Tuesday, November 1, 2022

Opiate overdose, without chest pain or shortness of breath. Cognitive dissonance.

I was reading EKGs on the system and saw this one.....

What did I put in as my interpretation?

Interpretation: "Acute LAD occlusion until proven otherwise. " 

There is non-diagnostic ST Elevation in V1-V3, with rather large T-waves but in the context of a deep S-wave (high voltage).  HOWEVER, lead V4 is diagnostic of OMI.  This is massive ST Elevation, huge hyperacute T-wave, and loss of S-wave (which in V4, unlike V2-3, can be normal but should greatly raise suspicion.)  There is ST depression in V5-6.  This alone could be due to LVH, but V4 could NOT be due to LVH.

There was an EKG from 5 years prior:

I went to check on the history:

History: It was the middle of the night.  The 50-something patient with history of coronary stenting and slightly reduced LV ejection fraction.  He had been smoking an opiate and suddenly collapsed.  He was ventilated with BVM on arrival.  He awoke with naloxone.  This EKG was recorded as part of a standing order for critical care.  

He denied any CP or SOB.

An EKG was repeated at 5 minutes

The T-wave is less hyperacute.  Maybe there is some spontaneous reperfusion?

"Pathway B" was activated, meaning that there is an immediate consultation with Cardiology.  The cardiologist was worried about the EKG, but did not want to activate the cath lab.    

The cardiologist wanted an emergent formal echo first.

Another ECG was recorded 25 minutes after first:

There is further diminution of the T-wave.  
The S-wave is making a comeback.
There is likely some spontaneous reperfusion

At this time, the first hs troponin I returned at 31 ng/L (Abbott Architect, URL for male = 34 ng/L).  So this is within the normal range, but getting close to the URL and this is unusual for an otherwise healthy person.  It is suggestive that the subsequent troponins will rise and the patient will rule in for acute MI.

60 minutes
Not much change from 25 minutes

Formal echo done at 120 minutes and shows that the estimated left ventricular ejection fraction is 40 %.  There was a new regional wall motion abnormality-apical septum, inferior, lateral, and anterior, akinetic with dyskinetic apex.  

This confirms LAD Occlusion.

Another ECG was recorded at 120 minutes, S-wave reconstituted

T-wave and STE are normalizing.  
The S-wave is reconstituted.  
There is definite reperfusion.

Here is the full evolution of lead V4 over 140 minutes
Note decreasing T-wave "bulk" and reconstitution of the S-wave

Troponin Profile:

0 hours: 31 ng/L (normal)

2 hours: 478 ng/L

4 hours: 3963 ng/L

6 hours: 11,279 ng/L (>10,000 ng/L)

ACS (culprit lesion) with a high sensitivity troponin I  5000-10,000 ng/L is our research definition of OMI, as OMI generally results in trop elevations above this threshold.  Of course this depends on many factors: 1) duration of occlusion, 2) whether full or near occlusion with zero flow or some flow -- the flow in the artery is the critical factor, measured by "TIMI" flow, 3) presence of collateral circulation and others.

Taken to cath lab next AM:


--LAD is a large-caliber vessel that wraps around the apex

--Tandem 70% stenoses are noted in the proximal LAD in conjunction with a

diffuse 70% stenosis in the mid vessel

--D1 is a small caliber vessel with 80% proximal stenosis

--D2 is a medium caliber vessel with diffuse 95% stenosis that appears to fill

predominantly by left to left collaterals

--The far apical LAD is occluded and fills by right to left collaterals from

the RCA, as above

"While there is no obvious culprit lesion for the patient's significantly elevated troponin, ACS cannot be fully excluded given multiple stenoses noted on today's angiogram.   In the setting of prior stenting and reduced left ventricular ejection fraction, would pursue a heart team revascularization approach Syntax score 28.5, which would suggest reduced rates of major adverse cardiac events with coronary artery bypass grafting."

2 days later

This is a typical LVH pattern, without ischemia

Patient underwent 4 vessel CABG.

Discharge Diagnosis was STEMI  (The STE did not meet "criteria," so "OMI" would be better, but "STEMI" is far better than what this could have been called: NonSTEMI)

Quotes from a note written by a really fine and knowledgable physician: 

"12-lead EKG was obtained initial 1 at time zero.  This showed subtle ST elevation from V1 all the way to V4 with ST depression in V5, V6 and minimally in lead I and II.  Upon questioning patient, he denies having any chest pain or chest tightness of any sort.  Subsequent EKGs were obtained at 5 min, 25 min, and 60 minutes.  Old EKG showed similar findings and there was No Evolution over the course of an hour which is unusual in the setting of acute coronary syndrome.  Initial troponin came back negative."


"Nonspecific ST elevation from V1-V4, question of early repolarization versus pericarditis, question of acute current of injury and ?  Sodium channel blockade effect from unidentified drug?"

"In the absence of chest pain and negative troponin, it appears less likely that he is having acute coronary syndrome though EKG appears concerning.  On the other hand, stable EKG over an hour in the setting of ongoing acute coronary syndrome is again unusual.  After discussing all of the above with ED staff, we have made a decision to get stat echocardiogram and assess overall LV function and wall motion abnormalities and defer cath lab activation at the time."

Smith comment: many of these observations are demonstrably erroneous.  

1. The ECG is VERY specific for OMI. 

2.  The old EKG did not show anything similar 

3.  There was definite evolution of the ECG.  It was not "Stable"

4. The initial troponin was NOT negative -- it just was not (yet) above the URL.  

5. Pericarditis would be even more unlikely in someone without chest pain.  

Why these comments from an excellent physician?  I suspect it is due to cognitive dissonance.  It is hard for many physicians to imagine that someone could have a complete coronary occlusion without any chest pain or SOB.  The history is so discordant with the objective data that the objective data does not register in the mind.  

But OMI does happen without specific symptoms!!

Fortunately for this patient, the artery spontaneously opened and the damage was limited.

Main Learning Point:  Use pre- and post- test probability.

Some ECGs are so specific for OMI that it is OMI regardless of the clinical context. Some ECGs are sufficiently ambiguous that the clinical context is crucial.  This is true for all tests for all pathologies: the pretest probability is crucial for interpreting the test.  But a test with 99% specificity is positive until proven otherwise, regardless of the pretest probability.   

1.  If the ECG is very specific, the symptoms need not be.

2.  If the ECG is NOT very specific, then there should be chest discomfort.

Later note:

"He notes that over the past 3-4 months he has a history of dyspnea with exertion and chest pain with exertion. He walks a few blocks to the store and these symptoms will become worse. Chest pain is squeezing or tight in nature. It lasts from 10-15 mins in duration. It does not radiate. It is relieved with rest."  



MY Comment, by KEN GRAUER, MD (11/1/2022):


Like Dr. Smith — I interpreted the initial ECG in today’s case without the benefit of any history. My impression was similar to his. Dr. Smith reviewed sequential changes over the course of the 7 tracings in today’s case. Instead — I decided to focus a bit more on KEY findings in the initial tracing = ECG #1). For clarity in Figure-1 — I've labeled this initial tracing, which I compare with the last tracing shown above = ECG #7).
  • The rhythm in ECG #1 — is sinus at ~65/minute. Intervals (PR, QRS, QTc) and the axis (about +75 degrees) are normal. Of note — the QRS “looks” wide in a few leads (especially in lead V5) — but it does not measure more than 0.10 second (which is the upper limit of normal for QRS width).
  • Voltage criteria for LVH are satisfied (ie, deepest S in V1 or V2 + tallest R in V5,V6 ≥35 mm).

Regarding Q-R-S-T Changes in ECG #1:
  • Q Waves — Small and narrow Q waves are seen in the inferior leads — and in the lateral chest leads ( = V5,V6). These most probably are normal septal q waves. Of note — normal septal q waves can be seen in the inferior leads with a relatively vertical frontal plane axis, as is seen here.
  • R Wave Progression — is normal, with Transition (where the R wave becomes taller than the S wave is deep) occurring normally (here, between V3-to-V4).

Regarding ST-T Wave Changes:
  • As per Dr. Smith — there is non-diagnostic ST elevation in leads V2 and V3. The shape of the elevated ST-T waves in anterior leads V2,V3 is the mirror-image opposite picture of what LV “strain” looks like in left-sided leads (I discuss and illustrate this concept in detail in My Comment — at the bottom of the page in the June 20, 2020 post of Dr. Smith's ECG Blog).

  • As per Dr. Smith — the KEY lead is lead V4. When I first saw ECG #1 — I thought the prominent notching in this lead (RED arrow in lead V4) might represent an ischemic-induced J-wave. Against this, however — is the absence of similar notching in other leads. It turns out that rather than a “J-point” — the RED-arrow notch that we see in lead V4 of ECG #1 is contained within the QRS complex in this lead. By means of the vertical dotted-RED line — I've identified the end of the QRS complex (which is clearly seen in leads V5 and V6). Therefore — the PURPLE arrow in lead V4 points to the S wave, which is clearly elevated above the baseline! 
  • KEY Point: The elevated S wave above the baseline qualifies as T-QRS-D (Terminal-QRS-Distortion). While clearly abnormal when T-QRS-D occurs in lead V2 or V3 — it is not always abnormal when seen in lead V4. That said, in the context of other abnormal findings on this tracing (especially the coved and markedly elevated ST segment in lead V4) — the finding of T-QRS-D in lead V4 strongly suggests LAD OMI(For more on T-QRS-D — Please see My Comment at the bottom of the page in the November 14, 2019 post in Dr. Smith's ECG Blog).

  • In support of our suspicion of acute LAD OMI in ECG #1 — is the presence of abnormal ST-T wave changes in a number of other leads. These include: i) ST segment coving (albeit without ST elevation) in neighboring lead V5ii) Nonspecific ST-T wave flattening in leads III, aVL and aVF — and especially the sagging ST depression in leads I and IIandiii) The suggestion of "Precordial Swirl" by the ST elevation in lead V1 — and the shelf-like ST depression in lead V6.

Precordial Swirl in ECG #1:
As discussed in the October 15, 2022 post in Dr. Smith's ECG Blog — Drs. Meyers and Smith coined the new term known as, "Precordial Swirl" — in which acute LAD occlusion proximal to the 1st septal perforator produces a unique form of ST elevation in lead V1 (and also in lead aVR) — with reciprocal ST depression in lateral lead V6 (and often also in lead V5)
  • The pattern of Precordial Swirl is easy to mistake for LVH (and vice versa) — because both of these entities may show anterior lead ST elevation with lateral chest lead ST depression.

As I suggest in My Comment at the bottom of the page in the October 15 post — I find the shape of the ST elevation in lead V1 — and the shape of the ST depression in lead V6 to be distinctive in most cases.
  • As shown in Figure-1 — the picture within the dotted-RED rectangle in ECG #1  — is unusual, not only because of the amount of ST elevation in lead V1 (which is 2 mm) — but because of the flattened shape of the elevated ST segment in this lead. The elevated ST segment of LV "strain" in lead V1 typically shows upward slanting (as is seen in leads V2 and V3) — and should not be expected to show a greater amount of J-point ST elevation in lead V1 than in leads V2 and V3 (especially when the S waves in leads V2,V3 are deeper than the S wave in lead V1).
  • Compare the appearance of the ST-T wave in lead V1 of ECG #1 — with the ST-T wave appearance in lead V1 of ECG #7, which was obtained 2 days later (after acute ST-T wave changes had almost completely normalized). Note in lead V1 of ECG #7 — that the ST segment is now upsloping, and that the J-point ST elevation is no longer present.

  • In lead V6 of ECG #1 — it once again is the shape of the ST depression that is atypical for LV "strain". The ST-T wave picture within the dotted-PURPLE rectangle in ECG #1 is essentially the mirror-image of the ST-T wave in lead V1 = 2.5 mm of J-point ST depression, with a flat instead of gradually downsloping depressed ST segment).
  • In comparison — the ST-T wave in lead V6 of ECG #7 looks much more like LV "strain", in that there is minimal J-point depression with now gradual downsloping of the ST segment.

  • BOTTOM Line: The ST-T wave appearance in leads V1 and V6 of ECG #7 looks exactly as expected for a patient with LVH. In contrast — the ST-T wave appearance in leads V1 and V6 of ECG #1 is distinctly atypical for LV "strain" — and, in the context of the marked ST elevation with T-QRS-D in lead V4 — strongly suggests a Precordial Swirl pattern of acute LAD OMI.

Figure-1: I’ve labeled the initial ECG in today’s case — and the last ECG (done 2 days later).

WHY is the QRS in Lead V4 so Notched?
Having established that the RED-arrow notch in lead V4 of ECG #1 is not a J-wave — but rather a part of the QRS complex — the question arises as to WHY we see this QRS notching only in lead V4 (and not in any of the other 11 leads)?
  • I believe the answer is that lead V4 marks the abrupt transition between the almost-all-negative QRS in lead V3 — and the almost-all-positive QRS in lead V5This is relevant to today's case — because knowing that the PURPLE arrow marks the S wave in lead V4 establishes the presence of T-QRS-D.

SUGGESTION: Take a moment to review the appearance of the QRS complex in lead V4 for each of the tracings shown above in today’s case. Note that the QRS in each of today's 7 tracings is notched in lead V4 (but in no other leads). Note that the S wave in each of today's 7 tracings tells the tale as to what is going on in the LAD. 
  • The baseline ECG from 5 years earlier ( = the 2nd tracing shown in Dr. Smith's above discussion) — shows a deep and completely normal S wave — which makes sense since there was no LAD occlusion at that time.
  • In contrast — the S wave is elevated above the baseline (ie, = T-QRS-D) in the 1st3rd4th and 5th tracings in today's case — during which time the LAD was occluded.
  • The 6th tracing (recorded at 120 minutes) — shows that the S wave in lead V4 has been reconstituted. This occurs simultaneous with normalizing ST segment and T wave morphology in other leads ( = ST-T wave changes of reperfusion!).
  • 2 days later ( = ECG #7 in Figure-1) — virtually all acute ST-T wave changes have resolved! As a result — a fragmented QRS complex with normal S wave is seen in lead V4.

  • BOTTOM Line: Even without a history of new chest pain — numerous clues were present on the initial ECG to at least raise strong suspicion of acute LAD OMI until proven otherwise.

P.S.: Did you notice that the P wave in ECG #7 is no longer upright? This is a change from the prior 6 tracings in today's case — and simply reflects that instead of sinus rhythm, there is now a low atrial rhythm. Of note — a low atrial rhythm does not change any clinical implications in this case.

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