A 50-something male had onset of chest pain 1 hour prior to ED arrival. It is constant, 9/10, left-sided CP that radiates into left arm and jaw. Endorses some associated SOB, but denies back pain, fever, cough, chills, leg swelling, or other new symptoms. Has never had this before. Takes metoprolol for HTN.
Here is the triage ECG:
This was not identified as OMI by either the conventional algorithm nor the triage faculty physician.
Smith: I think leads V3 and V4 are highly concerning, and all but diagnostic, for acute LAD occlusion. I would activate the cath lab, or at least look for an old one and/or obtain serial ECGs.
I would use the Queen of Hearts (which and the LAD vs. Early Repol formula.
You can see many examples of use of the Queen of Hearts AI Bot from PMCardio HERE; you can sign up to get it HERE.
Case Continued
There was an old ECG available from 1.5 years prior, but I do not know if the triage physician (who is VERY busy) looked for it. Here it is:
Let's look at them side by side:
Old ECG On presentation, with chest pain
Now you can easily see that the T-waves in V2-V5 are all much larger, both taller and "bulkier"
If you used the Queen of Hearts AI app, it would have been a false negative.
Case continued
The ECG was completed at 0952, ECG was not recognized by triage MD as being due to LAD OMI. The patient was put in triage waiting room, then roomed at 1028.
The patient and ECG were seen by a very good Physician Assistant and she was worried, so she sought out another staff MD who is very good at ECGs, and he agreed that this is anterior OMI. The patient was moved to the critical care area (stabilization room).
Cath lab was activated.
A 2nd ECG recorded 50 minutes after the first.
Significant change. Now more diagnostic of LAD OMI. Notice the diminution of the S-wave in V3, and increase in STE with more bulk to the T-wave also in V3. This is one of the features of LAD occlusion: loss of S-wave depth until there is full blown terminal QRS distortion (TQRSD). TQRSD is not present here (not yet anyway) and it is not always present in LAD OMI, but TQRSD is never present in normal ST Elevation)
I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:
While waiting for cath team to be ready, another was recorded 20 minutes after the 2nd
The first hs troponin I retuned much later at 125 ng/L.
Angiogram
Culprit Lesion (s):
ST elevation myocardial infarction due to 99% stenosis of the distal LAD
Formal echo:
Normal estimated left ventricular ejection fraction, 63%.
Regional wall motion abnormalities: mid-apical anteroseptum and apical inferior wall hypokinesis with apical dyskinesis.
Peak troponin not measured.
Post PCI ECG
Next day ECG:
Learning Points
1. Hyperacture T-waves can be very subtle
2. It is easy to miss acute LAD Occlusion
3. The Queen of Hearts (first version) is incredible, but not perfect.
4. We will make subsequent versions much better -- it can continuously learn and continuously be taught
5. Always compare with an old ECG if available (we will teach the Queen to do this in the future)
6. Always get serial ECGs in a patient with acute chest pain.
MY Comment, by KEN GRAUER, MD (9/1/2023):
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- For clarity and ease of comparison — I've put the first 2 tracings shown in today's case together in Figure-1.
-USE.png) |
| Figure-1: Comparison of the first 2 ECGs in today's case. |
- The single lead that immediately alerted me to the likelihood of an acute event — was lead V1. Normally — the ST segment in lead V1 is flat, often with slight T wave inversion. On occasion there may be slight ST segment coving, and even some ST elevation in V1 — but in my experience, there should virtually never be as much J-point ST elevation in lead V1 in a narrow-QRS, non-LVH tracing as we see in ECG #1 (RED arrow in lead V1 of Figure-1). The combination of this much J-point ST elevation and ST segment coving of the shape that we see in ECG #1 (ie, that does not look like LV "strain") — in a patient with new, worrisome CP made me immediately look closer at the remaining 11 leads.
- The 2nd-most worrisome lead to me in ECG #1 — was lead V3. Although the "shape" of the ST-T wave in lead V3 manifested gentle upsloping of the ST segment that is often seen as a normal finding — the amount of J-point ST elevation in this lead is clearly excessive (ie, at least 3 mm, as per the RED arrow in this lead). In that context — despite normal R wave progression and a QTc that is not prolonged — I thought the base of the ST-T wave in lead V3 looked wider-than-expected — and despite the deep S wave = 16 mm in V3, the 12+ mm tall T wave in this lead is disproportionately larger-than-expected.
- Surprisingly — the ST-T wave in neighboring lead V2 looked normal ...
- That said — In the context of a patient with new, worrisome CP — the clear ST-T wave abnormalities in leads V1 and V3 told me that the relative size of the T wave in the other neighboring lead V4 was clearly disproportionately enlarged (ie, hyperacute) with respect to R wave amplitude in that lead.
- To Emphasize: Looking at ECG #1 as a single, isolated tracing — there clearly are no acute ST-T wave changes in the limb leads of this tracing. That said — the ST-T waves in leads III, aVL and aVF of this initial tracing are not completely "normal". As per the BLUE lines that I drew in ECG #1 — these limb leads manifest nonspecific ST segment and T wave flattening. Given how hyperacute I thought the ST-T waves in leads V1, V3, V4 were — I wondered IF the reason for not seeing acute limb lead changes in ECG #1 might be: i) That the patient's baseline ECG might not be completely normal; and/or, ii) That this middle-aged man might have multi-vessel disease.
- The above said — Regardless of whether or not the limb leads in ECG #1 showed anything acute — prompt cath for presumed acute LAD OMI was already indicated on the basis of the history and the above-noted hyperacute ST-T waves changes in leads V1, V3, V4.
- NOTE: Reciprocal ST-T wave changes are more likely with proximal LAD occlusion — but not all LAD OMIs manifest reciprocal limb lead changes.
- The BLUE arrow in lead V1 of ECG #2 shows — that although ST segment coving in this lead V1 was present in the prior tracing — the excessive J-point ST elevation that I pointed out with my RED arrow in ECG #1 was not previously there.
- There also are limb lead changes in ECG #1 that were not present in the prior tracing. Despite very similar QRS morphology in the limb leads (ie, The frontal plane axis is not appreciably changed — so lead-to-lead comparison of ST-T wave changes will be valid!) — the T wave in lead III was previously inverted, whereas it now is slightly positive in lead III of ECG #1.
- The T wave in lead aVF is now also positive in ECG #1.
- The slight ST elevation that was present in the high-lateral leads (I, aVL) of the prior tracing — is no longer present in ECG #1.
- To Emphasize: None of these changes that I point out above in the limb leads between these first 2 ECGs in today's case alter management (ie, This patient clearly needed prompt cath with PCI based on history and hyperacute chest lead findings alone). But I always find it insightful (and for me, instructive) — to correlate as much as possible serial ECG findings with the clinical history. Not only did acute cath reveal 99% stenosis of the distal LAD ( = the "culprit" lesion) — but it also revealed disease in the LCx system — which to me explains the subtle limb lead abnormalities in the prior tracing — and which to me confirms that there were some subtle, acute limb lead changes in today's initial ECG.
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