Saturday, November 23, 2024

Chest (or abdominal?) pain and ECG artifact.

An elderly woman presented with one day of chest and right arm pain, and also abdominal pain.  There was associated tingling and numbness in the right hand and generalized weakness, worse on the right side.

A triage ECG was recorded:










Smith: there is widespread artifact, except in lead III.  Since lead III is not artifactual, one can deduce that the artifact is caused by movement of the right arm electrode, so that electrode should be moved and the ECG re-recorded.  This makes it difficult to assess. 

But one can see that there is some ST depression in lead III, which should always make you think that it is reciprocal to some, often minimal, STE in aVL (of high lateral OMI).  Thus, aVL, I, and V2 must be scrutinized, but they are distorted by artifact.  

This is extremely easy to overlook, unless there is a high suspicion of OMI.

Single limb lead electrode artifact is explained here, in a case of Arterial Pulse Tapping Artifact (APTA): Bizarre (Hyperacute??) T-waves


Clinical course: The provider recognized artifact, but did not see anything worrisome and regrets not ordering another.

Labs, including troponins, were ordered and the patient needed be placed in the waiting room pending a bed.

When the provider next looked up lab results, it was noticed that the first troponin was 45,000 ng/L.  This is then a large MI, but it is subacute.

There was a previous ECG available for review:
This shows baseline STE in inferior leads, including lead III.
At the time is was recorded, there was no a myocardial infarction; this was baseline STE (normal variant)
This previous ECG confirms that the STD in lead III is very abnormal


Due to the very high troponin, the patient was brought to the critical care area and another ECG was recorded:
Sinus rhythm with PVCs
There is inferior STD with STE and a coved ST segment in aVL.  There is STE in V5-6.  There are new Q-waves in aVL, V5-6.  
It is diagnostic of OMI, but this is SUBACUTE OMI

I sent this ECG to my "EKG Nerdz" friends, without any clinical info at all and they answered "OMI"


The Queen said: "STEMI-Equivalent with High Confidence:"

Notice she sees findings in both normal beats and PVCs.


There was some question of whether the patient was having abdominal pathology, and she also had a history of aortic pathology, so a chest abd/pelvic with aorta angiogram was ordered.

If this were ACUTE (vs. SUBACUTE) OMI, that would result in an undesirable delay.

But this is clearly a subacute MI, with most of the damage done.  How do I know?

1) Very high initial troponin of 45,000 ng/L

2) A full day of chest pain

3) Q-waves on the ECG, with some T-wave inversion

Here is one frame of the CT scan which includes the heart:

Can you spot the infarct?



Here is an arrow pointing to it:


The Cath Lab was activated.

Angiogram:

100% occluded ramus intermedius.  The ramus is an occasional artery between the circumflex and the LAD, and often takes the place of a large first diagonal, and has the same distribution.

It was opened and stented.

Here are the troponins:



Echo:

Normal LV size and hyperdynamic systolic function with an estimated EF of 77%.

Regional wall motion abnormality--mid anterior akinesis.


Compared to TTE from 7/3/24:  the anterior regional wall motion abnormality is new and is consistent with ischemia/infarction in the LAD territory





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MY Comment, by KEN GRAUER, MD (11/23/2024):

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There are several insightful aspects of today's case.
  • Marked artifact in the initial ECG (TOP tracing in Figure-1) — makes assessment of the limb leads difficult — since lead III (within the BLUE rectangleis the only undistorted lead. But in a patient with CP (Chest Pain) — the T wave in this single undistorted limb lead clearly looks to be hyperacute (disproportionately "bulky" considering modest size of the QRS in this lead)
  • I next looked at leads V2,V3,V4 for sign of posterior OMI — since CP + hyperacute T wave in lead III + suggestion of posterior OMI would be enough to greatly enhance my confidence of acute OMI in this initial tracing. Unfortunately — artifact distortion of the the ST segments in these 3 chest leads prevents drawing any conclusions. But, in this patient with CP — ECG #1 needs to be immediately repeated!
  • As per Dr. Smith — the fact that artifact in ECG #1 is maximal in leads I and II (with lead III undistorted) — points to the RA extremity as the "culprit" (See My Comment in the December 5, 2022 post of Dr. Smith's ECG Blog for review on how to determine the "culprit" extremity within seconds).

Figure-1: Comparison between the initial ECG and the repeat ECG in today's case.

The 2nd ECG:
Assessment of the next ECG in today's case (BOTTOM tracing in Figure-1) — provides its own set of insightful observations:
  • Overall — the artifact is decidedly less in ECG #2. That said — Note how the "culprit" extremity has changed! Here limb lead artifact is maximal in leads IIII and aVL — with lead II no more than minimally affectedNote also that instead of the artifact distorting the entire recording of 5/6 limb leads (as it did in ECG #1) — the artifact distortion in ECG #2 is primarily of the baseline! This localizes the source of artifact to the LA electrode (rather than pointing to a tremulous RA extremity — as was the case in ECG #1, in which large amplitude artifactual deflections were seen throughout in the affected limb lead recordings).

Although the artifact in ECG #2 should also prompt repeating the ECG — we nevertheless can draw important conclusions from this 2nd tracing.
  • The rhythm is ventricular bigeminy (each of the even-numbered beats in ECG #2 is a PVC).
  • That every-other-beat in ECG #2 is a PVC (and not a PAC conducted with RBBB aberration) — can be established by the fact that underlying sinus P waves continue throughout the tracing (YELLOW arrows in the long lead II rhythm strip showing on-time sinus P waves producing subtle distortion of the beginning of the ST segment of each PVC). In addition, the direction of the initial deflection in 4 of the chest leads is different for sinus beats and the PVCs (whereas sinus beats #9,11,13 in leads V1-thru-V4 all manifest an initial R wave — beas #8,10,12 all manifest an initial negative deflection).

PEARL:
 As we have occasionally seen in other cases in Dr. Smith's ECG Blog — it is the PVCs (and not the sinus-conducted beats) that provide more incriminating evidence of an ongoing acute event.
  • Consider lead aVL (within the PURPLE rectangle) — in which the most markedly abnormal ST elevation is seen in beats #4 and #6 (with the tricky aspect of beat #4 being the lead change marker that hides the QRS of beat #4).
  • Lead I appears to show abnormal ST elevation in both sinus beats and the PVC in this lead — although artifact make assessment difficult in this lead.
  • But BLUE arrows in lateral chest leads V5 and V6 show what appears to be disproportionately elevated J-point ST elevation in the PVC ( = beat #12).

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Links to Examples of ARTIFACT:
Artifact is a reality of clinical practice — so comfort in assessing tracings with artifact is essential. What follows below is my expanding list of technical "misadventures" — most from Dr. Smith's ECG Blog — some from other sources (NOTE: As I did not previously keep track of these — there are additional examples of artifact sprinkled through Dr. Smith's ECG Blog that I have not yet included here ... ).











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