its-peak and wide-at-its-base). Although the T waves in leads V5 and V6 are not particularly tall — they share the fatter-at-their-peak-than-they-should-be appearance that we have already seen in leads V2-thru-V4. NOTE: Confirmation that ST-T waves in all 6 chest leads were abnormal in ECG #1 is forthcoming through comparison with the last 2 tracings (obtained after reperfusion) in this case.
PEARL: When contemplating the likely location of acute LAD occlusion — I look for the following Clues, which when present suggest a more proximal LAD lesion:
  • Is there ST elevation (or at least acute-looking ST segment covingin lead aVL?Yes, in Figure-1 — as suggested by the coved BLUE line in lead aVL). Note that this ST coving in lead aVL ends with terminal T wave inversion. There is also a surprisingly wide q wave in lead aVL, which may reflect the ongoing acute process.
  • Is there reciprocal ST depression in the inferior leads?Yesin the form of scooped ST segments — as highlighted by curved BLUE lines in these inferior leads). Inferior lead T waves also look prominent in Figure-1 (a bit larger, and fatter-than-they-should-be at their peak).
  • How early in the chest leads do acute/hyperacute ST-T wave changes begin? ( = slight ST elevation with ST coving begins as early as in lead V1 in ECG #1).
  • Are there potentially acute ST-T wave changes elsewhere? ( = Yes  in the form of scooped and slightly depressed ST segments in leads V5,V6).
Bottom Line: Given the history of new-onset chest pain — You should be able within a minute (or less) of seeing this initial ECG in Figure-1 to: iBe confident in strongly suspecting acute proximal LAD occlusion until proven otherwise; andii) Know that you should contact the cardiologist on call as you are activating the cath lab!
  • As per Dr. Smith — the diagnosis of acute proximal LAD OMI is solidified beyond doubt by subsequent tracings — but these subsequent tracings were not needed to justify immediate cath lab activation in this case. All that was needed given the history of new chest pain — was a quick look at ECG #1 in Figure-1.


Sunday, June 23, 2019

2 ECGs texted to me. Minimal STE in inferior leads. How important is it?

These 2 ECGs were texted to me with the words "I think acute MI, but cardiology does not."

I believed these to be 2 serial ECGs:

ECG 1: (later found to be time zero):
Computer read: "minimal ST depression 0.025 mm"
There is a small amount of STE in II, III, aVF
From less than 0.5 mm - 0.5 mm.
There is les than 0.5 mm of reciprocal ST depression in aVL, and an inverted T-wave

And the other: (later found to be time 24 minutes):
Now there is more STE and more STD
One very telling finding are the ST segments in V2-V6:
ST depression has developed in V2-V6, downsloping in V4-V6.
Though minimal, this is very specific adjunctive data for ECG diagnosis of MI.

This was my response:

"It looks like a myocardial infarction...Does the patient have chest pain?"

History:

Syncope in clinic, some vague chest pain.

Not a great history, so we looked for a previous ECG:
From within the last year
No STE, no STD.
This makes the others diagnostic.

Cardiology had wanted the patient to be admitted, but had not seen evidence of acute MI and had not wanted the cath lab activated.

In spite of this, my partner and I agreed the cath lab should be activated, so he did activate.

Just before transport, another ECG was recorded at time 71 min, prior to cath:
Now obvious inferior and posterior STEMI.


The patient had a ventricular fibrillation arrest before the angiogram, and was resuscitated.

Angiogram: 100% distal RCA occlusion.

After cath, next day:
Reperfusion T-wave in III.
STE resolved.


Peak trop 47.4 ng/mL (large MI)


Echo: Regional wall motion abnormality-inferior, EF 60%. 

Learning Points:

1. In the original thrombolytic trials (the only placebo-controlled reperfusion trials!), especially GISSI-1, treatment of inferior MI with streptokinase did not have a measurable effect on mortality outcome.  Here we see what appears to be an electrocardiographically tiny inferior MI, which only later becomes large.  The patient arrests and has a very high troponin.  So don't be fooled by an apparently small inferior MI.
2. Do serial ECGs.
3.  Compare with a previous ECG.
4. You must push to get patients who need it to the cath lab.
5.  Cardiologists have a huge amount they have to know, spanning an enormous specialty.  They do not always have time to learn the subtleties of OMI on the ECG.  
6.  You have to be the expert!!



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Comment by KEN GRAUER, MD (6/23/2019):
===================================
The definition of the word subtle” is — so delicate or precise as to be difficult to analyze or describe (especially when referring to a change). Subtlety is the “theme” of this case.
  • For clarity — I’ve put the first 3 ECGs shown in this case together in Figure-1. Because of how subtle the findings are — I’ve enlarged one complex in leads II, III, aVF and aVL, that I’ve placed to the right of each of these tracings.
Figure-1: The first 3 ECGs shown in this case — with enlargement of leads II, III, aVF and aVL to the right of each tracing (See text).



The CASE: ECGs #1 and #2 in Figure-1 were texted to Dr. Smith with the words, “I think acute MI — but cardiology does not… “
  • The HISTORY  “Syncope in clinic; some vague chest pain … “ — which clearly is not strongly suggestive of acute MI — but which also does not rule out the possibility of MI, because there was new event (ie, syncope) — and this was followed by some type of chest discomfort that the patient did not have before the syncopal episode.

MTHOUGHTS on ECG #1  The rhythm appears to be regular, at a rate just under 50/minute. The QRS is narrow. This is sinus bradycardia.
  • The QTc is probably normal given the slow rate.
  • The frontal plane axis is normal (about +70 degrees).
  • There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are small q waves in a number of leads, including leads I, II, III, aVF; V4, V5, V6. The tiny, narrow lateral chest lead q waves are normal septal q waves. The significance of the inferior q waves is uncertain.
  • Transition occurs at a normal point (ie, between leads V2-to-V3). That said — I strongly suspect some technical problem because of lead V3appearance — because leads V1 and V2 are predominantly negative with reduced QRS amplitude — before abrupt development of a huge (26 mm) R wave in lead V3 — with reduction in R wave amplitude after lead V3. This pattern of R wave progression simply does not make physiologic sense.
  • There is subtle-but-real ST elevation in each of the inferior leads. There is shallow T wave inversion in lead aVL. The ST segment is uncharacteristically straight in lead V2 — with ST segment straightening (ie, before the T wave) in leads V3-thru-V6.
MIMPRESSION: I was not at all certain about what was going on after looking at this initial ECG ( ECG #1). My concerns were the following:
  • The q waves in the inferior leads were each small and narrow. This is not necessarily a pathologic finding (Occasionally, normal inferior “septal” q waves may be seen — especially when the frontal plane axis is relatively vertical).
  • The shape of the elevated ST segments in each of the inferior leads is gently upsloping. I was uncertain if this represented early infarction or a benign repolarization pattern.
  • Lead aVL does not clarify this situation — because shallow T wave inversion without ST depression that is isolated to lead aVL is not necessarily abnormal when the QRS in aVL is predominantly negative (as it is here).
  • The ST segment straightening in leads V3-thru-V6 is a nonspecific abnormality. The especially straightened ST segment in lead V2 is clearly abnormal — but not necessarily an acute finding.
  • Bottom Line: I was uncertain about ECG #1. I needed more information to arrive at a conclusion.

MTHOUGHTS on ECG #2  ECG #2 was done just 24 minutes later in the ED. Once again — lead V3 looks out-of-place” — so I suspected this tracing was done by the same ECG Tech who did ECG #1. Unfortunately — this meant some information in the anterior leads was likely to be misleading. That said — at least frontal plane axis & overall QRS morphology was comparable between ECGs #1 and #2 — which meant that lead-to-lead comparison for assessment of serial change would be valid!
  • Sinus bradycardia is again present.
  • I see no significant change in the chest leads between ECG #1 and #2.
  • do think there is a subtle-but-important change in leads II, III, aVF and aVL between the 2 tracings! So I magnified these key leads to better illustrate the findings!
Looking at the BLOW-UPS (magnified viewsof Leads IIIIIaVF and aVL for ECG #1 and ECG #2:
  • I thought the amount of inferior lead ST elevation in the Blow-Up of ECG #2 was more than it was in ECG #1. The point at which the ST segment begins to rise looks to be earlier — almost as if the T wave is now trying to "lift up" the ST segment.
  • There now looks to be some ST depression in lead aVL of ECG #2 — and, the T wave is more deeply inverted. The overall “picture” of the ST-T wave in lead aVL to me now looks much more like a “mirror-image” (ie, reciprocal change) of the elevated ST-T wave in lead III.
  • Bottom Line: I thought ECG #2 showed evidence of subtle-but-real serial change (ie, evolutionin each of these 4 leads — which to me (given the history), was diagnostic of acute inferior OMI until proven otherwise.
  • PEARL: The changes I describe above are much easier to recognize on the BLOW-UP magnification. GO BACK and take another look at the complete 12-lead of ECG #2. The image to “inscribe” in your brain is that the picture of these 4 leads (II,III,aVF; aVL) viewed together suggests acute inferior OMI until proven otherwise. In that context — the ST flattening in lead V2 is equally worrisome. Considering ST straightening in leads V3-thru-V6 + the sagging ST segment in lead I — this makes for a total of 10 out-of-12 leads that show ST-T wave abnormalities in ECG #2!

Icing othe CAKE: At this point — a prior ECG on this patient was found ECG #3). Comparing lead-by-lead the appearance of ECG #3 (in both the full 12-lead tracing, as well as in the Blow-Up) — with the findings we see for ECGs #1 and #2 — NOTE the following:
  • There was no ST elevation in the inferior leads of the earlier tracing ( = ECG #3).
  • There was no T wave inversion at all in lead aVL.
  • Lead V2 in the prior ECG ( = ECG #3) showed an upsloping ST segment. Therefore, the overly straight ST segment in lead V2 of ECGs #1 and 2 is new finding.
  • The ST segment straightening that we see in leads V3-thru-V6 for ECGs #1 and #2 was not present in the prior tracing.
  • Bottom Line: Any doubt about whether the serial changes in ECGs #1 and #2 are acute should be completely eliminated once the prior tracing ( = ECG #3) became available.
  • P.S.The small inferior q waves were already present on the prior tracing ( = ECG #3). They are therefore not a result of this acute event.
  • P.P.S. — Note the much more logical R wave progression is seen in ECG #3. This supports my suspicion of a problem with lead V3 placement in ECGs #1 and #2.


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