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):
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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!



2 comments:

  1. Steve...

    Excellent case and great comments from Ken.

    My take on this is that this is likely a proximal occlusion of a non-dominant LCx. The ST depressions in V1 - V3 are indicative of what we NOW know to be an infarction of the lateral wall of the LV. The obtuse marginals serve the lateral wall and the apicolateral region (V5 and V6). But there is no inferior involvement, so the RCA is dominant.

    This is an important piece of information because the apicolateral (lower lateral) wall of the LV is just about the BEST perfused area of the heart under normal circumstances. It is served by the LAD, the LCx, the RCA (when dominant) and the ramus intermedius (when present). When we see ischemia in this area due to a single occluded artery, you must surmise that the other arteries serving that area are also impaired (or else simply not present).

    Occlusions of either the LCx or a dominant RCA can cause STE in V5 and V6. It's actually more common with the LCx but not so much more that the information is useful diagnostically. STE in V5 and V6 should always make you suspicious of the integrity of the other coronary vessels.

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    1. Thanks, Jerry. Sorry for the delay. Was on vacation and then buried!

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